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chapter 32 diuretics, kidney diseases Flashcards

1
Q

What do diuretics generally do in terms of

1) urinary output
2) solutes
3) renal tubular absorption
4) water

A

1) increase the rate of urine output
2) increase urinary excretion of solutes (na and cl)
3) decrease renal tubular absorption (increased na output=naturesis)
4) water loss in urine secondary to inhibition of tubular reabsorption of na (other solutes may be lost as well)

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2
Q

what is most common use of diuretics

A

reduce extracellular fluid volume, especially in diseases such as edema and HTN

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3
Q

name 5 compensatory responses to chronic diuretic usage

*when do these compensatory mechanisms occur?

A

1) decreased ECF volume2) reduces arterial pressure and the 3)GFR leading to 4)increased renin and 5)angiotensin II
* these compensatory mechanisms generally occur only after decreases in BP and ECF volume have occured

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4
Q

What is mechanism of action of osmotic diuretics

A

decrease water reabsorption by increasing the osmotic pressure of the tubular fluid

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5
Q

name 3 major ingredients of osmotic diuretics, and how do they exert their effects

A

1)mannitol 2)urea 3)sucrose
exert increased osmotic pressure in tubules, which reduces water reabsorption, pulling water into urine via osmosis, as mannitol, urea, and sucrose are generally not reabsorbed

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6
Q

1) In diabetes, what sugar level in the plasma acts to cause osmotic diuresis of excess urine?
2) what are hallmark symptoms of DM?

A

1) 250mg/dl exceeds tubular reabsorption of glucose, resulting in excess glucose in filtrate(urine) which pulls water into filtrate (urine) via osmosis
2) polyuria, polydypsia

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7
Q

How do Loop Diuretics exert their effects?

A

decrease active 1na-2cl-1k cotransporter that normally causes reabsorption in the luminal membrane of the epithelial cells in the thick ascending loop of henle. Blocking the na, cl, k, cotransporter results in increased output of na, cl, and k in filtrate (urine) which pulls water via osmosis, and this causes disruption of countercurrent multiplication system by decreasing osmolarity of renal interstitium (normally salty), so kidneys cannot dilute or concentrate urine.

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8
Q

Name 3 examples of loop diuretics

A

1)furosimide 2)ethacynic acid 3)bumetanide

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9
Q

with loop diuretics, why is urinary 1)dilution and 2) concentration impaired

A

1) decreased solutes in medullary interstitum causes more solutes to be excreted than reabsorbed in LOH, and water follows the osmotic gradient of the solutes
2) reabsorption of water in collecting ducts is impaired

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10
Q

how much of GFR is delivered to urine after administration of loop diuretics

A

20-30% of GFR, causes UOP to be increased by 25% for at least a few minutes

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11
Q

1) How do thiazide diuretics work
2) name a common thiazide diuretic
3) how much of GFR can pass into urine

A

1) inhibit na/cl cotransporter, stoping reabsorption in the lumenal membrane (urine side) of early distal convoluted tubule
2) chlorothiazide
3) 5-10% of GFR passes into urine (which is same amount of Na normally reabsorbed in DCT)

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12
Q

1) How do carbonic anhydrase inhibitors work?
2) name an example
3) by decreasing HCO3 reabsorption and H secretion, what happens to na reabsorption
4) what do carbonic anhydrase inhibitors cause

A

inhibits carbonic anhydrase enzyme, which is necessary for reabsopriton of HCO3 PCT(primary effect) and intercalated cells of collecting tubule (minimal)

2) acetazolamide
3) na reabsorption decreases because in PCT na/H countertransport is coupled to HCO3 reabsorption and H secretion, resulting in more Na in urine that exerts osmotic diuretic effects by pulling water into urine
4) cause acidosis because of loss of HCO3 in urine

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13
Q

1) how do mineral corticoid receptor antagonists work
2) what happens to potassium with this type of diuretic
3) name 2 examples of this type of diuretic

A

1) compete with aldosterone for receptor binding sites in collecting tubule epithelial cells causing decrease na reabsorption in collecting tubules, and potassium secretion into collecting tubules, resulting in na remaining in tubules (urine side) pulling more water and na into urine
2) because aldosterone is blocked, K secretion does not happen, and K moves into ECF
3) sprinolactone, eplerenone

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14
Q

1) How do Na channel blockers work as diuretics
2) are Na channel blockers K sparing?
3) name 2 examples of Na channel blockers

A

1) inhibit na reabsorption and K excretion in collecting tubules, blocking na channels of lumenal membrane (urine side) and blocking na/k/atpase pump on basolateral side (blood side)=reduced K into cells, and decreased K into urine
2) na channel blockers are K sparing
3) amiloride and trianterene

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15
Q

Describe acute kidney disease

A

abrupt loss of kidney function within a few days-can be reversible.

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16
Q

describe acute renal failure

A

severe acute kidney injury where the kidneys may stop working necessitating dialysis

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17
Q

describe chronic kidney disease

A

progressive loss of function of nephrons that gradually decreases renal function

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18
Q

describe pre renal acute kidney injury, give some examples

A

prerenal=decreased blood supply to kidney, with issue originating in area before kidneys-heart failure with low CO and BP, severe hemorrhage

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19
Q

describe intrarenal acute kidney injury, give some examples

A

abnormalities inside of kidney such as blood vessels, glomeruli, and/or tubules

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20
Q

1) describe post renal acute kidney injury

2) give examples

A

1) obstruction of urinary collecting system anywhere from the calyces to outflow from bladder
2) examples-stones (urate, calcium, cystine)

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21
Q

How much blood supply do kidneys normally receive

A

1100ml/min or 20-25% of CO

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22
Q

why do kidneys receive such high blood flow volumes

A

provide enough plasma for the high rates of GFR needed for effective regulation of body fluid volumes and solute concentrations

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23
Q

what happens with decreased renal blood flow

A

1)decreased GFR 2)decreased urine output of solutes and water, which accumulate in the body

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24
Q

As long as blood flow does not fall to ____% of normal, AKI can usually be _____ if the cause of ischemia is corrected before damage to renal cells has occurred

A

20-25%, reversed

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25
Q

what are protective mechanisms in kidneys during times of reduced blood flow

A

GFR and filtered nacl, water and other electrolytes is reduced which decreases the amount of reabsorption (reabsorption requires the most energy), and thereby reduces the amount of O2 consumption

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26
Q

in times of no blood flow to kidney, what happens to renal cells and tubular epithelial cells

A
  • below 20-25% of blood flow, renal cells become hypoxic causing damage and death of renal cells and tubular epithelial cells.
  • ischemia >a few hours causes prerenal failure to evolve into intrarenal failure
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27
Q

name some examples of pre renal failure 4 categories

A
  • intravascular volume depletion (hemorrhage, diarrhea, vomiting, burns)
  • cardiac failure (MI, valvular damage)
  • Peripheral vasodilation/hypotension (anaphylactic shock, anesthesia, sepsis)
  • Renal artery stenosis, embolism, thrombosis of renal artery or vein
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28
Q

name some examples of intrarenal acute kidney injury

A
  • small vessel and/or glomerular injury (polyarteritis nodosa), cholesterol emboli, malignant hypertension, acute glomerular nephritis
  • tubular epithelial injury (tubular necrosis) ischemia, toxin ingestion
  • renal interstitial injry (acute polynephritis, acute allergic interstitial nephritis)
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29
Q

intrarenal acute kidney injury-what is it

A

abnormalities that originiate in kidney and abruptly diminish urine output

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30
Q

describe acute glomerulonephritis

A

damage to glomeruli resulting from infective process occurring outside of kidney, usually from group A beta strep. Antibody antigen complexes from insoluble immune complex that are entrapped in glomerulus in basement membrane of glomeruli, either blocking the glomeruli or increasing glomeruli permeability beyond normal causing protein and RBCs to leak from blood into urine. Can be self limiting, or progress to CRF

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31
Q

Describe acute tubular necrosis-what is damaged and what are 2 major reasons

A

destruction of epithelial cells in the tubules, caused by 1)severe ischemia and inadequate supply of O2 and nutrients to tubular epithelials, and 2)poisons

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32
Q

In renal ischemia that causes acute tubular necrosis, describe pathology, and what is most common cause

A

damaged tubular epithelial cells slough off, and plug nephrons, and nephrons that are plugged fail to excrete urine even when renal blood flow is restored to urine, even after blood flow is restored to normal-most common-circulatory shock

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33
Q

Describe acute tubular necrosis caused by toxins-what are common toxins

A

tubular epithelium on basement membrane are damaged and slough off and plug tubules, sometimes basement membrane is destoryed, can repair itself in some cases in 10-20 days
-carbon tetrachloride, heavy metals (mecury and lead) ethylene glycol (antifreeze), insecticides, tetracyclines, cis-platinum (cancer med)

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34
Q

Describe post renal AKI-what happens if only one kidney is effected, how long before irreversible damage occurs, and what are 3 causes

A

blockage or partial blockage of urine flow even if blood supply and kidney function is initially normal.
if only one kidney is effected, other kidney will compensate and no huge changes in body fluid composition
-if issue is corrected in a few hours, no major issues
-chronic blockage of urinary tract lasting several days or weeks can cause irreversible kidney damage
-common causes-blood clots or stones obstructing ureters or renal pelvises, 2)bladder obstruction 3)obstruction of urethra

35
Q

Name 4 major physiological effects of acute renal injury

A

retention of water
accumulation of waste products
accumulation of electrolytes in blood and ECF (especially K)
metabolic acidosis(can further cause hyperkalemia)

36
Q

how long after AKI will a patient die if anuric

A

8-14 days unless dialysis is initiated

37
Q

what defines CKD, when is CKD clincally apparent

A
  • kidney damage/decreased kidney function that persists at least 3 months
  • functional nephrons 70-75 percent of normal-no clinical symptoms
  • ECF and electrolytes until functional nephrons drop below 20-25 percent
38
Q

Name two adaptions to loss of functioning nephrons
what happens over time
what is best medication to use to prevent this

A

1) hypertrophy of remaining nephrons
2) decrease in vascular resistance and tubular reabsorption in surviving neprhons-functional vasodilation and increased pressure to glomerulus
* this adaption leads to further injury of surviving nephrons over time however due to sclerosis of glomeruli and arteroiles from increased pressure-use ace inhibitor to slow this process (lower glomerular hydrostatic pressure and arterial pressure)

39
Q

What are the most common causes of ESRD (5)

what is an important risk factor seen with two of these

A

1) DM 2)HTN 3)glomerulonephritis 4)Polycystic kidney disease 5)other/unknown
* excessive weight gain as seen with DM and HTN most important main risk factor for ESRD with HTN and DM

40
Q

Describe the vicious circle with primary kidney disease

A

primary kidney disease–>decreased nephrons–>hypertrophy and vasodilation of surviving neprhons–>increase in arterial pressure–>increase in glomerular pressure and filtration rate–>glomerular sclerosis–>leading to further decrease in nephron number

41
Q

Describe 3 causes of injury to the renal vasculature

A

1) atherosclerosis of larger renal arteries
2) fibromuscular hyperplasia of one or more of large arteries which occludes vessels
3) nephrosclerosis-sclerotic lesions of smaller arteries, arterioles, and glomeruli

42
Q

Describe atherosclerosis or hyperplastic lesions of large arteries

A

usually effect one kidney more than other, unilateral diminished kidney function, causes hypertension to kidneys

43
Q

describe the most frequent form of kidney disease

A

benign nephrosclerosis/glomerulosclerosis-begins with leakage of plasma through the intimal membrane of the smaller interlobular arteries and in afferent arterioles, resulting in fibrinoid deposits to develop in medial layers of these vessels, followed by progressive thickening of the vessel walls which can constrict/occlude them-no collateral circulation among smaller renal arteries, occusion of one or more causes destruction of many nephrons, replacing kidney tissue with fibrosis
HTN, DM worsens

44
Q

in healthy people how much does renal plasma flow and GFR decrease

A

40-50% by age 80

45
Q

Describe chronic glomerulonephritis

A

slowly progressive disease leading to irreversible renal failure, may be following acute episode, or accompanied by SLE. Antibody/antigen complexes precipitated accumulate in glomerular membrane, causing inflammation, decreasing capillary tufts due to thickened glomerular membranes, healthy kidney tissue replaced by fibrosis which cannot filter fluid

46
Q

Describe interstitial nephritis

A

results from vascular glomerular, or tubular damage that destroys nephrons, or it can result from damage to renal interstitum from bacteria, toxins, or drugs
bacterial=pyelonephritis (e.coli common culprit)-inability of bladder to empty, or obstruction of outflow

47
Q

describe cystitis

A

proliferation of bacteria within the bladder resulting in inflammation within bladder

48
Q

what is vasicoureteral reflux

A

urine going up ureter into kidney during urination due to failure of sphincter to close, can result in bacteria going up into renal pelvis

49
Q

describe pyelonephritis-where does pyelonephritis usually effect in kidney

A

renal medulla, can spread to cortex, impairs ability of countercurrent multiplication and ability to concentrate urine. Pyelonephritis effects renal medulla interstitium, tubules, glomeruli, and other structures, may lead to CKD

50
Q

Describe nephrotic syndrome 3 types

A

loss of large amounts of plasma proteins in urine because of increased glomerular permeability, can be due to chronic glomerularnephritis, amyloidosis (depositing of abnormal proteins or basement membrane of glomeruli 3)minimal change nephrotic syndrome
may be associated with CKD

51
Q

in chronic kidney disease describe waste product accumulation in proportion to functioning nephrons

A

accumulation is proportional to number of functioning nephrons that have been destroyed, because urea and creatinine depend largely on glomerular filtration to be excreted, and they are not reabsorbed as readily as electrolytes

52
Q

describe minimal change nephrotic syndrome

A

loss of negative charge in basement membrane of capillary can be due to antibodies, often occurs in kids b/t agens of 2 and 6-colloid osmotic pressure falls from 28-10 and plasma protein to less than 2

53
Q

describe solutes phosphate, urea, and hydrogen in CKD

A

maintained near normal range until GFR falls below 20-30 percent of normal
this is maintained by decreasing tubular reabsorption of increasing tubular secretion

54
Q

How are na and cl plasma concentrations maintained in CKD

A

decreasing tubular absorption of these electrolytes
with a 75% loss in functional nephrons, each surviving nephron must secrete 4 times as much na and 4 times as much volume
adaption from increased BF and increased GFR (hypertrophy of nephrons, dilation of blood vessels and glomeruli)

55
Q

With decreased GFR how are normal rates of excretion accomplished?

A

normal rates of excretion can be maintained by decreasing rate of reabsorption of water and solutes by tubules

56
Q

what is isosthenuria

A

inability of kidney to concentrate or dilute urine

57
Q

why is concentrating ability of kidney impaired in isosthenuria

A

1) rapid flow of tubular fluid through collecting ducts prevents water reabsorption
2) rapid flow through LOH and CD prevents countercurrent mechanism, losing concentrating ability of medullary interstitium

58
Q

name 2 factors that CKD has on body fluids

A

1) water and food intake

2) degree of impairment of renal function

59
Q

describe clinical findings in uremia

A

generalized edema
acidosis
high concentrations of non-protein nitrogens (urea, creatinine, uric acid)
high concentration of phenols, sulfates, phosphates, K, and guanidine bases

60
Q

why does fluid accumulation not occur until kidney function falls to 25% or lower

A

surviving nephrons excrete increased na and H2O, increased secretion of renin and angio II causing HTN

61
Q

describe acidosis in kidney disease

A

Body produces 50-80 mmols of acid more than metabolic alkoli each day, and this accumulates in the renal patient over time. Buffers in body fluids can buffer 500-1000mmols of acid without lethal increases in ECF, and phosphate in bones can buffer an additional few thousand mmols of acid, but when these are depleted, pt pH can quickly become deadly acidic

62
Q

Why do patients with renal disease develop anemia

A

erythropoeitin is produced in kidneys which stimulates bone marrow production of RBCs, with renal damage this is impaired

63
Q

Describe Osteomalacia in CKD 2 reasons

A

1)bones partially reabsorbed and weakened
Vitamin D is converted by a two stage process in liver then to kidneys into 1,25-dihydroxychelecalciferol before it can promote calcium reabsorption from intestine. Damage to kidneys reduces blood concentration of active vitamin D, which decreases intestinal absorption
2)rise in serum phosphate due to decreased GFR, which increases binding of phosphate with calcium in plasma, decreasing ionized calcium which stimulates PTH secretion, causing secondary hyperparathyroidism, stimulates release of ca from bones

64
Q

what type of renal lesions promote hypertension

A

those that reduce ability of kidneys to excrete na and water, ones that decrease GFR or increase tubular reabsorption

65
Q

describe how increases in renal vascular resistance cause HTN

A

increases in vascular resistance reduces RBF and GFR (htn caused by renal artery stenosis)

66
Q

describe how decreased glomerular capillary filtration coefficient reduces GFR

A

example-chronic glomerular nephritis causes inflammation and thickening of glomerular capillary membranes, thereby reducing glomerular capillary coefficient

67
Q

describe how excessive tubular reabsorption of na causes HTN

A

example is HTN caused by excessive aldosterone secretion which increases na reabsorption in cortical collecting tubules

68
Q

how can HTN be caused by patchy renal damage

A

if a part of kidney is damaged, renal tissue that is ischemic secretes renin which leads to angio II and increased BP (more na and water retention)

69
Q

Describe pharmacological interventions to optimize kidney function in the face of HTN

A

block effects of nervous and hormonal signals (beta blockers, ARBs, ACE inhibitors)
vasodilate kidneys and increase GFR (ca channel blockers)
diuretics (directly inhibit renal tubular absorption of na and water)

70
Q

describe renal glycosuria

A

failure of kidneys to reabsorb glucose

71
Q

aminoaciduria

A

failure of kidneys to reabsorb Amino acids-essential cystinuria (renal calculi from failure to reabsorb), glycinuria (no absorption of glycine)

72
Q

renal phosphatemia

A

failure to reabsorb phosphate, brittle bones refractory to vit D therapy

73
Q

renal tubular acidosis

A

failure of kidneys to secrete H ions, so lots of HCO3 lost in urine, resulting in metabolic acidosis

74
Q

nephrogenic diabetes insipidus

A

failure of kidneys to respond to ADH

75
Q

fanconi’s syndrome

A

generalized reabsorptive syndrome of AA, gluc, phosphate, sometimes HCO3, increased secretion of K and calcium, usually effects PCT if caused by tubular injury

76
Q

bartters syndrome

A

decreased na, cl and K reabsorption in LOH, due to impaired function of 1na, 2cl,1k transporter=hypokalemia, metabolic acidosis activates RAAS

77
Q

gitelmans syndrome

A

decreased na cl reabsorption in DCT activates RAAS

78
Q

Liddles syndrome

A

increased Na reabsorption, leading to HTN, metabolic alkalosis treated with amiloride

79
Q

what does the rate of movement of solute across teh dialyzing membrane depend on

A

1) concentration gradient of the solute between the two solutions
2) permeability of the membrane to the solute
3) surface area of the membrane
4) length of the time that the blood and fluid remain in contact with the membrane

80
Q

how much blood is in artifical kidney at one time

A

about 500 mL

total diffusion surface area is .6 to 2.5 square meters

81
Q

what is bulk filtration

A

mass transfer of solutes and water can be produced by applying hydrostatic pressure to force the fluid and solutes across the membranes of the dialyzer

82
Q

what does dialyzing fluid NOT contain

A

phosphate, urea, urate sulfate or creatinine, so they are readily absorbed into dialysate via concentration gradient

83
Q

what is rate of clearance of urea from plasma in comparison to normal kidney

A

100-225ml/min compared to 70 ml/min

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