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54 Cards in this Set
- Front
- Back
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location of kidneys
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retroperitoneal; right lower than left because of liver
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left renal artery location
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over inferior vena cava - prone to high pressure and compression
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cortex
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outermost portion of kidney; contains renal corpuscle
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renal corpuscle
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glomerulus + Bowman's capsule + tubules
functions to filter solutes/impurities out of blood and into urine |
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medulla
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contains collecting ducts which feed into minor calyces
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renal papillae
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extension of collecting ducts/tubules
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parietal layer of glomerular capsule
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outside
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visceral layer of glomerular capsule
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inside; forms podocytes for filtration
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juxtaglomerular apparatus
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monitors water and solute content of blood
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juxtaglomerular cells
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aka granular cells; release renin when water/solutes are decreased
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mesangial cells
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possess contractile and phagocytic functions
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glomerular basement membrane
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between podocytes and endothelium
-lamina rara interna externa -lamina densa |
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kidney functions
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-excretory
-regulatory (solute, volume content) -acid/base balance of plasma -endocrine (erythropoietin, renin, prostaglandins) |
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proximal convoluted tubule
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-permeable to water
-AA's glucose, HCO3, PO4 reabsorbed -passive reabsorption of NaCl |
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descending loop of henle
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-Na reabsorbed
-organic acids secreted -very permeable to water; most water reabsorbed, urine becomes very concentrated |
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ascending loop of henle
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-impermeable to water
-solutes get reabsorbed, so urine becomes dilute again -loop diuretics inhibit Na and K reabsorption |
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distal convoluted tubule
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-impermeable to water
-thiazide diuretics inhibit NaCl reabsorption |
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collecting duct
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-permeable to water ONLY with vasopressin
-Na reabsorbed via aldosterone -Na reabsorption inhibited by ANP |
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basement membrane permeability
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-impermeable to albumin
-semipermeable to some ions/other substances -when albumin present in urine, significant damage to BM and podocytes has occurred |
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glomerular capillary histologic alterations
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-hypercellularity
-BM thickening -hyalinization and sclerosis |
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hypercellularity
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-abnormal increase in amount of cells present
-mesangial, endothelial, epithelial, or inflammatory cells (neutrophils, macrophages) |
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BM thickening
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-due to inflammatory process
-deposits of immune complexes containing amyloid (protein) or fibrin tissues |
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hyalinization and sclerosis
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-due to buildup of precipitated, dead plasma proteins in the BM apparatus
-blanket term for BM thickening = focal segmental glomerulonephritis |
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inflammatory process sequence of events
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antibody-antigen too large to be filtered --> get stuck --> elicit inflammatory responce --> BM thickening and glomerular injury
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C5b-9
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part of complement that initiates the membrane attack sequence; punches holes in BM and destroys cells
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sequence of glomerular injury pathogenesis
KNOW THIS!!! |
1. immune complex/antibody deposition on BM structures (in situ)
2. circulating immune complex deposition 3. antibodies to glomerular cells 4. cell mediated immunity 5. alternative complement pathway activation 6. mediators released 7. epithelial injury |
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glomerular diseases
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1. nephrotic syndrome
2. nephritic syndrome |
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nephrotic syndrome signs and symptoms
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-proteinuria (3.5 g/day): protein spilling into urine
-hypoalbuminemia (<3 g/dL): protein spilling out of blood -hyperlipidemia/lipiduria: liver stimulated to synthesize more lipids -generalized edema: protein has colloidal nature - pulls water along with it; lots of protein in extracellular space means lots of water and thus edema |
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membranous glomerulonephritis/ glomerulopathy
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-leads to nephrotic syndrome
-diffuse thickening of glomerular capillary wall -accumulation of IgG deposits on EPITHELIAL (visceral) BM |
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renal bx in membranous glomerulonephritis/glomerulopathy would show...
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-diffuse thickening of capillary wall
-electron dense deposits in BM -obliteration of podocytes |
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membranous glomerulonephritis/ glomerulopathy caused by...
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-infections (hepB)
-systemic disease (diabetes) -malignancies (cancer) -autoimmune disease (lupus) -C5b-C9 injury (complement) |
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nephritic syndrome signs and symptoms
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-HTN
-edema -RBCs and RBC casts in urine -moderate proteinuria (less than in nephrotic syndrome) |
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acute proliferative glomerulonephritis
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-leads to nephritic syndrome
-neutrophil and monocyte infiltration -endothelium and mesangial cell proliferation -capillary lumen obliteration -red cell cast in tubules |
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renal bx in acute proliferative glomerulonephritis would show...
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-glomerular hypercellularity
-intracapillary leukocytes -intrinsic glomerular cell proliferation -may be immune complex mediated |
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acute pyelonephritis
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-caused by UTIs
-normal, happens often -most frequently bacterial or fungal |
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chronic pyelonephritis
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-caused by vesicoureteral reflux or obstruction; distorted/abnormal anatomy
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hematogenous infection
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blood infection; systemic
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ascending infection
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coliform infection; caused by normal flora (E.coli, enterobacter, proteus)
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acute pyelonephritis predisposing conditions
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-urinary obstruction (BPH, cervical cancer, stenting)
-instrumentation -vesicoureteral reflux -sex/age (the older you are, the more prone to UTI; women more prone than men bc shorter urethra) -diabetes -immunosuppression |
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acute pyelonephritis bx would show...
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-interstitial tubular necrosis (tubules more likely to be affected than glomerulus)
-interstitial patchy suppurative inflammation in later stages -papillary necrosis -pyonephrosis (infection of renal pelvis; pus builds up and causes renal distension) -perinephric abscess |
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chronic pyelonephritis predisposing conditions
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-chronic obstructive nephropathy (BPH, tumors, normal pregnancy): patient unable to void so leads to bacterial overgrowth...bacteria has adhesin proteins which enable it to ascend from urethra up the ureters into kidneys
-reflux nephropathy: if angle at which ureter enters bladder becomes obtuse (>45 degrees), valve mechanism malfunctions and urine can reflux back into kidneys |
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chronic pyelonephritis renal bx would show...
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-corticomedullary scarring
-blunted calyces -dilated ureter -thyroidization |
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brush border cells of tubules contain many___ and why?
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loaded with mitochondria to produce enough ATP to transport ions against their concentration gradient
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factors predisposing to tubular injury
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-charged surface
-active transport -high metabolic rate/oxygen consumption |
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types of tubular injury
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1. ischemic/toxic = acute tubular necrosis
2. inflammatory = tubulointerstitial nephritis |
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causes of ischemic ATN
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-polyarteritis nodosa (autoimmune attack of arteries)
-malignant HTN |
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causes of toxic ATN
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-radiocontrast dyes
-myoglobin (from muscle breakdown) |
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ischemic ATN morphology
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-focal tubular epithelial necrosis
-rupture of BM (tubulorrhexis) -occlusion of tubular lumens by casts (eosinophilic hyaline casts, pigmented granular casts, or tamm-horsfall proteins) -loss of PCT brush border -cell swelling/vacuolization -interstitial edema -leukocyte accumulation w/in vasa recta -epithelial regeneration |
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toxic ATN morphology
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-variable
-PCT affected more than other areas -tubular necrosis/non-specific |
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ATN clinical courses
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1. initiation phase: w/in first 36 hours; increased BUN, decreased renal function
2. maintenance phase: oliguria, hyperkalemia 3. recovery phase: water, Na, K lost; make sure patient is getting replenishment of fluids and K!!! |
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dominant etiological agents causing tubulointerstitial nephritis
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-e.coli
-proteus -kelbsiella -enterobacter -strep. faecalis |
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mechanisms associated with ascending infections
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-colonization in distal urethra and introitus (vaginal/penile orifice)
-multiplication in bladder -vesicoureteral reflux -intrarenal reflux |
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signs and symptoms of acute pyelonephritis
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-costovertebral angle (CVA) tenderness
-fever/malaise -dysuria, low frequency/urgency -leukocyte casts/neutrophils in urine *best diagnosis made by quantitative urine culture |
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what tests used to establish UTI with certainty
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1. positive leukocyte esterase
2. nitrite |
