3800 Final Exam LOs PDF

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3800 Learning Objectives Final Exam Reproductive Disorders (12 questions, 4 men/6 women/2 STI) 

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Define “cryptorchidism.” Describe 2 major complications. o Undescended testes directly related to low birth weight and gestational age, so screen pre-me’s and low birth weight babies  Increased risk of malignancy and infertility due to testes being exposed to heat inside the body  Placement of testes in scrotum required by 1 y/o Define “erectile dysfunction”. Name the most common causes, especially related to cardiovascular and diabetes. o Most common causes: anxiety, depression, stroke, spinal cord injury, neurologic disease, uncontrolled diabetes, hormonal changes, medications, street drugs, HTN o Marker for CV diseases in men, requires follow up for comorbidities o Lots of causes: any neuro/vascular changes Define “benign prostatic hypertrophy”. Name the clinical symptoms and possible complications. (HESI) o Common, age related, nonmalignant enlargement o s/s: weak urine stream, dribbling, frequency, nocturia, urinary retention o DRE and PSA test are diagnostic Know the risk factors for prostate cancer and name 2 recommended screening tests. o DRE and PSA are recommended screening tests o Similar s/s to BPH, or can be asymptomatic o Risk factors: aging, African American Define the pathophysiology of “endometriosis” o Endometrial tissue found outside uterus (in fallopian tubes, ovaries, pelvis, intestines…) o Multiple theories on how it gets there o Responds to menstrual cycle and causes a lot of pain; also bleeds like a period o Associated with infertility o Diagnosed with history, laproscopy o Treatment: medication, surgery Define “menometrorrhagia” and state its significance. o Heavy bleeding during and between periods Name the risk factors for breast cancer, including genetic mutations. o Risk factors: late child bearing, estrogen, BRCA 1 & 2, obesity (because fat cells produce estrogen), alcohol, smoking, heredity o Emphasis on clinical breast exam, also teach BSE o Mammography is only effective screening tool Define “menopause”. Name 3 conditions common to the post-menopausal woman, including risk for cardiovascular disease/MI. o No menses, decrease in estrogen, changes in bone health, cardiac and CAD risk  Because estrogen is protective against CAD o Insomnia irritability, depression o Vaginal dryness, dyspareunia

Diagnosis: 1 year of no menses, treat the symptoms (estrogen replacement no longer used due to cancer risk) State the most common cause of pelvic inflammatory disease (PID) o Infection of the upper reproductive tract with STI o Often starts with menstruation when cervix dilates and bacteria enter uterus, then fallopian tubes o Risk factors: < 25, not using condoms, new or multiple partners, pHx of PID Discuss the pathophysiology of polycystic ovarian disease o Too much male sex hormone (androgen) produced at ovary o Causes irregular periods, infertility, male hair growth, insulin resistance, acne, metabolic syndrome Know which STI that antibiotic ophthalmic ointment prevents in newborns. o Chlamydia, gonorrhea Know which STI has a classic “strawberry” appearance of the cervix. o Trichomoniasis Know which STI is caused by an overgrowth of yeast due to the use of antibiotic therapy. o Candidiasis o Also could be caused/exacerbated by changing hormones, BCPs, pregnancy, diabetes, immunosuppression Know which STI is the most common, can cause genital warts, can lead to cervical cancer, and which has a vaccine. o HPV o Gardasil 4 & 9, and bivalent cevarix o

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Musculoskeletal (12 questions) 

Differentiate types of fractures: especially oblique, comminuted, greenstick

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Know the stages of bone healing and goals of treatment. NOTE: Stages of bone healing may be worded slightly differently. Use these words: Hematoma, callous formation, ossification, remodeling.

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Describe nursing assessment of the neurovascular system to include the five “Ps”. Be able to apply to a clinical situation. o Pain – especially on passive motion o Pallor/cyanosis o Paresthesia – sensation of numbness/prickling/tingling o Paralysis o Pulseless-ness o Perform these assessments in any patient at risk for neurovascular compromises (surgery, cast, splint, traction)  Assess and document sensation, temperature, movement, cap refill, pulses, color, swelling of extremities  Early signs: pain, pallor, paresthesia  Late signs: paralysis, pulseless-ness Define the purpose of immobilization after a fracture. o The MAIN purpose is to prevent damage to blood vessels, nerves and soft tissues  Preserve/restore function by preventing pressure on nearby nerves/arteries o Hazards of immobility – DVT, atelectasis, pressure ulcers Differentiate a fracture caused by an injury from a pathologic fracture. Be able to apply. o Pathologic fracture – a fracture in a bone that is weakened by another disease process; not primarily due to an injury  Examples: inherited bone disease, bone cancer, infection, osteoporosis, compression fracture Identify and describe the functions of the musculoskeletal hormones – calcitonin, parathyroid hormone, and vitamin D. o Calcitonin – stimulates osteoblasts; increases calcium deposition in bones; released from thyroid gland o Parathormone – breaks down bones, stimulates osteoclasts; released from parathyroid o Vitamin D – calcium absorption; we get vitamin D from UV light and our diet

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 You have to have liver and kidney function to turn vitamin D into a usable form Describe the pathophysiology of osteoporosis o Simple explanation – rate of bone resorption exceeds the rate of bone formation Define osteomyelitis and its treatment. o Severe bone infection; involves soft marrow and soft tissue  Most commonly due to staph aureus  Acute or chronic (>1 month)  Fever, night sweats, malaise, bone pain  Swelling, tenderness, warmth at the site  Later may have purulent drainage from sinus tracts o May lead to bone ischemia/necrosis which is irreversible o Pathophysiology of osteomyelitis  Indirect injury – blunt trauma  Direct entry – open, pressure ulcer  WBCs release enzyme which lyses bone  Damaged bone has decreased blood supply so difficult to heal (natural and antibiotic)  Organisms sequester and bone can become necrotic – see purulent discharge at site  Can spread to brain or lungs o Clinical manifestations = fever, pain, poor incisional healing, wound drainage, pain on movement, loss of movement o Diagnosis = x-ray, CT/MRI, nuclear imaging, bone biopsy, if blood borne – C&S o Treatment = antibiotics, surgical intervention Describe the pathophysiology of compartment syndrome – symptoms and treatment. o Severe pain due to swelling and pressure (bleeding/inflammation) o Decreased sensation, skin pallor, increased cap refill time, tight/swollen/shiny skin o May lead to tissue death and nerve damage o Medical emergency! Differentiate between rheumatoid arthritis and osteoarthritis. (HESI) o Rheumatoid arthritis  Systemic inflammatory disease  Cause: uncertain, genetic predisposition (immunologically mediated trigger)  Affects small joints  Joints – stiff, swollen, tender, warm  Systemic – fever, weakness, fatigue, weight loss, thin skin, corneal ulcers, nodules, vasculitis  Exacerbations and remissions  BILATERAL o Osteoarthritis  Most common form of degenerative joint disease  Primary or secondary disorder  Localized, affects weight bearing joints  Degeneration of the articular cartilage and the subchondral bone of joints  Pain, aching  Pain worsens with use, relieved by rest  Crepitus and grinding

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Limited joint ROM; joint enlargement (new bone formation) NO CURE

Describe the pathophysiology of rhabdomyolysis (just the simple explanation – skeletal muscle break down leading to acute kidney injury). o An acute, sometimes fatal disease in which byproducts of skeletal muscle breakdown accumulate in the renal tubules (myoglobin, creatine kinase) o May result from: crush injuries, severe muscle strain/exertion toxic effect of drugs or chemicals on skeletal muscle sepsis, shock, or severe hyponatremia Describe the pathophysiology of gout (HESI). o Buildup of uric acid crystals in and around joints  Uric acid is a metabolic byproduct of nitrogen compounds (protein rich foods) o Decreased renal excretion (most common), increased production or increased intake of uric acid o Most common causing recurrent acute or chronic arthritis o Acute pain, tenderness, warmth, redness, swelling o Genetic and patients with metabolic syndrome at risk

Cardiovascular (9 questions) 

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Know modifiable and non-modifiable risk factors for atherosclerosis o Non-modifiable: increasing age, gender (male), family history of premature CAD, genetic disorder of lipid metabolism o Modifiable: cigarette smoking, HTN, hyperlipidemia with elevated LDL and low HDL, obesity, DM, decreased physical activity, stressful lifestyle Describe the pathophysiology of atherosclerosis. Which arterial layer is affected? o Stage 1: lipid accumulation and smooth muscle proliferation  Injury to ENDOTHELIAL LINING  Permeability is increased – smooth muscle cells enter the bloodstream  Body tries to repair damage using migration of inflammatory cells (monocytes)  Monocytes migrate into intima and transform into macrophages  Activated macrophages  Oxidize LDL  Ingest LDL – resulting in foam cells

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Foam cells are the primary component of atherosclerosis lesions – the “fatty streak” o Stage 2: fibrous plaque development  Plaque forms consisting of smooth muscle cells, macrophages, collagen and lipids  Covered by fibrous cap  As plaque grows, it occludes vessel lumen o Stage 3: complicated lesion – plaque rupture  Rupture, ulceration or erosion of cap may lead to  Hemorrhage into plaque  Platelet aggregation  Thrombotic occlusion of the vessel lumen  Leads to MI, CVA, or DVT Know the difference in LDL, HDL, VLDL & total cholesterol. Know normal values. o LDL – transports cholesterol from liver to artery walls, main carrier!  DEFINITELY contributes to atherosclerosis  < 130 or 70-100 in high risk people (INCEP)  < 100 mg/dL is optimal  100-129 is near optimal, acceptable in normal people but can be a concern for people with CAD  130-159 is borderline high  160-189 is very high o HDL – transports cholesterol from artery walls to liver for recycling  PROTECTIVE: reverses cholesterol transport; “good” cholesterol  > 45 (INCEP)  60 and above is considered protective against CAD  < 50 is a major risk for heart disease Know the action of the renin-angiotensin-aldosterone system. o Regulates salt/blood volume/blood pressure o INCREASES BP!

Define orthostatic hypotension. Who is most likely to have it? o When changing from lying or sitting to a standing position

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 Drop in systolic BP > 20 mmHg  OR drop in diastolic BP > 10 mmHg o Elderly are most likely to have it Know the risk factors and clinical signs of DVT and how to prevent? (HESI) o Venous thrombosis: blood clot attached to vessel wall (usually legs) o Major concern: PE!!! o Virchow’s triad  Venous stasis  Hypercoagulability  Vessel injury o s/s: tenderness, swelling, pain at site o Prevention  Compression stockings, blood thinners, avoid long periods of staying still, exercise! Describe the pathophysiology of acute myocardial infarction. (HESI) o Plaque ruptures and creates a hole, body tries to repair by clotting o Clotting blocks perfusion to myocardium o Conversion from aerobic to anaerobic metabolism o Striking loss of contractile function o Changes in cell structure – glycogen depletion and mitochondrial swelling o Irreversible cell death begins to occur 20-40 minutes of severe ischemia  Changes are reversible if blood flow is restored (TPA, PCI, CABG) o s/s: chest pain, rapid onset, “severe,” “crushing,” “discomfort”  May be accompanied by GI distress, N/V  Similar to angina but not relieved with rest/NTG  Women may present atypically; SOB/jaw/shoulder/epigastric/neck pain  Decreased blood supply may lead to SCD (sudden cardiac death) from ventricular dysrhythmias Differentiate clinical signs of stable angina from unstable angina and MI. Teach patient how to control stable angina. o Stable angina  Fixed clot obstructs blood flow  Has thick fibrous cap  Precipitated by the “3 E’s”  Exercise, emotions, eating  Also, exposure to cold weather  Pain relieved when O2 supply meets demand with rest or NTG  Patient sits up and leans forward relieves pain; 5-10 minutes  Pain begins slowly and worsens over the next few minutes o Unstable  Pain relieved only when blood clot is dissolved or removed  When a clot ruptures and has a thin fibrous cap over large lipid core  Causes platelet adhesion and thrombus formation  Most dangerous because can lead to MI, sudden cut off of blood supply to the heart Recognize that assessment of chest pain is a major priority. o Time is muscle

Sub-endocardial (non-STEMI) can turn into transmural (STEMI) if not treated and more irreversible damage can occur o Pericarditis, pleural chest pain: relieved when patient sits up and leans forward o Coronary disease:  Stable, pain is relieves when O2 supply meets demand (with rest) or NTG  Unstable, pain relieved when blood clot is dissolved or removed Differentiate a STEMI from a NONSTEMI. Which one represents damage of the entire wall thickness/partial wall thickness? o STEMI – ST elevated MI, acute injury, transmural MI (more dangerous – throughout entire muscle layer of heart = 0 electrical activity) o Non-STEMI – non-transmural, sub-endocardial MI, just the inner layer of the heart right below the endocardium (less dangerous but can cause complications) Know the meaning of elevated cardiac enzymes and which ones are significant. o Elevated Troponin – most specific for myocardial injury o Elevated CKMB o Elevated myoglobin o Elevated potassium – could cause cardiac dysrhythmias Describe the pathophysiology of heart failure and describe whether adaptive mechanisms are helpful in compensating. (HESI) Know the definition of systolic dysfunction in heart failure, defined by ejection fraction. o Systolic dysfunction – an excess volume state due to a weak ventricle o Systolic HF = EF < 40% o Ejection fraction – average percentage of blood ejected from the ventricle  Normal EF = > 60% Know the signs/symptoms of right sided heart failure and left sided heart failure. o Left heart failure – ischemia, MI, systemic HTN, valvular disorders (MS, MR, AS, AR), cardiomyopathy, anemia, thyroid disease  s/s: pulmonary edema, SOB, DOE, PND, orthopnea, crackles in lungs o Right heart failure – left heart failure (*most common*), valvular dysfunction (TS, TR, PS, PR), right sided MI, cardiomyopathy, pulmonary causes (pulmonary HTN, pneumonia, PE)  s/s: peripheral edema, weight gain, ascites, anorexia, JVD, hepatomegaly Describe the body’s response to hypovolemic shock. o Causes: external fluid losses (blood loss, plasma loss/burns, body fluid loss/n/v/d/diuresis) OR internal fluid shifts (hemorrhage, pooling of fluid/3 rd spacing/shift from intravascular to interstitial space) o Decreased intravascular volume, decreased venous return, decreased ventricular filling, decreased SV, decreased CO, decreased tissue perfusion o Hypovolemic shock – assessment findings  Hypotension  Tachycardia  Cool, clammy skin  Signs of hemorrhage and fluid loss  15-20% blood/fluid loss before hemodynamic instability – approximately 2 liters  Treated with replacement of fluid volume (IV/blood infusion)  Body’s SNS response: increased HR, contractility Recognize a normal sinus rhythm and a life-threatening rhythm (ventricular fibrillation) on an ECG. o

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Normal

Ventricular Fibrillation Hematology (4 questions) 

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Name the components of the CBC – especially RBC, HB and HCT and WBC -and their normal values. Relate to names of disorders of blood cells. o RBC: 3.6-5.4 o WBC: 4.4-11.3 o Platelets: 150-400 o Hemoglobin: 12-16.5 o Hematocrit: 37-50 Define “aplastic anemia” o Stem cells can’t grow and divide o Decrease in all cell components (decrease in RBC, WBC, platelets) o Also called pancytopenia Define “polycythemia” o RBC count is increased o From loss of fluids from the vascular space, disease of the bone marrow, or increased EPO from COPD, heart failure o Headache, backache, weakness, fatigue, HTN, joint pain, thrombosis Differentiate when the PT, INR and the PTT would be measured. Which one with heparin / warfarin? o PT: prothrombin time 9-12 seconds o INR: international normalized ratio, 1.5-2 times  Used to assess warfarin therapy o PTT: partial thromboplastin time 26-33 seconds  Used to assess heparin therapy

GI (7 questions)  

Know the most important common consequence of vomiting o Dehydration and loss of electrolytes State which class of drugs is used prophylactically in hospitalized patients to prevent stress ulcers. o Antacids: PPIs or H2 blocker typically used on ALL patients (ex. Pepcid, Zantac)

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Know the main cause and route of transmission of clostridium difficile enterocolitis. o Spore forming bacillus normally present in gut o Growth restricted by normal intestinal flora o Disruption of normal flora allows germination of spores with toxin production in gut o Toxins damage intestinal mucosa – diarrhea o Can lead to pseudomembranous colitis o Caused by BS antibiotics o Spread by contact Describe the role of the liver in the synthesis of clotting factors, bilirubin clearance, carbohydrate metabolism and conversion of ammonia to urea. o Liver functions: synthesis/storage of amino acids, proteins, vitamins, fats  Detoxification, blood circulation, filtration, bile drainage, BG regulation, makes proteins for blood clotting, synthesis of bile and bilirubin metabolism, carb metabolism, converts ammonia to urea Describe the clinical manifestations of liver failure. o Malnutrition/impaired glucose metabolism and protein synthesis o Hypoglycemia, insulin resistance, hypoalbuminemia o Edema/ascites o Bruising/bleeding (impaired clotting factors) o Jaundice/pruritus (impaired bile formation) o Portal hypertension (increased hydrostatic pressure, esophageal varices, splenomegaly) o Hepatic encephalopathy (ammonia buildup) Describe the pathophysiologic causes of hepatic encephalopathy, esophageal varices and ascites. o Hepatic encephalopathy – ammonia build up  Liver can’t detoxify substances and poisons built up in the bloodstream  Ammonia can build up and damage the nervous system – confusion/coma o Esophageal varices – abnormal veins on lower esophagus  Develop when blood flow from liver is blocked  From portal HTN and increased hydrostatic pressure  Due to cirrhosis as well o Ascites: edema of the abdomen  Due to decreased protein synthesis – hypoalbuminemia – third spacing of fluid and pressure from portal HTN  Caused by portal hypertension, decreased colloid osmotic pressure (hypoalbuminemia) and sodium retention by kidneys Discuss the relationship between decreased level of consciousness and ammonia levels in patients with liver failure. (HESI) Know the most common liver function tests. Know 2 common causes of liver cirrhosis. Define Laennec’s cirrhosis (HESI). Define jaundice and state 3 causes. Describe the pathophysiology and characteristics of pain in cholecystitis. (HESI) Name a common drug hidden in many OTC preparations which can be inadvertently overdosed and lead to liver failure.

Respiratory (5 questions)

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Recognize early clinical signs o...