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Pain/Palliative (2)
Metabolic/Respiratory/Acidosis/Alkalosis (2)
Delegation (3)
 RN to NA transfers responsibility only. RN still assumes accountability
 NA can perform: ADL’s, simple, repetitive, common activities that do not require nursing judgments such as
hygiene, feeding, ambulation etc.
 RN to RN transfers responsibility and accountability
 Must reevaluate to see if the nursing tasks are done properly
 Communicate a time frame- ask was the task done correctly?, was the task done in the proper time frame?, were the
clients needs met?
 Right patient, right task, right instructions, right circumstance, right time, right supervision
 ATI in fundamentals ATI for delegation
4. Medication Administration (8) (dosage, administration, skills)
5. Blood Transfusion (3)
6. Psoriasis (1)
 Immune mediated, red patches of scaly skin, not contagious, chronic.
 Caused by stress, depression, alcohol abuse
 Treat with topical corticosteroids and systematic medications, phototherapy- short, non-burning exposure to
sunlight, photochemotherapy, epsom salts, climatotherapy for Dead Sea, doctor fish in Turkey.
7. Herpes (2): viral infections
 HSV-I: Lips, mouth, face, common cold sore, fever blister
 HSV-II: STD, Genital ulcers, oral lesions, can lead to complications to the brain.
 Herpes Zoster: shingles, localized infection from varicella, painful blistering, rash (chicken pox)
 Treat Herpes Simplex with OTC treatments, antivirals (acyclovir, -vir), topical antibiotics ointments
 Treat Herpes Zoster with antivirals (acyclovir, -vir), analgesics, TCAs
8. Skin Cancer (2)
 Basal Cell: epithelial tumor, most common, least aggressive
 Squamous Cell: more aggressive, has affinity for metastasis
 Malignant Melenoma: fair skinned
 Asymmetry, Borders, Color, Diameter, Elevation
 Treat with radiation, surgery, curettage (scrape), electrodessication, surgical excision, chemo, immunotherapy
(inferons and interleukins to boost immune response), radiation therapy.
9. Pressure Ulcers (2)
10. Burns (5)
 Set water heaters at home to >120
 With chemical burns, tissue destruction can continue for 72 hours
 3 types of smoke and inhalation injuries: Carbon monoxide, inhalation injury above the glottis (caused by inhaling
hot air, steam, or smoke)-glottis closes and stops spread, inhalation injury below the glottis- most fatal
 Electrical injury can cause: fractures of long bones and vertebra, cardiac arrest or arrhythmias because of SA node,
severe metabolic acidosis because the muscle contractures causes lactic acid that the kidneys cant get rid of which
causes myoglobinuria (muscle enzymes cant breakdown, excreted through kidneys causing dark urine). Treat with
Ringers Lactate (hypervolemic) or other fluids to flush out the kidneys or an osmotic diuretic (mannitol) to maintain
urine output
 Cold thermal Injury (frostbite): tissue necrosis, do not massage
 If the client has burns to the face/neck/chest be concerned with the airways
 Burn percentages: 9% for entire arm. 18% entire leg. 9% head. 36% entire trunk. 1% inguineal.
 Lund-Browder chart is more accurate but rule of nines is used in emergent situations.
 Remove jewelry due to swelling
 Signs of airway injury is soot, singed nose hair, coughing up black sputum, blisters around oral mucosa
 More death with upper body burns
 Greatest initial threat is hypovolemic shock (loss of intravascular fluid volume) to a major burn patient. (S/S shock:
dilated pupil, hypotension, tachycardia, weak thready pulse, cold and clammy)
 Second spacing- fluid moves into interstitial tissues from capillaries causing edema
 Third spacing- large amount of fluid collecting in spaces they aren’t suppose to such as ascites.
 UOP: 30-50cc/hr
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Wound care waits until patent airway, adequate circulation and fluid replacement is in place.
Parkland Formula: 4mL x kg of pt x total body surface burned % - give half of this in first 8 hours and then the rest
over 16 hours
 If clients respirations are shallow, they are retaining CO2, and will have respiratory acidosis
 Albumin holds onto fluids in the vascular space which helps correct fluid volume deficit
 Start pain meds low and slow via IV
 Tetanus toxoid immunization will be given, takes 2-4 weeks to develop immunity
 Manifestations of shock: confusion, increased capillary refill time, UO <30mL/hr, rapid elevations in temperature,
decreased bowel sounds
 Drug of choice is Silver Sulfadiazine (topical to soothe area and prevent infection).
 Superficial: pink to red, no blisters, mild edema no eschar, painful; sunburns
 Superficial partial thickness: pink to red, mild to moderate edema, no eschar, painful; flame burns
 Deep partial thickness: red to white, with moderate edema, free of blisters and soft and dry eschar, painful
 Full thickness: red to tan, black, brown or white, free from blisters, severe edema, pain may or not be
present, as it heals pain senses return; grease, tar, chemical or electrical burns
 Deep full thickness: black, edema; chemical burns
11. Diabetes Mellitus (5)
 Ketones: accumulate in the blood due to breakdown of fatty acids when insulin is not available, resulting in
metabolic acidosis
 Kussmauls respirations to attempt to excrete CO2 and acid due to metabolic acidosis: have fruity breath, HA, N/V,
inability to concentrate, decreased level of consciousness, and seizures leading to coma
 Blood glucose > 200mg/dL, fasting >126 mg/dL
 Rapid acting: humolog, novolog; given right before means, administer with intermediate or long acting
 Short acting: regular (Can give IV), administer 30-60 minutes before meal
 Intermediate: NPH, humulin N, administers between meals and at night, only insulin to mix with regular. Clear
(regular) before cloudy (NPH)
 Long acting: glargine insulin, administer once daily during the day at the same time everyday, dissolves slowly over
24 hours without peaks and troughs
 Cold and clammy needs some candy, hot and dry sugars high
 When hypoglycemic (<70mg/dL), give 15-20 g of readily absorbable carbs with are: 4-6 ounces of fruit juice or
regular soft drink, 3-4 glucose tablets, 8-10 hard candies, 1 T of honey, then recheck blood glucose in 15 minutes
then repeat if not within normal limits then recheck in 15 minutes. If unconscious administer glucagon IM then
recheck in ten minutes and notify provider.
 DKA: hyperglycemia >300mg/dL, life-threatening, breakdowns body fat for energy, initaially give NS then give ½
NS and add dextrose when glucose reaches 250mg/dL and regular insulin
 hyperglycemic hyperosmolar state (HHS): life-threatening hyperglycemia >600mg/dL, leads to dehydration,
coma and death. Usually type 2. Also may have myoclonic seizures, and reversible paralysis. Don’t have ketones in
urine or serum, absence of acidosis. Monitor serum potassium levels for hypokalemia.
 For HHS administer isotonic fluids, then hypotonic fluids, glucose and regular insulin via IV.
 Dawn Phenomenon: rise in blood glucose between 0400-0800
 Symogi: hypoglycemia at night and rebound hyperglycemia in the morning.
12. Neutropenia (1): decreased neutrophils
13. Endocrine Disorders (8) (Hyper/Hypo, Cushing, Addison’s, SIADH, DI)
 Hyperthyroidism: excessive thyroid hormones.
 Graves: autoimmune antibodies results in hypersecretion of thyroid hormones.
 S/S Hyperthyroidism: nervousness, irritability, weakness, heat intolerance, weight change, insomnia,
warm skin, tremor, exopthalmus (Graves only), hair loss, goiter, tachycardia, facial flushing, fine hair,
splenomegaly
 Toxic nodular goiter: overproduction of thyroid hormone due to the presence of thyroid nodules.
 Thyroid Storm: sudden surge of large amounts of thyroid hormones caused by trauma, infection,
emotional stress, DKA, digitalis toxicity. Decreased TSH but increase T3, T4. S/S hyperthermia, HTN,
delirium, vomiting, abdominal pain, hyperglycemia, chest pain, dyspnea, palpatations. Give antithyroid
MMI (Tapazole, methamazole) drugs and Iodine then relieve respiratory distress first and stabilize cardio.
Reduce fever with Tylenol, give beta-blocker for cardio stabilization, and iodine solutions.
 RAI therapy: radioactive precautions, such as not using the same toilet as others for 2 weeks, flush three
times, wear washable clothing and was separate from others and run it before washing others clothes, don’t
share tooth brushes. It damages the thyroid tissues. Give with MMI’s and beta-blockers.
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Hypothyroidism:
 Primary: thyroid gland is not secreting enough (Hashimotos) (TSH is increased, t3, t4 are low)
 Secondary: pituitary isn’t secreting enough TSH (TSH is decreased, no t3,t4 low)
 Myexedema: accumulation of non-pitting edema in the connective tissues. First maintain airway, then do
ECG monitor, do ABGs, warm them up, then give synthyroid
 Creatinism: caused by thyroid hormone deficiencies in the neonatal and fetal life causing mental
retardation
 S/S: intolerance to cold, weight gain, pale skin, thinning hair, joint and muscle pain, bradycardia,
constipation, dry flaky skin
 Return them to euthyroid state, barbituates and sedatives are contraindicated.
 Treat: Synthroid is treatment of choice, and monitor for CV compromise, take 1-2 hours before breakfast
 Hyperparathyroidism: hypercalcemia, hypophosphatemia, causes the osteoclast to break down bone for
circulating calcium. Can cause kidney stones. Primary: gland is malfunctioning. Secondary: hypocalcemia all the
time causes it to produce more calcitonin. Tertiary: caused by chronic renal failure. Symptoms usually related to
hypercalcemia such as abdominal pain and constipation. Treat by increasing PO fluids, encourage activity (for
osteoblasts), avoid thiazide diuretics, avoid Vitamin A D, avoid antacids and calcium supplements.
 Hypoparathyroidism: check for Trousseaus signs (hypocalcemia) and Chvostek’s. Treat with calium gluconate,
supplemental calcium and vitamin D
 Cushing: Have a cushion of excess ACTH. Advise the client to take medications as instructed, may be
lifelong therapy, eat foods high in calcium and vitamin D, no alcohol and caffeine, monitor for gastric
bleeding (black tarry stools, hematemesis), need to avoid infection by practicing good hygiene.
 BBIIG: Blood pressure, Bone formation inhibition, Decrease anti-Inflammatory, Decrease Immunity,
Increase glycogenesis S/S: moon face, buffalo hump, HTN, osteoporosis, immune suppression, muscle
weakness with thin extremities and trunkal obesity, hyperglycemic
 Treat: Aminoglutethimide and Mitotane, administer glucocorticoids to prevent abrupt drop in cortisol
 Adrenal cortex secretes: Mineral corticosteroids, Androgens, Cortisol
 Cortisol is a stress hormone and a steroid hormone
 Addisons: Adrenocortical insufficiency due to damage or dysfunction of the adrenal cortex.
 S/S: hyperpigmentation (bronze), weight loss, weakness, dehydration, hyperkalemia, hypoglycemia,
hypercalcemia
 Primary: increase in ACTH because the gland wont work
 Secondary: decrease in ACTH because of pituitary tumor or abrupt withdrawal in steroids.
 Treat: hydrocortisone, prednisone and cortisone to replace an adrenal insufficiency and as an antiinflammatory. Fludrocortisone is a mineralocorticoid used to replace adrenal insufficiency
 Adisonian Crisis: occurs when there is an acute drop in adrenocorticoids due to sudden discontinuation of
glucocorticoids or trauma/stress. Administer insulin, calcium, kayexalate, loop or thiazide diuretics
 S/S of adisonian crisis: high fever, weakness, severe penetrating pain to abd, lower back and legs,
vomiting, diarrhea, hypotension, circulatory collapse, shock and coma as well as all the symptoms of
addisons disease.
 SIADH: Excessive ADH is released. Hold onto water. Weight gain without edema because water, not sodium, is
retained. Seizures, coma and death because decreased sodium. Blood is dilute and urine is concentrated.
 Restrict fluids. Flush with NS to add some sodium back.
 Declomycin may cause drug induced DI. Lithobid is used to block the renal response to ADH, may induce
DI. Lasix used to increase water excretion from the kidneys, can cause hyponatremia to worsen.
 Complications: water intoxication, cerebral edema, severe hyponatremia
 DI: deficiency of ADH from the posterior pituitary causes DI. Large quantity of diluted urine. Polydipsia and
polyuria, nocturia, fatigue, dehydration, tachycardia, hypotension, decreased skin turgor.
 Primary (neurogenic): problems in the hypothalamus and pituitary.
 Nephrogenic: is inherited and the body isn’t responding to ADH.
 Drug induced: may alter the way the kidneys respond to ADH.
 Need lifelong treatment of Desmopressin (DDAVP), which increases water absorption in from the kidneys
and decreased urine output. Tegretol stimulates the release of ADH (central DI). Vassopressin increases
water absorption form kidneys and decreased urine output.
 Vasopressin test determines what type of DI they have. Will only respond if they are neurogenic.
14. Multiple Myeloma (1)
15. Cancer (5)
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16. Thrombocytopenia (2): low platelets
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Platelet count less than 100,000
Idiopathic thrombocytopenia purpura (ITP) antibodies are attacking platelets prematurely, Petechiae, purpura
Thrombotic thrombocytopenia purpura (TTP) platelet aggregation, multiorgan involvement HA, seizure
Treat with Oral glucocorticoids (prednisone), immunosuppressive, platelet transfusion, plasmapharesis,
splenectomy
17. SLE (1)
18. Von Willebrand’s (1)
19. Hemophilia (2)
 Hemophilia A: problem with factor 8
 Hemophilia B: Christmas disease, affects factor 9
 Hemophilia C: Factor II is affected, jewish people
 Treat with DDAVP
 Hgb: 13-15
20. DIC (2)
 Depleted platelets and clotting factors followed by excessive clotting- if you’re pregnant, cancer, poisonous snakes,
head trauma or SEPTIC you’re at increase risk for developing DIC.
 Treat with fresh frozen plasma (gives back platelets and clotting factors), platelets (give quickly), heparin (when
youre clotting too much)
21. Lymphoma (3)
22. Leukemia (3)
23. HIV (3):
 After initial infection (fever, HA, sore muscles, stomach ache, swollen lymph glands, N/V), becomes asymptomatic
for 8-10 years but is still contagious. CD4+ is 500-1600 which drops dramatically in infected people
 <200: PCP
 <100: toxoplasmosis, cryptococcosis
 <75 MAC
 HIV becomes AIDs when the CD4+ is <200
 ELISA test: when you suspect aids, can cause false + or -; western blot
24. Infection (2)
25. Altered Immunity (hypersensitivity) (2)
 Natural active: chickenpox
 Natural acquired: immunization- vacines
 Passive natural: mother to child
 Acquired passive: serum injection
 Cell-mediated immunity: T cells respond and attack antigens directly (rejected transplant)
 Helper T: stimulate B cells to mature into plasma cells which secrete immunoglobulin or antibodies
 Humoral: produce antibodies from B cells
 Haptens: low weight substances that are harmless alone but clump together and cause antibodies which can later
elicit an immune response
 B cells: produce antibodies
 IgG: active against almost anything.
 IgM: active infection, first response
 IgA: found in saliva and tears, defends against pathogens on body surfaces, think smaller local immunity
 IgD: predominant antibody on the surface of B cells
 IgE: immediate hypersensitivity reactions or allergic reactions
 WBC: 4.5-11
 Type I: IgE mediated allergic reactions- anaphylactic shock with bronchial edema and angioedema, allergic rhinitis,
hives, bee sting
 Type II: cytotoxic reactions- binding of IgG or IgM antibodies to an antigen. Antibody-antigen complexes activate
complement system: ABO incompatabilities, transfusion reaction, hemolytic anemia,
 Type III: immune complex reactions- immune complexes are deposited in the kidney, skin, joints, blood vessels
and lungs. Local or systemic, lupus, RA, serum sickness (deposits of antigen-antibody complexes in the blood
vessels od the skins, joints, and renal glom)
 Type IV: cell mediated reactions-delayed hypersensitivity response: contact dermatitis, transplant rejection, poison
ivy
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Treat Anaphylactic shock: airway, epi 1/10,000, Benadryl, airway management, then give IV fluids, give
vassopresser, then steroids, then reassess, if clients not ok, repeat with epi, H2 blocker and reassess. *reverse
Trandelenberg
 Latex Allergies: Type IV allergic contact dermatitis caused by the chemicals, delayed occurs 6-8 hours later. Type
I allergic reactions, response to natural rubber latex proteins and occurs within minutes.
 Radioallergosorbent test (RAST): measures IgE
 Treatment of Autoimmune Disorders: Anti-inflammatory drugs (NSAIDS, corticosteroids), Antirheumatic drugs
(Gold salts, Plaquenil), Cytotoxic drugs (Cyclosporin, Imuran).
26. Transplants (2)
 Hyperacute Transplant Rejection: occurs immediately to 2-3 days after the transplant, transplant cannot be saved
 Acute Transplant Rejection: occurs days to months after transplant, impaired organ function
 Chronic Transplant Rejection: occurs 4 months to years after transplant, antibody mediated immune response
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Gastroenteritis (2)
Malnutrition (2)
GERD (2)
PUD (2)
Ostomy (2)
IBS (1)
Appendicitis (1)
Peritonitis (2)
Gastroenteritis (3)
Crohn’s (1)
Ulcerative Colitis (1)
Gall Bladder (2)
Hepatitis (4)
Cirrhosis (3)
Pancreatitis (2)
Repetitive Use Disorders (1)
Sprain/Strain (1)
Fracture (3)
Osteoporosis (3)
Paget’s (1)
Gout (2)
Osteoarthritis (2)
Rheumatoid Arthritis (2)
Perioperative (4)
Anemia (2)
Sickle Cell (2)
Treat Malignant Hyperthermia with Dantrolene