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Pathophys > Renal 4a > Flashcards

Renal 4a Flashcards

1
Q

renal anatomy

A

highly vascularized tissue surrounded by adipose and connective tissue capsule

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2
Q

functional unit =

A

nephron

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3
Q

_____nephrons per kidney

A

1 million

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4
Q

nephron anatomy

A

glomerulus + tubule, and associated capillaries

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5
Q

nephrons create ___ from blood

A

filtrate

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6
Q

useful substances are____ and returned to blood

A

reabsorbed

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7
Q

other substances (toxins, drug metabolites selectively ____

A

into tubule to exit the body as urine

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8
Q

porous membrane with large surface area allows for____

A

water/ solutes to be filtered

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9
Q

what anatomy allows for glomerular filtration

A
  1. fenestrasted endothelium (gaps)
  2. basment membrane
  3. podocytes with foot processes and filtration silts
    (only capillary bed fed AND drained by arterioles)
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10
Q

filtrate =

A

plasma- proteins
(entire plasma volume filtered 60 times each day! )

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11
Q

Glomerular filtration is a passive process driven by

A

hydrostatic pressure
-higher than other capillaries (55mmHg)

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12
Q

intrinsic control (autoregulation)

A

maintains constant GFR when MAP fluctuates (mean arterial pressure)
-Anything that affects BP or blood volume can impact GFR
-healthy kidneys maintain GFR; diseased kidneys cannot

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13
Q

extrinsic control )nervous system, endocrine)

A

Epi/ NE (neural), renin-angiotensin-aldosterone system (hormonal) indirectly regulates GFR by maintaining systemic BP, drives filtration to kidneys

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14
Q

increase in BP leads to ____

A

constriction of afferent arterioles which decreases flow to glomerulus
-GFR constant, protect glomeruli from damaging high BP

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15
Q

Decrease in BP leads to

A

dilation of afferent arterioles which increases flow of glomerulus
-helps maintain normal GFR when BP

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16
Q

Juxtaglomerular apparatus (JGA)

A

made up of :
-macula densa cells- of ascending limb of nephron loop
-extraglomerular mesangial cells
-granular cells
importance in regulation of filtrate formation and blood pressure

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17
Q

granular (jextaglomerular cells)

A

smooth muscle cells of afferent arteriole
mechanoreception: sense BP
secrete renin

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18
Q

macula densa

A

chemoreception: sense NaCl content of filtrate (indicate whether flow rate is too high or too low)

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19
Q

mesangial cells

A

modified SM cells, can contract to reduce surface area for filtration
allow communication between other 2 cell types

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20
Q

If GFR too high

A

macula densa cells sense increased NaCl in filtrate
signal to granular cells to constrict afferent arteriole

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21
Q

if GFR too low

A

too little NaCl sense by macular densa cells
signal granular cells to relax afferent arteriole

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22
Q

acute kidney injury

A

-sudden onset. may resolve or progress to chronic

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23
Q

chronic kidney injury

A

progressive damage, leads to kidney failure

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24
Q

kidney injury determined by

A

imaging
urinalysis
renal clearance
biopsy

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25
Q

Normal urine

A

-95% water and 5% solutes
-nitrogenous wastes: urea, uric acid and creatinine
-other norrmla solutes: Na, K, PO4, SO4, Ca, Mg, HCO
-pH 6.0 (range 4.6- 8.0 )

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26
Q

abnormal urine- albuminuria

A

damage to filtration membrane - too much albumin

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27
Q

glucosuria:

A

hyperglycemia, too much sugar in blood

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28
Q

hematuria

A

damage to filtration membrane; bleeding in urinary tract, blood in urine

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29
Q

renal clearance

A

volume of plasma cleared of a particular substance in a given time (1 min)
RC= GFR= 125 mL/ min

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30
Q

renal clearance test used to :

A

determine GFR
Detect glomerular damage
follow the progress of renal disease

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31
Q

general mechanisms of acute kidney injury

A

-vascular basis or tubular basis

32
Q

vascular basis

A

afferent arteriole constriction OR efferent arteriole dilation
-decrease in renal perfusion
-decrease GFR
caused by ischemia, hypoxia in renal medulla

33
Q

tubular basis

A

damaged cells –> cellular debris
genereal mechanisms of acute kidnety of tubule
incr intratubular pressure affects filtration upstream
decr GFR
damaged cells -> filtrate leaks out of tubule

34
Q

manifestation of acute kidney injury

A

all result from decreased GFR
Fatigue, malaise - from impaired waste clearance
dyspnea, orthopnea
peripheral edema
-altered mental status -prolonged impairment of excretory fxn
-azotemia

35
Q

Azotemia

A

build up of nitrogenous wastes in blood
-elevated ratio BUN (blood urine nitrogen level: creatinine

36
Q

tx for acute kidney injury

A

tx underlying reason for kidney damage

37
Q

tubular cells regenerate ->

A

nephron fxn return to normal

38
Q

chronic kidney dx progresses to

A

renal failure

39
Q

renal failure

A

-irreversible loss of nephrons
-greater burden on remaining nephrons -> hyperfiltration (local htn)
-glomerular sclerosis
-increase rate of nephron loss, glomerular scarring

40
Q

uremia

A

inadequate renal fxn
-functional reserve of nephrons lost
-s &S of chronic kidney dx

41
Q

functional reserve

A

kidneys can lose about 50% of nephrons before impairment
(reason why healthy ppl can donate a kidney)

42
Q

mechanism of uremia

A
  1. retention of products that are normally exerted ( nitrogenous wastes)
  2. normal renal hormones over-secreted (compensation for low GFR)
  3. Loss of normal kidney products (vit D, erythropoietin)
43
Q

hypernatremia and water retention

A

decr ability to excrete water and Na+
-made worse by dietary Na+
-htn, edema, hrt failure worsened

44
Q

hyperkalemia

A

decr GFR leads to incr aldosterone -> K+ retention

45
Q

metabolic acidosis

A

decr ability to excrete acid (H+, NH4+)
-put pt at risk of crisis in case of vommiting/ diarrhea)

46
Q

mineral and bone tissue (uremia)

A

decr vit D production, decr Ca2+ absorbed in gut
retention of phosphate

47
Q

-inadequate bone mineralization=

A

osteomalacia; cant rebuild bone but can break it down normally

48
Q

CV and pulmonary manifestations of uremia

A

htn, pulmonary edema
decr GFR -> increases secretion of renin which incr blood volume and BP

49
Q

Neuromuscular effects of uremia

A

mild: impaired concentration, memory loss
sever: asterixis (jerking of hands/wrists), seizures, coma
-altered nerve conduction (from abnormal K+ and Na+ levels)

50
Q

endocrine effects of uremia

A

females: low estrogen, amenorrhea (absence of menstruation), infertility
men: low testosterone, impotence (inability for a man to achieve erection of orgasm), low sperm count
-metabolism of insulin impaired (good for dm)

51
Q

derm manifestation of uremia

A

pallor (anemia)
-hyperpigmentation (accumulated pigmented metabolites)
-hematomas (clotting abnormalities)

52
Q

Causes of chronic kidney dx

A

-DM
-HTN
-Glomerulonephritis
-pyelonephritis
-polycystic kidney dx
-toxic nephropathy
-SLE

53
Q

Diabetes and kidney dx=

A

diabetic nephropathy

54
Q

Diabetic nephropathy characteristic changes

A

glomerulus enlarges
-alter filtration directly:
basement membrane thickens
loss of podocytes
-affect blood flow-> alters filtration:
mesangial cells proliferate
arteriole vasoconstriction

55
Q

htn and kidney dx

A

prolonged constriction of afferent arterioles (to regulate GFR)
-Hypertrophy of VSM cells in affernt arteriole
-narrowed vessel -> ischemia
injury to endothelial cells
-enhances vascontriction
-promotes VSM hypertrophy
glomerular sclerosis (scarring)
-decr GFR

56
Q

htn ____ kidney damage and kidney damage______ htn

A

promotes, promotes

57
Q

Glomerulonephritis

A

damage to glomerular capillary wall. altering filtration
-infiltration of inflamm cells
contraction of mesengial cells
decr GFR
Na+ and water retention
edema, htn, hematuria, proteinuria

58
Q

acute gn

A

abrupt onset on hematuria, proteinuria, decr GFR, Na+ and water retention
-infectious dx, often involves autoantbodies, deposition of immune complexes in glomerulus

59
Q

chronic gn

A

persistent urinary abnormalities with progressive decline in renal fxn

60
Q

nephrotic syndrome

A

proteinuria, hyperlipidemia, edema
-target podocytes

61
Q

pyelonephritis

A

inflammation due to bacterial infection
-ascedning UTI
-inflammation
-tubular obstruction and damage
-interstitial edema
more common in females (bc shorter ureters)

62
Q

pyelonephritis pathogens

A

KEEPS
Klebsiella, E. coli, enterococcus, pseudomonas, staphylococcus

63
Q

urine findings:

A

WBC in urine (incr blood count in blood)
-hematuria (maybe)
-foul-smell
-bacterial culture (+)

64
Q

polycystic kidney dx

A

-genetic condition:
95% inherited (autosomal dominant)
PKD1, PKD2, PKD3 mutation
-dysfunctional Ca 2+ channels on epithelial cells:
abnormal Ca2+ entry disrupts signaling

65
Q

_____develops cysts and abundance of cysyts ____tubules and organ architecture

A

nephrons, distorts

66
Q

polycystic kidney dx affecting other epithelial cells

A

brain-> berry aneurysms (death)
liver-> cyst formation
heart-> valvular dysfxn
seminal vesicles -> decreased sperm motility, infertility
(severity depends on mutation)

67
Q

manifestation of polycystic kidney dx

A

proteinuria: damages filtration membrane leaks protein
htn: compressed renal vasculature activates RAAS
Hematuria: altered renal vasculature + damages filtration
pain: inflammation if cysts begin harboring bacteria

68
Q

polycystic kidney dx diagnosed by

A

Imaging CT, MRI, ultrasounds
Genetic testing (less common)

69
Q

toxic nephropathy

A

=nephrotoxicity
damage induced by chemicals or drugs
-distal tubular cell injury
-impaired mitochondrial fxn -> incr oxidative stress and free radicals
-impaired ability to concentrate urine
-hematuria, pain
-damage resolved if drug stopped

70
Q

kidneys are vulnerable to drugs bc:

A
  1. they receive 25% of cardiac output, exposed to large amounts of chemical in blood
  2. hyperosmotic medulla allows concentration of drugs in kidney interstitium
  3. kidneys are common site of exertion; any renal insufficiency leads to the accumulation of the drug
71
Q

common classes of drugs that cause nephropathy

A

-pain relievers (naproxen)
-antimicrobials (pcn)
-psychiatric drugs
-cancer tx (methotrexate)
-cholesterol lowering drugs (statins)

72
Q

SLE and kidney dx - lupus nephritis

A

development of autoantibodies targeting glomerulus or tubule
-glomerular sclerosis
can occur with other autoimmune conditions: goodpasture syndrome (antibodies attack lungs and kidneys) or
progressive systemic sclerosis (of vasculature)

73
Q

progressive kidney damage , loss of functional nephrons=

A

renal failure

74
Q

med treatments for kidney dx

A

-treat underlying condition
htn, hrt failure= diuretics
autoimmune= immunosuppressors
infection= antimicrobials

75
Q

lifestyle tx

A

dietary regulation of
protein
k+ and na+
fluids

76
Q

transplant

A

better tissue matching and immunosuppresent tx, prevent rejection
-limited by donor avalibility

77
Q

dialysis

A

main tx
cannot replace hormone fxn of kidney

Pathophys (11 decks)

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