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2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct., Exams of Nursing

2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct.

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Download 2025-2026 Pathophysiology Final NUR 2063 final exam all 187 solutions correct. and more Exams Nursing in PDF only on Docsity!

2063 final exam all 187 solutions correct.

2025 - 2026 Pathophysiology Final NUR

2063 final exam all 187 solutions correct.

Gastritis and Etiology and patho - ANSWER-inflammation of stomach's mucolas lining (can involve entire stomach or region) can be acute or chronic.

may be caused by h. pylori infection (imbeds in mucosal layer activating toxins and enzymes that cause inflammation. NSAIDS, chronic alcohol consumption, stress, trauma, burns, or infections, autoimmune conditions

manifestations of gastritis - ANSWER-indigestion, heartburn, epigastric pain, abdominal cramping, nausea, vomiting, anorexia, fever, malaise.

hematemesis and dark, tarry stools indicate ulceration and bleeding. chronic gastritis increases risk for peptic ulcers, gastric cancer, anemia, and hemorrhage.

gastritis diagnosis/treatment - ANSWER-h&p, GI tract x ray, egd, serum h. pylori antibodies, h. pylori breath test, stool analysis (h. pylori and occult blood

treatment-acute is self limiting ususally resolves

meds-antacids, acid-reducing agents, and mucosal barrier agents

other strategies include those for GERD (diet, small meals, antacids)

Peptic ulcer disease (PUD) - ANSWER-refers to erosive lesions affecting the muscularis mucosa of the stomach or duodenum. ulcers vary in size and severity, ranging from superficial erosions to complete penetration through GI tract wall

peptic ulcer disease etiology and patho - ANSWER-ETIOLOGY: most commonly H. pylori and NSAID use.

PATHO: develops because of an imbalance between destructive forces and protective mechanisms

PUD duodenal ulcers - ANSWER-most commonly associated with excessive acid or H. pylori infections

typically present with epigastric pain relieved in the presence of food

2063 final exam all 187 solutions correct.

PUD gastric ulcers - ANSWER-less frequent-more deadly

typically associated with malignancy and NSAIDS

pain worsens with eating

PUD Stress ulcers - ANSWER-develop because of major physiological stressor on body due to local tissue ischemia, tissue acidosis, bile salts entering stomach, and decreased GI motility

most frequently develop in stomach; multiple ulcers can form within hours of the precipitating event

often hemorrhage is the first indication (vomiting blood or blood in stool)

PUD manifestations/treatment - ANSWER-epigastric, abd. pain, abd. cramping, heartburn, indigestion, chest pain, nausea/voimiting, melena (dark, tarry stools), fatigue, unexplained weight loss

Treatment: same as gastritis: antacids, mucosal barrier agents, acid-reducing agents

possible surgical repair

Iron-deficiency Anemia - ANSWER-Not enough iron for hemoglobin production

erythrocytes pale and small

Etiology: decreased iron consumption/absorption, increased bleeding

manifestations in addition to "anemia": brittle nails, headache/irritability, pica, cyanosis of sclera of eyes, delayed healing

Anemia - ANSWER-common acquired or inherited disorder of erythrocytes that impairs the bloods oxygen-carrying capacity.

ETIOLOGY: decrease in # of circulating erythrocytes, reduction in hemoglobin content, presence of abnormal hemoglobin

MANIFESTATIONS: weakness, fatigue, pallor, syncope, dyspnea, tachycardia

Pernicious anemia - ANSWER-B12 deficiency or megaloblastic anemia

large, immature erythrocytes.

usually lack of intrinsic factor (protein necessary for b12 absorption in stomach)

2063 final exam all 187 solutions correct.

b12 is needed for cell division and maturity.

too little b12 gradually causes neuro problems because of the breakdown in myelin, neuro effects may be seen before anemia is diagnosed.

Additional manifestations: bleeding gums, diarrhea, impaired smell, DTR loss, anorexia, personality/memory changes, + babinski sign, stomatitis, paresthesia of hands and feet, unsteady gait

aplastic anemia - ANSWER-bone marrow fails to make enough blood cells leading to pancytopenia

MANIFESTATIONS: general anemia, leukcytopenia, and recurrent infections

can be caused by cancers, cancer treatment, pesticides

Sickle cell anemia - ANSWER-genetic, hemoglobin-s trait vs. gene

crescent shape during times of hypoxia, can clump together and clog vessels.

MANIFESTATIONS: swelling in hands and feet, sickle cell crisis, abd. pain, bone pain, jaundice, skin ulcers, stroke, chest pain

tissue ischemia and necrosis.

electrophoresis and stem cell transplant may cure

thalassemia - ANSWER-genetic, not RBC problem, hemoglobin problem. lack one or 2 proteins that make up hemoglobin

MANIFESTATIONS: heart failure, splenomegaly, hepatomegaly, bone deformities, jaundice, fatigue, dyspnea

Idiopathic thrombocytopenia purpura (ITP) - ANSWER-hypocoagulopathy due to immune system destroying its own platelets (autoantibodies) Circulating IgG reacts with the platelets which are then destroyed in the spleen and liver.

can be acute or chronic

ETIOLOGY: idiopathic, autoimmune disease, live vaccines, immunodeficiency disorders, viral infections

Manifestations: abnormal bleeding (petechiae, epistaxis [nose bleed], hematuria)

ACUTE TREATMENT: glucocorticoid steroids, immunoglobulins, plasmapheresis and platelet pheresis

CHRONIC TREATMENT: splenectomy, blood transfusions, immunosuppressants

2063 final exam all 187 solutions correct.

Thrombotic thrombocytopenia purpura - ANSWER-coagulation disorter d/t deficiency of enzyme responsible for cleaving von Willebrand factor

increased clotting which decreases available platelets --> bleeding under skin and purple colored spots called "purpura"

manifestations: thrombi>thrombocytopenia>bleeding

purpura, LOC changes, confusion, fatigue, fever

Thrombocytopenia - ANSWER-a condition in which there is an abnormally small number of platelets circulating in the blood

hemostasis - ANSWER-stoppage of bleeding

  1. vasospasm (vasoconstriction)-brief reflex blood vessel narrows to decrease blood flow to injury and increase bp
  2. platelet plug formation-involves activation, aggregation, and adherence of platelets into a plug that serves as a barrier against blood flowing out of vessel.

3 coagulation-or clotting changes blood into gel through cascade of events. fibrin mesh is cleaved from fibrinogen. fibrin acts like glue during clot formation holding the platelet plug together. Once blood flow is stopped tissue repair can begin

parathyroid hormone (PTH) - ANSWER-Works in opposite way to calcitonin to regulate serum calcium levels. PTH secreted with Ca levels drop. PTH increases osteoclast activity which releases Ca from bone. Also increases absorption of Ca in GI tract and kidneys. PTH also regulates phosphate levels by reducing renal reabsorption of phosphate in proximal tubule and increasing the uptake from the intestines and bones into blood

hyperparathyroidism and etiology - ANSWER-condition of excessive PTH production by parathyroid glands

causes: tumors, hyperplasia, chronic hypocalcemia (renal failure)

2063 final exam all 187 solutions correct.

hyperparathyroidism manifestations/treatment - ANSWER-osteoporosis, renal calculi, polyuria, abd. pain, constipation, fatigue, weakness, flaccid muscles, dysrhythmias, hypertension, depression, forgetfulness,

Cushing's syndrome - ANSWER-excessive cortisol that results from the increased ACTH levels

Cushing's syndrome etiology - ANSWER-iatrogenic from ingestion of glucocorticoid meds, adrenal tumors that secrete glucocorticoids, pituitary tumors that secrete ACTH and cortisol, and paraneoplastic syndrome (rare disorders triggered by abnormal immune response to a cancerous tumor called neoplasm)

Cushing's syndrome treatment - ANSWER-gradual tapering of any glucocorticoids

tumors may need surgery and radiation

meds to control cortisol production

interventions to manage complications

Cushing's manifestations - ANSWER-moon face, obesity, buffalo hump, muscle weakness/wasting, delayed growth, acne, broad purple striae, thin bruisable skin, delayed healing, hyperpigmentation (due to ACTH), increased infections, osteoporosis, hirsutism (abnormail hair growth), glucose intolerance, hypertension, dyslipidemia, edema, hypokalemia, mood changes

Growth Hormone (GH) - ANSWER-stimulates cell growth and fat breakdown. primary targets are muscle and bone, where GH stimulates amino acid uptake and protein synthesis.

Anterior Pituitary gland

Type 1 diabetes mellitus, etiology - ANSWER-develops when body's immune system destroys pancreatic beta cells.

etiology-unknown, most likely viral or environmental trigger in genetically susceptible people.

manifestations of diabetes mellitus - ANSWER-polyuria, polydipsia, polyphagia

hyperglycemia, glucosuria, weight loss, blurred vision, fatigue

2063 final exam all 187 solutions correct.

hypoglycemia manifestations - ANSWER-weak, double or blurred vision, hunger, tachycardia, palpitations

hyperglycemia manifestations - ANSWER--urinary frequency, anorexia, dry mouth

long term complications of diabetes mellitus - ANSWER-hyperglycemia, DKA, hypoglycemia, heart disease, stroke, HTN, diabetic retinopathy, blindness, kidney disease, amputations, periodontal disease, preg complications, increase susceptibility to infections, erectile dysfunction.

high blood glucose can harden vasculature

Type 2 diabetes causes - ANSWER-starts out as insulin resistance. ofter overweight

treatment for diabetes mellitus - ANSWER-Type 1

Insulin therapy

Type 2

Lifestyle changes

Oral drug therapy

Insulin when the above no longer provide glycemic control

Diabetes insipidus etiology - ANSWER--almost half of the cases are idiopathic

-The other half are usually attributed to head trauma resulting in damage to the pituitary gland or hypothalamus

-Causes insufficient secretion of antidiuretic hormone (ADH)

-This allows excessive water to be excreted by the kidneys

Addisonian crisis/adrenal crisis - ANSWER-onset of severe symptoms usually triggered by acute infection, trauma, surgery, or sodium loss.

2063 final exam all 187 solutions correct.

manifestations: profound fatigue, dehydration, vascular collapse (decreased BP), renal shut down, decreased serum Na, increased serum K

Hyperthyroidism etiology - ANSWER-excessive iodine, graves disease (autoimmune stimulates thyroid hormone production), thyroid tumors nonmalignant, goiter, inflammation, thyroid hormone replacement meds, high levesls of serum human chorionic gonadotropin

hyperthyroidism manifestations and treatment - ANSWER-sudden weight loss, tachycardia, dysrhythmias, hypertension, increased appetite, nervousness/anxiety, diff. concentrating, tremor, diaphoresis, increased sensitivity to heat, diarrhea, goiter, exophthalmos

thyroid storm - ANSWER-a relatively rare, life-threatening condition caused by exaggerated hyperthyroidism. fever, decreased mental alertness, abdominal pain

hypothyroidism etiology - ANSWER-iatrogenic, hashimotos

hypothyroidism manifestations and treatment - ANSWER-fatigue, sluggishness, pale dry skin, hoarseness, hypercholesterolemia, myalgia, weakness, brittle fingernails, bradycardia, hypotension, constipation, depression, goiter

increased TSH, low t3 and t

hormones to treat-levothyroxine

stress hormones - ANSWER-Epinephrine and norepinephrine, secreted as part of the reaction of the nervous system to stress.

hormones that increase glucose - ANSWER-glucagon, epinephrine, growth hormones, cortisol

stress response - ANSWER-bodys effort to restore balance, damaging when repeatedly activated.

fight or flight, epinephrine, norepinephrine, cortisol

2063 final exam all 187 solutions correct.

tumor staging - ANSWER-T-tumor

N-nodes involved

M-metastasis

staging-location and patterns of spread, size, extent, lymph node and organ involvement, distant metastsis

Malignant tumors - ANSWER-can kill host

confirmed by invasive or metastasizing nature

tissue specific differentiation (does not closely resemble tissue of origin)

grows rapidly, established blood supply (angiogenesis)

may initiate tumor vessel growth

frequently necrotic

dysfunctional-invade and overrun neighbors, gain ability to migrate

Benign tumors - ANSWER-can be life threatening because of area or size

does not invade adjacent tissue or spread

many are encapsulated

more closely resemble original tissue type

slower growing

little vascularity

rarely necrotic

often retains original function

tumor grading (staging-tnm) - ANSWER-grading

histological characterization of tumor cells

degree of anaplasia

3 or 4 classes of increasing degrees of malignancy

greater degree of anaplasia=greated degree of malignant potential

2063 final exam all 187 solutions correct.

inflammatory response-innate defese - ANSWER-triggered by damate/trauma to body tissue

erythema, edema, heat, pain

leukocytes line vessels walls and migrate to interstitial space

phagocytosis begins

fibrinogen > fibrin which walls area of injury and contains foreigh substances

new cells formed as healing process begins

innate defenses - ANSWER-physical and chemical barriers

skin/mucous membrane

bacteriostatic layer on skin

hydrochloric acid in stomach

ters and saliva lysozyme (disolves bacteral cell walls)

inlammation

pyrogens-released by macrophages, travel to hypothal. cause fever

interferons-interefere with spread of viral spread-cells last dying protection

complement proteins-membrane attack complex, embeds in bacteria and allows water inflow and lysis. also stimulate vasodilation, increase cas. permeability, promote phagocytosis

adaptive (acquired defenses) - ANSWER-immune system, cellular and humoral

Cellular immunity - ANSWER-T cells produced in bone marrow, mature in thymus.

regular cells :

helper t cells activate b cells to produce antibodies

supressor t cells turn it off

Effector cells (killer cells/cytotoxic cells):

destroy infected cells by degrading cell walls

2063 final exam all 187 solutions correct.

humoral immunity - ANSWER-B cells mature in marrow-become memory cells or immunoglobulin secreting antibody cells

Each B cell has receptor for antigen

antibody-producing cells:

quicker response on subsequent exposure because memory cells recall antigen as foreign and response is quicker (acquired immunity)

capillary hydrostatic pressure - ANSWER-outward push of vascular fluid against capillary walls

interstitial fluid colloid osmotic pressure - ANSWER-inward-pulling force of particles in the interstitial fluid

antidiuretic hormone (ADH) - ANSWER-tap water hormone=kidneys reabsorb plain water

released from pituitary gland

secreted in response to increased osmolality of ECF, decreased circ. blood volume, pain, nausea, stress

ETOH (alcohol) decreased ADH release-promotes diuresis

Aldosterone - ANSWER-salt water hormone

secreted in response to decreased circulating blood volume and in response to hyperkalemia

kidneys reabsorb Na+ water; expands extracellular fluid volume, decreased urine volume

Natriuretic peptides (ANP and BNP) - ANSWER-stored in cardiac cells, released when tissue is streched from increased vascular volume

promotes Na secretion in urine

opposite action of aldosterone, not as strong

Normal serum Na+ - ANSWER-135-145 mEq/L

2063 final exam all 187 solutions correct.

Hyponatremia and causes - ANSWER-<135 mEq/L, ECF has too much water from amount of sodium ions present, more dillute than normal

Excessive ADH (SIADH)

excessive intake of hypotonic solution, causes cells to swell

diuretic use, GI losses, sweating, adrenal insufficiency, dietary sodium restrictions

excessive water, hyperlycemia (excess glucose in blood attracts water from the intracellular and interstitial spaces), excessive water ingestion, renal failure, heart failure

Hyponatremia manifestations - ANSWER-Mild: malaise, anorexia, nausea, vomiting, headache

Severe: confusion, lethargy, seizures, coma, fatal cerebral herniation

poor skin tugor, dry mucous membranes, BP changes, pulse changes, edema, headache, diminished DTRs, muscle weakness

treatment for Hyponatremia - ANSWER-treat underlying cause

restricting water, increase sodium, administering corticosteroids for addison's disease

Correction of sodium leves done slowly to not overload heard from fluid shifting into the intravascular space. Seizure precautions, neuro checks

Hypernatremia causes - ANSWER->145 mEq/L

ECF contains too little water from amt of sodium present, cells shrivel. also called water deficit, hypertonic syndrome, hyperosmolality

causes:

inadequate water intake or excess excretion

concentrated tube feedings

hypertonic saline infusion

loss of more water that salt: osmotic diuresis, diabetes insipidus

2063 final exam all 187 solutions correct.

Hypernatremia manifestions - ANSWER-mild: thirst, oliguria, confusion, lethargy

severe: seizures, coma, death

increased temp, warm flushed skin, dry and sticky mucous membranes, dysphagia, weak/thready pulse

edema

hypernatremia treatment - ANSWER-underlying cause. replace water and remedy electrolyte deficits. glucose-electrolyte solutions.

IV hypotonic solutions.

don't want to do too rapid because of cerebral edema

neuro checks

Normal potassium K levels - ANSWER-3.5-5 mEq/L

most potassium is inside cell

hypokalemia causes - ANSWER-decreased intake

shift into cell (insulin administration)

increased excretion, usually renal

v/d, ng suction, fistulas, laxatives, diuretics, cushing syndrome (decreases sodium excretion, with increases potassium excretion)

corticosteroids

alkalosis-decreased serum hydrogen causes potassium to shift into cells

hypokalemia symptoms - ANSWER-cardiac:

ectopic beats, alteration in conduction, dysrhythmias, cardiac arrest

abdominal symptoms:

distension, diminished bowel sounds, paralytic ileus

Muscle symptoms:

2063 final exam all 187 solutions correct.

bilateral muscle weakness, respiratory paralysis

hypotension, paresthisa, hyporeflexia,

hyperkalemia causes - ANSWER-deficient excretion: renal failure, addison's disease, excessive intake, increased release from cells with acidosis, burns

hyperkalemia manifestations - ANSWER-intestinal cramping, diarrhea

muscle weakness

cardiac dysrhythmias or cardiac arrest

hyperkalemia treatment - ANSWER-underlying cause prior to treating hyperkalemia.

calcium gluconate to minimize dysrhythmias

decrease K+ intake

kayexalate IVF

potassium-losing diuretics, dialysis

insulin infustion with glucose-containing IVF

Normal serum calcium range - ANSWER-8.6-10.2 mg/dL

or 4-5 mEq/L

Hypocalcemia causes - ANSWER-decreased intake or absorping/lack of Vitamin D

decreased physiologc availability-excessive phosphate, hypoparathyroidism

increased excretion: steatorrhea and pancreatitis (Ca+ binds to fat and excreted in feces

hypoparathyroidism, renal failure, hyperphosphatemia, hypomagnesemia, alkalosis, pancreatitis, calcitonin,

2063 final exam all 187 solutions correct.

hypocalcemia manifestations - ANSWER-decreases the threshold potential, causing hyperexcitability of neuromuscular cells

positve trousseau and chvostek sign

paresthesias, twitching/cramping, tetany, laryngospasm, hyperactive reflexes, siezures, cardiac dysrhythmias or heart failure

hypocalcemia treatment - ANSWER-underlying cause, oral supplement, IV calcium gluconate, Vitamin D supplements, limit phosphorus intake

hypercalcemia causes - ANSWER-increased intake or absorption, shift from bone to ECF- hyperparathyroidism, immobilization, bone tumors

hypercalcemia manifestations - ANSWER-muscle weakness, diminished reflexes, cardiac dysrhythmias

anorexia, nausea, emesis, fatigue, polyuria, constipation, headache, personality changes, renal calculi, pathologic fractures

hypercalcemia treatment - ANSWER-treat underlying cause.

manage dysrhythmias

oral phosphate

increase mobility

calcitonin

IVF

diuretics

Normal Serum magnesium levels - ANSWER-1.8-2.4 mEq/L

magnesium ions present in bound and unbound ionized forms

hypomagnesemia cuases - ANSWER-decreased intake/absorption: chronic alcoholism, malnutriton, diarrhea

2063 final exam all 187 solutions correct.

excessive excretion

hypomagnesemia manifestations - ANSWER-insomnia, hyperactive reflexes, muscle cramps, twitching, grimacing, positive Chvostek and Trousseau sign

nystagmus, dysphagia, ataxia, tetany, seizures, cardiac dysrhythmias

hypomagnesemia treatment - ANSWER-moral Mg++ supplements, IV Mg++, treat underlying cause

hypermagnesemia causes - ANSWER-increased intake/absorption: laxitives, antacids

decreased magnesium excretion: oliguric renal failure, adrenal insufficiency

hypermagnesemia manifestations - ANSWER-depression of neuromuscular function related to decreased release of acetylcholine at neuromuscular junctions

decreased DTRs

lethargy

hypotension

flushing

diaphoresis

drowsiness, flaccid paralysis, respiratory depression, bradycardia, cardiac dysrhythmias, cardia arrest

hypermagnesemia treatment - ANSWER-underlying cause, diuretics, hypotonic IVF dialysis IV calcium

neutrophils - ANSWER-A type of white blood cell that engulfs invading microbes and contributes to the nonspecific defenses of the body against disease.

Types of WBCs - ANSWER-monocyte-"clean up crew" remove debris

lymphocytes- B and T cells-live for years. immune protection

2063 final exam all 187 solutions correct.

Eosinophils-destroy/attack parasites, present in allergic responses. phagocytizes ANTIGEN-antibody complex

basophil-release histamine during inflammation (potent vasodilator)

Neutrophils-engulf bacteria, live 5-90 hours

RBCs function - ANSWER-transport oxygen and carbon dioxide

anemia - ANSWER-acquired or inherited, impairs bloods oxygen-carrying capacity. can result from

  1. a decrease in number of circulating erythrocytes

  2. a reduction in hemoglobin content

  3. presence of abnormal hemoglobin

anemia manifestations - ANSWER-weakness, fatigue, pallor, syncope, dyspnea, tachycardia

polycythemia vera - ANSWER-bone marrow produces too many blood cells >increase blood volume and viscosity > vessels distend and flow is sluggish

Complications: ischemia/necrosis, thrombosis, hypertension, heart failure

Manifestations: cyanotic or reddish skin, HTN, tachycardia, dyspnea, headaches, visual abnormalities

cause unknown. chemo and radiation sometimes

management of clotting and bleeding is key

Rheumatoid Arthritis (RA) - ANSWER-autoimmune-inflammatory response-immune cells attack tissue of joint, result in erosion, cyst, deformity

Classic presentation-bilateral symmetric polyarthritis involving small joints, malaise, fatigue, and diffuse musculoskeletal pain

2063 final exam all 187 solutions correct.

treatments: NSAIDS, corticosteroids, biological agents,

diease-modifying antirheumatic drugs (DMARDS), rest with regualr activity. alternate heat/ice. splints, braces, assistimve devices

Osetoarthritis - ANSWER-Overuse, local degenerative, not inflammatory but causes inflammation to surrounding tissues. aging, post menopausal, weat bearing joints most affected (knees, shoulders)

localized joint pain and crepitus, often unilateral, bony enlargement-heberden and bouchard nodes

morning joint stiffness

limited ROM

Treatment-physical therapy, rest, ice, topical agents, NSAIDS, weight reduction, hip/knee surgery

muscular dystrophy MD - ANSWER-genetically determined myopathies

progressive muscle weakness and deegeneration.

dystrophin causes muscle dysfunction, weakness, fiber loss and inflammation

Manifestations: intellectual disability, muscle weakness leads to hypotonia, muscle spasms, delayed development/motorskills/ poor cordination

calf elargement, falling

Treatment: muscle relaxers, immunosuppressants, corticosteroid therapy

preservation of function, ROM/PT

Assistive devices

osteoporosis etiology - ANSWER-progressive loss of bone calcium leaves bones brittle

risks: soda, caffeine, low intake of vitamin D, Hx gastrectomy or bypass. smoking, excessive etoh, certain meds, post menopausal

2063 final exam all 187 solutions correct.

manifestations of osteoporosis and treatment - ANSWER-osteopenia

bone pain/tenderness, fractures w/ little to no trauma, low back pain or neck pain, kyphosis, height reduction

biphosphanates to help stop breaking down

5 P's of compartment syndrome - ANSWER-pain, pulse, pallor, paresthesia, paralysis

increased pressure within compartment-fascia- restricts blood flow, circulation to tissue and nerves. extreme bleeding or swelling.

fasciotomy to relieve pressure

Gout - ANSWER-inherited disorder in which disturbance of uric acid metabolism leads to deposits of urate salts in articular, periarticular, and subcutaneous tissue

gout manifestations - ANSWER-inlammation and accumulation of tophi in bony and connective tissue, red, swollen, very tender to palpation, uric acid calculi (kidney stones)

causes of gout - ANSWER-high purine foods, alcohol, acute illness

avoid red meat, turkey

stress urinary incontinence (SUI) - ANSWER-occurs when urine involuntary loss

increases in intraabdominal pressure

weakening of pelvic muscles or intrinsic urethra sphincter deficiency

Urgency urinary incontinence (UUI) - ANSWER-involuntary leakage of urine accompanied by a sudden urgency to have to go to the bathroom

2063 final exam all 187 solutions correct.

result of overactive detrusor muscle

may be idiopathic, because of bladder infection, radiation therapy, tumors, stones, or CNS damage

neurogenic bladder - ANSWER-a urinary problem caused by interference with the normal nerve pathways associated with urination

cystitis - ANSWER-inflammation of the bladder, UTIs are common cause. or could be irritant. Same treatment as UTI unless not from infection

Acute pyelonephritis - ANSWER-infection of 1 or both kidneys. most common ascending UTI. obstruction or urethral reflux allows contaminated urine to enter kidney. usually involves renal tubules, pelvis, or calices; inflammation and edema, exudate > compress renal artery > accesses, infection, necrosis

Manifestations: CVA tenderness with fever, chills, dysuria urgency, frequency

n/v, anorexia

urosepsis

Nephrolithiasis (Kidney Stones) - ANSWER-hard masses of crystals compoased of minerals that the kidneys would normally excrete

generally form in renal pelvis, ureters and bladder

most commonly made of calcium with oxalate or phosphate

supersaturation of urine-stay hydrated

manifestaions: renal colic/flank pain radiates down back/groin, bloody/cloudy/foul-smelling urine

dysruia, frequency, genital discharge, n/v, fever and chills

filter urine, extracorporeal shock wave lithotripsy

percutaneous nephrolithotomy, ureterscopy, surgical removal

Bladder cancer - ANSWER-inner lining of bladder transitional cells

2063 final exam all 187 solutions correct.

smoking, aging caucasian men, exposure to chemicals, frequent UTIs, long term cath placement, previous chemo or radiation

manifestations: hematuria, dark/rusty or brown urine, frequency, dysuria, urge incontinence, UTIs, abd. or back pain

polycystic kidney disease PKD - ANSWER-inherited disorder

numerous grape-like clusters of fluid-filled cysts in both kidneys

cysts enlarge kidneys while compressing and eventually replacing the functional kidney tissue

manifestations of PKD - ANSWER-potter facies -pronounced epicanthic folds (skin folds at the corner of eyes on either side of nose), pointed nose, small shin, floppy, low-set ears

large, bilateral symmetrical masses on the flanks

respiratory distress (fluid accumulation from renal impairment)

uremia

HTN, lumbar pain, swollen, tender abdomen, hematuria, nocturia, drowsiness

chronic kidney disease CKD - ANSWER-permanent loss of functional nephrons

CKD-> chronic renal failure (CRF) -> end-stage renal disease (ESRD) which requires dialysis

CKD risk factors - ANSWER-diabetes, HTN, recurrent pyelonephritis, urine obstructions, glomerulonephritis, PKD, sickle cell disease, lupus, fam. history of CKD

CKD manifestations - ANSWER-systemic

hypertension, polyuria with pale urine, oliguria or anuria with dark-colored urine, anemia, bruising and bleeding, electrolyte impalances especially hyperkalemia, hypocalcemia, hypomagnesemia, hyperphosphatemia, muscle twitches/cramps, pericardidits, heart failure, resp. distress, edema, weight changes, malaise, flank pain, jaundice, pruritis

Chronic kidney disease treatment - ANSWER-stop or slow progression, underlying cause.

2063 final exam all 187 solutions correct.

CKD findings - ANSWER-decreased kidney function eGFR<60 mL/min/1.73 m2 for 3+ months

renal sonogram showing small kidney

severe anemia, hyperphosphatemia and hypocalcemia, subperiosteol erosions on radiography, fatigue, nausea, pruitis, nocturia, hypertension

Phases of acute tubular necrosis - ANSWER-prodromal phase: injury/damage has occured, normal or decreased urinary output, increased BUN and Cr

Oliguric: oliguria, anuria, volume overload, hyperkalemia, azotemia/uremia, metabolic acidosis

postoliguric phase: fluid volume deficit, labs begin to normalize

prerenal kidney injury causes - ANSWER-due to conditions that diminish kidney perfusion, happens BEFORE kidney

hypovolemia, hypotension, heart failure

renal artery obstruction

fever/vomiting/diarrhea

burns

overuse of diuretics

edema, ascites

drugs: ACE inhibitors, angiotensin II blockers, NSAIDS

Intrarenal kidney injury causes - ANSWER-affects kidney difectly. due to a primary dysfunction of the nephrons and the kidney itself

most commonly acute tubular necrosis (ATN)

may occur with glomerular inflammation, vascular clots, or interstitial etiolgoes (rhabdomyolysis)

ATN causes: nephrotoxic insult (contrast media)

ischemic insults (sepsis)

2063 final exam all 187 solutions correct.

Postrenal Kidney injury causes - ANSWER-obstruction within the urinary collecting system distal to the kidney, elevated pressure in Bowan capsule; impedes glomerular filtration

clinical findings based on duration of the obstruction

prolonged postrenal ARF leads to acute tubular necrosis (intrinsic) and if continues leads to irreversible kidney damage

Define amenorrhea - ANSWER-absence or suppression of menstruation (after age 16)

Causes for amenorrhea - ANSWER-hormonal disturbances (most common)

stress

sudden weight loss/extreme reduction in fat

anemia

neoplasms (ovarian, adrenal, pituitary tumors); chemo

treatment of amenorrhea - ANSWER-aimed at underlying cause

hormonal supplementation

surgery (tumor removal)

Syphilis etiology - ANSWER-spirocete bacterium Treponema pallidum

transmitted through skin or mucous membrane contact with infected/ulcerative lesion (chancre) and through placental transfer after 4 months

causes inflammation and fibrosis of vascular tissue systemically

Syphilis manifestations - ANSWER-primary-formation of chancre after 2-3 weeks

secondary-2-3 weeks after chancre forms, generalized, non-pruritic brown-red rash, low grade fever, malaise, patchy hair loss, sore throat, headache, lymphadenopathy

latent/tertiary phase: 2/3 asymptomatic, positive serologic assay, contagious only during early part of this stage. can lead to blindness, paralysis, dementia,CVD, pathological fractures, death

2063 final exam all 187 solutions correct.

Syphylis treatment - ANSWER-penicillin G (first choice)

tetracycline

doxycycline

response to antibiotics monitored by repeating laboratory testing at regular intervals up to 24 months after therapy

Gonorrhea Etiology "the clap" - ANSWER-Neisseria gonorrhoeae

transferable through sexual contact and from mother to infant during birth.

Gonorrhea pathophysiology - ANSWER-infects epithelia of vagina, mouth, anus, pharynx, or conjunctivae causing irritation and inflammation. Bacterium attaches to epithelia, microvilli surround it and draw it into the surface of the mucosal cell.

Gonorrhea Complications - ANSWER-PID

epididymitis, prostatitis

infertility

neonatal conjunctivitis

ectopic pregnancy

can spread to other locations in the body causing arthritis, dermatitis

gonorrhea manifestations - ANSWER-often asymptomatic. 2-10 days after infection

dysruia, frequency, urgency

penile, vaginal, rectal discharge (while, yellow, or green)

penile, scrotal, rectal, or lower abdominal pain and tenderness

redness or edema at urinary meatus in men

postcoital bleeding, intermenstrual bleeding

pharyngitis

2063 final exam all 187 solutions correct.

white blisters that darken and disappear

gonorrhea treatment - ANSWER-combination of antibiotics. ceftriaxone (cephalosporin), azithromycin (Zithromax), doxycycline, or gemifloxacin (Factive)

screening of sexual partners

Cervical cancer etiology - ANSWER-almost all caused by HPV

detected by pap smear

manifestations of cervical cancer - ANSWER-continuous vaginal discharge, abnormal vaginal bleeding between menstruatuion, after intercourse, or after menopause, and menorrhagia

late leaking of urine or feces from vagina; bone fractures; unilateral lower extremity edema

treatment for cervical cancer - ANSWER-loop electrosurgical excision procedure (LEEP)

cryotherapy

laser therapy

chemo

radiation

surgery

breast cancer manifestations - ANSWER-asymptomatic; mass in the breast or axillary that is hard, has uneven edges, and is usually painless

change in size/shape/feel of breast or nipple

nipple drainage that may be bloody/clear/yellow/green/purulent

edema or pitting of the breast "peau d'Orange"

breast cancer treatment - ANSWER-chemo/radiation

surgery

2063 final exam all 187 solutions correct.

hormone therapy

coping and support interventions

testicular torsion etiology - ANSWER-twisted spermatic cord and blood vessels

can be brought on by trauma or after strenuous exercise or spontaneously

testicular torsion manifestations - ANSWER-sudden, severe testicular pain (usually unilateral) with or without a predisposing event.

scrotal edema

nausea, vomiting, dizziness, hematospermia and testicular mass

cremasteric reflex (testicular contraction when inner thigh stroked) usually absent on affected side

testicular torsion treatment - ANSWER-emergency

manual manipulation and surgery to untwist testis

"pex" secure untwisted testis to the scrotal wall

"pex" contralateral testis

Increased intracranial pressure (ICP) and etiology - ANSWER-increased volume in limited space of cranial cavity.

increased ICP can occur from TBI and other conditions that increase volume in skull (tumor, hydrocephalus, cerebral edema, and hemorrhage)

ICP - Monro-Kellie hypothesis - ANSWER-Normal ICP is 60-200 mm h20 or 4-15 mm Hg

any increase in volume must be compensated for by decrease in volume of another component

compensation primarily accomplished by shifts in CSF and blood volume as brain tissue volume remains relatively constant