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Year 5 😊✌🏼 > MedEd Histopath 2 > Flashcards

MedEd Histopath 2 Flashcards

1
Q

Which pneumonia pathogen is associated with erythema multiforme?

A

Mycoplasma pneumonia

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2
Q

AKI - what is it?

A

acute decline in renal function
leads to fall in urine output
measured with Cr and Urea

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3
Q

CKD - what is it?

A

decline in renal function over >3 months
progressive damage
eGFR used to measure/stage it

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4
Q

eGFR - CKD staffing

A

1 - >90
2 60-89 (mild)
3A 45-59
3B 30-44
4 12-29
5 <15 (end stage)

no sx, no CKD

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5
Q

Causes of CKD

A

DM
HTN

ADPKD
untreated AKI (pyelonephritis, ATN, obstruction)

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6
Q

are AKI and CKD reversible?

A

AKI can be

CKD no

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7
Q

Causes of AKI

A

renal
- ischaemia
- nephrotoxins
- glomerulonephritis
- interstitial nephritis
- hepatorenal syndrome
- HUS/TTP

post-renal

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8
Q

Types of intrinsic renal pathology

A

Glomerulus
- nephrotic syndromes (minimal change, membranous, FSGS, secondary causes)
- nephritic syndromes (IgA, post streptococcal, rapidly progressive (crescentic) _>

add

Blood vessels
- HUS
TTP

Tubules
add

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9
Q

Mesangium (kidney)

A

ECM
EC-tissue

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10
Q

which cells do the filtering ?

A

podocytes (check)

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11
Q

nephrotic syndrome triad

A

peripheral oedema
proteinuria (3g/d or PCR >300mg)
low serum albumin

also increased cholesterol and clotting tendencies

issues with podocytes -> protein get out

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12
Q

nephrotic syndrome triad

A

peripheral oedema
proteinuria (3g/d or PCR >300mg)
low serum albumin

also increased cholesterol and clotting tendencies

issues with podocytes -> protein get out

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13
Q

Minimal change disease

A
  • affects children
  • normal on light microscopy
  • electron microscopy shows loss of food processes in podocytes
  • nothing on immunofluorescence
  • responds very well to steroids (90% poeple respond well to pred)
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14
Q

Membranous glomerulopathy

A
  • immune complexes attach evenly to basement membrane
  • responds poorly to steroids
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15
Q

Which antibodies are associated with membranous glomerulopathy?

A
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16
Q

FSGS

A

focal: only some glomeruli are damaged
segmental: only some regions of the glomerulus are damaged
sclerosis: scarring

affects adults

light microscopy shows focal and segmental scarring
EM: loss of foot processes
Responds less well to steroids (but better than)

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17
Q

secondary causes of nephrotic syndrome

A

Diabetes (kimmelstiel Wilson nodules)

Amyloidosis
- AA or AL
AA is chronic inflammation e.g. SLE, RA
AL is light chains -> multiple myeloma

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18
Q

Nephritic syndrome

A

haematuria
HTN
peripheral oedema

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19
Q

red cell casts in urine

A

red cells forced through the sieve
damage to kidney
…

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20
Q

IgA nephropathy

A

causes nephritic syndrome
post group A strep infection (1-2d, IgA = acute)

IgA immune deposits within glomeruli
IgA immune deposits in mesangium seen on IF

33% get better
33% get CKD
33% need dialysis

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21
Q

post strep glomerulonephritis

A

after group A strep infection (1-3w)
thought to be due to antigen mimicry and immune complex deposition

bloods: raised anti-streptolysin O titre, reduced C3

IF: granular IgG deposits in BM

Mx: supportive

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22
Q

Rapidly progressive (crescentic)

A

most aggressive form of glomerulonephritis causing renal failure in weeks

characterised by severity and presence of crescents (macrophages in Bowman’s capsules)

acute onset

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23
Q
A

Anti-GBM - Goodpastures
Immune complex mediated
Pauci immune (ANCA-assocaited)

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24
Q

Goodpastures syndrome

A

anti-GBM disease
presence of anti-glomerular BM Ab

credence seen on LM
IF: linear deposition of IgG in GBM

also see pulmonary haemorrhage

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25
Q

Immune complex mediated - rapidly progressive GN causes

A

SLE
IgAa nephropathy
post-infection
HSP

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26
Q
A

bumpy deposition of immune complexes in GBM or mesangium

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27
Q

Pauci-immune/ANCA associated

A

cANCA: GPA
pANCA: MPA/eGPA
vasculitis affecting small micro blood vessels

LM;
IF: no/scanty immune complexes

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28
Q

Alpert’s syndrome

A

hereditary cause of glomerulonephritis

X-linked causing problem with type 4 collagen

triad:

causes progressive end stage renal failure with some extra-renal sx

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29
Q

benign familial haematurua - genetic issue

A

AD gene causing problem with type 4 collagen

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30
Q

benignfamilial haematurua

A

causes

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31
Q

ATN

A
  • most common renal cause of AKI
  • tubules will die and she leading to presence of brown casts in the urine
  • caused by hypovolaemia
  • toxins (aaminoglycosdies ee.g. gentamicin, myoglobin (rhabdomyolysis), contrast)
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32
Q

commonest cause of renal AKI

A

ATN

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33
Q

Acute interstitial nephritis

A

interstitial infiltrate of

kind of like an allergic rection

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34
Q

causes of white and brown cell casts in urine

A

white: AIN
brown: ATN

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35
Q

AIN - causese

A

most often after starting

36
Q

HUS

A

eColi O157:H7

after petting zoo, after a bout of diarrhoea

37
Q

E coli O157:H7 - what does it cause?

38
Q

TTP - genetic mutation

A

ADAMTS13 protease deficiency (it cleared vWF)

40
Q

PKD

A

AD due to mutation in PKD gene encoding polycystic

extra renal
- liver cysts
- Berry aneurysms (SAH)

41
Q

Lupus nephritis

A

wire loop capillaries and lumpy immune complex deposotopm

42
Q

6 stages of lupus nephritis

A

1: minimal

early: only connective tissue affected, later on also kidney tissue finally advanced sclerosis(>90%)

43
Q

Portal triad

A

hepatic artery
portal vein
bile duct

-> central vein in the middle of lobule

44
Q

functional unit of liver

45
Q

Zone 1-3 liver

A

1: periportal (closest to BV)
- affected first in viral hepatitiss and toxic substance ingestion
- most oxygenation

2: Mid zone

add

46
Q

rouses transaminases 0 3 main causes

47
Q

causes of acute hepatitis

A
  • hep Aa/E (faeco oral route)
    drugs
48
Q

pattern of infallamtion in acute hepatitis

A

spotty ///////add

49
Q

Causes of chronic hepatitis

50
Q

pattern inflammation in chronic hep

A

piecemeal necrosis/interface hepatitis

loss of border between the portal tract and the surrounding parenchyma

bridging fibrosis
check

51
Q

nodule size in cirrhosis

A

micronodulaar: alcohol
macro nodular: everything else

52
Q
A

high resistance in fibrotic

intrahep

53
Q

intrahepatic shunting

A

bypasses hepatocytes

due to …..backflow due to restistance of hepatocytes?

54
Q

F1-F4 fibrosis

55
Q

Mallory denk bodies

A

seen in alcoholic hepatitis

56
Q

steatosis vs alcoholic hepatitis vs. alcoholic cirrhosis

57
Q

NAFLD

A

Histologicaally similar to ALD, distinguished via hx

Progression
1.
2.
3. cirrhosis

61
Q

stain in alpha 1 antitr

62
Q

Wilsons

63
Q

haemaachromatosis

64
Q

commonest liver tumours

65
Q

commonest liver tumour

A

haemangioma (most common, benign)

66
Q

liver cell adenoma

A

associated with cOCP

67
Q

antibodies in

A

anti-mitochondrial antibody

68
Q

inheritance pattern of hereditary haemochromatosis

69
Q

WIlson inheritance pattern

70
Q

alpha-1 antitrypsin deficiency inheritance pattern

71
Q

most common examination finding in a patient with portal HTN
splenomegaly
hepatomegaly
spider naevi
jaundice
liver flap

A

splenomegaly

72
Q

Which pathogens cause spotty necrosis in

A

hep A/E (what causes acute hepatitis)

73
Q

which tumours have keratin production of intercellular bridges?

A

aqueous cell carcinoma

74
Q

which malignant tumours have glands?

A

adenocarcinomas

75
Q

H&E stain full nam e

A

haematoxylin and eosin

purple:
pink:

76
Q

histopath in MI

A

<6 h: normal histology

6-24h: loss of nuclei, homogenous cytoplasm and necrotic cell death

1-4d” infiltration of polymorphs then macrophages (which clear up debris)

5-10d further removal of debris

1-2w has granulation tissues new BVs, myofibroblasts.

add

77
Q

FAP mutation

A

AD mutation in APC tumour suppressor gene

78
Q

FAP presentation

A

100s or 1000s of polyps

seen in childhood

adenoma -> polyp -> carcinoma

progression ot cancer is 10)%

79
Q

Garner’s syndrome

A

subtypes of FAP with extra-GI sx

more

80
Q

Lynch syndrome mutation

A

AD mutation in DNA mismatch repair gene

81
Q

What cancers in HNPCC associated with?

A

endometrial
ovarian
gastric
colon

82
Q

GI polyps higher risk of cancer

A
  • larger
  • more
  • higher villous component
  • dysplastic features
83
Q

Medullary thyroid carcinoma

A

parafollicular cells
measure calcitonin

84
Q

MEN syndrome

A

MEN 1: 3P

2P

1 P

85
Q

Gleason Score

A

/10

sum of worst grade seen and the most common grade seen (e.g. 3+5 = 8)

Year 5 😊✌🏼 (53 decks)

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