Endocrine System NCLEX
is shedding the stratum functionalis (functional layer)
Maternity Nursing Review: Menstrual Cycle
Purpose of the Menstrual Cycle: is to release an egg
for potential fertilization (from the ovary) so it can
implant into the endometrium…hence help develop a
baby. If this doesn’t happen, the 28 day cycle starts
all over (note cycle days vary among women).
Two structures that play a vital role in the
woman’s reproductive cycle:
Ovary & Uterus (they work together)
Each structure has three cycles (and these cycles
correspond with each other)
Ovarian Cycles: Follicular (occurs during the
menstrual and proliferative phase), Ovulation, Luteal
Phase
Uterine Cycles: Menstrual & Proliferative (both
occur during the follicular phase), Secretory Phase
Easy Recap of these Phases:
1. Follicular Phase (cycle day 1-13…ovarian
changes) happens during Menstrual (cycle days 1-
6…uterine changes) & Proliferative Phase (cycle days
7-14….uterin changes)
2. Ovulation (day 14…the mid-point of the 28 day
cycle)
3. Luteal Phase (cycle days 15-28….ovarian changes)
happens during Secretory Phase (cycle days 15-
28….uterine changes)
*Typical menstrual cycle is 28 days
Cycle Day: 1-13: First Part of the Menstrual Cycle
Menstrual (Cycle days 1-6)
Follicular Phase (Cycle days 7-13)
Proliferative Phase (Cycle days 7-14)
MENSTRUAL Phase: (uterine changes…cycle days 1-
6)
Goal: shed the stratum functionalis layer of the
endometrium
Woman has bleeding (consists of 1-6 days) where she
of the endometrium. If pregnancy did not occur
during the last cycle, the progesterone and estrogen
levels drop which causes the layer to shed.
During this same time, there are OVARY CHANGES
known as the:
FOLLICULAR PHASE: (ovarian changes…..cycle days
1-13)
Goal: prepare a follicle to release a mature egg
(ovum)
How does it do this? When hormone levels from the
previous cycle drop (specifically progesterone and
estrogen) the hypothalamus releasesGonadotropin-
Releasing Hormone (GnRH) and this causes the
anterior pituitary gland to release FSH (follicle
stimulating hormone) and LH (luteinizing
hormone).
The FSH released from the anterior pituitary
gland stimulates the follicles in the ovary to grow. A
woman has two ovaries (right and left) and each
contains MANY follicles.
Follicles are fluid-filled sacs in the ovary that contain
an immature egg known as an oocyte. NOTE: FSH will
cause several follicles to develop but only ONE turns
into a Graafian follicle (mature follicle) that will
release a mature egg (ovum). The other follicles that
didn’t release an egg will die.
As the follicle matures, it will produce hormones such
as ESTROGEN. The estrogen will steadily increase as
the egg reaches maturity. There will be a small dip in
the production of FSH and LH because the body
senses the extra estrogen which represents that the
egg must be mature and the follicle doen’t need to be
stimulated to grow. This is the negative feedback
loop where the estrogen will signal to the
hypothalamus to decrease production of GnRH so the
anterior pituitary gland will quit releasing so much
FSH and LH.
However, the mature follicle is producing massive
amounts of estrogen and the estrogen secretion from
the follicle will peak to a VERY HIGH POINT. This will
actually cause the anterior pituitary gland to release
a surge of LH (luteinizing hormone)…hence positive
feedback loop and this is what is called an LH surge
(cycle day 11-13).
LH plays a huge role in causing the egg to be released
from the follicle (which causes ovulation to happen).
LH causes the egg to mature and breaks down the
wall of the Graafian follicle allowing the follicle to
release the egg which is now called an ovum. 24-36
hours after the LH surge the ovary will release
the ovum (usually happens mid-cycle…hence day
14).
In addition, LH helps the Graaifan follicle that
released the egg turn into theCORPUS LUTEUM. The
corpus luteum will be responsible for releasing
progesterone and estrogen to maintain a potential
pregnancy until the placenta can take over. NOTE: the
development of the corpus luteum occurs in the
LUTEAL Phase…note why it is called
LUTEAL…the LUTE of luteal corresponds with the
word corpus LUTEum).
*The last 5 days of the follicular phase and during
ovulation is the most fertile time for a woman to get
pregnant…sperm live approximately 5 days and the
egg lives for 24 hours (so fertile cycle days would be
days 9 -16).
PROLIFERATIVE Phase (uterine changes…cycle
days 7-14)
Goal: to rebuild the stratum functionalis layer that
was just shed during the menstrual phase (in case the
ovum is fertilized) so it can implant into the uterus.
What causes the layer to rebuild? Remember how
during the follicular phase the maturing follicles are
secreting estrogen? The estrogen from the secretion
of the maturing follicles is ALSO causing the stratum
functionalis layer to rebuild. In addition, it causes
cervical mucous to thin which allows sperm to
migrate easier to the egg.
OVULATION: Cycle day 14
The egg is released from the ovary. The ovum enters
into the PERITONEAL CAVITY . It makes it journey
to the fallopian tube with the help of the fimbria
which have cilia to help sweep the ovum into the
fallopian tube. If sperm are present to fertilize the
egg, fertilization will occur in the fallopian tube most
likely in the AMPULLA.
The egg will only live for 24 hours and disintegrate, if
not fertilized. The woman will have a low basal body
temperature before ovulation and then increase 0.4-
1’F around ovulation.
Cycle Days 15-28: Second Part of the Menstrual Cycle
Luteal (cycle days 15-28)
Secretory (cycle days 15-28)
LUTEAL PHASE (ovary changes….cycle day 15-28)
Goal: prepare the endometrium for a potential
fertilized egg
Begins when the egg is releases from the ovary.
The corpus luteum forms which developed from the
Graaifan follicle that released the ovum. The corpus
luteum acts as a temporary endocrine structure
that secretes progesterone and estrogen.
Progesterone prepares the endometrium for
implantation of the embryo, if the ovum is fertilized.
Role of Progesterone:
stimulates estrogen production
allows the endometrium to receive the fertilized
ovum for implantation
stops production of LH and FSH (so possible
pregnancy can be maintained) and estrogen inhibits
the hypothalamus from releasing GnRH (hence new
reproductive cycle….if the ovum is fertilize you want
to prevent another menstrual cycle from occuring so
pregnancy can occur).
This will help prevent the hypothalamus from
releasing GnRH which will prevent LH and FSH from
being secreted in case fertilization has occurred.
Corpus luteum stays in place for about 14 days and if
fertilization hasn’t occurred it disintegrates. It will
turn into the corpus albicans. When the corpus
luteum dies, estrogen and progesterone will
decrease and this leads to a new reproductive
cycle….the hypothalamus will release GnRH which
will cause the anterior pituitary gland to release FSH
and LH and the woman will shed the uterine lining
and new follicle will be stimulated to produce a new
egg etc.
However, if fertilization occurs the fetus will start to
produce HcG Human chorionic
gonadotropin (hence what a pregnancy test picks
up) and this will prevent the corpus luteum from
dying. So, until the placenta becomes fully functional,
the
corpus luteum will help maintain steady levels of
progesterone and estrogen to maintain the
endometrium for the fetus. The placenta will take
over will progesterone and estrogen production at
approximately 8 weeks.
SECRETORY Phase: (uterine changes….cycle days 15-
28)
Goal: endometrium is receptive to the implantation
of a fertilized ovum
The progesterone being released from the corpus
luteum is allowing the endometrium to be receptive
for implantation of the fertilized ovum.
Pheochromocytoma
pheo: dark chromo: color cyt:
cell oma: tumor
Definition: It is a tumor found on the adrenal medulla
of the kidneys that secretes excessive amounts of
catecholamines.
Pathophysiology of Pheochromocytoma
Key Players:
Adrenal gland: the human body has two adrenal
glands that are cone-shaped that sit on the kidneys.
The outer layer is the adrenal cortex and the center
layer is the adrenal medulla (tumors are found here).
Adrenal Medulla: found in the adrenal gland and is
within the adrenal cortex. Its role is to secrete
epinephrine (adrenaline), norepinephrine
(noradrenaline), and low amounts of dopamine in
response to the body’s sympathetic nervous system
(fight or flight system) via chromaffin cells.
Chromaffin Cells: founds in the adrenal medulla and
secrete catecholamines. This is what the tumor is
made up of (tumors tend to be benign). These cells
are also found in the heart, head, neck, bladder, spine,
abdomen. If a tumor(s) develops in this area it is
known as paragangliomas rather than
pheochromocytoma
Catecholamines: have a huge influence on how
organs and tissues work. They cause the body to do
the following:
increase heart rate and blood pressure
increase glucose (stimulates the liver to release it
stores of glucose in the blood and blocks the role of
insulin)
increases fat metabolism for energy (breaking down
of fats for fuel)
increases basal metabolic rate (burns more calories)
increases thermogenesis (elevates body
temperature)
how you respond to stress (example: see a
bear…jump and feel fear/anxiety).
—All of this is produced because of stimulation of the
sympathetic nervous system in response to fight or
flight mechanism and happens normally in the body
when stiumalated to do so. However, in
pheochromocytoma a patient is experiencing these
signs and symptoms due to a tumor.
Pheochromocytomas wreak havoc the most on the
cardiovascular system (due to excessive
hypertension).
Tumor or tumors can be found in one or two glands
(most commonly affects one gland).
Causes…..genetic disposition and commonly found
in early to middle aged adults.
Signs & Symptoms of Pheochromocytoma
Remember the mnemonic: Fight & Flight (this helps
you remember it is stimulating the sympathetic
nervous system & symptoms are going to be
extreme)
Facial flushing (from hypertension), fluttering in
chest (palpitations)
*Increased blood pressure & heart rate
Glucose high
*Headaches (sudden and severe)
Tremors
*Frequent sweating (from hypertension)
Loss of weight
Increase anxiety and fear
Growing tumor can cause back or abdominal
pressure or pain
Heat intolerance
Tired and weak (from the constant stimulation)
*=most common signs and symptoms
***Signs and symptoms can happen in episodes or
triggered after an event:
Eating foods with Tyramine (plays a role in pressure
blood): foods that areaged, pickled, fermented like
cheeses, red wine, smoke/dried meat, bananas,
sauerkraut, chocolate.
Surgery, trauma injury, emotional stress, medications
such as Monoamine Oxidase Inhibitors: MAOIs
Diagnosed
24-hour urine for catecholamines and
metanephrines (are metabolites formed when the
body breaks down catecholamines)….if too many
metabolites are found then there are too many
catecholamines being produced). If this test comes
back positive the doctor may order a MRI or CT scan
of the adrenal glands to inspect for tumors.
Blood test to measure metaneprhines.
Treatment:
Adrenalectomy: remove the adrenal gland with the
tumor (may remove one or both depending on where
tumor is located)
Pre-opt: prescribed alpha-adrenergic blockers
Nursing Interventions for Pheochromocytoma
Monitor vital signs: blood pressure, heart rate
Monitor for hypertensive crisis: >180 systolic or
>120 diastolic…if blood pressure is too high for a
long period of time this can cause damage to vital
organs…kidneys, eyes, brain, heart.
Signs and symptoms of this: headache, vision
changes, neuro changes, seizures, shortness of breath
Monitor for chest pain (risk for MI), neuro status
(stroke), EKG changes, hyperglycemia
Provide a calm and cool environment….no
overstimulation!
Per MD order: Administer pre-opt (prior to
adrenalectomy) alpha-adrenergic
blockers (Cardura, Minipress, Hyrtin): work
by blocking noradrenaline, reduces catecholamines.
These medications help decrease blood pressure and
prevent a hypertensive crisis during surgery.
Alpha-adrenergic blockers can cause reflex
tachycardia (due to the decrease in blood pressure).
The heart rate increases in an attempt to increase the
blood pressure as a “reflex” response, and these
medications can causes orthostatic hypotension.
Doctor may also be prescribe patient a beta-
adrenergic blockers like Labetalol or Inderal to help
with hypertension and tachycardia
Education for patient with pheochromocytoma:
Eat high calorie diet: burning fats at a rapid rate
Avoid stimulant substances: energy drinks, caffeine
products, or smoking (due to vasoconstriction)
For patient going for an adrenalectomy: educate
about having to take hormone replacement
medications after surgery and taking alpha-
adrenergic prior to surgery (usually 2 weeks before
surgery)
If patient is having a bilateral adrenalectomy (both
glands removed ): will have to take glucocorticoids
and mineralocorticoid for life.
If patient is having a unilateral
adrenalectomy (only one gland removed): will have
to tak
Hyperthyroidism
Definition: High secretion of thyroid hormone
Key Players:
Thyroid: produces thyroid hormones that play a big
role in body metabolism, regulation of body
temperature, and growth/development.
These hormones are known
as: T3 Triiodothyronine, T4 Thyroxine (most
important when talking about hypo/hyper
thyroidism), and Calcitonin.
Thyroid can NOT make thyroid hormones
without iodine which comes from foods (if you don’t
have enough iodine in your diet…low t3 and t4…this
leads to hypothyroidism and if you have too much
hyperthyroidism)
T3 & T4: plays a huge role in:
burning calories
how new cells replace dying cells
how fast we digest food
stimulate sympathetic nervous system (alertness,
quick responsiveness/reflexes)
increases body temperature and heart rate
brain development
muscle contraction
fertility
regulates TSH (thyroid-stimulating hormones
through the negative feedback loop)
TSH: produced from the anterior pituitary gland
that stimulates T3 and T4 production
Negative Feedback Loop of Thyroid Hormone
Production
Hypothalamus produces -> TRH (Thyrotropin-
releasing hormone)…this causes the Anterior
Pituitary Gland to produce ->TSH (thyroid-
stimulating hormone)….this cause the thyroid
gland to produce-> T3 & T4
There can be problems with the feedback system
where the pituitary gland is not stimulating the
thyroid gland enough so hormones are not produced
or the thyroid is not receptive to the TSH from the
pituitary gland.
Thyroid problems diagnosed with blood tests that
look at T3, T4 (free) levels, and TSH to make a
conclusive diagnosis.
Signs & Symptoms Hyperthyroidism
Let the word of the condition help
you: HYPERthyroidism…everything is going to be
working at an accelerated or high of a rate.
Depending on how high the levels are and what is
causing the condition signs and symptoms can vary:
Weight loss (burning calories increased)
Heat intolerance (feel extremely hot…sweaty)
Tachycardia (sympathetic system in overdrive)
Hypertension (sympathetic system in overdrive)
Diarrhea (GI system working harder and faster)
Skin smooth (from increased blood flow)
Soft hair
Cardiac dysrhythmias: A-fib
Personality changes: irritable, moody, insomnia
Irregular menstruation in women
Causes of Hyperthyroidism
Grave’s Disease (most common cause): autoimmune
disorder due to the production of an
antibody/immunoglobulin TSI (thyroid stimulating
immunoglobulin) that has the same effect as
TSH…this stimulates the body to produce high
amounts of thyroid hormones (genetic).
NOTE UNIQUE S & S: Protruding eyeballs, goiter,
pretibial myxedema: waxy orange peel appearance of
the skin found in the feet and legs
TX: antithyroid meds, beta blockers (block the effect
of the high thyroid hormones on the body…slows
heart, decrease sweating) radioactive iodine therapy,
or thyroidectomy
Toxic Nodular Goiter (TNG): not
autoimmune…growths of nodular goiters that are
independently functioning to cause hypersecretion of
thyroid hormones
S & S: won’t see ophthalmic signs like the protruding
eye balls but the classic signs and symptoms of
hyperthyroidism
TX: antithyroid meds, beta blockers (block the effect
of the high thyroid hormones on the body…slows
heart, decrease sweating) radioactive iodine therapy,
or thyroidectomy
Thyroiditis: inflammation of the thyroid gland and
this can cause T3 and T4 leak into the body
Too much iodine: remember iodine helps make T3
and T4
Nursing Interventions for Hyperthyroidism
Keep the patient comfortable: cool, quiet
environment, calm (administer prescribed sedatives
as needed)
Obtain daily weights (need to watch weigh due to
weight loss from the increased metabolic rate)
Monitor EKG, heart rate, blood pressure
Educate about medications and treatment
(radioactive iodine therapy and thyroidectomy)
Monitor for Thyroid Storm: life-threatening that
presents with exaggerated signs/symptoms of
hyperthyroidism, such as fever, fast heart rate,
HTN
Cause of thyroid storm: complication from
uncontrolled hyperthyroidism or due to
thyroidectomy (caused from excessive thyroid
hormones leaking into the bloodstream after
removal)
Medications for Hyperthyroidism
Antithyroid medication: stops the thyroid from
synthesizing T3 and T4, doesn’t damaged thyroid
gland like radioactive iodine therapy
Methimazole “Tapazole” (most common…fewer
side effect)…common treatment for Grave’s Disease
PTU “Propylthiouracil” (safer during first trimester
of pregnancy)….liver failure
Other side effects of both medications:
agranulocytosis and aplastic anemia
Education for Antithyroid medications:
Never stop taking abruptly (takes a while before the
patients start seeing results)
Take at same time every day
Signs and symptoms of thyroid storm
Avoid iodine rich foods (sea foods like seaweed, dairy
eggs) or supplements
No aspirin (increases thyroid hormone)
Signs and symptoms of hypothyroidism (toxicity)
Beta Blockers:” Inderal” to treat patient signs and
symptoms (help decrease heart rate, blood pressure,
and decrease heat intolerance)
Treatment for Hyperthyroidism
Radioactive iodine: destroys the thyroid gland
overtime and is a permanent cure compared to
medications….not for pregnant or nursing women
Side Effects: Iodism: taste changes “metal taste”,
nausea, and swollen saliva glands
Surgical Treatment:
Thyroidectomy: Removal of the thyroid gland
Watch for thyroid storm due to the manipulation of
the gland causing extra T3 and T4 to leak into the
body….prevent by prepping with medications
of:antithyroid meds, sodium iodide solution, beta
blockers, glucocorticoids
Educate about post-opt care: coughing and deep
breathing and splinting neck when coughing
Monitor for parathyroid destruction problems
(common when a thyroid procedure is performed
due to the close proximity of the parathyroid to the
thyroid gland)…watch calcium levels
“hypocalcemia”…parathyroid responsible for
calcium regulation)
Watch for respiratory distress due to the nature of
the surgical site…keep patient in semi-fowler’s to
help with swelling and drainage at the site (keep at
bedside trach kit and supplies)
Hyperthyroidism
Definition: High secretion of thyroid hormone
Key Players:
Thyroid: produces thyroid hormones that play a big
role in body metabolism, regulation of body
temperature, and growth/development.
These hormones are known
as: T3 Triiodothyronine, T4 Thyroxine (most
important when talking about hypo/hyper
thyroidism), and Calcitonin.
Thyroid can NOT make thyroid hormones
without iodine which comes from foods (if you don’t
have enough iodine in your diet…low t3 and t4…this
leads to hypothyroidism and if you have too much
hyperthyroidism)
T3 & T4: plays a huge role in:
burning calories
how new cells replace dying cells
how fast we digest food
stimulate sympathetic nervous system (alertness,
quick responsiveness/reflexes)
increases body temperature and heart rate
brain development
muscle contraction
fertility
regulates TSH (thyroid-stimulating hormones
through the negative feedback loop)
TSH: produced from the anterior pituitary gland
that stimulates T3 and T4 production
Negative Feedback Loop of Thyroid Hormone
Production
Hypothalamus produces -> TRH (Thyrotropin-
releasing hormone)…this causes the Anterior
Pituitary Gland to produce ->TSH (thyroid-
stimulating hormone)….this cause the thyroid
gland to produce-> T3 & T4
There can be problems with the feedback system
where the pituitary gland is not stimulating the
thyroid gland enough so hormones are not produced
or the thyroid is not receptive to the TSH from the
pituitary gland.
Thyroid problems diagnosed with blood tests that
look at T3, T4 (free) levels, and TSH to make a
conclusive diagnosis.
Signs & Symptoms Hyperthyroidism
Let the word of the condition help
you: HYPERthyroidism…everything is going to be
working at an accelerated or high of a rate.
Depending on how high the levels are and what is
causing the condition signs and symptoms can vary:
Weight loss (burning calories increased)
Heat intolerance (feel extremely hot…sweaty)
Tachycardia (sympathetic system in overdrive)
Hypertension (sympathetic system in overdrive)
Diarrhea (GI system working harder and faster)
Skin smooth (from increased blood flow)
Soft hair
Cardiac dysrhythmias: A-fib
Personality changes: irritable, moody, insomnia
Irregular menstruation in women
Causes of Hyperthyroidism
Grave’s Disease (most common cause): autoimmune
disorder due to the production of an
antibody/immunoglobulin TSI (thyroid stimulating
immunoglobulin) that has the same effect as
TSH…this stimulates the body to produce high
amounts of thyroid hormones (genetic).
NOTE UNIQUE S & S: Protruding eyeballs, goiter,
pretibial myxedema: waxy orange peel appearance of
the skin found in the feet and legs
TX: antithyroid meds, beta blockers (block the effect
of the high thyroid hormones on the body…slows
heart, decrease sweating) radioactive iodine therapy,
or thyroidectomy
Toxic Nodular Goiter (TNG): not
autoimmune…growths of nodular goiters that are
independently functioning to cause hypersecretion of
thyroid hormones
S & S: won’t see ophthalmic signs like the protruding
eye balls but the classic signs and symptoms of
hyperthyroidism
TX: antithyroid meds, beta blockers (block the effect
of the high thyroid hormones on the body…slows
heart, decrease sweating) radioactive iodine therapy,
or thyroidectomy
Thyroiditis: inflammation of the thyroid gland and
this can cause T3 and T4 leak into the body
Too much iodine: remember iodine helps make T3
and T4
Nursing Interventions for Hyperthyroidism
Keep the patient comfortable: cool, quiet
environment, calm (administer prescribed sedatives
as needed)
Obtain daily weights (need to watch weigh due to
weight loss from the increased metabolic rate)
Monitor EKG, heart rate, blood pressure
Educate about medications and treatment
(radioactive iodine therapy and thyroidectomy)
Monitor for Thyroid Storm: life-threatening that
presents with exaggerated signs/symptoms of
hyperthyroidism, such as fever, fast heart rate,
HTN
Cause of thyroid storm: complication from
uncontrolled hyperthyroidism or due to
thyroidectomy (caused from excessive thyroid
hormones leaking into the bloodstream after
removal)
Medications for Hyperthyroidism
Antithyroid medication: stops the thyroid from
synthesizing T3 and T4, doesn’t damaged thyroid
gland like radioactive iodine therapy
Methimazole “Tapazole” (most common…fewer
side effect)…common treatment for Grave’s Disease
PTU “Propylthiouracil” (safer during first trimester
of pregnancy)….liver failure
Other side effects of both medications:
agranulocytosis and aplastic anemia
Education for Antithyroid medications:
Never stop taking abruptly (takes a while before the
patients start seeing results)
Take at same time every day
Signs and symptoms of thyroid storm
Avoid iodine rich foods (sea foods like seaweed, dairy
eggs) or supplements
No aspirin (increases thyroid hormone)
Signs and symptoms of hypothyroidism (toxicity)
Beta Blockers:” Inderal” to treat patient signs and
symptoms (help decrease heart rate, blood pressure,
and decrease heat intolerance)

Treatment for Hyperthyroidism

Radioactive iodine: destroys the thyroid gland

overtime and is a permanent cure compared to
medications….not for pregnant or nursing women

Side Effects: Iodism: taste changes “metal taste”,

nausea, and swollen saliva glands

Surgical Treatment:

Thyroidectomy: Removal of the thyroid gland

Watch for thyroid storm due to the manipulation of

the gland causing extra T3 and T4 to leak into the
body….prevent by prepping with medications
of:antithyroid meds, sodium iodide solution, beta
blockers, glucocorticoids

Educate about post-opt care: coughing and deep

breathing and splinting neck when coughing

Monitor for parathyroid destruction problems

(common when a thyroid procedure is performed
due to the close proximity of the parathyroid to the
thyroid gland)…watch calcium levels
“hypocalcemia”…parathyroid responsible for
calcium regulation)Watch for respiratory distress
due to the nature of the surgical site…keep patient
in semi-fowler’s to help with swellingand drainage
at the site (keep at bedside trach kit and supplies)

Key Points to Remember about SIADH and DI
Each condition is related the secretion of ADH (anti-
diuretic hormone also called vasopressin) which
plays a major role in how the body RETAINS water.
Each condition presents oppositely of each other (ex:
in SIADH the patient retains water vs. DI where the
patient loses water)—-Remember they are opposite
of each other!
Diabetes Insipidus and Diabetes Mellitus are two
separate conditions and are not related although they
share the name “Diabetes”.
How does the Anti-diuretic Hormone work?
ADH is produced in
the hypothalamus and secreted/stored by
the posterior pituitary gland. The function of ADH
is to cause the body to retain water and constrict
blood vessels.
How ADH cause the body to retain water? Through
the help for theKIDNEYS! ADH causes the renal
tubules to retain water (in a homeostatic way).
***But if you have too much ADH you will retain too
much water and if you have too little ADH you will
urinate all of the water our of your body!
How to Remember which one is Increased vs
Decreased?
Syndrome of Inappropriate Antidiuretic
Hormone (SIADH): There is a high level of ADH
(antidiuretic hormone) produced
I like to remember this by the acronym
SIADH….S Increased ADH (anti-diuretic hormone)
High Level of ADH equals low urinary output
Diabetes Insipidus: There is a low level of ADH
(antidiuretic hormone) produced
Low Level of ADH equals excessive urinary output
Diabetes Insipidus Key Concepts
Causes of Diabetes Insipidus:
Kidneys not receptive to ADH
Damage to the pituitary gland and/or hypothalamus
Brain trauma through stroke or head trauma
Tumors
Drugs… ex: Declomycin: this is a part of the
tetracyline antibiotic family and has properties to
inhibit ADH production and is also a treatment for
SIADH
Gestational due to the placenta producing
vasopressinase….too much vasopressinase causes
ADH to breakdown
Signs and Symptoms of DI
Polyuria: LOTS of urine 4L to 24 L per day
Polydipsia: body’s way of trying to keep water in the
body….crave water/ice
Dry mucous membranes, dry skin, decrease skin
tugor…very dehydrated
Urine diluted….low urinary specific gravity
Hypotension (due to the severe dehydration and
remember ADH is responsible for constricting blood
vessels…here the vessel will be dilated which causes
hypotension)
Extreme fatigue and muscle pain/weakness
Hypernatremic (due to the concentrate sodium in the
body from low water levels)
Nursing Management of Diabetes Insipidus
Strict I and O’s, daily weights, safety, watch other
electrolytes (hypokalemia)
Restrict foods that promote diuresis: watermelon,
grapes, garlic, berries etc and caffeine (tea, energy
drinks, coffee)
MD may order:
Mild cases: Chlorpropamide aka Diabinese (used in
type 2 diabetes…not used as much now but it has
properties that increases ADH hormone…watch
for hypoglycemia (blood glucose) and educate
patient about photo-sensitivity to the sun (mild)
Extreme cases: Desmopression (form of vasopressin
that naturally occurs in the body which the ADH) also
called Stimate or DDAVP…given PO, IV, nasally, or
subq. Side Effects: Watch for the patient to become
hyponatremic too and water intoxication
Syndrome of Inappropriate Antidiuretic Hormone
(SIADH)
Try to remember it by this:
S- Samatha’s
I- Increased
A- Anti
D- Diuretic
H- Hormone
Causes of SIADH
Lung cancer (may be a first sign a patient gets…then
finds out they have lung CA)
Nursing Management of SIADH
Daily weights and watch for weight gain, strict intake
and output, fluid restrictions, safety (confused from
brain swelling and low sodium)
Medical treatment per md order:
Loop Diuretics (Lasix): to remove the extra fluids
through the kidneys…watch K+ levels
Hypertonic IV solutions (3% Saline) to remove fluid
from the cell back into the vascular system so it can
be urinated out (watch for causing fluid volume
overload..give slowly and through central line per
hospital protocol)****NOTE: Loop Diuretics &
Hypertonic Solutions are usually order together.
Declomycin (tetracycline family) ADH inhibitor and
allow for diuresis…don’t give with calcium
containing foods like milk or antacids because it
affects absorption.

Damaged to the hypothalamus or pituitary gland

Infection/germs (PNA, meningitis)

Central neuro issues: strokes, gullian-barre syndrome

Drugs (Diabinese aka Chlorpropamide which has

properties to increase the ADH and is a treatment for
DI)

Signs and Symptoms of SIADH

Fluid overload (weight gain)

Hypertension

Fast HR

Low sodium (euvolemic hyponatremia…sodium is

watered down)

Confusion (due to brain swelling with extra fluid)

Seizures

Anorexia (full of water…doesn’t want to eat)

Low urine output with concentrated urine (high

urinary specific gravity)

Addison’s Disease vs Cushing’s
Major Players in these endocrine disorders:
Adrenal Cortex
Steroid Hormones
Corticosteroids (specifically Aldosterone
(mineralocorticoid) & Cortisol (glucocorticoid)
Role of Adrenal Cortex: releases steroid hormones
and sex hormones
Role of Aldosterone: regulates blood pressure
through renin-angiotensin-aldosterone system, helps
retain sodium and secretes potassium (balances
sodium and potassium levels).
Role of Cortisol: “STRESS Hormone” helps the body
deal with stress such as illness or injury, increases
blood glucose though glucose metabolism, break
downs fats, proteins, and carbs, regulates
electrolytes.
Cushing’s (Syndrome & Disease)
Cushing’s: hyper-secretion of CORTISOL (watch
video for clever ways to remember this)
Cushing’s Syndrome vs Cushing’s Disease
Cushing’s Syndrome: caused by an outside cause or
medical treatment such asglucocorticoid therapy
Cushing’s Disease: caused from an inside source due
to the pituitary gland producing too much
ACTH (Adrenocorticotropic hormone) which causes
the adrenal cortex to release too much cortisol.
Signs & Symptoms of Cushing’s
Remember the mnemonic: “STRESSED” (remember
there is too much of the STRESS hormone CORTISOL)
Skin fragile
Truncal obesity with small arms
Rounded face (appears like moon), Reproductive
issues amennorhea and ED in male(due to adrenal
cortex’s role in secreting sex hormones)
Ecchymosis, Elevated blood pressure
Striae on the extremities and abdomen (Purplish)
Sugar extremely high (hyperglycemia)
Excessive body hair especially in women…and
Hirsutism (women starting to have male
characteristics), Electrolytes imbalance: hypokalemia
Dorsocervical fat pad (Buffalo hump), Depression
Causes of Cushing’s
Glucocorticoid drug therapy ex: Prednisone
Body causing it: due to tumors and cancer on
the *pituitary glands or adrenal cortex, or genetic
predisposition
Nursing Management for Cushing’s Syndrome
Prep patient for Hypophysectomy to remove the
pituitary tumor
Prep patient for Adrenalectomy:
If this is done educate pt about cortisol replacement
therapy after surgery
Risk for infection and skin breakdown
Monitor electrolytes blood sugar, potassium, sodium,
and calcium levels
Addison’s Disease
Addison’s: Hyposecretion of Aldosterone &
Cortisol (watch the video for a clever way on how to
remember this and not get it confused with
Cushing’s)
Signs & Symptoms of Addison’s Disease
Remember the phrase: “Low STEROID Hormones”
(remember you have low production of aldosterone
& cortisol which are STEROID hormones)
Sodium & Sugar low (due to low levels of cortisol
which is responsible for retention sodium and
increases blood glucose), Salt cravings
Tired and muscle weakness
Electrolyte imbalance of high Potassium and high
Calcium
Reproductive changes…irregular menstrual cycle and
ED in men
lOw blood pressure (at risk for vascular
collapse)….aldosterone plays a role in regulating BP
Increased pigmentation of the skin
(hyperpigmentation of the skin)
Diarrhea and nausea, Depression
Causes of Addison’s Disease
Autoimmune due to the adrenal cortex becoming
damaged due to the body attacking itself:
Tuberculosis/infections
Cancer
Hemorrhaging of the adrenal cortex due to a trauma
Nursing Management of Addison’s Disease
Watching glucose and K+ level
Administer medications to replace the low hormone
levels of cortisol and aldosterone
For replacing cortisol:
ex: Prednisone, Hydrocortisone
Education: Patient needs to report if they are having
stress such as illness, surgery, or extra stress in life (
will need to increase dosage), take medication exactly
as prescribed….don’t stop abruptly without
consulting with MD.
For replacing aldosterone:
ex: Fludrocortisone aka Florinef
Education: consume enough salt..may need extra salt
Wearing a medical alert bracelet
Eat diet high in proteins and carbs, and make sure to
consume enough sodium
Avoid illnesses, stress, strenuous exercise
Addisonian Crisis
This develops when Addison’s Disease isn’t treated.
In addisonian crisis, the patient has extremely LOW
CORTISOL levels (life threatening).
Remember the 5 S’s
Sudden pain in stomach, back, and legs
Syncope (going unconscious)
Shock
Super low blood pressure
Severe vomiting, diarrhea and headache
NEED IV Cortisol STAT:
Solu-Cortef and IV fluids (D5NS to keep blood sugar
and sodium levels good and fluid status)
Watch for risk for infection, neuro status (confusion,
agitation), electrolyte levels (sodium and potassium,
glucose)
 helps the body deal with stress such as illness or
injury by increasing blood glucose though glucose
metabolism, breaking down fats, proteins, and carbs,
and regulating electrolytes.

Causes of Adrenal Crisis

Damage to the adrenal cortex:

Addison’s Disease which is under treated (not

taking medication properly or they are taking it
properly, but there is extra stress on the body and the
medication needs to be increased…surgery, illness,
emotional stress)

Adrenalectomy:

A treatment for Cushing’s (removal of the adrenal

gland) and patientmust take oral cortisol because
body isn’t producing it. If the patient fails to take the
medication or the medication isn’t enough they could
enter into adrenal crisis.

Pituitary gland is damaged and isn’t

producing enough ACTH. Remember the negative
feedback loop (watch the video for details on it)

Signs and Symptoms of Addisonian Crisis

Remember the 5’S & 3 H’s

Super low blood pressure (nothing will bring it up)

Sudden pain in stomach, back, and legs

Syncope (going unconscious)

Shock

Severe vomiting, diarrhea and headache

Adrenal crisis
Hyponatremia
in a nutshell is extremely low CORTISOL levels.
Hyperkalemia
Key Players in Adrenal Crisis:
Hypoglycemia
Adrenal Cortex: produces CORTISOL
Nursing management of Adrenal Crisis
Pituitary Gland (anterior): regulates CORTISOL
production by releasing ACTH (adrenocorticotropic Administer some cortisol STAT via fastest route
hormone)…when this is released it causes the which is IV!!
adrenal cortex to release cortisol.

CORTISOL: a steroid hormone which is a

glucocorticoid know as the “STRESS Hormone” . This
Most commonly prescribed is Solu-Cortef
“hydrocortisone”, along with IV fluids which will
help replenish sodium and glucose (D5NS).
Start on PO glucocorticoids and mineralocorticoid:
For replacing cortisol: ex: prednisone,
hydrocortisone
Education: patient to report if they are having stress
such as illness, surgery, or extra stress in life…… will
need to increase dosage, take medication exactly as
prescribed….don’t stop abruptly without consulting
with md.
For replacing aldosterone: Fludrocortisone aka
Florinef
Education: consuming enough salt..may need extra
salt
Diabetes Mellitus Lecture Notes for NCLEX
Review
Key Players:
Glucose:
“Sugar” (body needs it to survive) fuels the cells of
your body so they can work properly, BUT IT CAN
NOT ENTER THE CELL WITHOUT THE HELP
OF INSULIN
It is stored mainly in the liver in the form of glycogen
Insulin:
“deals with high blood sugar levels”
A hormone that helps regulate the amount of glucose
in the blood (too much glucose is very toxic to the
body).
It allows your body to use glucose by allowing it to
enter the cells (without insulin glucose would just
float around in your body)
Secreted by the BETA cells of the pancreas from the
islets of Langerhans
Glucagon:
“deals with low blood sugar levels”
A peptide hormone that causes the liver to turn
glycogen into glucose…does the opposite as insulin.
Also secreted by the pancreas
Pancreas:
Releases insulin and glucagon
Liver:
Sensitive to insulin levels and stores and turns
glycogen into glucose when the pancreas secretes
glucagon. Example: (if the body has increased blood
glucose/increased insulin in the blood the liver with
absorb and store the extra glucose for later….if there
is low blood sugar/low insulin levels the liver will
release glycogen which turns into glucose to help
increase the blood sugar level)
Glucagon and Insulin Feedback Loop
Increased blood sugar -> pancreas releases insulin ->
causes glucose to enter into the cells to be used or be
saved as glycogen for later (stored mainly in the
liver)
Decrease blood sugar -> pancreas release glucagon ->
causes the liver to release glycogen which turns into
glucose to increase the low blood sugar level
What happens in diabetes mellitus?
The body is unable to use glucose due to either
the absence of insulin or the body’s resistance to
use insulin. Therefore, the patient
becomesHYPERGLYCEMIA (the glucose just hangs
out in the blood stream which affects major organs of
the body)
The body starts to metabolize FATS for energy
(since it can’t get to the glucose…remember glucose
can NOT enter the cell without the help of
INSULIN)….which happens in Type 1 diabetics OR
there is a moderate amount of insulin to deal with
fats and proteins BUT carbs cannot be used (Type 2).
Causes of Diabetes Mellitus
Divided into types:
Type 1: the beta cells located in the islet of
Langerhans don’t work (been destroyed) therefore
the body doesn’t release anymore insulin. For
treatment, the patient MUST USE INSULIN.
Risk factors: Genetic, auto-immune (virus) NOT
RELATED TO LIFESTYLE (like type 2)
What do patients look like clinically? Patients are
young and thin….happens suddenly; ketones will be
present in the urine
Type 2: cells quit responding to insulin (won’t let
insulin do its job by taking the glucose into the cell).
Therefore, the patient has INSULIN RESISTANCE.
This leaves all the glucose floating around in the
blood and the pancreas senses there’s a lot of glucose
present in the blood so it releases even more insulin.
Due to this the patient starts to
experience hyperinsulinemia which caused
metabolic syndrome
Treatment: diet and exercise (first line
treatment)…when that doesn’t work oral medications
are started Note: The type 2 diabetic may NEED
INSULIN DURING STRESS, SURGERY, OR INFECTION
Risk Factors: Lifestyle- being obese, sedentary, poor
diet (sugary drinks), stress AND genetic
What do patients look like clinically? Patients are
overweight, it happens overtime, rare to have
ketones (remember issues with carb metabolism)
adult aged
Gestational: similar to type 2 diabetes where the
cells are not receptive to insulin…typically goes away
after birth
Complications of Diabetes Mellitus
Hypoglycemia:
Blood glucose less than 60 mg/dL or drops rapidly
from an elevated level.
Remember the mnemonic: “I’m sweaty, cold, and
clammy….give me some candy”
Signs and Symptoms: Sweating, clammy, confusion,
light headedness, double vision, tremors
Treatment: Need simple carbs if they can eat, or if
unconscious IV D50
Simple carbs include: hard candies, fruit juice,
graham crackers, honey
Organ Problems:
Hardens the vessel (atherosclerotic….makes vessels
hard from all the glucose that sticks on the proteins
of the vessels and it forms plaques). So the patient
can develop heart disease, strokes, hypertension,
neuropathy, poor wound healing (FROM DECREASE
circulation), eye trouble, infection.
DKA (Diabetic Ketoacidosis):
Happens in Type 1 diabetics (rare to happen in type
2)
There is no insulin in the body and the body starts to
burn fats for energy since it can’t get to the glucose
Due to this the ketones, which are acids, start to enter
into the body and this causes life-threatening
situation, such as acid/base imbalances
Signs and Symptoms of DKA: N&V, excessive thirst,
hyperglycemia, Kussmaul breathing
HHNS Hyperglycemic hyperosmolar nonketotic
syndrome:
Happens mainly in Type 2 diabetics
This presents with hyperglycemia without the
breakdown of ketones…so there isn’t
acidosis/ketosis because there is just enough insulin
present in the body to prevent the breakdown of fats
Signs and Symptoms of HHNS: very dehydrated,
thirsty, hyperglycemic, mental status changes
Assessment Findings of DM
3 of Hyperglycemia P’s & SUGAR
Hyperglycemia: Three P’s
Polyuria: (frequent urination)
Why? elevated levels of glucose in the body causes
the body to remove the water from inside the cell
(remember in the hypertonic, hypotonic video about
OSMOSIS). The water will move to an area of higher
concentration which will be the blood stream and
this causes more fluid to enter the blood stream. The
kidneys will secrete the extra water. HOWEVER,
normally your kidneys could handle all of the glucose
by reabsorption but there is too much so it leaks into
the urine…. GLYCOSURIA
Polydipsia: very thirsty
Why? the blood is trying to prevent the body from
becoming dehydrated from the excessive urination so
it signals to the patient to drink more water…but it
doesn’t work because the kidneys will remove the
excess water
Polyphagia: very hunger
Why? the body is burning FAT for energy since it
doesn’t have any glucose to use so the body signals to
the person to keep eating so there will be food to use
for energy. The patient will have WEIGHTLOSS!
*The 3 P’s present mainly in Type 1 Diabetics
Other Assessment findings of the Diabetic Patient
Remember “Sugar”
Slow wound healing
blUrry vision (damaged from glucose on eyes)
Glycosuria (kidneys can’t reabsorb all the extra
glucose)
Acetone smell of breath (from burning ketones) *type
1
Rashes on skin DRY and itchy, repeated vaginal
infections (yeast….loves glucose)
Diabetes Nursing Management
Nurse’s role: educating, monitoring, and
administering (medications)
Teach patient to follow the Triangle of Diabetes
Management
**Diet, medications, and exercise all work together
while monitoring blood glucose
Example: Patient wants to make sure their diet is
balanced with their medication (insulin/oral meds)
and they use exercise to manage glucose levels (doing
all this while monitoring blood glucose).
As the nurse you will be educating the diabetic…so
for the NCLEX know education pieces like:
Diet, exercising, oral medications, giving insulin
(peak times), drugs that increase blood glucose and
lower glucose etc.
Diabetic Diets
DIET: Diets are individualized due to physical activity
and medication therapy (they always need
tweaking)…recommend following American Diabetic
Association Diet (ADA)
Limitation of the following:
Carbs (45-60%) grains, vegetables with starches
potatoes, corn, sweets…cookies, soda, dried beans,
milk)
Fats (<20 %)….limit unhealthy fats saturated, trans
fats, cholesterol: lard, gravies, whole milk, bologna,
hot dogs, sausage, processed foods hydrogenated
oils…concentrate on mono & polyunsaturated
avocadoes, olives, peanuts, nuts
Proteins (15-20%) meats don’t increase the
glycemic index: meats chicken, turkey, fish, plant
based beans, peas, low fat cheese, eggs whites
Exercising Management
Exercise: Aerobic the best (helps the body use
insulin) ex: cardio running, walking, swimming etc.
Teach patient signs of hypoglycemia &
hyperglycemia
Signs of Hypoglycemia:
“I’m sweaty, cold, and clammy….give me some candy”
“Sweating, clammy, confusion, light headedness,
double vision, tremors”
Signs of Hyperglycemia: Three P’s
Polyphagia
I’m hot and dry…I must be on a sugar high!
Polydipsia
Polyuria
Always check blood sugar prior to exercising:
if lower than 100 eat a small carb snack and
carry SIMPLE carbs with you while exercising in case
of hypoglycemic attack
Example of simple carbs: hard candy, honey,
crackers/graham crackers, fruit juice
****If patient plans on exercising for an extended
period of time, check glucose prior, during, and after.
****If blood glucose is higher than 250 with ketones
present in urine prior to exercise avoid exercise until
glucose and ketones stabilize.
Diabetic Medications
NCLEX specific:
Oral medications (for patients with Type 2 diabetes
when exercise and diet doesn’t work to control blood
glucose):
Sulfonylureas: ides zides, mides, rides” (most
common) stimulate beta cells in pancreas to make
insulin (Glyburide, Glipizide, Diabinese,
Amaryl)AVOID ETOH….extreme hypoglycemia
Meglitinides: “glinide” Ex: repaglinide “Prandin”
stimulate beta cells in pancreas to make
insulin…instruct pts to take first bite with meal
Biguanides: Metformin (Glucophage)….causes the
liver to decrease its stores of glucose. Watch out if
patient is scheduled for surgery/procedure (heart
cath)…stop for 48 hours and watch renal
function…diarrhea
Alpha-glucoside inhibitors: Precose, Glyset lower
blood sugar by slowly down the breakdown of
starchy foods in the GI system which helps slowly
rise the blood sugar… instruct pts to take first bite
with meal
Thiazolidinedione: “glitazone” reduce glucose
production in the liver: Actos/Avandia watch liver
function and heart function increase risk of MIs
Medications that cause hypoglycemia
Remember from the hypertension lecture that Beta
Blockers (mask symptoms of hypoglycemia)
Other medication that cause it: ETOH, ASA,
Sulfonylureas (medications used to treat type 2:
Glyburide, Glipizide, Diabinese), and MAO inhibitors
(meds for depression) , Bactrim (common antibiotic)
Medications that cause hypergycemia
Thiazide diuretics (HCTZ), Glucocorticoids
(Prednisone, Hydrocortisone), estrogen therapy
Insulin
It is used for Type 1 regularly, and sometimes for
Type 2 diabetics if the patient is experiencing
stress on the body like surgery or illness.
Know the categories of insulin. Example: whether
they are rapid, short, intermediate, long acting and
the onset, peak, and duration.
Note: Peak is the most susceptible time for
hypoglycemia
Insulin Mnemonics
Note that if you use the word insulin you can divide
the word and separate it into specific categories of
insulin types. Watch the lecture above for a full in-
depth explanation about this mnemonic.
Rapid-Acting Insulin:
“15 minutes feels like
an hour during 3 rapid responses.”
Onset: 15 minutes
Peak: 1 hour
Duration: 3
Short-Acting Insulin:
“Short-staffed nurses went from 30 patient to
(2) 8 patients.”
Onset: 30 minutes
Peak: 2 hours
Duration: 8 hours
Intermediate-Acting Insulin:
“Nurses Play Hero to (2) eight 16 year olds.”
Onset: 2 hours
Peak: 8 hours
Duration: 16 hours
Long-Acting Insulin:
“The two long nursing shifts never peaked but
lasted 24 hours.”
Onset: 2 hours
Peak: NONE
Duration: 24 hours
Key Points to Remember about Administering Insulin
Rotate sites: do not use the same site more than
once in a 2-3 week period this PREVENTS
LIPODYSTROPHY (pitting of subq fat)
Sites include: abdomen, arms, and thighs
When mixing insulin (clear to cloudy) clean=regular,
cloudy=NPH
Don’t massage site after administration increase
hypoglycemia due to absorption
Dawn Phenomenon:
Watch for Dawn phenomenon (hence the name
dawn…crack of dawn means the waking hours) this is
a time when the body will increase the blood sugar in
preparation for waking. However, when you have
insulin problems (not enough of it) the increased
blood sugar causes HYPERGLYCEMIA
Typical time: 5am to 8 am
Treatment: may need a night time dose of NPH to
counteract.
Somogyi Effect:
Somogyi effect (remember S in Somogyi for sleeping
hours): This is a drop in blood sugar at the hours of 2
to 3 am. This happens when the body releases
hormones such as coristol, catecholamines, growth
hormones to increase the blood sugar. However, in
diabetics the body can’t cope with the increased
blood sugar and the sugar will be elevated.
Treatment: Eat a bedtime snack….a dose of bedtime
insulin will prevent it from dropping so low or
decreasing insulin amounts at night
nsulin Onset, Peak, and Duration Times Glucose: fuels the cells so it can function. However,
with DKA there is no insulin present to take the
Rapid-Acting Insulin: glucose into the cell…so the glucose is not used and
Onset: 15 minutes the patient will experience hyperglycemia >300
Peak: 1 hour mg/dL.
Duration: 3 Insulin: helps take glucose into the cell so the body
“15 minutes feels like an can use it for fuel. In DKA, the body isn’t receiving
hour during 3 rapid responses.” enough insulin…so the GLUCOSE can NOT enter into
the cell. The glucose floats around in the blood and
Short-Acting Insulin: the body starts to think it is starving because it
cannot get to the glucose. Therefore, it looks
Onset: 30 minutes elsewhere for energy.
Peak: 2 hours Liver & Glucagon: the body tries an attempt to use
Duration: 8 hours the glucose stores in the liver (because it doesn’t
know there is a bunch of glucose floating around in
“Short-staffed nurses went from 30 patient to the blood and thinks the body is experiencing
(2) 8 patients.” hypoglycemia). In turn, the liver releases glucagon to
turn glycogen stores into more GLUCOSE….so the
Intermediate-Acting Insulin: patient becomes even more hyperglycemic.
Onset: 2 hours Ketones: a byproduct of fat break down. In DKA, the
body needs FUEL to function so it starts to break
Peak: 8 hours
down FATS since it cannot use the glucose in the
Duration: 16 hours body. The patient will experience increased ketones
in the body which are LIFE-THREATENING to a
“Nurses Play Hero to (2) eight 16 year olds.” diabetic patient because it causes the blood to
become acidic (metabolic acidosis)
Long-Acting Insulin:
Kidneys: plays a role in reabsorbing glucose in the
Onset: 2 hours
renal tubules. However, there is too much glucose
Peak: NONE present in the blood and it cannot be reabsorbed. So,
it leaks into the urine and this causes OSMOTIC
Duration: 24 hours DIURESIS which causes polyuria and excretion of
electrolytes (sodium,potassium, chloride)
“The two long nursing shifts never peaked but
lasted 24 hours.” Happens mainly in TYPE 1 Diabetics…rare in type 2
but possible if they are experiencing a severe illness.
Diabetic Ketoacidosis
Causes of DKA
Define: a complication of diabetes mellitus that is life-
threatening, if not treated. It is due to the breakdown Undetected diabetes: patient doesn’t know they are
of fats which turn into ketones because there is no diabetic and this is the first sign, usually.
insulin present in the body to take glucose into the
cell. Therefore, you will seehyperglycemia and More Insulin needed by the body than normal: the
ketosis and acidosis. body needs more units of insulin than it is actually
receiving from injections.
Key Players of DKA:
Example: when a diabetic become sick (INFECTION)
with illness or recovering from surgery or
experiences some type of stress on the body like
certain drugs such as, corticosteroids or thiazide
diuretics.
Not eating (skipping meals): body starts to go into
“starvation” mode and begins to burn ketones
(normally in nondiabetics when the body goes into
starvation mode it can cope when ketones are
released by regulating insulin and glucagon to
maintain sugar levels…but in the diabetic they don’t
have that ability and ketones production is
dangerous).
Not taking insulin as scheduled: therefore the
blood glucose levels are not controlled…ketones are
produced and the cycle of acidosis starts to take place
in the body.
Signs & Symptoms of Diabetic Ketoacidosis:
Recap of what is going on:
Hyperglycemia (intracellular to extracellular
shifting takes place which will lead to electrolyte
imbalances)
Ketones in the blood (leads to metabolic acidosis,
weight loss because of all the fat burning, electrolyte
shifting as well)
Metabolic Acidosis (blood pH <7.35 and HCO3 <15
mEq/L)
Happens suddenly (there may be warning signs
present if the patient is monitoring their blood
glucose which will be elevated consistently (>300
mg/dL)
Polyuria: due to the extreme levels of glucose in the
body that causes the water inside the cells to shift to
the extracellular area. The kidneys try to compensate
by increasing urinary production to eliminate this
extra fluid but the kidneys cannot reabsorb all the
glucose so it leaks into the urine. This
causes OSMOTIC DIURESIS which causes SODIUM
AND POTASSIUM (along with calcium, phos) TO BE
EXCRETED.
*NOTE potassium levels typically stay normal or
elevated in DKA because of the shifting of potassium
from the inside of the cell to the outside BUT WHEN
TREATMENT STARTS TO BE INITATED WITH
INSULIN IT WILL CAUSES THE K+ TO MOVE BACK
INTO THE CELL. Therefore, you have to watch
POTASSIUM LEVELS closely during treatment.
Polydipsia: frequent drinking due to extreme
thirst….vicious cycle of frequent urination and the
body is trying to keep itself hydrated.
Dehydration: dry mucous membranes, decreased
skin turgor (the extreme drinking doesn’t work)
Nausea & vomiting, Abdominal pain-> (especially
children…causes not 100% known but could be due
to the ketones present in the blood)
Kussmaul Breathing: due to metabolic
acidosis….the respiratory system tries to compensate
by getting rid of extra acid in the body by blowing off
carbon dioxide which is an acid…this is rapid deep
breathing
Acetone Smell of the Breath “fruity”: due to the
breakdown of ketones
Ketones present in the urine
Tachycardia, hypotension, confusion, fatigue
Nursing Interventions of DKA
*Get treatment early because DKA is fatal*
Teach patient early signs and when to seek
treatment:
Monitor glucose and ketones during illness every 4
hours, especially if dealing with illness/infection
If vomiting and cannot eat food or drink liquids notify
doctor (if can tolerate drink liquids every hour)
Notify medical doctor if blood sugars are higher than
normal or greater than 300 mg/dL consistently
Ketones present in the urine
Excessive thirst, frequent urination, abdominal pain,
nausea and vomiting, acetone breath
Treatment of DKA
Goal: Hydrate, decrease blood glucose, monitor
Potassium level and cerebral edema (esp. in
children), correct acid-base imbalance
Administering IV fluids: (depending on MD order)
such as 0.9% normal saline (start out with a bolus
of this) and progress with 0.45% NS to hydrate the
cells (depends on how dehydrated the patient is)
5% dextrose may be added to the 0.45% NS when
glucose is around 250 to 300 mg/dL. This will help
gradually bring the blood sugar down and help the
insulin do its job by removing the ketones.
Administered insulin: REGULAR (only type given IV)
and make sure K+ is normal >3.3
Typically started out by giving unit IV bolus…then
start an infusion (checking blood glucoses around the
clock…hospital protocols)…you will be titrating the
insulin base on blood glucose checks.
NOTE: if you rapidly bring a patient’s blood glucose
down (or up) the brain can’t cope and water will be
moved from the blood to the CSF and you will get
cerebral edema and increased intracranial pressure
Tip for insulin administration: when priming tubing
for insulin infusion waste 50cc to 100cc (per
institution protocol) because insulin absorbs into the
plastic lining of the tubing.
Watch potassium levels very closely because insulin
causes K+ to move back into the cell
Administer Potassium solution IV to combat
this….note renal function before administering.
Hyperglycemic Hyperosmolar Nonketotic
Syndrome (HHNS) NCLEX Review
A.K.A: Hyperosmolar Hyperglycemic State (HHS)
Definition of HHNS: a life-threatening condition of a
hyperglycemic state that affects patients
with diabetes mellitus. It presents with an extreme
high blood glucose which causes the blood to become
very concentrated “hyperosmolar” but without the
breakdown of KETONES (fats)
Therefore, clinically the patient will have HEAVY-
DUTY HYPERGlYCEMIA and DEHYDRATION (due to
the hyperosmolar)
Key Players of HHS:
Glucose: fuels the cells so they can function.
However, the body is not using the glucose because
there isn’t enough insulin to take it into the cell or the
cells are insulin RESISTANT. Glucose levels will >600
mg/dL. The blood becomes very concentrated a.k.a.
“hyperosmolar” due to the extra glucose. This causes
water to pull from inside the cells which will result in
cell dehydration and an even higher glucose level.
Insulin: helps take glucose into the cell so the body
can use it for fuel. In HHNS, the cells are not receptive
to the insulin or there isn’t enough because of an
illness which limits its availability. Therefore,
GLUCOSE can NOT enter into the cell and glucose
floats around in the blood. However, because it
happens in mainly type 2 diabetes there is SOME
insulin present (but not all cells are not receptive to
use it but some do) which prevents the breakdown of
fats (you willnot see ketones).
Kidneys: plays a role in reabsorbing glucose in the
renal tubules. However, there is too much glucose to
be reabsorbed so it leaks into the urine. This
causesOSMOTIC DIURESIS which causes polyuria and
excretion of electrolytes (sodium, potassium,
chloride). This leads to MAJOR DEHYDRATION.
Important take-aways: NO KETOSIS or
ACIDOSIS in HHNS because there is just enough
insulin present that prevents the body from breaking
down fats for energy; therefore there is no build-up
of ketones.
Patients are going to present with HYPERGLYCEMIA
and DEHYRDATION.
CAUSES of Hyperglycemic Hyperosmolar Nonketotic
Syndrome:
Illness or infection (the patient isn’t aware their
blood glucose is high because they haven’t been
monitoring it)…most common in OLDER ADULTS
IMPORTANT: Happens gradually….remember
glucose is going to be VERY VERY high (higher than
glucose levels in DKA)
Remember the Mnemonics: HHNS (Heavy-
duty HYPERGLYCEMA)
Signs & Symptoms of HHNS
High glucose >600 mg/dL
Polyuria
Polydipsia
Dehydrated: dry mucous membranes
Fever
Fatigue
Mental status changes (confusion, seizures)
Coma
Nursing Interventions for HHNS
Goal: Hydrate, decrease blood glucose, monitor
potassium levels and for cerebral edema, correct
acid-base imbalance (similar to the treatment of
DKA)
However, HYDRATION will helps just as well as
insulin due to the severe hydration experienced in
HHNS. The fluids will help hydrate the cell which will
decrease glucose levels and help with electrolyte
balance.
Administering IV fluids: (depending on MD order)
such as 0.9% Normal Saline (start out with a bolus of
this) and progress with 0.45% NS to hydrate the cells
(depends on how dehydrated the patient is)…see the
lecture on hypotonic, isotonic, and hypertonic
solutions.
5% dextrose may be added to the 0.45% NS when
glucose is around 250 to 300 mg/dL. This will help
gradually bring the blood sugar down and help the
insulin do its job by removing the ketones.
Administered insulin REGULAR (only type given
IV) and make sure K+ is normal >3.3
Typically started out by giving unit IV bolus…then
start an infusion (checking blood glucose levels
around the clock…hospital protocols)…you will be
titrating the insulin base on blood glucose checks.
NOTE: if you rapidly bring a patient’s blood glucose
down (or up) the brain can’t cope and water will be
moved from the blood to the CSF and you will get
cerebral edema and increased intracranial pressure.
Tip: when priming tubing for insulin infusion waste
50cc to 100cc (per institution protocol) because
insulin absorbs into the plastic lining of the tubing.
Watch potassium levels very closely because insulin
causes K+ to move back into the cell
Administer Potassium solution IV to combat
this….note renal function before administering.
DKA vs HHNS
Diabetic Ketoacidosis
Affects mainly Type 1 diabetics
Ketones and Acidosis present
Hyperglycemia presents >300 mg/dL
Variable osmolality
Happens Suddenly
Causes: no insulin present in the body or
illness/infection
Seen in young or undiagnosed diabetics
Main problems are hyperglycemia, ketones,
and acidosis (blood pH <7.35)
Clinical signs/symptoms: Kussmaul
breathing, fruity breath, abdominal pain
Treatment is the same as in HHNS (fluids,
electrolyte replacement, and insulin)
Watch potassium levels closely when giving insulin
and make sure the level is at least 3.3 before
administrating.
Hyperglycemic Hyperosmolar Nonketotic Syndrome
Affects mainly Type 2 diabetics
No ketones or acidosis present
EXTREME Hyperglycemia (remember heavy-
duty hyperglycemia) >600 mg/dL sometimes four
digits
High Osmolality (more of an issue in HHNS than
DKA)
Happens Gradually
Causes: mainly illness or infection and there is
some insulin present which prevents the breakdown
of ketones
Seen in older adults due to illness or infection
Main problems are dehydration & heavy-duty
hyperglycemia and hyperosmolarity (because the
glucose is so high it makes the blood very
concentrated)
More likely to have mental status changes due to
severe dehydration due to hyperosmolarity
Treatments are the same as in DKA, however, fluid
administration helps just as much as insulin therapy
because of the correction of osmolarlity issue.
Blood pH will be normal (remember no acidosis as
in DKA)
No Kussmaul breathing and fruity breath (because
there is no KETOSIS)
Thyroid Storm
Definition: Life-threatening complication that
develops in someone who has hyperthyroidism
which is an excessive secretion of thyroid hormones
(T3 and T4).
It is usually because hyperthyroidism is not being
treated properly, the patient is undiagnosed, or the
patient experienced an illness.
In addition, thyroid storm can develop after a
thyroidectomy due to the thyroid being manipulated
during removal which can cause high amounts of T3
and T4 to enter into the blood stream. However, it is
rare because today patients are placed on
medications to help combat this.
Causes of Thyroid Storm
Patients will already have hyperthyroidism along
with any of the following:
got an illness or experienced trauma/stress (septic,
DKA, surgery, trauma to the gland)
suffers from Grave’s Disease that is under treated or
they became sick
not taking antithyroid medications properly
taking medications that increase thyroid hormones
(Salicylates: ASA)
pregnancy
radioactive iodine therapy (CT scan or as treatment)
remember the thyroid loves iodine and uses it to
make thyroid hormone
Signs & Symptoms of Thyroid Storm
The patient will have typical hyperthyroidism
symptoms but they will beSEVERE to the point of
death…remember the function of T3 and T4 is to
increase body’s metabolism and temperature and to
stimulate the sympathetic nervous system (this will
be happening at an accelerated rate).
Remember this condition as: A violent storm on the
body at an accelerated rate.
Fever (not just heat intolerance)
Hypertension—going to exhaust the heart to the
point of failure (CHF or MI)
Tachycardia— going to exhaust the heart to the point
of failure (CHF or MI)
Increase respirations—due to the body working so
hard and it needs more oxygen and nutrients…will
get respiratory failure if not treated fast
Very restless, irritable, confused …this will progress
to seizures, delirium, coma
Diarrhea
Nursing Interventions for Thyroid Storm
Monitor HR, BP, RR (respiratory failure…may need
mechanical ventilation), EKG, Temperature
Keep environment quiet and patient cool (cooling
blankets and sedatives as prescribed)
No foods containing iodine (seafood…seaweed, dairy,
eggs)
Pharmacological Management of Thyroid Storm
Goals:
Need to decrease the thyroid hormone:
Antithyroid medications (block synthesis) :
Tapazole “Methimazole”: has fewer side effects
than PTU…not for first trimester of pregnancy
PTU “Propylthiouracil”: can be used during 1st
trimester…watch for liver failure
Side Effects with these medications: Agranulocytosis
and thrombocytopenia and watch for toxicity which
will present as signs and symptoms
ofHYPOTHYROIDISM: slow heart rate, intolerance to
cold, drowsy
Iodide solution (block secretion)
Lugol’s solution: Side effects: taste changes metal
taste in mouth
2. Decrease fever:
Tylenol NO Salicylates or cooling blankets
3. Decrease effects of thyroid hormones on the
body by blocking peripheral conversion of T3 and
T4:
Beta Blockers: Inderal (not for people with asthma
or history of bronchospasm…watch in diabetics can
mask hypoglycemia)
4. Prevent further secretion and conversion of
thyroid hormones by suppressing immune
system with:
Glucocorticoids (Dexamethasone )
Grave’s Disease
Definition: Most common cause of hyperthyroidism
that is caused by an autoimmune condition. The
patient will have excessive thyroid hormone
secretion (T3 and T4) by the thyroid gland.
Cause: the body is producing an antibody called TSI
(thyroid stimulating immunoglobulin) that is
producing the same effects on the body as TSH
(thyroid stimulating hormone). TSH release causes
the thyroid gland to secrete T3 and T4.
Negative feedback system of thyroid hormone
release:
Hypothalamus->TRH (thyrotropin releasing
hormone)->Anterior pituitary gland—>TSH—
>stimulates the thyroid gland to secrete ->T3 and T4
T3 and T4: play a huge role on body metabolism,
increases body temperature, sympathetic nervous
system (increase heart rate, blood pressure,
alertness), how fast the body digests food etc.
Signs and Symptoms of Grave’s Disease
Typical signs and symptoms of HYPERTHYROIDISM
but there are UNIQUE signs and symptoms:
Weight loss (burning calories increased)
Heat intolerance (feel extremely hot…sweaty)
Tachycardia (sympathetic system in overdrive)
Hypertension (sympathetic system in overdrive)
Diarrhea (GI system working harder and faster)
Irritable
Smooth skin/hair (increase blood flow)
UNIQUE S&S:
Ophthalmopathy: protruding eye balls
Goiter: overstimulation of the thyroid gland which
causes it to swell
Pretibial Myxedema: red, swelling on the skin,
lower legs, and feet that has an orange peel
texture…can advance to face, chest, arms
Nursing Interventions for Grave’s Disease
Monitor HR, BP, EKG, weight (at risk for weight loss
and will need a high calorie diet)
Keep patient in a cool, quiet environment
Pharmacology Management:
Antithyroid medication: stop the thyroid from
synthesizing t3 and t4, doesn’t damage thyroid gland
like radioactive iodine therapy
Tapazole “Methimazole” (most common…fewer
side effect) common treatment for Grave’s Disease
PTU “Propylthiouracil” (safer during first trimester
of pregnancy)….liver failure
Other side effects for both
medications: agranulocytosis and aplastic anemia
Patient education for Antithyroid medications:
Never stop taking abruptly (takes a while before the
patient starts seeing results)
Take at same time every day
Signs and symptoms of thyroid storm
Avoid iodine rich foods (sea foods like seaweed, dairy
eggs) or supplements with iodine
No Aspirin or Salicylates (increases thyroid
hormone)
Signs and symptoms of hypothyroidism (toxicity)
Beta Blockers:
Inderal: prevents the hyperthyroidism effects on
the body by blocking peripheral conversion of T3 and
T4. This medication will help decrease heart rate,
blood pressure, and decrease heat intolerance (not
for people with asthma or history of
bronchospasm…watch in diabetics…. can mask signs
and symptoms of hypoglycemia).
Treatments for Grave’s Disease
Radioactive iodine: destroys the thyroid gland
overtime and is a permanent cure compared to
medications….not for pregnant or nursing women
Side Effects: Iodism- taste changes “metal taste”,
nausea, and swollen saliva glands
Surgical Treatment: Thyroidectomy (removal of
the thyroid gland)
Watch for thyroid storm due to the manipulation of
the gland causing extra T3 and T4 to leak into the
body….prevent by prepping with medications of:
antithyroid meds, sodium iodide solution, beta
blocker, glucocorticoids
Educate about post-opt care: coughing and deep
breathing and splinting neck when coughing
Monitor for parathyroid destruction
problems (common when a thyroid procedure is
performed due to the close proximity of the
parathyroid to the thyroid gland)…watch calcium
levels “hypocalcemia”…parathyroid is responsible
for calcium regulation.
Watch for respiratory distress due to the nature of
the surgical site…keep patient in semi-fowler’s to
help with swelling and drainage at the site and keep
at the bedside a trach kit, oxygen, and suction.
Myxedema Coma
Definition: life-threatening condition that occurs in
patients withhypothyroidism due to severely low
thyroid hormones (untreated or undiagnosed
hypothyroidism).
Causes of Myxedema Coma
Occurs mainly in elderly women with
hypothyroidism who have experienced:
illness (respiratory or urinary infection)
stressful event (MI)
medications (Lithium: inhibits thyroid hormone
release) or sedatives
toxicity of antithyroid medications…used to treat
hyperthyroidism
not taking thyroid replacement medications (some
patient will abruptly stop them because they think
they are not helping…medications take a while to see
effects)
Thyroidectomy (removal of the thyroid gland)
Signs and Symptoms of Myxedema Coma
Patients will have the
typical HYPOTHYROIDISM signs and
symptoms,BUT they will be more SEVERE….systems
of the body are slowing down to the point of death
Hypothermia (not just cold intolerance)
Myxedema: swelling of tissues that have a waxy
appearance or orange peel texture which will be
located on the eyes and face
Slow heart rate and low blood pressure
Respiratory failure (most likely will need mechanical
ventilation)
Hyponatremia (due to the increased antidiuretic
hormone which causes the body to conserve water &
decreased glomerular filtration rate because there is
decreased blood flow to the kidneys)
Hypoglycemia (due to the reduced metabolic rate
hence decreased gluconeogenesis)
Very confused/drowsy…may progress to a coma
Nursing Interventions for Myxedema Coma
Monitor HR, BP, EKG, temperature, respiratory status
(respiratory failure and maintain airway)
Administer IV solutions as prescribed (ex: normal
saline or hypertonic solutions…to
correct hyponatremia and correct cardiovascular
collapse) Learn more about isotonic, hypotonic, and
hypertonic solutions
IV thyroid hormones: Synthroid (this can cause
adrenal insufficiency because thyroid hormones
increase the metabolic clearance of
glucocorticoids….so corticosteroids may be
prescribed along with treatment)
****Watch for signs and symptoms of Synthroid
toxicity which would present as signs and symptoms
of hyperthyroidism (fast heart, feeling hot, sweating)
Administered glucose IV for hypoglycemia
Keep patient warm with warming blankets as
prescribed
NO sedatives or narcotics for these patients….very
sensitive to them
Fluid and Electrolytes
Metabolic Alkalosis
Metabolic alkalosis in simple terms: a metabolic
problem caused by the excessive loss of acids (H+) or
increased amount of bicarb (HCO3) produced in the
body that leads to an alkalotic state in the body.
Disease processes and drugs can cause metabolic
alkalosis.
When metabolic alkalosis happens in the body other
systems try to compensate by hopefully fixing the
blood’s pH and bicarb level. One system that does this
is the respiratory system by stimulating the
respiratory system to hypoventilate(decrease
respirations) which will retain PCO2 (carbon
dioxide) so it will decrease the pH back to normal,
hence you will start to see bradypnea in your patient.
If a patient is experiencing metabolic alkalosis they
will present with the following labs:
 HCO3: increases >26
 Blood pH: increases >7.45
 CO2: >45 or normal (may be normal but if
increased this is the body’s way of trying to
compensate. Remember the respiratory
system tries todecrease the pH from its
alkalotic state by causing hypoventilation (
bradypnea). The respiratory system hopes that
if the CO2 increase enough it will cause the pH
to decrease and the kidneys will start to
excrete the bicarb which will hopefully
decrease the overall HCO3.
Remember what normal values are:
 pH 7.35-7.45
 PaCO2 35-45
 HCO3 22-26
Causes of Metabolic Alkalosis
Remember: “Alkali” (**these are the most common
causes)
**Aldosterone production excessive
(hyperaldosteronism) activates renin-angiotensin-
aldosterone system : the adrenal cortex is releasing
too much aldosterone which causes the renal tubule
in the kidneys to keep sodium which wastes
hydrogen ions (ex: potassium) and this causes you to
keep bicarb (HCO3)
Loop **diuretics (Lasix) or thiazide therapy: causes
the kidneys to waste hydrogen ions and chloride
through the urine (ALSO LOSING K+) which in turn
increases the bicarb
alKali ingestion of food (baking soda, milk, antacids)
increases bicarb level in the blood
Anticoagulant “citrate” (used as a storage agent in
blood and during continuous forms of renal
replacement therapy) Caused from a massive
transfusion of whole blood (patient needs several
bags of blood) and the body metabolizes the citrate
used in the blood as bicarb which increases the HCO3
level in the body. Also, patients who undergo
continuous forms of renal replacement therapy
(CRRT) (an alternative therapy for patients who can’t
undergo hemodialysis) are affected by the citrate
used in the therapy.
Loss of fluids (**vomiting and **GI suctioning) hence
this fluids are rich in K+ and when you lose them you
are losing hydrogen ions and this causes the body to
increase the bicarb level, Low potassium levels cause
reabsorption of HCO3-
Increased sodium bicarb administration (trying to
correct metabolic acidosis)
Signs and Symptoms of Metabolic alkalosis
 Bradypnea (hypoventilation) <12 bpm
 Many symptoms due to low potassium
(dysrhythmia), tetany, tremors, muscle
weakness/cramping, tired, irritable,
 vomiting, Depression ST, flat or inverted
T wave and prominent u-wave)
Nursing Interventions for Metabolic Alkalosis
 Based on the cause: vomiting (give antiemetic
ex: Zofran, Phenergan), stop diuretics
 Doctor may order Diamox (Carbonic
anhydrase inhibitors): a diuretic which
reduces the reabsorption of bicarb
 Watch ABGs and signs of respiratory distress
 Monitor potassium and chloride levels (wasted
in this condition)
Metabolic Acidosis
Metabolic Acidosis in Simple Terms: a metabolic
problem due to the buildup of acid in the body fluids
which affects the bicarbonate (HCO3 levels) either
from:
 increased acid production (ex: DKA where
ketones (acids) increase in the body which
decreases bicarbonate)
 decreased acid excretion (ex: renal failure
where there is high amount of waste left in the
body which causes the acids to increase and
bicarb can’t control imbalance)
 loss of too much bicarb (diarrhea)
When this acidic phenomena is taking place in the
body other systems will try to compensate to
increase the bicarb back to normal. One system that
tries to compensate is the respiratory system.
In order to compensate, the respiratory system will
cause the body tohyperventilate by increasing
breathing through Kussmaul’s respirations.
Kussmaul respirations are deep, rapid breathes. The
body hopes this will help expel CO2 (an acid) which
will “hopefully” increase the pH back to normal.
Lab values expected in Metabolic Acidosis:
 HCO3: decreased <22
 Blood pH: decreased <7.35
 CO2: <35 or normal (may be normal but if it is
decreased this is the body’s way of trying to
compensate). **Remember the respiratory
system is causing hyperventilation. The
respiratory system tries to increase the pH
from its acidotic states through tachypnea with
Kussmaul’s breathing. The goal is to “blow off”
the CO2 which is acidic to help alleviate the
already acidotic conditions in the body.
Memorize these normal values for ABGs:
 pH 7.35-7.45
 PaCO2 35-45
 HCO3 22-26
Causes of Metabolic Acidosis
High anion gap & Normal anion gap problems:
What is an anion gap? Simplified this is where the
doctor look at various lab results from a patient’s lab
work (such as electrolytes (chloride, bicarbonate,
sodium) and calculates them to see the difference
between the anions and cations.
If there is a gap (>14 mEq/L from normal (normal
is: 10-14 mEq/L) there is high anion gap metabolic
acidosis going on. In other words the anion gap tells
us what type of acidosis we have going on which is Ostomy drainage (excessive) ileostomies,
important so it can be treated appropriately. Ureteroenterostomies (normal anion gap)…ostomies
are an opening of an organ to allow
High Anion Acidosis is conditions that cause the
drainage…depending on where the ostomy is these
body to produce too much acid or NOT enough bicarb
fluids are rich in bicarb and if loss directly at this spot
(DKA, Aspirin toxicity, renal failure, high-fat diet, low
(instead of travelling through the body to form into
carb diet, malnutrition)
stool (which doesn’t lose much bicarb)…it can
deplete the bicarb fast.
Normal Anion acidosis is loss of the bicarbonate
from the body. Examples: diarrhea via GI fluids,
fisTula (pancreatic fistula) (normal anion gap) fistula
ostomies or fistula drainage (ileostomies or
: a fistula is a passage between an hollow organ and
pancreatic fistula)…which are rich in alkalotic fluids,
body surface or between two organs….same concept
however when lost it causes acidosis, or drugs
with the ostomy…losing fluids where you shouldn’t
ingestion: Diamox (diuretic)…. carbonic anhydrase
be and they are not being absorbed by the body…you
inhibitor which reduces reabsorption of bicarb.
are wasting the bicarb

Combine all of this to form the Mnemonic “Acidotic”

Intake of high-fat diet: eating too much fat leads to
the building-up of waste product which in turn leads
Aspirin toxicity: (high anion gap) which increases the
to buildup of ketones and acids
acid in the body and this also causes respiratory
alkalosis (hyperventilation)
Carbonic anhydrase inhibitors (Diamox): diuretic
which reduces the reabsorption of bicarb
Carbohydrates not metabolized (high anion gap):
when there isn’t enough oxygen to break down carbs Signs & Symptoms of Metabolic Acidosis
the pyruvic acids (that supplies the cells with energy)
starts to turn into lactic acid and when you get acid  ****Kussmaul’s respiration (body’s way of

building up you get acidosis trying to compensate by exhaling the excessive

CO2…in hopes of increasing bicarb and blood
Insufficiency of kidneys (high anion gap): kidneys are pH)
failing to filter out metabolic waste products, acids
 Confused, weak, low blood pressure, cardiac
increase, and bicarb cannot keep up so it depletes
changes (if hyperkalemic …can happen

Diarrhea (normal anion gap): profuse diarrhea leads EXCEPT with diarrhea or with Diamox usage

to loss bicarbonate, DKA (diabetic ketoacidosis) body which causes hypokalemia), n & v

is breaking down ketones and is not metabolizing Nursing Interventions for Metabolic Acidosis

glucose correctly which leads to high blood glucose

Vary depending on the causes of acidosis:
levels and breakdown of acids in the blood
  Watch respiratory system and ABGs closely…if 2. down through the Pharynx
too bad may need intubation
3. into the Larynx (the throat)
 Assess other electrolyte levels (esp. potassium
4. then into the Trachea
because during active acidosis it will be
high…however when it resolves there is an 5. and the Bronchus (right and left) which

extracellular to intracellular shift of K+ back branches into the bronchioles and ends in

into the cell which will causes hypokalemia) alveoli sac

 Watch neuro status, safety, and place in seizure *The alveolar sacs are where gas exchange takes

precaution place (oxygen and carbon dioxide diffuse across

the membrane). The oxygen enters into your blood
 Dialysis may be needed if they patient is
stream and CARBON DIOXIDE CO2 is exhaled
experiencing acidosis (high anion gap issue ex:
through your nose or mouth.
renal failure)
The diaphragm also plays a role in allowing lungs
 Diabetic ketoacidosis: administer prescribed
into inflate and deflate.
insulin to help glucose go back into cell which
will help the body start regulating how it
Note: if there is any problem with the patient
metabolizes glucose…hence not more ketones
breathing rate (too fast), alveolar sacs (damaged),
(acids)
hyperventilation, or a brain injury that affects the
respiratory center a patient is at risk for respiratory
alkalosis

*Main cause of respiratory alkalosis is

tachypnea (fast respiratory rate >20 bpm which
causes CO2 to decrease in the lungs)

When this happens the following lab values are

affected:

 Blood pH increases (>7.45)

 Carbon dioxide levels increase (<35)

 **To compensate for this the Kidneys start to

Respiratory Alkalosis
excrete bicarbonate (HCO3) to hopefully

What’s involved:…let’s look at normal breathing: decrease the blood’s pH back to normal…..so
HCO3 becomes <22.
1. Oxygen enters through the mouth or nose
REMEMBER (memorize) these lab values:
  pH 7.35-7.45 Pain…rapid breathing (blowing off too much carbon
dioxide), Pregnancy (especially in 3rd trimester due
 PaCO2 35-45
to changes of the respiratory tract), Pneumonia
 HCO3 22-26
Neurological injuries from a head injury or stroke
(affects the respiration system of the brain which is
located in the medulla and pons)

Embolism or Edema in the lungs

Asthma due to hyperventilation (however, asthma

can cause respiratory acidosis as well due to
bronchospasms which is causing the alveoli to not
Causes of Respiratory Alkalosis properly deflate)

Signs and Symptoms of Respiratory Alkalosis

Remember: TACHYPNEA (fast breathing leads to
“hyperventilation” which leads to respiratory
 ***Classic Assessment Sign is fast respiratory
alkalosis)
rate (normal for adult is 12-

Temperature increase (fever) due to increased 20) TACHYPNEA (>20 bpm)

metabolic needs of the body which causes the  Neuro changes: Tired, lethargy, fast heart rate
respiratory center (medulla and pons) to try to
 **Tetany, dysrhythmias, muscle cramps,
compensate by making the respiratory rate
positive Chvostek’s sign due
increased…hence exhaling too much carbon dioxide
tohypocalcemia and hypokalemia
(CO2)
Nursing Interventions for Respiratory Alkalosis
Aspirin toxicity: too much aspirin in the body leads to
hyperventilation due to the stimulation of the  Teach patient breathing techniques to slow

respiratory center and fever down breathing, holding breath…”rebreathing

into a paper bag or re-breather mask
Controlled ventilation (excessive usage)…mechanical
 Watch potassium levels
ventilation****hyperventilates the patient with too
(hypokalemia..remember hyperkalemia in
much oxygen and depletes carbon dioxide
respiratory acidosis & hypocalcemia) and for

Hyperventilation (excessive respirations) expelling signs and symptoms of low calcium and

too much carbon dioxide potassium levels.

 **Closely watch patients on mechanical

hYsteria (anxiety) leads to rapid breathing and
ventilation to ensure breaths are not
expelling of carbon dioxide
hyperventilating the patient
  **To compensate for this the Kidneys start to
conserve bicarbonate (HCO3) to hopefully
increase the blood’s pH back to normal…..so
HCO3 becomes >26.
What’s involved:…let’s look at normal breathing:
REMEMBER (memorize) these lab values:

1. Oxygen enters through the mouth or nose

 pH 7.35-7.45
2. down through the Pharynx
 PaCO2 35-45
3. into the Larynx (the throat)
 HCO3 22-26
4. then into the Trachea

5. and the Bronchus (right and left) which

branches into the bronchioles and ends in
alveoli sac

*The alveolar sacs are where gas exchange takes

place (oxygen and carbon dioxide diffuse across
the membrane). The oxygen enters into your blood
stream and CARBON DIOXIDE CO2 is exhaled
through your nose or mouth.
The diaphragm also plays a role in allowing lungs
into inflate and deflate.
Causes of Respiratory Acidosis
Remember “DEPRESS” Breathing (anything that
causes you to breathe slowly, blocks the airway, or
causes the diaphragm not to work properly will cause
respiratory acidosis)

Note: if there is any problem with the patient
breathing rate (too slow), alveolar sacs (damaged), or
diaphragm (weak) the patient can experience
respiratory acidosis.
*Main cause of respiratory acidosis
is bradypnea (slow respiratory rate <12 bpm which
causes CO2 to build-up in the lungs)
Drugs (opioids (fentanyl, morphine), sedation
(versed), ….causes respiratory depression
“hypoventilation….retain carbon dioxide….increase
PaCO2 and decreased pH” ) & Diseases of the
neuromuscular system…Myasthenia gravis, Guillain–
Barré syndrome (weakness of voluntary muscles
affects the diaphragm….can’t expelled the carbon
dioxide)

When this happens the following lab values are

Edema (pulmonary) extra fluid in the lung causes
affected:
impaired gas exchange

 Blood pH decreases (<7.35)

 Carbon dioxide levels increase (>45)

Pneumonia…excessive mucous production affect gas  may need endotracheal intubation if CO2 rise
exchange…the alveoli are majorly affected because above 50 mmhg or respiratory distress is
they are filled with pus and fluid present

Respiratory center of brain damaged (brain injury,

stroke)

Emboli (blocks the pulmonary artery or branch of the

lungs causes carbon dioxide to increase)

Spasms of bronchial tubes (asthma) bronchioles

constrict and you have decreased gas exchange

Sac elasticity of alveolar sac are damaged and this Hypophosphatemia

restricts air flow in and out of the lungs and this
increases carbon dioxide (Emphysema & COPD) Hypo: “below”

Signs and Symptoms of Respiratory Acidosis Phosphat: prefix for phosphate

 Major neuro changes: Confused, very drowsy, Emia: blood

and reports a headache
 respiration rate less than 12
 low blood pressure
Nursing Interventions for Respiratory Acidosis
 Administer oxygen
 encourage coughing and deep breathing
Meaning of Hypophosphatemia: Low levels of
phosphate in the blood
Normal Phosphate levels: 2.7 to 4.5 mg/dL (<2.7 is
hypophosphatemia)
Role of phosphate in the body: helps build
bones/teeth and nerve/muscle function.

 suction (pneumonia)
Stored mainly in the bones. The kidneys and
 may need respiratory treatment (asthma) parathyroid play a role in the regulation of calcium

 hold respiratory depression drugs (know the and phosphate.

category of drugs used opiods, sedatives etc)

 ****Watch potassium levels that are
>5.1…remember in hyperkalemiavideo we
talked about how respiratory acidosis caused
increase potassium ….can cause dysrhythmias)
**Calcium and phosphate influence each other in
opposite way. For example, when calcium levels
increase in turn phosphate levels decrease (vice
versa).

 administer antibiotics for infection

Vitamin D plays an important role in phosphate
absorption.
Causes of Hypophosphatemia
Remember phrase: Low “Phosphate”
Pharmacy: drugs such as aluminum hydroxide-based
or magnesium based antacids cause malabsorption in
the GI system, so no phosphate is absorbed through
the GI track and the lack of vitamin d (which plays a
role in phosphate absorption).
Hyperparathyroidism: due to over secretion of
parathyroid hormone (parathyroid plays a role in
maintaining calcium and phosphate levels and it
normally inhibits re-absorption of phosphate by the
kidneys). However, in hyperparathyroidism there is
an over secretion of PTH which causes phosphate
to NOT be reabsorbed at all.
Oncogenic osteomalacia: kidneys start to waste
phosphate which leads to low phosphate levels and
softening of the bones (this puts the patient at risk
for bone fractures).
Syndrome of Refeeding (aka Refeeding Syndrome):
causes electrolytes and fluid problems due to
malnutrition or starvation.
**Watch patients who are on TPN (total parenteral
nutrition). This happens when food is reintroduced
after the body being in starvation mode (hence the
body went into survival mode and is depleted of
almost everything). When the nutrition is introduced,
the body releases insulin due to the increased blood
sugar from the food which causes the body to rapidly
use the already low stores of phosphate, magnesium,
and potassium to help with synthesizing. This
depletes phosphate levels.
Pulmonary issues such as respiratory alkalosis
(under alkalotic conditions phosphate moves out of
the blood into the cell which causes phosphate blood
levels to decrease)
Hyperglycemia leads to symptoms of glycosuria,
polyuria, ketoacidosis which causes the kidneys to
waste phosphate
Alcoholism: alcohol affects the body’s ability to
absorb phosphate and many alcoholics are already
malnourished (hence already have low phosphate
level to begin with)
Thermal Burns due to the shifting of phosphate
intracellularly
Electrolyte imbalances: hypercalcemia,
hypomagnesemia, hypokalemia also cause phosphate
levels to decrease
Signs & Symptoms of Hypophosphatemia
Remember the word: “BROKEN”
These patients are at risk for broken bones and the
systems of the body are breaking down (respiratory,
muscles, neuro, immune etc.)
Breathing problems due to muscle weakness
Rhabdomyolysis which is caused by an electrolyte
disorder. This happens which there is rapid necrosis
of the skeletal muscles which leads to renal failure.
**These patients will have tea-colored looking
urine due to myoglobin in the urine and will have
muscle weakness/pain. The renal failure occurs
because when the muscle dies, myoglobin is released are failing the patient won’t be able to clear
into the blood which is very toxic to the phosphate). Place on cardiac monitor and watch for
kidneys. Reflexes (deep tendon) decreased EKG changes.

Hyperphosphatemia
Osteomalacia (softening of the bones) fractures and
decreased bone density (alteration in bone shape),
Hyper: “excessive”
cardiac Output decreased
Phosphat: prefix for phosphate
Kills immune system with immune suppression and
decreases platelet aggregation (which leads to Emia: blood
increased bleeding)
Meaning of Hyperphosphatemia: High levels of
Extreme weakness, Ecchymoses from decreased phosphate in the blood
platelets
Normal Phosphate levels: 2.7 to 4.5 mg/dL (>4.5 is
Neuro status changes (irritability, confusion, hyperphosphatemia)
seizures)
Role of phosphate in the body: helps build bones
Nursing Interventions for Hypophosphatemia
and teeth and nerve/muscle function.

**Administer oral phosphorus with Vitamin-D

Stored mainly in the bones. The kidneys and
supplement (remember vitamin-d helps with
parathyroid play a role in the regulation of calcium
absorbing phosphate)
and phosphate.

If patient is receiving TPN watch for patient

**Calcium and phosphate influence each other in
complaints of muscle pain or weakness (may be due
opposite way. For example, when calcium levels
to rhabdomyolysis or refeeding syndrome)
increase in turn phosphate levels decrease (vice
versa).
Ensure patient safety due to risk of bone fractures

Vitamin D plays an important role in phosphate

Encourage foods high is phosphate but low in
absorption.
calcium: **Foods high in phosphate are fish, organ
meats, nuts, pork, beef, chicken, whole grains Causes of Hyperphosphatemia (**main cause is
Renal Failure)
If phosphate levels less than 1mg/dL, the doctor
may order IV phosphorous which affects calcium Remember “PhosHi” (there is a drug called Phoslo

levels causing hypocalcemia or increase phosphate (calcium acetate) which is prescribed for patients in
levels (Hyperphosphatemia). ***Also, assess renal end stage renal failure (ESRF) to help keep phosphate

status (BUN/creatintine normal) before levels low. Phoslo is a phosphate binder and it

administering phosphorous because if the kidneys prevents the GI system from absorbing phosphate.
Phospho-soda overuse: phosphate containing Remember CRAMPS (same mnemonic used for
laxatives or enemas (Sodium Phosphate/Fleets hypocalcemia)
Enema) ….do not administer to patients with renal
Confusion
failure

Reflexes hyperactive
Hypoparathyroidism due to under secretion of
parathyroid hormone. The parathyroid plays a role in
Anorexia
maintaining calcium and phosphate levels and it
normally inhibits reabsorption of phosphate by the Muscle spasms in calves or feet, tetany, seizures
kidneys. In hypoparathyroidism, there is under
secretion of PTH which causes phosphate to become Positive Trousseau’s Signs, Pruritis

over absorbed by the kidneys.

Signs of Chvostek

Overuse of Vitamin D (remember Vitamin D helps Nursing Interventions of Hyperphosphatemia

with phosphate absorption. Too much vitamin-d
would cause too much phosphate to be absorbed)  **Administer phosphate-binding drugs
(PhosLo) which works on the GI system and
Syndrome of Tumor Lysis is a metabolic problem that causes phosphorus to be excreted through the
mainly occurs with treatment of cancer with stool.***NCLEX: Give with a meals or right
chemotherapy. It causes the electrolytes to imbalance after eating meal
due to the cell dying and releasing intracellular
 Avoid using phosphate medication such as
contents into the blood, hence too much phosphate is
laxatives and enema
released into the blood
 Restrict foods high is phosphate ***eat,
rHabdomyolysis is rapid necrosis of the muscles and
poultry, fish, dairy, nuts, sodas, oatmeal
this leads to myoglobin being released into the
 Prepare patient for dialysis if patient in renal
bloodstream which affects the kidneys and causes
failure
renal failure. In renal failure, you start to have
phosphate excretion decreased.

Insufficiency of Kidneys (end renal failure) causes

Hypermagnesemia
phosphate to not be excreted

Signs & Symptoms of Hyperphosphatemia Hyper: “excessive”

Will have many of the same symptoms as Magnes: prefix for magnesium
hypocalcemia because remember phosphate and
Emia: blood
calcium function oppositely.

Meaning of Hypermagnesemia: High levels of
magnesium in the blood
Normal Levels of Magnesium: 1.6 to 2.6 mg/dL (>2.6
hypomagnesemia)
Magnesium plays a role in: major cell functions like
transferring and storing energy, regulation of
parathyroid hormone PTH (which also plays a role
in calcium levels). In hypermagnesemia, the release
of calcium is inhibited and that is why you will
see hypocalcemia if you have low magnesium level.
Magnesium also plays a role in the metabolism of
carbs, lipids, and proteins, and blood pressure
regulation.
Magnesium is absorbed in the small intestine and
excreted via the kidneys (any issues with these
systems can cause magnesium level issues).
Causes of Hypermagnesemia
Remember “MAG”
Hypermagnesemia is less common than
hypomagnesemia. It typically happens when you are
trying to correct hypomagnesemia with magnesium
sulfate IV infusion. However, other causes can
include:
Magnesium containing antacids and
laxatives***(Mylanta, Maalox)
Addison’s disease (adrenal insufficiency)
Glomerular filtration insufficiency (<30mL/min)
renal failure. This is because the kidneys are keeping
too much magnesium.
Signs & Symptoms Hypermagnesemia
Remember: Every system of the body is “Lethargic”
(opposite of hypomagnesemia where the body
systems are experiencing hyper-excitability)
Note: You will typically only see symptoms in severe
cases of hypermagnesemia (mild cases patient will be
asymptomatic)
Lethargy (profound)
EKG changes with prolonged PR & QR interval and
widened QRS complex
Tendon reflexes absent/grossly diminished
Hypotension
Arrhythmias (bradycardia, heart blocks)
Respiratory arrest
GI issues (nausea, vomiting)
Impaired breathing (due to skeletal weakness)
Cardiac arrest
Nursing Interventions for Hypermagnesemia
 Monitor cardiac, respiratory, neuro system,
renal status. Put patient on cardiac monitor
(watch for EKG changes)
 Ensure safety due to lethargic/drowsiness
 Prevention:
1. Avoid giving Magnesium containing
antacids/laxative to patients with renal failure
 2. Assess for hypermagnesemia during IV
infusions of magnesium sulfate for
hypomagnesemia (sign and symptom would be
diminished/absent deep tendon reflexes)
3. Withhold foods high in magnesium, such as:
Remember:
“Always Get Plenty Of Foods Containing Large Numb
ers ofMagnesium”
 Avocado
 Green leafy vegetables
 Peanut Butter, potatoes, pork
 Oatmeal
 Fish (canned white tuna/mackerel)
 Cauliflower, chocolate (dark)
 Legumes
 Nuts
 Oranges
 Milk
 Administer diuretics that waste magnesium (if
patient is not in renal failure) such as Loop and
Thiazide diuretics
 Patient in renal failure patient prep for dialysis
 IV calcium may be order to reverse side effects
of Magnesium (watch IV for infiltration…prefer
central line)
Hypomagnesemia
Hypo: “under”
Magnes: prefix for magnesium
Emia: blood
Meaning of Hypomagnesemia: Low levels of
magnesium in the blood
Normal Levels of Magnesium: 1.6 to 2.6 mg/dL (<1.6
hypomagnesemia)
Magnesium plays a role in: major cell functions like
transferring and storing energy, regulation of
parathyroid hormone PTH (which also plays a role
incalcium levels). In hypomagnesemia, the release of
calcium is inhibited and that is why you will see
hypocalcemia if you have low magnesium level.
Magnesium also plays a role in the metabolism of
carbs, lipids, and proteins, and blood pressure
regulation.
Magnesium is absorbed in the small intestine and
excreted via the kidneys (any issues with these
systems can cause magnesium level issues).
Causes of Hypomagnesemia
Remember “Low Mag”
Limited intake Mg+ (starvation)
Other electrolyte issues cause low mag levels
(hypOkalemia, hypOcalcemia)
Wasting Magnesium kidneys (loop and thiazide
diuretics & cyclosporine…stimulates the kidneys to
waste Mag)
Malabsorption issues (Crohn’s, Celiac, proton-pump
inhibitors drugs “Prilosec, Nexium, Protonix”…drug
family ending in “prazole” Omeprazole,
diarrhea/vomiting)
 Nursing Interventions for Hypomagnesemia
Alcohol (due to poor dietary intake, alcohol
stimulates the kidneys to excreted mag, acute
 Monitor cardiac, GI, respiratory, neuro status.
pancreatitis)
Place on a cardiac monitor (watching for any

Glycemic issues (Diabetic Ketoacidosis, insulin EKG changes prolonging of PR interval and

administration) widening QRS complex)

Signs & Symptoms of Hypomagnesemia  May administer potassium supplements due to

hypokalemia (hard to get magnesium level up
Remember “Twitching” because the body is if potassium level is down)
experiencing neuromuscular excitability. This is
 Administering calcium supplements (oral
the OPPOSITE in hypermagnesemia where
calcium supplements w/ Vitamin-D or 10%
everything system of the body is lethargic.
Calcium Gluconate)

Trouesseau’s (positive due to hypocalcemia)  Administer Magnesium Sulfate IV route.

Monitor Mg+ level closely because patient can
Weak respirations
become magnesium toxic (***Watch for

Irritability depressed or loss of deep tendon reflexes)

 Place patient in seizure precautions

Torsades de pointes (abnormal heart rhythm that
leads to sudden cardiac death…seen in  Oral forms of Magnesium may cause diarrhea

alcoholism) Tetany (seizures) which can increase magnesium loss so watch

out for this
Cardiac changes (moderate loss: Tall T-waves and
 Watch other electrolyte levels like calcium and
depressed ST segments*** severe loss: prolonged PR
potassium
& QT interval (prolong of QT interval increases
patient’s risk for Torsades de pointes) with widening  Encourage foods rich in Magnesium:
QRS complex, flattened t-waves, Chvostek’s sign
“Always Get Plenty Of Foods Containing Large Numb
(positive which goes along with hypocalcemia)
ers of Magnesium”

Hypertension, hyperreflexia
 Avocado

Involuntary movements  Green leafy vegetables

 Peanut Butter, potatoes, pork

Nausea
 Oatmeal
GI issues (decreased bowel sounds and mobility)
 Fish (canned white tuna/mackerel)

 Cauliflower, chocolate (dark)

 Causes of Hypernatremia
 Legumes

 Nuts Remember the phrase “HIGH SALT”

 Oranges
Hypercortisolism (Cushing’s Syndrome),
 Milk hyperventilation
Hypernatremia
Increased intake of sodium (oral or IV route)

Hyper: “excessive”
GI feeding (tube) without adequate water

Natr: Prefix for Sodium supplements

Emia: blood Hypertonic solutions

Meaning of Hypernatremia: excessive sodium in Sodium excretion decreased (body keeping too much

the bloodisotonic, hypotonic, and hypertonic tonicity. sodium) and corticosteroids

Normal sodium levels: 135 to 145 mEq/L (>145 Aldosterone overproduction (Hyperaldosteronism)

sodium is hypernatremic)
Loss of fluids (dehydrated) infection (fever),

Hypernatremia is a water problem rather than a sweating, diarrhea, and diabetes insipidus

sodium problem. This is because when the body

Thirst impairment
collects sodium it causes a lot of water retention and
this is what causes the patient problems. Signs & Symptoms of Hypernatremia

Role of sodium in the body: It’s an important Remember: “No FRIED foods for you!” (too much
electrolyte that helps regulate the amount of water salt)
inside and outside of the cell (water and sodium
Fever, flushed skin
loves each other).

Restless, really agitated

Where ever sodium goes, so does water. Watch my
video on hypotonic, hypertonic, and isotonic tonicity.
Increased fluid retention

For example, in hypernatremia there is a lot of

Edema, extremely confused
sodium outside the cell and this attracts the water
from inside the cell which will cause water to move Decreased urine output, dry mouth/skin
outside the cell and dehydrate the cell. Sodium also
Nursing Interventions for Hypernatremia
plays a role in muscle, nerves, and organ function.

 Restrict sodium intake! Know foods high in

salt such as bacon, butter, canned food,
 cheese, hot dogs, lunch meat, processed
food, and table salt.
 Keep patient safe because they will be
confused and agitated.
 Doctor may order to give isotonic or hypotonic
solutions such as 0.45% NS (which is
hypotonic and most commonly used). Give
hypotonic fluids slowly because brain tissue is
at risk due to the shifting of fluids back into the
cell (remember the cell is dehydrated with
hypernatremia) and the patient is at risk
for cerebral edema. In other words, the cell
can lyse if fluids are administered too quickly.
 Educate patient and family about sign and
symptoms of high sodium level and proper
foods to eat.
Hyponatremia
Hypo: “under/beneath”
Natr: Prefix for Sodium
Emia: blood
Meaning of Hyponatremia: low sodium in the blood
Normal sodium levels: 135 to 145 mEq/L (<135 =
hyponatremia)
Role of sodium in the body: An important
electrolyte that helps regulate water inside and
outside of the cell. Remember that water and sodium
loves each other and where ever sodium goes so does
water.
Learn about Hypertonic, Hypotonic, & Isotonic
Solutions. For example, in hyponatremia sodium
outside of the cell is very low and this causes water to
move inside the cell. In turn, the cell will swell and
you will start to see problems in the body, especially
with brain cells (confusion).
Sodium also play a role in muscle, nerves, and organ
function.
Types of Hyponatremia
Euvolemic Hyponatremia is where the water in the
body increases but the sodium stays the same. The
causes include: SIADH (Syndrome of inappropriate
antidiuretic hormone secretion) which is due to the
increased amount of secretion of antidiuretic
hormone. This hormone retains water in the body
which dilutes sodium. Other causes: diabetes
insipidus, adrenal insufficiency, Addison’s disease etc.
Hypovolemic Hyponatremia is where the patient
has lost a lot of fluid and sodium. Causes: vomiting,
diarrhea, NG suction, diuretic therapy, burns,
sweating
Hypervolemic Hyponatremia is where the body has
increased in fluid and sodium. However, sodium
decreases due to dilution and because total body
water and sodium are regulated independently in the
body. Causes: congestive heart failure, kidney failure,
IV infusion of saline, liver failure etc.
Causes of Hyponatremia
Remember “NO Na+”
Na+ excretion increased with renal problems, NG
suction (GI system rich in sodium), vomiting,
diuretics, sweating, diarrhea, decreased secretion of
aldosterone (diabetes insipidus) (wasting sodium)
Overload of fluid with congestive heart failure,
hypotonic fluids infusions, renal failure (dilutes
sodium)
Na+ intake low through low salt diets or nothing by
mouth
Antidiuretic hormone over secreted **SIADH
(syndrome of inappropriate antidiuretic hormone
secretion…remembers retains water in the body and
this dilutes sodium)
Signs & Symptoms of Hyponatremia
Remember “SALT LOSS”
Seizures & Stupor
Abdominal cramping, attitude changes (confusion)
Lethargic
Tendon reflexes diminished, trouble concentrating
(confused)
Loss of urine & appetite
Orthostatic hypotension, overactive bowel sounds
Shallow respirations (happens late due to skeletal
muscle weakness)
Spasms of muscles
Nursing Interventions for Hyponatremia
 Watch cardiac, respiratory, neuro, renal, and GI
status
 Hypovolemic Hyponatremia: give IV sodium
chloride infusion to restore sodium and fluids
(3% Saline hypertonic solution….harsh on the
veins…given in ICU usually through central line
very slowly…must watch for fluid overload)
 Hypervolemic Hyponatremia: Restrict fluid
intake and in some cases administer diuretics
to excretion the extra water rather than
sodium to help concentrate the sodium. If the
patient has renal impairment they may need
dialysis.
 Caused by SIADH or antidiuretic hormone
problems: fluid restriction or treated with an
antidiuretic hormone antagonists
called Declomycinwhich is part of the
tetracycline family (don’t give with food
especiallydairy or antacids…bind to cations
and this affect absorption).
 If patient takes Lithium remember to monitor
drug levels because lithium excretion will be
diminished and this can cause lithium toxicity.
 Instruct to increase oral sodium intake and
some physicians may prescribe sodium tablets.
Food rich in sodium include: bacon, butter
canned food, cheese, hot dogs, lunch meat,
processed food, table salt
Hypercalcemia
Hyper: excessive
Calc: prefix for calcium
Emia: blood
Meaning of Hypercalcemia: excessive calcium in the
blood
Normal calcium levels in the blood: 8.6 to 10.0
mg/dL (>10.0 is hypercalcemia)
Calcium plays a huge role in bone and teeth health Absent reflexes, absent minded (disorientated),
along with muscle/nerve function, cell, and blood abdominal distention from constipation
clotting.
Kidney Stone formation
Calcium is absorbed in the GI system and stored in
Nursing Interventions for Hypercalcemia
the bones and then excreted by the kidneys.
Mild cases of Hypercalcemia
Vitamin D helps play a role calcium absorption.
 Keep patient hydrated (decrease chance of
Causes of Hypercalcemia
renal stone formation)

Remember “High Cal”  Keep patient safe from falls or injury

Hyperparathyroidism (high parathyroid hormone  Monitor cardiac, GI, renal, neuro status

causes too much calcium to be released into the  Assess for complaints of flank or abdominal
blood) pain & strain urine to look for stone formation

Increased intake of calcium (excessive use of oral
calcium or Vitamin D supplements)
Glucocorticoids usage (suppresses calcium
absorption which leaves more calcium in the blood)
Hyperthyroidism
Calcium excretion decreased
with Thiazide* diuretics & renal failure, cancer of the
bones
 Decrease calcium rich foods and intake of
calcium-preserving drugs likethiazides,
supplements, Vitamin D
To help you remember foods high in calcium
remember the phrase:
“Young Sally’s calcium serum continues to randomly
mess-up”
Yogurt

Sardines
Adrenal insufficiency (Addison’s Disease)

Cheese
Lithium usage (affects the parathyroid and causes
phosphate to decrease and calcium to increase)
Spinach
Signs & Symptoms of Hypercalcemia
Collard greens
“The body is too WEAK”
Tofu
Weakness of muscles (profound)
Rhubarb
EKG changes shortened QT interval (most common)
Milk
and prolonged PR interval
Moderate cases of Hypercalcemia
Administer calcium reabsorption
inhibitors: Calcitonin, Bisphosphonates,
prostaglandin synthesis inhibitors (ASA, NSAIDS)
Severe cases of Hypercalcemia
Hypocalcemia
Hypo: low
Calc: pre-fix is calcium
Emia: blood
Meaning of hypocalcemia: Low calcium in the blood
Normal calcium level: 8.6 mg/dL to 10.0 (<8.6
mg/dL)
Role of Calcium: plays a huge role in bone and teeth
health along with muscle/nerve function, cell, and
blood clotting. Calcium is absorbed in the GI system
and stored in the bones and then excreted by the
kidneys.
Vitamin D helps play a role in calcium absorption.
In addition, phosphorus and calcium affect each
other in the opposite way. For instance, if
phosphorus levels are high in the blood, calcium will
decrease and vice versa. They are always doing the
opposite (remember this because it is important for
the causes of hypocalcemia.
Causes of Hypocalcemia
Remember “Low Calcium”
Low parathyroid hormone due. This is due to the
destruction or removal parathyroid gland (any
surgeries of the neck ex: thyroidectomy you want to
check the calcium level) Professors love to ask this on
an exam.
Oral intake inadequate (alcoholism, bulimia etc.)
Wound drainage (especially GI System because this is
where calcium is absorbed)
Celiac’s & Crohn’s Disease cause malabsorption of
calcium in the GI track
Acute Pancreatitis
Low Vitamin D levels (allows for calcium to be
reabsorbed)
Chronic kidney issues (excessive excretion of calcium
by the kidneys)
Increased phosphorus levels in the blood
(phosphorus and calcium do the opposite of each
other)
Using medications such as magnesium supplements,
laxatives, loop diuretics, calcium binder drugs

Mobility issues
Signs & Symptoms of Hypocalcemia
Remember “CRAMPS”
Confusion
Reflexes hyperactive
Arrhythmias (prolonged QT interval and ST
interval) Note: definitely remember prolonged QT
interval…another major test question
Muscle spasms in calves or feet, tetany, seizures
Positive Trousseau’s! You will see this before
Chvostek’s sign or before tetany. This sign may be
positive before other manifestations of hypocalcemia
such as hyperactive reflexes.
(KNOW How to elicit a positive Trousseau’s. You
do this by using a blood pressure cuff and place it
around the upper arm and inflate it to a pressure
greater than the systolic blood pressure and hold it in
place for 3 minutes. If it is positive the hand of the
arm where the blood pressure is being taken will
start to contract involuntarily (see the teaching
tutorial on a demonstration).
Signs of Chvostek’s (nerve hyperexcitability of the
facial nerves. To elicit this response you would tap at
the angle of the jaw via the masseter muscle and the
facial muscles on the same side of the face will
contract momentarily (the lips or nose will twitch).
Nursing Interventions for Hypocalcemia
 Safety (prevent falls because patient is at risk
for bone fractures, seizures precautions, and
watch for laryngeal spasms)
 Administer IV calcium as ordered (ex: 10%
calcium gluconate)….give slowly as ordered
(be on cardiac monitor and watch for cardiac
dysrhythmias). Assess for infiltration or
phlebitis because it can cause tissue sloughing
(best to give via a central line). Also, watch if
patient is on Digoxin cause this can cause
Digoxin toxicity.
 Administer oral calcium with Vitamin D
supplements (given after meals or at bedtime
with a full glass of water)
 If phosphorus level is high (remember
phosphorus and calcium do the opposite) the
doctor may order aluminum hydroxide
antacids (Tums) to decrease phosphorus level
which in turn would increase calcium levels.
 Encourage intake of foods high in calcium:
Young Sally’s calcium serum continues to randomly
mess-up.
 Yogurt
 Sardines
 Cheese
 Spinach
 Collard greens
 Tofu
 Rhubarb
 Milk

Hypokalemia
You will learn the following:
 Causes (easy mnemonics to remember it)
 Signs & Symptoms (tricks on how to easily
remember)
 Nursing Intervention…things that NCLEX and
lecture exams look for
Hypo= low
Kal= root word for potassium….. don’t get it confused
with cal= calcium
Emia=blood
Meaning of hypokalemia: Low Potassium in the
Blood
Normal Potassium Level 3.5-5.1 (2.5 or less is very
dangerous)
Most of the body’s potassium is found in the
intracellular part of the cell compared to the
extracellular which is where sodium is mainly found.
Blood tests measure potassium levels via the outside
of the cell (extracellular fluid).
Remember potassium is responsible for nerve
impulse conduction and muscle contraction.
Causes of Hypokalemia
“Your Body is trying to DITCH potassium”
Drugs (laxatives, diuretics, corticosteroids)
Inadequate consumption of Potassium (NPO,
anorexia)
Too much water intake (dilutes the potassium)
Cushing’s Syndrome (during this condition the
adrenal glands produce excessive amounts of cortisol
(if cortisol levels are excessive enough, they will start
to affect the action of the Na+/K+ pump which will
have properties like aldosterone and cause the body
to retain sodium/water but waste potassium)…hence
hypokalemia
Heavy Fluid Loss (NG suction, vomiting, diarrhea,
wound drainage, sweating)
(Other causes: when the potassium moves from the
extracellular to the intracellular with alkalosis or
hyperinsulinism (this is where too much insulin in
the blood and the patient will have symptoms of
hypoglycemia)
Signs & Symptoms of Hypokalemia
Try to remember everything is going to be SLOW and
LOW. Don’t forget potassium plays a role in muscle
and nerve conduction so muscle systems are going to
be messed up and effect the heart, GI, renal, and the
breathing muscles for the lungs.
 Weak pulses (irregular and thread)
 Orthostatic Hypotension
 Depression ST, flat or inverted T wave and
prominent u-wave
  Shallow respirations with diminished breath
sounds….due to weakness of accessory muscle
movement to breath)
 Confusion, weak
 Flaccid paralysis
 Decrease deep tendon reflexes
 Decreased bowel sounds
Easy way to Remember 7 L’s
1. Lethargy (confusion)
2. Low, shallow respirations (due to decreased
ability to use accessory muscles for breathing)
3. Lethal cardiac dysrhythmias
4. Lots of urine
5. Leg cramps
6. Limp muscles
7. Low BP & Heart
Nursing Interventions for Hypokalemia
Watch heart rhythm (place on cardiac monitor…most
are already on telemetry), respiratory status, neuro,
GI, urinary output and renal status (BUN and
creatinine levels)
Watch other electrolytes like Magnesium (will also
decrease…hard to get K+ to increase if Mag is low),
watch glucose, sodium, and calcium all go hand-in-
hand and play a role in cell transport
Administer oral Supplements for potassium with
doctor’s order: usually for levels 2.5-3.5…give with
food can cause GI upset
IV Potassium for levels less 2.5 (NEVER EVER GIVE
POTASSIUM via IV push or by IM or subq routes)
-Give according to the bag instruction don’t increase
the rate…has to be given slow…patients given more
than 10-20 meq/hr should be on a cardiac monitor
and monitored for EKG changes
-Cause phlebitis or infiltrations
Don’t give LASIX, demadex , or thiazides (waste more
Potassium) or Digoxin (cause digoxin toxicity) if
Potassium level low…notify md for further orders)
Physician will switch patient to a potassium sparing
diuretic Spironolactone (Aldactone), Dyazide,
Maxide, Triamterene
Instruct patient to eat Potassium rich foods
Remember POTASSIUM to help you remember the
foods
 Potatoes, pork
 Oranges
 Tomatoes
 Avocados
 Strawberries,
 Spinach
 fIsh
 mUshrooms
 Musk melons: cantaloupe
Hyperkalemia
You will learn the following:
  Causes (easy mnemonics to remember it)
Signs & Symptoms (tricks on how to easily
remember)
Nursing Intervention…things that NCLEX and
lecture exams look for
Hyper= excessive
Kal= root word for potassium
Emia=blood
Meaning of hyperkalemia: excessive potassium in
the blood
Normal Potassium is 3.5 to 5.1. Anything higher 7.0
or higher is very dangerous!
Most of the body’s potassium is found in the
intracellular part of the cell compared to the
extracellular which is where sodium is mainly found.
Blood tests that measure potassium levels are
measuring the potassium outside of the cell in the
extracellular fluid.
Remember that potassium is responsible for nerve
impulse conduction and muscle contraction.
Causes of Hyperkalemia
Remember the phrase “The Body CARED too much
about Potassium”
Cellular Movement of Potassium from Intracellular to
extracellular (burns, tissue damages, acidosis)
Adrenal Insufficiency with Addison’s Disease
Renal Failure
Excessive Potassium intake
Drugs (potassium-sparing drugs like aldactone
(spiroaldactone), Triamterene, ACE inhibitors,
NSAIDS
Signs & Symptoms of Hyperkalemia
Remember the word MURDER
Muscle weakness
Urine production little or none (renal failure)
Respiratory failure (due to the decreased ability to
use breathing muscles or seizures develop)
Decreased cardiac contractility (weak pulse, low
blood pressure)
Early signs of muscle twitches/cramps…late
profound weakness, flaccid
Rhythm changes: Tall peaked T waves, flat p waves,
Widened QRS and prolonged PR interval
Nursing Interventions for Hyperkalemia
 Monitor cardiac, respiratory, neuromuscular,
renal, and GI status
 Stop IV potassium if running and hold any PO
potassium supplements
 Initiate potassium restricted diet and
remember foods that are high in potassium
 Remember the word POTASSIUM for food rich
in potassium
Potatoes, pork
Oranges
Tomatoes
Avocados
Strawberries,
Spinach
fIsh
mUshrooms
Musk Melons: cantaloupe
Also included are carrots, cantaloupe, raisins,
bananas.
 Prepare patient for ready for dialysis.
Most patient are renal patients who get
dialysis regularly and will have high
potassium.
 Kayexalate is sometimes ordered and
given PO or via enema. This drug
promotes GI sodium absorption which
causes potassium excretion.
 Doctor may order potassium wasting
drugs like Lasix or Hydrochlorothiazide
 Administer a hypertonic solution of
glucose and regular insulin to pull the
potassium into the cell
Isotonic, Hypotonic, & Hypertonic Fluids for
Nursing Students
First, let’s get familiar with the cell and how tonicity
works through osmosis.
The cell is divided into two parts: (intracellular &
extracellular). Each part is made up of a solution
and depending on the tonicity of the fluid you can
having shifting of fluids from outside of the cell to the
inside via osmosis.
The cell loves to be in an isotonic state and when
something happens to make it unequal (like with
hypotonic or hypertonic conditions) it will use
osmosis to try to equal it out.
Osmosis allows molecules of the solvent to pass
through a semipermeable membrane from a less
concentrated solution to a higher concentrated
solution. The key thing to remember here is that
everything will move from aLOW concentration to
a HIGH concentration.
Remember when we are talking about isotonic and
hypo/hypertonic we are talking about how it looks
outside of the cell compared to inside.
Easy Overview of Isotonic, Hypotonic, &
Hypertonic Solutions
Isotonic
Iso: same/equal
Tonic: concentration of a solution
The cell has the same concentration on the inside and
outside which in normal conditions the cell’s
intracellular and extracellular are both isotonic.
It is important to be familiar with what fluids are
isotonic and when they are given.
Isotonic fluids
 0.9% Saline
  5% dextrose in water (D5W)**also used as a
hypotonic solution after it is administered
because the body absorbs the dextrose BUT it
is considered isotonic)
 5% Dextrose in 0.225% saline (D5W1/4NS)
 Lactated Ringer’s
Isotonic solutions are used: to increase the
EXTRACELLULAR fluid volume due to blood loss,
surgery, dehydration, fluid loss that has been loss
extracellularly.
Hypotonic
Hypo: ”under/beneath”
Tonic: concentration of a solution
The cell has a low amount of solute extracellularly
and it wants to shift inside the cell to get everything
back to normal via osmosis. This will cause CELL
SWELLING which can cause the cell to burst or lyses.
Hypotonic solutions
 0.45% Saline (1/2 NS)
 0.225% Saline (1/4 NS)
 0.33% saline (1/3 NS)
Hypotonic solutions are used when the cell is
dehydrated and fluids need to be put back
intracellularly. This happens when patients develop
diabetic ketoacidosis (DKA) or hyperosmolar
hyperglycemia.
Important: Watch out for depleting the circulatory
system of fluid since you are trying to push
extracellular fluid into the cell to re-hydrate it. Never
give hypotonic solutions to patient who are at risk
for increased cranial pressure(can cause fluid to
shift to brain tissue), extensive
burns, trauma (already hypovolemic) etc. because
you can deplete their fluid volume.
Hypertonic
Hyper: excessive
Tonic: concentration of a solution
The cell has an excessive amount of solute
extracellularly and osmosis is causing water to rush
out of the cell intracellularly to the extracellular area
which will cause the CELL TO SHRINK.
Hypertonic solutions
 3% Saline
 5% Saline
 10% Dextrose in Water (D10W)
 5% Dextrose in 0.9% Saline
 5% Dextrose in 0.45% saline
 5% Dextrose in Lactated Ringer’s
When hypertonic solutions are used (very
cautiously….most likely to be given in the ICU due to
quickly arising side effects of pulmonary edema/fluid
over load). In addition, it is prefered to give
hypertonic solutions via a central line due to the
hypertonic solution being vesicant on the veins and
the risk of infiltration