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Capstone FINAL EXAM 1.

GIB with cardiac pathology: pharmacotherapy Nonselective beta-blocker, such as Propranolol (Inderal), to decrease heart rate and consequantly reduce hepatic venous pressure Vasoconstrictors, such as Vasopressin (Desmopressin) and Octreotide (Sandostatin), to decrease portal outflow 2. Stable angina: patient education (PE) page 331-336 for more Decrease stress, rest, take nitro. If unrelieved by nitro, see PCP 3. Esophageal varices: nursing care priorities (NCP) Monitor for S+S: hematemesis, melena, hypotension, tachycardia If the client is bleeding, establish IV access, monitor vital signs and hematocrit, type and crossmatch for blood transfusions, and monitor for overt and occult bleeding 4. Abdominal surgery: risk ID (RID) Indications: ineffective management of PUD, emergency surgical intervention for perforation and hemorrhage, surgical removal/reduction of gastric cancer 5. Tumor lysis syndrome: NCP Maintain adequate hydration Provide emotional support Treat metabolic imbalances/monitor F+E increased potassium, uric acid, phosphate, & decreased calcium Potassium: kayexalate Uric acid: allopurinol Prevent life-threatening complications (severe electrolyte imbalances) 6. Immunity: mechanisms Innate Immunity Pathogen recognized by receptors encoded in the germline Adaptive Immunity Pathogen recognized by receptors generated randomly

Receptors have broad specificity, i.e., recognize many Receptors have very narrow specificity;

related molecular structures called PAMPs (pathogenassociated molecular patterns) PAMPs are essential polysaccharides and polynucleotides that differ little from one pathogen to another but are not found in the host. Receptors are PRRs (pattern recognition receptors)

i.e., recognize a particular epitope Most epitopes are derived from polypeptides (proteins) and reflect the individuality of the pathogen. In jawed vertebrates, the receptors are B-cell (BCR) and T-cell (TCR) receptors for antigen Slow (35 days) response (because of the need for clones of responding cells to develop Memory of prior exposure

Immediate response Little or no memory of prior exposure

Under Adaptive:
cell-mediated immunity (CMI), cellular immunity acquired immunity in which the role of T lymphocytes is predominant. humoral immunity acquired immunity in which the role of circulating antibodies is predominant.

7. Acute pancreatitis: PA y S+S o Sudden onset of severe, boring pain     o N/V o Weight loss o Signs and symptoms of inflammation or peritonitis o Seepage of blood-stained exudates into tissue   Ecchymoses on the flanks (Turners sign) Bluish periumbilical discoloration (Cullens sign) Epigastric, radiating to back, left flank, or left shoulder Worse when lying down or with eating Not relieved with vomiting Some relief in fetal position

o Generalized jaundice o Paralytic ileus o Hyperglycemia Assess & Monitor: pain level, nutritional status, bowel function, blood glucose levels, diet and alcohol intake history, F+E status 8. Intestinal obstruction: PA
Small bowel and large intestine obstructions Obstipation: the inability to pass a stool and/or flatus for more than 8 hrs despite feeling the need to defecate Abdominal distention High-pitched bowel sounds before site of obstruction with hypoactive bowel sounds after, or overall hypoactive; absent bowel sounds later in process Small bowel obstruction Pain is spasmodic and colicky Large intestine obstruction Pain is diffuse and constant

Visible peristaltic waves Profuse, (projectile) sudden vomiting with feculent odor; vomiting relieves pain

Significant abdominal distention Infrequent vomiting; the client can have diarrhea around an impaction.

9. Tension pneumothorax: PA Monitor for S+S: pleuritic pain, signs of respiratory distress (tachypnea, tachycardia, hypoxia, cyanosis, dyspnea, and use of accessory muscles), tracheal deviation to unaffected side, reduced or absent breath sounds on affected side, asymmetrical chest wall movement, anxiety, hyperresonance on percussion 10. Procedural sedation: RID
y Before, during, and after the procedure, emergency equipment is to remain at the bedside. Some complications that can arise from conscious sedation include: o Airway obstruction: insert airway, suction o Respiratory depress: administer oxygen and reversal agents, such as naloxone (Narcan) and flumazenil (Romazicon) o Cardiac arrhythmias: set up 12-lead ECG, provide antidysrhythmics and fluids o Hypotension: Provide fluids, vasopressors o Anaphylaxis: administer epinephrine Most hospitals and facilities require that for conscious sedation the RN needs to be certified in advanced cardiac life support or pediatric advanced life support (PALS) in case of emergency. In all instances of complications, the sedation needs to be stopped and care given to end the problem.

11. Hepatitis: PA Monitor for S+S: influenza-like symptoms, hepatomegaly, signs of obstruction (light-colored stools, dark urine, jaundice, elevated bilirubin and liver enzymes); inspect overall color of skin, eyes, and mucous-membranes; skin irritations d/t pruritus; pain in muscles, joints, abdomen; fever, malaise, increased fatigue, N/V 12. Immunosuppression: RID

13. CRF: PA y y y y y y y y y Renal-polyuria, nocturia (early), oliguria, anuria (late), proteinuria, hematuria, and dilute urine color when present. Cardio-HTN, peripheral edema, pericardial effusion, congestive heart failure, cardiomyopathy, and orthostatic hypotension Respiratory-dyspnea, tachypnea, uremic pneumonitis, lung crackles, Kussmaul respirations, and pulmonary edema Hematologic-anemia, bruising, and bleeding Neurologic-lethargy, insomnia, confusion, encephalopathy, seizures tremors, ataxia, paresthesias, and coma. GI-nausea, anorexia, vomiting, metallic taste, stomatitis, diarrhea, uremic halitosis, and gastritis Musculoskeletal-osteomalacia, muscle weakness, pathologic fractures, and muscle cramps Reproductive-erectile dysfunction Other general symptoms include: o Fatigue o Lethargy o Restless leg syndrome o Depression o Intractable hiccups Abnormal findings: o Urinary elimination patterns (amount, color, odor, and consistency) o Vital signs (especially BP) o Weight -1kg daily weight increase is approximately 1 L of fluid retained o Assess/monitor vascular access or peritoneal dialysis insertion site.

14. Type 2 diabetes: patient outcomes (PO)


y Complications o CVD:  The leading cause of death in diabetics. Three out of four diabetes-related deaths are caused by CVD. People with diabetes are 2 to 4 times more likely to have heart disease. Clients with T2D who do not have heart disease still have an increased risk of having a heart attack. Due to other risk factors for heart disease, they may have high blood pressure and atherosclerosis. o Blindness:  Caused by diabetic retinopathy o Kidney Failure:  Elevated blood glucose levels can damage the kidneys. Even with good dietary and medical management, diabetes can cause kidney disease (diabetic nephropathy) and kidney failure o Foot Ulcers:  People with diabetes need to take special precautions with their feet. They are at risk for foot injuries because of the numbness experienced secondary to nerve damage (diabetic neuropathy) and decreased blood flow to the legs and feet. Clients with foot ulcers should off load their wounds and apply wound dressings, skin substitutes, consider hyperbaric therapy, or other treatments to protect and heal their skin.

15. Type 1 Diabetes: nursing interventions Provide information regarding importance of foot care (common sense nursing interventions, p 584). Encourage clients to take measures to reduce risk of injury (wear shoes, adequate lighting). Refer clients to dietician. Teach guidelines to follow when sick (SICK DAY RULES - monitor blood glucose q4h, continue to take insulin or oral agents, consume 8 oz of fluid every hour to prevent dehydration, meet carbohydrate needs through solid foods if possible, test urine for ketones, rest). Teach measures to take in response to hypoglycemia symptoms (check glucose level, treat with juice prn). Teach measures to take in response to hyperglycemia symptoms (encourage oral fluid intake, administer insulin, restrict exercise when levels are >250, test urine for ketones, consult PCP if symptoms progress). Know onset, peak, and duration of administered insulin; monitor for signs of hypoglycemia accordingly. Provide information regarding self-administration of insulin, observe pt performance.

Insulin administration: NRRN (air in NPH, air in REGULAR, pull up REGULAR, pull up NPH) Provide information regarding oral antidiabetic medications take 30 minutes before a meal for most meds, or with first bite of a meal 16. HHNS: RID
y y HHNS is more common in older adult clients and in individuals with untreated or undiagnosed type 2 diabetes mellitus Caused by Serve hyperglycemia from: o A lack of sufficient insulin (new onset diabetes, lack of compliance with diabetes treatment plan). o An increased need for insulin (stress, illness, infection, surgery, trauma) Serum glucose levels o > 600 mg/dL Serum Electrolytes o Sodium: Na increased due to water loss o Potassium: K initially low due to dieresis Serum Renal Studies o BUN/ Creatinine: Increased secondary to dehydration Ketone Levels o Serum : Absent o Urine: Absent Serum Osmolarity o VERY HIGH Serum pH (ABG) o Absence of acidosis

y y

y y

y y

17. DM with cardiac pathology: pharmacotherapy

18. Solid organ transplantation: PA


y Assess/Monitor o Vital signs continually o Intake and output at least hourly (urine output should be greater than 30mL/hr) o Urine appearance and odor hourly (initially pink and bloody, gradually returning to normal in a few days to several weeks) o Daily Weight o Daily urine tests, including urinalysis and glucose determinations o Renal function, specially for oliguria (100 to 400 mL output in 24 hr) o For fluid and electrolyte imbalances, such as hypervolemia, hypovolemia, hypokalemia, and hypnatremia o For signs of infection (respiratory, surgical site) o For signs of organ rejection

19. Nephrotic syndrome: PA S+S: hematuria, edema, irritability, malaise/fatigue, hypertension, anemia, anorexia/nausea, azotemia (elevated BUN and creatinine), uremia 20. Anemia: pharmacotherapy Iron supplements (ferrous) take with meals if GI side effects occur Vitamin C improves absorption Do not take within 2 hours of milk or antacid Stools will be black; constipation may occur Use a straw to avoid staining teeth Administer parenteral iron using Z-track method Erythropoietin (Procrit) Vitamin B12 Folic acid supplements Oxygen Vitamin C IV fluids 21. Sickle Cell Disease: PA Jaundice and anemia; results in tissue ischemia, promoting development of pain. Stroke & priapism (prolonged painful ERECTIONNNN)

Organ damage to spleen, kidneys, and liver can results from sickle cell crisis 22. Bacterial pneumonia: pharmacotherapy
y Antibiotics are given to destroy the infectious pathogens o Commonly used antibiotics include the penicillins and cephalosporins o They are often initially given by IV and then switched to an oral form as the client s condition improves o It is important to obtain any culture specimens prior to giving the first dose of the antibiotic. Once the specimen has been obtained, the antibiotics can be given while waiting for the results of the ordered culture. Bronchodilators o Short acting beta 2 agonist, such as albuterol (Proventil, Ventolin), quickly provide bronchodilation o Methylxanthines, such as theophylline (Theo-Dur), require close monitoring of serum medication levels due to narrow therapeutic Corticosteriods, such as prednisone, decrease airway inflammation. If given systemically, monitor for serious side effects (immunosuppression, fluid retention, hyperglycemia, hypokalemia, poor wound healing).

23. Sepsis: PA A systemic response to infection, manifested by 2 or more of the following a temperature of > 100.4F, a HR of >90, RR of >20, or PaCO2 <32, WBC >12,000 or <4,000 24. Renal status: PA NORMAL Values:
y y y UO >30 ml/hr No protein, glucose, ketone, nitrate, bacteria, leukocyte, esterase, crystals and stones ADH: A relatively small (peptide) molecule that is released by the pituitary gland at the base of the brain after being made nearby (in the hypothalamus). ADH has an antidiuretic action that prevents the production of dilute urine (and so is antidiuretic). Regulates BP Syn, releases, and activates: erythropoietin, renin, and Vit. D

y y

25. ARF: PA Clinical manifestations occur abruptly, and if chronic leads to S+S in #13 3 phases o Oliguria: begins with the renal insult and continues for 3 weeks

o Diuresis: Begins when the kidneys begin to recover and continues for 7 to 14 days o Recovery: Continues until renal function is fully restored and requires 3 to 12 months. 26. Graves disease: pharmacotherapy
y Administer antithyroid medications as prescribed, which may include: o Propylthiouracil (PTU) or methimazole (Tapazole)-blocks thyroid hormone synthesis. o Beta-adrenergic blockers-treats sympathetic nervous system effects (tachycardia, palpitations) o Iodine-containing medications-inhibits the release of stored thyroid hormone and retards hormones synthesis. Use of these medications is contraindicated in pregnancy. o Clients receiving antithyroid medications should be monitored for signs of hypothyroidism, which can occur with overmedication Eye inflammation o Certain medications, such as steroids, reduce the swelling (inflammation) behind the eyes to relieve discomfort. Prescription strength eyedrops also may help relieve some symptoms.

27. HHNS (hyperglycemic hyperosmolar nonketotic syndrome): PE Take measures to decrease risk of dehydration. Monitor glucose q4h when ill and continue to take insulin. Consume liquids with carbs and electrolytes (ex. sports drinks) when unable to eat solid food. Notify PCP if illness lasts more than a day. 28. Cushings disease: PA y y Neurologic, cardiovascular, dermal, and endocrine system assessments are indicated. S+S include: o Evidence of decreased immune function and decreased inflammatory response o HTN (sodium and water retention) o Changes in fat distribution, including the characteristic fat distribution of moon face, truncal obesity, and fat collection on the back of the neck (buffalo hump) o Emotional lability o Fractures (osteoporosis) o Impaired glucose tolerance o Hirsutism o Bruising and petechiae (fragile blood vessels)

o Muscle wasting 29. HTN: pharmacotherapy Diuretics Thiazide diuretics (hydrochlorothiazide) Loop diuretics (Lasix) Potassium-sparing diuretics (Spironolactone) CCB (Verapamil, diltiazem) ACE-Inhibitors (-pril) ARBs (-sartan) Beta Blockers (-olol) Alpha agonists (clonidine) 30. Shock: NI Give IV fluids (combo of crystalloids and colloids) Medications: vasopressors and positive inotropes Decrease oxygen consumption (rest, pain relief, anxiolytics, hypothermia) Optimize O2 delivery (nasal cannula, mask, vent) 31. Head Injury: PA Open: skull integrity is lost (penetrating trauma) Closed: Skull integrity is maintained (blunt trauma). Head traumas are classified as mild, moderate, or severe; depending on the Glasgow Coma scale ratings and loss of consciousness Assess: respiratory status is the priority assessment, changes in the LOC is the earliest indication of neurological deterioration; alcohol or drug use at the time of injury can mask IICP; amnesia before or after injury; loss of consciousness and length; Cushings reflex (late sign of increased ICP); posturing, cranial nerve functioning; pupillary changes (PERRLA, pinpoint, fixed/nonresponsive, dilated); signs of infection (nuchal rigidity with meningitis), cerebrospinal fluid leakage from nose and ears (halo sign-yellow stain surrounded by blood, test positive for glucose), GCS rating (15= normal, 3=deep coma)

32. IICP: PA Symptoms include severe h/a, decreased LOC, dilated or pinpoint pupils, altered breathing pattern, decreased motor function sometimes accompanied by abnormal posturing, Cushings triad is a LATE sign (HTN, bradycardia, widening pulse pressure) 33. Stroke: PE Risk factors: HTN, atherosclerosis, hyperlipidemia, DM, cocaine use, a.fib, smoking, use of oral contraceptives, obesity, hypercoagulability, cerebral aneurysm, arteriovenous malformation 34. Stroke: pharmacotherapy For an ischemic stroke: Systemic or catheter-directed thrombolytic therapy restores cerebral blood flow. It must be administered within hours of the onset of symptoms. It is contraindicated for treatment of hemorrhagic stroke and for clients with an increased risk for bleeding. Rule out hemorrhagic stroke with an MRI prior to initiation of thrombolytic therapy. o Anticoagulants: sodium heparin, warfarin (Coumadin) o Antiplatelets: Ticlopidine (Ticlid), clopidogrel (Plavix) o Antiepileptic medications: Phenytoin (Dilantin), gabapentin (Neurontin) 35. Head Injury: PA See #31 36. Hospice care: PA 37. GCS: PA Score based on eye opening, verbal and motor response Mild (13-15) Moderate Disability (9-12): loss of consciousness greater than 30 mins, physical or cognitive impairments which may or may not resolve, benefit from rehab Severe Disability (3-8): Coma Vegetative State (Less than 3) Eye Opening Response (E)Verbal Response (V) 4 = spontaneous 5 = normal conversation 3 = to voice 4 = disoriented conversation 2 = to pain 3 = words, but not coherent 1 = none 2 = no words, only sounds Motor Response (M) 6 = normal 5 = localizes to pain 4 = withdraws to pain 3 = decorticate posture

1 = none E score V score E + V + M = total score

2 = decerebrate 1 = none M score

38. IICP: pharmacotherapy 39. MODS: pharmacotherapy Prophylactic abx; if fever continues with abx, use antipyretics IV fluids (crystalloid or colloids) If significant blood loss, administer blood products 40. MODS: PA Cardiovascular: tachycardia, hypotension, ventricular arrhythmias, peripheral edem with bounding or diminished pulses Pulmonary: tachypnea, PaO2 <70 mm Hg, SaO2 <90%, dyspnea with increased work of breathing Liver: jaundice levels, increased enzymes, decreased albumin, and increased PTT GI: anorexia, N/V, upper/lower GI bleed, diarrhea, bacterial overgrowth in stool CNS: altered LOC, confusion, psychosis, hyperthermia/hypothermia Renal: increased serum/creatinine/BUN; oliguria, anuria, or polyuria 41. MODS: PA See #40 42. Shock: PA Vitals are Key! Temperature (decreased in hypovolemia, increased in sepsis; hypothermia is a late sign) BP decreases HR initially increases; except in neurogenic shock, bradycardia exists. Evidence of decreased CO (cold, clammy, pale skin; UO <30 mL/hr) Respirations depend on stage of shock; hyperventilation is during the compensatory stage.

43. ARF: nutritional intervention Supply nutrition oral, enteral, or parenteral nutrition is needed to combat catabolism in critically ill patient with renal dysfunction Diet: restrict dietary intake of protein, sodium, and potassium during oliguric phase. Restrict fluid intake during oliguric phase.

44. F+E: NI ATI pages 379-387 45. Shock: NCP ABCs: open airway, start the breathing, stop the bleeding, chest compressions Treat the underlying cause (septic, neurogenic, cardiogenic, hypovolemic, anaphylactic) 46. Anaphylaxis: NCP Refer to #30 for shock interventions Administer epinephrine and antihistamines 47. ABGs: interpretation Acid renal imbalances are a result of insufficient compensation. Compensation refers to the process by which the body attempts to correct changes and imbalances in pH levels. Full compensation occurs when the pH level of the blood returns to normal (7.35-7.45). If the pH is not able to normalize, then it is referred to as partial compensation. Respiratory acidosis: results from hypoventilation/respiratory depression, airway obstruction; results in increased CO2 and increased H+ concentration Respiratory alkalosis: results from hyperventilation or hypoxemia; results in decreased CO2 and decreased H+ concentration Metabolic acidosis: results from excess production or inadequate elimination of H+ ions, inadequate production of or excess elimination of bicarb; results in decreased HCO3, increased H+ concentration Metabolic acidosis: results from base excess or acid deficit; results in increased HCO3, decreased H+ concentration * Step 5: Determine Compensation. Uncompensated: the pH will be abnormal and either the HCO3 or the PaCO2 will be abnormal. Partially compensated: the pH, HCO3 and PaCO2 will be abnormal. Fully compensated: the pH will be normal but the PaCO2 and the HCO3 will both be abnormal.

48. ATN: NCP Caused by lack of O2 to kidney tubules, resulting in ARF Assessment: decreased LOC, decreased or no urine output, general edema, N/V, increased BUN and creatinine Nursing: identify and assist with correcting the underlying cause; prevent prolonged episodes of hypotension and hypovolemia 49. Abdominal aneurysm: NCP Priority: reduce and maintain systolic BP between 100 & 120 Administer anti-hypertensive medications as prescribed 50. Pneumothorax: PA Monitor for S+S: pleuritic pain, signs of respiratory distress (tachypnea, tachycardia, hypoxia, cyanosis, dyspnea, and use of accessory muscles), tracheal deviation to unaffected side, reduced or absent breath sounds on affected side, asymmetrical chest wall movement, anxiety, hyperresonance on percussion 51. MI: PA Monitor S+S, can be asymptomatic chest pain, dyspnea, pallor and cool/clammy skin, tachycardia and/or palpitations, anxiety/fear/feeling of doom, diaphoresis, N/V, dizziness, decreased LOC 52. Thyroidectomy: PA Post-op assessments: observe for signs of respiratory distress, assess for signs of hemorrhage, watch for hypocalcemia, and be alert for thyroid storm (tachycardia, diaphoresis, increased BP, anxiety) 53. CHF: pharmacotherapy Diuretics (loop, thiazide, potassium sparing) Afterload-reducing agents (ACEs, BBs, ARBs) Inotropic agents (digoxin, dopamine) Vasodilators (nitrates) Anticoagulants (warfarin, heparin) 54. HTN: pharmacotherapy See #29

55. Chest pain: NCP Administer O2 4-6 L Obtain and maintain IV access Promote energy conservation Teach client to avoid straining, strenuous exercise, or emotional stress Educate client regarding response to chest pain Prepare for diagnostic exams Encourage lifestyle modifications 56. HTN: pharmacotherapy See #29 57. COPD: NCP Position client in high-fowlers Encourage coughing; suction Encourage deep breathing, use of incentive spirometer Administer breathing treatments and meds as prescribed Bronchodilators Anti-inflammatorys Combination agents (bronchodilator & anti-inflammatory) Administer heated and humidified O2 therapy Instruct client to practice breathing techniques (diaphragmatic, abdominal, purse-lipped breathing) Provide O2 therapy (2-4 L); if chronic, 1-2 L Include periods of rest Promote adequate nutrition; encourage smoking cessation as needed Provide support; encourage verbalization of feelings 58. ARDS: RID

Risk factors for ARDS: anything that may result in direct injury to lung tissue or affects other systemic problems Aspiration, PE, pneumonia, sepsis, trauma, nervous system injury, smoke or toxic gas inhalation, drug ingestion (heroin, opioids, ASA), near-drowning victims 59. Pneumonia: PO Complications: atelectasis, acute respiratory failure, bacteremia/sepsis 60. Edema: PA Can be assessed by applying fingertip pressure on the skin over a bony prominence; if indentation does not disappear within 15 seconds, pitting edema is present Ratings: +1: 2-mm in depth +2: 4-mm in depth, lasting up to 15 seconds +3: 6-mm, lasting up to 60 seconds +4: 8-mm, lasting longer than 60 seconds 61. Communicable disease: patient assignment Per Dunn Who would you isolate? Who would you not allow in a room with someone who has a communicable disease (ie. kids, elderly, immunocompromised, pregnant) Who can you delegate these patients to? 62. Chest pain: pharmacotherapy Administer medications as prescribed Vasodilators (nitro) Analgesics (morphine) Beta Blockers (-olol) Thrombolytic agents, only if given within first 6 hours Antiplatelet agents (aspirin) Anticoagulants (heparin)

Glycoprotein IIB/IIIA inhibitors 63. Hypovolemia: PA Thready pulse, poor capillary refill, hypotension, decreased UO, dizziness (orthostasis), cool skin, pallor 64. DKA: pharmacotherapy (SATA) Isotonic fluid replacement IV regular insulin IV Sodium-bicarbonate for severe acidosis 65. Immune dysfunction: pathophysiology (SATA) 66. Immune suppression: NCP (SATA) 67. PE: NCP (SATA) Assess and monitor respiratory status Administer O2, place in high-fowlers, collect and interpret ABGs Assess and monitor cardiovascular status Assess and monitor pain Initiate and maintain IV access Administer meds as prescribed Anticoagulants Fibrinolytic therapy Provide education for treatment and prevention of PE Avoid long periods of immobility, monitor intake of foods high in vitamin K, adhere to and schedule for monitoring of PT and INR Provide emotional support Surgical management Embolectomy and/or insertion of filter in the vena cava 68. Thrombocytopenia: RID (SATA)

Definition: decrease in circulating platelets Disorders that involve low production of platelets in the bone marrow include:
y y y y y y y

Aplastic anemia Cancer in the bone marrow Cirrhosis (chronic liver disease) Folate deficiency Infections in the bone marrow (very rare) Myelodysplasia Vitamin B12 deficiency

Use of certain drugs may also lead to a low production of platelets in the bone marrow (heparin, NSAIDs, histamine blockers, most chemo agents, allopurinol and alcohol) Disorders that involve the breakdown of platelets include:
y y y y y y

Disseminated intravascular coagulation (DIC) Drug-induced nonimmune thrombocytopenia Drug-induced immune thrombocytopenia Hypersplenism Immune thrombocytopenic purpura (ITP) Thrombotic thrombocytopenic purpura

69. Hypothyroidism: PA (SATA) Early S+S: weakness, fatigue; intolerance to cold, decreased bowel motility, weight gain, joint and/or muscle pain, brittle thinning hair, thin brittle fingernails, pale skin, depression Late S+S: slow thought processes and speech, thickening of skin, thinning eyebrows, dry flakey skin, swelling in hands and feet, decreased acuity of taste and smell, hoarse raspy speech, abnormal menstrual periods, decreased libido 70. Shock: pathophysiology decreased CO, vasodilation (decreased BP), decreased venous return, decreased stroke volume 71-75: Med Math