HYPOTHYROIDISM

Definition: Low 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 and Symptoms Hypothyroidism
• Let the condition’s name help you: everything is going to be LOW and SLOW due to the body
working at a very slow metabolism rate
• Weight Gain
• Unable to tolerate cold
• Possible goiter from constant thyroid stimulation to get the thyroid gland to produce T3 and
T4 MOST COMMON SIGN IN HASHIMOTO’S
• Extremely tired and fatigued
• Slow heart rate
• Thinning and brittle hair
• Depression
• Constipation
• Memory loss
• Myxedema: swelling of the skin (eyes and face) that gives it a waxy appearance
• Dry skin
• Joint, muscle pain
• Menstrual problems (irregular or heavy periods)
***early signs are feeling tired and fatigue…then as hypothyroidism progresses the patient starts to
exhibit other symptoms
Causes of Hypothyroidism
• Affects mainly women (middle-aged to older-aged)
• Hashimoto’s thyroiditis (most common cause): autoimmune
disorder where the body attacks the thyroid gland which
causes it to stop releasing T3 and T4. GOITER LIKELY
• Iodine deficiency: not consuming enough foods with iodine
• Pituitary Tumor: stops the anterior pituitary from secreting
TSH which stimulates the thyroid gland to secrete T3 and T4.
Treatment for hypothyroidism:
•Thyroid Hormone replacement (Synthroid,
Thyrolar, Cytomel)
•Avoid sedatives and narcotics because these
patients are very sensitive to them and they
increase the chances of myxedema coma
Nursing Interventions for Hypothyroidism
• Monitor for Myxedema Coma: caused from uncontrolled
low thyroid production usually due to illness, abrupt
stopping thyroid replacement medication, or removal of
thyroid gland
- Presents with everything shutting down (or slowing down to
the point of death)
- Temperature regulation doesn’t work (hypothermia)
- Extreme drowsiness
- Respiratory failure, bradycardia (remember t3 and t4 play a
role in sympathetic system)
- Low blood glucose, sodium levels…progress to a coma
•Monitor vitals sign: HR, BP, EKG
•Monitor weight
•Keep patient warm and assess for
constipation (very
uncomfortable)…encourage fluids
Medications for Hypothyroidism
• Thyroid hormone replacement:
• Cytomel “Liothyronine sodium”
• Thyrolar “Liotrix”
• Synthroid “Levothyroxine” MOST COMMON
Patient education:
• Don’t abruptly stop taking (takes a while for signs and
symptoms to improve)
• Take at the same time every day in the morning
without food
• Don’t take within 4 hours of multivitamins, GI
medications like Carafate, aluminum hydroxide,
simethicone….decreases absorption of thyroid
medication
• Watch for signs and symptoms of toxicity which would
present as signs and symptoms of hyperthyroidism
(fast heart, feeling hot, sweating)
• Note patients with hypothyroidism are sensitive to
narcotics like opioids (avoid dilaudid, morphine,
fentanyl) and other sedatives (could lead to
myxedema coma). Instead use alternatives for pain as
prescribed like non-narcotics (Tylenol, Ibuprofen)
 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)
Hypoparathyroidism

Definition: low production of parathyroid

hormone (PTH) by the parathyroid gland
Key Players:
• Parathyroid Gland: located in the neck, behind the thyroid gland.
There is a total of 4 parathyroid glands and they secrete parathyroid
hormone.
• Parathyroid hormone (PTH): regulates calcium and phosphate blood
levels. It regulates calcium levels by acting on the bones (stimulates
osteoclasts which break down the bones and this causes bone
resorption which releases calcium into the blood), kidneys (reabsorb
calcium and activates vitamin D), and GI system (vitamin d activated
by the kidneys cause the small intestine to reabsorb calcium from
food intake), and it regulates phosphate by inhibiting the kidneys
from reabsorbing phosphate, and is therefore excreted into the urine.
• Kidneys: reabsorb Ca+ and excrete phosphate, and activate
vitamin D
• Bones: causes osteoclasts in the bones to break down bone
and release calcium through bone resorption
• Small Intestines: the activation of vitamin D by the kidneys
causes the gut to absorb calcium from the food
• PTH Negative feedback Loop: Low levels of calcium detected
in the blood causes the parathyroid gland to release PTH
which stimulates the bones and kidneys to increase calcium
levels.
• In HYPOparathyroidism, there isn’t enough PTH being released by the
parathyroid gland to cause the kidneys and bones to release or
absorb calcium so calcium levels fall. The patient will
experience: HYPOcalcemia and HYPERphosphatemia (this is because
the kidneys start to conserve phosphate).
• Hypocalcemia: low calcium levels (calcium plays a role in muscle and
nerve conduction, bone health and needs vitamin D to help the body
absorb calcium)
• Hyperphosphatemia: high phosphate levels (phosphate plays a role in
bone health, muscle and nerve function….the kidneys regulate the
amount of phosphate in the body)
Causes of Hypoparathyroidism
• Destruction or manipulation of the parathyroid
glands (most common): Thyroidectomy or treatment of
cancer of the neck/throat…due to the close proximity and
sharing of blood supply of the thyroid gland and parathyroid.
• Hypomagnesemia: low levels of magnesium can cause the
parathyroid gland to not work properly
• Autoimmune: body produces antibodies that attack the
gland
• Body is resistant to PTH: parathyroid works great but the
bones and kidneys do not respond to it being released.
Signs and Symptoms of Hypoparathyroidism
• Signs and symptoms are mainly due to the low calcium level
• Remember “PTH” for parathyroid hormone to help you remember S
&S
• Paresthesia (tingling sensation on the mouth, face, and
finger/toes), Positive Trousseau’s sign or Chvostek’s sign (due to
hypocalcemia)
• KNOW how to elicit a positive Trousseau’s Sign. 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.
 • KNOW how to elicit a positive Chvostek’s Sign (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) if positive.
• Tetany (severe) due to low calcium and high phosphate level
which is involuntary muscle cramping and contraction:
bronchospasm and laryngospasms, hand/feet spasms,
seizures, EKG changes
• Hypocalcemia and Hyperphosphatemia
Nursing Interventions for Hypoparathyroidism
• Monitor calcium (normal 8.6 to 10.0 mg/dL) and
phosphate levels (normal 2.7 to 4.5 mg/dL)
• Monitor airway due to tetany and seizures
(bronchospasm/laryngospasms)…prepare for the
worst…have a trach kit, oxygen, suction at bedside)
• Ensure patient eats a diet high in calcium (dairy, green
leafy vegetables) and low in phosphate (organ meats,
soft drinks, eggs)
Administering Medications per physician’s order:
• Goal of medications are to increase calcium levels and
decrease phosphate levels.
• IV Calcium (if very low): (ex: 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 because this can
cause Digoxin toxicity.
• Oral calcium with Vitamin D: Calcium Carbonate “Os-cal with vitamin
D” (patient education: GI upset, constipation…renal calculi…flank
pain)
• ***Calcium supplements interfere with the absorption of iron and thyroid
hormone so give at separate times
• Phosphate-binders may be ordered to increase excretion of
phosphate by GI system into the stool: Aluminum carbonate (Gelusil
Amphojel) ADMINISTER after meals
• Parathyroid Hormone Replacement: Natpara
• Monitor calcium levels: can increase calcium levels too high, GI issues nausea
vomiting, paresthesia
 Hyperparathyroidism
• Definition: excessive secretion of parathyroid
hormone by the parathyroid gland which
causes HYPERcalcemia and HYPOphosphatemia.
Normal calcium: 8.6 to 10.0 mg/dL (>10.0 is hypercalcemia)
Normal phosphate: 2.7 to 4.5 mg/dL (<2.7
hypophosphatemia)

Causes of Hyperparathyroidism
• Primary Hyperparathyroidism: There is a problem with the
parathyroid gland itself.
- Noncancerous growths: Adenoma (most common)
- Hyperplasia of the glands (enlargement)
- Cancerous growths
Secondary Hyperparathyroidism: A disease is causing the
parathyroid gland to mess up.
• Hypocalcemia (very severe): causes the parathyroid to
become overworked in trying to keep the calcium levels up.
• Vitamin D deficiency: low absorption of calcium (remember
vitamin d helps with calcium absorption ) so the parathyroid
gland overworks to produce PTH (with the intention of
increasing calcium levels but can’t increase them).
• Chronic renal failure: kidneys aren’t able to activate the
vitamin D so the small intestines can’t absorb calcium and
the kidneys don’t absorb calcium (most common cause)
Signs and Symptoms of Hyperparathyroidism
Main reason for signs and symptoms is due to the high
calcium levels: remember calcium plays an important role in
bone health, muscle contraction, and nerve function….too
much calcium causes the bones to become fragile (because
calcium has left the bones), muscles and nerve function will
slow down as well.
• Bones fractures (osteoporosis): PTH causing excessive
stimulation of bone osteoclasts which causes major bone
resorption where calcium leaks into the blood in excessive
amounts and it causes the bones to become very fragile
• Calculi formation: increased calcium levels causes the
kidneys to reabsorb calcium which can form stones (plus
dehydration increases this risk).
• Constipation: high calcium levels slow down the GI system
• GI problems: nausea, vomiting, epigastric pain: (from
calcium effects of causing increased GI acid)
• Frequent urination: high amounts of calcium cause the
kidneys to work harder and put out more urine
• EKG changes: short QT interval
Nursing Interventions for Hyperparathyroidism
• Monitor vitals, EKG, renal stones (strain urine), calcium and
phosphate levels
• Monitor intake and output and fluid status (encourage
fluids….patients are risk for dehydration and kidney stone
formation, however watch fluid status on patients with
congestive heart failure and renal failure.
• Diet low is calcium and high in phosphate…watch phosphate
in renal patients
Treatments and Medications (depend on the cause):

• Parathyroidectomy: main treatment for primary

hyperparathyroidism
• Monitor respiratory status due to nature of surgery, Semi-
Fowler’s position, trach kit, oxygen, and suction at bedside
for emergency
• Watch for low calcium levels: tingling or numbness or
excessive twitching in extremities or face, tetany, positive
Trousseau’s or Chvostek’s Sign
• Monitor patient for laryngeal nerve damage: voice
changes (hoarseness), problems swallowing or speaking
Medication Goals: to decrease parathyroid and calcium levels and keep
patient hydrated
• IV fluids: normal saline for hydration
• Calcimimetics: “Senispar” decreases PTH, calcium, and phosphate
levels (usually prescribed for patients with secondary
hyperparathyroidism with CKD…patients with renal failure struggle
with high phosphate levels so this medication helps with this as well)
• It mimics the role of calcium in the blood and deceives the parathyroid gland
into thinking there is enough calcium in the blood so it will quit secreting PTH.
Note: Take with food or right after meal….side effects: GI issues and
hypocalcemia
• Calcitonin (injection or nasal sprays): naturally produced by the
thyroid gland and helps lower calcium levels (suppresses osteoclast
activity of the bones (helps protect bones) and increases the kidneys
excretion of calcium).
• Loop diuretics “Lasix”: decreases calcium levels by inhibiting calcium
reabsorption in the renal tubules (watch potassium levels)
• Bisphosphonates: “Pamidronate (Aredia) or Alendronate (Fosamax)”
helps protect bones from losing calcium by slowing down osteoclasts
(which break down bones) and allow osteoblasts to work (to help
build bones)
• Patient education for Fosmax: take on empty stomach, by itself, with a full
glass of water, and sit-up right for 30 minutes after taking (very hard on the
esophagus and stomach and can cause ulcers)…wait 30 minutes before taking
antacids, vitamins
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
Cushing’s Syndrome vs Cushing’s Disease
•Cushing’s Syndrome: caused by an outside cause
or medical treatment such as glucocorticoid
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

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
Watch for 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
1. Sudden pain in stomach, back, and legs
2. Syncope (going unconscious)
3. Shock
4. Super low blood pressure
5. 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)
What is Diabetes Insipidus (DI) and SIADH (Syndrome of
inappropriate antidiuretic hormone secretion)?
This is where the body has a problem producing ADH
(either too much or not enough). What is ADH? It is
anti-diuretic hormone. This hormone is produced in the
hypothalamus, and stored and eventually released in
the posterior pituitary gland. In order to understand
diabetes insipidus and SIADH, you MUST understand
how ADH works because ADH plays an important role
in both DI an SIADH.
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 the KIDNEYS! 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
You would 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- Sara’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)
• 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)
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.
Here is a chart comparing the two. You can use this as a study aid in
helping you remember. Sometimes, seeing the differences side by side
between the two helps.
MULTIPLE SCLEROSIS

- Refer to the old notes I gave

you.
Parkinson’s Disease

• What is Parkinson’s Disease? It’s a neuro disease that

gradually starts to affect movement.
• What is happening in Parkinson’s disease to cause
movement to become affected? The dopaminergic neurons
in the part of the brain called substantia nigra have started
to die.
• Significance of this area? This area is part of the basal
ganglia which is part of the midbrain that controls
movements.
• What is the role of these dopaminergic neurons? They release the
neurotransmitter dopamine, which allows us to have accuracy with
movement. Therefore, if they are dying this will lower the amounts of
dopamine available to our body for normal movement.
• Why is there the signs and symptoms of tremors,
rigidity etc.? Normally in the nervous system there is
a balance between acetylcholine (an excitatory
neurotransmitter) and dopamine (an inhibitory
neurotransmitter).
• Therefore, the loss of dopamine leads to more
acetylcholine being able to produce more excitatory
affects to the neurons in the basal ganglia and this
leads to overstimulation…..tremors, rigidity
(increased cholinergic activity) etc.
Key Points about Parkinson’s Disease
• The disease tends to occur in older age 60+ (however it can
affect younger people…example: Michael J. Fox was
diagnosed with PD at the age of 29).
• There is currently no cure (there are medications to relieve
signs and symptoms).
• Signs and symptoms are subtle (some patients don’t notice
them at first) and they will become worse overtime.
• Signs and symptoms may present on one side or one
extremity and progress to the others overtime.
Signs and Symptoms of Parkinson’s Disease

• Mainly motor symptoms: affects how the patient is able to

move
• Tremors at rest (most common): hands, arms, legs (even lips
and tongue)… improves with movement
• Pill-rolling: tremors of the hands and fingers….looks like
the patient is rolling a pill between fingers and hands.
• Stiffness of extremities (arms DON’T swing with
gait)…. akinesia: inability to move the muscles
voluntarily….”freeze up”
• Shuffling of gait (extremities can freeze while walking)
• Cogwheel rigidity: when moving the patient’s arms
passively toward the body they jerk or push back slightly
• Bradykinesia: movements are slow, difficulty swallowing
(drooling), Face mask-like: expressionless
• Coordination issues…..so the patient will stoop to
compensate.
• Issues with the muscles used for chewing food, swallowing,
and speaking: soft or slurred speech, problems swallowing
(aspiration)
Other signs and symptoms that are non-motor:

•Depression
•Constipation: digestion slows down
•Loss of smell
Nursing Interventions for Parkinson’s Disease

What is going on?

• Safety issues (balance coordination, swallowing, freezing
episodes can lead to falls)
• Psychosocial issues (low self-esteem, loses ability to care for
self, depression, isolation)
• Digestion issues/nutrition issues
• Side effects and teaching with medications
Safety Issues:
• Patient needs to wear low heel shoes and avoid rubber
soles (they tend to stick to the floor and can cause
tripping). The soles should be smooth (not slick).
• For balance: move slowly when changing positions…rubber
tip cane that is single point can help.
• Education on how to deal with freezing episodes (some
patients have them and they can occur randomly). For
example, it can occur in the legs, and it feels like the shoes
suddenly become stuck to the ground and they can’t move.
• Try to change direction of movement….rather then continue going to
the side go forward.
• Use cane or walker with a laser…it provides a laser line on the floor
that will help the patient find a landmark for when freezing episode
happens and helps the patient coordinate their next step.
• Consciously lift the legs (as in marching) with each step or pretend
they are walking over an object.
• DON’T push through the freeze up.
Use handrails in bathroom and shower, elevated toilet seat, non-slip
shoes and socks, removes rugs and make sure pets are away from feet
etc.
• Psychosocial Issues: autonomy very important!
Help them with locating utensils for eating, cooking etc….. there are
special types of cookware for PD like spoons, forks, bowls, knives to
maintain autonomy
isolation:
• local support groups with other people who have PD
• exercise
Don’t stress patient about activities or hurry them…stress increases
symptoms….wait for medication to peak so the most dopamine will be
the most available.
Dress patient in shirts without buttons or zippers…easy to put
on…replace articles of clothing with Velcro and shoes that don’t have
to be tied.
Digestion/Nutrition:
• Avoid taking antiparkinson’s medication (Carbidopa/Levodopa) with
a high protein meal (meats, eggs, dairy, beans) because they interfere
with how the body can absorb the medication (makes medication less
effective).
• At risk for weight loss because of the struggle with swallowing,
chewing, depression, and hard to feed self due to rigidity
• Needs foods that are soft, easy to swallow, and chew…speech therapy
to evaluate…recommend consistency of fluids
• Prevent constipation: drink plenty of fluids 2 L per day (unless
contraindicated) with high fiber foods….example fresh fruits and
vegetable and stool softner per MD order
• Assess last bowel movement and bowel sounds along with palpation
of abdomen.
Medications for Parkinson’s Disease (side effects and teaching)

NO cure but medications can help make signs and symptoms

more manageable
• Carbidopa/Levodopa (combination)….most
common “Sinemet”: adds more dopamine to the brain
• Carbidopa helps to prevent levodopa from being broken
down in the blood before it enters the brain (hence more
enters the brain) and lessens the side effect of nausea and
when levodopa enters the brain it turns into dopamine
Education:
• takes up to 3 weeks to notice a decrease in symptoms when beginning
treatment
• don’t be alarm if body fluids turn a dark color
• after long term usage the drug may wear off before next dose and cause
signs and symptoms
• Entacapone “Comtan”: a COMT can be prescribed to help decrease this from
happening
• Don’t take with MAO inhibitors….hypertensive crisis!!
• Don’t take with high amounts of food or supplements with Vitamin B6:
decreases effectiveness
• Avoid taking with high protein foods like cheese, milk, meat
etc…decreases the amount of drug absorbed (competes with protein in the
small intestines)

Side effects: nausea, involuntary movements

• Ropinirole “Requip”: stimulates dopamine receptors ….dopamine
agonists: helps with improving movement
Side effects: drowsiness major side effect (educate NOT to take when
about to drive, cook, or operative machinery etc.)
• Amantadine (antiviral: prevents influenza A…antiparkison as well):
helps with symptoms by stimulating dopaminergic activity in the CNS
• Anticholinergic:
Remember acetylcholine (causes cholinergic activity) is exceeding
dopamine, which is producing an excitatory affect on the neurons.
Therefore, ANTIcholinergics can be prescribed to decrease these
effects. These medications are usually for younger adults who have
extreme tremors and avoided in older adults because for the side
effects.
• Benztropine “Cogentin”: blocks acetylcholine by decreasing rigidity, saliva
(drooling), improved movements
NOT for people with GLAUCOMA!!
Education: never abruptly stop taking (increases signs and symptoms seen in
Parkinson disease), dry mouth (sugar less candy or gum), NO alcohol.
• MAO Inhibitor Type B (Monoamine Oxidase Inhibitor Type B):
asagiline “Azilect”: increases dopamine by stopping the activity of
MOA…improvement of symptoms
-Educate about limiting foods with tyramine: hypertensive crisis
-aged cheese
-smoked or cured meats (pepperoni, bacon, hot dogs)
-fermented food
-beer
• COMT Inhibitors
• Entacapone “Comtan” (catechol-O-methyltransferase inhibitors) used with
levodopa/carbidopa to prevent the “wearing off” of the drug before the next
dose is due….blocks COMT enzyme that will break down the levodopa in the
blood to allow it to last longer.
 Myasthenia Gravis

What is Myasthenia Gravis? It’s an autoimmune

condition where the body attacks the receptors that
allow for voluntary muscle control, which leads
to muscle weakness.
What voluntary muscles are involved?
• Eyes: most likely will be the first sign something is
wrong
• Throat: another common sign…hoarse voice and
problems swallowing
• Face
• Arms/Legs
• Respiratory muscles for breathing (in severe cases)
Key Players Involved:
Neuromuscular Junction:
• Nicotinic Acetylcholine Receptors (NAChRs) or the function of
Muscle-Specific Kinase (MuSK). MuSK helps with maintaining and
building the neuromuscular junction
• Neurotransmitter: Acetylcholine
• Immune System: produces the anti-bodies against the nicotinic
receptors.
• Thymus gland
• Acetylcholinesterase: an enzyme that breaks down acetycholine
(remember this substance because it plays a role in the treatment of
MG with anticholinesterace medications).
• In myasthenia gravis the issue arises at the neuromuscular junction.
This is the place where the motor neuron and muscle fiber meet and
the neurotransmitter acetylcholine is released.
• At this junction are receptors on the muscle fiber called nicotinic
acetylcholine receptors that become stimulated when acetylcholine
is released and cause contraction of the muscle fiber.
• However, in myasthenia gravis the nicotinic acetylcholine receptors
are being attacked by antibodies the immune system has created and
are not working properly. These receptors can NOT access the release
of acetylcholine and cause muscle contraction, so there is muscle
weakness.
• The thymus gland (found anteriorly in the upper part of the chest
behind the sternum in between the lungs) plays a very important role
in our immune system health. It’s the creator of T-cells, which are
super important for immune health by fighting viruses and bacteria.
In children the thymus is large (remember it will produce most
of the body’s T-cells by the time a person attains puberty). It
should shrink by adulthood and then in older age be like a
fatty tissue. But in people with myasthenia gravis, the thymus
gland tends to stay large and develops tumors or collection of
immune cells in the gland. It is thought that the thymus
erroneously causes immune cells to produce antibodies that
will attack receptor sites on these voluntary muscle
neuromuscular junctions.
Signs and Symptoms of Myasthenia Gravis
• **HALLMARK: muscle weakness becomes worse
with activity (especially repetitive activity) but will
improve after resting the muscle.
• Patients tend to notice symptoms in the eyes due to
eye muscle weakness of the extraocular muscles or
have problems with speaking (slurred) or
swallowing….signs and symptoms vary among
patients.
“WEAKNESS”
• Weakness neck, face, arms/legs/hands
• Eyelid drooping…can be one eye or both (Ptosis)

• Appearance mask-like: no expression…looks very sleepy

• Keeps choking or gagging when eating (difficulty
swallowing)…many muscles help with the swallowing
process and have become weak
• No energy…very fatigued…gets worse throughout the day as muscles
are used
• Extraocular muscle involvement leading to double vision…strabismus

• Slurred speech (voice may be hoarse and very soft)

• Short of breath (can extend to respiratory muscles)
Complications of Myasthenia Gravis
• Myasthenia gravis can go into remission where the patient
doesn’t have signs and symptoms, but some patients can
experience severe acute exacerbation with a complication
called Myasthenic Crisis. This is where the disease is becoming
worse and the patient may need intubation and mechanical
ventilation to breathe.
• Risk factors for experiencing Myasthenic Crisis: improper dosage
(not enough) of anticholinesterase meds to treat this condition,
stress (physical…surgery or mental), and respiratory infection.
• That patient will have severe weakness of muscles that cause
respiratory failure.
How is it diagnosed?
• Edrophonium (Tensilon test): During this test a medication is
given called Edrophonium.
• How does the medication work? It prevents the
breakdown of acetylcholine at the neuromuscular
junction, which allows more of the neurotransmitter to be
present at the neuromuscular junction.
• It is used to diagnose Myasthenia Gravis AND differentiate
between a myasthenic crisis and cholinergic crisis (see
more about cholinergic crisis in the pharmacology part of
this lecture).
IMPORTANT:
• What will happen if Edrophonium is given to a patient with
myasthenia gravis or to a patient in myasthenic crisis? The patient’s
signs and symptoms will temporarily improve. Hence, the test is
positive.
• What will happen if Edrophonium is given to a patient with cholinergic
crisis? The patient’s signs and symptoms will become worse….NO
improvement. Hence, the test is negative.
• If this happens the nurse (per MD order) will administer the antidote
for Edrophonium, which is ATROPINE! It is also important to have the
patient on a cardiac monitor during the test and a crash cart within
reach if an emergency arises.
Nursing Interventions & Medications for Myasthenia Gravis
• Monitor respiratory status: effort of breathing, respiratory
rate, oxygen saturation, does the patient feel like it’s hard to
breathe? If hospitalized with exacerbation needs
resuscitation equipment close by: suction etc.
• Monitor neuromuscular status:
• Assessing vision (double vision?), quality of voice, swallowing
(important for medication administration…ALWAYS check
swallowing before giving meds), facial appearance, strength
with arms/legs, cranial nerves
• Safety: at risk for injury….needs assistance at all times
(remember the patient may have double vision (eye patch to
help with this), arm and leg weakness)
• Speech pathologist will evaluate and recommend treatment
based on findings. Patient may need or have a feeding tube
and you will be managing this as the nurse.
• Monitor for aspiration
• Education about food because patient may have difficulty chewing
and swallowing:
• smaller meals that are easy to chew foods…pick food options that are
soft and require minimal effort to chew
• try scheduling meals during peak time of medication (30 minutes to 1
hour before eating) so chewing and swallowing muscle will have the
most access to acetylcholine
• Thicken liquids for swallowing
• Take small bites and rest while eating and before a meal
• It’s best to have large meals at the beginning of the day than at the
end (remember patients with MG becomes progressively weaker
throughout the day)
• Educate about performing most of their activities
early in the day when the patient will have the most
energy.
• Help patient identify things that makes symptoms
worst: menstrual cycle, sickness, stress, extreme
temperatures
Medications for Myasthenia Gravis:
• Anticholinesterase: “Pyridostigmine” …improves symptoms…there
is no cure!
• How does the anticholinesterase medication work? Remember the
substance we talked about earlier called acetylcholinesterase? This
medication will prevent it from working. Therefore, there will NOT be
the breakdown of acetylcholine. Therefore, more of it will be available
at the neuromuscular junction site. This will help improve muscle
strength.
• Patient should take 30 to 60 minutes before a meal to help increase
muscle strength with swallowing and chewing.
• Monitor: Myasthenic crisis (from not enough medication) or
cholinergic crisis (too much of the medication): ….both will have
respiratory failure and severe muscle weakness but from different
causes.
Signs and Symptoms of Cholinergic Crisis:
Think of the signs and symptoms experienced during cholinergic crisis
similar to the parasympathetic nervous system being in overdrive:
• Pupil constriction
• Bronchoconstriction….eventually respiratory failure
• Increased salivation and mucous production
• GI problems: abdominal cramping, vomiting, diarrhea
• Bladder incontinence
• Bradycardia
Treatment: No anticholinesterase medications and atropine to reverse
symptoms.
Other drugs used to treat MG: corticosteroids and
immunosuppressants
Other treatments for MG:
• Thymectomy: removal of the thymus gland (improves
symptoms in some patients…NOT a cure)
• Plasmapheresis with administration of IV immunoglobulins
(severe cases): filters blood by removing antibodies that
attack the receptors at the neuromuscular junction
(temporary improvement for about 4 weeks to a couple of
months….NOT a cure).
 Cerebrovascular Accident
(CVA) Stroke
What is a stroke? It is a condition that develops when
blood rich in oxygen can NOT reach brain cells (due to
either a blockage or bleeding). This causes the brain
cells to die.
Type of Strokes
Ischemic (most common): due to a blood clot within a blood
vessel or stenosis of an artery that feeds the brain tissue. This
limits the blood that can reach the brain cells. This type of
stroke can happen due to:

• Embolism: where a clot has left a part of the body (example

the heart: this can happen due to a heart valve problem
or atrial fibrillation). The clot develops in the heart and
travels to the brain, which stops blood flow.
• Thrombosis: Clot forms within the artery wall within the
neck or brain. This is seen in patients with hyperlipidemia or
atherosclerosis
• Hemorrhagic: this occurs when there is bleeding in the brain
due to a break in a blood vessel. Therefore, no blood will
perfuse to the brain cells. In addition, this can lead to
excessive swelling from the leakage of blood in the brain.
Causes of this type of stroke includes: rupture of a brain
aneurysm, uncontrolled hypertension, or aging blood vessels
(older age).
• TIA (transient ischemic attack) also called a mini-stroke. This
is where signs and symptoms of a stroke occurs but last only
a few minutes to hours and resolves. It is a warning signs an
impending stroke may occur. If this occurs the patient needs
to seek treatment.
To understand strokes, let’s talk about the
BRAIN’S function and anatomy.
Blood supply to the brain? The blood supply
to the brain comes for the carotid and
vertebral arteries, which then branch into
other arteries that feed the brain. If any of
these areas of the artery become blocked or
burst open it decreases the blood supply to
the brain cells. Brain cells are very sensitive
and within 5 minutes these cells start to become damaged, and the
damage can become IRREVERSIBLE.
The cells in the brain control how our
body functions and depending on
where the cells are located they are
responsible for specific functions.
Therefore, it is super important to
be familiar with the function of each
lobe and the difference between the
right and left hemispheres of the brain.

Let’s look at the lobes of the brain and their functions:

Now strokes tend to affect ONE side of the body. So be familiar with
the functions of the right side vs the left side:
• The right side of the brain is the CREATIVE side while the left side is
the LOGICAL side.
Right Side’s Functions:

• Attention span
• Showing emotions
• Ability to solve every day problems by making decisions/plans
• Reasoning (understanding jokes…reading in between the lines)
• Making judgement calls
• Memory
• Music/art awareness
• Control the left side of the body
If a patient has right side brain damage, what do you think the patient will
experience?
• Left side weakness: Hemiplegia
• Impairment in creativity: arts and music
• Confused on date, time, place
• Cannot recognize faces or the person’s name
• Loss of depth perception
• Trouble staying on topic when talking
• Can’t see things on left side: LEFT SIDE NEGLECT (unilateral neglect)
• (Ignores left side of body)
• Trouble with maintaining proper grooming
• Emotionally: not going to think things through….very impulsive
• Poor ability to make decisions and assessing spatial qualities….shapes
• Denial about limitations
• Not able to read nonverbal language or understand the hidden meaning of
things
• Very short attention span
Left Side’s Functions:
• Speaking
• Writing
• Reading
• Math skills
• Analyzing info
• Planning
If a patient has left side brain damage, what do you think the patient
will experience?:
• Right side Hemiplegia
• Aphasia (trouble formulating words and comprehending them)
• Aware of their limits…experiences depression, anger, frustration
• Trouble understanding written text
• Can’t write (agraphia)
• Impaired math skills
• Memory intact
• Issues with seeing on the right side
So, as you can see when there is brain cell death in a certain area it will
cause specific signs and symptoms. The amount of brain damage
depends on how long it took for blood to return to the affected brain
cells.
Risk Factors for stroke
-be familiar the risk factors and which ones are modifiable (things a
person can change) vs. unmodifiable (things a person CAN’T change
• “Strokes Happen”
• Smoking Hypertension
• Thinners (blood) Atherosclerosis
• Rhythm changes (a-fib/flutter) Physical inactivity
• Oral Contraceptive Previous TIA
• Kin (family history) Elevated blood sugar (diabetes
mellitus) aNeurysm (brain)
• Excessive weight
• Senior citizens
Signs and Symptoms of a Stroke
• Happens suddenly: need to act fast as the nurse to
help save brain cells
• call rapid response so patient can receive appropriate
treatment or call 911 (if outside of the hospital in the
United States)
• NOTE the exact time the signs and symptoms
appears…important for stroke treatment
“FAST”
• Face: drooping or uneven smile
• Arm: numbness, weakness, drift (raise both arms)
• Speech: can’t repeat a phrase, slurred speech
• Time: to call rapid response and note the time

**National Stroke Association recommends using the

mnemonic F.A.S.T. to help assess for signs and symptoms
quickly.
The patient can also have the following as well:
• Bowel and bladder incontinence or retention
Important Stroke Terms:
• remember these terms because exams love to ask you about them.
• Aphasia: unable to speak (comprehending or producing it)
• Receptive Aphasia: unable to comprehend speech (Wernicke’s area)
• Expressive Aphasia: comprehends speech but can’t respond back
with the correct words, if at all (Broca’s area)
• Mixed Aphasia: combination of the two types of aphasia.
• Global Aphasia: complete inability to understand speech or produce
it.
• Dysarthria: unable to hear speech clearly due to weak muscles (hard
to understand the patient’s speech….it may be slurred)
• Apraxia: can’t perform voluntarily movements (winking/moving arm
to scratch an itch) even though muscles function is normal.
• Agraphia: loss the ability to write
• Alexia: loss the ability to read…doesn’t understand or recognize the
words
• Agnosia: doesn’t understand sensations or recognize known objects
or people
• Dysphagia: issues swallowing (weak muscles)
• Hemianopia: limited vision in half of the visual field

• Hemiparesis: weakness on one side of the body

Diagnosed?

CT scan
MRI
Medication for Ischemic Strokes:

• tPA (tissue plasminogen activator): for ischemia strokes

ONLY not hemorrhagic!
How does it work? It dissolves the clot within the blood vessel
by activating the protein that causes fibrinolysis.

REMEMBER: It must be given within 3 hours from the onset

of stroke symptoms. It can be given 3 to 4.5 hours after onset
IF strict criteria is met.
To receive tPA the patient should have a:
• CT of head that is NEGATIVE for hemorrhage
• labs within normal limits (glucose, INR, platelets)
• BP needs to be controlled SBP <185 and DBP <110
• glucose controlled (increases rise of hemorrhage)
• not receiving heparin or other types of anticoagulants

Nurse’s Role: monitor for BLEEDING, neuro checks around the

clock, blood pressure medication if needed for hypertension,
vital signs, labs, glucose, preventing injury (bedrest), avoid
unnecessary venipunctures, avoid IM injections, will go to ICU
to be monitored
Nursing Interventions for Stroke

• Monitor vital signs and neuro status:

• especially blood pressure (notify MD is hypertensive)
• airway (difficulty swallowing….at risk for aspiration HOB 30’
with suction at bedside)
• turn every 2 hours with proper alignment and watch for
increased ICP (intracranial pressure) during acute stage
• headache, nausea and vomiting, increased blood pressure
and decreased HR and decreased RR, decrease in mental
status from baseline, pupils don’t respond
Assess with NIH Stroke Scale
• Score ranges from 0 to 42
• 0: no stroke symptoms
• 21-42: severe symptoms
• 11 assessments area are scored
• Assesses:
• Level of consciousness, gaze, visual, facial palsy, motor function of
extremities, sensory, best language, dysarthria, extinction/inattention
• Check cranial nerves: pupil responses, motor function, gag reflex
• Monitor bowel and bladder function (may be incontinent or retaining)
• Passive ROM with extremities and preventing contractions
Interventions for aphasia
• Communication is key (just because the patient can’t communicate doesn’t
mean they have a mental deficit). They just can’t get it out and it takes
them time. The nurse’s role is to help bridge the gap and make it less
frustrating for the patient.
1. Receptive Aphasia: unable to comprehend speech (Wernicke’s area)
• -use short phrases
• -use gestures or point while giving a command
• -be patient and not expect a fast response
• -remove distractions
2. Expressive Aphasia: comprehends speech but can’t respond back with
speech (Broca’s area)
• -be patient and let them speak
• -be direct and simple when asking questions…..give opstions
• -communication via a dry erase board
Stroke care is a multidisciplinary approach: need to involve
family as much as possible because they will be providing care
when patient is discharged. In addition, it is important to be
always be communicating with the speech language
pathologist, physical therapy, occupational therapy etc.

Diet: evaluated by speech language pathologist

• may need thicken liquids and mechanical soft foods
• assist with eating and monitor for pouching of food in cheek
(on the affected side). This increases risk of aspiration.
• Have patient tuck in chin to their chest while swallowing.
Watch for neglect syndrome: (tends to happen in right side
brain damage). The patient is at risk for injury because patient
ignores the affected side.
• Remind patient to use and touch both sides of body daily
(must make a conscious effort to do so).
• Educate the patient about the importance of turning head
side-to-side to prevent injuring the affected side.

Hemianopsia interventions: turning head side-to-side to see

all visual fields to prevent injury
 End.

THANK YOU ☺