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BHP Exam 4 > Genitourinary 1 > Flashcards

Genitourinary 1 Flashcards

1
Q

vitamin D

A

absorption of Calcium

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2
Q

renal activation of vit D

A

secondary to hyperparathyroidism and bone disease (renal osteodystrophy) w/out kidney

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3
Q

renal osteodystrophy

A

bone mineralization deficiency

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4
Q

nephrotic syndrome

A
  • glomerular filtration increases
  • abnormality in GBM/mesangium
  • glomerulus loses capacity for selective retention of proteins in blood
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5
Q

nephrotic syndrome leads to

A

1 proteinemia (mostly albumin)
2 hypoalbuminemia causing generalized edema by decreasing plasma colloid pressure or oncotic pressure
3 hyperlipidemia bc of reduced serum apolipoproteins (proteins that bind lipids)

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6
Q

nephritic syndrome

A
  • disturbance of glomerular structure that involves reactive cellular proliferation
  • reduced glomerular flow
  • oliguria, hematuria, proteinuria, uremia (retention of waste prdts)
  • activation of renin-angeiotensin system w/ fluid retension and mild hypertension
  • mild edema, not as prevalent as nephrotic syndrome
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7
Q

glomerular perfusion failure

A

nephritic syndrome

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8
Q

3 signs of nephrotic syndrome

A

1 massive proteinuria
2 hypoalbuminemia
3 generalized edema

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9
Q

Interruption of the capillary walls of the glomeruli which leads to increase permeability of plasma proteins leads to

A

nephrotic syndrome

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10
Q

structural or physiochemical alteration of the GBM allows protein to escape from blood…this occurs in

A

nephrotic syndrome

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11
Q

edema

A

extension of salt and water in kidneys

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12
Q

Good pasture syndrome

A

a rare autoimmune disease in which antibodies attack the basement membrane in lungs and kidneys, leading to bleeding from lungs and to kidney failure

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13
Q

primary causes of nephrotic syndrome

A

1 minimal change nephropathy - everything looks normal under a microscope but in an electron microscope, there’s a problem with the nephrons
2. membranous neuropathy- slowly progressive disease of the kidney affecting adults 30-50 yrs

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14
Q

membranous nephropathy

A
  • slowly progressive
  • 30-60 yrs
  • subepithelial Ig deposits along GBM, -thickening capillary wall
  • 85% idiopathic
  • antibodies reacting to endogenous or implanted glomerular antigens
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15
Q

minimal change nephropathy (lipid nephropathy)

A

1 pathology is detected only w/ electron microscope

2 T cells produce a cytokine that attacks foot processes and nephrins so proteins can seep through

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16
Q

Nephritic syndrome**

A

1 hematuria= elevation of blood urea
2 azotemia= high creatine or N-compds in blood
3 oliguria= little urine
4 crescent shaped

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17
Q

what has an acute onset, hypertension, and proteinuria, but not like nephrotic

A

nephritic syndrome!

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18
Q

chronic glomerulonephritis**

A

develops insidiously, discovered late in its course after onset of renal insufficiency, compensatory metabolic regulation hides the disease until late

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19
Q

nephritic vs. nephrotic

A 
nephritic= acute diffuse proliferative glomerulonephritis, crescent glomerulonephritis
nephrotic= membranous glomerulopathy and minimal change glomerulopathy
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20
Q

Glomerular diseases

A
  • structural changes in GBM

- damage to both basement membrane and cell proliferation (mixed nephritic and nephrotic syndrome)

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21
Q

benign nephrosclerosis

A
  1. hyaline thickening of small arteries and arterioles
  2. leads to decreased blood flow
  3. ischemia + diffuse tubular atrophy
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22
Q

malignant nephrosclerosis

A
  1. leads to malignant hypertension
  2. rapid increase in BP
  3. the glomerular capillary netowrk–> segmental tufts necrosis
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23
Q

fibrinoid necrosis

A

looks like onion skin, malignant hypertension or malignant nephrosclerosis

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24
Q

most common cause of renal infarction

A

1 emboli going down renal arterial branches like emboli from a mural thrombus (recent MI)
2 thrombotic vegetations on mitral/aortic valves /prosthesis
3 thrombus from left atrium of patients with atrial fibrillation

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25
Q

wedge shaped subscapular areas of necrosis with broad base at capsular surface

A

renal infarction

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26
Q

wedges of renal infarction

A
  • first, wedge intially red and slightly raised
  • 4-5 days later, wedge is yellow white center with rim of hyperemia
  • old infarcts are narrow, wedge shaped, depressed sacs
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27
Q

**what is the most common cause of end stage renal disease?

A

diabetusssss!

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28
Q

complications of diabetic vascular disease

A

1 increase severity of small, med, large arteries (general renal ischemia)
2 hyaline atherosclerosis in afferent arterioles (ischemic glomerular damage)

29
Q

diabetic glomerular damage

A

red stained coagulated fibrin protein (“protein cap”) on the surface of glomerulus

30
Q

kimmelstiel-wilson nodules only seen in

A

Diabetes!!!

31
Q

kimmelstiel wilson nodules description

A

excess mesangial matrix formation first as an even pattern throughout the glomerulus, but later as laminated spheres or nodules

32
Q

diabetic renal disease

A
  • BM thickens
  • exudative lesions as fibrin like material (fibrin caps
  • fibrin caps over tips of glomerular capillary loops
33
Q

adult polycystic disease

A

autosomal dom, manifestation in adults, 2 genes on chrom #2 and #16, kidneys enlarged bilaterally, partial parenchyma replaced w/ cysts

34
Q

In what disease do cysts enlarge over the years but are asymptomatic until # and size become so great that abdominal mass is observed

A

adult polycystic disease

35
Q

Wilm’s tumor

A

nephroblastoma, tumor of kidney in children (1-4 yrs)

36
Q

renal adenocarcinoma symptoms

A

hematuria (blood in urine)
flank pain (dull pain in lower part of body)
after 50 years; men
-palpable mass

37
Q

renal adenocarcinoma

A
  1. 90% of primary malignant renal tumors in adults
  2. from tubular epithelium
  3. majority are sporadic
  4. molecular classification advances help us understand etiology, often in poles (especially upper)
38
Q

gross renal adenocarcinoma

A

round, yellow cut surface w/ hemorrhage + necorsis

39
Q

histiology of renal adenocarcinoma (SEEN IN ADULTS)

A

polygonal clear cell

40
Q

Wilms tumor description

A

from primitive metanephros w/ at least 3 diff genetic alterations

  • less frequently hematuria
  • abdominal palpable, often huge mass
41
Q

reflux nephropathy

A
  • chronic reflux- associated pyelonephritis
  • scarring and atrophy results from superimposition of a UTI on congenital vesiculouretal reflux
  • unilateral or bilateral
42
Q

vesiculouretal reflux

A

constant UTI b/c valves stop functioning

43
Q

**What is the most comomn cause of acute renal failure?

A

acute tubular necrosis

44
Q

*How old is the peak incidence of Wilm’s tumor?

A

peaks incidence 1-4 yrs (children!)

45
Q

glomerular damage associated with proliferation of endothelial or mesangial cells is associated with

A

microhematuria or nephritic syndrome

46
Q

deposition of excessive mesangial matrix leads to

A

abnormal loss of protein in urine or to nephrotic syndrome

47
Q

If glomerular damage is RAPID, what develops?

A

acute renal failure

48
Q

diverticula of urethra

A

outpouching of bladder mucosa

49
Q

megaureter

A

enlarged ureter, dilated, dilation of pelvicalyceal system (dydronephrosis)

50
Q

end stage hydronephrosis

A
  • unilateral obstruction of ureter

- renal fxn maintained by nonobstructed kidney

51
Q

bilateral obstruction

A

usually w/ lesions of bladder base or retroperitonial tissues

52
Q

What occurs before severe atrophy of both kidneys?

A

renal failure

53
Q

bilateral kidney obstruction also predisposes to

A

infection and stone formation

54
Q

urinary calculi

A

kidney stones

55
Q

predisposing factors of urolithiasis

A
  1. increase solute in urine
  2. metabolite or low fluid
  3. reduced solubility bc abnormal PH
  4. stony concentrations in bladde or urinary tract
56
Q

What is the second most common type of urinary calculi made of ?

A

struvite ( Mg, NH4+, Calcium Phosphate)

57
Q

What is the most common symptom of transitional cell carcinoma of the bladder ?

A

hematuria

58
Q

transitional cell carcinoma of the bladder

A
  • most common tumor of urinary collecting system (calyces, pelvis, ureter, bladder)
  • often multifocal
59
Q

What causes transitional cell carcinoma of the bladder?

A

environmental agents excreted in high concentration in urine like aniline dye, cigarettes, cyclophosphamide

60
Q

are multiple tumors common in transitional cell carcinoma of the bladder

A

yes, field change in all of urothelium so multiple tumors are common

61
Q

what is the men:female of transitional cell carcinoma of the bladder

A

3:1

62
Q

what is the growth pattern of transitional cell carcinoma of the bladder

A

papillary growth pattern with cauliflower appearance

63
Q

Susceptibilities of nephrotic syndrome

A

1 susceptibility of infection b/c low Ig and complement

2 susceptibility to thrombosis bc increased fibrinogen in blood

64
Q

most frequent cause of nephrotic syndrome in children

A

minimal change nephropathy (lipid nephropathy)

65
Q

What does malignant nephrosclerosis do to large muscular vessels?

A

large muscular vessels w/ loose fibroelastic proliferation of the intima- the afferent arterioles exposed to sudden high prressure frequently undergo necrosis, w/ fibrin in damaged walls (fibrinoid necrosis)

66
Q

acute renal failure- when sufficient nephrons are destroyed (damage to tufts and afferent arterioles) leads to

A

malignant nephrosclerosis

67
Q

What nodules are seen in diabetic renal disease?

A

kimmelstiel wilson nodules

68
Q

infarction

A

is tissue death (necrosis) caused by a local lack of oxygen, due to an obstruction of the tissue’s blood supply

BHP Exam 4 (4 decks)

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