Phys 31

Front 1

osmotic diuretics

Back 1

add substances not easily absorbed by renal tubules and water follows

Front 2

examples of osmotic diuretics

Back 2

urea, mannitol, sucrose

Front 3

loop diuretics that block sodium 2-chloride potassium co-transporter in thick ascending limb

Back 3

furosemide, ethacrynic acid, bumetanide

Front 4

net result of these loop diuretics

Back 4

raise urine Na+ ,Cl-, K+, water, and other electrolytes

Front 5

why do loop diuretics impair ability to either dilute or concentrate urine

Back 5

decrease osmolarity of medullary interstitial fluid

Front 6

why is dilution impaired in loop diuretics

Back 6

inhibition of Na and Cl reabsorption causes more of these ions to be excreted along with water

Front 7

why is concentration impaired in loop diuretics

Back 7

renal medullary interstitial fluid concentration of these ions is reduced

Front 8

thiazide derivatives

Back 8

act mainly on early diatal tubules to block Na+ Cl- cotransporter in luminal membrane of tubular cells

Front 9

carbonic anhydrase inhibitors

Back 9

acts mostly in proximal tubule; decrease bicarb reabsoption and Na+ reabsorption; can cause acidosis

Front 10

example of carbonic anhydrase inhibitor

Back 10

acetazolamide

Front 11

competitive inhibitors with aldosterone net action

Back 11

decrease Na+ reabsorption and Potassium secretion

Front 12

example of aldosterone competitive inhibitors

Back 12

spironolactone and eplerenone

Front 13

where do they compete for receptors with aldosterone

Back 13

cortical collecting tubule epithelial cells

Front 14

amiloride and triamterene

Back 14

inhibit Na+ reabsorption and potassium secretion in collecting tubules; act to block Na+ from Na+ channel in luminal membrane

Front 15

how do amiloride and triamterene cause increase K+ secretion

Back 15

decrease activity of Na+/K+ pump

Front 16

two main categories of kidney diseases

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1) acute but may eventually recover near normal fxn 2) chronic progressive loss

Front 17

Causes of acute renal failure

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1) decrease blood supply (in system before kidneys) 2) intrarenal acute renal failure 3) Postrenal acute renal failure (obstruction in urinary colleting system)

Front 18

what are kidney stones typically caused from

Back 18

precipitation of calcium, urate, or cysteine

Front 19

oliguria

Back 19

diminished urine output below level of intake of water and solutes

Front 20

basal blood flow requirement for kidney

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1/4 normal (20-25%)

Front 21

subdivisions of intrerenal acute renal failure

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1) injure glomerular capillaries or small renal vessels 2) damage tubular epithelium 3) damage to renal interstitium

Front 22

glomerulonephritis

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intrarenal acute failure caused by abnormal immune rxn that damages glomeruli

Front 23

when does glomerulonephritis generally occur in 95% of cases

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1-3 weeks after infection elsewhere in body; usually group A beta streptococci

Front 24

long term prognosis of glomerulonephritis

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subsides in about 2 weeks and return to almost normal fxn within weeks/months

Front 25

tubular necrosis

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destruction of epithelial cells in tubules caused by ischemia or poisons (meds, toxins)

Front 26

what determines recovery of tubular necrosis

Back 26

if basment membrane intact, cells can proliferate and repair within 10-20 days

Front 27

what can be a fatal consequence of acute renal failure

Back 27

K+ elevation in plasma then acidosis

Front 28

when do clinical symtoms of chronic renal failure occur

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number of fxnal nephrons falls 70-75% below normal

Front 29

net results of mechanisms of adaptation of fxnal nephrons in chronic kidney failure

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hypertrophy, decreased vascular resistance, tubular reabsorption decrease; exact mechanisms unknown

Front 30

what is chronic increase in P and stretch of small arterioles believed to cause

Back 30

sclerosis of the vessels

Front 31

only proven method of slowing progressive loss of kidney fxn in chronic renal disease

Back 31

lower arterial P and glomerular hydrostatic P

Front 32

what accounts for 70% of all chronic renal failures

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diabetes and hypertension

Front 33

most common lesions that can lead to ischemia and death of kidney tissue

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1) atherosclerosis 2) fibromuscular hyperplasia 3) nephrosclerosis

Front 34

chronic glomerulonephritis causes

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from acute form or secondary to systemic dieases like lupus erythematosus

Front 35

result of accumulation of antibody-antigen complexes in glomerular membrane

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inflammation, progressive thickening of membranes, eventual invasion of glomeruli by fibrous tissue

Front 36

pyelonephritis

Back 36

renal interstitial injury caused by bacterial infection; esecially E Coli form fecal contamination of urinary tract

Front 37

what clinical conditions interfere with normal flushing of bacteria from bladder

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1) inability to completely empty 2) obstruction of flow

Front 38

cystitis

Back 38

inflammed bladder

Front 39

vesicoureteral reflux

Back 39

urine propelled up ureters during micturition

Front 40

what issue would present first in patients with pyelonephritis

Back 40

inability to concentrate urine as medulla would be affected first

Front 41

nephrotic syndrome

Back 41

excretion of protein in urine because of increased glomerular permeability

Front 42

what diseases can cause nephrotic syndrome

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1) chronic glomerulonephritis 2) amyloidosis 3) minimal change nephrotic syndrome

Front 43

who is minimal change nephropathy most common in

Back 43

children btwn 2-6 years

Front 44

what occurs to waste products of metabolism like urea and creatinine in kidney failure

Back 44

accumulate almost in proportion to number of nephrons destroyed

Front 45

how is noraml renal excretion maintained as more and more nephrons become nonfunctional

Back 45

decrease the rate at which the tubules reabsorb water and solutes

Front 46

isothenuria

Back 46

inability to concentrate urine and dilute urine

Front 47

why is concentration impaired in renal failure

Back 47

1) rapid flow through both loop of henle and collecting ducts prevents countercurrent mechanism from working effectively 2) rapid flow prevents water reabsorption

Front 48

what occurs to specific gravity as renal failure progresses

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approaches specific gravity of glomerular filtrate

Front 49

why is dilution impaired in kidey failure

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rapid flushing and high load of solutes (like urea) cause relatively high solute concentration

Front 50

important test of renal fxn

Back 50

how well kidneys can concentrate urine in 12 hour water restriction

Front 51

azotemia

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increase in urea and other nonprotein nitrogens

Front 52

why is osteomalacia caused in renal failure

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decreased production of active vit D and phosphate retention

Front 53

why is anemia observed in renal failure

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erythropoietin production decline

Front 54

what does increased phosphate levels do

Back 54

binds with Ca2+ in plasma reducing serum ionized Ca2+ which stimulated PTH release

Front 55

what kidney diseases tend to cause hypertension

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renal artery stenosis (increase renal vascular resistance), decrease glomerular capillary filtration coefficient, excessive tubular sodium reabsorption

Front 56

what are the net affects of kidney diseases that cause hypertension

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decrease GFR or increase tubular reabsorption

Front 57

renal glycosuria

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failure of kidneys to reabsorb glucose; relatively benign

Front 58

aminoaciduria

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failure of kidneys to reabsorb aas; generally with specific transporter

Front 59

examples of aminoaciduria

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1) essential cystinuria (renal stone forming) 2) simple glycinuria 3) beta-aminoisobutyricaciduria (no major clnical significance, 5% all people)

Front 60

renal hypophosphatemia

Back 60

failure of kidneys to reabsorb phosphate; no immediate effect, long term bone formation impaired

Front 61

renal tubular acidosis

Back 61

failure of tubules to secrete hydrogen ions; large amounts of bicarb lost in urine; metabolic acidosis

Front 62

nephrogenic diabetes insipidus

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failure of kidneys to respond to ADH; person becomes rapidly dehydrated if not enough water supplied

Front 63

Fanconi's syndrome

Back 63

generalized reabsorptive defect of renal tubules; increased urinary secretion of all aas, glucose, phosphate

Front 64

what occurs in severe cases of Fanconi's syndrome

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1) failure to reabsorb bicarb 2) increased excretion of K+ and sometimes Ca2+ 3) nephrotic diabetes insipidus

Front 65

multiple causes of Fanconi's syndrome

Back 65

1) hereditary defect in cell transport 2) toxins/drugs that injure renal tubular epithelial cells 3) injury to renal tubular cells from ischemia