1

what test must be done prior to radial artery catheter

placement in a pt with acromegaly? Why?

Allens test- carpal ligament enlargement may cause

inadequate ulnar artery flow

Pre-op workup of acromegalic patient reveals

impairment of adrenal and/or thyroid axis. What should
be implemented in perioperative period?

stress-level glucocorticoid therapy ; thyroid replacement

What two important peptide hormones does the posterior

pituitary hormone secrete?

ADH (Vasopressin)
Oxytocin

What is the function of ADH?

ADH controls water excretion and reabsorption in the kidney

and is a majorregulator of serumk osmolarity

What effect does ADH have on renal collecting ducts?

Decreases permeability

What stimulates the release of ADH?

Na and plasma osmolality

What effect does ADH have on the vasculature?

Potent vasoconstriction

What effect does ADH have on blood volume?

Increases

How does ADH affect hemostasis?

promotes hemostasis by increasing vWF and FVIII

Will ADH release be increased, decreased or unchanged

in the perioperative period?

Increased D/T stress, hemmorrhage, anemia, medications,

hypotension

What is diabetes insipidus? (DI)

what are the two types?

Neurogenic DI-Inadequate ADH secretion from the posterior

pituitary
Nephrogenic DI-inability of renal collecting duct tubule
receptors to respond to ADH

What are causes of DI?

genetic,
hypercalcemia
hypokalemia
medication-induced nephrotoxicity
ETOH

What perioperative management will be taken with DI?

electrolyte evaluation
volume status-SLOW restoration of volume pre-op (24-48
hrs)

What is SIADH?

High vasopressin level despite hyponatremia and plasma

hypotonicity

What are clinical manifestations of SIADH?

cerebral edema->lethargy, H/A, N/V, seizures coma

How is SIADH managed?

Mild SIADH: fluid restriction

Na<115: SLOW IV infusion of hypertonic saline (no more
than 5-7mEq/hr)

What negative sequelae may result from rapid infusion

of hypertonic saline?

Central Pontine Demyelination Syndrome-permanent

neurologic damage

What % of body Ca++ exists in the bone?

99%

In what three forms does serum CA++ exist, and in what

percentage each?

Plasma protein bound -40%

Nonionized (bound to anion)-10%
Ionized Ca++-50% (only part that counts!)

What is the effect of alkalosis on Ca++?

Alkalosis (think hyperventilation) reduces ionized Ca++ by

allowing more to bind with proteins

What three hormones work in concert to regulate the

plasma concentratin of calcium?

Vit D
Parathyroid Hormone (PTH)
Calcitonin

What effect does decreased PTH have on CA++?

decreases CA++

How does a decreased PTH affect nerve function?

decreased Ca++ -> lowered threshold potential>neuromuscular excitability->muscle spasm and tetany

What sx will be seen in hypocalcemia?

variable severity: cramps, perioral perissthesias, numbness in

feet or toes, hyperactive deep tendon reflexes
Acute laryngeal muscle spasm->stridor

What are two classic manifestations of latent

hypocalcemia?

Chvostek's sign-ipsilateral twitching when facial nerve is

tapped at angle of jaw
Trousseau's Sign-inflation of BP cuff->aggravation of muscle
yielding irritability and spasm at the wrist

following parathyroid surgery for hyperparathyroidism,

the anesthetist would be alert for ...?

Transient (1-2 day) hypocalcemia D/T "bone hunger"

Monitor Ca++ level regularly

What mainifestations of neuromuscular compromise

secondary to hypocalcemia may be seen s/p parathyroid
surgery?

Laryngeal spasm (unilateral or bilateral)

Prolonged QT interval -> hypotension, decreased contractility

What interventions may cause an abrupt decline in levels

of ionized calcium?

Hyperventilation
NaHCO3 administration
Blood transfusion

What affect does hypocalcemia have on NDMR?

Altered response-consider shorter acting NDMR

How is the QT interval measured?

Begins with the start of the Q wave , lasts thru the QT interval
and ends with the end of the T wave, and is corrected for heart
rate

what is the primary cause of hyperparathyroidism?

Increased PTH despite high serum Ca++ levels

90% from parathyroid adenoma

When will sx of hyperparathyroidism be seen?

Asymptomatic until Ca++ =11-12 mg/dL

"Stones, Bones and Groans"- stones, bone damage, pain
weakness, confusion, pathologic fx

What is a significant diagnostic feature of

hyperparathyroidism?
Why does this occur?

Elevated alkaline phosphatase (secreted by osteoblasts as they

try to rebuild bone destroyed by osteoclast exagerated activity
in response to PTH)
(Rich had this wrong in the notes, see N&Z pg 749)

What are sx of hyperparathyroidism?

1)"Stones, Bones and Groans"- stones, bone damage, pain

weakness, confusion, pathologic fx

Distinguish clinical features of hyper vs hypo

poarathyroidism

CV
HYPER=HTN, conduction disturbances, shortened QT
HYPO=hypotension, decreased contractility,prolonged QT
MUSCULOSKELETAL

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HYPER=bone pain, pathologic fx, muscle weakness,
&atrophy
HYPO=NM excitability
NEUROLOGIC
HYPER=somnolence, cognitive impairment, depression,
hypotonia
HYPO=tetany, paresthesias, numbness in fingers/toes,
seizures
GI
HYPER=anorexia, N?V, constipation, abd pain, pancreatitis ,
peptic ulcer
HYPO=None
RENAL
HYPER=tubular resorption defects, dim renal function,
kidney stones, polyuria
HYPO=None
What is the surgical treatment for hyperparathyroidism?

Removal of abnormal thyroid tissue

Is nerve monitoring required for parathyroid surgery?

No

What type of blood loss is anticipated with parathyroid

surgery?

minimal

Anesthetic medication doseages and selection may be

affected by impairments in which system of a pt
undergoing parathyroid surgery for secondary
hyperparathyroidism?

Renal impairment-> volume overload, anemia, electrolyte

derangements

In a hyperparathyroid pt, how is severe hypercalcemia

(>14mg/dL) treated perioperatively?

isotonic salione and loop diuretics

What CV effects does hypercalcemia have?

HTN,arrhythmias, short QT interval

Why might the hypercalcemic pt be dehydrated?

N/V, anorexia

In the hyperparathyroid pt who is hypercalcemic, what

considerations are there regarding sedation and NMB?

Avoid pre-op sedative in lethargic/confused pt. NDMR may

be prolonged due to muscle wekness

Where are the adrenal glands located?

above the kidneys

What are the three zones of the adrenal cortex? what

hormones are secreted by each?

Zona glomerulosa(outer)-mineralocorticoid
Zona Fascibulata (middle)-cortisol (ACTH)
Zona Reticularis (inner)-adrenal androgenic hormones
All are corticosteroids

ACTH from the _________ gland stimulates the adrenal

gland to make_________.

Pituitary
Cortisol

As the level of cortisol________, the amount of

___________ made by the pituitary is turned ________.

rises
ACTH
down

What are 4 specific actions of cortisol?

Guconeogenesis
Stimulates protein metabolism

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Oxidizes fatty acids
decreases inflammatory process

What are the stimulants of aldosterone release?

a)Hypokalemia
b)AngiotensinII
c) Hyponatremia
d)ACTH

what is the primary mineralocorticoid?

Aldosterone

What is the major role of mineralocorticoids?

Regulation of extracellular Na and K and total body fluid

balance

What is primary aldosteronism?

Adrenal adenoma->increased aldosterone secretrion->renal

excretion of K (hypokalemia)in wxchange for Na
(hypernatremia)->HTN

What are the anesthetic implications in management of

hyperaldosteronism?

1)Correct electrolyte, glucose imbalance

2)Hypokalemia ->prolonged NDMR
3) Hypertension controlled with K sparing diuretics
(spironolactone)

What syndrome does excess glucocorticoid cause?

Cushings

Cushings syndrome is an excess of ________.

Glucocorticoid (cortisol)

What causes Cushings syndrome?

1)therapeutic administratin of glucocorticoids

2)endogenous:
a-pituitary tumor (Cushings disease)
b-adrenal tumor
c-hypothalamic tumor
d-ectopic hormone production

What are clinical features of Cushings syndrome?

Truncal obesity, HTN, glucose intolerance, striae,

weakness(fat and muscle broken down), fluid retention,
hypokalemic alkalosis, inhibition of immune
system,increased incidence of DVT, hirsutism, trun

What is the primary treatment for Cushings ?

transphenoidal hypophysectomy

What are anesthetic considerations for Cushings pt?

Control HTN & glucose

Adm glucocorticoid steroids

What is the pathophysiology of Pituitary Cushing's

Syndrome?

Pituitary hyperfunction(adenoma of microadenoma)>produce ACTH->adrenal cortial hyperplasia->cortisol

release, acts on pituitary->suppression of normal pituitary
60-70% of Cushing's have elevated plasma cortisol and
ACTH with loss of normal diurnal variation

What 2 systems maintain homeostasis?

nervous
endocrine

Choose one: a)endocrine or b)exocrine glands

secrete their hormone products directly into the
surrounding extracellualr fuid?

endocrine glands
exocrine secrete through ducts

What three major categories of hormones are there?

1) peptide or protein

5
2)amines or amino acid derivatives
3) steroids
Most hormones are of which structure? Can you name
some?

peptide: insulin, growth hormone, vasopressin, angitensin,

prolactin, erythropoeitin, calcitonin, somatostatin, ACTH,
oxytocin, glucagon, and parathyroid hormone

where are prehormones stored? what causes their

relsease?

stored in secretory cells in the exocrine gland, and released

upon stimulation that causes exocytosis

what are steroid hormones derived from? where are

steroid hormones stored?

cholesterol
in contrast to most other hormones, steroid hormones are not
stored in discrete secretory granules, but are
compartmentalized in the endocrine cell and released into the
extracellular fluidby simple diffudion thru the cell membrane

where are most hormones broken down?

liver and kidneys

What is the effect of protein binding on hormones?

longer duration

what general effect does the binding of a hormone to a

cellular receptor have?

activates a second messenger

what is downregulation?

receptor # is inversel proportional to circulating hormone

what is upregulation?

low circulating hormone causes an increase in receptors to

amplify cellular response

1. Neural control(pain, stress)

2. Biorhythms (intrinsic oscillations-genetic)
what three general control mechanisms regulate hormone
3. Feedback control
secretion?
a)negative
b)positive
What is the nickname of the pituitary gland?

The Master Gland

what is the largest portion of the pituitary?

Anterior

the syntesis of what 6 hormones are directed by the

hypothalamus?

1. Growth hormone-skeletal muscle development

2. Adrenocorticotropic hormone (ACTH)-adrenal
development
3. Thyroid stimulting hormone (TSH)- metabolism
4. follicle Stimulating Hormone (FSH)- gonadal development
5. Lutinizing hormone (LH)- ovulation
6. Prolactin mammary development

Is the vsacular supply of the pituitary primarily arterial

or venous?

Primarily venous

What conditions may cause hypopituitary disorders?

1. large pituitary tumors(macroadenomas)

2. Sheehan's syndrome(postpartum shock)
3. irradiation
4. trauma
(according to Rich, most tumors cause hypersecretion and
infarcts cause hyposecretion)

what is panhypopituitarism?

generalized pituitary hypofunction (as opposed to reduced

6
output of a single pituitary hormone)
what can cause Sheehan's syndrome?

an infarct of the pituitary following postpartum shock or

hemmorrhage. It resultsin hypopituitarism

what is the significance of damage to the anterior

pituitary gland?

damage to the anterior pituitary causes partial or complete

lossof thyroid, adrenocortical and gonadal function

What is the ususal surgical approach to the anterior

pituitary?

transphenoidal, less often:sublabial

What are the implications for the transphenoidal

approach usually used for pituitary surgery/

"half-sitting" position
potentialy large blood loss
post op nasal packing-don't extubate till full return of airway
reflexes
need smooth and rapid wake up for post op neuro exam

what is often the cause of hypersecrtion from the

pituitary?

tumor

What are the three most common hypersecreting

pituitary tumors?

1. prolactin-infertility
2. ACTH-Cushing's disease
3. GH-acromegaly

Tell me what you know about growth hormone :)

peaks in childhood, declines with age

no target receptor, affects alltissue
stimulates bone growth

Hyposectretion of growth hormone causes

dwarfism

hypersecretion of growth hormone causes

acromegaly

what physiologic changes are seen in acromegaly?

massive bone growth

increased soft tissue- LARGE LIPS, TONGUE,
EPIGLOTTIS!
osteoarthrits
glucose intolerance
skeletal muscle weakness
CV/CAD/HTN
decreased corticosteroids-May need a stress dose of steroids

What % of people with acromegaly have a difficult

airway?

31%

what features will cause a difficult airway with

acromegaly?

facial deformities, large jaw, subglottic narrowing, large lips,

tongue and epiglottis

What complication can result from rapid Na+ correction?

central pontine demyelination syndrome-permanent

neurologic damage

What % of body Ca++ is found in bone?

99%

In what three forms is serum Ca++ found ?

1. protein + Calcium=40%
2. diffusable ion + Calcium = 10%
3. IONIZED CALCIUM=50% (this is the only one that
counts!)

What effect does alkalosis have on ionized Calcium?

reduces ionized calcium by allowing more to bind with

7
proteins
Which three hormones operate in concert to regulate the
plasma concentration of calcium?

1. Vit D (inactive prohormone from sun and milk)

2. Parathyroid hormone (PTH)
3. Calcitonin

What is the effect of decreased parathyroid on calcium

levels? wha teffect does this have?

Low serum calcium levels which causes

1. hyperexcitability of the nerve and muscle cells(muscle
spasm and tetany) (cramps, numbness in feet)
2. ACUTE LARYNGEAL SPASM!!!(stridor)

What are the two classic signs of latent hypocalcemic

tetany and how do you test for htem?

1. Chvostek's sign-ipsilateral twitching when tap facial nerve

at the angle of the jaw
2. Trousseau's sign-inflate BP cuff->aggravation of muscle
yielding irritability and spasm at the wrist

How is Calcium replacement administered?

slow IV (CaGluconate over 1/2hr; Cacl will cause profound

sustained brady-push over 1-5 minutes)

What altertion in Calcium is frequently observed s/p

parathyroid surgery for hyperparathytoidism?

hypocalcemia within hours or 1-2 post op days, resulting from

rapid bone uptake of Ca (bone hunger)

What sx of hypocalcemia may alert the anesthetist ?

1. laryngeal spasm (unilateral=stridor; bilat =inability to move

air)
2. prolonged QT interval (delayed veentricular
rrpolarization)may lead to hypotension, decreased
contractility

The pt is hypocalcemic. In planning anesthesia for

surgery, the anesthetist may consider...

using a shorter acting NDMR-hypocalcemia prolongs

response to NDMR

What type of lines are necessary for parathyroid surgery

Large Ivs or Aline-frequent Ca levels will need to be drawn

and pt will be 180 degrees away form you

Name differential dx in someone presenting with

headache, HTN, elevated RR, BP, HR

Pheo, hypo/hyper glycemia, MI, thyroid storm, HTN, stroke

What is the normal percent of circulating epi to norep?

80% and 20%

What is the ratio of circulating catecholamines in

pheochromocytomas?

9:1, more norepi

Name the symptom triad found in pheo

headache, diaphoresis, tachycardia

What is the conclusive (but subjective) test for pheo

elevated plasma norepi

What is another test for pheo?

24 hr urine for metanephrines. 95% of pheo have increased

levels. If elevated, test for free catecholamines. If all 3
negative, - pheo.

What drug can be given to test for pheo?

Clonidine bc of A2 antagonism. If BP doesn't go down= +

pheo
Also phentolamine (regitan)

What is MIBG scintography?

test where dye will concentrate in cromaffin cells bc of

similarity to NE. 85% sensitive, 97% specific

What drug must be stopped 1-2 weeks before pheo

MAOI- blocks breakdown of dopamine and norepi.

8
removal?
Name minimul preoperative criteria for pheo surgery

BP <160/90 for 48 hrs before surgery, no ST changes for 1

wk, no more than 1 PVC/5 mins

What to avoid during pheo surgery

histamine releasing drugs, possibly Des, pancuronium,

droperidol (toursades) ketamine, narcan, succ contraversial d/t
catecholamine release

Name possible anesthetic plan for pt with pheo surg

GETA + epidural, preoperative benzos, deep induction for

DL, succ contraversial, use of nitroprusside, narcotics.

What do you anticipate post tumor removal?

hypo/hyperglycemia, hypotension treated with direct A1

agonist, HTN if residual catecholamines

Name S/S of Cushing's disease

Truncal obesity, thin extremities, buffalo hump, osteopenia,

hyperglycemia, HTN from fluid overload, emotional liability,
increased risk of infection

Name S/S of Addison's

primary adrenal insufficiency- skeletal muscle weakness,

hypoglycemia, hemoconcentration, wt loss, hypotension,
dehydration, needs steroid dose before surgery

Characteristics of T3 and T4

T3- more potent, in peripheral tissues

T4- more in circulation overall, less potent

Drugs used in hyperthyroidism

Thioamindes to inhibit thyroid peroxidase, PTU,

methimazole. Iodides inhibit production and release of
thyroid hormone. T3 and T4 because of negative feedback
mechanism

What is the role of beta blockade in hyperthyroidism?

Inhibits peripheral conversion of T4 to T3 and decreases

tachycardia associated with increased SNS activity

What is the role of corticosteroids in hyperthyroidism?

Inhibits TSH and peripheral conversion of T4 to T3

Name intraoperative considerations during

thyroidectomy

thiopental (dose dependent antithyroid activity), propofol,

etomidate, (no ketamine), positioning, des contraversial, N20
ok, DL can cause ball valve obstruction

Name S/S of thyroid storm

hyperthemia, tachycardia, tachydysrythmias, altered

mentation (part of differential)

Name causes of thyroid storm

6-18 hrs postop. Precipitating factors- infection, surgery,

DKA, CHF, pregnancy, extreme stress.

What disease is thyroid storm linked to?

Non-euthyroid preoperative Grave's disease

Name differential dx of MH

hyperthermia, tachycardia, HTN, hypercarbia, elevated CO2,

Masseter spasm

Name differential dx of thyroid storm

hyperthermia, tachycardia, tachydysrythmias, HTN, altered

mentation

Name differential dx of pheo

Tachycardia, paroxysmal HTN, headaches

Why is ASA dangerous in thyroid storm?

Displaces thyroid hormone from protein and increases

circulating free levels

Name postoperative complications of thyroidectomy

RLN damage, acute hypoglycemia (parathyroid removal),

pneumo, hematoma (airway compression, especially in
tracheomalacia)

Name S/S hypothyroidism

lethargy, cold intolerance, decreased CO and HR, peripheral

vasoconstriction, decreased platelet adhesion, anemia,
impaired renal concentration, adrenal cortex suppression

Preop concerns of hypothyroidism

low cardiac reserve and stress response, possible CV collapse

with CHF, down regulation of baroreceptors, chronic
hypovolemia, more sensitive to hypotension causing meds,
less response to hypoxia and hypercapnea, delayed gastric
empyting

anesthetic concerns of hypothyroidism

anemia, hypothermia, low dose induction agent with no

change in MAC, delayed emergence from low drug
metabolism. Respond weill to direct acting agents when
treating hypotension

Myxedema coma

Extreme hypothyroidism, impaired mentation,

hypoventilation, hyponatremia, CHF, hypoglycemia, may
have bowel obstruction. 80% mortality

Hyperparathyroidism

adenoma, CA, hyperplasia of parathyroid that causes

hypersecretion. Hypercalcemia= kidney stones, confusion,
HTN, arrythmias

What is amitiza?

prokinetic with no anticholinergic effects

Transphenoidal Adenohypophysectomy

Possiblity of DI,steroid prep, Rae tube, mouth pack, avoid

hyperventilation, mannitol, and N20, awake extubation

What is the only organ that does not require insulin to

utilize glucose

brain

What are the actions of insulin?

1. moves glucose into muscle and adipose

2. conversion of glucose into glycogen and triglycerides
3. stim hepatic glycogen synthesis
4. inhibits muscle and fat breakdown, decreasing release of
FA, glycerol and AA
5. Inhibits glycogenolysis and gluconeogenesis

What is the primary organ of glucose homeostasis?

Liver

When will parenteral (IV) Regular insulin have peak

effect?

30 min

If IV access is not available, which route of

administration should you choose for fastest onset and
most reliable absorption?

IM>SQ

How much will 1 unit Reg insulin decrease blood sugar?

1unit-> decrease 25mg/dl IV

What is the mechanism of action of Sulfonylureas?

Increase endogenous insulin secretion

Name 3 sulfonylureas

Glyburide, Tolbutamine, Chlorpropamide

What is the duration of action of Glyburide?

18-24 hrs

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What is the duration of action of Tolbutamide?

6-10hrs

What is the duration of action of Chlorpropamide?

24-72 hrs

What are the contraindications to sulfonylureas?

severe insulin deficiency, concurrent illness, perioperative

Name a Biguanide

Metformin

What is the mechanism of action of Biguanides

(metformin)?

Reduces GI glucose absorption, inhibits production, enhances

insuylin sensitivity.
Does NOT stimulate insulin secretion

What drug impairs excretion of metformin?

cimetidine

What is the plasma half life of metformin?

6 hrs

What is the side effect that anesthesai providers should

be aware of (of Metformin?)

lactic acidosis, especially in renal/hepatic failure

The diabetic patient shows metabolic acidosis and severe

hyperglycemia. What is the cause? What is a
predisposing factor?

hyperglycemic ketoacidosis, predisposed by infection

What electrolyte defieciency may be masked in DKA?

Total body K+ may be depleted yet serum K+ levels normal

Why is an RSI indicated for diabetics?

Autonomic neuropathy causes gastroparesis-considered full

stomach

What drug can be given to prevent aspiration with

diabetics?

metoclopramide (reglan)

What is the danger of cardiac autonomic neuropathy

(with coexisting HTN) in the OR?

Can lead to hypotension unresponsive to ephedrine-give

epinephrine 10mcg IV
Can lead to bradycardia unresponsive to atropine-give
epinephrine 10 mcg IV

What position is risky for a diabetic with retinopathy?

Prone

Why is sit important to give a diabetic an antacid pre-op?

30ml of gastric contents with pH< 2.5 is sufficient to cause

chemical pneumonitis if aspirated. cimetidine is very effective

What period of time in the OR is the diabetic at greatest

risk of CV instability due to autonomic neuropathy?

between intubation and incision-period of no stimulation

How can airway difficultly be assessed in diabetics

1. prayer sign-inability to approximate palms D/T stiff joint

syndrome
2. Limited atlanto -occippital joint motion
3. limited TMJ motion

When should oral hypoglycemic agents be held pre-op?

AM of surgery (48-72 hrs prior if long acting)

What test is mandatory for pre-op workup of diabetic?

EKG-most common peri-operative morbidity in DM is

ischemic heart disease

What is the recommended pre-op blood glucose

parameter?

<200mg/dL

What is a normal A1C (glycosylated hemoglobin)

5-7% shows estimated blood glucose control for past 4-6

weeks

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How should pre-op insulin be managed?

Hold regular insulin AM of surgery, give 1/4 to 1/2 dose

NPH; alternatively , hold all insulin and check blood sugar

What are the intra -op sx of hypoglycemia?

What is the BS level where you will treat?

tachycardia, sweating, HTN, cold clammy skin

50 mg/dL
To raise BS 30mg/dL, give 15 ml D50(=to 7.5 Gm)

How is hypoglycemia treated intra-op?

Bolus with D50 followed by D10 gtt and insulin gtt to prevent
rollercoaster

How does DKA lead to acidosis?

DKA begins with hyperglycemia, leads to osmotic diuresis,

dehydration, and acidosis

Describe 4 cell types of pancreas and what they secrete

and what percent of total?

Alpha-glucagon-25%
Beta-insulin-60%]
Delta-somatostain-10%
PP release pancreatic polypeptide

Describe glucagon, insulin feedback control system.

A decrease in BG stimulates glucagon secretion which can

increase BG in minutes. It stimulates liver to break down
glycogen and increase gluconeogenesis. After this is
exhausted glucagon can increase the rate of amino acid
uptake by liver and then convert the amino acids to glucose

Large amounts of glucagon do what four things?

increase cardiac contractility

enhance bile secretion
inhibits gastic acid secretion
increase blood flow in some tissues especially the kidneys

What are insulins effects of carbohydrate metabolism?

promotes muscle glucose uptake and metabolism

promotes liver uptake, storage, and use of glucose
*CAUSES INCREASED STORAGE OF GLYCOGEN IN
THE LIVER-IMPORTANT BC HELPS TO KEEP
GLUCOSE LEVELS STEADY INBETWEEN MEALS
*iNHIBITS GLUCONEOGENSIS BY DECREASING
QUANTITIES AND ACTIVITIES OF LIVER ENZYMES
NEEDED
*LACK OF INSULIN CAUSES LIVER TO CONVERT
FATTY ACIDS INTO PHOSPHOLIPIDS AND
CHOLESTEROL, THEN TRIGLYCERIDES PLUS
PHOSPHOLIPIDS AND CHOLESTEROL ARE RELEASED
INTO BLOOD AND THIS LEADS TO
ARTHEROSCLEROSIS IN DIABETICS

What causes the increased risk of strokes, heart attacks,

and vascular isues in diabetics?

A lack of insulin which causes the liver to convert fatty acids

into phopholipids and cholesterol. Then triglycerides plus
phospholips and cholesterol are released into the blood and
this high lipid concentration leads to atherosclerosis in
diabetics

What is one of the most serious effects and most

damaging to organs in patients with diabetes?

lack of insulin which leads to protein wasting

What contols secretion of insulin?

increase in BG

What is normal BG range?

80-90mg/100ml

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How much does insulin increase after an increse in BG?

10-fold within 3-5 minutes after increase

When does insulin decrease after an increase and by how

much?

Decreases about halfway back to normal in 5-10minutes

When does insulin rise a second time after an intial

increase and when does it reach a plateau?

rises a second time in about 15 minutes and reaches plateau in

2-3hrs

Describes effects of somatostatin and where created?

Created Delta cells

Inhibits glucagon and insulin secretion
Decreases motility of stomach, dudenom, and gallbladder,
decreases both secretion and absorption in GI tract so
prolongs period of time over which food nutrients are
assimilated into blood

What are symptoms of Type 1 diabetes

increased thirst
increased urination
constant hunger
weight loss
blurred vision
extreme fatigue

When type 2 diabetes is diagnosed what is the problem?

pancreas usually producing enough insulin, but body is

resistant to it
After several years the insulin production decreases

What drug inhibits insulin release?

Alpha 1 agonist

What drug increases it release and uptake of glucose and

potasium glococortoids so it also increases insulin
release

beta agonist

What drug causes hyperglycemia secondary to decreased

insulin secretion?

Beta blockers

How is diabetes diagnoses, what does the ADA

recommend, and what are normal/abnormal results?

ADA recommends Fasting blood glucose test, pt fasts for 8

hrs
100-125=prediabetes
>125=diabetes
2nd test Oral glucose test
drink 75 grams Glucose
>or= 200=diabetic
140-199=prediabetes

What is the average BG level over a 3 month period?

How ofter to check and what is normal/abnormal?

Glycosylated Hemoglobin or Hg A1C test

Check two times a year
goal<7
Normal 6 or less

What is NPH also called?

protamine zinc insulin

When do you worry about giving NPH insulin and why?

Worry when giving it to pts undergoing open heart surgery or

other vascular surgeries when protamine will be given to
reverse heparin
Can have life threating allergic reaction to protamine
Low dose antigenic stimulation from the protamine
containing insulin evokes the production of antibodies to
protamine

13

Signs and symptoms of DKA are?

nausea and vomiting

dehydration, hypotension and tachycardia
kussmauls respirations
abdominal pain
illeus
somnolence or coma
acidosis, high anion gap

What are the essential components for the treatment of

DKA?

insulin administration, fluid replacement, and potassium

repletion

With a patient with DKA what is the fluid, K, and bicarb

deficit?

fluid-5-8hrs
K-200-400meq
Bicarb-350-600meq

Who does Hyperosmolar non-ketonic syndrome usually

to, how does it occut to and why?

Occurs mostly in pts over age of 50 and w/ DM type 2

More insidiuos in nature and usally appear sicker
Higher incidence in nursing home patients and have dementia
related diminished thirst and this causes more dehydration

With HNKS what is Glc, Osmolality, pH, and other

symptoms...6 total

Glucose.600-1000
Hyperosmolarity>350
Normal pH
Osmotic diuresis with hypokalemia
Hypovolemia with hemoconcentration
CNS depression

Hypoglycemia is defined by a BG less than what?

less than 50mg/dl

What are signs and symptoms of hypoglycemia?

diaphoresis, tremulousness, tachycardia, impaired cognition,

confusion, headache, irritability, retrograde amnesia, seizures,
unconciousness, alcohol ingestion

In case of loss of consciousness due to hypoglycemia

what do you give?

10-25 g (20-50ml) of 50% Dextrose IV, maybe Glucagon 1mg

IV

What is the earliest sign for DM 2 nephropathy and what

is it a predictor of?

microalbuminuria earliest sign

strong predictor of death from sstroke or MI

What type of intubation with diabetic patients? WHy?

RSI, due to diabetic autonomic neuropathy and gastric reflux

What are major anesthetic considerations for pts with

diabetes?

Check BG,
Have A1C
lab work
resp, CV status
Gastric motor dysfunction so have Gerd and reflux-use pepcid
Infection increased
kidney involvement
Joint issues

When do you treat Glucose Intra Op ?

If BG >250 treat with IV bolus insulin or start on insulin drip

Every 7.5gm will increase BS how much?

30mg/dl

A B-islet umor of the pancreas that secretes large

amounts of insulin is called?

insulinomas

What are three layers of the adrenal gland?

zona glomerulosa

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zona fasciculata
zona reticularis
Outermost layer of adrenal gland and secretes
mineralocorticoid?

zona glomerulosa

what is a mineralcorticoid

aldosterone

Middle and widest layer of adrenal gland and secretes

glucocortoids and adrenal androgens and estrogen?

zona fasciculata

What are glucocortoids?

cortisol and corticoesterone

Deepest layer of adrenal gland and secretes DHEA,

androstenedione as well as small amounts estrogens and
glucocortoids?

zona reticularis

All hormones from the adrenal cortex are synethisized

from what?

from cholesterol

What ion greatly increases aldosterone secretion?

increased K

Increased activity of what increases aldosterone

secretion?

renin-angiotension system

What ion very slightly decreases aldosterone secretion?

increased Na+

What is necessary for aldosterone secretion but has little

effect in controlling the rate of secretion?

ACTH

What are the most important roles in regulation of

aldosterone?

K and renin angiotensin system

What is chiefly involved with fluid and electrolyte

balance?

aldosterone from adrenal cortex

Aldosterone causes what in kidneys and explain?

secretion causes Na to be reabsorbed in distal renal tubules in

exchange for potassium and hydrogen ions

The net expansion in extracellular volume from

aldosterone is caused by what 3 things?

fluid retention, a decrease in plasma potassium, and metabolic

alkalosis

What secretes hormones which help regulate chemical

balance, regulate metabolism, and supplement other
glands?

Adrenal glands

Describe renin-angiotension sytem?

Renin is made and stored in inactive form called prorenin in

juxtaglomerula cells
When BP falls kidneys cause prorenin to be split into renin
Renin leaves kidneys through blood stream
Renin acts enzymatically on Angiotensinogen to release
angiotensin1
Ace in the lung converts antiotensin1 to angiotension2
Angiotensin 2 is a powerful vasoconstrictor and also decreaes
the excretion of salt and water

What causes Conn's syndrome?

hypersecretion of aldosterone from the zona glomerulosa of

adrenal cortex

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What are the causes of Conns syndrome?

benign adenoma
hyperplasia of adrenal gland
Adrenal cancer

What are the causes of Conns syndrome?

benign adenoma
hyperplasia of adrenal gland
Adrenal cancer

What are the two primary clinical manifestatins of conns

syndrome

hypertension and hypokalemia

What is another name for hyperaldosteronism?

conns syndrome

What are the two types of hypoaldosteronism?

primary due to deficiency due to adrenal gland

secondary due to kidney problem and called hypoeninemic
hypoaldosteronism or renal tubular acidosis type 4

What type of acid base balance do you have with

hyperaldosteronism?

hypokalemic metabolic alkalosis

What type of acid base balance do you have with

hypoaldosteronism?

mild metabolic acidosis

What is secreted by zona fasciculata and is a

glucocorticoid?

cortisol

What are the physiological effects of cortisol?

maintenance of BP, increases sensitivity of vasculature to epi

and norepi
required bronchial and vascular smooth muscle to respond to
catecholamines
gluconeogenesis
inhibits peripheral use of glucose
antiinflammatory effects
facilitates retention of Na and excretion of K
increases glomerular filtration and decreases reabsorption of
water by renal tubules and therefore increases volume of
urine

In the absence of cortisol what happens to your BP?

widespread vasodilation

What are signs and symptoms of Cushings?

protein catabolism, skeletal muscle weakness, osteroporosis,

purpura, ecchmosis
suppressed imune system
increased glucose
alterations in fat metabolism, leads to uncal obesity, moon
face, pendulous abdomen, fat hump on back
HTN, dt cortisol effect on blood vessels
increased Na and decreased K
increased intravascular volume

clinical manifestations of cushings are...fourt things?

psychiatric changes, cognitive difficulities, sleep

disturbances, fatique

What hormones are critical for life?

cortisol and aldosterone

What is one of the most significant consequences of

Addisons?

failure of body to adapt to stresses such as surgery, trauma, or

serious infection, and without adequate steroid coverage, this
may result in a state of shock known as Addisons crisis

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What two drugs can cortisol be inhibited by?

etomidate, ketoconazole

When is addsisons disease apparent?

usually not until 90% of adrenal cortex has been destroyed.

Sometimes pt is in crisis when medical attention if sought

signs and symptoms of addisons disease are?

severe fatique and weakness, loss of weight, increased

pigmentation of skin, faintness and low bp, nausea and
vomiting, abdominal pain, salt cravings, cravings for licorice,
painful muscles and joints, mouth leasions on the inside of
cheek

What causes secondary addisons disease?

most cases secondary hormone control is still maintained

can be caused by pituitary problem
can be caused by long term dose steroid drugs which cause
temporary or permanent loss of adrenal function

What are signs and symptoms of addisons crisis?

sudden penetrating pain in lower back, abdomen, or legs

severe nausea and vomiting
dehydration
low bp
loss of consciousness
difficulty breathing

Treatment of addisons disease is?

hydrocortisone

Hydrocortisone 20mg is equal to what in other steroids?

Cortisone acetate 25mg

prednisone 5mg
dexamethazone 0.75mg

What is treatment of hypoaldosteronism?

fludrocortisone if patient is hypotensiove or has orthastatic

hypotension
can also give lasix alone or with mineralocorticoids

What is treatment of hyperaldosteronism?

Na restriction, K sparing diuretics, surgery only with

hypokalemia cannot be controlled
spironolactone which produces increase in K
Amiloride K sparing diuretic
supplement K
antihypertensives

What is secreted adrenal medulla and in what

percentage?

epi-80%
norepi-20%

What are effects of Norepinephrine?

constriction of all blood vessels of body

increased heart rate
gi tract is inhibited
pupils dilate
greatly increases total peripheral resistance which greatly
increases arterial BP

What is the normal resting rate of secretion of norepi?

0.05g/k/min

What is the manifestations of Epinephrine?

similar to norepi
greater effect on cardiac stimulation
greater beta receptor stimulation effect
less constriction of muscle blood vessels
increases arterial bp to a lesser extent than norepi
increases cardiac output more than norepi

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Rare catecholamine secreting tumors derived from
chromaffin cells of the embryonic neural crest?

pheochromocytoma

Where do pheos arise? How about PGLs or

paragangliomas?

Pheos arise from adrenal medulla

PGLs are from adomen, pelvis, thorax, and neck

What produces significant amounts of catecholamines

and give rise to the classic PHEO clinical picture?

adrenal and extra adrenal paragangliomas(PGL)

What rarely produce signifant amounts of

catecholamines?

parasympathetic PGLS of head and neck

In 9-23% of cases of pheo, the tumors develop from

what?

Develop from extra adrenal chromaffin tissue and are referred

to as PGLS

Malignant Pheos account for what percentage ?

26-35%

About 10% of pts with PHEOs present with what at

inital workup?

metastatic disease

What is MEN 1?

Austosomal dominant syndrome characterized by primary

hyperparathyrodism, pancreatic islet cell neoplasms, and
pituitary adenomas

When MEN1 is associated with PHEOs what are the

manifestations?

rarely associated
all unilateral
rarely malignant
most characterized by HTN
Predominant NE production

Clinical presentation of pheo is?

sudden rise in BP with episodic headache, palpitations, and

sweating

What was one of the main drugs to treat pheo? Why has
it fallen out of favor?

alpha blocker phenoxybenzamine

fallen out of failure due to it producing significant orthostatic
hypotension and reflex tachycardia which causes hypotension
intraop and post op

Nonselective alpha adrenergic blockage can lead to

what? How do you treat it?

reflex tachycardia
Use beta blocker to lower HR

What should you never give a beta blocker before an

alpha blocker?

Non selective beta blockers lead to loss of beta receptor

mediated vasodilation and the unopposed effects of alpha
receptors cause vasoconstriction leading to arterial HTn and
increased afterload, causing MI and pulmonary edema

What is a major concern for preop and intraop control

during PHEO surgery?

volume expansion using colloid and crystalloids to prevent bp

fluctuations, very high fluid volume needed
Intraop BP control with calcium channel blocers, NTg,
Nitroprusside, Phentolamine, cardiac tachyarrythmias treat
with esmolol or labetalol

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What are safe medications to use with Pheos

midazolam
etomidate
propofol
lidocaine
fentanyl
sufentanil
remifentanil
nitrous
iso
sevo
vec
roc
cistacurium

What drugs to avoid with Pheos?

morphine,atracurium, atropine, pan, ketamine, Sux,

halothane, droperidol, reglan, des

What are the periods of greatest danger intraoperative

with Pheos?

Induction, Intubation
exploration of tumor
after venous ligation of tumor

Preferred method of removal of Pheo tumors is?

Laproscoptic

Benefits of Laproscoptic tumor removal of Pheo tumors?

shorter hospital stay and recovery time

decreased requirements for analgesics
cosmetically better result

Syndrome that occurs from tumors that may occur in

small intestine, colon, bronchial tubes, or appendix
These are from enterochromaffin cells.

carcinoid tumor