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Z MD1 Renal block > kidney pathology > Flashcards

kidney pathology Flashcards

0
Q

what is special about the collagen in the kidney

A

it has a strong negative charge - repels negatively charged species in the kidney - stopping their filtration

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1
Q

what type of collagen is in the glomerulus

A

special type of type 4 (reticular fibres)

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2
Q

3 cell types in the glomerulus

A 
endothelial cells lining the internal surface of the capillaries
mesangial cells in the stalk 
epithelial cells (podocytes) that cover the urinary surface of the basement membrane
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3
Q

4 presentations in a patient presenting with nephrotic syndrome

A

oedema - typically whole body oedema
proteinuria
hypoalbuminaemia
hyperlipidaemia

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4
Q

what is another word for nephrotic syndrome

A

severe proteinuria

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5
Q

what causes nephrotic syndrome

A

when proteins (particularly albumin) escape into the urine

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6
Q

3 reasons why proteins are not normally filtered into the filtrate of the glomerulus

A
  • negative charge repelled by the BM of the glomerulus
  • physical structure of the membrane of collage type 4
  • slit membrane between the podocytes
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7
Q

what are the key proteins of the slit membrane

A

nephrine, podocin and F1 and F2

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8
Q

what are the common causes of nephrotic syndrome

A

diabetes mellitus
some forms of glomerulonephritis
amyloid deposition
inherited abnormalities in those proteins that make up the slit membrane

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9
Q

proteinuria results from a ________ abnormality

A

glomerular filtration

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10
Q

acute renal failure definition

A

an acute reduction in glomerular filtration rate reflected as reduced creatinine clearance, and as a result an increasing serum urea and creatinine

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11
Q

what is the most commonest renal cause of acute renal failure

A

acute tubular necrosis

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12
Q

what is glomerulonephritis

A

injury to the glomerulus, most often immune mediated (eg. Type 3 hypersensitivity - depositing immune complexes)

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13
Q

what is the syndrome called when you have glomerulonephritis with no immune complexes involved

A

pauci-immune

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14
Q

when do you get crescents in the kidney

A

when there is acute glomerulonephritis associated with necrosis of part of the glomerulus leading to clumps of monocytes and epithelial cells and exuded fibrin = crescents

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15
Q

what is the commonest form of glomerulonephritis

A

IgA nephropathy

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16
Q

what is and what does membranous nephropathy lead to

A

proteinuria

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17
Q

how do glomeruli react to damage by the immune system

A

glomerular cells proliferate (epithelial, endothelial and mesangial)
inflammatory cells arrive (neutrophils, lymphocytes, monocytes)
BM may proliferate to make new layers of BM

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18
Q

what is the most common cause of end stage renal failure in australia

A

diabetic nephropathy

19
Q

what causes diabetic nephropathy

A

hyperglycaemia

20
Q

3 most important outcomes of tubulointerstitial injury

A 
acute tubular necrosis (ischaemia)
acute pyelonephritis (infection)
acute/chronic tubulointerstitial nephritis
21
Q

what causes acute tubular necrosis

A

blood supply falls to the nephron and therefore tubular epithelium dies –> degenerate and detach from the BM –> slough and leaving behind naked BM

22
Q

what are some drugs that can lead to acute tubular necrosis

A

heavy metals
some antibiotics
some cancer chemotherapy drugs

23
Q

what causes acute interstitial nephritis

A

allergic inflammation of the interstitium due to a drug

24
Q

histological presentation of acute interstitial nephritis

A

lots of lymphocytes in the interstitium of the kidney

25
Q

what is the histological presentation of acute pyelonephritis

A

bacteria in the medullary pyramids and foci of acute inflammation (necrosis)

26
Q

what causes analgesic nephropathy

A

long standing use of compounds containing phenacetin with caffeine and aspirin lead to direct toxic effects of phenacetin metabolites

27
Q

what does a kidney that has chronic renal failure look like macroscopically

A

rubbery, scarred, shrunken, knobbly kidney

28
Q

what does a kidney with chronic end stage kidney disease look like histologically

A

most of the kidney has turned into collagen, interstitium is expanded and fibrotic and tubules are atrophied

29
Q

at what stage of renal failure do you tend to have symptoms

A

when GFR is at 10%

30
Q

decision to treat hypertension in based on…

A

the level of absolute risk and evidence of end-organ damage (not levels of BP alone)

31
Q

classification of hypertension

A

primary/essential - no specific identifiable cuase
secondary - identifiable cause

benign - slow onset, doesnt go extremely high
malignant - fast onset (acute) and can go extremely high

32
Q

what factors create BP

A

cardiac output

resistance of arterioles

33
Q

what are the age related changes of the vesells

A

arteriosclerosis and arteriolosclerosis

34
Q

what happens during arteriosclerosis in large and small/medium vessels

A

large:
- media - fragmentation of elastin, increased collagen
- intima: increased collagen
small and medium arteries:
- media - fragmentation of elastin, increased collagen and sometimes calcification
- intima: increased collagen –> thickening

35
Q

what causes the pathology of arteriolosclerosis

A

deposition of plasma proteins in the wall, with increased collagen and smooth muscle atrophy

36
Q

how does arteriosclerosis lead to hypertension

A

loss of elasticity –> elevation of the SBP and widening of the pulse pressure

37
Q

what is the main reason for secondary systolic hypertension

A

renal disease

38
Q

what is the mechanism behind renal failure causing hypertension

A

decreased capacity to excrete sodium –> excessive renin secretion –> excessive sympathetic activity –> contraction of the vessels –> HT

39
Q

why cant atherosclerosis on its own lead to hypertension

A

because BP is determined by the resistance in the arterioles, not the large arteries

40
Q

when can atherosclerosis lead to HT

A

if the atherosclerosis is in the renal artery –> ischaemia –> renin released –> fluid retention and constriction of arterioles –> HT

41
Q

what are some outcomes of HT

A
  • LV hypertrophy –> MI, angina, sudden death, cardiac failure
  • atherosclerosis
  • aortic dissection
  • berry aneurysm
  • hyaline arteriolosclerosis
  • renal failure
  • stroke
  • retinopathy
42
Q

what is the histology in a kidney with benign nephrosclerosis

A
  • chronic inflammation due to ischaemia
  • more intersitital CT
  • fewer tubules due to atrophy
  • sclerosed glomeruli
43
Q

what are the effects of malignant hypertension

A

hyperplastic arteriosclerosis of the media in the blood vessels
fibrinoid necrosis as a result of chronic stress on the walls –> thrombus

44
Q

what are the possible outcomes for secondary hypertension

A

retinopathy
deteriorating renal function
microangiopathic hemolytic anaemia
encephalopathy

Z MD1 Renal block (8 decks)

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