CPR Exam #2 Flashcards
COPD: Chronic Bronchitis
3 months of chronic cough in a row, repeated over 2 years.
COPD: Emphysema
Persistent smoking elevates neutrophils and elastase levels. This leads to destruction of elastic fibers and the permanent dilation of alveoli. Alveoli no longer stretch.
Restrictive Lung Disease: Pulmonary Fibrosis
Excess buildup of connective tissue in the lungs.
Pulmonary Edema
Several causes: Increased capillary hydrostatic pressure (due to increased CVP), decreased capillary oncotic pressure malnourishment), increased alveolar surface tension (Hyaline membrane disease), reduced lymphatic drainage (obstruction).
Freshwater Drowning
Aspirating hypertonic solution, causing pulmonary edema. Cause of death is asphyxia.
Saltwater Drowning
Aspirating hypertonic solution, causing pulmonary edema. Cause of death asphyxia.
Carbon Monoxide Poisoning
Carbon monoxide inhalation forms carboxyhemoglobin which shifts the O2-Hb curve to the left, causing ischemic injury.
Sickle Cell Anemia (Hemoglobin S)
Autosomal recessive inheritance pattern. Caused by a mutation in beta-globin gene. Missense mutation, E6V.
Hemoglobin C Disease
Missense, E6K, on beta globin gene. Moves slowest toward anode on hemoglobin electrophoresis.
Alpha-Thalassemia
Deficiency in alpha-globin chain synthesis. Caused by a deletion caused by unequal crossing over during homologous recomb.
Hb Bart Hydrops Fetalis Syndrome
Most severe form of alpha-thalassemia. Hb Bart is the aggregation of four gamma chains into a tetramer, b/c no copies of alpha-globin.
Hemoglobin H Disease
alpha-thalassemia where 3 of 4 alpha-globin genes are deleted. This leads to the formation of HbH which is the formation of 4 beta-chains into a tetramer.
Beta-thalassemia Major (“Cooley’s Anemia” or “Mediterranean Anemia”)
A severe mutation in both beta-globin genes OR compound heterozygotes for B-o and B+ genes.
Beta-Thalassemia intermedia
One severe mutation on beta-globin gene and a less severe on the other gene, OR 2 less severe mutations.
Beta-Thalassemia Minor
Mostly heterozygotes-one normal and one mutant beta-globin.
Hemophilia A
Deficiency of Factor VIII, causing a defect in the intrinsic coagulation pathway. X-linked recessive inheritance.
Hemophilia B
Deficiency of Factor IX, causing a defect in the intrinsic coagulation pathway. X-linked recessive inheritance.
Pentavalent Arsenate Poisoning
Consumption or inhalation of pentavalent arsenate causes inhibition of glyceraldehyde 3 phosphate dehydrogenase.
Fluoride Poisoning
Consumption or inhalation of fluoride inhibits enolase.
Pyruvate Kinase Deficiency
Deficiency of pyruvate kinase causes a defect in glycolysis. RBCs only get ATP via glycolysis and will lyse if there is a defect in glycolytic pathway. Can’t maintain ionic gradients!
Lactic Acidosis
Observed in increased conversion of pyruvate to lactate, deficiency of pyruvate dehydrogenase, decreased blood supply to peripheral tissues resulting in anaerobic metabolism.
Hypoxemia
Too little oxygen in blood, resulting in hypoxia. Detrimental long-term effects include pulmonary hypertension, RV failure, and polycythemia.
Hydronephrosis
Obstruction of urinary tract system leads to the backing up of urine into the kidneys. Usually caused by stones. Accessory renal arteries can also cause.
Unilateral Renal Agenesis
Early degeneration of failure of formation of the ureteric bud. Left kidney is usually the absent one.
Bilateral Renal Agenesis
Early degeneration or failure of formation of the ureteric bud. Left kidney is usually the absent one.
Supernumerary Kidney
Very rare. If supernumerary kidney has its own separate ureter (rather than a bifid ureter), there were probably two separate ureteric buds on that side.
Horseshoe Kidney
Fusion of inferior poles of kidney while still in pelvis. Ascent of the horseshoe kidney is interrupted by the IMA.
Bifid Ureter
Due to early, incomplete division of the ureteric bud, a split ureter to a single kidney is formed.
Cross-fused Renal Ectopia
Left kidney fused with right kidney while in the pelvis and was then carried along with the ascent of the right kidney
Nephrolithiasis
Aggregates of calcium, phosphate, oxalate, urate, and other soluble salts form due to urine saturation.
Nutcracker Syndrome
Left renal vein gets compressed between the superior mesenteric artery and the aorta, shunting blood into the left gonadal vein, causing pain and edema in testicular region.
AD Polycystic Kidney Disease
Autosomal dominant. Usually presents in adults. Cysts develop slowly overtime. Due to defective polycystin.
AR Polycystic Kidney Disease
Autosomal recessive. Presents in infancy or childhood. Cysts are radially arranged, dilated CDs. Due to defective Fibrocystin.
Cystocele
Prolapse of the bladder into the vaginal canal. Common in multiparity, straining for bowel movements, violent coughing, heavy lifting, and obese women.
Acute Proliferative Glomerulonephritis (Post-Strep)
Granular deposits immune complexes on the glomerular basement membrane (IgG and complement), often following a streptococcal throat infection.
Membranous Nephropathy
Can be primary/idiopathic (most cases) or secondary (SLE, malignant tumors, or medications). Diffuse thickening of the glomerular capillary basement membrane by reactive deposition of add’l BM material, leading to “spikes” on the outer surface of the basement membrane.
Minimal change disease
Likely cell mediated immunity, causing effacement of the podocyte foot processes.
Diabetic Glomerulosclerosis
Occurs in diabetics. Glomerular basement membrane thickens, and mesangial matrix. Afferent/efferent arterioles hyalinize, leading to decreased blood flow to the glomerulus.
Acute Tubular Necrosis
Most common cause is acute ischemia due to hypotension. Also NSAIDS, iodine contrast agents, heavy metals, toxins, infections, ischemia/hypovolemic shock, and obstruction.
Acute Pyelonephritis
Acute suppurative bacterial infection of the renal interstitium and tubules, ascending from the lower urinary tract.
Chronic Pyelonephritis
Obstruction of the drainage system (pyelonephrosis), urinary reflux, and recurrent acute pyelonephritis leads to permanent scarring on the kidneys.
Chronic Renal Hypertension
Increased tension in renal vessel walls leads to hyalinization of the walls and reduction in the caliber of the vessel.
Acute vs. chronic renal failure
Acute: Reversible changes. Symptoms develop within 7 days. Chronic: Irreversible changes. Symptoms are prolonged and are the end result of all chronic renal disease.
Renal Artery Stenosis
Major cause is atheromatous plaques. Causes refractory hypertension due to renal production of renin in response to low plasma volume entering through stenosed renal artery.
Hypoalbuminemia
Caused by either decreased synthesis of albumin (ex. kwashiorkor and liver cirrhosis) or increased loss of albumin (ex. kwashiorkor and liver cirrhosis) or increased loss of albumin (ex. kidney disease and severe burns).
Alpha-1 Antitrypsin Deficiency
Autosomal recessive inheritance pattern. Deficiency in alpha-1 antitrypsin, due to lack of glycosylation of an Asp.
Wilson’s Disease
Deficiency of a copper-transporting ATPase (ATPase 7-B), which is needed to link copper to apoceruloplasmin and to release copper into bile.
Addison’s Disease
Atrophy of the adrenal glands, causing adrenal insufficiency.
Conn’s Syndrome
Hyperaldosteronism, due to excess secretion by adrenals.
Syndrome of Inappropriate ADH
Excessive levels of ADH are secreted by the posterior pituitary, causing excess water reabsorption by the kidneys.
Central Diabetes Insipidus
No ADH is released from the posterior pituitary, leading to excess water excretion.
Nephrogenic Diabetes Insipidus
ADH is released by kidneys are not responding to it, leading to excess water excretion.
Dipsogenic Diabetes Insipidus
A defect in the thirst mechanism, causing excessive thirst and fluid intake that suppresses ADH secretion and increases urine output.
Gestational Diabetes Insipidus
Pregnant mother produces vasopressinase in the placenta, which breaks down ADH. This can cause low plasma ADH.
Metabolic Syndrome
Clustering of atherosclerotic and cardiovascular disease risk factors including visceral adiposity, insulin resistance, low level of HDL, a systemic proinflammatory state.
Metabolic Acidosis
Decreased bicarbonate in the blood
Metabolic Alkalosis
Increased bicarbonate in the blood.
“Alkalosis Begets Alkalosis”
ECF volume contraction increases bicarbonate reabsorption in the proximal tubule and proton secretion by alpha intercalated cells. Thus, alkalosis with an ECF volume contraction causes runaway alkalosis.
Respiratory Acidosis
Increased CO2 retention due to hypoventilation.
Respiratory Alkalosis
Decreased CO2 due to hyperventilation.
Salicylate Poisoning
Due to large dose of salicylates (aspirin). Causes excess stimulation of respiratory center, leading to hyperventilation.
