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MedEd Path > MedEd Histo 2 > Flashcards

MedEd Histo 2 Flashcards

1
Q

what is AKI

A

acute decline in renal function leading to fall in urine output

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2
Q

how is AKI captured in clinical setting

A

rise in creatinine / urea seen on U&Es

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3
Q

what is CKD

A

decreased kidney function or kidney damage, present for more than 3 months

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4
Q

how is CKD captured in clinical setting

A

fall in eGFR

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5
Q

normal eGFR

A

> 90

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6
Q

eGFR of each stage of kidney disease

A

1 = >90 (normal)
2 = 60 - 89 (mild)
3A = 45 - 59 (mod)
3B = 30 - 44 (mod)
4 = 15 - 29 (severe)
5 = <15 (ESRF)

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7
Q

2 most common causes of CKD

A

DM
HTN

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8
Q

other causes of CKD except DM and HTN

A

ADPKD (PCKD)
untreated AKI
- pyelonephritis
- ATN
- obstruction

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9
Q

how do categorise AKI

A

pre renal
renal
post renal

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10
Q

general cause of pre renal AKI

A

decreased blood flow to kidneys

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11
Q

causes of pre renal AKI

A

hypovolaemia
sepsis
CCF
renal artery stenosis
ACEi

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12
Q

general cause of renal AKI

A

direct damage to nephrons

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13
Q

causes of renal AKI

A

ischaemia
nephrotoxins
GN
interstitial nephritis
hepatorenal syndrome
HUS / ITP

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14
Q

general cause of post renal AKI

A

physical blockage to outflow

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15
Q

causes of post renal AKI

A

stones
tumours
prostate problems
blocked catheter

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16
Q

of the 3, which type of AKI is the most to least common

A

most common = pre renal
2nd = post renal
3rd = renal

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17
Q

what diseases affect the glomerulus

A

nephrotic and nephritic syndromes

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18
Q

name 4 nephrotic syndromes

A

minimal change
membranous
FSGS
secondary causes

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19
Q

name 5 nephritic syndromes

A

IgA vasculitis
post strep GN
Alports syndrome
benign familial haematuria
rapidly progressive GN - goodpastures, pauci immune, immune complexes

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20
Q

name 2 conditions which can affect BVs of kidney

A

HUS
TTP

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21
Q

name 2 tubule disorders

A

acute tubular necrosis
acute interstitial nephritis

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22
Q

what is mesangium

A

connective tissue (ESM) between capillaries in kidneys

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23
Q

what cells actually do the filtering in kidney

A

podocytes

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24
Q

triad of nephrotic syndrome

A

peripheral oedema
proteinuria
low serum albumin

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25
Q

define proteinuria

A

3g/day or PCR >300mg

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26
Q

what other 2 associated features often come with nephrotic syndrome

A

increased cholesterol
increased clotting tendency

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27
Q

what is the actual issue in nephrotic syndromes

A

issue with podocytes which form the filtration barrier

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28
Q

treatment of nephrotic syndromes

A

steroids

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29
Q

who gets minimal change disease

A

kids

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30
Q

Ix of minimal change disease

A

light microscopy
electron microscopy
immunoflurescence

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31
Q

what does light microscopy / immunoflurescnce of minimal change disease show

A

NOTHING

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32
Q

what does electron microscopy of minimal change disease show

A

loss of podocyte foot processes

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33
Q

tx and prognosis of minimal change disease

A

steroids (prednisolone) - very good response

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34
Q

what does immunoflurescence look for

A

immune complexes

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35
Q

who gets membranous GN

A

adults

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36
Q

histology of membranous GN

A

diffuse basement membrane thickening

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37
Q

what can you see on EM of membranous GN

A

spikey immune complexes deposited

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38
Q

what can you see on immunoflurescence of membranous GN

A

immune complexes across all the BM

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39
Q

tx and prognosis of membranous GN

A

poor response to steroids

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40
Q

2 associations of membranous GN

A

SLE
anti phospholipase a2 ABs

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41
Q

what is FSGS

A

focal segmented glomerulonephritis

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42
Q

characteristic finding of FSGS

A

only SOME parts of kidney affected (focal)

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43
Q

who gets FSGS

A

adults

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44
Q

histology of FSGS

A

focal and segmental scarring

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45
Q

EM of FSGS

A

loss of foot processes

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46
Q

immunoflurescence of FSGS and why

A

NOTHING - no immune complexes involved

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47
Q

steroid response to FSGS

A

not great but not as bad as membranous

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48
Q

secondary causes of nephrotic syndromes

A

DM
amyloidosis

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49
Q

buzzword for DM causing nephrotic syndrome

A

Kimmelsteil Wilson nodules

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50
Q

buzzword for amyloidosis

A

apple green birefringence with Congo red stain

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51
Q

2 types of amyloidosis & what they are

A

AA (chronic inflam eg RA)
AL (light chains -> MM)

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52
Q

triad of nephritic syndrome

A

HTN
haematuria
peripheral oedema

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53
Q

what do you see in urine of nephritic syndrome

A

red cell cast

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54
Q

what is the actual problem with nephritic syndrome

A

large proteins / immune complexes causing damage to delicate kidney BVs

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55
Q

what is the commonest cause of GN worldwide

A

IgA nephropathy

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56
Q

what preceeds IgA nephropathy

A

group A strep infection

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57
Q

how long after strep infection do you get IgA nephropathy

A

1-2 days

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58
Q

what is the problem in IgA nephropathy

A

deposition of IgA immune complexes within glomeruli

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59
Q

immunoflurescence of IgA nephropathy

A

IGA immune deposits in MESANGIUM

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60
Q

what is the 1/3rds rule with IgA nephropathy

A

1/3 get better
1/3 get CKD
1/3 need dialysis

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61
Q

difference between IgA nephropathy and post strep GN presentation

A

same Sx but post strep GN occurs 1-3 WEEKS after group A strep, but IgA nephropathy is 1-2 days

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62
Q

what is the problem in post strep GN

A

antigen mimicry and immune complex deposition

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63
Q

2 blood results seen in post strep GN

A

reduced c3
raised anti streptolysin O titre

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64
Q

immunoflurescence of post strep GN

A

granular IgG deposits in BASEMENT MEMBRANE

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65
Q

mx of post strep GN

A

supportive

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66
Q

name cresentic (rapidly progressive) GN

A

goodpastures
immune complex mediated
pauci-immune (ANCA-associated ie vasculitis)

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67
Q

what are cresentic (rapidly progressive) GN

A

most aggressive type of GN, causing renal failure in weeks

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68
Q

what is characteristic of cresentic (rapidly progressive) GNs on histology (inc what this actually is)

A

severity and presence of crescents (macrophages in Bowman’s space)

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69
Q

buzzword for goodpastures

A

anti glomerular BM ABs

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70
Q

what does histology of goodpastures show

A

crescents

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71
Q

what does immunoflurescence of goodpastures show

A

linear deposition of IgG in GBM

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72
Q

sx of goodpastures

A

nephritic syndrome
pulmonary haemorrhage

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73
Q

causes of immune complex mediated GN

A

SLE
IgA nephropathy
post infectious
HSP

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74
Q

histology of immune complex mediated GN

A

crescents

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75
Q

immunoflurescence of immune mediated GN

A

bumpy deposition of immune complexes in GBM or mesangium

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76
Q

name 2 pauci-immune / ANCA associated GNs

A

granulomatosis with polyangiitis
eosinophilic granulomatosis with polyangiitis

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77
Q

buzzword for granulomatosis with polyangiitis

A

cANCA

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78
Q

buzzword for eosinophilic granulomatosis with polyangiitis

A

pANCA

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79
Q

where do pauci-immune GNs effect

A

vasculitis affecting small micro blood vessels

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80
Q

immunoflurescence of pauci-immune GN

A

no / scanty immune complexes
–> this one isnt immune complex mediated

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81
Q

sx of pauci-immune GN

A

skin rashes
pulmonary haemorrhage
nephritic syndrome

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82
Q

what is alports syndrome

A

hereditary cause of CKD

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83
Q

how is alports inherited

A

X linked (affects boys)

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84
Q

what is the defect in alports

A

type 4 collagen problem

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85
Q

triad of alports sx

A

nephritic syndrome
bilateral sensorineural deafness
lens dislocation

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86
Q

prognosis of alports

A

progressive
causes ECKD in young adults

87
Q

inheritance of benign familial haematuria

A

AD

88
Q

what is the defect in benign familial haematuria

A

type 4 collagen

89
Q

aka benign familial haematuria

A

thin basement membrane disease

90
Q

sx of benign familial haematuria

A

asymptomatic haematuria
no other issues generally

91
Q

most common cause of renal AKI

A

acute tubular necrosis

92
Q

sign of acute tubular necrosis and why

A

brown casts in urine
- tubule cells die and shed into urine

93
Q

causes of acute tubular necrosis

A

hypovolaemia
toxins
- gentamicin
- myoglobin (rhabdomyolysis)
- IV contrast

94
Q

what is acute interstitial nephritis

A

kind of like an allergic reaction
-see interstitial infiltrate and eosinophils

95
Q

what sign is seen in acute interstitial nephritis

A

sterile pyuria
(white cell casts / white cells in urine with no infection)
also rash / fever

96
Q

what causes acute interstitial nephritis

A

penicillins
allopurinol
NSAIDs

97
Q

when can you get chronic interstitial nephritis

A

taking paracetamol / NSAIDs for ages

98
Q

triad of HUS

A

progressive renal failure
MAHA
low platelets

99
Q

most common specific cause of HUS (esp in kids <5)

A

e.coli O157:H7

100
Q

describe the 4 steps of pathophysiology of HUS

A

gastroenteritis (e.coli) - produces toxins
endothelial damage
thrombosis, platelet consumption, fibrin strand deposition
destruction of RBCs - schistocytes / anaemia

101
Q

where can kids get e.coli O157:H7 from

A

petting zoos

102
Q

what is TTP

A

thrombotic thrombocytopaenic purpura

103
Q

pentad of TTP

A

MAHA
thrombycytopaenia
uraemia
fever
neuro Sx
(ie HUS + fever + neuro sx)

104
Q

mortality of TTP if untreated

A

> 90%

105
Q

describe pathophysiology steps of TTP

A

deficiency of protease that cleaves vWF
large vWF multimers form
platelet aggregation and fibrin deposition
microthrombi

106
Q

how are the microthrombi different in TTP and HUS

A

HUS - microthrombi just in liver
TTP - microthrombi occur everywhere esp in CNS

107
Q

what protease enzyme is deficient in TTP

A

ADAMTS13

108
Q

inheriatnce of PCKD

A

AD

109
Q

defect in PCKD

A

PKD gene defect encoding polycystin

110
Q

sx of PCKD

A

haematuria
kidney failure

111
Q

extra renal manifestations of PCKD
** buzzwords

A

liver cysts (most common)
berry aneurysms ** key buzzword
–> SAH

112
Q

what is lupus nephritis

A

damage due to immune complex deposition

113
Q

buzzwords of histology seen in lupus nephritis

A

wire loop capillaries
lumpy immune complex deposition

114
Q

6 stages of lupus nephritis

A

1 = minimal mesangial disease only
2 = mesangial disease
3 = focal deposits
4 = diffuse deposits
5 = subepithelial membranous disease
6 = advanced sclerosis (>90%)

115
Q

ABs to phsopholipase a2 R are associated with which form of GN

A

membranous

116
Q

ABs to minimal change disease

A

none

117
Q

ABs to goodpastures

A

anti BM

118
Q

histology of kidney biopsy of MM pt

A

amyloid deposition

119
Q

describe the liver anatomy zones from portal triad to central vein

A

portal triad: hepatic artery, portal vein, bile duct
zone 1 (periportal)
zone 2
zone 3 (periventricular)
central vein

120
Q

which zone is least / most oxygenated

A

zone 1 is most
zone 3 is least

121
Q

which zone does viral hepatitis / toxins affect first

A

zone 1

122
Q

which zone is most sensitive to metabolic toxins and why

A

zone 3 - has the most hepatocytes

123
Q

which zone is most sensitive to ischaemia and why

A

zone 3 - least oxygenated

124
Q

3 causes of massively raised LFTs

A

viral hepatitis
ischaemia
metabolic toxins eg paracetamol

125
Q

causes of acute hepatitis

A

viral - A&E
drugs
AID

126
Q

what is the pattern of inflammation in acute hepatitis
*** buzzword

A

spotty necrosis

127
Q

what is spotty necrosis

A

small foci of inflammation and necrosis with inflammatory infiltrates

128
Q

causes of chronic hepatitis

A

viral (C)
drugs
PBC, PSC
Wilsons / haemachromatosis

129
Q

what is the pattern of inflammation in chronic hepatitis
*** buzzword

A

piecemeal necrosis / interface hepatitis

130
Q

what is piecemeal necrosis / interface hepatitis

A

loss of border between portal tract and surrounding parenchyma

131
Q

what histological sign in lvier signals evolution to cirrhosis
**buzzword

A

bridging fibrosis (portal triad to central vein)

132
Q

what are the causes of micronodular vs macronodular replacement of hepatocytes

A

micro = alcohol
macro = everything else

133
Q

describe the pathophysiology of cirrhosis

A
  1. hepatocyte damage leads to necrosis
  2. fibroblasts replace hepatocytes, some areas of regenerating hepatocytes remain
  3. increased resistance to blood flow within liver leads to portal HTN
  4. increases resistance causes fibrotic bridges to form –> intrahepatic shunting (bypasses the hepatocytes)
  5. portal HTN causes extrahepatic shunts due to backlog of blood
134
Q

where are the portal anastomoses

A

oesophagus
anorectal
umbilicus
spleen

135
Q

3 main histological patterns of alcoholic liver disease

A

hepatic steatosis –> alcoholic hepatitis –> cirrhosis

136
Q

3 key features of hepatic steatosis

A

fully reversible if ETOH stopped
large, pale, yellow, greasy liver
fat droplets in hepatocytes

137
Q

3 key histological features of alcoholic hepatitis
**buzzwords

A

hepatocyte ballooning
mallory denk bodies
fibrosis

138
Q

which zone is most affected in alcoholic hepatitis

A

3

139
Q

features of alcoholic cirrhosis

A

shrunken brown organ
micronodular cirrhosis

140
Q

how is NAFLD distinguished from alcoholic liver disease

A

history - histology is the same

141
Q

cause of NAFLD

A

insulin resistance associated with obesity / DM

142
Q

who gets PSC

A

males

143
Q

buzzwords for histology of PSC

A

periductal intra / extra hepatic bile duct fibrosis

144
Q

3 associations of PSC
** buzzwords

A

UC
cholangiocarcinoma
pANCA

145
Q

who gets PBC

A

females with other AIDs

146
Q

histology buzzwords of PBC

A

chronic BD inflammation
granulomas

147
Q

buzzword for AB association of PBC

A

anti mitochondrial ABs

148
Q

who gets AI hepatitis

A

young / post menopausal women with other AIDs

149
Q

2 AB associations buzzwords for AI hepatitis

A

anti smooth muscle AB
anti liver kidney microsomal (LKM) Ig

150
Q

inheritance of haemochromatosis

A

AR

151
Q

sx of haemachromatosis

A

bronzed skin
DM
hepatomegaly

152
Q

buzzword histology stain for haemachromatosis

A

prussian blue stain

153
Q

pathophysiology of haemochromotosis

A

increased gut iron absorption

154
Q

pathophysiology of wilsons

A

failure of copper excretion by hepatocytes to bile

155
Q

buzzword histology stain for wilsons

A

rhodanine stain

156
Q

buzzword ix result for wilsons

A

reduced serum caeroplasmin
reduced serum copper

157
Q

alpha 1 antitrypsin deficiency pathophysiology

A

failure to secrete alpha 1 antitrypsin into blood –> massive build up in hepatocytes –> forms globules in hepatocytes –> chronic hepatitis

158
Q

buzzword histology stain and result for alpha 1 antitrypsin deficiency

A

periportal red hyaline globules using periodic acid schiff stain

159
Q

most common form of liver cancer

A

mets

160
Q

3 benign liver cancers

A

haemangioma
liver cell adenoma
bile duct adenoma

161
Q

association of liver cell adenoma

A

OCP

162
Q

most common benign liver cancer

A

haemangioma

163
Q

2 malignant liver cancers

A

HCC
cholangiocarcinoma

164
Q

tumour marker for HCC

A

AFP

165
Q

RFs for HCC

A

viral hepatitis
alcoholic cirrhosis
NAFLD
aflatoxin
haemochromatosis

166
Q

association of cholangiocarcinoma

A

PSC

167
Q

histology of cholangiocarcinoma

A

capillary ingrowth

168
Q

inheritance for
haemochromatosis
wilsons
alpha 1 antitrypsin

A

AR
AR
AD

169
Q

most common examination finding in someone with portal HTN

A

splenomegaly

170
Q

liver biopsy reveals spotty necrosis, which is most likely cause?
hep A
hep B
hep C
TB
HIV

A

Hep A

171
Q

what are neutrophils raised in

A

acute inflam

172
Q

what do neutrophils look like

A

multilobed and granulated

173
Q

what are macrophages released in

A

late acute inflammation to clear debris
chronic inflammation

174
Q

what are lymphocytes released in

A

chronic inflam

175
Q

what are eosinophils raised in

A

allergy
parasitic infection

176
Q

what do eosinophils look like

A

bi-lobed nuclei with red granules

177
Q

what are mast cells raised in

A

allergy

178
Q

what do mast cells look like

A

large cells with lots of granules

179
Q

key buzzwords of SCC

A

keratin production
intercellular bridges
NOT gland forming

180
Q

where can you get SCC

A

skin
H&N
oesophagus - upper/middle 1/3
anus
cervix / vagina

181
Q

buzzwords of adenocarcinomas

A

forms glands
secretes mucin

182
Q

where can you get adenocarcinomas

A

viscera
- lung / breast / stomach / colon / pancreas

183
Q

where can you get transitional cell carcinoma

A

kidney pelvis
ureters
bladder

184
Q

2 key histo stains

A

haematoxylin
eosin

185
Q

what does haematoxylin and eosin stain and what colour

A

haematoxylin = basic parts PURPLE
eosin = acidic parts PINK

186
Q

MI histopath at <6hrs

A

normal
CK-MB also normal

187
Q

MI histopath at 6 - 24hrs

A

loss of nuclei
homogenous cytoplasm
necrotic cell death

188
Q

MI histopath 1-4 days

A

infiltration of polymorphs then macrophages to clear up debris

189
Q

MI histopath 5 - 10 days

A

further removal of debris

190
Q

MI histopath 1-2 weeks

A

granulation tissue
new blood vessels
myofibroblasts
collagen synthesis

191
Q

Mi histopath weeks to months

A

strengthening
decellularising scar tissue

192
Q

inheritance of FAP

A

AD

193
Q

where is the mutation in FAP

A

APC TSG

194
Q

how does FAP present

A

100s to 1000s of polyps in childhood

195
Q

prognosis of untreated FAP

A

100% risk of adenocarcinoma in early adulthood

196
Q

what is gardeners syndrome

A

subtype of FAP with extra-intestinal features

197
Q

what are the extra-intestinal features of gardner’s syndrome

A

osteomas of skull
epidermoid cysts
desmoid tumours
dental caries

198
Q

inheritance of gardners

A

AD

199
Q

inheritance of lynch

A

AD

200
Q

what is the gene defect in lynch

A

DNA mismatch repair gene

201
Q

number of polyps in lynch vs FAP

A

much less in lynch in the 10s
FAP in 100s-1000s

202
Q

why does lynch progress to cancer even if there are less polyps than FAP

A

can’t repair errors as defect is in DNA mismatch repair gene

203
Q

extra-colonic cancers seen in lynch

A

endometrial (2nd most common)
ovarian
small bowel
gastric

204
Q

how are FAP / lynch / gardners mx

A

regular monitoring
+/- colectomy

205
Q

what features of polyps increases the risk of cancer

A

larger polyps (key one)
more polyps
higher villous component
dysplastic features

206
Q

what % of colorectal cancers are adenocarcinomas

A

98%

207
Q

what is the medical name of colon polyps

A

adenoma

208
Q

3 types of neoplastic polyps

A

tubular
tubulovillous
villous

209
Q

features of MEN1

A

pituitary adenoma
parathyroid hyperplasia
pancreatic tumour

210
Q

features of MEN2a

A

parathyroid hyperplasia
medullary thyroid carcinoma
pheochromocytoma

211
Q

features of MEN2b

A

mucosal neuromas
marfanoid body habitus
medullary thyroid carcinoma
phaeochromocytoma

212
Q

what hormone can be monitored in MEN2a to assess treatment response

A

calcitonin

213
Q

what type of cancer is prostate cancer

A

adenocarcinoma

214
Q

how do you work out the gleason score for prostate cancer

A

1-5 based on differentiation of cells on histology (1 = normal looking, 5 = poorly differentiated and aggressive)
take a biopsy and classify the most common and worst pattern seen
add these 2 numbers together to get score /10

MedEd Path (10 decks)

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