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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.
Typology: Exams
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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
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)
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
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
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)
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
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.
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
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
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
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
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
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:
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,
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
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
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
a decrease in number of circulating erythrocytes
a reduction in hemoglobin content
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
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
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
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
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.
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)
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
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
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
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