Renal Physio

Item: 1 of 27 ~ 1 • M k -<:J 1>- Jil ~· !
:';-~
QIO: 2330 ..L ar Pre v ious Next Lab fli!ltues Not es Calcula t o r
•1 & &
A 56- year -old male, recently diagnosed with nephrolithiasis, presents for recent fatigue and "slowed thought processes." On further
•2 questioning, the patient states he has had constipation, intermittent abdominal pain, and weakness for 1 month . He denies any history of
•3 endocrine disorders in the family . On physical examination, there is no neck swelling, and the abdomen is soft and nontender. There is no
focal neurologic deficit. Blood tests reveal an elevated calcium and parathyroid hormone (PTH) level. Renal function tests are unremarkable.
·4
•5
Which of the following is an effect of this hormone on the kidney?
•6
:
•7 A. Activation of adenylate cyclase v ia nuclear transcription activation
·8
B. Conversion of 1,25-0H vitamin D to 25 -0H vitamin D
.9
• 10 C. Decreased phosphate reabsorption by the kidney
• 11 0. Inactivation of !a-hydroxylase
• 12
E. Increased calcium excretion by the kidney
• 13
• 14
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• 16
• 17
• 18
• 19
• 20
• 21
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Item: 1 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2330 ..L ar Prev ious Next Lab fli!ltues Not es Calculat o r
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1
Th e co rrect an sw er i s C. 730/o ch ose this .
•2
PTH acts to protect the serum ionized calcium concentration by increasing calcium levels and decreasing phosphate levels in the extracellular Ruid
•3 (ECF) . PTH stimulates bone resorption, releasing calcium and phosphate to the ECF. However, this effect alone would not increase free calcium
·4 levels as phosphate complexes with calcium . Hence, PTH also acts to decrease phosphate reabsorption by the kidney, producing a net effect of
calcium release from bone. PTH also indirectly stimulates calcium absorption by the intestine by stimulating !a-hydroxylase to produce 1,25- 0H
•5 vitamin 0 {the active form of vitamin D) .
•6 V'tamon D calcium E trace lular fluid Kidney Phosphate Bone resorption Extracel ular Gastroontestinal tract Vitamin Reabsorption Bone Blood plasma
•7 A is not correct. 70fo ch ose th is.
·8 PTH produces its actions on the kidney by binding to a basolateral hormone r eceptor in proximal tubu le cells that is coup led to adenylate cyclase
v ia a G5 protein. Increased renal ca lcium reabsorption, increased urinary cAMP, and phosphaturia result.
.9 Pro imal convoluted tubule Adenylyl cyclase Cyclic adenosine monophosphate Protein Kidney Hormone Calcium Receptor (biochemistry) Nephron
• 10 Anatomical terms of location
• 11 B is not co r rect. 120/o c hose t his .

• 12 PTH stimulates !a-hydroxylase in the kidney to produce the active form of vitamin D (1,25-0H vitamin D) from 25-0H vitamin D. !a-Hydroxylase
activity is also stimulated by low serum calcium and low serum phosphate levels. 1,25-0H vitamin D acts to increase both serum calcium and
• 13
phosphate levels primarily by increasing intestinal absorption of both phosphate and calcium and stimulating bone resorption.
• 14 Vitamin 0 Bone resorption Kidney Calcium Phosphate Blood plasma Vitamin Bone Serum calcium Serum (blood)
• 15 D is not co rrect. 30/o c hose this .

• 16 !a - Hydroxylase located in the kidney is d irectly responsible for conversion of 25-0H vitamin D to its active form 1,25-0H vitamin D. Activation of
this enzyme is mediated by PTH .
• 17 Vitamin 0 Enzyme Kidney Vitamin
• 18
E i s n ot correct. solo ch ose t his •
• 19
PTH increases calcium reabsorption in the kidney via a basolateral receptor that is coupled to adenylate cyclase. Th is hypocalciuric action is
• 20 distinct from the phosphaturic action, which is also mediated by adenylate cyclase .
Adenyly cyclase Kidney calcium Receptor (biochemistry)
• 21
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Item: lof27 ~. , . M k <:] t> al ~· ~
QIO: 2330 .l. ar Previous Next lab 'lifllues Notes Calculator
1 via a Gs protein . I ncreased renal calcium reabsorption, increased urinary cA MP, and ph osphaturia resu lt.
Proximal convoluted tubule Adenylyl cyclase Cyclic adenosine monophosphate Protein Kidney Hormone Calcium Receptor (biochemistry) Nephron
. 2
Anatomical terms of location
•3
B is n o t co rrect . 1 20/o c h ose t his.
.4
PTH stimulates 1a-hyd roxy lase in the kidney to produce the active form of vitamin D (1,25-0H vitamin D) from 25-0H vitamin D. 1a-Hyd roxy lase
•5 activity is also stimulated by low serum calcium and low serum ph osphate levels. 1,25-0H vitamin D acts to increase both serum calcium and
•6 ph osphate levels primarily by increasin g intestinal absorption of both ph osphate and calcium and stimulating bone resorption .
Vitamin D Bone resorption Kidney Calcium Phosphate Blood plasma Vitamin Bone Serum calcium Serum (blood)
.7
0 is n o t co rrect . 30/o c h ose t his •
•8
1a-Hyd roxy lase located in the kidney is d irectly respons ible for conversion of 25-0H vitamin D to its active form 1, 25-0H vitamin D. Activation of
•9 this enzyme is mediated by PTH.
Vitamin D Enzyme Kidney Vitamin
• 10
· 11 E is n o t co rrect . 50/o c h ose t his.

PTH increases calcium reabsorption in the kidney via a basolateral receptor that is coupled to adenylate cyclase . This hypocalciuric action is
• 12
d istinct from the ph osphaturic action, which is also mediated by adenylate cyclase .
• 13 Adenylyl cyclase Kidney Calcium Receptor (biochemistry)
• 14
• 15
Bo tto m Lin e :
• 16
PTH acts on the kidney to maintain calcium homeostasis by decreasin g ph osphate reabsorption in the proximal convoluted tubule, increasin g
• 17 calcium reabsorption in the d istal convoluted tubule, and promotin g conversion of 25-hyd roxycholecalciferol to 1, 25-0H vitamin D (the
biolog ically active form of vitamin D) .
• 18
Distal convoluted tubule Proximal convoluted tubule Vitamin D Homeostasis Calcium Calcium metabolism Kidney Calcifediol Phosphate Reabsorption Nephron
• 19 Vitamin Anatomical terms of location
• 20
• 21
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Item: lof27 ~. , . M k <:] t> al ~· ~
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Bo tto m Line :
. 2
PTH acts on the kidney to maintain calcium homeostasis by decreasin g ph osphate reabsorption in the proximal convoluted tubule, increasin g
•3 calcium reabsorption in the d istal convoluted tubule, and promotin g conversion of 25-hyd roxycho lecalciferol to 1, 25-0H vitamin D {the
.4 biolog ically active form of vitamin D).
Distal convoluted tubule Proximal convoluted tubule Vitamin D Homeostasis Calcium Calcium metabolism Kidney Calcifediol Phosphate Reabsorption Nephron
•5 Vitamin Anatomical terms of location
•6
.7
•8 lijl;fiiJI•J fo r ye ar:l 20 17 ..
FI RST AID FAC T S
•9
• 10 FA17 p 559.2
· 11 Hormones acting on kidney
• 12
Atria natriuretic peptide
• 13 Secreted in response toi atrial pressure. Causes i GFR
and i Na• filtration with no compensatory Na· reabsorption
• 14 in distal nephron. Net effect: Na· loss and volume loss. Distal
• 15 Glomerulus convoluted
tubule C.' '
• 16 Afferent !
• 17
• 18
S"')3rs K·
• 19 Amino acids H'
N.J• Secreted in response to
• 20 Angiotensin II J. blood volume (via AT II) and
Synthesized in response to J. BP. Causes efferent arteriole i plasma (K'I: causes iNa·
• 21 constriction ~ i GFR and i FFbut with compensatory Na' reabsorption, i K• secretion•
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Item: 1 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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•2
FA17p320.1
•3
Parathyroid hormone
·4
SOURCE Chief cells of paralh) roid.
•5
FUNCTION t bone resorption of Ca 2.,. and P0 4~-. PTH t serum Ca 2-, ! serum (P04 3-), t urine
•6
t kidney reabsorption of Ca 2+ in distal (P0-1 3 ), t urinecAl\IP.
•7
com·oluted tubule. t RA K-L (receptor acti,·ator of NF-KB ligand)
·8 ! reabsorption of ro ..3- in pro'\imal convoluted secreted by osteoblasts and osteocytes. Binds
.9 tubule. lv NK (receptor) on osteoclasis and their
• 10 t 1.25-(0 H)z D 3 (calcitriol) production by precursors to stimulate osteoclasts and t Cah
stimulating kidney !a-hydroxylase in pro-.:imal ..... bone resorption. lntennittent PTl l release
• 11
com·oluted tubule. can also stimulate bone formation .
• 12
PTll = P hosphate-Trashing H ormone.
• 13 PTI-1-rclated peptide (PTHrP) funct ions
• 14 like PTII and is commonly increased in
• 15 malignancies (eg, squamous cell carcinoma of
the lung, renal cell carcinoma).
• 16
• 17 REGULATION l serum Ca 2+ ..... t PTJ-1 secretion.
t serum P0 43- .... t PTH secretion .
• 18
l serum Mg 2.. ..... t PTII secretion .
• 19
U serum J\ lg2+ ..... l PT H secretion.
• 20 Common causes of l lg2+ include diarrhea,
• 21 aminoglycosides, diuretics, alcohol abuse.
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Item: 2 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 380 3 ..L ar Pre v ious Next Lab fli!ltues Not es Calcula t o r
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1
A 23-year-old man is brought in to the emergency department with a gunshot wound to his right abdomen, which has been bleeding
•2 profusely for 20 minutes. There is no known comorbidity nor drug allergies. The patient is unconscious and has a pulse of 135/min and blood
•3 pressure of 85/60 mm Hg.
·4
If plasma renin were measured in this patient before resuscitation, it would likely be similar to that for a patient with which of the following enzyme
•5
deficiencies?
•6
: ~
•7 A. 11~-Hydroxylase
·8
B. 17o-Hydroxylase
.9
• 10 C. 21o-Hydroxylase
• 11 0. So-Reductase
• 12
E. Aromatase
• 13
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• 17
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Item: 2 of 27 ~. , . M k <:] t> al ~· ~
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2 The co rrect a nswe r is C. SOO/o c hose t his.

•3 The patient is sufferin g from hypovolem ic sh ock . He has suffered massive blood loss an d is tachycard ic an d hypot ensive. The renal response t o
hypovolem ia is t o increase plasma renin levels, which in turn both increases th e conversion of an g iot ensin I t o an g iot ensin II (in order t o
•4 vasoconstrict an d maintain blood pressure), an d stim ulates th e release of aldosterone, which increases th e rate of sod ium reabsorption from
.s nephrons. I n 2 1a-hyd roxylase deficiency, th e ability t o make min eralocorticoid horm ones (th e most important of which is aldosterone) is
decreased . Thus th e patient does not make adeq uate aldosterone, sod ium is not reabsorbed, an d intravascular volume is not properly
•6 maintain ed, so th ere is no feed back for renin levels t o decrease. Thus renin levels will consistently be elevated in th ese patients.
•7 Hypovolemia Aldosterone Renin Angiotensin Mineralocorticoid Angiotensin II Tachycardia Angiotensin I Hypotension Nephron Blood pressure Sodium
Blood plasma Bleeding Renal sodium reabsorption Hormone Kidney Blood vessel
•8
•9 A is not co rrect. 2 1 Ofo c hose t his .

I n 1113- hyd roxylase deficiency, th e ad renal g land s are unable t o make aldosterone or cortisoL How ever, th e precursor of aldosterone, 11 -
• 10
deoxycorticosterone, is still a pot ent min eralocorticoid, which lead s t o increased ret ention of sod ium an d thus hypertension. As a result, th e
· 11 plasma renin levels in th ese patients are actually low, despite th eir inability t o synth esize aldosterone.
Cortisol Aldosterone 11-Deoxycorticosterone Mineralocorticoid Renin Hypertension Sodium Blood plasma Adrenal gland
• 12
B is not co rrect. 200/o c hose t his .
• 13
I n 17a-hyd roxylase deficiency, th e ad renal g land s are unable t o synth esize g lucocorticoid s, such as cortisol, or sex horm ones. Rath er than
• 14
havin g decreased levels of min eralocorticoid s, th eir levels of aldosterone are actually increased d ue t o all precursors movin g down th e
• 1S min eralocorticoid pathway, an d th ese patients often present with hypertension, hypernatremia, an d hypokalemia. Due t o th e hig h aldosterone
levels, th ese patients will have low renin levels, in contrast t o th e elevated renin levels observed in hypovolemic sh ock .
• 16
Hypokalemia Hypovolemia Hypernatremia Cortisol Aldosterone Renin Mineralocorticoid Hypertension Glucocorticoid Adrenal gland Sex steroid Hormone
• 17
0 is not co rrect. 60/o c hose t his .
• 18 I n Sa-red uctase deficiency, th e ability t o convert t estosterone t o d ihyd rot estosterone is decreased . This results in child ren wh o are biolog ically
• 19 male bein g born with female ext ernal genitalia. At puberty, th e need for Sa-red uctase is overcome, an d th e in d ivid uals' t estes descend an d th ey
appear male. This enzym e deficiency has no effect on th e renin -an g iot ensin -aldosterone axis, an d thus plasma renin levels sh ould not be elevated
• 20
in th ese in d ivid uals.
• 21 Dihydrotestosterone Testosterone Enzyme Renin Testicle Puberty Sex organ Blood plasma
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Item: 2 of 27 ~. , . M k <:] t> al ~· ~
1 • deoxycorticosterone, is still a potent m in eralocorticoid, which leads to increased retention of sodium and thus hypertension . As a resu lt, the
plasma ren in levels in these patients are actually low, despite their inability to synthesize aldosterone.
2 Cortisol Aldosterone 11-Deoxycorticosterone Mineralocorticoid Renin Hypertension Sodium Blood plasma Adrenal gland
•3
B is no t co rrect. 2 0 0/o c hose this.
•4
I n 17a-hyd roxy lase deficiency, the adrenal g lands are unable to synthesize g lucocorticoids, such as cortisol, or sex hormones. Rathe r than
.s having decreased levels of mineralocorticoids, their levels of aldosterone are actually increased due to all precu rsors moving down the
mineralocorticoid pathway, and these patients often present with hypertension, hypernatremia, and hypokalemia. Due to the high aldosterone
•6
levels, these patients will have low ren in levels, in contrast to the elevated ren in levels observed in hypovolemic shock.
•7 Hypokalemia Hypovolemia Hypernatremia Cortisol Aldosterone Renin Mineralocorticoid Hypertension Glucocorticoid Adrenal gland Sex steroid Hormone
•8 0 is no t co rrect. 6 0/o c hose this.

•9 I n Sa-reductase deficiency, the ability to convert testosterone to d ihyd rotestosterone is decreased . This resu lts in children who are biolog ically
male bein g born with female external gen italia. At puberty, the need for Sa-reductase is overcome, and the in d ividuals' testes descend and they
• 10
appear male. This enzyme deficiency has no effect on the ren in -ang iotensin -a ldosterone axis, and thus plasma ren in levels should not be elevated
· 11 in these in d ividuals.
Dihydrotestosterone Testosterone Enzyme Renin Testicle Puberty Sex organ Blood plasma
• 12
E is no t co rrect. 30/o c hose this .
• 13
Aromatase is the enzyme that converts testosterone to estrad ioL It is present in adipose tissue, as well as developin g ova rian follicles . A
• 14
deficiency of this enzyme would not affect plasma ren in or aldosterone levels, which should be normal in these in d ividuals.
• 1S Aldosterone Estradiol Aromatase Testosterone Adipose tissue Renin Enzyme Ovarian follicle Blood plasma
• 16
• 17 Bo tto m Line :
• 18 I n hypovolemic shock, such as that seen with massive blood loss, plasma ren in and aldosterone levels are elevated in order to retain sodium
• 19 and thus intravascular volume . I n 21a-hydroxyalse deficiency, the ability to synthesize mineralocorticoids in the adrenal g lands is lost, resu lting
in chronically elevated ren in levels .
• 20 Hypovolemia Aldosterone Renin Mineralocorticoid Sodium Adrenal gland Blood plasma Bleeding
• 21
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Item: 2 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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2
Adre nal steroids and congenital adrenal hyperplasias
•3
Ketoconazole blocks several steps m steroidogPne<~s)
r ..,m~_
ACTH
·4
•5
•6
t± r ~l 1 Anastrozole. exemestane
.7
Pregnenolone
17a hydro ~"~ 17u hydroxylase
17-hydroxypregneoolone tl
I.Jehydroepandrosterone !DHEAJ
·8
.9
• 10
1
Progesterone
17a hydroxylase ! 17u
17-hydroxyprogesterone
hydrox~ Androstenedoone __::.:..:;::.:::::.::..++-+ Estrone
• 11
• 12
• 13
ll·deoxycortKosterone ll·dcoxycortosol
1Testosterone
Aromatase
!
Estr1diol
• 14
• 15
• 16
1
Corticosterone
!
Cortisol
S<~·reouctase
Dihydrotestosterone
• 17
. 18
11--0- Glycyrrhetonoc acod
IDHT)
• 19
• 20 Angiotensin II
Aldosterone Cortisone
II Fonasterode
• 21
•
ZONA GLOMERULOSA II ZONA FASCICULATA ZONA RETICULARIS
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f 11-deoxycorti- &
2 costerone
•3 (results in
f BP)
·4
aAII congenital adrenal enzyme deficiencies are characterized by an enlargement of both adrenal glands due to f ACT H
•5
stimulation (in response to l cortisol) and by skin hyperpigmentation .
•6
•7
FA17 p 299.1
·8
.9
Shock Inadequate organ perfusion and dcli, er) of nutrients necessary for normal tissue and cellular
function. Initially mar be re, ersible but life threatening if not treated promptly.
• 10
PCWP SVR
• 11
CAUSED BY SKIN (PRELOAD) co (AFTERLOAD) TREATMENT
• 12
Hypovolemic Hemorrhage, dehydration, Cold, ll l f lV Au ids
• 13 burns cl a mm y
• 14
Cardiogenic Acute Ml, HF, valvular lnotropes, diuresis
• 15 dysfunction, arrhythmia
Cold,
• 16 Obstructive Cardiac tamponade, f orl ll f Relieve obstmction
clammy
• 17 pulmonary embolism,
tension pneumothorax
• 18
Distributive Sepsis, anaphylaxis \Varm l f ll lV Au ids, pressors
• 19
C 'S injury Dry l l ll
• 20
• 21
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Item: 3 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 3799 ..L ar Pre v ious Next Labfli!llues Notes Calcula t o r
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1
A 57-year-old man with a 15-year history of type 2 diabetes mellitus and hypertension who is on insulin therapy presents with complaints of
2 fatigue and swollen feet. Physical examination reveals 3 + pitting edema bilaterally in both feet, and loss of pain and temperature sensation in
•3 all toes. Vital signs are normal except for a blood pressure of 150/95 mm Hg. Blood tests show an LDL level of 154 mg/dL, blood glucose
level of 213 mg/dl, and a hemoglobin Ate level of 9.2%. A basic metabolic panel shows a blood urea nitrogen level of 67 mg/dL and creatinine level
·4 of 2.6 mg/dl. Urinalysis shows 4+ protein with no casts.
•5
•6 Which of the following antihypertensive medications may have helped prevent this patient's current kidney disease?
•7 :
·8 A. A selective 13-blocker
.9 B. An antagonist of cardiac and vascular calcium channels

• 10
C. An inhibitor of a thick ascending limb t ransport protein
• 11
D. An inhibitor of the sodium-chloride symporter in the distal convoluted tubule
• 12
• 13 E. Angiotensin receptor blocker
• 14
• 15
• 16
• 17
• 18
• 19
• 20
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Item:3of27 ~. , . M k <:] t> al ~· ~
QIO: 3799 .l. ar Previous Next Lab 'lifllues Notes Calculator
2 The co rrect a nswe r is E. 720/o c hose t his .

3 This patient has nephropathy, as evidenced by the lowe r -extremity swelling (as a resu lt of hypoalbuminemia), hyperlipidemia, and proteinuria.
I n this case the most likely explanation is d iabetic nephropathy. Diabetic nephropathy leads to changes in the efferent arteriole of the g lome rulus .
.4
A variety of hormonal and nonen zymatic g lycosy lation factors come into play to cause an ove rall d ilation in the efferent arteriole. This increases
•5 the g lomerular filtration rate, which can initially help to preserve renal function, though ove r time the increase leads to intrag lomerular
hypertension and subsequent renal damage. One of the main therapies aimed at prevention of d iabetic nephropathy is the use of an angiotensin -
•6
converting enzyme {ACE} inhibitor or angiotensin receptor blocker (eg, losartan) . These act by d ilating the efferent arteriole, which can help to
.7 decrease this intrag lomerular pressu re to prevent hyperfiltration injury to nephrons.
Efferent arteriole Hypoalbuminemia Arteriole Glomerulus (kidney) Angiotensin II receptor antagonist Diabetic nephropathy Proteinuria Glomerulus Renal function
•8
Angiotensin-converting enzyme Hyperlipidemia Enzyme Hypertension Kidney disease Nephron Angiotensin Diabetes mellitus Glomerular hyperfiltration Hormone
•9
Angiotensin receptor Enzyme inhibitor
• 10
A is not co rrect. 50fo c hose t his .
· 11 Metoprolol is a specific 131- receptor - block in g agent used to treat hypertension and congestive heart failure . Blockade of 131- receptors leads to the
• 12 inhibition of sympathetic stimulation of heart rate, then to a slower heart rate and decreased cardiac muscle contractility. 13 1- receptor blockade
also lowe rs blood pressure by acting at the juxtaglomerular apparatus {JGA} in the kidney; 13 1- receptor stimulation of JGA cells promotes ren in
• 13
production, thus activating the ren in -angiotensin -aldosterone signaling (RAAS} cascade . However, metroprolol does not have any renal-
• 14 protective effects in d iabetes. I mportantly, 13- blockers must be used with caution in d iabetics because they can mask the effects of hypoglycemia .
Metoprolol Hypoglycemia Heart failure Congestive heart failure Cardiac muscle Renin Diabetes mellitus Hypertension Kidney Heart rate Blood pressure
• 15
Contractility Sympathetic nervous system Muscle
• 16
B is not co rrect. 4 0fo c hose t his .
• 17
Am lod ipin e is a calcium -channel blocker that is used often as first- line antihypertensive therapy . I nhibition of calcium channels leads to decreased
• 18 ability of vascular smooth muscle to contract, lead in g to less vasoconstriction and lowe r blood pressu re. However, it does not offer renal
• 19 protective effects in d iabetic patients .
Calcium channel blocker Amlodipine Antihypertensive drug Vasoconstriction Smooth muscle tissue Blood pressure Calcium channel Vascular smooth muscle
• 20
Voltage-dependent calcium channel Diabetes mellitus Calcium Kidney Blood vessel
• 21
C: ic; n nt rn rrPrt4 1 0 0/n r h nc:P t hic; 4
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• Metoprolol Hypoglycemia Heart failure Congestive heart failure Cardiac muscle Renin Diabetes mellitus Hypertension Kidney Heart rate Blood pressure
1
Contractility Sympathetic nervous system Muscle
2
B is not co rrect. 4 0fo c hose t his.
3
Am lod ipin e is a calcium -channel blocker that is used often as first- line antihypertensive therapy . I nhibition of calcium channels leads to decreased
•4 ability of vascular smooth muscle to contract, lead in g to less vasoconstriction and lowe r blood pressu re. However, it does not offer renal
•5 protective effects in d iabetic patients.
Calcium channel blocker Amlodipine Antihypertensive drug Vasoconstriction Smooth muscle tissue Blood pressure Calcium channel Vascular smooth muscle
•6
Voltage-dependent calcium channel Diabetes mellitus Calcium Kidney Blood vessel
•7
C is not co rrect. 100/o c hose t his .
•8
Furosemide is a loo p d iuretic that acts by inhibiting sodium reabsorption in the loo p of Hen le. It is used in the treatment of volume ove rload in
•9 patients with congestive heart failure as well as in d ru g-resistant hypertension . It does not offer d iabetics any renal protective effects.
loop diuretic Furosemide Diuretic Heart failure Congestive heart failure loop of Henle Hypertension Volume overload Sodium Renal sodium reabsorption
• 10
Diabetes mellitus Kidney
· 11
0 is not co rrect. 90fo c hose t his .
• 12
Hyd roch loroth iazide is a thiazide d iuretic that works by inhibiting sodium reabsorption in the d istal convoluted tubule . It is used often as first- line
• 13 treatment of hypertension . However, it offers no renal protective effects in d iabetic patients or others .
• 14 Distal convoluted tubule Hydrochlorothiazide Thiazide Diuretic Hypertension Sodium Diabetes mellitus Nephron Tubule Renal sodium reabsorption
• 15
• 16 Bottom Li ne :
• 17 Diabetics are at risk for d iabetic nephropathy because of hyperfiltration inj ury to the g lome rulus ove r time . For this reason the primary
treatment of hypertension in d iabetic patients is with angiotensin -converting enzyme {ACE} inhibitors {drugs end in g in - pril, such as captopril}
• 18
or angiotensin receptor blockers {drugs end in g in -sartan, such as losartan) .
• 19 Captopril losartan Diabetic nephropathy Glomerulus (kidney) Angiotensin-converting enzyme Glomerulus Enzyme Angiotensin II receptor antagonist Hypertension
Kidney disease Angiotensin Diabetes mellitus Angiotensin receptor Glomerular hyperfiltration
• 20
• 21
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FA17p577.1
2
Angiotensin- Captopril, enalapril, lisinopril, ramipri l.
3 converting enzyme
·4 inhibitors
•5 MECHANISM Inhibit ACE - l AT II - l C FR b) pre,cnting
•6 constriction of efferent arterioles. f renin due
.7 to loss of negati,·e feedback. Inhibition of CE
also prevents inacti\'ation of brad) kinin, a
·8
potent vasodilator.
.9
CliNICAL USE Hypertension, HF (l mortality), proteinuria, In chronic kidney disease (eg, diabetic
• 10
diabetic nephropathy. Pre, entunfmorable nephropathy), l intraglomerular pressure,
• 11
heart remodeling as a result of chronic slowing CBYl thickening.
• 12 hypertension .
• 13 ADVERSE EFFECTS Cough, Angioedema (due to f bradykinin; Captopril's CATCllll.
• 14 contraindicated in Cl esterase inhibitor
• 15 defi ciency), Teratogen (fetal renal
• 16
ma lfo rmations), f C reatinine (l CFR),
llyperkalemia, and llypotension. Used with
• 17
caution in bilateral renal artery stenosis
. 18 because ACE inhibitors will furt her l C FR
• 19 - renal fa ilure .
• 20
• 21 FA17p304.1
•
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Item: 3 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1 FA17 p 304.1
2 Hypertension treatment
3 Primary (essential) Thiazide diuretics, ACE inhibitors, angio tensin
·4 hypertension l1 receptor blockers (ARBs), dihydropyridine
•5 Ca2+ channel blockers.
•6 Hypertension with Diuretics, ACE inhibitors/ARBs, ~-blockers ~-blockers must be used cautiously in
.7 heart failure (compensated HF), aldosterone antagonists. decompensated HF and are contraindicated in
cardiogenic shock.
·8
Hypertension with ACE inhibitors/. RBs, Ca 2+ channel blockers, ACE inhibitors/ARBs are protective againsl
.9
diabetes mellitus thiazide diuretics, ~-blockers. diabetic nephropathy.
• 10
Hypertension in Hydralazine, labetalol, methyldopa, nifedipine.
• 11
pregnancy
• 12
• 13
FA17 p 558.1
• 14
Renin-angiotensin-aldosterone system
• 15
• 16 I BP (JG cells)
• 17 I Na' delivery Acts at angiotensin II
{macula densa cells) - -+ Vasoconstriction I BP
receptor. type 1 {AT1) on
. 18
I sympathetic tone vascular smooth muscle
• 19 {~1 -receptors)
• 20 Constricts efferent I FF to preserve renal function {GFR)

/ artenole of glomerulus in low-volume states {ie, when RBF ~ )
• 21
• !
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Item: 3 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1
FA17 p 558.1
2
3
·4 I BP (JG cells)
•5 I Na• delivery Acts at angiotensin II

(macula densa cells) - -+ Vasoconstriction I BP
receptor. type 1(AT1) on
•6 vascular smooth muscle
I sympathetiC tone
.7 -receptors)
Constricts efferent I FF to preserve renal functiOn (GFRl
·8
artenole of glomerulus 1n low-volume states (ie. when RBF ~ )
.9
~ B dyk' .
ACE ____.. ra 1111n Aldosterone
• 10 Renin I Na' channel insertion and - -+ Creates
--") breakdown (adrenal cortex) I activity of Na'/K' pump; favorable Na·
• 11 't
Angiotensinogen Angiotensin I - -+ enhances K' and H· gradient for
• 12 excretion by way of principal Na' and Hp
cell K' channels and reabsorption
• 13
ex-intercalated cell H' ATPases
• 14 ...-~ AOH
• 15 (posterior ------~ I aquaporin insertion in - --+ H20

pituitary) principal cells reabsorption
• 16
- --+ Na•. HC01·, and Hp reabsorption
• 17 1 PCT Na'/H ' activity (can permit contraction alkalosis)
. 18 Stimulates hypothalamus ----+ Thirst
• 19
• 20 Renin Secreted by JG cells in response to l renal arterial pressure, t renal S)111pathetic discharge (~ 1
• 21 effect), and l N<C delivery to macula densa cells.
•
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QIO: 3874 ..L ar Pre v ious Next Labfli!llues Not es Calcula t o r
1
A 56-years-old male was chopping wood outside when he accidentally chopped into his arm, causing it to bleed profusely. A friend drives him
2 to the hospital, 30 minutes away. Although pressure is applied to the wound, there is continued blood loss. Upon arrival to the emergency
department, he appears lethargic and pale.
3
.4
Total
•5 Heart peripheral
Choice Renin Vasopressin
rate resistance
•6
.7
·8
A ~ t t t
.9 8 t ~ t t
• 10 c t t ~ t
• 11
• 12
D t t t ~
• 13 E t t t t
• 14
• 15
Which of the following chan ges w ou ld most likely be seen in this patient as he is being transported t o t he hospit al?
• 16
:
• 17
A
. 18
B
• 19
• 20 c
• 21 D
•
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Item: 4 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 3874 ..L ar Pre v ious Next Labfli!ltues Not es Calcula t o r
& &
1
2 Total
Heart periphera l
Choice Renin Vasopressin
3 rate res istance
•4
•5 A ~ f f f
~
•6
•7
B f f f
·8
c f f ~ f
.9 0 f f f ~
• 10
• 11
E f f f f
• 12
• 13 Which of the following changes would most likely be seen in this patient as he is being transported to th e hospit al?
• 14 :
• 15 A
• 16 B
• 17
c
• 18
D
• 19
• 20 E
• 21
•
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QIO: 3874 ..L ar Prev ious Next Labfli!ll ues Not es Calculat o r
& &
1
2 Th e correct an swer is E. 680/o chose this.
3 The man is going into hypovolemic shock due to hemorrhage. The body's normal response to hypovolemia in the short term results from a
decreased blood volume that is sensed by baroreceptors, which leads to an increased sympathetic output. The response is an increased heart
4
rate and vasoconstriction to increase cardiac output so that the body can continue to perfuse vital organs. The kidney senses decreased volume
•5 and increases renin production, which will lead to increased angiotensin II and aldosterone levels. In addition, the body will increase levels of
•6 vasopressin, or ADH, which will conserve sodium and water by facilitating water reabsorption in the distal collecting duct .
Hypovolemoa Mldosterone Vasoconstriction Vasopressin Angiotensin II Cardiac o otpo Re Angiotenson Collecting duct system Bleeding Kidney Heart rate
•7
Blood vol orne Sodium Tachycardia Baroreceptor Anatomical terms of location Perfusion
·8
A i s not correct. 6 0/o chose this.
.9 Although it is correct that the total peripheral resistance, renin, and vasopressin should be increased, the heart rate is increased in hypovolemic
• 10 shock, not decreased. This occurs due to increased sympathetic stimulation .
Hypovolemia Vascular resistance Vasopressin Renin Heart rate Sympathetic nervous system
• 11
B is not correct. 170/o chose this .
• 12
Although it is correct that the heart rate, renin, and vasopressin should be increased, the total peripheral resistance is increased, rather than
• 13 decreased, in response to hypovolemia in order to increase effective cardiac output to the vital organs.
• 14 Hypovolemia Vascular resistance Vasopressin Renin Cardiac output Heart rate
• 15 C is not correct. JO/o c hose this •
• 16 Total peripheral resistance, heart rate, and vasopressin will be increased in hypovolemia. However, renin will be secreted by the kidney due to
decreased blood volume and increased sympathetic stimulation. Thus, renin levels will increase, not decrease .
• 17 Hypovolemia Vascular resistance Renin Vasopressin Kidney Heart rate Blood volume Sympathetic nervous system
• 18 D i s n ot correct. 60fo ch ose this •
• 19 Total peripheral resistance, heart rate, and renin levels will be increased in hypovolemia. However vasopressin levels will be increased, rather
• 20 than decreased, to increase water reabsorption in hypovolemia .
Hypovolemoa Vascular resistance Vasopressin Renin Heart rate
• 21
•
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Item:4of27 ~. , . M k <:] t> al ~· ~
1 • Hypovolemia Aldosterone Vasoconstriction Vasopressin Angiotensin II Cardiac output Renin Angiotensin Collecting duct system Bleeding Kidney Heart rate
Blood volume Sodium Tachycardia Baroreceptor Anatomical terms of location Perfusion

2
3 A is not co rrect. 60/o c hose t his.
A lthough it is correct that the total peripheral resistance, ren in, and vasopressin should be increased, the heart rate is increased in hypovolemic
4
shock, not decreased . This occu rs due to increased sympathetic stimulation .
•5 Hypovolemia Vascular resistance Vasopressin Renin Heart rate Sympathetic nervous system
•6 B is not co rrect. l JOfo c hose t his.

•7 A lthough it is correct that the heart rate, ren in, and vasopressin should be increased, the total peripheral resistance is increased, rath er than
decreased, in response to hypovolemia in order to increase effective cardiac output to the vital organs .
•8
Hypovolemia Vascular resistance Vasopressin Renin Cardiac output Heart rate
•9
C is not co rrect. 30fo c hose t his .
• 10 Tota l peripheral resistance, heart rate, and vasopressin will be increased in hypovolemia. However, ren in will be secreted by the kidney due to
· 11 decreased blood volume and increased sympathetic stimulation . Thus, ren in levels will increase, not decrease.
Hypovolemia Vascular resistance Renin Vasopressin Kidney Heart rate Blood volume Sympathetic nervous system
• 12
0 is not co rrect. 60/o c hose t his .
• 13
Tota l peripheral resistance, heart rate, and ren in levels will be increased in hypovolemia. However vasopressin levels will be increased, rath er
• 14 than decreased, to increase water reabsorption in hypovolemia.
• 15 Hypovolemia Vascular resistance Vasopressin Renin Heart rate
• 16
• 17 Bottom Line :
• 18 I n hypovolemic states, perfusion of vital organs is maintained through compensatory mechanisms; the heart rate is increased and the
• 19 vasculature vasoconstricts. Ren in and vasopressin secretion are increased, causing vasoconstriction and increased water reabsorption in the
kidneys .
• 20 Vasopressin Vasoconstriction Renin Heart rate Perfusion Kidney Circulatory system Reabsorption Hypovolemia
• 21
•
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Item: 4 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
& &
1 FA17 p 558.1
2
3
4 l BP (JG cells)
•5 l Na• delivery Acts at angiotensin II

- -+ Vasoconstriction
,
I BP
(macula densa cells) receptor. type 1(AT1) on
•6 vascular smooth muscle
I sympathetJc tone
.7 IP,-receptorsl
..----) Constricts efferent I FF to preserve renal functiOn (GFRl
·8 artenole of glomerulus 1n low-volume states (ie, when RBF ~ )
.9
~ B A-.!.' .
ACE ____.. ra...1 nlllln Aldosterone
• 10 Renin I Na' channel insertion and - -+ Creates
breakdown
~ (adrenal cortex) I activity of Na'/K' pump; favorable Na·
• 11 i'
Angiotensinogen Angiotensin I - -+ enhances K' and H- gradient for
• 12 excretion by way of principal Na' and Hp
• 13
ex-intercalated cell H' ATPases
• 14 ...-~ ADH
(posterior _ _ _ _ _ _,.. I aquaporin insertion in _ _,.... H p
• 15 pituitary) principal cells reabsorption
• 16
1 PCT Na'/H' activity
- --+ Na', HCQ~-· and Hp reabsorption
• 17 (can permit contraction alkalosis)
• 19
• 20 Renin Secreted by JG cells in response to 1 renal arterial pressure, t renal S)111pathetic discharge (~ 1
• 21 effect), and 1 N<C delivery to macula densa cells.
•
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1 l renin. Dilates afferent arteriole, constricts efferent arteriole, promotes natriuresis.
2 ADH Primarily regulates osmolarity; also responds to low blood ,-olume states.
3 Aldosterone Primarily regulates ECF volume and 1 a+ content ; responds to low blood ,·olume states. Responds to
4 hyperkalemia by t K+ excretion.
•5
•6 FA17 p 272.1
.7
Cardiac output CO= stroke volume (SV) x heart rate (IIR) During the early stages of exercise, CO is
·8
Fick principle: maintained by t HR and t SV. During the late
.9 stages of exercise, CO is maintained by t HR
CO = rate of 0 2 consumption
• 10 on ly (SV plateaus).
arterial 0 2 content- ,·enons 0 2 content
Diastole is preferentially shortened with t IIR;
• 11
\!lean arterial pressure (\1 P) =COx tota l less fil ling time - l CO (eg, ventricular
• 12
periphera I resista nee (TPR) tachycardia).
• 13
\1AP = 2;{ diastolic pressure+ Xsystolic pressme
• 14
• 15 Pulse pressure= systolic pressure - diastolic pressure t pulse pressure in hyperthyroidism, aortic
Pulse pressure is proportional to S , inversely regurgitation, aortic stiffening (isolated systolic
• 16
proportional to arterial compliance. hypertension in elderly), obstructive sleep
• 17
apnea (t sympathetic tone), exercise (transient).
S =end-diastolic '·olume (EDV) - end-systolic
. 18 l pulse pressure in aortic stenosis, cardiogenic
,-olume (ESV)
• 19 shock, cardiac tamponade, advanced heart
• 20 failure (H F').
• 21
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Item: 5 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1
A 25-year-old man comes to the emergency department complaining of several days of abdominal pain and multiple loose stools that began
2 shortly after a recent camping trip. He appears lethargic, and physical examination shows decreased skin turgor, heart rate of 120/min, and
respiratory rate of 22/min. Oxygen saturation is 99% on room air (normal: 95%-99%) .
3
4
Which of the following arterial blood gases is the patient most likely to have?
•5
•6
A. pH 7.18, Pco 2 88, Po 2 68, HC03- 24, Na+ 138, Cl- 110
•7
·8 B. pH 7.28, Pco2 32, Po2 88, HC03 - 17, Na+ 137, Cl- 112
•9 c. pH 7.28, Pco 2 42, Po 2 88, Hco3 - 16, Na+ 140, cl- 104
• 10
D. pH 7.50, Pco2 42, Po 2 88, HC03 - 32, Na+ 140, Cl- 108
• 11
E. pH 7.52, Pco 2 22, Po 2 94, HC03- 26, Na+ 139, Cl- 111
• 12
• 13
• 14
• 15
• 16
• 17
• 18
• 19
• 20
• 21
•
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Item:5of27 ~. , . M k <:] t> al ~· ~
2 The co rrect ans w e r is B. 6 20/o c hose this.

Non-anion gap metabolic acidosis. The primary acid-base insult in this scenario is d iarrhea, and one can infer that this should lead to metabolic
3
acidosis even without knowing the laboratory values . Several organ ic anions, inclu d in g HCo3- , are excreted in the stool, which we should expect
4 to lead to a low serum pH and low plasma HC03- . I n addition, the resu lting loss of fluids promotes reabsorption of NaCI and thus water in the
kidneys to maintain extracellular fluid volume . This increase in Cl- reabsorption helps to replace the loss of HCo3- , thus creating a non-anion gap
5
metabolic acidosis. Moreover, the decreased delivery of Na+ to the d istal tubule due to extensive reabsorption in the proximal nephron can impair
•6 renal acid excretion . To compensate for the acidosis, the body hyperventilates to blow off C02 and by doin g so will increase the serum pH .
.7 Resp iratory alkalosis with or without metabolic compensation is not the correct answer here as the vignette in d icates that it is not the primary
insult. Moreover, the normal oxygen saturation for this patient is another clu e, suggesting that tachypnea in this case is not due to a pulmonary
•8 cause . This patient's anion gap is 8 .0, a value between 8 .0 and 12.0 is considered normaL
•9 Anion gap = sodium - (cl- + HCo3- )
• 10 The cause of metabolic acidosis is generally either an increase in acid (eg, d iabetic ketoacidosis) or a decrease in base (eg, d iarrhea, kidney
· 11 failure) . Metabolic acidosis can be further subdivided into non-anion gap and anion gap metabolic acidosis. Other examples of an non-anion gap
metabolic acidosis can be recalled with the HAROASS mnemonic: Hyperalimentation, A dd ison d isease, Renal tubular acidosis, D iarrhea,
• 12
A cetazolamide, S pirono lactone, Saline infusion .
• 13
Diabetic ketoacidosis Nephron Respiratory alkalosis Distal convoluted tubule Metabolic acidosis Tachypnea Anion gap Extracellular fluid PH Blood plasma Acidosis
• 14 Diarrhea Ketoacidosis Kidney Sodium Chloride Alkalosis Anion Serum (blood) Oxygen saturation Mnemonic Anions Diabetes mellitus Metabolism Oxygen
• 15 Oxygen saturation (medicine) Bicarbonate Sodium chloride Excretion Feces Chlorine
• 16 A is no t co rrect. 4 0fo c hose this.

• 17 Resp iratory acidosis resu lts from a decrease in ventilation and an increase in serum C02 levels, lead in g to a decrease in pH . Causes include
inadequate ventilation (eg, depressed respiration by d ru gs or neurologic inj ury) or impaired gas exchange (eg, pulmonary edema). This would
• 18
not occu r in the setting of tachypnea .
• 19 Respiratory acidosis Tachypnea Pulmonary edema Hypoventilation Respiration (physiology) Acidosis Edema Gas exchange Ventilation (physiology)
• 20 Cellular respiration Blood plasma Serum (blood)
• 21 C is no t co rrect. 1 50/o c hose this .
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1 • inadequate ventilation (eg, depressed respiration by d ru gs or neurologic injury) or impaired gas exchange (eg, pulmonary edema). This would
not occu r in the setting of tachypnea .
2
Respiratory acidosis Tachypnea Pulmonary edema Hypoventilation Respiration (physiology) Acidosis Edema Gas exchange Ventilation (physiology)
3 Cellular respiration Blood plasma Serum (blood)
4
C is no t co rrect. 150/o c ho s e this.
5 An ion gap metabolic acidosis. The calculated anion gap is equal to 18.0 . This patient's d iarrheal illness would not resu lt in an anion gap metabolic
•6 acidosis. However, in general, patients with metabolic acidosis compensate for this condition by increasin g ventilation to blow off excess carbon
d iox ide and increase pH. For anion-gap acidosis use the MUOPILES mnemonic: Methanol; U rem ia; D iabetic ketoacidosis; Propylene g lycol/
•7
Paraldehyde, I nfection, I ron, Isoniazid, I nborn errors of metabolism; Lactic acidosis; Ethylene g lycol/Ethanol; Salicylates.
•8 Inborn error of metabolism Metabolic acidosis Anion gap Carbon dioxide Ethanol Paraldehyde Ketoacidosis Acidosis Anion Isoniazid Mnemonic Metabolism
•9 0 is no t co rrect. 90fo c hose this.

• 10 Metabolic alkalosis is not seen in excessive d iarrhea, and the compensation for metabolic alkalosis is hypoventilation .
Metabolic alkalosis Hypoventilation Diarrhea Alkalosis Metabolism
· 11
• 12
Res piratory alkalosis resu lts from an increase in ventilation, lead in g to a decrease in serum C02 and excess HC03- . This occu rs in cases of
• 13 increased respiratory d rive (eg, by d ru gs or central nervous system d isorders, anxiety, and fear) . Res piratory alkalosis would not be caused by
• 14 d iarrhea .
Respiratory alkalosis Central nervous system Diarrhea Ventilation (physiology) Alkalosis Anxiety Nervous system Blood plasma Control of ventilation
• 15
• 16
Severe d iarrhea resu lts in a non-anion gap metabolic acidosis. Res piratory compensation can be expected, resu lting in an increased respiratory
• 18
rate and below normal Pco2. To calculate the anion gap in a metabolic acidosis use this formula : An ion gap = Na+ - (cl- + HCo3- ) . A normal
• 19 anion gap is 8 .0-12.0 .
Metabolic acidosis Anion gap Respiratory compensation Diarrhea Acidosis Chloride Anion Metabolism Respiratory rate
• 20
• 21
•
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Item: 5 of 27 ~ 1 • Ma r k -<:J I> ~ £!1}>'
• !!":-~
QIO: 1780 ..L Pre v ious Next Lab lues Not es Calcula t o r
& &
1
FA17 p 561.2
2
Acidosis and alkalosis
3
4 Check arterial pH
5 pH< 7.35 pH> 745
•6
Acidemia Alkalemia
.7
·8 Pco1 > 44 mm Hg HC~- < 20 mEq/l Pco1 < 36 mm Hg
.9
• 10 Respiratory Respiratory
Metabolic acidosis Metabolic alkalosis
acidosis alkalOSIS
• 11
• 12
Hypoventilation Check anion gap Hy~rv~ntilation H• loss/HC05- excess
• 13 =Na •- (Cl +HC01 )
Airway obstruction Hysteria l oop diuretics
• 14 Acute lung disease Hypoxemia (eg, high altitude) Vomiting
Chronic lung disease Salicylates (early) Antacid use
• 15 Oploids, sedatives Tumor Hyperaldosteronism
• 16 Weakening of respiratory Pulmonary embolism
muscles
• 17
. 18
> 12 mEq/l 8-12 mEq/l
• 19 Pco1 •
• 20 I 45
40 Resporatory
40mmHg
--
I Anion gap Normal inion gip acidosis
• 21
• UIIOPII r~· IUD !\A~~· ~ 35
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lactic acidosis Resporatory
Ethylene glycol (.... oxalic acid) Metabolic alkalosiS
2 Salicylates (late) acidosis
3 69 70 71 72 7.5 74 75 76 77 78 79
4 pH
5
•6 FA17 p 561 .1
•7 Acid-base physiology
·8 pH Pco, (HC0 I COMPENSATORY RESPONSE

1
.9
• 10
Metabolic acidosis
Metabolic alkalosis
l
f
l
f
'
f
Hypen·entilation (immediate)
llypoventilation (immediate)
• 11 Respiratory acidosis l f f f renal [HC03-] reabsorption (delayed)
l renal (HC03-Jreabsorption (delayed)
• 12
• 13
Respiratory alkalosis f
'
Ker: f l = 1" disturbance; l f =compensatory response .
l
• 14
• 15
• 16
Henderson-Hasselbalch equation: p i I = 6. 1+ log 6~~~~~~
2
• 17 Pred icted respiratory compcns~1t ion for a simple metabolic acidosis can be calculated using the
Winters formula. If measured Pco2 > predicted Pco2 - concomitant respiratory acidosis; if
• 18
measured Pc~ <pred icted Pco2 - concomitant respiratorr alkalosis:
• 19
• 20
Pco2 = 1.5 [HC03-] + 8 :t 2
• 21
•
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1
A 7 - year- old boy presents to the physician with acute-onset edema and facial swelling. Dipstick urinalysis reveals 4+ proteinuria. Renal
2 biopsy shows no appreciable changes under light and fluorescence microscopy, but electron microscopy shows effacement of glomerular
epithelial cell foot processes. A diagnosis of minimal change disease is made.
3
4
How does this disease affect the pressures governing the flow of fluid across the glomeruli?
5
•6
A. Bowman space hydrostatic pressure will be decreased
•7
·8 B. Bowman space hydrostatic pressure will be increased
.9 C. Bowman space oncotic pressure will be decreased

• 10
D. Glomerular capillary hydrostatic pressure will be increased
• 11
E. Glomerular capillary oncotic pressure will be decreased
• 12
• 13
• 14
• 15
• 16
• 17
• 18
• 19
• 20
• 21
•
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Item: 6 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2321 ..L ar Prev ious Next Labfli!ll ues Notes Calculat o r
& &
1
3 Minimal change disease results in nephrotic syndrome, which is manifested primarily in the loss of significant protein in the urine. As a result of
4 this protein loss, the plasma protein concentration will decrease, thus decreasing the oncotic pressure in th e glomerular capillary. According to
the Starling equation (glomerular filtration rate = Kt [(PGc- PBs)- (nGC - nBs)]), this change will lead to a higher glomerular filtration rate by
5 decreasing the oncotic forces that normally oppose ultrafiltration.
6 Neph otic ~t ,J ome U trafoltration Minimal change disease Oncotic pressure Renal function Ultrafi1tration (renal) Proteinuria Starling equation Blood plasma
Protein Gl me ulus Urine Blood proteins Glomerulus {kidney) Cap1 .ary
0 7
o8 A i s not correct . 9 0fo chose this.
The Bowman space hydrostatic pressures are not affected by nephrotic syndrome. In general, Bowman space hydrostatic pressure does not
.9
decrease.
• 10 Neph otic syndrome Hydrostatic pressure
• 11 B is not correct. 11 Ofo chose this.

• 12 The Bowman space hydrostatic pressures may be increased secondary to an obstruction of urinary flow (st on es, cancer or prostate
enlargement). The patient has minimal chan ge d isease and this condition does not affect the Bowman space hyd rostatic pressures .
• 13 Minimal change disease Benign prostatic hyperplasia Prostate cancer Prostate Cancer
0 14
C is n ot co rrect. 130/o c hose this •
• 15 Bowman space oncotic pressure will increase, not decrease, as protein is filtered into Bowman space and thus increases the protein concentration
0
16 there.
Oncotic pressure Protein
0
17
Dis n ot co rrect. 110/o chose this •
• 18
Hydrostatic pressures are not affected in minimal change disease. The glomerular capillary hydrostatic pressure could be increased with
• 19 constriction of the efferent arteriole, for example.
• 20 Efferent artenole Artenole Hydrostatic pressure Glomerulus Glomerulus (kidney) capillary Starling equation
• 21
•
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Item: 6 of 27 ~. , . M k <:] t> al ~· ~
.- ... .. .. .. .- .. .- . .. .. .. .. .- .- ..
1 •
Nephrotic syndrome Ultrafiltration Minimal change disease Oncotic pressure Renal function Ultrafiltration (renal) Proteinuria Starling equation Blood plasma
2 Protein Glomerulus Urine Blood proteins Glomerulus (kidney) Capillary
3 A is not co rrect. 90fo c hose t his.

4 The Bowman space hydrostatic pressu res are not affected by nephrotic syndrome. I n general, Bowman space hydrostatic pressu re does not
decrease.
5
Nephrotic syndrome Hydrostatic pressure
6
B is not co rrect. 11 Ofo c hose t his.
•7
The Bowman space hydrostatic pressu res may be increased secondary to an obstruction of urinary flow (stones, cancer or prostate
•8 en largement). The patient has minimal change d isease and this condition does not affect the Bowman space hydrostatic pressu res .
Minimal change disease Benign prostatic hyperplasia Prostate cancer Prostate Cancer
•9
C is not co rrect. 130/o c hose t his .
• 10
Bowman space oncotic pressu re will increase, not decrease, as protein is filtered into Bowman space and thus increases the protein concentration
· 11 there .
• 12 Oncotic pressure Protein
• 13 0 is not co rrect. 11 Ofo c hose t his .

• 14 Hyd rostatic pressu res are not affected in m inimal change d isease. The g lomerular capillary hydrostatic pressu re could be increased with
constriction of the efferent arteriole, for exam ple .
• 15 Efferent arteriole Arteriole Hydrostatic pressure Glomerulus Glomerulus (kidney) Capillary Starling equation
• 16
• 17
Bottom Line :
• 18
S ign ificant proteinuria in nephrotic syndrome leads to decreased g lomerular capillary oncotic pressu re, which in turn causes an increase in
• 19 g lomerular filtration rate.
Nephrotic syndrome Oncotic pressure Proteinuria Renal function Glomerulus Capillary Glomerulus (kidney)
• 20
• 21
•
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1 FA17 p 566.1
2 Nephrotic syndrome I'\ephrO tic syndrome-massive prO teinuria (> 3.5 g/day) with hypoalbuminemia, resulting
3 edema, hyperlipidemia. Frothy urine" ith fatty casts. Due to podocyte damage disrupting
4 glomerular filtration charge barrier. \llay be 1° (eg, direct sclerosis of podocytes) or 2° (systemic
process [eg, diabetes] secondarily damages podocytes). Associated with hypercoagulable state (eg,
5
thromboembolism) due to antithrombin ( T ) Ill loss in urine and t risk of infection (due to loss of
6
immunoglobulins in urine and soft tissue compromise by edema).
0 7 se,·ere nephritic syndrome may present with nephrotic srndrome features (nephritic-nephrotic
o8 syndrome) if damage to CB I is se,·crc enough to damage charge barrier.
.9 Minimal change LVI-normal glomeruli (lipid may be seen in \!lost common cause of nephrotic S)11drome
• 10 disease (lipoid PCT cells). in children. Often 1° (idiopathic) and ma) be
• 11
nephrosis) IF 8 . triggered by recent infection, immunization,
EM -effacement of foot processes []. immune stimulus. Rarely, may be 2° to
• 12
lymphoma (eg, cytokine-medialed damage). I0
• 13 disease has excellent response to corticosteroids.
14
Focal segmental LM-segmental sclerosis and hyalinosis : . Mo~l common cause of nephrotic syndrome in
0
• 15 glomerulosclerosis IF - often 8, but may be Ef> for nonspeci fi e focal African Americans and Hispanics. Can be ]0
0
16 deposits of Ig r, C3, C l. (idiopathic) or 2° to other conditions (eg, H IV
0
17 EM-effacement of foot process sim ilar to infection, sickle cell disease, heroin abuse,
minimal change disease. massive obesity, interferon treatment, ch ronic
. 18
kidney disease due to congenital malformations).
• 19 0
) disease has inconsistent response to steroids.
• 20 ~lay progress to chronic renal disease.
• 21 Membranous LM-diffuse capillary and CB'vf thickening 'vtost common cause of 1° nephrotic syndrome
•
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Item: 6 of 27 ~ 1 • Ma r k -<:J I> ~ £!1}>'
• !!":-~
QIO: 2321 ..L Pre v ious Next Lab lues Notes Calcula t o r
& &
1
FA17 p 552.2
2
Glomerular filtration Inulin clearance can be used to calculate CFR 14
3 rate because it is freely filtered and is neil her
4 reabsorbed nor secreted. 12
5
. x V/P.mu1•m =C.111111•111
· = U.mu11n
CFR
6 10
= Kr [(Pcc - Pss>- (7tcc - 7tss>l
.7 ~
·c ::; 8
(CC =glomerular capillary; BS = Bowman space.) :::~0E
·8 ::.~
7tss normally equals zero; Kr = filtration constant. "'-
.9 E en
., E 6
.!! -
• 10
Normal CFR = 100 mL/min. Q.
Creatinine clearance is an approximate measure 4

• 11
of CFR. Slightly overestimates CFR because
• 12 creatinine is moderately secreted by renal 2
• 13 tubules.
• 14 Incremental reductions in CFR define the stages
of chronic kidney disease. 25 50 75 100 125 150
• 15
Glomerular filtration rate
• 16 (ml/min)
• 17
. 18 FA17 p 551 .2
• 19 Glomerular filtration Responsible for filtration of plasma according to Charge barrier-all 3 layers contain 8 charged
• 20 barrier size and charge selectivity. gl)eOproleins preventing <±> charged molecule
• 21
Composed of: entry (eg, albumin).
• • ~or..oc+r..,f--o~ ""'"';)).,'"' ' onAn•l... o J; .. _, ("; __ .. ___;__ t"----•-•-..1 ---:11 - - . - ·-:•l. - 1:..•_
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Item: 6 of 27 ~ 1 • Ma r k -<:J I> ~ £!1}>'
• !!":-~
QIO: 2321 ..L Pre v ious Next Lab lues Notes Calcula t o r
1 (CC =glomerular cap.Jlary; BS = Bowman space.) :::: E 8
.. - 6
~0
rr8s normally equals zero; Kr = filtration constant b~
2
E en
., E
.!! -
3 I orrnal CFR = 100 mL/min. a..
4 Creatinine clearance is an approximate measure 4
5 of GF'R. Slightly o,·erestimates GF'R because
6
creatinine is moderately secreted b) renal 2
tubules.
•7
Incremental reductions in GF'R define the stages
·8 of chronic kidney disease. 25 50 75 100 125 150
.9 Glomerular filtration rate
(mUmin)
• 10
• 11
FA17 p 551 .2
• 12
Glomerular filtration Responsible for filtration of plasma according to Charge barrier-all 3 layers contain 8 charged
• 13
barrier size and charge selectivity. glycoprotcins preventing<±> charged molecule
• 14 Composed of: entry (eg, albumin).
• 15 • Fenestrated capillary endothelium Size barrier-fenestrated capillary epithelium
• 16 Basement membrane with type I collagen (prc\'ent entry of > 100 nm molecules/blood
• 17
chains and heparan sulfate cells); podocyte foot processes interpose with
• Epithelial layer consisting of podocyte foot basement membrane; slit diaphragm (prevent
• 18
processes · entrr of molecules> 50-60 nm).
• 19
• 20
• 21
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1
A 19- year -old male presents to his general physician . He is training for an upcoming mountain climb an d he wants to know if there are any
2 medications that can help with adjusting to high altitu des. The patient is notcurrently taking any medications. He has no known allergies, and
3 his past medical history is unremarkable. The physician considers an appropriate medication that is also used for treatment of glaucoma.
4
This medication causes which of the following side effects that helps to alleviate the symptoms of high altitud e?
5
6
A. Metabolic acidosis
0 7
o8 B. Metabolic alkalosis
.9 C. Mixed metabolic acidosis and respirat ory alkalosis

• 10
D. Respiratory acidosis
• 11
E. Respiratory alkalosis
• 12
• 13
0 14
• 15
0
16
0
17
• 18
• 19
• 20
• 21
•
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Item: 7 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 180 5 ..L ar Prev ious Next Lab fli!ltues Not es Calculat o r
& &
1 Th e co rrect a n s wer is A. 61 Ofo ch ose this.
2 Acetazolamide can be taken prophylactically or therapeutically to alleviate the symptoms of acute mountain sickness. It acts by inhibiting carbonic
anhydrase, which is important for HCo3- reabsorption in the proximal tubule of the kidney, and thus causes excretion of HC03- in the urine. This
3
leads to alkalinization of the urine and a m etabolic acidosis. The drop in the plasma pH results in an increased breathing drive and higher oxygen
4 levels in the body, helping to reverse the effects of hypoxemia. Acetazolamide is also used for treatment of glaucoma and pseudotumor cerebri. It
5 should be avoided in patients with an allergy to sulfa drugs. It may cause type 2 (proximal) renal tubular acidosis as an adverse effect.
Acetazolamode Glaucoma Metabolic acidosis carbonic anhydrase Pro ima1 convoluted tubule Idoopathoc ntracranial hypertension Sulfonamide medicine
6 Renal tubular acidosis PH Hypoxemia Blood plasma Preventive healthcare Altitude sickness Urine Kidney Acidosis Oxygen Adverse effect Allergy Metabolism
t
7 Chronic mo 1ntain sic ness
·8 B is not correct . 180/o chose this.

.9 Acetazolamide does not cause metabolic alkalosis. Loop diuretics and thiazides both cause metabolic alkalosis. Furosemide has the opposite effect
of acetazolamide in that it lowers urine pH and raises blood pH .
• 10
Acetazolamide Furosemide Metabolic alkalosis Thiazide PH Loop diuretic Diuretic Alkalosis Urine Metabolism
• 11
C is no t co rrect. 6 0fo chose this .
• 12
Acetazolam ide does not cause a mixed metabolic acidosis and respiratory alkalosis. This combination can be seen with aspirin toxicity, but
• 13 respiratory alkalosis is not an effect of acetazolamide .
Acetazolamide Respiratory alkalosis Metabolic acidosis Aspirin Acidosis Alkalosis Metabolism Toxicity
• 14
• 15 D is not co rrect. 70fo c hose this .
Acetazolamide does not ca use respiratory acidosis. Respiratory acidosis results from impaired respiration and can be seen with chronic
• 16
obstructive pulmonary disease, sedative or oropiate use, pneumothorax, and acute respiratory distress syn d rom e, among others.
• 17 Acute respiratory distress syndrome Respiratory acidosis Chronic obstructive pulmonary disease Pneumothorax Sedative Respiration (physiology) Dyspnea Acidosis
Cellular respiration Infant respiratory distress syndrome Respiratory disease
• 18
• 19 E is n ot correct . 80/o ch ose this .
• 20 Respiratory alkalosis results from respiratory carbon dioxide output in excess of normal for the metabolic production of carbon dioxide by tissue .
This can be seen with hyperventilation in a patient with anxiety or pain, salicylate toxicity, or central nervous system lesions, among other
• 21 factors .
•
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Item: 7 of 27 ~. , . M k <:] t> al ~· ~
- - + + - + -- - -
1 •
Acetazo lam ide does not cause metabolic alkalosis. Loo p d iuretics and thiazides both cause metabolic alkalosis. Furosemide has the opposite effect
2 of acetazo lamide in that it lowe rs urine pH and raises blood pH.
Acetazolamide Furosemide Metabolic alkalosis Thiazide PH loop diuretic Diuretic Alkalosis Urine Metabolism
3
C is not co rrect. 60/o c hose t his.
4
Acetazo lam ide does not cause a mixed metabolic acidosis and respiratory alkalosis. This combination can be seen with aspirin toxicity, but
5
respiratory alkalosis is not an effect of acetazo lamide.
6 Acetazolamide Respiratory alkalosis Metabolic acidosis Aspirin Acidosis Alkalosis Metabolism Toxicity
7 0 is not co rrect. 70/o c hose t his.

•8 Acetazo lamide does not cause respiratory acidosis. Res piratory acidosis resu lts from impaired respiration and can be seen with chronic
obstructive pulm onary d isease, sedative or oropiate use, pn eumothorax, and acute respiratory d istress syndrome, among others .
•9
Acute respiratory distress syndrome Respiratory acidosis Chronic obstructive pulmonary disease Pneumothorax Sedative Respiration (physiology) Dyspnea Acidosis
• 10 Cellular respiration Infant respiratory distress syndrome Respiratory disease
· 11 E is not co rrect. SO/o c hose t his .

• 12 Res piratory alkalosis resu lts from respiratory carbon d iox ide output in excess of normal for the metabolic production of carbon d iox ide by tissue .
This can be seen with hyperventilation in a patient with anxiety or pain, salicylate toxicity, or central nervous system lesions, among other
• 13
factors .
• 14 Respiratory alkalosis Carbon dioxide Hyperventilation Central nervous system Aspirin poisoning Alkalosis Salicylic acid Nervous system Anxiety Toxicity
• 15 Metabolism
• 16
• 17 Bottom Li ne :
• 18 Acetazo lamide is a carbonic anhydrase inhibitor that can be used to in duce metabolic acidosis, lead in g to an increased breathin g d rive. This
• 19 property may be useful for prevention and treatment of acute mountain sickness .
Acetazolamide Carbonic anhydrase inhibitor Carbonic anhydrase Metabolic acidosis Altitude sickness Acidosis Chronic mountain sickness Metabolism
• 20 Enzyme inhibitor
• 21
•
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Item: 7 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1 FA17 p 575.2
2 Acetazolamide
3 MECHANISM Carbonic anhydrase inhibitor. Causes self-
4 limited 'aHC03 diuresis and l total body
5
HC0 3- stores.
6 CliNICAl USE Glaucoma, urinary alkalinization, metabolic
alkalosis, altitude sickness, pscudotumor
7
cerebri.
·8
.9
• 10
• 11
• 12
ADVERSE EFFECTS Proximal renal tubular acidosis, parcsthesias, "AClD"azolamide causes ACIDosis.
• 13
NH3 toxicity, sulfa allergy, hypokalemia .
• 14
• 15
FA17p561 .1
• 16
Acid-base physiology
• 17
pH Pco IHCD COMPENSATORY RESPONSE
. 18
Metabolic acidosis l l l l lyperventilation (immediate)
• 19
Metabolic alkalosis t t f I lypo\'entilation (immediate)
• 20
Respiratory acidosis l f f t renal (HC03-J reabsorption (delayed)
• 21
• ..... _ --1-- - --· - ·· ~ · --! - • t rt • ~'"' _, ' 1 1
"
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Item: 7 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1
FA17p561 .1
2
Acid-base physiology
3
pH P<oz IHC01 I COMPENSATORY RESPONSE
4
Metabolic acidosis l l l llyperventilation (immediate)
5
Metabolic alkalosis t t t I lypo"entilation (immediate)
6
Respiratory acidosis l t t t renal (I-IC03-Jreabsorption (delayed)
7
Respiratory alkalosis t l l l renal [I-IC03-Jreabsorption (delayed)
·8
.9 Ke): t l = I" disturbance: l t =compensatory response.
• 10
. [IICO -]
• 11 Henderson-Hasselbalch equahon: pi I = 6. 1 +log 0.0 P~Oz
3
• 12
Predicted respiratory compensation for a simple metabolic acidosis can be calculated using the
• 13
Winters formula. If measured Pco2 >predicted Pco2 - concomitant respirator)' acidosis; if
• 14 measured Pco2 < predicted Pco2 - concom itant respiratory alkalosis:
• 15
Pco2 = 1.5 IHC03- ] + 8 :!: 2
• 16
• 17
FA17 p 561 .2
. 18
• 19
• 20 Check arterial pH
• 21 pH< 7.35 pH> 745
• l
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Item: 8 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2336 ..L ar Pre v ious Next Lab fli!ltues Notes Calcula t o r
& &
1
A 76-year-old male patient with hepatocellular carcinoma develops severe ascites. Medical management was attempted, but was
2 unsuccessful. He was advised that 3- 5 L of fluid must be drained from his peritoneal cavity every 3 days, but th e procedure may have
3 detrimental effects on kidney function, and monitoring of glomerular filtration rate is required . After a few days of drainage, renal laboratory
values show:
4
5 Creatinine clearance: 120 ml/min

Glomerular capillary hydrostatic pressure: 40 mm Hg
6 Bowman capsule hydrostatic pressure: 12 mm Hg
7 Plasma inulin: 1.5 mg/ml
Urinary inulin : 50 mg/ml
·8 Urine para-aminohippiuric acid (PAH): 100 mg/ ml
.9 Plasma PAH: 0.4 mg/ml
• 10
Which of the following is his urine flow rate?
• 11
• 12 :
A . 0.48 mL/min
• 13
• 14 B. 0.96 mL/min
• 15 C. 1.6 mL/min
• 16
D. 1.8 mL/min
• 17
E. 3.6 mL/min
• 18
• 19
• 20
• 21
•
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Item:8of27 ~. , . M k <:] t> al ~· ~
1 •
2 The correct answer is E. 4J Ofo chose this.

3 I nulin is freely filtered across the g lomerular capillary wall and is neither reabsorbed nor secreted . It is therefore used to calculate the g lomerular
filtration rate {GFR}, otherwise kn own as clearance of inulin . Creatinin e clearance can also be used as a physiolog ic approximation of GFR. GFR is
4
calculated as : (urinary concentration of inulin x urinary flow rate}/plasma concentration of inulin . Using this equation, urine flow rate= {GFR x
5 plasma concentration of inulin}/urinary inulin concentration = {120 m l /min x 1.5 mg/m l }/ 50 mg/m l = 3 .6 m l /min . Glomerular capillary and
Bowman capsule hydrostatic pressu res, listed in the table of laboratory values, are d istracters that are not used for what is bein g calculated .
6
A is not correct. 100/o chose this.
7
This answer underestimates the urine flow rate. The answer uses concentrations of para -aminohippuric acid {PAH} to calculate urine flow rate
8 that would be incorrect in this case . PAH is used to calculate effective renal plasma flow because it is both filtered and secreted in the proximal
•9 collecting tubule {PCT}, resu lting in near 100% excretion of all PAH enterin g the kidney. To calculate urine flow rate from the values g iven, we
also need to kn ow the effective renal plasma flow (eRPF} . The calculation for eRPF is eRPF = UrinePAH x Urine flow rate/PiasmaPAH .
• 10
B is not correct. 120/o chose this.
· 11
This answer underestimates the patient's urine flow rate, which is 3 .6 m l /min .
• 12
Cis not correct. 190/o chose this .
• 13 This answer underestimates the patient's urine flow rate, which is 3 .6 m l /min . Urine flow rate= {Glomerular filtration rate x plasma
• 14 concentration of inulin}/urinary inulin concentration .
• 15 0 is not correct. 120/o chose this .

This answer underestimates the patient's urine flow rate, which is 3 .6 m l /min .
• 16
• 17
Bottom Line:
• 18
Urine flow rate can be calculated using three param eters {GFR, plasma, and urinary inulin concentrations) in the following equation : Urine flow
• 19
rate = GFR x [ inulin ] p I [ inulin ] u
• 20
• 21
•
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Item: 8 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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FA17 p 552.2
2
3
rate because it is freely filtered and is neil her
5
. x V/P.mu1.m =C.111111·111
· = U.mu11n
CFR
6 10
= Kr [(Pcc - Pss>- (1tcc - 1tss>l
7 ~
·;: ::; 8
8
(Ce =glomerular capillary; BS = Bowman space.) :::~0E
0~
1tss normally equals zero; Kr = filtration constant. "'-
.9 E en
., E 6
• 10 Normal CFR = 100 mL/min. "'
0.: -
• 11
of C FR. Slightly overestimates C FR because
• 12
creatinine is moderately secreted by renal 2
• 13 tubules.
• 14 Incremental reductions in GFR define the stages
• 15 of chronic kidney disease. 25 50 75 100 125 150
• 16 (mUmin)
• 17
. 18 FA17 p 552.1
• 19 Renal clearance e x= uxV/PX= \·olumc of plasma from \\ h ich the ex= clearance of X (mL/min).
• 20 substance is completely cleared per unit time . Ux = urine concentration of X (eg, mg/mL).
If e x< C FR: net tubular reabsorption of X. P~ =plasma concentration ofX {eg, mg/mL) .
• 21
• .. rv ' ' __ . __ a _~ -- •-- '-- ' , __ : _,
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Item: 9 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1
A 35-year-old man with controlled diabetes is enrolled in a stu dy examining the difference between serum glucose levels and urine glucose
2 levels in type 2 diabetes mellitus. As part of this study the patient eats a large carbohydrate-rich meal and then has serial serum and urine
3 glucose levels drawn. Although his serum glucose level begins to rise rapidly, glucose only becomes detectable in his urine several hours
later.
4
5 Glucose does not become immediately detectable in his urine because of the:
6
:
7 A. Impermeability of occluding proteins in the tight junctions of glomerular capillary endothelial cells
8
B. Kinetics of the sodium -dependent glucose symporter in the distal convoluted tubule
.9
• 10 C. Kinetics of the sodium-dependent glucose symporter in the proximal convoluted tubule
• 11 0. Kinetics of the sodium-potassium exchange pump in the distal convoluted tubule

• 12
E. Kinetics of the sodium-potassium exchange pump in the proximal convoluted tubule
• 13
• 14
• 15
• 16
• 17
• 18
• 19
• 20
• 21
•
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Item: 9 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2347 ..L ar Previous Next Lab fli!ltues Not es Calculat or
& &
1
2 Th e correct a n s wer is C. 860/o chose this.
3 Glucose is reabsorbed from the proximal tubule by a sodium-dependent glucose symporter located at the luminal membrane of the proximal
convoluted tubule . These transporters are able to handle filtered glucose concentrations in the healthy physiologic range. At a glucose
4
concentration of 200 mg/dl, threshold for glucose reabsorption is reached . It is at this value that glucose may start to appear in the urine.
5 Threshold occurs when some but not all of the nephrons start to reach their maximum transport level. At 300 mg/dl (or a transport rate of 375
mg/min), however, all the transporters become saturated and some glucose is not resorbed back from the proximal tubules. This is called
6
transport maximum and occurs when no more glucose will be absorbed and all the excess will be secreted in the urine. This difference between
7 threshold and transport maximum is due to the fact that some nephrons excrete glucose at a lower transport maximum level. The transport
maximum for the kidney is reached when all nephrons are at their maximal capacity.
8
Pro imal convoluted tubule Glucose Lumen (anatomy) Symporter Kidney Nephron U ine Rena• glucose reabsorption Physiology Cell membrane
9 Anatomical te ms of location Reabsorption
• 10
A is not c orrect. 4 0/o chose this .
• 11 Glomerular capillaries are made of fen est rated epit helial cells that do not contain tight junctions. Tight j unct ions are normally found in the blood-
• 12 brain barrier of the brain and retina .
Retina Blood-brain barrier Capillary Tight junction Epithelium Glomerulus Glomerulus (kidney) Fenestra (histology) Brain
• 13
B is n ot c o rre c t. 50/o c hose this •
• 14
The sodium-glucose symporters are o nly located in th e prox imal tubule. Glucose is not resorbed in othe r pa rt s of t he ne phron .
• 15 Nephron Proximal convoluted tubule Symporter Glucose Anatomical terms of location Tubule
• 16 D is n ot c o rre c t. 20/o c hose this •
• 17 ATP-driven sodium-potassium exchan ge p u m ps are responsible for creating the sodium grad ient that allows for cotransport of many molecules,
• 18 including glucose, as sodium travels d own its concentration gradient from the tubular lumen into the tubular epith elial cells . These pumps are
located in all parts of the nephron, but g lucose r esorption can only take place in the proximal convoluted tubule, wh ere the sodium - glucose
• 19 cotransporters (sympo1·ters) are located .
• 20 Nephron Proximal convoluted tubule Co-transport Glucose Cotransport Molecular diffusion Sodium Epithelium Symporter Lumen (anatomy) Na+/K+-ATPase
Electrochem•cal gradient Anatomical terms of location Gradient
• 21
•
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Item:9of27 ~. , . M k <:] t> al ~· ~
: '
1
The sodium -g lucose symporters are on ly located in the prox imal tubule . Glucose is not resorbed in other parts of the nephron .
2 Nephron Proximal convoluted tubule Symporter Glucose Anatomical terms of location Tubule
3
0 is n ot co rrect. 20/o c h ose t his.
4 ATP-d riven sodium - potass iu m exchan ge pumps are respons ible for creating the sodium g rad ient that allows for cotransport of many molecu les,
5 inclu d in g g lucose, as sodium travels down its concentration g rad ient from the tubular lumen into the tubular epith elial cells . These pumps are
located in all parts of the nephron, but g lucose resorption can on ly take place in the proximal convoluted tubule, where the sodium -g lucose
6 cotransporters (symporters) are located .
7 Nephron Proximal convoluted tubule Co-transport Glucose Cotransport Molecular diffusion Sodium Epithelium Symporter lumen (anatomy) Na+/K+-ATPase
Electrochemical gradient Anatomical terms of location Gradient
8
9 E is n ot co rrect. 30/o c h ose t his.
The sodium - potassium exchange pump in d irectly prov ides the energy for g lucose resorption in the proximal convoluted tubule . By moving
0 10
sodium from the epith elial cells into the interstitial fluid/blood, the pump creates a g rad ient that promotes entry of sodium in the tubular lumen
o ll into the tubular epith elial cells . As the sodium travels down its g rad ient, it passes through the sodium -g lucose symporter and supplies energy for
the resorption of g lucose. An increase in serum g lucose will increase the concentration of g lucose filtered into tubules and transport by the
0
12
sodium -g lucose symporter, but this should not change the function of the sodium - potassium exchange pump.
0
13 Proximal convoluted tubule Glucose Sodium Nephron lumen (anatomy) Epithelium Blood plasma Blood sugar Symporter Anatomical terms of location
0 14 Interstitial fluid Gradient
0 15
0
16 Bottom Lin e :
0 17 Serum g lucose of up to 300 mg/d l (corresponds to transport rate of 375 mg/min) can be reabsorbed in the proximal tubule by a sodium -
0
18 g lucose cotransport system . At a g lucose level >300 mg/d l , these transporters become saturated, and g lucose beg ins to spill into the urine.
Threshold for g lucose reabsorption is reached at 200 mg/d l . This d ifference between threshold and transport maximum is due to the fact that
0 19 some nephrons excrete g lucose at a lowe r transport maximum leveL
0 20 Proximal convoluted tubule Glucose Co-transport Blood sugar Nephron Urine Anatomical terms of location Blood plasma Reabsorption Renal glucose reabsorption
Cotransport liver function tests
0
21
•
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Item: 9 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1 FA17 p 554.2
2
Glucose clearance Glucose at a normal plasma level (range 60-120 G lucosuria is an important clinical clue to
3 mg/dL) is completely reabsorbed in proximal diabetes mellitus.
4 convoluted tubule (PCT) by 1 a•tglucose Splay is the region of substance clearance
5 cotransport. between threshold and T111; due to the
In adults, at plasma glucose of- 200 mg/d 1., heterogeneity of nephrons.
6
glucosuria begins (threshold). At rate of
7 600 F1ltered
- 375 mg/min, all transporters are full)
8 saturated (T m>·
9 Normal pregnancy may decrease abilit) of
• 10 PCT to reabsorb glucose and amino acids
• 11
- glucosuria and aminoaciduria .
Sodium-glucose cotransporter 2 (SGLT2)
• 12
inhibitors (eg, -Aozin drugs) permit glucosuria
• 13 at plasma concentrations< 200 mg/dL .
• 14
Normal Plasma glucose (mg/dll
• 15
• 16
FA17 p 555.1
• 17
Nephron physiology
. 18
• 19
l
Dislal
lnlt<SIWm- Wmen- lnle<st>Wm-
convoltMd
• 20 unne blood
blood IUbu~
• 21
• .... _._(_
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Item: 10 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
& &
1
A 53 - year -old woman is undergoing r enal function testing to evaluate proteinuria detected by her prima•·y care physician at a routine visit.
2 The patient's glomerular filtration rate ( GFR) is initially estimated at 100 mL/min by inulin clearance. Subsequ ently, as part of a research
3 study, the patient's GFR is determined using a novel marker (compound X) and is found to be 125 ml/min .
4
Which mechanism most likely explains th e difference noted between these two GFR estimates?
5
6
A. Compound X is not freely filtered at the glomerulus
7
8 B. Compound X is reabsorbed in t he descending limb of the loop of Henle
9 C. Compound X is reabsorbed in t he proximal convoluted tubule

• 10
D. Compound X is secret ed in t he prox imal convoluted tubule
• 11
E. Inulin is reabsorbed in th e prox imal convoluted tubule
• 12
• 13
• 14
• 15
• 16
• 17
• 18
• 19
• 20
• 21
•
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Item: 10 of 27 ~. I • M k <:] t> al ~· ~
1 •
2 The correct answer is 0. 760/o chose this.

3 I nulin clearance is an accurate estimate of GFR because it is freely filtered and neither reabsorbed nor secreted in the nephron . Because it
ove restimates true GFR, compound X must therefore undergo net secretion in the nephron . That is, more compound X is excreted in the urine
4
than is filtered at the g lome rulus . I ndeed, it is precisely this mechanism that is respons ible for the characteristic ove restimation of GFR by
5 measuring creatinine clearance.
Nephron Inulin Creatinine Renal function Urine Glomerulus Glomerulus (kidney)
6
7 A is not correct. 50fo chose this.
If compound X w ere not freely filtered at the g lome rulus, its clearance w ou ld underestimate GFR.
8
Glomerulus (kidney) Glomerulus
9
B is not correct. 30fo chose this.
10
The descend in g limb of the loo p of Hen le is poo rly perm eable to solute and instead allows passive efflux of water from the filtrate. Furthermore,
· 11 compound X cannot undergo net reabsorption in the nephron .
Nephron loop of Henle Descending limb of loop of Henle Solution Reabsorption Semipermeable membrane Friedrich Gustav Jakob Henle Filtration
• 12
C is not correct. 80fo chose this .
• 13
The proximal convoluted tubule is respons ible for most ultrafiltrate reabsorption . How ever, if compound X underwent net reabsorption, its
• 14
clearance would underestimate, not ove restimate, the inulin -calculated GFR.
• 15 Proximal convoluted tubule Ultrafiltration (renal) Ultrafiltration Nephron Anatomical terms of location Reabsorption
• 16 E is not correct. 80fo chose this.

• 17 I nulin is freely filtered and neither reabsorbed nor secreted in the nephron . It is these characteristics that allow its use as an accurate measure of
GFR.
• 18
Nephron Inulin
• 19
• 20
Bottom Line:
• 21
• r..... , . l; ..... ..-I...-. .............. ,.,..,.. ........ 1-. ...-. . . .... ...-...-! ~...... ..--.1..-• . 1.... ~...... ~h..-. ..-. 1..-.. .............. .... . 1....... &01~ ...... ~; ...... ...., ...... ~...... , , ,...;....,....,~h..-. ~...... 11.....,,.,, ;...., ...., ........... . . .... ~; ...... ...., . r-; -=-n - 1 t. . . "'\tin, .. - r . ..
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Item: 10 of 27 ~. I • M k <:] t> al ~· ~
1 • ove restimates true GFR, compound X must therefore undergo net secretion in the nephron . That is, more compound X is excreted in the urine
than is filtered at the g lome rulus . I ndeed, it is precisely this mechanism that is responsible for the characteristic ove restimation of GFR by
2
measuring creatinine clearance.
3 Nephron Inulin Creatinine Renal function Urine Glomerulus Glomerulus (kidney)
4 A is not correct. 50fo chose this.

5 If compound X were not freely filtered at the g lome rulus, its clearance would underestimate GFR.
Glomerulus (kidney) Glomerulus
6
B is not correct. 30fo chose this.
7
The descend in g limb of the loo p of Hen le is poo rly perm eable to solute and instead allows passive efflux of water from the filtrate. Furthermore,
8 compound X cannot undergo net reabsorption in the nephron .
9 Nephron loop of Henle Descending limb of loop of Henle Solution Reabsorption Semipermeable membrane Friedrich Gustav Jakob Henle Filtration
10 C is not correct. 80fo chose this.
· 11 The proximal convoluted tubule is respons ible for most ultrafiltrate reabsorption . However, if compound X underwent net reabsorption, its
clearance would underestimate, not ove restimate, the inulin -calculated GFR.
• 12 Proximal convoluted tubule Ultrafiltration (renal) Ultrafiltration Nephron Anatomical terms of location Reabsorption
• 13
E is not correct. 80fo chose this .
• 14 I nulin is freely filtered and neither reabsorbed nor secreted in the nephron . It is these characteristics that allow its use as an accurate measure of
• 15 GFR.
Nephron Inulin
• 16
• 17
• 18 Bottom Line:
• 19 I nulin clearance can be used to calculate the g lomerular filtration rate, using the following equation : GFR = Uinulin x V/Pinulin = Cinulin
Inulin Renal function Glomerulus Glomerulus (kidney) Filtration
• 20
• 21
•
6
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Item: 10 of 27 ~. I • M k <:] t> al ~· ~
2
3 liil;fii!1J•J
FI RST AID FA CTS
fo r ye ar:l 2 0 17 "
4
5
FA11 p 552.2
6
Glomerular filtration Inu lin clearance can be used to calculate GFR 14
7 rate because it is freely filtered and is neither
9
GFR = U.mu1.111 x VfP.mu1m
. =C.mu1.111
10 10
= Kr [(P cc - Pss) - (nee - nss)J ...c:
· 11 ·c ::r
(GC =glomerular capillary; BS = Bowman space.) := E 8
:o
..E""-E 6
• 12 -o
v_.
1tss normally equals zero; Kr =filtration constant.
• 13
• 14
I ormal GFR"' 100 mL/min. .. -
~
<>:
• 15
of GFR. Slightly overestimates GFR because
• 16 creatinine is moderately secreted by renal 2
• 17 tubules.
• 18 Incremental reductions in GFR define the stages
• 19
• 20 (ml/min)
• 21
•
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Item: 11 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
& &
1
A 3-year-old boy is brought to the em er gency department after playing outside for 2 hours on a hot an d humid summer day. Upon physical
2 examination, the physician notices the symptoms of extreme dehydration and immediately takes action to correct th e problem. He also
3 notices that the child is small for his ag e, an d a review of systems reveals frequent lung infections and greasy stools.
4
The volume status and pH of the patient upon arrival to the emergency department would be similar to a patient with which of the following?
5
6
A. Administration of excess bicarbonate
7
8 B. Diabetic ketoacidosis
9 C. Excessive diuresis with a loop diuret ic

10
D. Existence of an aldosteronoma
• 11
E. Posthypercapnic alkalosis
• 12
• 13
• 14
• 15
• 16
• 17
• 18
• 19
• 20
• 21
•
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Item: llof27 ~. , . M k <:] t> al ~· ~
1 •
2 The correct answer is C. 580/o chose this.

3 The patient described has become dehyd rated through excessive sweating . Patients with cystic fibrosis have a defective chloride channel and
consequently release a high -chloride, low-bicarbonate solution through their sweat. Their stools are also low in bicarbonate. As a resu lt, this
4
patient is los in g volume without los in g bicarbonate and would have a contraction alkalosis. Add itiona lly, aldosterone secretion is increased due to
5 hypovolemia, causing sodium reabsorption and consequent hydrogen ion secretion . The patient is unable to compensate for the alkalosis because
of this volume -de pleted state, causing further alkalosis. Patients treated with excessive d iuretics lose bicarbonate-free fluid, lead in g also to
6
contraction alkalosis.
7 Cystic fibrosis Hypovolemia Aldosterone Alkalosis Bicarbonate Sodium Hydrogen ion Perspiration Diuretic Ion Hydrogen Chloride channel Dehydration Chloride
8 A is not correct. 100/o chose this.

9 Adm inistration of excess bicarbonate can lead d irectly to alkalosis, but it does not lead to loss of bicarbonate-free fluid and volume contraction .
Thus there is no contraction alkalosis associated with it.
10
Contraction alkalosis Bicarbonate Alkalosis
11
B is not correct. 160/o chose this .
• 12
Diabetic ketoacidosis resu lts in an acidotic state. Patients with d iabetic ketoacidosis present with lethargy, hyperventilation, mental status
• 13 changes, vomiting/nausea, pain, and often a fruity smell on the breath, which is in d icative of acetone production. This patient has a contraction
alkalosis, and thus while he may be letharg ic, he is not in d iabetic ketoacidosis .
• 14
Diabetic ketoacidosis Hyperventilation Acetone Acidosis Ketoacidosis Diabetes mellitus Alkalosis
• 15
0 is not correct. 100/o chose this .
• 16
The existence of an aldosteronoma leads to excessive primary mineralocorticoid secretion . The mineralocorticoid acts both by d irectly stimulating
• 17 the secretory H+-ATPase pump, and via the stimulation of sodium reabsorption, by making the lumen more electronegative, thereby minimizin g
the back -d iffusion of hydrogen out of the lumen. Hence there is an alkalosis, but there is retention of water, not loss of it. Thus there exists no
• 18
volume contraction .
• 19 Mineralocorticoid Sodium lumen (anatomy) Hydrogen Electronegativity
• 20 E is not correct. 60/o chose this.

• 21 Posthypercapnic alkalosis is caused by renal retention of bicarbonate after a period of hypercapnia that has stabilized . It does not resu lt in any
6
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Item: llof27 ~. , . M k <:] t> al ~· ~
1
A is no t co rrect. 100/o c hose this.
2
Adm inistration of excess bicarbonate can lead d irectly to alkalosis, but it does not lead to loss of bicarbonate-free fluid and volume contraction .
3 Thus there is no contraction alkalosis associated with it.
Contraction alkalosis Bicarbonate Alkalosis
4
5 B is no t co rrect. 160/o c hose this.
Diabetic ketoacidosis resu lts in an acidotic state. Patients with d iabetic ketoacidosis present with lethargy, hyperventilation, mental status
6
changes, vomiting/nausea, pain, and often a fruity smell on the breath, which is in d icative of acetone production . This patient has a contraction
7 alkalosis, and thus while he may be letharg ic, he is not in d iabetic ketoacidosis.
Diabetic ketoacidosis Hyperventilation Acetone Acidosis Ketoacidosis Diabetes mellitus Alkalosis
8
9 0 is no t co rrect. 100/o c hose this.
The existence of an aldosteronoma leads to excessive primary m in eralocorticoid secretion . The mineralocorticoid acts both by d irectly stimulating
10
the secretory H+-ATPase pu m p, and via the stimulation of sodium reabsorption, by makin g the lu men more electronegative, thereby m inimizin g
11 the back -d iffusion of hydrogen out of the lumen . Hence there is an alkalosis, but there is retention of water, not loss of it. Thus there exists no
volume contraction .
• 12
Mineralocorticoid Sodium lumen (anatomy) Hydrogen Electronegativity
• 13
• 14
Posthypercapnic alkalosis is caused by renal retention of bicarbonate after a period of hypercapnia that has stabilized . It does not resu lt in any
• 15 sort of fluid loss, so there is no volume contraction associated with it.
Hypercapnia Alkalosis Bicarbonate Kidney
• 16
• 17
• 19 While cystic fibrosis is classically associated with frequent lun g infections, it is a systemic d isease with other manifestations. Volume depletion
without corresponding loss of bicarbonate will cause contraction alkalosis; alkalosis can blunt respiratory d rive .
• 20 Cystic fibrosis Bicarbonate Fibrosis Alkalosis Hypovolemia lung Control of ventilation
• 21
6
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Item: 11 of 27 ~ 1 • Ma rk -<:J I> ~ £!1}>'
• !!":-~
QIO: 380 5 ..L Prev ious Next Lab lues Not es Cal culat o r
& &
1
FA17 p 561 .2
2
3
4 Check arterial pH
5 pH< 7.35 pH> 745

6
Ac.idemia Alkalemia
7
8
9
10 RespiratOf}' Respiratory
MetaboUc acidos1s Metabolic alkalOSIS
acidosis alkalosis
11
• 12
Hypowntilation Check anion gap Hyptrvtntilation H• loss/HC0 1- excess
• 13 =Na' - (Ct· +HCO; l
Airway obstruction Hysteria loop diuretics
• 14 Acute lung disease Hypoxemia (eg, high altitude) Vomiting
Chronic lung disease Sallcylates (early) Antacid use
• 15 Opioids, sedatives Tumor Hyperaldosteronism
• 16 Weakening of respiratory Pulmonary embolism
muscles
• 17
. 18
> 12 mEq/L 8-12 mEq/l
• 19 Pco.•
I 4S 40 mm Hg
• 20 40 Resporatory
I Anion gap Nonnal anion gap :::1
ac1dosls
---
3S
• 21
• MUOPILE5: HARDASS: ~
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Item: 11 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
& &
1
FA17 p 56.3
2 Cystic fibrosis
3 GENETICS Autosomal recessive; defect in CFTR gene on chromosome 7; commonly a deletion of Ph608.
4 Most common lethal genetic disease in Caucasian population.
5 PATHOPHYSIOlOGY CFTR encodes an ATP-gated CJ- channel that secretes CJ- in lungs and G l tract, and reabsorbs
6 CJ- in s"eat glands. lost common mutation ..... misfolded protein ..... protein retained in RER
7 and not transported to cell membrane, causing l CJ- (and H10 ) secretion; t intracellular CJ-
8
results in compensatory t 1 a+ reabsorption via epithelial Na+ channels ..... t 1120 reabsorption
..... abnormally thick mucus secreted into lungs and Gl tract. t t a+ reabsorption also causes more
9
negati\·e transepithclial potential difference.
10
DIAGNOSIS t Cl- concentration (> 60 mEq/L) in S\\eat is diagnostic. Can present with contraction alkalosis
11
and hypokalemia (ECF effects analogous to a patient taking a loop diuretic) because of ECF
• 12 H20/J'\a+ losses and concomitant renal K+fJJ+ wasting. t immunoreacti\·e trypsinogen (newborn
• 13 screening).
• 14 COMPliCATIONS Recurrent pulmonary infections (cg, S aureus [early infancy), P aeruginosa [adolescence]), chronic
• 15 bronchitis and bronchiectasis ..... reticulonodular pattern on CXR, opacification of sinuses.
• 16 Pancreatic insufficiency, malabsorpt ion wit h steatorrhea, fat-soluble vitamin deficiencies (A, D, E,
K), bi liary cirrhosis, liver disease. Meconium ileus in newborns.
• 17
Infertil ity in men (absence of vas deferens, spermatogenesis may be unaffected) and subfertility in
. 18 women (amenorrhea, abnormally thick cen ical mucus).
• 19 lasal polyps, clubbing of nails.
• 20 IREAIMENT J\lultifactorial: chest physiotherapy, albutcrol, aerosolized dornase alfa (DNAse), and hypertonic
• 21 saline facilitate mucus clearance. zithromycin used as anti-inflammatory agent. Ibuprofen slows
•
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Item: 12 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
& &
1
A 70-year-old female with a history of chronic, poorly controlled type 2 diabetes mellitus presents with lower extremity and periorbital
2 edema. Urine test reveals a protein - to -creatinine ratio greater than 3500 mg/g.
3
4 In non pathologic states, what properties of the glomerular filtration barrier prevent albumin from being freely filtered into the urine?
5 :
6 A. A combination of small pore size and negatively charged pore-forming molecules prevents albumin filtration
7 B. A combination of small pore size and positively charged pore-forming molecules prevents albumin filtration
8
C. Albumin is freely filtered across the basement membrane but is readily reabsorbed along the nephron
9
D. The positive charge of proteoglycans in the basement membrane repels albumin
10
11 E. The small size of the glomerular basement membrane pores excludes albumin molecules
• 12
• 13
• 14
• 15
• 16
• 17
• 18
• 19
• 20
• 21
•
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Item: 12 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2326 ..L ar Prev ious Next Labfli!ll ues Notes Calculat o r
& &
1
Th e correct an sw er is A . 7 8 0/o ch ose this .
2
The glomerular basement membrane is composed of endothelial fenestrae with filtration slits lined with anionic glycoproteins. The small diameter
3 of the filtration slits is a mechanical block to albumin filtration, but the anionic charge of the barrier provid es the largest obstacle to filtration by
electrostatically repelling the negatively charged albumin molecules.
4
Glomerular basement membrane Podocyte Basement membrane Albumin Human serum album1n Endothelium Glomerulus Glycoprotein Glomerulus (kidney}
5 Biologica membrane Fenestra (histology}
6 B is not correct . 11 Ofo chose t his.
7 Th is choice is incorrect because the filtration slits are lined w ith negatively charged anionic g lycoproteins and are not positively charged. Positive
8 charges wou ld attract albumin and cong lomerate, thereby impeding further filtration. It is correct, however, t hat the small d iameter of filtration
slits on the g lomerular basement membrane prevents albumin filtration.
9 Podocyte Glomerular basement membrane Basement membrane Albumin Glome ulus Glycoprotein Glomerulus (kidney} Ion Human serum albumin
10 Cis not correct. 20/o c hose t h is.
11 Albumin is neither freely filtered by the glomerulus nor reabsorbed along the nephron. Examples of substances reabsorbed along the nephron
12 are glucose and amino acids. I n contrast, factors that prevent albumin filtration are the small diameter of filtration slits and negatively charged
molecules on the glomerular filtration barrier.
• 13 Nephron Podocyte Albumin Glomerulus Human serum albumin Glomerulus (kidney} Glucose Amino acid Renal function
• 14 D is not correct. 4 0fo c hose this •
• 15 Basement membrane proteoglycans are negatively charged, as is albumin. The negatively charged molecules and small filtration slits on
• 16 glomerular basement membrane prevent albumin leaking into the urine .
Podocyte Glomerular basement membrane Basement membrane Albumin Urine Glomerulus (kidney} Glomerulus Proteoglycan Cell membrane
• 17 Human serum albumin
• 18
E i s n ot correct. solo ch ose this •
• 19
The size selectivity of the endothelial filtration slits provides an obstacle to albumin filtration, but size selectivity alone does not account for the
• 20 complete absence of albumin filtration in nonpathologic states .
Podocyte Albumm Endothel urn Human serum albumin
• 21
•
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Item: 12 of 27 ~. I • M k <:] t> al ~· ~
1
B is not co rrect. 11 Ofo c hose t his.
2 This choice is incorrect because the filtration slits are lined with negatively charged anionic g lycoproteins and are not positively charged . Positive
3 charges would attract albumin and conglomerate, thereby im ped in g further filtration . It is correct, however, that the small d iam eter of filtration
slits on the g lomerular basement membrane prevents albumin filtration .
4 Podocyte Glomerular basement membrane Basement membrane Albumin Glomerulus Glycoprotein Glomerulus (kidney) Ion Human serum albumin
5
6 Albumin is neither freely filtered by the g lome rulus nor reabsorbed along the nephron . Examples of substances reabsorbed along the nephron
7 are g lucose and amino acids. I n contrast, factors that prevent albumin filtration are the small d iam eter of filtration slits and negatively charged
molecules on the g lomerular filtration barrier.
8 Nephron Podocyte Albumin Glomerulus Human serum albumin Glomerulus (kidney) Glucose Amino acid Renal function
9 0 is not co rrect. 4 0fo c hose t his.
10 Basement membrane proteog lycans are negatively charged, as is albumin . The negatively charged molecules and small filtration slits on
11 g lomerular basement membrane prevent albumin leakin g into the urine.
Podocyte Glomerular basement membrane Basement membrane Albumin Urine Glomerulus (kidney) Glomerulus Proteoglycan Cell membrane
12 Human serum albumin
• 13
E is not co rrect. 50/o c hose t his .
• 14
The size selectivity of the endothelial filtration slits prov ides an obstacle to albumin filtration, but size selectivity alone does not account for the
• 15 complete absence of albumin filtration in non path olog ic states .
Podocyte Albumin Endothelium Human serum albumin
• 16
• 17
• 18 Bottom Line :
• 19 The g lomerular basement membrane prov ides selective filtration on the basis of size and charge via filtration slits and an anionic (negative)
charge barrier.
• 20 Glomerular basement membrane Basement membrane Podocyte Glomerulus Glomerulus (kidney)
• 21
6
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Item: 12 of 27 ~ 1 • Ma r k -<:J I> ~ £!1}>'
• !!":-~
QIO: 2326 ..L Prev ious Next Lab lues Notes Cal culat o r
& &
1
FA17 p 551 .2
2
Glomerular filtration Responsible for fil tration of plasma according to C harge barrier-all 3 layers contain 8 charged
3 barrier size and charge selectivity. gl)COproleins preventing <±> charged molecule
4 Composed of: entry (eg, albumin).
5 • Fenestrated capillary endothelium ize barrier- fenestrated capillary epithelium
6 Basement membrane with type IV collagen (pre, ent entrr of > 100 nm molecules/blood
chains and heparan sulfate cells); podocyte foot processes interpose "it h
7
Epithelial layer consisting of podoc) te foot basement membrane; slit diaphragm (prevent
8 processes · entrYof molecules> :>0- 60 nm).
'
9
10
11
FA17 p 553.1
12
• 13 Filtration Filtration fraction (FF) =CFR/RPF. CFR c<m be estimated with creatinine
• 14 Normal FF = 20%. clearance.
Filtered load (mg/min) = C F'R (mL/min) RPF is best estimated with PAH clearance.
• 15
X plasma concentration (mg/ml .). Prostaglandins Dilate Afferent arteriole (POA)
• 16 AC E inhibitors Constrict Efferent arteriole
• 17 (ACE)
. 18 Prostaglandinspreferentially
NSAIDs -0-i dilate afferent arteriole / Parietal layer of
• 19 / Bowman capsule
(i RPF. i GFR. so no tJ. FF)
• 20
• 21
~o'l"lman space r Podocytes
/ (YISCerallayerJ
•
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Item: 12 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
1 ~
2 r Angiotensin II preferentially
ACE inhibitors - { ; H I constricts efferent arteriole
3 (! RPF, i GFR. so i ff}
4
5 FA17 p 552.2
6
9
C FR = U.lllU1•Ill x V/P.lOll1.Ill = C.IIlli1.111
10 10
= Kr [(Pcc - Pss) - (7tcc- 7tss)J 4>
11 -c:c:...J-
·-=e
(CC =glomerular capillary; BS Bowman space.) = 8
12
7tss normally equals zero; Kr = filtration constant.
:
."'. -..
~o
o
E c:n
• 13 ., E 6
.!!l-
Normal C F R == 100 mL/min. 0..
• 14
• 15
• 16 creatinine is moderately sccrctccl by renal 2
• 17 tubules.
• 19
• 20 (mUmin}
• 21
•
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Item: 13 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
A 55-year-old male with a history of type 2 diabetes mellitus presents to his physician for follow-up . In his previous visit four weeks ago, his
&
1
blood pressure was found to be 150/90 mm Hg . This was subsequently confirmed by measurements obtain ed at home. He denies any other
2
medical history, including dyslipidemia. He takes metformin and he has no known drug allergies. The physician r echecks his blood pressure,
3 which is 155/90 mm Hg today. The physician wants to prescribe a drug that will decrease the production of angiotensin II.
4
Net Net
5 Choice HCO,- H•
resorption resorption
6
7 A ~ ~
8 B no effect no effect
9
10
c no effect
t
11
D
t no effect
12 E
t t
• 13
• 14 Using the table above, which of th e followin g sh ows the normal actions of angiotensin II in the prox imal t ubule?
• 15 :
• 16 A
• 17 B
. 18
c
• 19
D
• 20
• 21 E
•
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Item: 13 of 27 ~. I • M k <:] t> al ~· ~
1 •
2 The correct answer is 0. 420/o chose this.

3 Ang iotensin -converting -e nzyme converts angiotensin I to angiotensin II (AT II) . AT II increases the activity of the sodium - hydrogen {Na+-H +)
exchanger in the proximal tubule to facilitate salt and water reabsorption. As a resu lt, increased H+ is pumped into the tubular lu men. Luminal
4 H+ is then returned to the tubular cell in the process of bicarbonate {HC03-) resorption, asH+ and HC03- join and form water and carbon d iox ide
5 after catalysis by brush border carbonic anhydrase. Water and carbon d iox ide d iffuse back into the tubular cell and again liberate H+ and HC03-
after carbonic anhydrase catalysis. Here, the HC03- is transported into the bloodstream, whereas the H+ is free to participate in another round of
6 HCo3- resorption via the Na+-H + exchanger. Thus the net resu lt of increased Na+-H + exchange is an increase in HCo3- resorption and no net
7 change in H+ reabsoprtion. I ncreased HCo3- resorption after AT II stimulation accounts for the contraction alkalosis that occu rs as a resu lt of
volume depletion.
8 Angiotensin Proximal convoluted tubule Carbon dioxide Angiotensin II Carbonic anhydrase Bicarbonate ACE inhibitor lumen (anatomy) Hypovolemia Nephron
9 Brush border Alkalosis Anatomical terms of location Catalysis Circulatory system

11 AT II increases Na+-H + exchange in the proximal tubule lead in g to increased delivery of H+ to the tubular lumen, which is then used to shuttle
HC03- back into the tubular ceiL Hence HC03- resorption is increased, rath er than decreased. Net H+ resorption remains unchanged, rath er than
12
decreased.
13 Proximal convoluted tubule Nephron lumen (anatomy) Anatomical terms of location Bone resorption
• 14 B is not correct. 21 Ofo chose this.

• 15 AT II increases Na+-H + exchange in the proximal tubule lead in g to increased delivery of H+ to the tubular lumen, which then is used to shuttle
HC03- back into the tubular cells . Hence HC03- resorption is increased, whereas net H+ resorption remains unchanged .
• 16
Proximal convoluted tubule Nephron lumen (anatomy) Anatomical terms of location Bone resorption
• 17
C is not correct. 130/o chose this .
• 18
AT II increases Na+-H + exchange in the proximal tubule lead in g to increased delivery of H+ to the tubular lumen, which is then used to shuttle
• 19 HC03- back into the tubular cells . Hence HC03- resorption is increased, whereas net H+ resorption remains unchanged . There is no net increase
in H+ resorption, as the H+ in the lumen is returned to the cell in the process of HC03- resorption .
• 20
Proximal convoluted tubule lumen (anatomy) Nephron Anatomical terms of location Bone resorption
• 21
I= ic: nnt- rnrr,:..rt- 1 0 0/"' rllnc:,:.. t-hic:
6
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Item: 13 of 27 ~. I • M k <:] t> al ~· ~
1
A is not co rrect. 140/o c hose t his.
2 AT II increases Na+-H + exchange in the proximal tubule lead in g to increased delivery of H+ to the tubular lumen, which is then used to shuttle
3 HC03- back into the tubular ceiL Hence HC03- resorption is increased, rath er than decreased . Net H+ resorption remains unchanged, rath er than
decreased .
4 Proximal convoluted tubule Nephron lumen (anatomy) Anatomical terms of location Bone resorption
5
B is not co rrect. 2 1 Ofo c hose t his.
6 AT II increases Na+-H + exchange in the proximal tubule lead in g to increased delivery of H+ to the tubular lumen, which then is used to shuttle
7 HC03- back into the tubular cells . Hence HC03- resorption is increased, whereas net H+ resorption remains unchanged .
Proximal convoluted tubule Nephron lumen (anatomy) Anatomical terms of location Bone resorption
8
9
AT II increases Na+-H + exchange in the proximal tubule lead in g to increased delivery of H+ to the tubular lumen, which is then used to shuttle
10 HC03- back into the tubular cells . Hence HC03- resorption is increased, whereas net H+ resorption remains unchanged . There is no net increase
11 in H+ resorption, as the H+ in the lumen is returned to the cell in the process of HC03- resorption .
12
E is not co rrect. 100/o c hose t his.
13
AT II increases Na+-H + exchange in the proximal tubule lead in g to increased delivery of H+ to the tubular lumen . However, there is no net
• 14 increase in H+ resorption, as the H+ in the lu men is returned to the tubular cell in the process of HC03- resorption . However it is correct that AT II
• 15 increases net HC03- resorption .
• 16
• 17
Bottom Line :
• 18
AT II stimulates HC03- reabsorption in the proximal tubule by increasin g the rate of H+ recyclin g across the lu m inal cell membrane via the Na+-
• 19
H+ exchanger.
• 20 Proximal convoluted tubule Cell membrane lumen (anatomy) Anatomical terms of location Bicarbonate Reabsorption Nephron
• 21
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Item: 13 of 27 ~ 1 • Ma rk -<:J 1>- Jil ~· !:';-~
QIO: 2322 ..L Pre v ious Next Labfli!llues Notes Calcula t o r
1
FA17 p 555.1
2
Nephron physiology
3
4
5 l Na'
J lnll<Sw.om-
blood
6
Ang-ll I Glue~
7
8 HC0 - t
5
"":rr._
tr W HCQs--,.J...._+ K'
'---V--= I
9 H;z(OJ H;z(Os
10
11
12 HzOtCOl
13
Early OCT -reabsorbs a+, Cl- . ~akes urine
• 14 ful ly dilute (hypotonic).
( JYrt-l - t Ca 2+fNa+ exchange - Ca 2+
• 15
reabsorption .
• 16
Early PCT -conlains brush border. 5- 10% Na+ reabsorbed.
• 17 Reabsorbs all glucose and amino acids and
. 18 most HC03-, la+, Cl-, PO/-. K+, H20,
• 19
and uric acid. Isotonic absorption. Generates L =- l
c~~~ng J lnt:;:m-
and secretes 11 3, "hich enables the kidney a·~==~~~-
• 20 Principal cell
to secrete more JJ+.
• 21
•
PTH-inhibits Na+fP0-13- cotransport
" '"' l ..
Hzo--==+ _o•
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Item: 13 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2322 ..L ar Pre v ious Next Labfli!ltues Notes Calcula t o r
& &
1 FA17 p 558.1
2 Renin-angiotensin-aldosterone system
3
I BP (JG cells)
4
I Na• delivery Acts at angiotensin II
5
6 I sympathetK: tone vascular smooth muscle
7 -receptors)
Constricts efferent I FF to preserve renal functiOn (GFRl
8 arteriOle of glomerulus 1n low-volume states (ie, when RBF ~ )
9
~ B dyk' .
ACE ----+ ra 1r11n Aldosterone
10 Renin I Na' channel insertion and - -+ Creates
breakdown
~ (adrenal cortex) I activity of Na'/K· pump; favorable Na·
11 't
Angiotensinogen Angiotensin I - -+ enhances K- and H- gradient for
12 excretion by way of principal Na' and Hp
13 ex-intercalated cell H' ATPases
• 14 ...-~ AOH
_ _ _ _ _ _,.. I aquaporin insertion in - --+ H20
(posterior
• 15 pituitary) principal cells reabsorption
• 16
1 PCT Na'/H ' activity
- --+ Na•, HCOJ-. and Hp reabsorption
• 17 (can permit contraction alkalosis)
. 18 Stimulates hypothalamus ~ Thirst
• 19
• 21 effect), and l N;,c deli\'ery to macula densa cells.
•
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Item: 14 of 27 ~. I • M k <:] t> al ~· ~
1
A 56-year -o ld male with a 60-pack-year smoking history and normal fluid intake presents to his physician with 2 months of fatigue,
2 weakness, and weight loss accompanied by cough and m ild dyspn ea. On exam ination, the patient looks cachetic, his vital signs are normal,
and there is no proximal myopathy. A lowe r left lobe mass is noted on X-ray of the chest. Biopsy leads to the d iagnosis of small cell
3
carcinoma .
4
Laboratory tests show :
5
Plasma sodium : 125 m Eq/L
6 Plasma potass iu m : 3 .9 m Eq/L
7 Plasma C02: 24 m Eq/L
Plasma osmo lality : 253 mOsm/L
8 Urine sodium : 48 m Eq/L
9 Urine osmo lality : 350 mOsm/L
10
11 The hormone most likely respons ible for this patient's abnormal laboratory values has which of the following d irect effects?
12
:
13
• 14
A. Activation of G-protein -cou pled receptors in the hypothalamus resu lts in elevated cA MP levels and inhibition of hypothalamic-induced
• 15 thirst mechan ism
• 16 B. Activation of G-protein -cou pled receptors in the adrenal cortex elevates cA MP levels and leads to increased production and secretion
• 17 of corticosteroids
C. Activation of V2-receptors leads to a decrease in total periph eral resistance; activation of V 1 - receptors resu lts in the concentration of
• 18
urine .
• 19
0 . Activation of V2-receptors leads to an increase in total periph eral resistance; activation of V 1 - receptors resu lts in the concentration of
• 20 urine
• 21 E. Activation of V2-receptors resu lts in the insertion of aquaporins into the collecting duct; activation of V 1 - receptors leads to a decrease
6
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Item: 14 of 27 ~. I • M k <:] t> al ~· ~
1 Laboratory tests show :
2 Plasma sodium : 125 m Eq/ L

Plasma potass iu m : 3 .9 m Eq/ L
3
Plasma C02: 24 m Eq/ L
4 Plasma osmo lality : 253 mOsm/ L
Urine sodium : 48 m Eq/ L
5
Urine osmo lality : 350 mOsm/ L
6
7
The hormone most likely respons ible for this patient's abnormal laboratory values has which of the following d irect effects?
8
9 :
10
11 A. Activation of G-protein -cou pled receptors in the hypothalamus resu lts in elevated cA MP levels and inhibition of hypothalamic-induced
thirst mechan ism
12
B. Activation of G-protein -cou pled receptors in the adrenal cortex elevates cA MP levels and leads to increased production and secretion
13 of corticosteroids
• 14 C. Activation of V2- receptors leads to a decrease in total periph eral resistance; activation of V 1 - receptors resu lts in the concentration of
• 15 urine .
• 16 0 . Activation of V2- receptors leads to an increase in total periph eral resistance; activation of V 1 - receptors resu lts in the concentration of
urine
• 17
E. Activation of V2- receptors resu lts in the insertion of aquaporins into the collecting duct; activation of V 1 - receptors leads to a decrease
• 18 in total periph eral resistance
• 19 F. Activation of V2- receptors resu lts in the insertion of aquaporins into the renal collecting duct; activation of V 1 - receptors leads to an
increase in total periph eral resistance
• 20
• 21
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Item: 14 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
& &
1
2 Th e correct an sw er i s F. 600/o ch ose this.
3 In healthy people, osmoreceptors in the wall of the third ventricle sense increased body fluid osmolarity and trigger the release of antidiuretic
hormone (ADH) from the posterior pituitary. ADH exerts its main effects on the V2-receptors located in the principal cells of the late distal tubule
4
and collecting duct, where a Gs-protein- coupled mechanism directs the insertion of aquaporin water channels into the luminal wall, as shown in
5 the image. These channels are permeable only to water and result in a reabsorption of water, concentration of urine, and dilution of body fluids.
Activation of the Vt-receptor found in the vascular smooth muscles results in activation of Gq protein second - messenger cascade and contraction
6
of vascular smooth muscle, leading to an increase in total peripheral resistance. In patients with the syndrome of inappropriate ADH secretion
7 (SIADH), which can be caused by central nervous system disturbances (eg, stroke, hemorrhage, infection), small cell lung carcinoma,
intracranial neoplasms, and occasionally by pancreatic tumors, the unregulated release of ADH leads to the persistent excretion of concentrated
8
urine high in sodium. This causes hyponat remia and decreased serum osmolality without potassium or acid - base disturbances. Furthermore, in
9 the context of decreased serum osmolality, a urine osmolality > 100 mOsm demonstrates that the urine is submaximally dilute, which helps
10 confirm ADH excess. Plasma C02, which is different from Pco2, is measured as plasma HC03- since C02 is t ransported as HC03- in plasma and is
normal in this scenario.
11
KEY: Collecting duct, A = sodium chann el; B = chloride channe l; C = calcium channel; D = intracellular mineralocort icoid receptor; E =
12 Na+jK+/ATPase; F = V2
13
Lumen: urine
14
• 15
• 16
II II (1-
i't------t'l~'it------..
• 17
• 18
• 19
• 20
Water t
channel • • Collecting
• 21 molecules .._ tubule
•
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Item: 14 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1 of vascular smooth muscle, leading to an increase in total peripheral resistance. In patients with the syn drom e of inappropriate ADH secretion
2 (SIADH), which can be caused by central nervous system disturbances (eg, stroke, hemorrhage, infection), small cell lung carcinoma,
intracranial neoplasms, and occasionally by pancreatic tumors, the unregulated release of ADH leads to th e persistent excretion of concentrated
3 urine high in sodium. This causes hyponatremia and decreased serum osmolality without potassium or acid - base disturbances. Furthermore, in
4 the context of decreased serum osmolality, a urine osmolality > 100 mOsm demonstrates that the urine is submaximally dilute, which helps
confirm ADH excess. Plasma C02, which is different from Pco2, is measured as plasma HC03- since C02 is transported as HC03- in plasma and is
5 normal in this scenario.
6 KEY: Collecting duct, A = sodium channel; B = chloride channel; C = calcium channel; D = intracellular mineralocorticoid receptor; E =
7 Na.."/K .."/ATPase; F = V2
8 Lumen: urine
9
10
11
II II o-
12 1t------.....
i t - - - - - - 1 1l l t - - - - - - - i l
13
14 Water t
• 15 channel • • Collecting
molecules tubule
• 16
• 17
0
• 18
• 19
• 20
• 21 Interstitium: blood
•
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Item: 14 of 27 ~. I • M k <:] t> al ~· ~
1 A is no t co rrect . 4 0fo c hose t his.

2 This patient likely has paraneoplastic ADH production associated with small cell lun g carcinoma . I n this case, the ADH production is not related to
the hypothalamus. I n normal circumstances, ADH is regu lated by the osmo receptors in the hypothalamus, which is stimulated by increased
3 plasma osmo lality.
4 Hypothalamus Plasma osmolality Osmolality Osmoreceptor Blood plasma Small-cell carcinoma Vasopressin Paraneoplastic syndrome lung Carcinoma
5 B is no t co rrect . 50fo c hose t his.

6 This describes the mechanism of hormones inclu d in g ACTH, FSH, LH and TSH . A lthough ACTH can be produced by small cell lun g carcinomas,
this patient does not have any symptoms or signs of hypercortisolism (hypertension, weight gain, buffalo hump, truncal obesity, striae,
7 hyperglycemia, and osteoporos is). I n fact, the weight loss, hyponatremia, and lack of proximal myopathy is not suggestive of hypercortisolism .
8 C is no t co rrect . 50fo c hose t his.
9 V 2-receptors are coupled to the insertion of aquaporins, lead in g to increased water reabsorption and concentration of urine. I n contrast, V 1-
receptors are coupled to the contraction of vascular smooth muscle, which would increase total peripheral resistance.
10
0 is no t co rrect . 80fo c hose t his.
11
The appropriate descriptions of V 1- and V2-receptors are switched . V2-receptors are coupled to the insertion of aquaporins; V 1- receptors are
12 coupled to the contraction of vascular smooth muscle, lead in g to an increase in total peripheral resistance.
Vascular resistance Smooth muscle tissue Aquaporin Vascular smooth muscle Muscle Blood vessel
13
14 E is no t co rrect . 180/o c hose t his.
• 15 A lthough it is correct that activation of V2-receptors leads to insertion of aquaporins into the renal collecting duct, activation of V1- receptors leads
to an increase, not a decrease, in total peripheral resistance .
• 16
• 17
Bo tto m Line :
• 18
Small cell carcinoma is associated with a paraneoplastic S IADH . ADH acts on V 1- receptors in vascular smooth muscle to cause contraction; it
• 19 acts on V 2-receptors in the nephron late d istal tubule and collecting duct cells to increase water reabsorption via increased luminal aquaporin
• 20 density .
Nephron Distal convoluted tubule Aquaporin Small-cell carcinoma Collecting duct system lumen (anatomy) Vasopressin Smooth muscle tissue
• 21 Vascular smooth muscle Anatomical terms of location Carcinoma Blood vessel Reabsorption Muscle Paraneoplastic syndrome
6
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Item: 14 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2338 ..L ar Pre vious Next Lab fli!ltues Not es Calcula t o r
:.: I. : • • "'
3
lii! ;fil;1i•J fo r year: 20 17 ...
4 F I RST A ID FA CTS
5
6 FA17 p 317.3
Antidiuretic hormone
7
8
SOURCE Synthesized in hypothalamus (supraoptic
nuclei). stored and secreted by posterior
9
pituitary.
10
FUNCTION Regulates serum osmolarity (V2-receptors) ADH le\·el is ! in central diabetes insipidus (01),
11
and blood pressure ( 1-receptors). Primary normal or t in nephrogenic 0 1.
12 funct ion is serum osmolarity regulation (J\011 Nephrogenic 0 1can be caused by mutation in
13 ! serum osmolarity, t urine osmolarity) via \1 2-receptor.
14 regulation of aquaporin channel insertion in Dcsmopressin acetate (ADH analog) is a
principal cells of renal collecting duel. t ret~ t ment for central DI and nocturnal
• 15
enures1s .
• 16
REGULATION Osmoreceplors in hypothalamus ( I0 );
• 17
hypovolemia.
. 18
• 19
• 20
• 21
•
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Item: 15 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
A 35-year-old man arrives at the emergency department. He was found by a pedestrian who noticed a penetrating wound in the patient's
&
1
upper left quadrant. His hea•·t rate on arrival is 135/min, and blood pressure is 65/40 mm Hg. His extremities are pale in color and cold to
2
touch. His blood urea nitrogen and creatinine values are significantly elevated . He is sent to the surgical suite, where his wounds are
3 repaired, and his vital signs are stabilized after administration of 6 L normal saline and transfusion of 5 units of blood.
4 Afferent Efferent
Released from the
5 juxtaloglomerular arteriole arteriole
apparatus response response
6
A Aldosterone Constricts Constricts
7 B Angiotensin I Dilates Constricts
c Atrial natriuretic Dilates Constricts
8 . oeotide
D Renin Constricts Constricts
9
E Angiotensin II Dilates Dilates
10 F Vasopressin Dilates Constricts
11
12 While in the emergency department prior to any fluid resuscitation, which of the following would be released from juxtaloglomerular apparatus (JGA)
cells and ultimately lead to the responses shown in the table above in the afferent and efferent arterioles due to the patient's severe blood loss?
13
:
14
A
0 15
B
0
16
0
17 c
0
18 D
• 19
E
0 20
F
• 21
•
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Item: 15 of 27 ~. I • M k <:] t> al ~· ~
1 •
2 The co rrect a nswe r is 0. 750/o c hose t his.

3 This patient has a penetratin g wound to the abdomen with vital signs and a physical exam suggestive of severe volume loss. When perfusion
4 pressu re to the kidney falls, initially intrinsic regu latory mechan isms (stretch receptors in afferent arteriole} will attempt to maintain the
g lomerular filtration rate {GFR} by d ilating the afferent arteriole and constricting the efferent arteriole. However, as blood volume continues to be
5 depleted, these intrinsic mechanisms are superseded by other regu latory mechanisms, inclu d in g sympathetic inn ervation and the ren in -
6 angiotensin-aldosterone system . Decreased perfusion pressu re leads to ren in secretion by the juxtaglomerular apparatus {JGA} in response to
the loca l production of prostag lan d ins synthesized by baroreceptors in the wall of the afferent arteriole. Ren in then acts to initiate the RAS
7
pathway by cleavin g angiotensinogen to the decapeptide angiotensin I (AT ! } . AT I is then converted by angiotensin-converting enzymes {ACE}
8 located primarily in pulm onary endothelial cells to angiotensin II (AT II) . AT II then acts to cause four main effects : (1) periph eral
vasoconstriction, {2} increased secretion of aldosterone from the adrenal cortex, {3} increased reabsorption of NaCI from the proximal tubule and
9
other kidney segments, and ( 4 ) stimulation of thirst and antidiuretic hormone secretion, all of which lead to an increased blood volume and blood
10 pressu re. Furthermore, increased sympathetic nervous stimulation in states of hypovolemia also can increase release of ren in by JGA cells and
will lead to constriction of the afferent arteriole > efferent arteriole. Ultimately in states of severe hypovolemia, the afferent and efferent arteriole
11
both become constricted, which leads to a decrease in GFR, FF, and urine output.
12 Angiotensinogen Juxtaglomerular apparatus Efferent arteriole Arteriole Hypovolemia Aldosterone Adrenal cortex Afferent arterioles Proximal convoluted tubule
Renal function Renin Angiotensin II Prostaglandin Angiotensin Vasoconstriction Vasopressin Angiotensin I Renin-angiotensin system Kidney Endothelium
13
Blood pressure Baroreceptor Blood volume Urine Hormone Glomerulus Glomerulus (kidney) Nephron Perfusion Mechanoreceptor Sympathetic nervous system
14
Sodium chloride Vital signs
15
A is no t co rrect . 4 0fo c hose t his .
• 16
Although the ultimate response to severe, continuous volume loss is constriction of the afferent and efferent arterioles, the initial hormone
• 17 produced by the juxtaglomerular cells of the kidney is ren in . A ldosterone is produced by the zona g lomerulosa of the adrenal g land, rath er than
• 18 the j uxtaglomerular cells .
Adrenal gland Zona glomerulosa Aldosterone Renin Juxtaglomerular cell Kidney Efferent arteriole Hormone Arteriole
• 19
B is no t co rrect . 90fo c hose t his .
• 20
Angiotensin I (AT ! }is the product of the ren in d riven conversion of angiotensinogen, an inactivate precu rsor produced in the liver. S ince AT I is
• 21 not produced by the juxtaglomerular cells of the kidney, this answer choice is incorrect. AT I has minimal effects, it needs to be activated by the
•
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Item: 15 of 27 ~. I • M k <:] t> al ~· ~
1 • produced by the juxtaglomerular cells of the kidney is ren in . A ldosterone is produced by the zona g lomerulosa of the adrenal g land, rath er than
the j uxtaglomerular cells .
2 Adrenal gland Zona glomerulosa Aldosterone Renin Juxtaglomerular cell Kidney Efferent arteriole Hormone Arteriole
3
B is no t co rrect . 90fo c hose t his.
4 Ang iotensin I (AT ! }is the product of the ren in d riven conversion of angiotensinogen, an inactivate precu rsor produced in the liver. S ince AT I is
5 not produced by the juxtaglomerular cells of the kidney, this answer choice is incorrect. AT I has minimal effects, it needs to be activated by the
angiotensin-converting enzyme to angiotensin II (AT II) . AT II has several effects, inclu d in g constricting of efferent arterioles and stimulating
6 aldosterone release.
7 Angiotensinogen Aldosterone Angiotensin Angiotensin-converting enzyme Renin Angiotensin II Angiotensin I Juxtaglomerular cell Enzyme Efferent arteriole
Arteriole Kidney liver
8
9 C is no t co rrect . 50fo c hose t his.
Atrial natriuretic peptide {ANP} is released from atrial myocytes in response to increased blood volume, which leads to d ilation of afferent renal
10
arterioles and constriciton of efferent renal arterioles. ANP has a natriuretic effect. It is not released in states of hypovolemia, therefore this is not
11 correct.
Atrial natriuretic peptide Hypovolemia Peptide Cardiac muscle Blood volume Myocyte Arteriole Atrium (heart) Kidney Afferent nerve fiber Efferent nerve fiber
12
Vasodilation
13
E is no t co rrect . 4 0fo c hose t his.
14
Ang iotensin II (AT II) is produced from the conversion of angiotensin I by AC E in the pulm onary endothelium . Therefore, this answer is incorrect
15 as AT II is not produced by the j uxtaglomerular cells in the kidney. Furthermore, the ultimate response to severe blood loss is constriction of both
• 16 the afferent and efferent arterioles .
Angiotensin II Angiotensin Angiotensin I Juxtaglomerular cell Endothelium Efferent arteriole Arteriole Kidney Efferent nerve fiber
• 17
F is no t co rrect . 30fo c hose t his .
• 18
Vaso pressin (ADH} is released from the posterior pituitary, rath er than the j uxtaglomerular cells . ADH release is on ly stimulated by a substantial
• 19 loss of effective arterial blood vo lume. The main effect is regu lated by the V2 receptor, which mediates aquaporin insertion into the principal cells
• 20 on the renal collecting duct lead in g to increased water reabsorption . It also causes vasoconstriction, mediated by the V1 receptor.
Aquaporin Vasopressin Posterior pituitary Vasoconstriction Juxtaglomerular cell Collecting duct system Nephron Pituitary gland Blood volume
• 21
•
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Item: 15 of 27 ~. I • M k <:] t> al ~· ~
QIO: 2328 .l. ar Previous Lab 'lifllues
Next Notes Calculator
.. .. .. .. . .-... .. .- . .. .- .. .. .- .- ..
.. .- . .- .. .
1 angiotensin-converting enzyme to angiotensin II (AT II) . AT II has several effects, inclu d in g constricting of efferent arterioles and stimulating
2 aldosterone release.
Angiotensinogen Aldosterone Angiotensin Angiotensin-converting enzyme Renin Angiotensin II Angiotensin I Juxtaglomerular cell Enzyme Efferent arteriole
3
Arteriole Kidney liver
4
C is no t co rrect . 50/o c hose t his.
5
Atrial natriuretic peptide {ANP} is released from atrial myocytes in response to increased blood volume, which leads to d ilation of afferent renal
6 arterioles and constriciton of efferent renal arterioles. ANP has a natriuretic effect. It is not released in states of hypovolemia, therefore this is not
correct.
7
Atrial natriuretic peptide Hypovolemia Peptide Cardiac muscle Blood volume Myocyte Arteriole Atrium (heart) Kidney Afferent nerve fiber Efferent nerve fiber
8 Vasodilation
t
9
E is no t co rrect . 4 0fo c hose t his.
10 Angiotensin II (AT II) is produced from the conversion of angiotensin I by AC E in the pulm onary endothelium . Therefore, this answer is incorrect
11 as AT II is not produced by the j uxtaglomerular cells in the kidney. Furthermore, the ultimate response to severe blood loss is constriction of both
the afferent and efferent arterioles.
12 Angiotensin II Angiotensin Angiotensin I Juxtaglomerular cell Endothelium Efferent arteriole Arteriole Kidney Efferent nerve fiber
13 F is no t co rrect . 30/o c hose t his.

14 Vasopressin (ADH} is released from the posterior pituitary, rath er than the j uxtaglomerular cells . ADH release is on ly stimulated by a substantial
15 loss of effective arterial blood volume . The main effect is regu lated by the V2 receptor, which mediates aquaporin insertion into the principal cells
on the renal collecting duct lead in g to increased water reabsorption . It also causes vasoconstriction, mediated by the V1 receptor.
• 16 Aquaporin Vasopressin Posterior pituitary Vasoconstriction Juxtaglomerular cell Collecting duct system Nephron Pituitary gland Blood volume
• 17
• 18
Botto m Line :
• 19
When renal perfusion decrease (eg, hypovolemia), initially intrinsic mechanisms allow for maintenance of GFR. I n severe hypovolemia,
• 20 sympathetic and ren in -ang iotensin -a ldosterone systems are activated and afferent and efferent renal arteriole constriction occu rs .
Arteriole Hypovolemia Perfusion Kidney
• 21
6
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Item: 15 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1
FA17 p 558.1
2
3
4 I BP (JG cells)
5 I Na• delivery Acts at angiotensin II

6 vascular smooth muscle
I sympathetiC tone
7 IP,-receptorsl ,I
..----) Constricts efferent I FF to preserve renal functiOn (GFRl
8
artenole of glomerulus in low-volume states (ie. when RBF ~ )
9
~ B dyk' .
ACE ____.. ra 1111n Aldosterone
10 Renin I Na' channel insertion and - -+ Creates
breakdown
~ (adrenal cortex) I activity of Na'/K' pump; favorable Na·
11
Angiotensinogen
... Angiotensin I - -+ enhances K' and H· gradient for
12 excretion byway of principal Na' and Hp
13
a-intercalated cell H' ATPases
14 ...-? AOH
(posterior - - - - --+ I aquaporin insertion in - --+ Hp
15 pituitary) principal cells reabsorption
• 16
- --+ Na•. HC01· , and Hp reabsorption
• 17 1 PCT Na'/H' activity (can permit contraction alkalosis)
• 19
• 20 Renin Secreted by JG cells in response to 1 renal arterial pressure, t renal sympathetic discharge (~ 1
• 21 effect), and 1 N;c delivery to macula densa cells.
•
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1
FA17 p 553.1
2
Filtration Filtration fraction (FF) = C FR/ RP F. C FR can be estimated with creatinine
3
t\ormal FF = 20%. clearance.
4 Filtered load (m g/mi n) = CFR (m L!m in) RPF is best estimated with PAH clearance.
5 X plasma concentration (mg/m L). Prostaglandins D ilate Afferent arteriole (PO\)
6 ACE inhibitors C onstrict Efferent arteriole
(ACE)
7
PrOS1agland1ns preferentially
8 / Parietal layer of
NSAIDs -G-1 dilate afferent artenole
9 (i RPF. i GFR. so no ~ FFJ / Bowman capsule
10 ~ ~ov-Jroan space Podocytes

<:!?. IV1sc~allay~l
11 <;,..
12 ~~ . /
13 '6~
Juxtaglomerular~
14 cells I ~ ltc.c_...:,__ • • •
. I· . !·
15 - - + Excreted
Macula densa -------..
• 16
• 17
Distalrenal~ Reabsorbed ~ecreted
. 18 tubule Peritubular
• 19 capillary
Net filtration pressure
• 20 Endothelial cells_ / - = (Pc.c + rtas) - (Pas + rtG£)
• 21
n ...... _ .. _ •
•
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Item: 15 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
1 ~
2 r Angiotensin II preferentially
ACE inhibitors - { ; H I constricts efferent arteriole
3 (! RPF, i GFR. so i ff}
4
5 FA17 p 552.2
6
9
C FR = U.lllU1•Ill x V/P.lOll1.Ill = C.IIlli1.111
10 10
= Kr [(Pcc - Pss) - (7tcc- 7tss)J 4>
11 -c:c:...J-
·-=e
(CC =glomerular capillary; BS Bowman space.) = 8
12
7tss normally equals zero; Kr = filtration constant.
:
."'. -..
~o
o
E c:n
13 ., E 6
.!!l-
Normal C F R == 100 mL/min. 0..
14
15
• 16 creatinine is moderately sccrctccl by renal 2
• 17 tubules.
• 19
• 20 (mUmin}
• 21
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1
A 66-year-old male diagnosed with type 2 diabetes mellitus 15 years ago presents to his prima•·y care physician for a routine check-up. Over
2 the past 3 years his serum creatinine levels have increased from 1.3 to 2.2 mg/dl. In an effort to slow diabetes- induced damage to his
3 kidneys, he was sta•·ted on an angiotensin - converting enzyme inhibitor, but only has minimal change in his nephropathy. His current
laboratory values indicate:
4
Potassium: 5.5 mEq/l
5 Urine pH: 5.2
6 Sodium: 140 mEq/l
Bicarbonate: 18 mEq/l
7 Chloride: 110 mEq/l
8 Arterial blood pH: 7.33
Partial pressure of carbon dioxide: 40 mm Hg
9
10
Which of the following conditions does this patient most likely have?
11
12 :
A . Acute kidney injury
13
14 B. Hyperreninemic hyperaldosteronism
15 C. Type I renal tubular acidosis

• 16
D. Type II renal tubular acidosis
• 17
• 18 E. Type IV renal tubular acidosis
• 19
• 20
• 21
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1

3 Renal tubular acidosis (RTA ) is a disorder characterized by a non-anion gap,
hyperchloremic metabolic acidosis. His anion gap (calculated as [Serum Na+]- Type I Type II Type IV
4
([Serum cl-] + [Serum HC03-]) is 12, which is normal. In particular, this patient has
5 type IV RTA, which is marked by hyperkalemia, as opposed to hypokalemia in the Proximal
Distal
other types. Type IV RTA is also characterized by hypoaldosteronism, caused by either Location (collecting
(proximal Adrenal OR
6 convoluted collecting tubule
insufficient adrenal secretion of aldosterone or resistance to aldosterone in the renal tubule)
tubule)
7 collecting tubule. This leads to decreased Na+ reuptake in the distal convoluted tubule
and collecting duct and, therefore, decreased excretion of K~ into the urine. The
8 K• Low Low High
resulting hyperkalemia generates a shift in H+ to the extracellular fluid to maintain K ..
9 balance, thus producing a metabolic acidosis. Urinary pH is also low in type IV RTA Hypoaldosteronism
10 because hyperkalemia inhibits urinary ammonia excretion, leading to decreased Mechanism
NoW NoHC03 (low aldosterone
urinary buffering capacity. Clinically, hypoaldosteronism therefore manifests with secretion reabsorption secretion QB lack
11 of response)
elevated serum K+ levels. pH is also low in RTA type IV. Recall that 21 - hydroxylase
12 deficiency can manifest similarly, but it is not common in adults.
13 It should be noted that the most common causes of hypoaldosteronism are diabetic nephropathy and chronic tubulointerstitial nephropathies.
Angiotensin -converting enzyme inhibitors, spironolactone, trimethoprim, and heparin can similarly red uce aldosterone production.
14
Distal convoluted tubule Renal tubular acidosis Hyperkalemia Spironolactone Hypokalemia Metabolic acidosis Aldosterone Diabetic nephropathy Hypoaldosteronism
15
Anion gap Trimethoprim Enzyme Heparin Connecting tubule ACE inhibitor Angiotensin -converting enzyme Collecting duct system Ammonia Extracellular fluid PH
16 Urine Acidosis Congenital adrenal hyperplasia due to 21-hydroxylase deficiency Hyperchloremic acidosis Blood plasma Kidney disease 21-Hydroxylase
• 17 Diabetes mellitus Chloride Anion Bicarbonate Metabolism Adrenal gland Anatomical terms of location Nephron Chlorine Secretion Serum (blood) Kidney
• 18 A i s not co rrect . solo ch ose this.

• 19 Acute kidney injury is sudden decline in kidney function in a short period of time, typically measured as a significant rise in creatinine over a
patient's baseline. Although the patient's creatinine rose from 1.3 to 2.2 mg/dl, it was over a period of 3 years, which constitutes a chronic
• 20
progression. The changes in creatinine seen in acute kidney injury are seen within 1-2 days, not months or years .
• 21 Acute k dney injury Creatimne Kidney Renal function
•
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A is n ot co rrect. 50fo c h ose t his.
2 Acute kidney inj ury is sudden declin e in kidney function in a short period of time, typically measu red as a significant rise in creatinine ove r a
3 patient's baseline. A lthough the patient's creatinine rose from 1.3 to 2. 2 mg/ d l , it was ove r a period of 3 years, which constitutes a chronic
prog ression . The changes in creatinine seen in acute kidney inj ury are seen within 1-2 days, not months or years .
4
Acute kidney injury Creatinine Kidney Renal function
5
B is n ot co rrect. 4 0fo c h ose t his.
6 Hyperaldosteron ism likely would lead to metabolic alkalosis, not acidosis as seen in this patient, and would be accompanied by h y p o kalem ia.
7 Other common causes of alkalosis inclu de vomiting secondary to gastrointestinal acid loss, d iuretics (thiazides, loo p d iuretics), congenital
syndromes such as Bartter and Gitelman, and milk -alkali syndrome caused by in gestion of calcium antacids. Hyperren in em ic hyperaldosteronism
8 is seen when the renal vasculature is compromised, for exam ple, bilateral renal artery stenosis. A lthough d iabetic nephropathy typically affects
9 renal parenchyma, d iabetes is commonly seen with atherosclerotic d isease, which could cause this presentation in another patient.
Metabolic alkalosis Renal artery stenosis Diabetic nephropathy Hyperaldosteronism Thiazide Parenchyma loop diuretic Acidosis Diabetes mellitus Diuretic
10
Alkalosis Atherosclerosis Kidney disease Stenosis Vomiting Congenital disorder Circulatory system Calcium Metabolism Renal artery Kidney
11
C is n ot co rrect. 220/o c h ose t his.
12
Type I RTA is characterized by hypokalemia, not hyperkalemia as seen in this patient. It is caused by in effective H+-K + adenosine triphosphatase
13 pump in the renal collecting tubules, which prevents secretion of H+ ions, lead in g to the metabolic acidosis with low serum potassium . There is a
14 tendency for kidney stone formation because the urine is alkaline as a resu lt of the lack of H+ ions in the urine. Predom inant clinic features of type
1 RTA in infants and children are failure to thrive and g rowth retardation .
15 Kidney stone Hyperkalemia Hypokalemia Metabolic acidosis Urine Acidosis Kidney Collecting duct system Failure to thrive Blood plasma Alkalinity Potassium
16 Adenosine Serum (blood) Metabolism Secretion
• 17 0 is n ot co rrect. 250/o c h ose t his •

• 18 Type II RTA is characterized by hypokalemia, not hyperkalemia as seen in this patient. The metabolic acidosis in type II RTA is caused by
impaired bicarbonate reabsorption in the proximal tubule . It is typically observed in childhood with other features of Fanconi 's syndrome and can
• 19
lead to hypophosphatemic rickets and osteoma lacia.
• 20 Fanconi syndrome Hyperkalemia Osteomalacia Hypokalemia Rickets Metabolic acidosis Proximal convoluted tubule Acidosis Bicarbonate
X-linked hypophosphatemia Nephron Anatomical terms of location Metabolism
• 21
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1 • Hyperaldosteron ism likely would lead to metabolic alkalosis, not acidosis as seen in this patient, and would be accompanied by hypokalem ia. •
Other common causes of alkalosis inclu de vomiting secondary to gastrointestinal acid loss, d iuretics (thiazides, loo p d iuretics), congenital
2 syndromes such as Bartter and Gitelman, and m ilk -alkali syndrome caused by in gestion of calcium antacids. Hyperren in em ic hyperaldosteron ism
3 is seen when the renal vasculature is compromised, for exam ple, bilateral renal artery stenosis. A lthough d iabetic nephropathy typically affects
renal parenchyma, d iabetes is commonly seen with atherosclerotic d isease, which could cause this presentation in another patient.
4 Metabolic alkalosis Renal artery stenosis Diabetic nephropathy Hyperaldosteronism Thiazide Parenchyma loop diuretic Acidosis Diabetes mellitus Diuretic
5 Alkalosis Atherosclerosis Kidney disease Stenosis Vomiting Congenital disorder Circulatory system Calcium Metabolism Renal artery Kidney
6 C is not correct. 220/o chose this.

7 Type I RTA is characterized by hypokalemia, not hyperkalemia as seen in this patient. It is caused by in effective H+-K + adenosine triphosphatase
pump in the renal collecting tubules, which prevents secretion of H+ ions, lead in g to the metabolic acidosis with low serum potassium . There is a
8
tendency for kidney stone formation because the urine is alkaline as a resu lt of the lack of H+ ions in the urine. Predom inant clinic features of type
9 1 RTA in infants and children are failure to thrive and g rowth retardation.
Kidney stone Hyperkalemia Hypokalemia Metabolic acidosis Urine Acidosis Kidney Collecting duct system Failure to thrive Blood plasma Alkalinity Potassium
10
Adenosine Serum (blood) Metabolism Secretion
11
0 is not correct. 250/o chose this.
12
Type II RTA is characterized by hypokalemia, not hyperkalemia as seen in this patient. The metabolic acidosis in type II RTA is caused by
13 impaired bicarbonate reabsorption in the proximal tubule . It is typically observed in childhood with other features of Fanconi's syndrome and can
14 lead to hypophosphatemic rickets and osteoma lacia.
Fanconi syndrome Hyperkalemia Osteomalacia Hypokalemia Rickets Metabolic acidosis Proximal convoluted tubule Acidosis Bicarbonate
15
X-linked hypophosphatemia Nephron Anatomical terms of location Metabolism
16
• 17
Bottom Line:
• 18
Rena l tubular acidosis (RTA} is a hyperchloremic metabolic acidosis. There are three major types of RTA : Type I RTA has decreased d istal H+
• 19
secretion and hypokalemia; type II has impaired proximal HCo3- reabsorption and hypokalemia; and type IV is hypoaldosteronism, lead in g to
• 20 hyperkalem ia .
Hypokalemia Metabolic acidosis Renal tubular acidosis Hypoaldosteronism Hyperchloremic acidosis Acidosis Metabolism Anatomical terms of location Kidney
• 21
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FA17 p 562.1
2
Renal tubular acidosis A disorder of the renal tubules that leads to normal anion gap (hyperchloremic} metabolic acidosis.
3 RTA TYPE NOTES
4 Distal renal tubular Urine pH > 5.5. Defect in abil ity of a intercalated cells to secrete H+ .... no new HC0 3- is
5 acidosis (type 1) generated .... metabolic acidosis. Associated with hypokalemia, t risk for calcium phosphate
6 kidney stones (due to t urine pH and t bone turnover}.
7 Causes: amphotericin B toxicity, analgesic nephropathy, congenital anomal ies (obstruction) of
urinary tract.
8
9
Proximal renal tubular Urine pl"i < 5.5. Defect in PCT HC03- reabsorption .... t excretion ofliC03- in urine and
acidosis (type 2) subsequent metabol ic acidosis. Urine is acidified by a-intercalated cells in collecting tubule.
10
Associated with hypokalemia, t risk for hypophosphatemic rickets.
11 Causes: Fanconi srnclrome and carbonic anhydrase inhibitors.
12 Hyperkalemic renal Urine pH < 5.5. Hypoaldosteronism .... hyperkalemia .... l H3 synthesis in PCT .... l I H4+
13 tubular acidosis excretion.
14 (type 4) Causes: l aldosterone production (eg, diabetic hyporcninism, ACE inhibitors, ARBs, NSAIDs,
15 heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (eg, K+-sparing diuretics,
nephropathy clue to obstruction, TMP/SMX).
16
• 17
• 18 FA11 p 561 .2
• 19 Acidosis and alkalosis

• 20
Check arterial pH
• 21
• n~~7~E\ I n!-1.,. 7 .ac;; •
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QIO: 2360 ..L Prev ious Next Lab fli!ltues Notes Cal culat o r
1 FA17 p 555.1
2
Nephron physiology
3
4
5 l J lnCt<SWJm·
blood
6
7
8
9
10
11
12
13 Early OCT-reabsorbs 'a+, CJ- . Makes urine
14 ful ly dilute (hypotonic).
( PTH- t Ca 2+fNa+ exchange ..... Ca 2+
15
reabsorption.
16 5-10% Na+ reabsorbed.
Early PCT -con lains brush border.
• 17 Reabsorbs all glucose and amino acids and
most I IC03 , Ia • , CJ-, PO/-, K+, H20,
. 18
• 19
and uric acid. Isotonic absorption. Generates Lumen-
urine
l
.
Collecung
tubule
J lnterstotoum-
b4ood
and secretes H3, which enables the kidney a- ~~~~=*--
Prooopat cell
• 20 to secrete more 1-1 +.
• 21
•
PTTI- inhibits N;r'iP0-13- cotransport
- Of'"\ l- -~ ·--- ...:- ....
. . : ::-. -•o
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1
A 32 - year -old female presents to her physician for some advice on fluid replacement during and after running a marathon . She has no known
2 medical history and does not take any regular medications. She has no known allergies and she denied any family history of cardiac diseases,
3 including sudden cardiac death. On examination, blood pressure is 120/70 mm Hg, heart rate 65/minute, and oxygen saturation is normal.
Auscultation with a stethoscope shows no murmurs, and there is no palpable left ventricular apical impulse.
4
5
If this patient drank an excessive amount of pure distilled water after the marathon, which of the following effects could be seen?
6
:
7 A. Decreased urine osmolarity
8
B. Increased aquaporin transport in the distal tubule and collecting duct
9
C. Increased hormonal secretion from the posterior pituitary
10
11 D. Increased plasma osmolarity
12 E. Stimulation of osmoreceptors in the hypothalamus

13
14
15
16
• 17
• 18
• 19
• 20
• 21
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2
Th e correct a n s w e r is A. 6 50/o ch ose this.
3 During a marathon, ADH is secreted from the posterior pituitary to conserve volume. It inserts aquaporin channel into the collecting duct to
4 increase water resorption from urine. In this runner, rapid ingestion of a large volume of free water can lead to hyponatremia. If the change in
plasma osmolarity is rapid, it can cause a potentially fatal cerebral edema when fluid moves from the extracellular to the intracellular fluid
5 compartment. To maintain plasma osmolarity, ADH release is inhibited, causing fewer aquaporin channels to be inserted in the collecting duct
6 and resulting in less water resorption from urine, reduced urine osmolarity, and increased urine volume. The half- life of ADH is 24 minutes.
Hyponatremoa Aquaporn Osmotic concentration Cerebral edema Posterior pito ;ta f I ace lular fluod Collecting duct system Blood plasma Half- "fe ur·ne
7
Vasop essin Pituitary gland Edema Plasma osmolality Intracellular Extracellular
8
B is not correct . 100/o chose this.
9
Inhibition of ADH secretion has t he effect of reducing the number of aquaporin molecules that are mobili zed in t he principal cells of the late distal
10 tubule and collecting duct. As a result, wat er resorption is decreased and the urine is diluted.
Distal convoluted tubule Aquaporin Collecting duct system Vasopressin Urine Secretion Nephron Tubule Anatomical terms of location
11
C is not co rre ct. 70fo c hose t his .
12
ADH and oxytocin are the two hormones secret ed by the posterior pituitary. Neither hormone is secret ed in response to volume expansion and
13 decreased plasma osmolarity, an d ADH secretion would specifically be decreased.
14 Oxytocin Posterior pituitary Osmotic concentration Blood plasma Hormone Pituitary gland Plasma osmolality Vasopressin
15 D is not co rre ct. 6 0/o c hose this .

16 When ingested water is d istribut ed t hroughout t he bod y's fluids, plasma osmolarity decreases due to d ilution of osmotic particles. This decreases
ADH secretion from the posterior pitu it ary, facilitating excretion of excess water.
17 Posterior pituitary Osmotic concentration Blood plasma Pituitary gland Plasma osmolality vasopressin Osmosis Excretion Secretion
. 18
E is n ot co rre ct. 1 20/o ch ose this .
• 19 In hypo- osmolar states, the osmoreceptors of the hypothalamus are inhibited, resulting in the suppression of thirst, as well as inhibited secretion
• 20 of ADH .
Hypothalamus Osmoreceptor
• 21
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.- ... .- .. .. .. .. .. ..
.- . .- .- ..
. .- .. -
1 Hyponatremia Aquaporin Osmotic concentration Cerebral edema Posterior pituitary Intracellular fluid Collecting duct system Blood plasma Half-life Urine
2 Vasopressin Pituitary gland Edema Plasma osmolality Intracellular Extracellular
3 B is no t co rrect. 100/o c hose this.

4 I nhibition of ADH secretion has the effect of reducing the number of aquaporin molecu les that are mobilized in the principal cells of the late d istal
tubule and collecting duct. As a resu lt, water resorption is decreased and the urine is d iluted .
5
Distal convoluted tubule Aquaporin Collecting duct system Vasopressin Urine Secretion Nephron Tubule Anatomical terms of location
6
C is no t co rrect. 70/o c hose this.
7
ADH and oxytocin are the two hormones secreted by the posterior pituitary. Neither hormone is secreted in response to vo lume expansion and
8 decreased plasma osmo larity, and ADH secretion would specifically be decreased .
Oxytocin Posterior pituitary Osmotic concentration Blood plasma Hormone Pituitary gland Plasma osmolality Vasopressin
9
0 is no t co rrect. 6 0/o c hose this.
10
When in gested water is d istributed throughout the body 's fluids, plasma osmo larity decreases due to d ilution of osmotic particles. This decreases
11 ADH secretion from the posterior pituitary, facilitating excretion of excess water.
12 Posterior pituitary Osmotic concentration Blood plasma Pituitary gland Plasma osmolality Vasopressin Osmosis Excretion Secretion
13 E is no t co rrect. 1 20/o c hose this.
14 I n hypo-osmolar states, the osmo receptors of the hypothalamus are inhibited, resu lting in the suppression of thirst, as well as inhibited secretion
of ADH .
15 Hypothalamus Osmoreceptor
16
17
Bo tto m Line :
• 18
Ra pid in gestion of water after significant vo lume contraction can resu lt in hyponatremia, which causes the kidneys to d ilute the urine. Ra pid
• 19 changes in osmo lality can cause cerebral edema.
Hyponatremia Cerebral edema Urine Edema Osmolality Kidney Volume contraction
• 20
• 21
•
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1 When ingested water is distributed throughout the body's fluids, plasma osmolarity decreases due to dilution of osmotic particles. This decreases
2 ADH secretion from the posterior pituitary, facilitating excretion of excess water.
Posterior pituitary Osmotic concentration Blood plasma Pituitary gland Plasma osmolality vasopressin Osmosis Excretion Secretion
3
E i s n o t correct . 120/o ch ose this .
4
In hypo-osmolar states, the osmoreceptors of the hypothalamus are inhibited, resulting in the suppression of thirst, as well as inhibited secretion
5 of ADH.
Hypothalamus Osmoreceptor
6
7
8 B ottom Line:
9 Rapid ingestion of water after significant volume contraction can result in hyponatremia, which causes t he kidneys to dilute the urine. Rapid
changes in osmolality can cause cerebral edema.
10
Hyponatremia Cerebral edema Urine Edema Osmolality Kidney Volume contraction
11
12
13 lill;fi£1!•] fo r y ear: 20 1 7 '"
FIRST AID FAC T S
14
15
FA17 p 552.1
16
Renal clearance ex= UXV/Px = ,·olume of plasma from which the ex= clearance of X (mL/min).
17
substance is completely cleared per unit lime. Ux =urine concentration of X (cg, mg/mL).
. 18 If ex< GFR: net tubular reabsorption of X. P, =plasma concentration of X (eg, mg/mL).
. 19 If e, >CPR: net tubular secretion of X. V =urine Aow rate (mL/m in).
• 20 If e, = GFR: no net secretion or reabsorption .
. 21
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A 45- year -old woman undergoes a routin e complete blood cell count and is found to have a WBC count of 156,000/mm3, with 96%
2 granulocytes. A basic metabolic panel is within normal limits. She undergoes bone marrow biopsy and is diagnosed with acute myelogenous
3 leukemia. She immediately begins chemoth erap y with a course of methotrexate and cytarabine. Four days after initiating therapy, she
presents to her physician with complaints of fatigue, nausea, vomiting and muscle cramps. In addition, she r eports barely making any urine despite
4 taking more than adequate amounts of fluid. laboratory tests show:
5
Na+: 139 mEq/ l
6 K+: 5.6 mEq/ l
7 cl-: 96 mEq/ L
HC03-: 18 mEq/ l
8 Blood urea nitrogen: 72 mg/ dl
9 Creatinine: 3.3 mg/ dl
ca 2+: 7.2 mg/ dl
10 P04 : 5.5 mg / dl
11
12 Which of the following medications could have prevented this patient's current condition?
13
:
14 A. Allopurinol
15
B. Colchicine
16
C. Furosemide
17
• 18 D . Mesna
• 19 E. Pyridoxine
• 20
• 21
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2
The correct answer is A. 4 30/o chose this.
3 This patient is presentin g with signs of acute kidney inj ury, with oligu ria, elevated blood urea nitrogen and creatinine and hyperkalemia. The
4 most likely cause in this case, due to her leu kem ia and administration of cytotoxic chemotherapy, is tumor lysis syndrome. This also inclu des
symptoms of metabolic acidosis (as evidenced by this patient's anion gap and decreased HCo3- level), hypocalcemia, and hyperphosphatemia.
5 When rapid ly d ivid in g leu kem ic cells d ie, they dum p their cellular contents into the bloodstream, inclu d in g large amounts of ph osphate and
6 purin es derived from their DNA. These purin es are metabolized and eventually are secreted in the form of uric acid . However, this massive
amount of uric acid, ph osphate, and other metabolites overwh elms the kidney, and resu lts in acute kidney inj ury. One of the key methods of
7 protectin g a patient's kidneys from tumor lysis syndrome is the administration of allopurinol (a d ru g also used in the treatment of gout) with
8 chemotherapy . This d ru g inhibits the enzyme xanth in e ox idase, which is respons ible for the final step of converting purin es to uric acid . The
prevention of uric acid synthesis spares this load on the kidney and can prevent renal failure .
9 Xanthine oxidase Tumor lysis syndrome Hyperkalemia Hypocalcaemia Allopurinol Oliguria Hyperphosphatemia Blood urea nitrogen Uric acid Metabolic acidosis
10 Urea Creatinine Enzyme Gout Xanthine Acute kidney injury leukemia Purine Chemotherapy Kidney Anion gap Acidosis Cytotoxicity Neoplasm Phosphate Anion
11 DNA Nitrogen Metabolism lysis Circulatory system Metabolite
12 B is not correct. 100/o chose this.

13 Co lchicine is an anti - inflammatory d ru g that works by inhibiting neutrophil chemotaxis. It is used to treat gout and other inflammatory conditions.
It is not used in the prevention of tumor lysis syndrome.
14 Neutrophil Colchicine Tumor lysis syndrome Chemotaxis Gout Anti-inflammatory Neoplasm lysis
15
C is not correct. 200/o chose this.
16 Furosemide is a loo p d iuretic used in the treatment of hypertension, congestive heart failure, and other fluid-overload states. It leads to rapid
17 decreases in fluid volume . The administration of furosemide to this patient would almost certainly have lead to dehyd ration, which would worsen
the tumor lysis syndrome. Part of adequate prevention and treatment of tumor lysis syndrome inclu des adequate hydration with intravenous
18 fluids, which is physiolog ically the opposite of furosemide therapy . I n addition, furosemide may cause an increase in uric acid, serum BUN, and
• 19 creatinine levels. You can remem ber furosemide 's side effects with the mnemonic OH DANG! (Ototoxicity, Hypokalemia, Dehydration, A llergy,
Nephritis (interstitial}, Gout) .
• 20 loop diuretic Furosemide Tumor lysis syndrome Diuretic Uric acid Heart failure Congestive heart failure Creatinine Hypertension Intravenous therapy
• 21 Blood urea nitrogen Dehydration Blood plasma Hypokalemia Neoplasm Interstitial fluid Mnemonic Adverse drug reaction Serum (blood)
•
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1
C is no t co rrect. 200/o c ho se this.
2 Furosemide is a loop d iuretic used in the treatment of hypertension, congestive heart failure, and other fluid-overload states. It leads to rapid
3 decreases in fluid volume . The administration of furosemide to this patient would almost certainly have lead to dehyd ration, which would worsen
the tumor lysis syndrome. Part of adequate prevention and treatment of tumor lysis syndrome inclu des adequate hydration with intravenous
4 fluids, which is physiologically the opposite of furosemide therapy . I n addition, furosemide may cause an increase in uric acid, serum BUN, and
5 creatinine levels. You can remem ber furosemide 's side effects with the mnemonic OH DANG! {Ototoxicity, Hypokalemia, Dehyd ration, A llergy,
Nephritis (interstitial}, Gout).
6 loop diuretic Furosemide Tumor lysis syndrome Diuretic Uric acid Heart failure Congestive heart failure Creatinine Hypertension Intravenous therapy
7 Blood urea nitrogen Dehydration Blood plasma Hypokalemia Neoplasm Interstitial fluid Mnemonic Adverse drug reaction Serum (blood)
8 Dis no t co rrect. 170/o c ho se this.

9 This patient's presentation is suggestive of tumor lysis syndrome. Mesna is not effective for the prevention nor treatment of this condition . Mesna
is a chemoprotective agent used with cyclophosphamide to prevent hemorrhagic cystitis. It is not used for cytarabine nor methotrexate.
10
Chemoprotective agent Tumor lysis syndrome Methotrexate Cyclophosphamide Cytarabine Hemorrhagic cystitis Mesna Urinary tract infection Neoplasm lysis
11
E is no t co rrect. 100/o c ho se this.
12
Pyridoxin e (vitamin B6 ) is an essential cofactor involved in transamination and decarboxy lation reactions. It is requ ired in the synthesis of niacin
13 from tryptophan . It is often administered in supplementation with ison iazid therapy (to treat tuberculosis) to prevent periph eral neuropathy. It is
not useful in the prevention of tumor lysis syndrome.
14
Isoniazid Niacin Cofactor (biochemistry) Pyridoxine Peripheral neuropathy Tryptophan Tuberculosis Transamination Decarboxylation Neoplasm
15
16
Bo tto m Line:
17
Tumor lysis syndrome inclu des the symptoms of acute renal failure, accompanied by hypocalcemia, hyperphosphatemia, and metabolic
18 acidosis. It resu lts from the dum pin g of intracellular contents of tumor cells after beg innin g cytotoxic therapy . It can be prevented with the use
• 19 of allopurinol, a xanth in e ox idase inhibitor typically used in the treatment of gout.
Xanthine oxidase Tumor lysis syndrome Hypocalcaemia Allopurinol Hyperphosphatemia Metabolic acidosis Xanthine oxidase inhibitor Gout Xanthine
• 20 Acute kidney injury Acidosis Neoplasm Cytotoxicity Chemotherapy Intracellular Kidney Metabolism lysis
• 21
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1 FA17 p 457.2
2 Gout drugs
3 Chronic gout drugs (preventive)
4 Allopurinol Competiti,·e inhibitor of xanthine oxidase. Diet - - Purines Nucleic adds
5 l conversion of hypoxanthine and xanthine to
6 urate. AJso used in lymphoma and leukemia
Hypoxanthine
to pre,·ent tumor lysis-associated urate
7 Xanthine
nephropathy. t concentrations of uathioprine
8 oxidase )
and 6-~ I P (both normally metabolized by Xanthine - Allopurinol
9 xanthine oxidase). - febuxostat
Xanthine
10 Febuxostat Inhibits xanthine oxidase. oxidase
11 Plasma - - Urate crystals - - Goot

Pegloticase Recombinant uricase that catalyzes metabolism uric acid depoSited
12 of uric acid to allantoin (a more \\aler-soluble in JOints
13 product).
14 Probenecid Inhibits reabsorption of uric acid in proximal Tubular
~
convoluted tubule (also inhibits secretion of reabsorption
15
penicill in). Can precipitate nric acid ca lc11li. Probenecid and
16
high-dose salicylates
Acute gout drugs
17 ~t----=,....---- Tubular
~ secretion
18 NSAIDs Any full-dose NSAID (cg, naproxcn,
• 19
indomethacin). Avoid salicylatcs (may decrease Diuretics and
Urine low-dose saUcylates
uric acid excretion, particularly at low doses) .
• 20
Glucocorticoids OraJ, intra-articular, or parenteral.
• 21
• ,.._._&.. :-=--
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1 FA17 p 440.1
2 Gout
3 FINDINGS Acute inflammatory monoarthritis caused by precipitation of monosodium urate crystals in
4 joints rJ. Ytore common in males. Associated with hyperuricemia, which can be caused by:
5 Underexcretion of uric acid (90% of patients)-largely idiopathic, potentiated by renal failure;
can be exacerbated by certain medications (eg, thiazide diuretics).
6
Q,·erproduction of uric acid (10% of patients)- Lesch-1\:yhan syndrome, PRPP e"\cess, t cell
7
turnover (eg, tumor lysis S) ndrome), von Gierke disease.
8 e
Crystals are needle shaped and birefringent under polarized light (yellow under parallel light,
9 blue under perpendicular light ).
10 SYMPTOMS Asymmetric joint distribution. Joint is swollen, red, and painful. Classic manifestation is painful
11 MTP joint of big toe (podagra). Tophus formation (often on external ear, olecranon bursa,
12
or Achilles tendon). Acute attack tends to occur after a large meal with foods rich in purines
(eg, red meat, seafood), trauma, surgery, dehydration, diuresis, or alcohol consumption (alcohol
13
metabol ites compete for same excretion sites in kidney as uric acid -+ l uric acid secretion and
14 subsequent buildup in blood).
15
TREATMENT Acute: 1 SAIDs (eg, indomethacin), glucocort icoids, colchici ne.
16 Chronic (preventive): xa nthine oxidase inhibitors (eg, allopurinol, febuxostal).
17 ' .;;;?~ ~~··"!·· ... ~ ;.-,-.
~""'~ ~ •.. .'L.,. .
18 n ...
, ~:"·)~·.•~.!'J~· ~-~~
... ~~ .. ~~rt
. ·
• 19 {;-~~~ ilf;t••J.,
'.. ';<r.,: ~-
.:"';
• 20 ~~~-
• 21
·'t.:-=><
,
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Item: 18 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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1
2 FA17 p 571 .2
3 Acute kidney injury Acute kidney injury is defined as an abrupt decline in renal function as measured by t creatinine
4 (acute renal failure) and t BU N or by oliguria/anuria.
5 Prerenal azotemia Due to l RBF (eg, hrpotension) - l CFR. l\a+f H20 and BUN retained by kidney in an attempt to
6 consen·e volume - t BUN/creatinine ratio (BU is reabsorbed, creatinine is not) and l FE'-Ja·
7 Intrinsic renal failure Cenerallr due to acute tubular necrosis or ischemia/toxins; less commonly due to acute
8 glomerulonephritis (eg, RPC l, hemol} tic uremic syndrome) or acute interstitial nephritis.
9
In AT~. patchy necrosis - debris obstructing tubule and Auid backAow across necrotic tubule
- l GFR. Urine has epithelial/granular casts. BUN reabsorption is impaired - l BUI\/creatinine
10
ratio and t FENa·
11
Postrenal azotemia Due to outAow obstruction (stones, BPI I, neoplasia, congenital anomalies). Develops only with
12 bilateral obstruction.
13
Pre renal Intrinsic renal Postrenal
14
15
Urine osmolality > 500 < 350 < 350
(mOsm/kg)
16
Urine Na+ (mEq/L) <20 >40 >40
17
FENa <I% >2% < 1% (mild)
18
> 2% (severe)
. 19
Serum BUN/Cr > 20 < 15 Varies
• 20
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1
An 83-year-old man visits his doctor for a checkup, and he is found to have hypertension. The physician wants to avoid the use of ~-blockers
2 and a-blockers with this patient because of the unpleasant adverse effects of these medications on the elderly, so he prescribes an
3 angiotensin-converting enzyme inhibitor instead. This drug is known to decrease the formation of angiotensin II in the body.
4
Aside from increasing aldosterone levels, how else does angiotensin II directly act?
5
6
A. Increases acid reabsorption in the proximal tubule
7
8 B. Increases glomerular filtration rate
9 C. Increases levels of bradykinin

10
D. Increases renal plasma flow
11
E. Increases sodium reabsorption in the distal tubule
12
13
14
15
16
17
18
. 19
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Item: 19 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 3571 ..L ar Prev ious Next Lab fli!ltues Notes Calculat o r
& &
1
2 Th e correct an swer is B. 550/o chose this.

3 Angiotensin II is responsible for vasoconstriction and the release of aldosterone, but this key regulator has many other functions. It is known to
4 cause the kidneys to increase the glomerular filtration rate through constriction of the efferent arteriole. This also leads to reabsorption of
bicarbonate in the proximal tubule and simultaneous secretion of acid into the tubular fluid.
5 Effe ent arte• ole Arter;ole A1dosterone Angiotensin Proximal convoluted tubule Vaso• o st 1ctJon Rena function Angiotensin II Tubular fluid Glomerulus (kidney)
6 Glome• ulus 'id1 ey Nephron Bicarbonate
7 A i s not correct. 60/o chose this.
8 Ang iotensin II would cause the increased secretion (not absorption) of acid by stimulating Na+JH+ exchange.
Ang•otensm II Angiotensin Absorption (chemistry) Secretion
9
Cis not correct. 150/o chose this.
10
Angiotensin II breaks down bradykinin and would consequently decrease bradykinin levels. This is actualy why angiotensin-converting enzyme
11 (ACE) inhibitors can lead to unusually high levels of bradykinin in the body and cause patients to develop cough as an adverse effect.
12 Bradykinin Angiotensin Angiotensin II Angiotensin-converting enzyme Enzyme ACE inhibitor Cough Adverse effect
13 D is not correct. 11 Ofo c hose this.
14 Angiotensin II constricts the efferent arteriole, which leads to a decrease in renal plasma flow an d an increase in the glomerular filtration rate.
However, a constriction of either the afferent arteriole or the efferent arteriole will lead to a decrease in renal plasma flow.
15 Efferent arteriole Arteriole Angiotensin II Afferent arterioles Angiotensin Renal function Blood plasma Glomerulus Glomerulus (kidney) Renal blood flow Kidney
16 E is not correct. 1 30/o ch ose this.

17 Angiotensin does not directly act on the distal tubule, although it does stimulate aldosterone, which acts to increase sodium reabsorption in the
distal tubule.
18
Aldosterone Distal convoluted tubule Angiotensin Sodium Nephron Reabsorption Anatomical terms of location Tubule Renal sodium reabsorption
19
• 20
Bottom Lin e :
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Item: 19 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
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bicarbonate in the proximal tubule an d simultan eous secretion of acid into the tubular fluid. &
Efferent arteriole Arteriole Aldosterone Angiotensin Proximal convoluted tubule Vasoconstriction Renal function Angiotensin II Tubular fluid Glomerulus (kidney)
2
Glomerulus Kidney Nephron Bicarbonate
3
A i s n o t correct . 6 0fo ch ose this.
4
Angiotensin II would cause the increased secretion (not absorption) of acid by stimulating Na+f H+ exchange.
5 Angiotens•n II Angiotensin Absorption (chemistry) Secretion
6 C i s not co rrect . 1 5 0/o chose t his.

7 Angiotensin II breaks down bradykinin and would consequently decrease bradykinin levels. This is actualy why angiotensin -converting enzyme
(ACE) inhibitors can lead to unusually high levels of bradykinin in the body and cause patients to develop cough as an adverse effect.
8
Bradyl•inon Angiotensin Angiotensin II Angiotensin-converting enzyme Enzyme ACE innibitor Cough Adverse effect
9
0 i s not correct. 11 Ofo chose t his .
10
Angiotensin II constricts the efferent arteriole, which leads to a decrease in renal plasma flow and an increase in t he glomerular filtration rate.
11 However, a constriction of either the afferent art eriole or the efferent arteriole will lead to a decrease in renal plasma flow.
Efferent arteriole Arteriole Angiotensin II Afferent arterioles Angiotensin Renal function Blood plasma Glomerulus Glomerulus (kidney) Renal blood flow Kidney
12
E is not correct. 1 30/o c hose this.
13
Angiotensin does not directly act on th e d istal tubule, although it does stimulate aldosterone, which acts t o increase sod ium reabsorption in the
14 distal tubule.
15 Aldosterone Distal convoluted tubule Angiotensin Sodium Nephron Reabsorption Anatomical terms of location Tubule Renal sodium reabsorption
16
17 Bottom Lin e:
18 Angiotensin II increases the levels of aldosterone, causes constriction of the efferent a1·teriole leading to an increase in GFR, and breaks down
19 bradykinin.
Efferent arteriole Bradykinin Arteriole Aldosterone Angiotensin Angiotensin II Efferent
• 20
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FA17 p 558.1
2
3
4 I BP (JG cells)
5 I Na• delivery Acts at angiotensin II

6 vascular smooth muscle
I sympathetiC tone
7 -receptors)
Constricts efferent I FF to preserve renal functiOn (GFRI
8
artenole of glomerulus 1n low-volume states (ie. when RBF ~ I
9
~ B dyk'.
ACE ____.. ra 1r11n Aldosterone
10 Renin t Na' channel insertion and - -+ Creates
breakdown
~ (adrenal cortex) t activity of Na'/K' pump; favorable Na·
11 i'
Angiotensinogen Angiotensin I - -+ enhances K' and H· gradient for
12 excretion by way of principal Na' and Hp
13 cell K' channels and reabsorption
a-intercalated cell H' ATPases
14 ...-~ AOH
_ _ _ _ _ _,.. t aquaporin insertion in _ ___. H 0
15 (posterior 2
pituitary) principal cells reabsorption
16
- --+ Na•. HC01· , and Hp reabsorption
17 1 PCT Na'/H' activity (can permit contraction alkalosis)
18 Stimulates hypothalamus ---+ Thirst
19
• 21 effect), and l N~c delivery to macula densa cells.
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2 FA17p577.1
3 Angiotensin- Captopril, enalapril, lisinopril, ramipril.

4 converting enzyme
5 inhibitors
6 MECHANISM Inhibit ACE - l AT II - l CFR b) prc,enting
7
constriction of efferent arterioles. f renin due
to loss of negati,·e feedback. Inhibition of CE
8
also prevents inacti\'ation of brad) kinin, a
9 potent vasodilator.
10
CLINICAL USE Hypertension, IIF (l mortality), proteinuria, In chronic kidney disease (eg, diabetic
11 diabetic nephropathy. Pre,ent unfmorable nephropathy), ' intraglomerular pressure,
12 heart remodeling as a result of chronic slowing CB.\11 thickening.
13 hypertension.
14 ADVERSE EFFECTS Cough, Angioedema (due to f bradykinin; Captopril's CATC llll.
15
contraindicated in Cl esterase inhibit·or
deficiency), Teratogen (fe tal renal
16
ma lfo rmations), f C reatinine (l CFR),
17 llyperkalemia, and llypotension . Used with
18 caution in bilateral renal artery stenosis
19 because ACE inhibitors will further ' CFR
• 20 - renal failure .
• 21
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1
A 60-year-old homeless alcoholic man is brou ght to the emergency department by an acquaintance from th e sh elter in which he is staying .
2 The acquaintance states that the patient has been complaining of a persistent and worsening productive cou gh lasting for 2 weeks,
3 headache, lack of appetite, and vomiting. The patient is clearly disoriented and drifts in and out of consciousn ess. Physical examination shows
a disheveled, malnourished man who is arousable, but incoherent. He is normocephalic, with no palpable cervical lymph nodes and no jugular
4 venous distention . His heart sounds are normal. Crackles are heard in the right lower lung fields. His abdom en is nondistended and nontender.
5 Clubbing, cyanosis, and edema are not present. A blood metabolic panel reveals a serum sodium level of 110 m Eq/ l and a plasma osmolality of 265
mOsm/l. Plasma cortisol levels are in the normal range.
6
7
Which of the following best explains his symptoms?
8
:
9 A. Addison disease-associat ed hyponat remic volume contraction
10
B. Central diabetes insipidus
11
12 C. Hepatic cirrhosis
13 D. Nephrogenic diabetes insipid us

14
E. Syndrome of inappropriate ADH secretion
15
16
17
18
19
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2 The correct answer is E. 580/o chose this.

3 The syndrome of inappropriate ADH secretion (S IADH } is a d isorder characterized by abnormally high ADH concentrations, causing water
retention that leads to hyponatremia and decreased plasma osmo larity. The causes include pulmonary d isease, ectopic production secondary to
4
malignancy, and CNS d isorders (such as men in g itis, brain abscess, or trauma) . I n any scenario manifesting in an obtun ded alcoholic, aspiration
5 pn eumon ia should be at the top of the d ifferential d iagnosis. A lthough it is not the most common cause, pn eumon ia can lead to SIADH . I n this
case, findings such as a normal cortisol level and no edema on physical exam ination enable us to reduce the list of potential d iagnoses. It should
6
be noted that although neoplasms are the classic teaching exam ple, adverse effects of d ru gs and central nervous system and pulm onary
7 d isturbances are more common causes of SIADH .
Hyponatremia Brain abscess Cortisol Aspiration pneumonia Central nervous system Osmotic concentration Meningitis Abscess Pneumonia Vasopressin Edema
8
Cancer Differential diagnosis Neurodegeneration Neoplasm Malignancy Blood plasma Nervous system Physical examination Brain Secretion Alcoholism
9
Human brain Major trauma
10
11
I n the setting of hyponatremia, Add ison d isease must be d istingu ished from syndrome of inappropriate ADH secretion . A lthough tuberculosis is
12 classically a common cause of adrenal insufficiency, the cause of Add ison d isease remains primarily an autoimmune ph enomenon . This patient's
normal cortisol level eliminates Add ison d isease as a poss ibility.
13
Addison' s disease Hyponatremia Cortisol Adrenal insufficiency Tuberculosis Vasopressin Autoimmune disease Autoimmunity Secretion
14
B is not correct. 8 0/o cho se this.
15
Central d iabetes insipidus (DI ) would cause polyuria and rapid dehyd ration . A patient's basic metabloic pan el would show hypernatremia (> 145
16 m Eq/ L} and an increased plasma osmo lality (> 295 mOsm/kg). Add itiona lly the patient would likely show signs of volume contraction such as d ry
mucous membranes. Common causes of central DI include pituitary tumor, autoimmune conditions, trauma, surgery, ischem ic encephalopathy,
17
and id iopathic conditions. ADH is decreased in central DL The water deprivation test can be used to aid in d iagnosis and would show g reater than
18 50% increase in urine osmo lality after administration of ADH analog .
Hypernatremia Polyuria Diabetes insipidus Neurogenic diabetes insipidus Dehydration Diabetes mellitus Blood plasma Plasma osmolality Urine Osmolality
19
Pituitary tumour Vasopressin Pituitary gland Idiopathy Autoimmunity Neoplasm Ischemia
20
C is no t co rrect. 140/o cho se this .
• 21
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Item: 20 of 27 ~. I • M k <:] t> al ~· ~
1 •
Central d iabetes insipidus (DI ) would cause polyuria and rapid dehyd ration. A patient's basic metabloic panel would show hypernatremia (> 145
2 m Eq/L} and an increased plasma osmo lality (> 295 mOsm/kg). Add itiona lly the patient would likely show signs of volume contraction such as d ry
mucous membran es. Common causes of central DI inclu de pituitary tumor, autoimmune conditions, trauma, surgery, ischem ic encephalopathy,
3 and id iopath ic conditions. ADH is decreased in central DL The water deprivation test can be used to aid in d iagnosis and would show g reater than
4 50% increase in urine osmo lality after administration of ADH analog .
Hypernatremia Polyuria Diabetes insipidus Neurogenic diabetes insipidus Dehydration Diabetes mellitus Blood plasma Plasma osmolality Urine Osmolality
5
Pituitary tumour Vasopressin Pituitary gland Idiopathy Autoimmunity Neoplasm Ischemia
6
C is not correct. 140/o chose t his.
7
Ch ron ic alcoholism and cirrhosis may cause many of the symptoms in this patient, but his hyponatremia and low osmo larity are most consistent
8 with syndrome of inappropriate ADH secretion . Hyponatrem ia due to cirrhosis man ifests in a hypervolemic state, and there is no edema, j ugular
venous d istention, or wet-sounding breath sounds in this case .
9
Hyponatremia Cirrhosis Alcoholism Edema Vasopressin Osmotic concentration Jugular venous pressure Hypervolemia Jugular vein
10
0 is not correct. 100/o chose t his.
11
Nephrogenic d iabetes insipidus (DI ) would cause polyuria and rapid dehyd ration. A patient's basic metabloic panel would show hypernatremia
12 (> 145 m Eq/L} and an increased plasma osmo lality (> 295 mOsm/kg). Add itiona lly the patient would show signs of volume contraction such as
d ry mucus membran es. ADH levies would be normal in nephrogenic DI, and pathology is due to failure of kidney to respond to ADH. Nephrogenic
13
DI may be d istingu ished from a central DI by administration of desmopressin, a vasopressin analog . I n central DI, desmopressin should increase
14 urine osmo larity and decrease urine volume .
Desmopressin Hypernatremia Polyuria Diabetes insipidus Plasma osmolality Vasopressin Nephrogenic diabetes insipidus Osmotic concentration Diabetes mellitus
15
Kidney Urine Osmolality Dehydration Mucus Blood plasma
16
17
Bottom Line:
18
Laboratory findings of hyponatremia and decreased plasma osmo larity in the context of an underlying neurologic or pulmonary d isorder are
19
consistent with SIADH.
20 Hyponatremia Blood plasma Osmotic concentration Plasma osmolality
• 21
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2 FA11 p 334.2
3 Syndrome of Characterized by: SIADH causes include:

4
inappropriate • Excessive free water retention • Ectopic ADH (eg, small cell lung cancer)
antidiuretic • Euvolemic hyponatremia with continued • C1 S disorders/head trauma
5
hormone secretion urinary Na+ excretion • Pulmonary disease
6 • Urine osmolality> serum osmolality • Drugs (eg, cyclophosphamide)
7 Body responds to water retention with Treatment: Auid restriction, salt tablets, IV
8 ~ aldosterone and t A P and BI P hypertonic saline, diuretics, conivaptan,
9 - t urinary Na+ secretion - normalization tolvaptan, demeclocycline.
of extracellular Auid ,·olume - euvolemic Increased urine osmolality during water
10
hyponatremia. Very low serum Na • levels deprivation test indicates psychogenic
11 can lead to cerebral edema, seizures. Correct polydipsia.
12 slowly to prevent osmotic demyelination
13 syndrome (formerly known as central pontine
14 myelinolysis).
15
16 FA11 p217.1
Paraneoplastic syndromes
17
MANIFESTATION DESCRIPTION/MECHANISM MOST COMMONLY ASSOCIATED CANCER(S)
18
Cutaneous
19
Acanthosis nigricans l lyperpigmented velvety plaques in axilla and Castric adenocarci noma and other visceral
20
neck malignancies (but more commonly associated
• 21 with obesity and insulin resistance) •
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2 Alcoholic liver disease
3 Hepatic steatosis J\1acrovesicular fatty change · that ma) be
4 re,·ersible with alcohol cessation.
5 Alcoholic hepatitis Requires sustained, long-term consumpl ion. lake a toAST with alcohol:
6
Swollen and necrotic hepatocytes with AST > ALT {ratio usually> 2:1 ).
neutrophilic infiltration. ~ fallory bodies
7
(intracytoplasmic eosinophilic inclusions of
8 damaged keratin filaments).
9
Alcoholic cirrhosis Final and usually irre,·ersible form.
10 Regenerati,·e nodules surrounded by fibrous
11 bands in response to chronic liver injury
-+ portal hypertension and end-stage liver
12
disease. Sclerosis around central vein (arrows
13
in [!j) may be seen in early dise<~SC.
14
15
16
17
18
19
20
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An anxious young woman presents to the emer gency department because of acute-onset severe abdominal pain . She consumed eight or
2 nine alcoholic drinks earlier in the evening . She also admits to using diuretics to "lose water weight." Physical examination reveals
3 periumbilical tenderness to palpation . Her stool is guaiac negative. Arterial blood gas analysis reveals a pH of 7 .55, a bicarbonate level of 21
mEq/l, and a partial pressure of carbon dioxide of 25 mm Hg . Her sodium level is within normal limits.
4
5
Which of the following is the most likely cause of her primary acid-base disturbance?
6
:
7 A. Electrolyte imbalance due to diuret ic use
8
B. Hyperventilation secondary t o pain and anxiety
9
10 C. Hypoventilation due to t he respiratory depression caused by alcohol ingestion
11 0. Prolonged diarrhea due to abdominal pain

12 E. Vomiting due to alcohol toxicity
13
14
15
16
17
18
19
20
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Item: 21 of 27 ~. I • M k <:] t> al ~· ~
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2
The co rrect answe r is B. 530/o c hose this.
3
Acco rd in g to her lab data, this patient has an acute respiratory alkalosis. Res piratory alkalosis is caused by respiratory loss of C02, which is
4 compensated for by increased renal excretion of HC03- . The keys to answering this question are to use the data g iven to identify respiratory
alkalosis as the primary d isturbance, and recogn izin g that respiratory alkalosis can be caused on ly by an increase in ventilation . This classically
5
occu rs when there is low oxygen (such as at high altitudes) or by sympathetic stimulation, such as anxiety, panic attack, or pain . This patient is
6 described as anxious and presents with severe abdominal pain, which is most likely the resu lt of acute alcohol-induced pancreatitis. Both the
anxiety and the pain could be causing her to hyperventilate.
7
I n respiratory acidosis or alkalosis, there are two phases of compensation . (1) A rapid, small change in serum HCo3- occu rs in the same d irection
8
as the Pco2 change as a resu lt of carbonic anhydrase activity. {2} Afte r a longe r period of time (minutes to hours), the kidneys respond by
9 increasin g or decreasin g serum HC03- if the pH d isturbance persists . This compensation in serum HC03- is also in the same d irection as the Pco2.
10 Respiratory alkalosis Respiratory acidosis Carbonic anhydrase Panic attack Pancreatitis PH Hyperventilation Alkalosis Acidosis Blood plasma Abdominal pain
11 Anxiety Kidney Ventilation (physiology) Oxygen Excretion Sympathetic nervous system
12 A is no t co rrect. 180/o c hose this.

13 Diuretic use can cause metabolic alkalosis by volume contraction . This causes the kidney to compensate by reabsorbin g sodium and excretin g
hydrogen ions. A metabolic alkalosis would manifest with elevated pH, elevated carbon d iox ide, and elevated bicarbonate.
14 Metabolic alkalosis Diuretic Carbon dioxide PH Sodium Bicarbonate Alkalosis Kidney Hydrogen Metabolism
15
C is no t co rrect. 11 Ofo c hose this.
16 Hypoventilation causes a reduction in pH due to C02 retention . The excess retain ed C02 leads to a respiratory acidosis. The compensatory
17 mechanism for respiratory acidosis is an increase in HCo3- retention by the kidneys to normalize the pH.
Respiratory acidosis Hypoventilation PH Acidosis Kidney
18
0 is no t co rrect. 4 0fo c ho s e this.
19
Prolonged d iarrhea would produce a metabolic acidosis due to d irect loss of bicarbonate from the gut. The decrease in pH would then stimulate
20 chemoreceptors to cause hyperventilation and blow off C0 2. The acid base profile for a patient with prolonged d iarrhea would be metabolic
21 acidosis, with decreased bicarbonate and decreased Pco 2.
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Item: 21 of 27 ~. I • M k <:] t> al ~· ~
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1 •
A is not co rrect. 180/o c hose t his.
2
Diuretic use can cause metabolic alkalosis by volume contraction . This causes the kidney to compensate by reabsorbin g sodium and excretin g
3 hydrogen ions. A metabolic alkalosis would manifest with elevated pH, elevated carbon d iox ide, and elevated bicarbonate.
4 Metabolic alkalosis Diuretic Carbon dioxide PH Sodium Bicarbonate Alkalosis Kidney Hydrogen Metabolism
5 C is not co rrect. 11 Ofo c hose t his.
6 Hypoventilation causes a reduction in pH due to C02 retention. The excess retain ed C02 leads to a respiratory acidosis. The compensatory
mechanism for respiratory acidosis is an increase in HCo3- retention by the kidneys to normalize the pH.
7 Respiratory acidosis Hypoventilation PH Acidosis Kidney
8 0 is not co rrect. 4 0fo c hose t his.

9 Prolonged d iarrhea would produce a metabolic acidosis due to d irect loss of bicarbonate from the gut. The decrease in pH would then stimulate
10 chemoreceptors to cause hyperventilation and blow off C0 2. The acid base profile for a patient with prolonged d iarrhea would be metabolic
acidosis, with decreased bicarbonate and decreased Pco 2.
11 Metabolic acidosis Hyperventilation Diarrhea PH Bicarbonate Acidosis Chemoreceptor Metabolism
12 E is not co rrect. 140/o c hose t his.

13 Vomiting causes a metabolic alkalosis secondary to the loss of H+ and c l- from the stomach . If this were the cause, this patient's lab resu lts would
14 show a high pH, a high HCo3- , and (with respiratory compensation) a high C0 2. The causes of metabolic alkalosis inclu de vomiting, d iuretic
therapy, and c l- restriction. The compensation for metabolic alkalosis is hypoventilation .
15 Metabolic alkalosis Diuretic Respiratory compensation PH Hypoventilation Vomiting Alkalosis Chloride Stomach Metabolism
16
17
Bottom Line :
18
Hyperventilation leads to respiratory alkalosis, which is characterized by high pH and low carbon d iox ide levels on blood gas analysis. Be able to
19 identify a patient's primary pH d isturbance using lab data and supporting clinical information.
Respiratory alkalosis Hyperventilation Carbon dioxide PH Arterial blood gas Alkalosis Blood gas
20
21
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Item: 21 of 27 ~ 1 • Ma r k -<:J I> ~ £!1}>'
• !!":-~
QIO: 1787 ..L Pre v ious Next Lab lues Not es Calcula t o r
& &
1
FA17 p 561 .2
2
3
4 Check arterial pH
5 pH< 7.35 pH > 745
6
Acidemia Alkalemia
7
Pco1 > 44 mm Hg HC~- < 20 mEq/l Pco1 < 36 mm Hg
8
9
10 Respiratory Respiratory
MetaboUc acidosis Metabolic alkalosis
acidoSIS alkalOSIS
11
12
Hypowntilation Check anion gap Hy~rv~ntilation H• loss/HC05- excess
13
Airway obstruction
=Na•- (CI t HC01 )
Hysteria loop diuretics
14 Acute lung disease Hypoxemia (eg, high altitude) Vomiting
15 Oploids, sedatives Tumor Hyperaldosteronism
Weakening of respiratory Pulmonary embolism
16 muscles
17
18
> 12 mEq/l 8-12 mEq/l
19 Pco,•
20
I 45
40 Resporatory
40mmHg
~ -· ........_
21 35
• MUDPILES: HARDASS:
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2 Salicylates (late) acidosis
3 69 70 71 72 7.5 74 75 76 77 78 79
4 pH
5
6 FA17 p 561 .1
7 Acid-base physiology
8 pH Pco, (HC0 I COMPENSATORY RESPONSE

1
9 Metabolic acidosis l l l Hypen·entilation (immediate)
10 Metabolic alkalosis f f f llypoventilation (immediate)
11 Respiratory acidosis l f f f renal [HC03-] reabsorption (delayed)
12 Respiratory alkalosis f l l l renal (HC03-Jreabsorption (delayed)
13 Ker: f l = 1" disturbance; l f =compensatory response.
14
15
16
Henderson-Hasselbalch equation: p i I = 6. 1+ log 6~~~~~~
2
17 Pred icted respiratory compcns~1t ion for a simple metabolic acidosis can be calculated using the
Winters formula. If measured Pco2 > predicted Pco2 - concomitant respiratory acidosis; if
18
measured Pc~ <pred icted Pco2 - concomitant respiratorr alkalosis:
19
20
Pco2 = 1.5 [HC03-] + 8 :t 2
21
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Item: 22 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 •
A 2-year-old girl is brought to the emergency department by her mother after ingesting a bottle of unmarked pills from the family medicine
7
cabinet. On examination, the child appears agitated and is breathing quickly. Urgent blood chemist•·y measurements are taken and reveal the
8 following:
9
Na+: 143 mEq/L
10 K+: 4.0 mEq/L
cl-: 104 mEq/L
11
HC03-: 19 mEq/L
12 pH: 7.28
13
14 Which of the following medications did t his patient most likely ingest?
15 :
16 A. Aldosterone antagonist
17 B. Antacid
18
C. Iron supplement
19
D . Loop diuretic
20
21 E. Opiate analgesic
• 22
• 23
• 24
• 25
• 26
•
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Item: 22 of 27 ~. I • M k <:] t> al ~· ~
6 •
7
The correct answer is C. 47 0fo chose this.
8 This patient is suffering from a severe metabolic acidosis, as in d icated by low serum pH, a low plasma bicarbonate level, and compensatory
9 hyperventilation and tachypnea . Next, note that the anion gap is elevated at 20 mmoi/L. The normal ran ge for the anion gap is somewhat
dependent on the analytical instruments used, but values of> 12 mmoi/L are generally considered high . Of the choices, on ly iron toxicity (the I in
10
the mnemonic MUOPILES} is associated with elevated anion gap metabolic acidosis. I ron ove rload causes d irect mitochondrial toxicity by
11 damag in g its membrane. Decreased number of mitochondria resu lts in increased production of lactate, which causes the anion gap metabolic
acidosis. The symptoms described in this stem are fairly typical for patients with iron toxicity, as they can easily develop hypovolemic shock with
12
an associated metabolic acidosis (seen by pH and blood chemistry) within the first few hours after in gestion . Furthermore, gastrointestinal
13 symptoms, inclu d in g abdominal pain, vomiting, and d iarrhea, can be present between 30 minutes and 6 hours.
Metabolic acidosis Hypovolemia Mitochondrion Hyperventilation Tachypnea PH Diarrhea Blood plasma Anion gap Acidosis lactic acid Bicarbonate Vomiting
14
Abdominal pain Iron overload Anion Serum (blood) Metabolism Gastrointestinal tract Mnemonic Iron
15
16
A ldosterone normally functions to increase sodium reabsorption, potassium excretion, and proton excretion in the d istal nephron . Thus,
17 aldosterone antagonists cause d iminish ed proton excretion and metabolic acidosis. However, unlike this case, the acidosis would be expected to
18 occu r in the setting of a normal anion gap.
Nephron Aldosterone Metabolic acidosis Anion gap Sodium Acidosis Potassium Proton Antimineralocorticoid Anatomical terms of location Anion
19
Distal convoluted tubule Excretion Metabolism
20
21
Most simple antacids are alkaline and operate by neutralizin g the low pH of the stomach . Thus, ove rdose would be expected to cause a metabolic
22 alkalosis, not an acidosis.
Metabolic alkalosis PH Antacid Acidosis Alkalinity Alkalosis Metabolism Stomach
• 23
• 24
0 is not correct. 130/o chose this .
Loo p d iuretic toxicity is associated with metabolic alkalosis, not acidosis. This is due to loo p d iuretics increasin g sodium delivery to the d istal
• 25
segment of the d istal tubule . The higher sodium concentration stimulates the aldosterone -sensitive pump to increase sodium reabsorption in
• 26 exchange for potassium and hydrogen ions. Thus, the increase in hydrogen ion loss leads to a metabolic alkalosis .
• I'"''"" rlit•rotir Mot-:ahnlir -:all.--:alncic f""'it•rotir f""'ict-:al rnnHnl••torl h•h••lo C:nrlilll"r'\ Lhtrlrn,on inn 1\.rirlncic Ont-:accil•l"r'\ 1\ll.--:alncic Tnviriht f\lonhrnn Tnn Mot-:ahnlicl"r'\ Lhtrlrn,on
6
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Item: 22 of 27 ~. I • M k <:] t> al ~· ~
6
A is n ot correct. 160/o chose this.
7
A ldosterone normally functions to increase sodium reabsorption, potassiu m excretion, and proton excretion in the d istal nephron . Thus,
8 aldosterone antagonists cause d iminish ed proton excretion and metabolic acidosis. However, unlike this case, the acidosis would be expected to
occu r in the setting of a normal anion gap.
9 Nephron Aldosterone Metabolic acidosis Anion gap Sodium Acidosis Potassium Proton Antimineralocorticoid Anatomical terms of location Anion
10 Distal convoluted tubule Excretion Metabolism
11 B is not correct. 120/o chose this.

12 Most simple antacids are alkaline and operate by neutralizin g the low pH of the stomach . Thus, ove rdose would be expected to cause a metabolic
alkalosis, not an acidosis.
13
Metabolic alkalosis PH Antacid Acidosis Alkalinity Alkalosis Metabolism Stomach
14
0 is not correct. 130/o chose this.
15
Loo p d iuretic toxicity is associated with metabolic alkalosis, not acidosis. This is due to loo p d iuretics increasin g sodium delivery to the d istal
16 segment of the d istal tubule . The higher sodium concentration stimulates the aldosterone -sensitive pump to increase sodium reabsorption in
exchange for potassium and hydrogen ions. Thus, the increase in hydrogen ion loss leads to a metabolic alkalosis.
17
loop diuretic Metabolic alkalosis Diuretic Distal convoluted tubule Sodium Hydrogen ion Acidosis Potassium Alkalosis Toxicity Nephron Ion Metabolism Hydrogen
18 Reabsorption
19
E is not correct. 120/o chose this.
20 I ngestion of opiates resu lts in reduced respiratory d rive and subsequent hypoventilation . I n this situation, a respiratory acidosis would have been
21 expected, and tachypnea would not be observed .
Respiratory acidosis Tachypnea Hypoventilation Acidosis Control of ventilation Opiate
22
• 23
• 24 Bottom Line:
• 25 Determin e the anion gap {Na+ - [ c l- + HC03-)) in the patient who presents with metabolic acidosis to pinpoint the cause .
Metabolic acidosis Anion gap Acidosis Anion
• 26
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Item: 22 of 27 ~ 1 • Ma r k -<:J I> ~ £!1}>'
• !!":-~
QIO: 4518 ..L Prev ious Next Lab lues Not es Cal culat o r
6 A
FA17 p 561 .2
A
7
8
Check arterial pH
9
10 pH<735 pH>745
,r~--------------------~----------------------~,
11
Acidemia Alkalemia
12
Pco1 > 44 mm Hg HC~- < 20 mEq/L Pco2 < 36 mm Hg
13
14
MetaboUc acidOSIS Metabolic alkalosiS
acidoSIS alkalOSIS
16
17
18
Airway obstruction
=Na•- (Cl t HC01 )
Hysteria loop diuretics
21 muscles
22
• 23
> 12 mEq/l 8-12 mEq/l
• 24 Pco,•
• 25
I 45
40 Resporatory
acidosis
40mmHg
t Anion gap Normal ilnion gilp

• 26
•
MUDPILES: HARDASS: i
c:
35
30 .____
Mixed
all<alosas
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Item: 22 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 A Oploids, sedatives Tumor Hyperaldosteronism A

7 muscles
8
9
> 12mEq/L 8-12 mEq/L
Pcol •
10 45 40mmHg
11 40 Respo-atcwy
I Anion gap NOI'IMI inion 9iiP acidosis
~
35 Mixed
12 MUDPILES: HARDASS:
30 alkalo!is
Methanol (formic acid) Hyperalimentation .§
13
Uremia Addison disease 0- 25
u
14 Diabetic ketoacidosis Renal tubular acidosis :5 20
Propylene glycol Diarrhea
15 Iron tablets or INH Acetazolamide j 15
Lactic acidosis Sptronolactone 10 Resporatory
16 Metabolic
Ethylene glycol (...... oxalic acid) Saline infusion alkaloSIS
5 acidos1s
Salicylates (late)
17
..
18 69 70 71 72 7.3 74 7.5 76 77 78 79
pH 1:1
19
20
FA17 p404.1
21
22 Iron poisoning High mortality rate with accidental ingestion by children (adult iron tablets may look like candy).
. 23 MECHANISM Cell death due to peroxidation of membrane lipids.
. 24 SYMPTOMS/SIGNS 1'\ausea, vomiting, gastric bleeding, lethargy, scarring leading to G I obstruction.
• 25 TREATMENT Chelation (eg, IV deferoxamine, oral deferasirox) and dialysis.
. 26
•
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Item: 23 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 •
A 68-years-old male with a history of gout presents to his physician for a follow-up. He has been taking allopurinol for many years, however
7
he gets one or two attacks of acute gouty arthritis a year. The physician counsels him on the importance of avoiding precipitants for acute
8 gout, and prescribes indomethacin for treatment of acute gout. He explained that nonsteroidal anti-inflammatory drugs {NSAIDs) are used
frequently for their anti-inflammatory, antipyretic, and analgesic effects. However, there is a known risk of acute kidney injury, particularly in
9
patients with pre-existing chronic kidney disease.
10
11 Which of the following is the most likely underlying mechanism of kidney damage caused by NSAID administration?
12
:
13 A. Decreased glomerular filtration rate due to constriction of the afferent arteriole
14
B. Decreased glomerular filtrat ion rate due to dilation of the afferent arteriole
15
C. Decreased glomerular filtration rate due to dilation of the efferent arteriole
16
17 D. Increased glomerular filtration rate due to constriction of the afferent arteriole
18 E. Increased glomerular filtration rate due to constriction of the efferent arteriole

19
F. Increased glomerular filtration rate d ue to d ilation of the afferent arteriole
20
21
22
. 23
. 24
• 25
. 26
•
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Item: 23 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 3876 ..L ar Prev ious Next Lab fli!ltues Notes Calculat o r
6 A A
7
Th e cor r ect an sw er i s A. 750/o ch ose this .
8 NSAIDs reversibly inhibit cyclooxygenases, which in turn blocks the synthesis of prostaglandins. Prostaglandins function at the level of the kidney
9 to dilate the afferent arteriole in order to increase glomerular filtration rate (GFR) . Thus, upon NSAID administration the afferent arteriole will
constrict and GFR will decrease. In a normally functioning kidney, this adverse effect is relatively mild . However, in an already compromised
10 kidney, this effect can be detrimental to kidney function.
11 Nonste oid ant -inflammatory drug Arteriole Renal function Afferent arterioles Prostaglandin Kidney Glomerulus Glomerulus (kidney)
12 B i s not correct. 6 0/o chose t his.
13 NSAIDs decrease GFR by disrupting prostaglandin - mediated vasod ilation of afferent arteriole, which causes vasoconstriction, rather than
vasodilation of afferent arteriole. Additionally, dilation of the afferent arteriole will increase, not decrease, GFR.
14 Arte •ole Va;oconstriction Afferent arterioles Vasodilation Nonsteroida• anti-inflammatory drug Afferent nerve fiber Renal function
15
C is not correct. 7 0/o c h ose t h is.
16 Dilation of the efferent arteriole indeed will cause a decrease in GFR. However, NSAIDs decreases GFR by inhibiting prostaglandin-mediated
17 vasodilation of afferent, rather than efferent arteriole.
Arteriole Efferent arteriole Vasodilation Nonsteroidal anti-inflammatory drug Renal function
18
D is not co rrect. JO/o c hose t his .
19
NSAIDs do cause vasoconstriction of th e afferent arteriole by inhibiting prostaglandin-mediated vasod ilation. How ever, this leads to a decrease,
20 rather than increase, in GFR.
21 Arteriole Vasoconstriction Afferent arterioles Vasodilation Nonsteroidal anti-inflammatory drug Afferent nerve fiber
22 E is no t co rrect. 4 0fo c hose this .
23 Constriction of the efferent arteriole will indeed increase GFR. This process occurs physiologically when an giotensin II acts to preferentially
constrict the efferent a•·teriole in the setting of low blood pressures. This causes an increase in GFR with an associated increase in sodium and
. 24 water reabsorption . However, this is not the mechanism of NSAID-induced renal injury.
• 25 Efferent arteriole Arteriole Angiotensin Angiotensin II Sodium Efferent nerve fiber Kidney
. 26 F i s n o t correct . solo ch ose this .

• 1"\ : 1 ... ... : . - ., Ca,.L .. - " - - - - "' _ _ _ _ ; .. I .. . . . :11 ;_ J .... J :----- - - r-rn ... L : .. L : ..... L .. - · .. .. L ..,_; ___ .. C _ _ ...; __ .. c ____ .., __ t __ J; _ _ n ...... . . .. .. a lr""A1'1"\ .. : - L : L : ....
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Item: 23 of 27 ~. , . M k <:] t> al ~· ~
6
C is no t co rrect . JOfo c hose t his.
7
Dilation of the efferent arteriole in deed will cause a decrease in GFR. However, NSA!Ds decreases GFR by inhibiting prostaglandin-mediated
8 vasodilation of afferent, rath er than efferent arteriole.
Arteriole Efferent arteriole Vasodilation Nonsteroidal anti -inflammatory drug Renal function
9
10 0 is no t co rrect . 30/o c hose t his.
NSA!Ds do cause vasoconstriction of the afferent arteriole by inhibiting prostaglandin-mediated vasodilation . However, this leads to a decrease,
11
rath er than increase, in GFR.
12 Arteriole Vasoconstriction Afferent arterioles Vasodilation Nonsteroidal anti -inflammatory drug Afferent nerve fiber
13 E is no t co rrect . 4 0fo c hose t his.

14 Constriction of the efferent arteriole will in deed increase GFR. This process occu rs physiologically when angiotensin II acts to preferentially
constrict the efferent arteriole in the setting of low blood pressures. This causes an increase in GFR with an associated increase in sodium and
15 water reabsorption . However, this is not the mechanism of NSAI D-in duced renal inj ury.
16 Efferent arteriole Arteriole Angiotensin Angiotensin II Sodium Efferent nerve fiber Kidney
17 F is no t co rrect . 50/o c hose t his.
18 Dilation of the afferent arteriole will in deed increase GFR, which is the mechanism of action of prostaglandins. Because NSA!Ds inhibit
prostaglandin production, the opposite of this scenario occu rs .
19 Arteriole Afferent arterioles Prostaglandin Nonsteroidal anti-inflammatory drug Afferent nerve fiber Mechanism of action Vasodilation Renal function
20
21
Bo tto m Line :
22
NSA!Ds reversibly inhibit cyclooxygenase and decrease prostaglandin synthesis. At the g lome rulus, prostaglandins d ilate the afferent arteriole
23 to increase the GFR. Consequently, with NSAI D administration the afferent arteriole will constrict and GFR will decrease. This decrease in
• 24 peritubular blood flow may increase the risk of acute kidney inj ury .
Nonsteroidal anti-inflammatory drug Arteriole Prostaglandin Glomerulus (kidney) Acute kidney injury Cyclooxygenase Glomerulus Afferent arterioles Kidney
• 25 Blood flow
• 26
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Item: 23 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 A A
FA17 p 456.3
7
Nonsteroidal Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac, meloxicam, piroxicam.
8
anti-inflammatory
9 drugs
10
MECHANISM Re,·ersibly inhibit cyclooxygenase (both COX-I and COX-2). Block prostaglandin synthesis.
11
CLINICAL USE Antip)Tetic, analgesic, anti-inAammatory. Indomethacin is used to close a PDA.
12
ADVERSE EFFECTS Interstitial nephritis, gastric ulcer (prostaglandins protect gastric mucosa), renal ischemia
13 (prostaglandins \<ISodilate afferent arteriole), aplastic anemia.
14
15
FA17 p 553.2
16 Changes in glomerular dynamics
17 Effect GFR FF (GFR/ RPF)
RPF
18
19
Afferent arteriole constriction
•t •
Efferent arteriole constriction
t plasma protein concentration
• t
20
l plasma protein concentration
•t •t
21
22
Constriction of ureter
Dehydration
• •t
23 •
• 24
• 25 FA17 p553.1
• 26 Filtration Filtration fraction (FF) = CFR/RPF. CFR can be estimated with creatinine
•
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Item: 24 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 A A
A 44-year-old man stumbles into the emerg ency department after having been lost in the woods without food or drink for 4 days. His basic
7 metabolic panel shows:
8
Na+: 144 mEq/L
9
K+: 4.5 mEq/L
10 Cl·: 108 mEq/L
HC03·: 24 mEq/L (normal range: 20 - 29 m Eq/L)
11
Blood urea nitrogen: 79 mg/dl
12 Creatinine: 2.3 mg/dl
Glucose: 105 mg/dl
13
14
15 The physician gives the patient IV fluids t o treat his acute kidney injury. In addition, she considers administ ering a trial medication to help increase
renal blood flow.
16
17
A medication with which of the following mechanisms is likely to have the most benefit?
18
19 :
20
21 A. Stimulation of afferent a -ad renerg ic receptors alone
22 B. Stimulation of afferent angiotensin II receptors alone
23
C. Stimulation of angiotensin II receptors and opening of vascular smooth muscle stretch-activated calcium channels in the renal
• 24 vasculature
• 25 D. Stimulation of renal a-adrenergic and angiotensin II receptors
• 26
• E. Stimulation of renal dopamine and bradykinin receptors
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Item: 24 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
r.TA1
7
Na+: 144 mEq/L
8 K+: 4.5 mEq/L
9 Cl·: 108 mEq/L
HC03·: 24 mEq/L (normal range: 20- 29 m Eq/L)
10 Blood urea nitrogen: 79 mg/dl
11 Creatinine: 2.3 mg/dl
Glucose: 105 mg/ dl
12
13
The physician gives the patient IV fluids to treat his acute kidney injury. In addition, she considers administering a trial medication to help increase
14 renal blood flow.
15
16
A medication with which of the following mechanisms is likely to have the most benefit?
17
:
18
19
20 A . Stimulation of afferent a-ad renerg ic receptors alone
21 B. Stimulation of afferent an g iot ensin II receptors alone

22
C. Stimulation of angiotensin II r eceptors an d opening of vascular smooth muscle stretch-activated calcium channels in the renal
23 vasculature
• 24 D. Stimulation of renal a-adrenergic and angiotensin II receptors
• 25 E. Stimulation of renal dopamine and bradykinin receptors

• 26
•
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Item: 24 of 27 ~. I • M k <:] t> al ~· ~
6 •
The co rrect a nswe r is E. 4 30/o c hose t his.
7
This patient has prerenal acute kidney inj ury as evidenced by the lack of hyd ration, increased creatinine, and blood urea nitrogen :creatinine ratio
8 > 20. The trial medication should increase blood flow to the kidneys. Rena l blood flow is determin ed by regu lation of the g lomerular afferent and
9 efferent arterioles. Low levels of dopamin e d ilate both the afferent and efferent arterioles as well as intralobular arteries in the kidney, increasin g
ove rall renal blood flow . Low levels of dopamin e also d ilate cerebral, cardiac, and splanchnic arterioles. S imilarly, bradykinin in duces the
10 vasodilation of arterioles. The combined actions of these substances will decrease vascular resistance and increase renal blood flow . {Of note, at
11 interm ed iate doses, dopamin e exerts a 13-agonist effect. At higher doses it exerts an a-agon ist effect. The a-agon ist effect of high-dose dopamin e
causes vasoconstriction, which would reduce renal bloodflow and worsen this patient's kidney function . )
12 Bradykinin Dopamine Vasoconstriction Urea Acute kidney injury Creatinine Vasodilation Glomerulus Vascular resistance Kidney Renal function Artery
13 Glomerulus (kidney) Arteriole Pharmaceutical drug Circulatory system Renal blood flow Blood flow Blood vessel
14 A is no t co rrect . 100/o c hose t his.

15 Stimulation of afferent a 1-ad renerg ic receptors acts to vasoconstrict both renal arterioles. This would worsen this patient's kidney inj ury.
Arteriole Kidney Afferent nerve fiber Receptor (biochemistry)
16
17 B is no t co rrect . 1 60/o c hose t his.
Angiotensin II is a peptide molecule that causes vasoconstriction and is active when blood pressu re is low. Rece ptors for angiotensin II are found
18 on both afferent and efferent renal arterioles, though it acts primarily on the efferent arterioles, thus increasin g g lomerular filtration fraction .
19 Stimulation of afferent angiotensin II receptors will act to vasoconstrict the arteriole and cause decreased renal blood flow, worsening his kidney
injury.
20
Arteriole Angiotensin Angiotensin II Vasoconstriction Blood pressure Efferent arteriole Kidney Angiotensin receptor Glomerulus Peptide Glomerulus (kidney)
21 Molecule Renal function Renal blood flow Blood flow
22 C is no t co rrect . 1 70/o c hose t his.

23 I n autoregulation of renal blood flow, the myogenic hypothesis suggests that increased stimulation of stretch-activated calcium channels in the
24 vascular smooth muscle causes an increase in intracellular calcium and a contraction of the muscle and in this case, the renal vasculature. This
causes a constriction of the vasculature and would lead to reduced renal blood flow .
• 25 Calcium Circulatory system Smooth muscle tissue Autoregulation Calcium channel Voltage-dependent calcium channel Vascular smooth muscle
• 26 Myogenic contraction Muscle Kidney Intracellular Blood vessel

•
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Item: 24 of 27 ~. I • M k <:] t> al ~· ~
6 B is no t co rrect . 1 60/o c hose t his.
7 Ang iotensin II is a peptide molecu le that causes vasoconstriction and is active when blood pressu re is low. Rece ptors for angiotensin II are found
on both afferent and efferent renal arterioles, though it acts primarily on the efferent arterioles, thus increasin g g lomerular filtration fraction .
8
Stimulation of afferent angiotensin II receptors will act to vasoconstrict the arteriole and cause decreased renal blood flow, worsening his kidney
9 inj ury.
Arteriole Angiotensin Angiotensin II Vasoconstriction Blood pressure Efferent arteriole Kidney Angiotensin receptor Glomerulus Peptide Glomerulus (kidney)
10
Molecule Renal function Renal blood flow Blood flow
11
C is no t co rrect . 1 70/o c hose t his.
12
I n autoregulation of renal blood flow, the myogenic hypothesis suggests that increased stimulation of stretch-activated calcium channels in the
13 vascular smooth muscle causes an increase in intracellular calcium and a contraction of the muscle and in this case, the renal vasculature. This
14 causes a constriction of the vasculature and would lead to reduced renal blood flow .
Calcium Circulatory system Smooth muscle tissue Autoregulation Calcium channel Voltage-dependent calcium channel Vascular smooth muscle
15
Myogenic contraction Muscle Kidney Intracellular Blood vessel
16
0 is no t co rrect . 140/o c hose t his.
17
a 1 -Ad renerg ic stimulation will cause vasoconstriction . Rece ptors are found on both the afferent and efferent arterioles, but there are far more
18 receptors on the afferent vessels . Ang iotensin II is a potent constrictor of both afferent and efferent arterioles, but the efferent arterioles are
more sensitive to low levels of angiotensin IL Stimulating both adrenergic and angiotensin receptors causes both afferent vasoconstriction
19
(decreases renal blood flow) and efferent vasoconstriction (increases filtration fraction), neither of which would benefit this patient's acute kidney
20 inj ury.
Vasoconstriction Acute kidney injury Angiotensin Angiotensin II Kidney Efferent arteriole Arteriole Renal blood flow Angiotensin receptor Filtration fraction
21
22
23 Bo tto m Line :
24 Low doses of dopamin e and bradykinin act to increase renal blood flow, whereas a-ad renerg ic stimulation vasoconstricts and reduces renal
blood flow .
• 25
Dopamine Bradykinin Kidney
• 26
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Item: 24 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 A A
FA17 p 553.1
7
Filtration Filtration fraction (FF) = CFR/ RPF. CFR can be estimated with creatinine
8
r\ormal FF = 20%. clearance.
9 Filtered load (mg/min) = CFR (mL/min) RPF is best estimated with PAH clearance.
10 X plasma concentration (mg/m L). Prostaglandins D ilate Afferent arteriole (PO\)
11 ACE inhibitors C onstrict Efferent arteriole
(ACE)
12
PlOS1agland1ns preferentially
13 / Parietal layer or
NSAIDs ~ dilate afferent artenole
14 (i RPF. i GFR. so no a FFl / Bowman capsule
15
~ ~0v-~roan space
~
16
~,...
17 ~~.
18 '6~
Juxtaglomerular~ •
19 cells J ---..... ltc.c--'---
. I· . !·
20 Filtered - - + Excreted
Macula densa ~
21
22
Distalrenal~ Reabsorbed ~ecreted
23 tubule Peritubular
24 capillary
Net filtration pressure
• 25 Endothelial cells_ / - = (Pc.c + rtes) - (Pes + ltc.c)
• 26
• ··-----·-·
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Item: 24 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
QIO: 2357
6 A
..L ar Pre v ious Next Labfli!llues
ACE inhibitors -e--t

' . .
Not es
. . ..
constricts efferent arteriole
Calcula t o r
A
7 (.! RPF, t GFR. so t FF)

8
9 FA17 p 553.2
10 Changes in glomerular dynamics
11 Effect GFR RPF FF (GFR/ RPF)
12 Afferent arteriole constriction l l
13 Efferent arteriole constriction I l I
14 I plasma protein concentration l l
l plasma protein concentration I I
15
Constriction of ureter l l
16 Dehydration l I
17
18
FA1 7 p 554.1
19
20 Calculation of Filtered load= GFR X Px.
reabsorption and Excretion rate= V x Ux.
21
secretion rate Reabsorption rate = fi ltercel - excreted.
22 Secretion rate= excreted- fi ltered.
23
Fe = la+ excreted = x U'Sa - Pc, X U Na
24 3
Na+ filtered GFR(u Cr x -p ) x p\ a Uc,x p 'a
• 25
Cr
. 26
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8
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Item: 25 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 A A
A 37-year -old man complains of constant, insatiable thirst. He says he drinks water all day and is constantly going to the bathroom. His blood
7
glucose level is 95 mg/dl and urine dipstick is negative for glucose. Results of laborato•·y tests after 24 hours of fluid restriction are within
8 normal limits, except for a serum osmolality of 310 mOsm/kg (normal: 275-295 mOsm/kg) and a urine osmolality of 105 mOsm/kg (normal:
>850 mOsm/kg) . The physician suspects this patient has a problem with a specific hormone.
9
0
10
11
12
13
14
15
16
17
18
19
20
21
22
Which of the sites labeled on the diagram indicates the primary site of action for the hormone that is not functioning adequately in this patient?
23
24 :
A
• 25
• 26 B
•
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8
End Bl ock
16
17
Which of the sites labeled on the diagram indicates the primary site of action for the hormone that is not functioning adequately in this patient?
18
19 :
A
20
21 B
22 c
23
D
24
E
• 25
• 26
•
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8
End Block
Item: 25 of 27 ~. , . M k <:] t> al ~· ~
6 •
The correct answer is E. 870/o chose t his.
7
This patient is presentin g with the symptoms of d iabetes insipidus (DI ), which resu lts from either a lack of antidiuretic hormone (ADH} production
8 by the hypothalmus (central DI) or a lack of response to ADH by the nephron ( nephrogenic DI). ADH normally functions primarily at the
9 collecting tubule {labeled "E" in the d iag ra m), though exerts lesser effects on the principal cells of the late d istal tubule . ADH signals for the
insertion of aquaporins into the cell membrane to allow for the passage of water out of the urine and back into the bloodstream. Of note, ADH
10 also functions at the ascending loo p of Hen le by increasin g sodium absorption, which leads to increased water reabsorption at the collecting
11 tubule . ADH is the main hormone regu lating the osmo lality of the blood. When a patient is fluid restricted, ADH should be released to conserve
water, keepin g the serum osmo lality normal and the urine osmo lality high . I n this case, the patient has a high serum osmo lality and an
12 inappropriately low urine osmo lality after fluid restriction, suggesting he is not properly retainin g water. A water- restriction protoco l can also
13 d ifferentiate true DI from psych ogen ic polyd ipsia in which a patient consumes too much water. I n psych ogen ic polyd ipsia, water restriction will
lead to appropriate concentration of urine once the plasma osmo larity is normalized. If a normalization is not seen, this in d icates the patient may
14
have DL
15
To d ifferentiate between nephrogenic and central DI, fluid restriction followed by administration of an exogenous ADH bolus is perform ed. I n
16 nephrogenic DI (often due to lithium toxicity), no change is seen in urine or plasma osmo lality in response to an ADH bolus since the nephron
itself is damaged and cannot respond to ADH signaling . I n central DI, an ADH bolus will resu lt in normalization of serum and urine osmo lalities
17
since the kidney remains respons ive to ADH but not enough ADH is bein g produced in the hypothalamus.
18
Nephron Distal convoluted tubule Hypothalamus Diabetes insipidus Plasma osmolality Vasopressin Polydipsia Cell membrane loop of Henle Osmotic concentration
19 Aquaporin Kidney Collecting duct system Diabetes mellitus Osmolality Sodium Urine Primary polydipsia Hormone Blood plasma Urine osmolality
20 Anatomical terms of location Antidiuretic Connecting tubule Ascending limb of loop of Henle Circulatory system Fluid restriction Exogeny
21 A is not correct. 2 0/o chose t his.

22 This area is the thick ascending limb after the loo p of Hen le, where the sodium - potassium -chloride cotransporter is actively removin g solute from
the tubule . The thick ascending limb is imperm eable to water and thus makes urine less concentrated as it ascends. antidiuretic hormones does
23
not act at this location.
24 loop of Henle Urine Ascending limb of loop of Henle Solution Cotransporter Nephron Hormone
25 B is not correct. 1 Ofo chose t his.

• 26 This area is the thin descend in g limb before the loo p of Hen le, where water is passively reabsorbed. However, this reabsorption is not under
•
6
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0
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Item: 25 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 •
A is no t correct. 2 0/o ch ose t his .
7
This area is the thick ascending limb after the loop of Henle, where the sodium-potassium-chloride cotransporter is actively removing solute from
8 the tubule. The thick ascending limb is impermeable to water and thus makes urine less concentrated as it ascends. antidiuretic hormones does
not act at this location.
9
Loop of Henle Urine Ascending limb of loop of Henle Solution Cotransporter Nephron Hormone
10
B i s not correct. 1 Ofo chose t his.
11
This area is the thin descending limb before the loop of Henle, where water is passively reabsorbed. However, this reabsorption is not under
12 hormonal control; it is driven by the osmotic gradient set up by the countercurrent ion multiplier of the kidney. Hence, this area of the nephron is
not the site of action of antidiuretic hormone.
13
Neph on _oop of Henle Vasopressin Descending limb of loop of Henle Kidney Hormone Osmosis Countercurrent exchange Reabsorption Ion Gradient AntidiuretiC
14 Rena. reab ;orption
15 C is not correct. 4 0fo c h ose this.
16 This area is the proximal convoluted tubule. Most substances, including sodium, glucose, amino acids, are reabsorbed from the primary filtrate
17 here. However, it is not the site of action of antidiuretic hormone.
Proximal convoluted tubule Vasopressin Amino acid Sodium Hormone Nephron Glucose Filtration Anatomical terms of location
18
D is not co rrect. 6 0fo c hose t his .
19
This area is the distal convoluted tubule ( DCT}. The DCT is the primary site of action of parathyroid hormone, which prompts the kidney to
20 conserve calcium. It is not, however, th e primary site of action of antidiuretic hormone.
Distal convoluted tubule Parathyroid hormone Vasopressin Kidney Hormone Parathyroid gland Anatomical terms of location Nephron Calcium
21
22
23 Bo tto m Lin e :
24 Antidiuretic hormone (ADH, also known as vasopressin) acts on the collecting tubule of the nephron; lack of ADH production results in central
DI, whereas lack of response to ADH causes nephrogenic DI.
25
Nephron Vasopressin Connecting tubule Collecting duct system Hormone Antidiuretic
. 26
•
a
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8
End Block
Item: 25 of 27 ~ 1 • Ma rk -<:J 1>- Jil ~· !:';-~
QIO: 3800 ..L Prev ious Next Lab fli!ltues Not es Cal culat o r
6 •
FA17 p 574.1
7
Diuretics site of action
8
9 Distal
convoluted
Glomerulus
10 0
N.l'
tubule Cal'
Proximal
11 Afferent convoluted a ~ \
tubule
12
Efferent
13
"
14 H,O
15
16
17
Cortex _______ ,_, ' .·.... Na'
18
Medulla
19 Na' @)
K· ...._
20 20 '
0 Mannitol Descending limb,
21
8 Acetazolamide loop of Henle Ascending limb,
22 (permeable to water) loop of Henle
@) loop diUretiCS (permeable to salts)
23
24
0 Thlaz1de
25
0 K• spar ng d1urebcs
Collecting
duct
• 26
•
a
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s
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8
End Bl ock
Item: 25 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 A A
FA17 p 334.1
7
8
Diabetes insipidus Characterized by intense thirst and polyuria with inability to concentrate urine due to lack of ADIJ
(central) or failure of response to circulating AD II (nephrogenic).
9
Central Dl Nephrogenic Dl
10
ETIOLOGY Pituitary tumor, autoimmune, trauma, surgery, Hereditary (ADH receptor mutation), 2°
11
ischemic encephalopathy, idiopathic to hrpcrcalcemia, hypokalemia, lithium,
12
demeclocycline (ADH antagonist)
13
FINDINGS ~ ADH l\ormal or t ADH b·els
14
Urine specific gravity< 1.006 Urine specific gra,·ity < 1.006
15 Serum osmolality> 290 mOsm/kg Serum osmolality> 290 mOsm/kg
16 Hyperosmotic ,·olume contraction Hyperosmotic ,·olume contraction
17 WATER DEPRIVATION TEST' >50% t in urine osmolality only after linimal change in urine osmolality, even after
18 ad ministration of ADH analog administration of ADH analog
19 TREATMENT Desmopressin acetate HCTZ, indomethacin, amiloride
20 Hyd ration Hydration, dietary salt rest riction, avoidance of
offending agent
21
"! o water intake for 2-3 hr followed by hourly measurements of urine vol ume and osmolarity and plasma Na+ concentration
22
and osmolarity. AD! I analog (desmoprcssin acetate) is administered if serum osmolality> 295-300 mOsm/kg, plasma
23
a+ ~ 145, or urine osmolality does not rise despite a rising plasma osmolality.
24
25
FA17 p 317.3
• 26
• Antidiuretic hormone
a
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8
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Item: 25 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 A A
TREATMENT Desmopressin acetate I-ICTZ, indomethacin, amiloride

7
Hydration Hydration, dietary salt restriction, avoidance of
8 offending agent
9
a o water intake for 2-3 hr foiiO\\·ed by hourly measurements of urine volume and osmolarity and plasma 1 a+ concentration
1
10 and osmolarity. AD!! analog (desmopressin acetate) is administered if serum osmolality> 295-300 mOsm/kg, plasma
11 1a" ~ 145, or urine osmolality does not rise despite a rising plasma osmolality.
12
13 FA1 7 p 317.3
14 Antidiuretic hormone
15 SOURCE Synthesized in hypothalamus (supraoptic
16 nuclei). stored and secreted by posterior
17 pituitary.
18 FUNCTION Regulates serum osmolarity ( 2-receptors) ADII bel is ! in central diabetes insipidus (01),
19 and blood pressure (V1-receptors). Primary normal or t in neph rogenic OJ.
funct ion is serum osmolarity reguh1tion (AOil ephrogenic 01 can be caused by mutation in
20
! serum osmolarity, t urine osmolarity) via V2-receptor.
21 regulation of aquaporin channel insertion in Dcsmopressin acetate (AOH analog) is a
22 principal cells of renal collecting duct. treatment for central or and nocturnal
23 enuresis.
24 REGULATION Osmoreceptors in hypothalamus (1°);
25 hypovolemia.
. 26
•
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Item: 26 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
6 •
After 3 days of flu-like symptoms, a patient is feeling unsteady on her feet and dizzy when she attempts to stand up. During her illness she
7
has eaten very little and has had frequent emesis. Blood tests reveal an arterial pH of 7 .5 and a partial pressure of carbon dioxide of 53 mm
8 Hg .
10 In addition to the a primary alkalosis from vomiting, how does the kidney contribute to the acid-base disturbance?
11
A. Decreased bicarbonate reabsorption by the proximal tubule
12
13 B. Decreased sodium reabsorpt ion in t he collecting duct
14 C. Effect of antidiuretic hormone (ADH) on collecting duct

15
D. Increased activity of Na/K/2CI transporter in ascending limb
16
17 E. Increased excretion of H+ in the collecting duct
18
19
20
21
22
23
24
25
• 26
•
a
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8
End Bl ock
Item: 26 of 27 ~. I • M k <:] t> al ~· ~
6
The correct answer is E. 42 0/o chose this.
7
This patient has a metabolic alkalosis, consistent with a pH > 7.4 and partial pressure of C0 2 > 4 0 mm Hg . This is secondary to volume depletion
8 and losses of H+ and c l- in the gastric contents. H+ loss from emesis leads to an "alkaline tide " of plasma HCo3- that is not compensated for. I n
addition, reduction of the extracellular volume from fluid losses leads to a relative concentration of HCo3-, termed a "contraction alkalosis. " The
9
significant volume depletion seen with severe vomiting will lead to activation of the ren in -angiotensin -aldosterone system (RAAS}. This causes (1)
10 an angiotensin - mediated increase in H+ secretion/HCo 3- reabsorption in the proximal tubule via stimulation of the sodium - hydrogen antiporter,
and (2} aldosterone - mediated reabsorption of Na+ in the cortical collecting ducts with increases in K+ and H+ excretion . The reabsorption of
11
HC03- and the excretion of H+ propagates the initial metabolic alkalosis.
12 Metabolic alkalosis Partial pressure PH Proximal convoluted tubule Vomiting Alkalosis Extracellular fluid Contraction alkalosis Collecting duct system Chloride
13 Blood plasma Renin-angiotensin system Hypovolemia Metabolism Nephron Antiporter Millimeter of mercury Chlorine

15 HC03- reabsorption in the setting of metabolic alkalosis and volume depletion is likely to be increased . First of all, in the setting of vomiting and
alkalosis, H+ loss from emesis leads to an "alkaline tide " of plasma HCo3- that is not compensated for. I n addition, reduction of the extracellular
16 volume from fluid losses leads to a relative concentration of HC03-. These lead to an increased filtered load of HC03-. I n the setting of volume
17 depletion, we have increased Na+ reabsorption in the proximal tubule mediated by angiotensin II stimulation of the Na/H exchanger, which
d rives increases in HC03- reabsorption in the proximal tubule .
18 Metabolic alkalosis Proximal convoluted tubule Vomiting Angiotensin II Angiotensin Hypovolemia Blood plasma Extracellular fluid Alkalosis Nephron Metabolism
19
20 Dehyd ration causes an increase, not decrease, in Na+ absorption in the collecting duct. This is d riven largely by renal exchanger activity toward
21 Na+ reabsorption and H+ excretion .
Collecting duct system Dehydration Excretion Reabsorption
22
C is not correct. 90fo chose this.
23
ADH acts on V2- receptors in the collecting duct. It does not have d irect effects on acid - base status because the aquaporin channels it mobilizes to
24 the cell membrane are permeable on ly to water.
25 Aquaporin Cell membrane Collecting duct system Vasopressin Semipermeable membrane
26 0 is not correct. JOfo chose this.
6
lock
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Item: 26 of 27 ~. I • M k <:] t> al ~· ~
6 • 3• p g I p y g g
alkalosis, H+ loss from emesis leads to an "alkaline tide " of plasma HCo3- that is not compensated for. I n addition, reduction of the extracellular
7
volume from fluid losses leads to a relative concentration of HC03- . These lead to an increased filtered load of HC03- . I n the setting of volume
8 depletion, we have increased Na+ reabsorption in the proximal tubule mediated by angiotensin II stimulation of the Na/H exchan ger, which
d rives increases in HC03- reabsorption in the proximal tubule .
9
Metabolic alkalosis Proximal convoluted tubule Vomiting Angiotensin II Angiotensin Hypovolemia Blood plasma Extracellular fluid Alkalosis Nephron Metabolism
10
B is n ot co rrect. 60/o c h ose t his.
11
Dehyd ration causes an increase, not decrease, in Na+ absorption in the collecting duct. This is d riven largely by renal exchanger activity toward
12 Na+ reabsorption and H+ excretion .
Collecting duct system Dehydration Excretion Reabsorption
13
C is n ot co rrect. 90fo c h ose t his.
14
ADH acts on V2- receptors in the collecting duct. It does not have d irect effects on acid - base status because the aquaporin channels it mobilizes to
15 the cell membrane are perm eable on ly to water.
16 Aquaporin Cell membrane Collecting duct system Vasopressin Semipermeable membrane
17 0 is n ot co rrect. JOfo c h ose t his.

18 The Na/K/2CI cotransporter creates an osmotic g rad ient in the ascending limp of the loo p of Hen le. This does not actively contribute to acid - base
balance in metabolic alkalosis. This transporter is blocked by furosemide, which leads to natriuresis and loss of potassium, calcium, and
19 magnesium .
20 Furosemide Metabolic alkalosis loop of Henle Magnesium Potassium Osmosis Alkalosis Acid dissociation constant Calcium Cotransporter
21
22 Bottom Lin e :
23 Emesis leads to loss of volume and protons, resu lting in a "contraction " in which HC03- is more concentrated in the blood ( "contraction
24 alkalosis " ) . Decreased renal perfusion in volume depletion will also activate the RAAS, which increases Na+ absorption in exchange forK+ and
H+, thereby worsening the metabolic alkalosis.
25 Metabolic alkalosis Vomiting Contraction alkalosis Hypovolemia Alkalosis Proton Kidney Metabolism Perfusion
26
•
6
lock
s
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0
End Block
Item: 26 of 27 ~ 1 • Ma r k -<:J I> ~ £!1}>'
• !!":-~
QIO: 236 1 ..L Pre v ious Next Lab lues Not es Calcula t o r
6 A A
FA17 p 561 .2
7
8
9 Chec.k arterial pH
10 pH<735 pH>745
,r~--------------------~----------------------~,
11
Acidemia Alkalemia
12
13 Pco1 > 44 mm Hg HC~- < 20 mEq/L Pco2 < 36 mm Hg
14
MetaboUc acidOSIS Metabolic alkalos1s
acidoSIS alkalOSIS
16
17
18 =Na•- (CI t HC01 )
Airway obstruction Hysteria loop diuretics
21 Weakening of respiratory Pulmonary embolism
muscles
22
23
> 12 mEq/l 8-12 mEq/l
24 Pco, •
25 I 45
40 Resporatory
40mmHg
~
26 35 Mixed
• MUDPILES: HARDASS: M '-----
•llr.lln<o<
a
Lock
s
Suspend
8
End Bl ock
7 acidosis
Salicylates (late)
8
69 70 71 72 7.5 74 75 76 77 78 79
9 pH
10
11 FA17 p 561 .1
12 Acid-base physiology
13 pH Pco, (HC0 I COMPENSATORY RESPONSE
1
14 Metabolic acidosis l l l Hypen ·entilation (immediate)
15 Metabolic alkalosis f f f llypoventilation (immediate)
16 Respiratory acidosis l f f f renal [HC 0 3-] reabsorption (delayed)
17 Respiratory alkalosis f l l l renal (HC 0 3-Jreabsorption (delayed)
18
Ker: f l = 1" disturbance; l f =compensatory response.
19
6~~~~~~
2
20
Henderson-Hasselbalch equation: p i I = 6. 1+ log
21
22 Pred icted respira tory compcn s~1t ion for a simple metabolic acidosis can be calculated using the
23 Winters formula. If measured Pco2 > predicted Pc o 2 - concomitant respira tory acidosis; if
24
measured Pc~ < pred icted Pco2 - concomitant respiratorr alkalosis:
25 Pc o 2 = 1.5 [HC 0 3-] + 8 :t 2

26
•
a
Lock Suspend
s 8
End Block
Item: 27 of 27 ~ 1 • M k -<:J 1>- Jil ~· !:';-~
A A
7 The following graph was obtained by collecting and assaying urine from a healthy volunteer given va•·ying amounts of glucose by intravenous
8 infusion.
10
11
12
13
14
15
16
0 200 400
17
Serum glucose (mgldL)
18
19
Which statement concerning the graph is most accurate?
20
:
21 A . Glomerular filtration of glucose is saturated at 375 mg/dL
22
B. Proximal convoluted tubule glucose reabsorption is saturated at 375 mg/d l
23
C. Proximal convoluted tubule glucose secretion begins at 200 mg/dL
24
25 D. Proximal convoluted tubule glucose secretion begins at 375 mg/dL
26 E. Urine glucose begins to be detectable at 375 mg/dL

• 27
a
Lock
s
Suspend
8
End Bl ock
Item: 27 of 27 ~. I • M k <:] t> al ~· ~
•
7 The correct answer is B. 600/o chose this.
8 Glucose is freely filtered at the g lome rulus and, in healthy in d ividuals, is completely reabsorbed in the prox imal convoluted tubule (PCT} .
However, as the filtered load of g lucose increases, the reabsorption ability of the nephron is eventually saturated, and g lucose beg ins to be
9 excreted in the urine. Due to significant variability in nephron physiology, certain nephrons are saturated at lowe r filtered loads than others .
10 Thus, between 200 and 375 mg/d l g lucose beg ins to appear in the urine, but not all nephrons are saturated . A bove 375 mg/d l , all nephrons'
transport maxima are reached, and any additional g lucose is excreted in the urine.
11
Nephron Glomerulus (kidney) Proximal convoluted tubule Glomerulus Glucose Urine Physiology Tubule Anatomical terms of location Reabsorption
12
A is not correct. 11 Ofo chose this.
13 Glomerular filtration is never saturated because it does not depend on carrier- mediated transport. Furthermore, even if g lucose were bein g
14 incom pletely filtered, this would tend to decrease (not increase) urine g lucose levels.
Glucose Urine Membrane transport protein Glomerulus Renal function Filtration
15
C is not correct. 180/o chose this.
16
To whatever extent poss ible, the kidney attempts to fully reabsorb g lucose in the proximal tubule . Thus, it is never secreted in the PCT.
17 Proximal convoluted tubule Kidney Glucose Nephron Anatomical terms of location
18 0 is not correct. 60/o chose this.

19 To whatever extent poss ible, the kidney attempts to fully reabsorb g lucose in the proximal tubule . Thus, it is never secreted in the PCT.
Proximal convoluted tubule Kidney Glucose Nephron Anatomical terms of location
20
21 E is not correct. 50/o chose this.

The g raph shows that the urine g lucose level beg ins to rise at a serum g lucose level of 200 mg/d l and is therefore detectable well before 375
22
mg/d l .
23 Glucose Urine Blood sugar Blood plasma liver function tests Serum (blood)
24
25
Bottom Line:
26
Glucose is freely filtered at the g lome rulus, and at normal plasma levels it is completely reabsorbed in the proximal convoluted tubule . At
27 ~
plasma levels of 200-375 mg/d l , g lucose beg ins to appear in the urine, and at levels exceed in g 375 mg/d l , transport becomes saturated .
6
lock
s
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0
End Block
Item: 27 of 27 ~. I • M k <:] t> al ~· ~
• However, as the filtered load of g lucose increases, the reabsorption ability of the nephron is eventually saturated, and g lucose begins to be •
7
excreted in the urine. Due to significant variability in nephron physiology, certain nephrons are saturated at lowe r filtered loads than others .
8 Thus, between 200 and 375 mg/d l g lucose beg ins to appear in the urine, but not all nephrons are saturated . A bove 375 mg/d l , all nephrons'
transport maxima are reached, and any additional g lucose is excreted in the urine.
9
Nephron Glomerulus (kidney) Proximal convoluted tubule Glomerulus Glucose Urine Physiology Tubule Anatomical terms of location Reabsorption
10
A is not co rrect. 11 Ofo c hose t his.
11
Glomerular filtration is never saturated because it does not depend on carrier- mediated transport. Furthermore, even if g lucose were bein g
12 incom pletely filtered, this would tend to decrease (not increase) urine g lucose levels.
Glucose Urine Membrane transport protein Glomerulus Renal function Filtration
13
14
To whatever extent poss ible, the kidney attempts to fully reabsorb g lucose in the proximal tubule . Thus, it is never secreted in the PCT.
16
0 is not co rrect. 60/o c hose t his.
17 To whatever extent poss ible, the kidney attempts to fully reabsorb g lucose in the proximal tubule . Thus, it is never secreted in the PCT.
19 E is not co rrect. 50/o c hose t his.

20 The g raph shows that the urine g lucose level beg ins to rise at a serum g lucose level of 200 mg/d l and is therefore detectable well before 375
mg/d l .
21 Glucose Urine Blood sugar Blood plasma liver function tests Serum (blood)
22
23
Bottom Line :
24
Glucose is freely filtered at the g lome rulus, and at normal plasma levels it is completely reabsorbed in the proximal convoluted tubule . At
25 plasma levels of 200-375 mg/d l , g lucose beg ins to appear in the urine, and at levels exceed in g 375 mg/d l , transport becomes saturated .
Glomerulus (kidney) Proximal convoluted tubule Glomerulus Glucose Urine Blood plasma Nephron Anatomical terms of location
26
27 ~
6
lock
s
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0
End Block
Item: 27 of 27 ~ .I • M k <:] t> al ~· ~
• plasma levels of 200-375 mg/d l , g lucose beg ins to appear in the urine, an d at levels exceed in g 375 mg/d l , transport becomes saturated .
7
Glomerulus (kidney) Proximal convoluted tubule Glomerulus Glucose Urine Blood plasma Nephron Anatomical terms of location
8
9
10 liill;fiiJI•J fo r year:[ 2017 "

FIRST AID FACTS
11
12
FA17 p 554.2
13
Glucose clearance Glucose at a normal plasma level (range 60-120 Glucosuria is an important clinical clue to
14
mg/dL) is completely reabsorbed in proximal diabetes mellitus.
15 convoluted tubule (PCT) by Na+Jglucose Splay is the region of substance clearance
16 cotransport. between threshold and T111; due to the
17 Tn adults, at plasma glucose of- 200 mg/dL, heterogeneity of nephrons.
18
glucosuria begins (threshold). At rate of
600
- 375 mg/min, all transporters are fully Filtered
19 c Excreted/
saturated cr.,). 'E
- 450 Tm~ 75mg/min ,,''
20
'ormal pregnancy may decrease ability of .§ ,/ Reabsorbed
PCT to reabsorb glucose and amino acids
,--::)~~~----- ,/,/,,•
21
__
22 - glucosuria and aminoaciduria.
23
Sodium-glucose cotransporter 2 (SGLT2) Renal / /
inh ibitors (eg, -Aozin drugs) permit glucosuria threshold /
24
at plasma concentrations < 200 mg/dL.
"'--~---- 1 ,--
__.,.,.
__::....
_ ---,-
25 1 200 400 600 800

Normal Plasma glucose (mg/dl)
26
27 ~
6
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0
End Block

Renal Physio

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Item: 1 of 27 ~ 1 • M k -<:J 1>- Jil ~· !

•7 A is not correct. 70fo ch ose th is.

• 11 B is not co r rect. 120/o c hose t his .

• 15 D is not co rrect. 30/o c hose this .

· 11 E is n o t co rrect . 50/o c h ose t his.

2 The co rrect a nswe r is C. SOO/o c hose t his.

•9 A is not co rrect. 2 1 Ofo c hose t his .

•8 0 is no t co rrect. 6 0/o c hose this.

.9 B. An antagonist of cardiac and vascular calcium channels

• 13 E. Angiotensin receptor blocker

2 The co rrect a nswe r is E. 720/o c hose t his .

• 20 Constricts efferent I FF to preserve renal function {GFR)

•5 I Na• delivery Acts at angiotensin II

• 15 (posterior ------~ I aquaporin insertion in - --+ H20

• 15 C is not correct. JO/o c hose this •

Blood volume Sodium Tachycardia Baroreceptor Anatomical terms of location Perfusion

•6 B is not co rrect. l JOfo c hose t his.

•5 l Na• delivery Acts at angiotensin II

2 The co rrect ans w e r is B. 6 20/o c hose this.

• 16 A is no t co rrect. 4 0fo c hose this.

• 20 Cellular respiration Blood plasma Serum (blood)

• 21 C is no t co rrect. 1 50/o c hose this .

•9 0 is no t co rrect. 90fo c hose this.

·8 pH Pco, (HC0 I COMPENSATORY RESPONSE

·8 B. Bowman space hydrostatic pressure will be increased

.9 C. Bowman space oncotic pressure will be decreased

• 11 B is not correct. 11 Ofo chose this.

3 A is not co rrect. 90fo c hose t his.

• 13 0 is not co rrect. 11 Ofo c hose t his .

Creatinine clearance is an approximate measure 4

1 (CC =glomerular cap.Jlary; BS = Bowman space.) :::: E 8

.9 C. Mixed metabolic acidosis and respirat ory alkalosis

·8 B is not correct . 180/o chose this.

7 0 is not co rrect. 70/o c hose t his.

· 11 E is not co rrect. SO/o c hose t his .

5 Creatinine clearance: 120 ml/min

2 The correct answer is E. 4J Ofo chose this.

• 15 0 is not correct. 120/o chose this .

• 11 0. Kinetics of the sodium-potassium exchange pump in the distal convoluted tubule

0 14 Interstitial fluid Gradient

8 B. Compound X is reabsorbed in t he descending limb of the loop of Henle

9 C. Compound X is reabsorbed in t he proximal convoluted tubule

2 The correct answer is 0. 760/o chose this.

• 16 E is not correct. 80fo chose this.

4 A is not correct. 50fo chose this.

10 C is not correct. 80fo chose this.

9 C. Excessive diuresis with a loop diuret ic

2 The correct answer is C. 580/o chose this.

8 A is not correct. 100/o chose this.

• 20 E is not correct. 60/o chose this.

5 pH< 7.35 pH> 745

2 The correct answer is 0. 420/o chose this.

10 A is not correct. 140/o chose this.

• 14 B is not correct. 21 Ofo chose this.

1 Laboratory tests show :

2 Plasma sodium : 125 m Eq/ L

1 A is no t co rrect . 4 0fo c hose t his.

5 B is no t co rrect . 50fo c hose t his.

2 The co rrect a nswe r is 0. 750/o c hose t his.

13 F is no t co rrect . 30/o c hose t his.

5 I Na• delivery Acts at angiotensin II

10 ~ ~ov-Jroan space Podocytes

15 C. Type I renal tubular acidosis

• 18 E. Type IV renal tubular acidosis