V.

ENDOCRINE
A. Thyroid Gland:
Produces 3 hormones (T3, T4,
Calcitonin)
Calcitonin DECREASES serum
Ca+ levels by taking the calcium out
of the blood and
pushing it back into the bone.
You need IODINE to make
hormones. (This is dietary iodine)
Thyroid hormone gives us
ENERGY!
1. Hyperthyroid: TOO MUCH
ENERGY!! (Graves Disease)
a. S/S:
Nervous
Weight DECREASE
Sweaty/hot
Exophthalmos
Attention span DECREASE
Appetite INCREASE
Irritable
GI FAST
BP UP
Thyroid UP
b. Dx:
If you drew a serum T4 (thyroxine)
or T3 (triiodothyronine)level on this
client
would it be increased or decreased?
INCREASED
Thyroid scan
Client must discontinue any iodine
containing medication ONE week
prior to
the thyroid scan.
c. Tx:
1) Anti-thyroids: Propylthiouracil
(PTU), Methimazole (Tapazole)
Stops the thyroid from making
thyroid HORMONE.
Its used PREOP to stun the
thyroid.
We want this client to become
euthyroid (eu=NORMAL)
2) Iodine Compounds: Potassium
Iodine (SSKI), Strong Iodine
Solution
(Lugols solution)
DECREASE the size and the
vascularity of the gland
ALL endocrine glands are VERY
VASCULAR!
Give in milk, juice, and use straw.
Why? STAIN THE TEETH
3) Beta Blockers:
PROPRANOLOL(Inderal)
Decreases myocardial contractility

Could decrease cardiac output

Decreases HR, BP
DECREASE anxiety.
4) Radioactive Iodine ( ONE dose)
Given P.O. (liquid or tablet form)
**Rule out pregnancy first**
Destroys thyroid cells
HYPOTHYROID
Follow radioactive precautions.
Stay away from BABIES for 24 hours.
Dont anyone for 24 hours.
Watch for thyroid storm
(thyrotoxicosis, and thyrotoxic crisis).
It is hyperthyroidism multiplied by
100.
Could be rebound effect postradioactive iodine
*TESTING STRATEGY*
Do not give beta blockers to
asthmatics or diabetics.
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5) Surgery: thyroidectomy
(partial/complete)
Post op:
Teach how to support neck.
Put personal items NEXT to them.
Positioning:
HOB? ELEVATED TO DECREASE
EDEMA
Check for bleeding where?
BEHIND THE NECK.
Nutrition (pre & post op) need
MORE calories.
Assess for recurrent laryngeal
nerve damage by listening for
HOARSNESS AND WEAK VOICE.
Could lead to vocal cord paralysis,
if there is paralysis of both cords
LARYNGEAL obstruction will occur
requiring immediate OPERATION.
Teach to report any c/o
PRESSURE.
Trach set at bedside
1) Swelling
2) Recurrent laryngeal nerve damage
(vocal cord paralysis)
3) Hypocalcemia
Assess for removal.
How? S/S of SEIZURE, RIGID
MUSCLE, LARYNGOSPASM.
Eye care is important for a client with
hyperthyroidism. If client cant close
their eyelids,
hypoallergenic tape may be applied to
close lid (to help prevent injury or
irritation). Dark glasses may
be worn if photosensitivity is present.
Artificial tears are used to prevent
drying of the eyes.

Treatment of hyperthyroidism DOES

NOT correct any eye or vision
problems.
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2. Hypothyroid (Myxedema):
a. S/S:
No ENERGY
When this is present at BIRTH its
called cretinism (very dangerous, can
lead to slowed mental and physical
development if undetected).
Fatigue
GI INCREASE
Weight INCREASE
Hot or cold? COLD
Speech SLOW/SLURRED
No expression
You may be taking care of a totally
immobile client
b. Tx:
Levothyroxine (Synthroid),
Thyroglobulin (Proloid),
Liothyronine
(Cytomel)
Do they take these meds forever?
YES
What will happen to their energy
level when they start taking these
meds?
INCREASE
c. People with hypothyroidism tend to
have CORONARY ARTERY
DISEASE.
B. Parathyroid Problems:
The parathyroids secrete PTH
which makes you pull
calcium from the UP and place it in
the blood. Therefore, the serum
calcium level goes HIGH.
If you have too much
parathormone in your body the serum
calcium level will be
HIGH.
If you do not have any
parathormone in your body the serum
calcium level will be
LOW.
1. Hyperparathyroidism =
Hypercalcemia =
Hypophosphatemia:
a. S/S:
Too much PTH
Serum calcium is HIGH. Serum
phos is LOW.
Other S/S LOOKS SEDATED
b. Tx:
Partial parathyroidectomy when
you take out 2 of your parathyroids.
PTH
secretion DECREASE.

What are you going to monitor post

op? HYPOCALCIMIC
2. Hypoparathyroidism =
Hypocalcemia =
Hyperphosphatemia:
a. S/S:
Not enough PTH,
Serum calcium is LOW. Serum phos is
HIGH.
Other S/S: NOT SEDATED
b. Tx:
IV CALCIUM
Phosphorus binding drugs
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C. Adrenal Glands:
Need your adrenals to handle
STRESS
You have two parts to your adrenal
gland: adrenal medulla and the adrenal
cortex.
1. Adrenal medulla: (epinephrine, nor
nonepinephrine)
Adrenal Medulla Problems:
Pheochromocytoma
Benign tumors that secrete epi and
norepi in boluses
a. S/S:
BP? UP
HR and Pulse? UP
Flushing/diaphoretic
b. Dx:
VMA (vanillylmandelic acid) test:
a 24 hour urine specimen is done
and you are looking for increased
levels EPI and NOREPI
(also called catecholamines).
With a 24 hour urine you should throw
AWAY the first
voiding and KEEP the last voiding.
c. Tx:
Surgery to remove TUMORS
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2. Adrenal cortex: (Glucocorticoids,
Mineralocorticoids, and Sex
hormones)
a. Adrenal Cortex Steroids:
1) Glucocorticoids:
Change your mood.
Example: insomnia, depressed,
psychotic, euphoric
Alter defense mechanisms
Immunosuppressed
High risk for INFECTION
Breakdown FAT and proteins
Inhibit insulin
H y p e rglycemic
Do accuchecks
2) Mineralocorticoids: Aldosterone
Make you retain SODIUM &
POTASSIUM

Make you lose POTASSIUM

Too Much Aldosterone.
Fluid volume excess
Serum Potassium: DOWN
Not Enough Aldosterone.
Fluid volume deficit
Serum Potassium: INCREASE
3) Sex hormones:
**See Cushings notes**
Adrenocorticotropin hormones
(ACTH) are made in the pituitary and
they stimulate cortisol to be made.
Cortisol is a hormone of the adrenal
cortex.
So no matter what fancy word
NCLEX Lady usesyou will still
get the same resultthink steroids.

ACTH = Cortisol level

Too many steroids = Hypercortisolism
(just another word).
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b. Adrenal Cortex Problems:
1) Addisons disease: (Adrenocortical
insufficiency-not enough steroids)
a) Pathophysiology:
They do not have enough
glucocorticoids, mineralocorticoids, or
sex hormones.
Aldosterone (mineralocorticoids)
Normally, aldosterone makes us
retain SODIUM and WATER
and lose POTASSIUM......Now we
dont have enough (insufficient)
so we will lose SODIUM and WATER
and retain POTASSIUM.
The serum K+ will be HIGH.
b) S/S:
Initially, the majority of the S/S are
a result of the hyperkalemia.
Beginning with muscle twitching, then
proceeds to weakness,
then flaccid paralysis.
Other S/S:
Anorexia/nausea
Hyperpigmentation-bronzing color
of the skin and mucous
membranes
Decreased bowel SOUNDS
GI upset
White patchy area of depigmented
SKIN (vitiligo)
Hypotension
Decrease Na, increased K+ and
WATER
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c) Tx:
Combat shock (losing SODIUM
and WATER)
INCREASE sodium in their diet

Processed fruit juice/broth (has lots

of SODIUM)
I & O and daily weight
If this client is losing Na and water
their BP will probably be
LOW.
They will probably be
gaining/losing weight? LOSING
Nursing DX: Fluid Volume
DEFICIT
Will be placed on the
mineralocorticoid drug
Fludrocortisone
(Florinef) (aldosterone)
Rule: When on a medicine where
weight has to be monitored,
keep weight within 2-3 lbs (+ or -) of
their normal weight.
WEIGHT is very important in
adjusting their medication.
Critical Thinking Exercise:
If you have a client at home taking
Fludrocortisone (Florinef) and the
following
occurswhat should the CLIENT do?
(1) Overnight gain of 7 lbs. what do
they do with their AM
dose? DECREASE or HOLD
(2) Overnight loss of 7 lbs. what do
they do with their AM
dose? HOLD IT, AND CALL THE
DOCTOR
If the nurse is taking care of the
client in the hospital on
Fludrocortisone (Florinef)
and the following occurswhat
should the NURSE do?
(1) Client has edema or their BP is
up INCREASE DOSE
(2) Clients BP is steadily going
down DECREASE
*TESTING STRATEGY*
Addisonian Crisis = severe
hypotension and vascular collapse
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2) Cushings:
a) S/S:
These clients have too many
glucocorticoids, mineralocorticoids,
and sex
hormones.
Growth arrest
Thin extremities/skin (lipolysis)
Increased risk of infection
Hyperglycemia Too
Psychosis to depression Many
Moon faced (fat redistribution or fluid
retention)
Truncal obesity (fat redistribution;
lipogenesis)
Buffalo hump (fat redistribution)

Oily skin/acne Too

Women with male traits Many
Poor sex drive (libido)
High BP
CHF Too
Weight gain Many
Fluid Volume EXCESS
Since the client has too much
mineralocorticoid (aldosterone), the
serum K+ will be LOW.
If you did a 24 hour urine on this
client the cortisol levels would be
HIGH.
b) Tx:
Adrenalectomy (unilateral or
bilateral)
*If both are removed lifetime
replacement
Quiet environment
Diet pre-treatment?
K+ INCREASE Na DECREASE
Protein INCREASE Ca INCREASE
Avoid infection.
What might appear in their urine?
KETONES, GLUCOSE
Hint: Steroids decrease serum
Calcium by excreting it through the GI
tract.
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D. Diabetes:
1. Classification:
a. Type 1: (IDDM)
They have little or no insulin.
Usually starts in childhood
First sign may be DKA.
Appears ABRUPTLY
1) Pathophysiology:
You have to have INSULIN to carry
glucose out of the vascular space
into the cellsince there is no insulin,
the glucose just builds up in the
VASCULAR space, the blood
becomes hypertonic and pulls fluid
into
the vascular spacethe kidney filter
excess glucose and fluids (polyuria
and polydipsia) the cells are starving
so they start breaking down protein
and fat for energy (polyphagia)
when you break down fat you get
KETONES (acids)Now this client is
METABOLIC ACIDOS (respiratory
or metabolic?)
2) S/S:
Polyuria
Polydipsia
Polyphagia
3) Tx:
Will oral hypoglycemia agents
work for this client? NO

They have to have insulin.

Normal Lab Value
Blood Glucose: 70-110 mg/dL
Hyperglycemia = 3 Ps
Polyuria think shock first.
Hurst Review Services 63
b. Type II: (NIDDM)
1) Pathophysiology:
These clients dont have enough
INSULIN or the insulin they have
is no good.
These clients are usually
OVERWEIGHT.
They cant make enough insulin to
keep up with the GLUCOSE load the
client is taking in.
This type of diabetes is not abrupt
as Type I.
Its usually found by accident; or
the client keeps coming back to the
doctor for things like a wound that
wont heal, repeated vaginal
INFECTION, etc.
Individuals with Type II diabetes
should be evaluated for
METABOLIC syndrome.
This includes: insulin resistance,
obesity, increased triglycerides,
decreased HDL, increased BP, and
CAD.
2) Tx:
Start with diet and exercise, then
add oral agents, then some clients take
INSULIN.
c. Gestational Diabetes:
Resembles Type II
Mom needs 2-3x more CALORIES
than normal.
If mom is over 25 or has family
history, screen at _______ weeks
gestation.
Complication to baby:
Increased birth weight anD
PROTEINURIA
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2. General Treatment of Diabetes:
(Type I and Type II)
a. Diet:
Majority of calories should come
from: *complex carbohydrates 5560% *fats
20-30% *protein 12-20%
Diabetics tend to have CAD disease.
Why are diabetics prone to CAD?
Sugar destroys vessels just like FAT.
High FIBER diet (keeps blood
sugar steady; client may have to
decrease
insulin)

High fiber slows down absorption in

the intestines,
therefore, eliminating the sharp
rise/fall of all blood sugar.
b. Exercise:
Wait until blood sugar
NORMALIZES to begin exercise.
What should the client do preexercise to prevent hypoglycemia?
EAT
Exercise when blood sugar is at its
highest or lowest? HIGHEST
Exercise SAME time and amount
daily.
c. Medications:
How do oral hypoglycemic agents
work? STIMULATE pancreas to
make insulin.
*Note: not all oral hypoglycemic
agents stimulate the pancreas to make
insulin.
Oral Anti-Diabetic Agents: Glipizide
(Glucotrol), Metformin
(Glucophage), Pioglitazone
(Actos)
Only give to Type II
How is the insulin dose
determined?
The dose is increased until the
BLOOD SUGAR is normal and until
there is no more GLUCOSE &
KETONES in
urine.
Reg (CLEAR).NPH (CLOUDY)
Lantus is also clear and is
considered a LONG ACTING insulin.
What is the only type of insulin
you can give IV? REGULAR
When drawing up regular and
NPH, which one do you draw up first?
REGULAR
*TESTING STRATEGY*
Extreme blood sugar =
Vascular damage
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d. Client Teaching Education:
Glycosylated Hemoglobin (Hb
A1c): blood test; gives an average of
what your
blood sugar has been over the past 3
MONTHS.
Client should eat when insulin is at
its PEAK.
What happens to your blood sugar
when you are sick/stressed?
INCREASED
Normal pancreas can handle these
fluctuations; an
increase in the blood sugar when
sick/stressed is a normal reaction

to help us fight the illness/stressor.

ILLNESS = DKA
Rotation of sites (Rotate WITHIN
an area first)
Aspirate? NO
e. Insulin Infusion Pumps:
Alternative to daily insulin
injections
Obtain better control: receiving a
basal level of insulin from pump along
with
additional insulin as needed with
MEAL, and if they have an
ELEVATED
blood sugar.
f. Hypoglycemic/Hyperglycemic
Episodes:
What are the S/S of hypoglycemia?
If hypoglycemic, what should the
client do? EAT SUGAR
After the blood sugar is up, what
should they do? COMPLEX CARBS
You enter a diabetic clients room
and they are unconscious do you
treat
this client like he is hypo or
hyperglycemic? HYPOGLYCEMIC
D50W (hard to push; and if you have a
choice you need a large bore IV)
Injectable glucagon (GlucaGen)
(used when there is no IV access;
given IM)
Prevention: (1)EAT
(2)TAKE INSULIN
(3)EXERCISE
For people with
diabetes, the ideal
goal for their
HbA1c is 4-6 % or
less.
ADA < 7%
*TESTING STRATEGY*

Illness = DKA
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3. Complications of Diabetes:
a. Diabetic Ketoacidosis (DKA):
1) Pathophysiology:
Anything that increases blood
sugar can throw a client into DKA
(infection, illness, skipping insulin).
DKA may be the first sign of
DIABETES.
Have all the usual S/S of Type I
diabetes
Patho: Absent or inadequate
insulin blood sugar goes sky high
Polyuria, Polydipsia, Polyphagia
Fat breakdown (acidosis)
Kussmauls respirations (trying to
blow off CO2 to compensate for the
metabolic acidosis). Also, as the client
becomes more acidotic the LOC
goes down.
2) Tx:
Find the cause.
Hourly blood sugar and K+
IV insulin-Insulin decreases
HYPOGLYCEMIA &
HYPOKALEMIA
by driving them out of the vascular
space into the cell.
ECG
Hourly OUTPUT
ABGs
IVFs Start with NSthen when
the blood sugar gets down to about
300 switch to D5W to prevent
throwing the client into
HYPOGLYCEMIA.
Anticipate that the doctor will want
us to add POTASSIUM to the IV
solution at some point.
Hurst Review Services 67

b. Hyperosmolar hyperglycemic
nonketosis (HHNK) or
Hyperosmolar hyperglycemic
nonketosis coma (HHNC):
Looks like DKA, but NO
ACIDOSIS
Making just enough insulin so they
are not breaking down body FAT
No fat breakdown.no KETONES
No ketonesno ACIDS
Will this client have Kussmauls
respirations? NO
c. Vascular Problems:
Will develop poor circulation
everywhere due to VESSEL damage
(sugar
irritates the vessel lining;
accumulation of sugar will decrease
the size of
vessel lumen therefore decreasing
blood flow)
1) Diabetic retinopathy
2) Nephropathy
d. Neuropathy:
1) Sexual problems:
impotence/decreased sensation
2) Foot/leg problems:
pain/paresthesia/numbness
Review of Diabetic Foot Care
3) Neurogenic bladder: bladder does
not empty properlythe bladder may
empty spontaneously,
INCONTINENCE or may not empty
at all, RETENTION.
4) Gastroparesis: stomach emptying is
delayed so there is an increased risk
for
ASPIRATION.
e. Increased Risk for INFECTION
*TESTING STRATEGY*
In the NCLEX world: Type I
DKA Type II HHNK