Clinical V Renal Flashcards

1
Q

what are histological alterations of the filtration mechanism associated with glomerular injury?

A

hypercellularity
thickening of the BM
hyalinosis and sclerosis

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2
Q

what are causes of glomerular kidney disorder?

A

immunological

toxic or infectious agents

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3
Q

what are example of glomerular kidney disorders?

A

glomerulonephritis

IgA nephropathy

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4
Q

what are some causes of tubular kidney disorders?

A

toxic
ischemia
mechanical

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5
Q

what are some causes of interstitial kidney disorders?

A

infectious

medication

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6
Q

what are examples of vascular kidney disorders?

A

hypertension

vasculitis

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7
Q

what is acute proliferative (post streptococcal Post infectious) glomerular nephritis

A

inflammation reaction = injury of the capillary wall
there is an escape of RBCs

leads to nephrotic syndrome

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8
Q

what are the symptoms associated with nephrotic syndrome?

A
hematuria
oliguria
HTN
proteinuria
edema
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9
Q

where might you find Ag-Ab complexes - electron dense deposits?

A

subendothelial - circulating, granular
subepithelial - in situ, granular
membranous - in situ, linear
mesangial

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10
Q

what occurs with hypercellularity in post streptococcal GN?

A

endothelial and mesangial cells
infiltration of neutrophils
crescent formation

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11
Q

what can you see with immunoflourescence in post streptococcal GN?

A

GRANULAR deposits of IgG, IgM and complement along BM

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12
Q

what can you see using electron micrograph in post streptococcal GN?

A

subendothelial intramembraneous and subepithelial hump against the GBM

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13
Q

what is Mesangial proliferative GM (IgA nephropathy)? What population is it commonly found in? What type of injury?

A

upper respiratory tract infection
young children and adults
diffuse and global injury

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14
Q

what are histological symptoms of Mesangial proliferative GM (IgA nephropathy)

A

increased mesangial maxtrix and cellularity
EM = electron dense deposits in the mesangium
IF = deposits of IgA (HALLMARK)*

associated with nephrotic syndrome

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15
Q

what is nephrotic syndrome?

A

increase in permeability of the capillary wall to plasma proteins

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16
Q

what are characteritstics of the PCT?

A

resorption
excretion
Mv

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17
Q

what is the function of the loop of Henle in relation to the tubules?

A

create a hypertonic environment surrounding the tubules

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18
Q

what are characteristics of the DCT?

A

macula densa

well developed basal foldings

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19
Q

what can cause tubular and interstitial injury?

A
drugs
iodine containing contrast agents
metals
infections
hypovolemic shock
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20
Q

what protein is affected in the adolescent congenital polycystic disease of the kidney?

A

fibroystin

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21
Q

what type of disease is the kind that affects kids congenital polycystic disease of the kidney?

A

autosomal recessive PKD

22
Q

what protein is defective in adult congenital polycystic disease of the kidney?

A

polycystin

23
Q

what type of disease is adult congenital polycystic disease of the kidney?

A

autosomal dominant PKD

24
Q

what is the most common cause of acute tubular necrosis?

A

acute ischemia

25
Q

what can you see with light microscopy of acute tubular necrosis(tubular injury)?

A

PCT - dilated tubules and flat epithelium

loss of brush borders and infoldings

26
Q

what are common causes of acute pyelonephritis?

A

acute suppurative bacterial infection
BPH
pregnancy

27
Q

what will you find in light microscopy of acute pyelonephritis?

A

neutrophil infiltration of the renal interstitum and tubules

28
Q

chronic inflammation and obstruction of the drainging system (calyces, ureters) associated with acute pyelonephritis may result in what?

A

hydronephrosis /hydroureters

29
Q

what does chronic pyelonephritis result in?

A

vesicourethral reflux
corticomedullary scaring
papillary necrosis

30
Q

what is hydronephrosis/ hydroureters? What can it lead to?

A

obstruction of the collecting system draining the kidney

maintained pressure in the system can lead to permanent kidney damage

31
Q

what is one of the principle causes of renal failure?

A

untreated HTN

32
Q

what does increased tension in the vessels lead to?

A

thickening of the walls and reduction in the calibre of the vessel

33
Q

what can you see using light microscopy of htn?

A

thickened and eosinophilic vessel walls

34
Q

what are the risks associated with DM in kidneys?

A

infections

atherosclerosis

35
Q

what are the histological changes seen in the kidney with DM?

A

icrease mesangial matrix (KIMMELSTEIL-WILSON NODULES)

increase thickness of the basement membrane with EM

36
Q

what is the frequency of renal cell carcinoma

A

80-85% adults

37
Q

who is at risk for renal cell carcinoma?

A

males , 60-70 yo, smokers, obesity, htn

38
Q

where is the common location of renal cell carcinoma?

A

cortex - renal tubular epithelium

39
Q

how often is hematuria present with renal cell carcinoma?

A

50% of cases

40
Q

what are the symptoms of renal cell carcinoma?

A
flank pain
ab mass
prolonged fever
polycythemia
paraneoplastic symptoms
metastases - lung, bone etc.
41
Q

where is the origin of renal cell carcinoma?

A

renal tubular epithelial cells (adenocarcinoma)

42
Q

what are the subtypes of renal cell carcinoma?

A

clear cell
papillary (chromophil)
chromophobe

43
Q

what is the growth patterns of renal cell carcinoma?

A

trabeculae or cordlike or tubular

44
Q

what kind of cells are present with renal cell carcinoma?

A

rounded or polygonal with clear or granular cytoplasm

45
Q

what types of cells are found in papillary carcinoma?

A

cuboidal or low columnar cells

46
Q

what types of cells are found in chromophobe carcinoma?

A

pale eosinophilic cells with perinuclear halo

47
Q

what is the major cause of renal artery stenosis?

A

atheromatous plaques - atherosclerosis

48
Q

what is a less common >1% cause of renal artery stenosis??

A

htn

49
Q

what will untreated renal artery stenosis result in?

A

renal atrophy

50
Q

is renal artery stenosis curable?

A

yes

51
Q

what is the htn effect due to with renal artery stenosis?

A

increased production of renin and subsequent circulation of angiotensin II