TISSUE INTEGRITY
Phases of wound healing:
 Inflammatory: 3-6 days. Deposits of fibrin and microphage migration
 Proliferation: 3-21 days. Collagen and granulation tissue
 Maturation: day 21 – 1-2 years
Pressure wound staging: 394
 Stage 1: skin intact but does not blanch.
Treatment is just a covering.
 Stage 2: top layer of skin is gone, shallow
wound bed. Pink and moist. Can’t see
subcutaneous tissue. Treatment is
Mepilex (promotes healing)
 Stage 3: full thickness skin loss, damage
to sub q, fat is visible. Can tunnel, but
muscle and bone are not exposed.
Treatment is wet to dry dressing, with a
goal of pulling out dead tissue.
 Stage 4: all the way to the bone exposing
ligaments, muscle, and cartilage.
Treatment is debridement and packing.
 Eschar tissue creates an unstageable
wound.
Braden Scale is imperative for nursing management. Score of 18 or below poses a greater risk for skin
breakdown.
SENSORY:
Multiple Sclerosis: 360inflammatory disease that attacks the myelin sheaths of neurons. Macrophages and
lymphocytes pass through the blood brain barrier and destroy the myelin, which causes lesions. Once
pathways are damaged, signals can’t pass through and symptoms begin.
 Relapsing-remitting MS (RRMS)- Most common form. Periods of remission and recovery
 Primary progressive MS- about 15% of cases. Gradual progressive, symptoms all the time, no
remission.
 Secondary progressive MS- starts with RRMS then gradually they become continuing progressing.
About ½ of RRMS convert to secondary.
 Progressive relapsing MS- symptoms all the time, no remission but will have periods of exacerbations
on top of current symptoms.
 Extreme heat/cold, menstruation, and fever can cause relapse or flareups
S/SX: muscle weakness, visual disturbances (blurred/diplopia/nystagmus), fatigue are common first
symptoms. Paresthesia, lack of coordination, unsteady gait, tremors, bladder, and bowel disfunction,
dizziness, sexual disfunction, pain, depression, and anxiety.
Risk factors: women 20-40s. Further away from the equator, smoking, obesity, high sodium intake as a teen,
low vitamin D.
Parkinson’s: 364 progressive neurological degenerative movement disorder causes by dopamine deficiency.
S/SX: divided into motor and nonmotor.
 Motor: tremors, shuffled gait, rigidity (tightened muscles), bradykinesia, postural instability, difficulty
swallowing/ drooling.
 Nonmotor: autonomic disorders (excessive sweating), cognitive decline, emotional changes, sleep
problems, RLS
Teaching: heal to toe walking, small frequent meals that are easy to chew, orthostatic hypotension. Keep
their muscles as active as possible. Speech therapy to help with dysphasia. Emotional support.
Meds: Does not cure but helps to reduce severity of symptoms and improve quality of life. Levodopa leaves
dopamine in the brain (increases levels). It helps reduce tremors, bradykinesia, and rigidity but not balance
and nonmotor function. Carbidopa conserves dopamine produced by levodopa- prevents it from being
metabolized before it reaches the brain.
Carbamazepine (Tegretol): seizure medication. Anticonvulsant that is also a mood stabilizer. Toxic effects are
severe skin rash, blood dyscrasias (disorders), hepatitis
Muscular dystrophy: progressive muscle weakness and wasting disease due to genetic mutation on X
chromosome. Absence of dystrophin protein. Most common is Duchenne’s Muscular dystrophy. Affects all
voluntary muscles as well as cardiac and respiratory.
S/SX: delayed walking, large calves and wide stance in toddlers, gross motor delays, waddling gait. School
aged kids will walk on the balls of their feet. Disturbed balances. Posture changes. Normally lose the ability to
walk by age 7-12.
Prednisone improves muscle strength and pulmonary function and slows the progression of
dystrophy/weakness. Be aware of osteoporosis, weight gain, and supplement with Calcium and Vit D
NUTRITION:
GERD: 246 gastroesophageal reflux disease. Backflow of gastric or duodenal contents or both into the
esophagus. The lower esophageal sphincter is dysfunctional. Gastric emptying is delayed and causes an
increase in the volume and pressure of the stomach. Heartburn
Nursing care/teaching: Small frequent meals. Identify trigger foods. Prop up on pillows or elevate HOB.
 Spicy, high fat, caffeine, smoking, and high alcohol intake can decrease lower esophageal sphincter
pressure, which can exacerbate symptoms. (Same things that could decrease muscle mass)
 Protein, carbs, nonfat milk, low dose ethanol increase lower esophageal sphincter pressure, which
can lessen symptoms. (Same things that can increase muscle mass)
 Barrett Esophagus is precancerous cells in the esophagus.
PPI: Proton pump inhibitors (end in “ZOLE”). Reduces gastric secretions, promote healing, and relieve
symptoms. Take 30 minutes to an hour before eating/ first thing in the morning. Drink plenty of liquids
throughout the day. Long term use can cause osteoporosis.
Peptic ulcer disease: 250 can occur anywhere in the GI tract that is exposed to acid-pepsin secretions.
 Gastric Ulcers: pain occurs WITH eating or within 30 minutes of eating. (gast = fast) Dull, gnawing
pain. Burning sensation in HIGH epigastric. Risk factor: Type A blood (gAstric). Hematemesis can
occur with gastric.
 Duodenal Ulcers: pain 3-4 hours AFTER eating. (duo = slow) Dull, gnawing pain. Burning sensation in
mid epigastric (because duodenum is lower in GI) and back. Sometimes eating can help the pain. Risk
factor: Type O blood (duOdenal)
 Complications: complete obstruction will lead to excessive vomiting and loss of electrolytes.
Perforation occurs when the acid eats through the lining completely and spills into the gut. The
abdomen will have a bored like appearance, patient doesn’t want to be touched, lots of pain, and no
bowel sounds.
Sucralfate is used to treat and prevent duodenal ulcers. It works by forming a barrier or coat over the ulcer.
This protects the ulcer from the acid of the stomach, allowing it to heal. Take on an empty stomach.
H. Pylori treatment:
 Triple therapy: Clarithromycin + Amoxicillin + PPI “triple CAP”
 Quad therapy: Tetracycline + metronidazole (antibiotic) + PPI + bismuth subsalicylate “Tet & Met +
PPI & Pepto”
CELLULAR REGULATION:
Cirrhosis: 264 permanent damage to the liver. Scarring can change the shape. The liver is gradually destroyed
and eventually loses function. Restricted blood flow = hepatic hypertension. Three types: alcoholic, biliary,
and post hepatic from chronic hepatitis. 50% is related to alcohol.
 Early stages: liver is enlarged and tender. Weight loss occurs due to not wanting to eat/ feeling full
because of enlarged liver.
 Chronic stage: scar tissue forms in the liver.
 Compensated: Liver maintains its function. Abdominal pain, ankle edema, flatulent, intermittent/
mild fever, palmer erythema, splenomegaly, unexplained epistaxis (nose bleeds), vague morning
indigestion, vascular spiders.
 Decompensated: Liver cannot preform important function. Ascites (protein dense fluid), clubbed
fingers, continuous mild fever, epistaxis, gonadal atrophy, HYPOtension, jaundice, muscle wasting,
weight loss, white nails, sparse body hair, purpura (red dotty rash), spontaneous bleeding, freaking
MELENA/hematemesis, esophageal varices and stomach varices.
o
Varices are ruptured blood vessels due to portal HT. Straining while having a BM, sneezing,
and vomiting can increase risk of bleeding. Esophageal and gastric varices are medical
emergencies.
 Labs: AST, ALT, Alkaline phosphatase, BUN, Bilirubin, and Ammonia will be HIGH. Albumin will be
LOW. EGD can show esophageal varices and stomach varices.
o High ammonia levels can cause delusions. Lactulose will help pull out the ammonia and it
will be excreted through the stool. 3-4 bowel movements per day is optimal.
o Just to tie it all together: When protein is digested (protein metabolism) it produces
nitrogen. From that, nitrogenous waste is made which is ammonia, urea (BUN), creatinine,
and uric acid. That’s why they need a LOW protein diet and why the liver labs are HIGH.
DIABETES: Criteria = glucose level ≥ 200 mg/dl + the classic “P” symptoms (polyuria, polydipsia, polyphagia)
and unexplained weight loss. OR a fasting glucose ≥ 126 mg/dl. OR A1C ≥ 6.5%
 Pre diabetes = fasting glucose of 100-125 mg/dl or A1C of 5.5-6%. Lose weight, change eating habits,
HPC may order metformin.
 Anything that affects the pancreas could potentially lead to DM.
Type 1: 302Insulin dependent and ketone prone. Its genetic and autoimmune. “Type one can pass to your
son and your body makes none.” Diagnosed in younger years. Sometimes triggered by a virus/autoimmune
reaction.
 S/SX: polyuria, polyphagia, polydipsia, sudden weight loss, fatigue, frequent infections, rapid onset,
tingling in hands/feet.
 Treatment: Insulin, diet, exercise
DKA: 296 biggest complication of Type 1. Caused by overeating, not taking insulin, and/or being sick. Blood
sugars can be elevated between 250-800+ mg/dl. Rapid onset.
 S/SX: DKA = Dehydration, Ketones in serum, high K+, Kussmaul respirations, Acidosis, Acetone
breath, Anorexia (from nausea)
 Treatment: fluid replacement, insulin, electrolyte replacement. Hourly I&O and glucose checks
Type 2: 300 non-insulin dependent. Non-ketosis prone. Decreased sensitivity to insulin or not enough
produced.
 S/SX: 3 Ps, fatigue, recurrent infections, history of HT, tingling in hands and feet, obese,
hyperpigmentation in neck.
 Risk factors: normally diagnosed over 50 unless family history. Triglycerides ≥ 250, HDL ≤35, BP
≥140/90, history of gestational diabetes or babies over 9 lbs.
 Treatment: diet is most important, oral hypoglycemic, activity
 Teaching: A1C less than 7% and BMI less than 25. Alcohol doesn’t get absorbed so large amount of it
can increase fat (which can also cause DKA). Exercise lowers blood sugar- so think exercise can act as
insulin therefore someone may need carb/snack before exercising to prevent hypoglycemia. Check
blood glucose before meals and bedtime.
HHS 306: hyperglycemic hyperosmolar syndrome. Main complication of type 2 diabetics. There are no
ketones spilt because there is some insulin therefore no breakdown of fat.
 Main issue is dehydration. Rehydration is more important than insulin because acidosis doesn’t
occur. Very emergent with high mortality rate.
Thyroid: when you think of thyroid think of metabolism. The presence of goiter (in hyper and hypo) is the
result of lack of iodine in the diet. The main purpose of iodine hormone is cellular metabolic activity.
Calcitonin helps regulate calcium deposits. If calcium levels are too high, it tells the kidneys to not reabsorb
more calcium.
HYPERthyroid 312: hyper metabolism. Everything is increased or in excess. Caused by excessive delivery of
TH. It continually releasing T3 and T4. More common in women. Graves’ disease.


S/SX: because its HYPER, all signs and symptoms will be related to high metabolism. Weight loss,
tachycardia, increased BP, increased appetite, heat intolerance + excessive sweating, hyperactive
bowels, sleep disturbances, hyper personality, thin hair/nails. Exophthalmos/bulging eyes.
Remember our hyper crackhead running to the Grave.
Thyroid storm is major complication. Caused by hyperparathyroidism, extreme stress/trauma,
infection, or potential complication of sub thyroidectomy. Occurs when thyroid secretes way too
much thyroid hormone in a short amount of time. Abrupt onset. Very serious.
o Hyperthermia with temps up to 106º, stroke level BP, severe tachycardia, shock, heart
failure, irritability, and coma.
o Treatment is to bring body temp down with cooling blankets and stay with patient
HYPOthyroid 314: hypo metabolism, so everything is slowed down and/or decreased. Thyroid produces
insufficient amounts of thyroid hormone. Primarily related to tissue being destroyed. Atrophy of thyroid
tissue is most common. Thyroid STIMULATING hormone will be elevated because the body is trying to
compensate.
 S/SX: Same as hypo metabolism. Obesity, slow HR, low BP, cold intolerance, slowed thinking,
constipation, poor appetite, dry skin, slow breathing, muscle stiffness, pallor
 Treatment: Synthroid taken on empty stomach with water in the morning 30 minutes- 1 hour before
breakfast.
 Complications: myxedema coma- opposite of thyroid storm. Decreased mental status, hypothermia,
bradycardia, slowing of organ function. Medical emergency. Synthroid IV.
FLUID/ELECTROLYTE: just winging it here y’all
Potassium: cardiac arrythmias, muscle contraction
Sodium: water distribution
Calcium: nerve function/ muscle contraction
Magnesium: heart rhythm, muscle contraction
Phosphate: muscle function, RBCs, ATP
Chloride: fluid balance
SODIUM: responsible for water distribution in the body. Most abundant electrolyte in ECF. Correction of
sodium imbalance must be done slowly to prevent neurological damage/cerebral edema.
Hyponatremia: serum sodium level less that 135 mEq/L. Commonly the result of fluid overload. (hypo =
overload… hypo/hippo = overload)
 S/SX: Nausea and vomiting, headache, lethargy, dizziness, confusion, muscle
cramps/twitching/weakness, seizures, high HR, low BP, edema
 Treatment: focused on clinical symptoms and lab values. Treating the underlying cause will normally
bring the sodium level back to normal. Sodium replacement: oral, NG tube, parenteral, LR or 0.9% NS
IV. Water restriction
Hypernatremia: serum sodium levels higher than 145 mEq/L. Hyper – dehydration (You get thirsty when
you’re hyper and running around) “High and dry”
 S/SX: thirst, elevated body temp, irritability, seizures, pulmonary edema, hallucinations, swollen and
dry tongue
 Treatment: gradual infusion of hypotonic solution
 Nursing mgmt: fluid losses and gains are carefully monitored in patients at risk for hypernatremia.
Monitor intake of OTC with high sodium like Alka seltzer. Monitor thirst level, elevated body temp,
and behavior changes.
POTASSIUM: 98% of the body’s potassium is inside the cell. I think of “okay” ⓚ. The remaining 2% is in the
ECF and is important in cardiac and neuromuscular function.
Kalemias do the same as the prefix EXCEPT heart rate and urine output.
Hypokalemia: deficit in potassium stores. Or with normal K+ stores, it can happen with alkalosis (alKLOWsis).
 S/SX: Kalemias do the same as the prefix EXCEPT heart rate and urine output. All systems will be
DOWN except heart rate and urine output. Don’t confuse HR with wave formation. Rate will be HIGH
(tachycardia) but wave patterns will be DOWN. PVCs (premature ventricular contractions)
 Treatment: oral K+ supplements, IV replacement of 40-60 mEq/DAY. Older people have lower total
body potassium levels therefore require less with treatment. High K+ diet include most fruits and
vegetables, legumes, whole grains, milk, and meat. Salt substitutes contain 50-60 mEq per teaspoon
 Nursing mgmt: Know at risk patients (patients taking Digoxin/ digitalis) who can have digitalis
toxicity because hypokalemia potentiates the action of digitalis. Monitor patient with telemetry,
monitor for decreased systemic effects. Only give potassium with adequate urine output. If less than
20/mL hour for 2 consecutive hours, stop infusion and notify HCP
Hyperkalemia: seldomly occurs in patients with normal renal function.
 S/SX: Kalemias do the same as the prefix EXCEPT heart rate and urine output. All systems will be
high/increased except HR and urine output will be LOW. Again, don’t confuse rate with wave form.
Bradycardia with tall T waves.
 Treatment: EKG should be obtained immediately. IV calcium gluconate. (calcium antagonizes the
action of potassium on the heart, but doesn’t reduce serum concentration) IV insulin and D50 will
cause the potassium to shift into the cells (happens quickly) Kayexalate increases excretion of fecal
potassium, but happens very slowly over hours. Think “k exits late”.
 Nursing mgmt: Monitor signs of muscle weakness and arrhythmias. Apical pulse.
Hypocalcemia
 S/SX: Calcium does opposite of prefix, so all systems will be UP. (But remember Cal follows Maggie,
so low Cal = low Maggie) Chovostek (cheek) and Trousseaus (hand) is a CLASSIC sign of
hypocalcemia. As well as TETANY which is muscle spasms/ neural excitability.
 Treatment: IV administration of calcium salt. Vitamin D increases calcium absorption. Calcium
supplements.
 Nursing mgmt: seizure precautions. Calcium replacements can cause orthostatic hypotension.
Educate on calcium rich foods: milk, leafy greens, canned salmon/sardines, fresh oysters. Alcohol and
caffeine inhibit calcium absorption and cigs increase calcium secretion.
Hypercalcemia:
 S/SX: Calcemias do the OPPOSITE of the prefix, so this will be a sedative like effect. Weakness,
constipation, lethargy, deep bone pain. (However the book says thirst and polyuria will be present).
 Treatment: IV NS temporarily dilutes calcium levels. Furosemide increases calcium secretion and
diuresis. Calcitonin (tones Calcium) reduces bone resorption and increases urinary excretion of
calcium.
 Nursing mgmt: Increasing patient mobility and encouraging fluids. Fluids with sodium unless
contraindicated. Calcium increases effect of digoxin, so monitor for symptoms of digoxin toxicity.
MAGNESIUM: plays major role in carbohydrate and protein metabolism and neuromuscular function. Mag
(like calcium) can also have a sedative effect. Magnesium does the OPPOSITE of the prefix.
Hypomagnesemia: frequently associated with hypokalemia and hypocalcemia
 S/SX: Mag does the opposite of the prefix, so all systems will be UP. Neuromuscular excitability,
increase deep tendon reflexes, PVCS
 Treatment: Diet (green leafy vegetables, beans, PB). Mag salts.
 Nursing mgmt: monitor for digitalis toxicity. In severe cases, seizure precautions. Patient education
plays major role in treating.
Hypermagnesemia:



S/SX: Mag does the opposite of the prefix, so all systems will be DOWN. Tachycardia that turns into
bradycardia.
Treatment: limiting mag intake, fluids and diuretics
Nursing mgmt: monitor hypotension, shallow breathing, bradycardia, arrhythmias, check with PCP
before taking OTC supplements, monitor I&Os
PHOSPHORUS: essential in muscle function, RBCs, and ATP (adenosine triphosphate)
Hypophosphatemia:
 S/SX: weakness, bone pain, chest pain, seizures
 Treatment: sources of phosphorus are dairy, meats, and beans
 Nursing mgmt: monitor malnourished patients receiving parenteral nutrition, monitor vit d levels,
calcium and phosphate levels checked every 6 hours.
Hyperphosphatemia:
 S/SX: tetany, tachycardia, signs of hypocalcemia
 Treatment: reduce phosphate intake
 Nursing mgmt: avoid phosphorus foods like dairy, nuts, whole grain, dried fruits and veggies,
sardines.
Chloride: helps maintain water balance and acid base balance. Sodium and chloride exert osmotic pressure.
Hypochloremia:
 S/SX: all symptoms increased except respirations
 Treatment: treating the acid base imbalance
 Nursing mgmt: monitor I&O, ABGs, and electrolyte levels
Hyperchloremia:
 S/SX: same as metabolic acidosis plus tachycardia and tachypnea
 Treatment: correcting the acid base balance
 Nursing mgmt: monitor vitals, ABG, I&O
ACID BASE:
Rules of acid base:
First determine if they are acidotic or alkalotic by pH level.
The rule of the Bs will help determine metabolic or respiratory. If pH and Bicarb BOTH in the same direction,
its metaBolic. Otherwise its respiratory.
As the pH goes, so goes the patient EXCEPT potassium. Meaning if the pH is high all systemic symptoms will
be high and low K+. If pH is low all systemic symptoms will be low and high K+.
Causes of acid base imbalance:
 IS it LUNG? If yes, then its respiratory. (duh)
 Over ventilating? Alkalosis
 Under ventilating? Acidosis
 DO NOT CONFUSE RESPIRATORY RATE WITH VENTILATION. Totally different.
 If it’s not lung, then its metabolic. (duh)
 Prolonged gastric suctioning: alkalosis.
 Everything else that isn’t lung or gastric suctioning: metabolic acidosis
 If you don’t know, pick metabolic acidosis.
GAS EXCHANGE:
Asthma 177: chronic disease of REVERSIBLE airflow obstruction. Chronic inflammatory disease of the lungs.
Mostly related to allergies.



S/SX: abrupt or delayed onset. Coughing, wheezing, SOB are classic symptoms. Chest tightness,
tachycardia, tachypnea, anxiety, and apprehension. LOTS of mucous production. Forced expiration.
Teaching: early intervention is key. Avoid allergen and environmental triggers. Monitor peak flow
readings.
o Peak flow meter: determines airflow limitations or if asthma is worsening. Green 80-100%.
Personal best. Yellow 50-80%. Need treatment. Red < 50%. Medical emergency.
o “Incentive spirometry id one of the best diagnostic tools for asthma.”
Medications: First line is daily long-acting inhaled corticosteroid (Fluticasone). SABAs like Albuterol
are used in acute situations. They allow airways to open by relaxing smooth muscle but can cause
jitteriness. Anticholinergics reduce bronchospasms.
COPD 170: Preventable and irreversible slowly progressive respiratory disease. Airway destruction involves
airways and/or pulmonary parenchyma (lung tissue).
 Teaching: Avoid others with respiratory infections, avoid crowds during peak risk season, avoid dairy
because is can increase mucous production. Small frequent high protein/ high calorie meals.
o O2 therapy: do not give COPD patient more than 2L/min unless specifically ordered. COPD
patients’ respiratory drive is hypoxia.
 Chronic bronchitis: disease of the airway. Cough and sputum production for at least 3 months in a
row for 2 consecutive years. Chronic bronchitis = chronic cough.
o Blue bloater: hypercapnia, hypoxia, mild cyanosis, constant cough
 Emphysema: impaired O2 and CO2 exchange due to overdistended walls of the alveoli (NOT
COLLAPSE) creating abnormal airspaces. Emphysema = physical change
o Pink puffer: barrel chested, dyspneic, prolonged expiration, tripod position, pursed lip
breather.
Bronchodilators: relax the smooth muscle of the airway. Long acting or short acting
 Long acting bronchodilators should always be taken with corticosteroids.
 Theophylline tablets: for long term control and prevention of symptoms in mild persistent asthma.
Serum concentrations should be between 5 and 15 mcg/mL. Toxicity symptoms include tachycardia,
N&V, tachyarrhythmias (SVT), CNS stimulation, headache, seizures, hematemesis, hyperglycemia,
and hypokalemia. Discontinue if toxicity occurs.
SIDs: Incidence peaks between 2 and 4 months with 80% of deaths occurring before 6 months. Risk factors:
siblings who died of SIDs, low birth weight, prematurity, respiratory or GI illness, maternal
smoking/alcohol/drug use, secondhand smoke, inadequate prenatal care, prone or side lying position,
hyperthermia, loose bedding, soft sleep surface, bed sharing, REM sleep abnormalities, absence of pacifier,
crib bumpers, blankets and stuffed animals in sleep space, LOW SOCIOECONOMIC STATUS, domestic
violence.
PERFUSION:
Cardiac Output is the amount of blood pumped out in one minute. Normally 4-6 liters.
 SV x HR = cardiac output
Cardiac Index = cardiac output / body surface area (BSA)
DVT 79: deep vein thrombosis. Usually in the calves.
 S/SX: dull aching pain in the affected extremity, especially when walking. Tenderness, warmth,
erythema, cyanosis, edema of affected extremity.
 Diagnostics: d-dimer positive when clot is present. Shows fragments of clots ≥250 indicates a clot.
 Nursing care: measure the affected leg and compare to unaffected. Do not ambulate unless going to
the bathroom. Ted hose for prevention. “Ted in the bed”

Heparin: binds to antithrombin and inactivates clotting factor. Prevents the extension of thrombus
and prevents development of new thrombus.
o Can be given sub q or IV.
o Assess for bleeding.
o Protamine sulfate is the antidote.
o PTT and platelet count must be monitored. Normal aPTT is 23-35 seconds, on heparin it will
be 1.5-2.5 times normal.
HYPERTENSION 75: normal is 110/70
 Prehypertension: 120-139/80-90
 Hypertension Stage 1: 140-159/90-99
 Hypertension Stage 2: ≥160/≥100
 Hypertensive crisis: medical emergency 180/120
Primary Hypertension: persistent elevated systemic blood pressure. Develops through interaction between
overstimulation of alpha- and beta-adrenergic receptors. Altered in RAAS. Insulin resistance,
hyperinsulinemia, endothelial function.
 85% of all HT is primary. Underlying cause may not be determined.
Secondary Hypertension: Elevated blood pressure from underlying disorder. Kidney disease, coarctation of
aorta, endocrine disorders, neurological disorders, drug use, pregnancy, hypothyroidism, obstructed sleep
apnea.
DASH diet: low sodium 1500-2300 mg/day, low fat proteins (chicken, fish), limit fats
“First line of therapy for uncomplicated hypertension is thiazide diuretics.”
Beta blockers: Metoprolol
 Selectively blocks the beta 1 adrenergic receptors of the sympathetic nervous system, which will
slow the heart rate and lower the blood pressure.
 Not recommended as the first line therapy for hypertension unless the patient has HF or CAD
 Can cause bradycardia.
 Avoid sudden discontinuation.
 You can still give BB even when BP is low if HR is really high.
 Beta blockers are contraindicated for asthma and COPD patients. “Beta blockers = bronchospasms.”
Loop Diuretics: Lasix (Furosemide)
 Decreases fluid volume by blocking the reabsorption of sodium, chloride, and water in the renal
tubules.
 Preferred diuretic for patients with symptomatic HF and patients with moderate to severe chronic
kidney disease.
 Risk of volume and electrolyte depletion. Monitor for hypokalemia. Risk for orthostatic hypertension
in geriatric population.
PVD: peripheral vascular disease. Blood can’t get down to the peripheral extremities.
 Risk factors: Atherosclerosis- thickening, loss of elasticity, calcification of arterial walls. High
cholesterol- over 200. We can high HDL and low LDL
 S/SX: pain in the calves or thighs, intermittent claudication. When disease is severe, they will have
pain at rest. Peripheral pulses are decreased or absent (because the arteries have no flow)
 Teaching: We want the blood to go down, so we want them to dangle legs on side of bed. DO NOT
put compression hose on. No crossing legs or tight clothing.
CVI: chronic venous insufficiency. Valves in the legs do not work, so blood can’t come back up efficiently.
They veins don’t work, thus venous insufficiency.
 Elevate feet as much as possible.
 Ted hose for immobile patients. Ted in the bed.
 Compression stockings start with high compression in the foot and gradually lighten up. These are
for patients that ambulate.
Inflammation: an adaptive response. Non specific.
Cardinal signs: redness, warmth, swelling, pain, possible impaired function. Kids brady first, then go tachy.
Adults are tachy first, then brady.
Celiac Disease 253: disorder of the small intestine. Autoimmune response to gluten. Antibodies attack gluten
protein in the small intestine which in turn destroys the microvilli/mucosa/lining of the small intestine. Less
microvilli = less surface area for absorption = malnutrition. They need water soluble forms of ADEK
 S/SX: abdominal bloating, pain, diarrhea, steatorrhea
o Anemia, vitamin deficiency, poor fat and protein absorption, problems with weight loss,
Rickets (lack of vit D)
 Risk factors: genetic, white, first degree relative
 Teaching: gluten free diet, wheat/rye/barley label checking. NPO during an attack. Corticosteroids
should be taken during the refractory period. IV nutrition for refractory. Steroids taken in the
morning with breakfast.
Gallbladder disease 254: cholecystitis= inflammation in the gall bladder Supersaturation of bile in the
gallbladder. Bile + cholesterol = biliary sludge or gallstones. Cholelithiasis = gallstones.
 S/SX: abrupt RUQ pain that radiates to the back or right shoulder. Pain is aggravated by movement.
Biliary colic (body is trying to “milk” it through by increased peristalsis. Dark/clay colored stool. (Clay
color = no bile) N&V, jaundice, vitamin deficiency.
 Teaching: 80% of patients with acute gallbladder inflammation achieve remission with rest, IV fluids,
gastric suction, analgesics, and antibiotics. Unless patient condition deteriorates, surgery is delayed
until the acute symptoms subside (few days).
 The diet immediately following an episode is usually low-fat liquids. These can include powdered
supplements high in protein and carbs stirred into skim milk. Cooked fruits/vegetables, rice, lean
meat, mashed potatoes, non-gas forming vegetables, bread, coffee, tea may be added as tolerated.
Patient should avoid eggs, cream, pork, fried foods, cheese, gas forming vegetables, and alcohol.
Fatty foods may induce an episode of cholecystitis.
Crohn’s 238 (regional enteritis) can affect any part of the GI system, but 80% involves the small intestine in
distal ilium and proximal colon. Slow and progressive. Extends through all layers of intestinal wall. Periods of
relapse and remission. Altered immune response to intestinal bacteria.
 S/SX: RLQ pain. Pain is not relieved by pooping. May have fever. Diarrhea and weight loss from
malnutrition.
 Teaching: stress reduction. Avoid trigger foods. If problems with blockage, raw fruits and vegetables
should be avoided because they are harder to digest. Low fat, high protein. Can have antidiarrhea
meds. No cure.
 Complications: abscesses and peritonitis can occur from perforated bowel. Fistulas and vitamin
deficiency. Colon cancer is more in small intestine.
Ulcerative colitis 238: rectal area up to sigmoid. Causes ulcerations in the mucosa of the intestines. Because
its closer to the booty hole, more blood will be seen in the stool.
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S/SX: LLQ pain. Diarrhea. Stool may contain blood, pus, and mucus. 6-10 bloody stools per day.
Risk factors: Jewish, 12-25 and 55-65
Complications: Toxic megacolon, hemorrhage, perforation, nutritional deficiencies
Teaching: High intake of vegetables can prevent. Probiotics can help maintain remission. No dairy.
Dietary fiber may reduce diarrhea. NPO during exacerbations- TPN or elemental diet (ensure)
Only cure is surgery.
Pancreatitis 102: inflammation of the pancreas. Enzymes that the pancreas makes are secreted early and
they aren’t excreted like they are supposed to. Then can auto digest that will breakdown pancreatic tissues.
80% are caused by alcohol or gall stones.
 Acute happens suddenly and can last days and is reversible. Onset normally occurs within 24-48
hours of heavy meal or overindulgence of alcohol.
o Risk factors for acute: alcoholism, gallstones, smoking, obesity.
o S/SX: abrupt onset of continuous severe epigastric/abdominal pain. Pain can radiate to their
back. Some relief can come from sitting up and leaning forward. Bloating, diarrhea,
tachycardia, hypotension, elevated temp, N&V, cold/clammy skin. Pain is aggravated by
fatty foods and alcohol, walking, or laying down.
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Chronic can last months or years and lead to fibrosis and permanent structural damage. It can be
stopped where it is, but it cannot be reversed.
o Risk factors for chronic: alcohol abuse, smoking, recurrent acute pain, hypertriglyceridemia.
o S/SX: intermittent or constant dull pain in left upper abdomen that can radiate to the back.
Pain can be aggravated by fatty foods or alcohol. Weight loss, constipation, steatorrhea.
o Complications: pancreatic abscess or pseudocyst, diabetes, pancreatic cancer
Nutrition: NPO in acute episode. IV fluids to maintain vascular volume. IV pain medicine. TPN. When
oral foods are resumed, low fat diet with pancreatic enzyme sprinkles on every meal. Avoid spicy
foods because it stimulates pancreatic inflammation.
Mgmt: O2 to keep sats up, pain mgmt, lay on side with HOB at 45, blood sugar checks. Treat
symptoms.
INFECTION: any disease caused by microbes in the body. Communicable disease. Caused by bacteria, viruses,
fungi, and parasites.
Flu 118: highly contagious viral respiratory disease. Epidemic is regional. Pandemic is global. Transmitted by
inhaling droplets (surgical mask precaution). Virus invades epithelium of respiratory tract.
 Flu A and B cause seasonal epidemics. Flu A is the only one that can cause pandemics. Flu C is
generally mild.
 S/SX: rapid onset respiratory and systemic. Fever, muscle aches, chills, headache, sore throat, cough,
fatigue, malaise. Possible crackles and dyspnea. Lethargy and weakness in elderly. Pneumonia is a
complication.
 We DO NOT give Aspirin to young people because it can cause Reyes Syndrome- which progresses to
encephalopathy/ loss of consciousness, seizures. So treat fever with Tylenol or NSAIDs for kids.
 Vaccine needs to be taken yearly. Injection contains killed virus. Nasal spray contains weakened live
virus.
Pneumonia 180: inflammation of lung parenchyma. Respiratory open to infection. Affects the ability to
ventilate, respirations, and ability to maintain airways. Can be bacterial, viral, or aspiration.
 Community-acquired: Pneumonia occurring in the community or LESS THAN 48 hours after hospital
admission or of patients who do not meet the requirements for healthcare associated pneumonia.
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Health care associated: Pneumonia occurring in a non-hospitalized patient with extensive health
care contact. Resident of nursing home or long care facility, antibiotic therapy/chemotherapy, or
wound care within 30 days of current infection. Hemodialysis treatment at hospital or clinic. Home
infusion or home wound care. Family member with infection due to multi drug resistant bacteria.
 Hospital associated pneumonia: Pneumonia occurring GREATER THAN 48 hours after hospital
admission that did not appear to be incubating at time of admission.
 Ventilator associated pneumonia: A type of HAP that develops greater than 48 hours after
endotracheal tube intubation.
S/SX: nonproductive cough, chills, dyspnea, fever, tachypnea, green/yellow/rust sputum, fatigue,
diaphoresis, anorexia, headache, abdominal pain.
Children’s airway is shorter and narrower which causes increased resistance. Pneumonia often resolves
sooner. Children under 6 use diaphragm to breathe. Retractions are early symptom.
Older adults- number of cilia decreases, gag and cough reflexes diminish, greater risk for dehydration,
immune function declines.
Medications: Antibiotics (amoxicillin is most common). Bronchodilators for inflammatory response. Agents to
break up mucus. O2 therapy for hypoxia.
Tuberculosis 179: chronic recurrent infectious disease caused by mycobacterium tuberculosis. Multi drug
resistance is an issue.
 Risk factors: immigrants, HIV/AIDs, homeless or those in shelters, disadvantaged populations,
minorities under 15, overcrowded institutions.
 Latent TB in infants, children, and adolescents won’t have symptoms.
 S/SX Active infection: fatigue, cough, diminished appetite, weight loss, night sweats, chills, low
grade fever, enlarged lymph nodes, wheezing.
 Nursing care: airborne precautions (n95 mask), negative pressure room, patient door closed at all
times. Weekly sputum cultures, 3 negative TB cultures to be considered controlled and come off
precautions. TB gold test is becoming more common than subdermal test. Cough into tissue or cup.
Compliance is biggest thing.
Urinary Tract Infection 120: includes kidneys, ureters, urinary bladder, and urethra. Cystitis, inflammation of
the urinary bladder, is most common.
 Upper UTI (Pyelonephritis) occurs in the ureters, pelvic area or renal parenchyma. Need antibiotics
for 7-10 days once infection reaches bed of the kidney.
 Lower UTI (Cystitis) occurs in the urethra and bladder. Only need antibiotics for 3ish days.
Risk factors: women (shorter urethra) and 20-40. Diaphragm and spermicidal gel contraceptives can alter the
vaginal flora and increase the risk of UTIs. Inability to empty bladder. Obstructed urinary. Catheterization.
Older adults.
S/SX: dysuria, nocturia, frequency, urgency, foul odor, pyuria, hematuria. In older adults, confusion.
ELIMINATION:
BPH 272: Benign Prostatic Hyperplasia: non-cancerous, enlargement of prostate because of too many cells.
Having more estrogen causes the prostate to be less sensitive to testosterone, thus making it grow.
 Risk factors: genetics, erectile dysfunction, diabetes, age- rare before age 40, 50% of men in 60s
have symptoms, 90% by age 85. Smoking, heavy alcohol consumption, western diet (high animal
fat/protein, refined carbs, low fiber.
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S/SX: frequency, nocturia, hesitancy, decreased and intermittent force, abdominal straining,
decreased volume, dribbling. Fatigue, anorexia, N&V, pelvic discomfort. Overall quality of life is
biggest issue.
Medication:
o Alpha-adrenergic blocker: Tamsulosin relaxes the smooth muscle of the bladder neck and
prostate. This improves urine flow and relieves symptoms of BPH. Side effects include
dizziness, headache, asthenia/fatigue, orthostatic hypotension, rhinitis, and sexual
dysfunction.
o The 5-alpha-reductase inhibitors are used to prevent the conversion of testosterone to DHT
and decrease prostate size. Side effects include decreased libido, ejaculatory dysfunction,
erectile dysfunction, gynecomastia (breast enlargement), and flushing.
Teaching: drink plenty of fluids 2000-3000 mL day spaced out. Urinate at first urge. Avoid alcohol
and caffeine. Avoid OTC cold and sinus medications.
Transurethral resection of the prostate (TURP) main surgical treatment for BPH. Done in severe cases. It
involves the surgical removal of the inner portion of the prostate through an endoscope inserted through the
urethra; no external skin incision is made. It can be performed with ultrasound guidance. The treated tissue
either vaporizes or becomes necrotic and sloughs. The procedure is performed in the outpatient setting and
usually results in less postoperative bleeding than a traditional surgical prostatectomy.
 3-way irrigation after surgery to prevent clots. Bloody urine is normal post-surgery. For output you
need to subtract the amount of irrigation bag- it’s not included in intake. Don’t flush too often
because of bladder spasms.
 Practice Kegels to strengthen pelvic floor.
 Monitor for hemorrhage. Observe for symptoms of urethral stricture (dysuria, straining, weak
urinary stream).
Encopresis: voluntary or involuntary retention of stool leading to constipation and dilation of lower bowel.
Child soiling clothes beyond toilet training. (4-5 yo). Could be physiological issue, like sphincter problem. Or it
can be behavioral, like not wanting to stop playing to go to the bathroom.
 Teaching: changes in diet- more fruits/vegetables, high fiber foods, avoid dairy/yogurt, make sure
child drinks plenty of water. Have child sit on toilet for about 15 minutes after breakfast and dinner.
 Offensive body odor may cause social, behavioral, school performance problems.
Enuresis: bed wetting during sleep for children older than 7. May be caused by developmental delay, lack of
ADH, sexual abuse, hard sleeping. Limit items that cause irritation like chocolate and caffeine. Limit fluids
before bed. Reward system. At bedtime, have them urinate then do routine then urinate again before getting
in bed.
Hypospadias : urethral opening is on ventral surface of penis. Surgery is dependent on severity. Maybe
cosmetic or to ensure normal sexual function.
 Child will not be circumcised and surgery is normally done until 1 year old.
 If not repaired, child may have to sit to urinate. Also may have fertility issues when older
 Double diapering after surgery. Typically goes home with catheter.
 No straddle toys
Urinary calculi: kidney stones. Can lodge anywhere in the urinary tract.
 Lithiasis = stone formation. Nephrolithiasis = stones form in kidney. Urolithiasis = stones form
elsewhere in urinary tract.
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Risk factors: Hyperparathyroidism. Too much Vitamin D/Calcium intake. Too much aspirin. High
doses of antacids. More common ages 30-50 in men.
Prevention: Most important is adequate fluid intake. Calcium stones and uric acid stones can be
prevented by reducing sodium and animal intake.
S/SX: vary with size and location.
o Calculi affecting kidney calyces and pelvis have few symptoms.
o If urinary flow is obstructed, dull achy flank pain.
o Bladder calculi is dull suprapubic pain with exercising and voiding and hematuria.
o Stones obstruction ureter causes renal colic- severe pain with accompanying sympathetic
response, ureteral spasms, and potentially UTI.
Complications: Obstruction. Hydronephrosis when kidneys produce urine behind the obstruction,
pressure builds up. Causes colicky pain on the affected side, hematuria, and/or UTI.
o Nephrostomy tube would be inserted. Drains the urine directly from the kidney. Fluid would
be included in output, but also measured separately.
Lithotripsy: stones greater than 1 cm need to be busted up. Lithotripsy is done from the outside of
the body with shock waves to break up the stone. Urine must be strained after procedure and
contents sent for testing. Stones can be busted up to be as small as grains of sand.
Bowel Obstruction 258:
Small intestine obstruction:
Adhesions – intestine adheres to slow healing
areas after surgery. Most common
Intussusception – one segment of the bowel
moves into another (A)
Volvulus – twisting of sigmoid colon (B)
Hernia – intestine protrudes through weakened
area of abdominal muscle wall (C)
Tumor – tumor within the intestinal wall extends
into intestinal lumen or tumor outside intestines
causes pressure on the intestinal wall.
S/SX: crampy colicky pain, abdominal distention, fecal vomiting, will pass mucous or blood but no stool,
dehydration.
Management: NPO, NG tube, bowel decompression, surgery if necrosis is present, hernia repair, division of
adhesion, partial colectomy.
Large bowel obstruction: accumulation of gas or intestinal contents above the area that’s obstructed.
Sigmoid is most common. Cancer, diverticular disease, volvulus, benign tumors, strictures, impaction.
 S/SX: slow progression, constipation, shape of stool is altered, weakness, weight loss, anorexia,
crampy lower abdominal pain.
 Management: Fluid replacement, colonoscopy, cecostomy, surgical resection, colostomy.
Oral care is very important with NG tubes because they are mouth breathers. Turn off suction when
auscultating. Leave it in place and clamp it off for a day or so to make sure they are tolerating clear liquids
okay. If tolerated well, advance diet to soft foods. Make sure they are passing gas.