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1
Q

MI 30m-12h microscopic

A

necrosis - karyolysis
RBCs
wavy myocytes
hypereosinophilia

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2
Q

macroscopic 30m-12h

A

nothing

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3
Q

12-24h whats happening

A

necrosis, start of acute inflammation

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4
Q

12-24h microscopic

A

contraction band necrosis, some neutrophils

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5
Q

12-24h macroscopic

A

mottled haemorrhagic

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6
Q

1-3 days whats happening

A

acute inflammation, troponin peak

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7
Q

1-3 days microscopic

A

neutrophils

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8
Q

1-3 days macroscopic

A

yellowing of walls - puss

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9
Q

3-7 days whats happening

A

end of acute inflam, start of early granulation

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10
Q

3-7 days microscopic

A

macrophages, vessels of granulation

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11
Q

3-7 days macroscopic

A

central yellowing, red rim

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12
Q

1-8 weeks whats happening

A

early to late granulation tissue, start of collagen

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13
Q

1-8 weeks microscopic

A

initially high cellularity, high vascularity, increasing collagen, fibroblasts

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14
Q

1-8 weeks macroscopic

A

white grey translucence

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15
Q

> 8 weeks whats happening

A

fibrosis and scar

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16
Q

> 8 weeks microscopic

A

fibroblasts, collagen

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17
Q

> 8 weeks macroscopic

A

white

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18
Q

what are complications of 30-12h and >8 weeks

A

arrhythmia and CF

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19
Q

complications 12-24h

A

arrythmia and pericarditis

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20
Q

complications 1-3 days and 3-7 days

A

mural thrombus, arrhythmia, rupture

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21
Q

complications 1-8 weeks

A

mural thrombus, aneurysm, arrhythmia

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22
Q

what type of nucleus do smooth msucle cells have

A

cigar shaped

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23
Q

what are nexus junctions

A

same as gap junctions but in heart (part of intercalated disk)

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24
Q

what is dense pink area, central in MI

A

necrotic cardiomyocytes - necrotic island - myocytes heal from outside in, dont take central necrosis into account when getting age of infarction

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25
Q

what do nuclei of granulation tissue vessels look like

A

puffed up

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26
Q

fibrinous exudate

A

plasma and protein exudate - typical reaction of pericardium or pleura on inflammation

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27
Q

dressler’s syndrome

A

presence of pericarditis after MI

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28
Q

purulent/suppprative exudate

A

exudate from blood vessels rich in neutrophils

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29
Q

fibrinous exudate

A

exudate from blood vessels rich in protein (fibrin) (fibrin looks like fairy floss)

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30
Q

serous exudate

A

fluid/plasma exudate from blood vessels rich in plasma

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31
Q

difference between lobar and bronchopneumonia

A

lobar - throughout a lobe, spreads through alveoli

broncho - patchy, spreads through airways

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32
Q

microscopic features of asthma

A
  • goblet cell hyperplasia/hypertrophy
  • smooth muscle cell hypertrophy
  • bright red eosinophils, bilobed
    thickened BM - fibrosis
  • lots of lymphocytes
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33
Q

what microscopically tells you asthma and not chronic bronchitis

A

presence of eosinophils and smooth muscle

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34
Q

microscopic features of proximal tubules

A
  • big cells - far apart nuclei

brush border with microvilli

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35
Q

how do you tell difference between distal and proximal tubules

A

distal tubules - nuclei closer together (smaller cells), not as eosinophilic, no brush border

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36
Q

microscopic appearance of collecting duct

A

cuboidal

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37
Q

microscopic features of pylonephritis

A

neutrophils in tubules, nutrophils in interstitium
normal glom
dilated capillaries

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38
Q

microscopic features of ATN

A

necrotic/karyolysis of tubule cells
casts of tubular cells
normal glom

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39
Q

microscopic features of benign nephrosclerosis

A
  • glomerulosclerosis
  • tubule atrophy - no real tubule lumen
  • interstitial fibrosis - space between tubules (shouldnt be any space)
  • mononuclear chronic infiltration in interstitium
  • arteriosclerosis
  • hyaline arteriolosclerosis
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40
Q

how can you tell difference between ATN and renal infarct

A

renal infarct - tubules AND glom are dead

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41
Q

63 yr old woman, history of recurrent UTIs, intermittent vague right flank pain and occasional mild haematuria. afebrile, high BP, urine dipstick RBC positive, but no WBC or protein, creatinine is 114 (quite high)

A

hydronephrosis - urine backed up in kidney due to blockage of calyces by calculi
dull visceral pain bc pain in kidney

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42
Q

what is polycystic kidney disease

A

diffuse cysts throughout kidney, genetic, linked to cilia immotility in prox tubule

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43
Q

38 yr old with haematuria after sharp pain in left flank. describes long history of vague dragging pian in lower back. afebrile, doesnt seem unwell, BP high. Urine dipstick RBC positive, but neg for WBCs and protein. High serum creatinine, slim build, abdo exam reveals bilateral palpable kidneys

A

polycystic kidney disease

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44
Q

42 yr old man, fatigue, SOB on exertion, nocturia, peripheral oedema worsening over several months. pale, tired, mild oedema to mid calf, high BP, hypertensive changes in fundoscopy. urine dipstick - mild proteinuria, neg for RBCs, WBCs a. v v high serum creatinine

A

glomerulosclerosis

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45
Q

tissue oxygen delivery equation

A

tissue O delivery = CO x Hb x %satn X 1.34 ml/min

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46
Q

initiation of secondary haemostasis

A

extrinsic pathway

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47
Q

amplification of secondary haemostasis

A

intrinsic pathway

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48
Q

measure of extrinsic pathway

A

PT

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49
Q

measure of intrinsic pathway

A

APTT

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50
Q

what do you measure of warfarin checking

A

PT

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51
Q

what do you measure for heparin checking

A

APTT

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52
Q

what is PT meausre of

A

extrinsic pathway, warfarin

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53
Q

what is APTT measure of

A

intrinsic pathway, heparin

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54
Q

2 components of hyaline arteriolosclerosis

A

smooth muscle cells produce too much Ecm

proteins from blood leak into damaged endothelium into wall of vessel

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55
Q

3 sequelae of hyaline arteriolosclerosis

A
  1. cerebral haemorrhage
  2. benign nephrosclerosis
  3. hypertensive retinopathy
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56
Q

3 sequelae of atherosclerosis

A
  1. embolic event
  2. chronic ischeamia
  3. aneurysm
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57
Q

type of calcification in atherosclerosis

A

dystrophic calcification

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58
Q

what is metastatic calcification

A

serum Ca and P too high adn start to precipitate out of solution

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59
Q

what is dissection

A

weakening in intima of blood vessel results in tear and blood between intima and media

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60
Q

squelae of dissection

A

rupture into pericardium - cardiac tamponade
rupture into thorax - exanguination
track to coronary arteries - MI
track to carotid arteries - stroke

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61
Q

what is T wave inversion indicative of

A

hypertrophy

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62
Q

when is AF v bad bc patients need atrial kick

A

in diastolic dysfunction

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63
Q

when does LV remodelling occur

A

post MI

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64
Q

what is LV remodelling

A

increased volume, more spherical, hypertrophy, interstitial fibrosis

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65
Q

what stimulates cardiac remodelling

A

angiogensin, symp on B1Rs

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66
Q

what is hypertrophic cardiomyopathy

A

autosomal dom mutation in sarcomere proteins causing increase LV thickness (particularly septum)
myocyte disarray, LV outflow obstruction from septum, diastolic dysfunction, ventricular arrhythmias and sudden death

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67
Q

what is dilated cardiomyopathy

A

idopathic, most common cardiomyopathy

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68
Q

what does normal endothelium produce thats anticoagulant

A

thrombomodulin, protein C and S

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69
Q

what is arterial thrombus associated with pathologically

A

endothelial dysfunction

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70
Q

virchow’s triad

A

abnormal endothelium
abnormal blood flow
abnormal coagulation

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71
Q

4 things that can happen to thrombus

A
  1. dissolution
  2. organisation - granulation tissue
  3. propogation
  4. embolus
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72
Q

7 Ps of ischaemia

A

pale, pulseless, purple, painful, paralysed, paraesthetic, perishingly cold

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73
Q

what is tissue factor also known as

A

thromboplastin

74
Q

how is fibrinolysis activated

A

protein C inactivates inhibitor of tPA, converts plasminogen to plasmin, breaks down clot

75
Q

microscopic features of cardiac hypertrophy

A

enlarged rectangular nuclei, bi-nucleated, increased connective tissue

76
Q

how does hypertrophy lead to cardiac failure

A

impaired perfusion and increased O demand - ischaemia - myocyte death and fibrosis - cardiac failure

77
Q

two consequences of cardiac failure

A

pulmonary oedema, nutmeg liver

78
Q

where is first area targeted in MI

A

subendocardium

79
Q

most common cause of MI

A

acute plaque event from atherosclerosis in coronary arteries

80
Q

symptoms of angina start at __% stenosis

A

70

81
Q

troponin and CK time to initial elevation adn peak

A

initial - 6h

peak - 1-3 days

82
Q

what is a respiratory acinus

A

resp bronchiole and alveoli

83
Q

what is a respiratory lobule

A

terminal bronchiole and 3-4 acini

84
Q

define emphysema

A

abnormal permanent enlargement of air spaces distal to terminal bronchiole, caused by alveolar wall destruction w/out fibrosis

85
Q

define chronic bronchitis

A

persistent cough productive of sputum for at least 3 months in 2 consecutive years

86
Q

components of chronic bronchitis

A

chronic irritation causes increase mucous production, mucous gland hypertrophy, increased goblet cells
- inflammation, peribronchial fibrosis, narrowing of airways, +/- metaplasia

87
Q

pink puffer

A

emphysema - increased breathing so no decreased O

88
Q

blue bloater

A

chronic bronchitis - tolerates hypoxia, don’t increase breathing

89
Q

causes of bronchiectasis

A

necrotising infection (staph a, flu), CF, cilia disorders

90
Q

what is usual interstitial pneumonitis

A

fibrosis and inflam that appears to be of different ages - key feature in idiopathic pulmonary fibrosis

91
Q

what is restrictive lung disease

A

chronic diffuse non-infectious inflammation and fibrosis of inter-alveolar septa

92
Q

what has rusty red sputum

A

pneumonia

93
Q

dull or stony dull is consolidated lung in pneumonia

A

dull

94
Q

what is stony dull

A

pleural effusion

95
Q

what do angry macs release in TB and what they called

A

epitheloid macs release ROS and MMPs

96
Q

ghon focus

A

sub-pleural, mid lung

97
Q

ghon complex

A

lymph node lesion

98
Q

what occurs in primary TB

A

ghon focus and ghon complex

99
Q

what occurs in secondary TB

A

granulomatous inflammation and caseous necrosis at apex of lungs

100
Q

describe granulomatous inflammation

A

epithelioid macrophages surrounding necrosis in some cases, surrounded by lymphs and fibroblasts
may be giant multi-nucleate cells

101
Q

what do you use to ‘guess’ if likely to be DVT or not

A

well’s DVT score

102
Q

what is pleural rub

A

rough sound of lung rubbing on pleura - sign of pulmonary infarction from PE

103
Q

buzz words for neoplasia

A

large nuclei, nuclear pleomorphism, choarse chromatin, prominent nucleoli, hyperchromatic nuclei, mitotic figures, architectural atypia/disorganisation

104
Q

signet ring cells what origin

A

glandular tissue

105
Q

mucin forming carcinoma

A

glandular - adenocarcinoma

106
Q

sarcoma suffix indicates

A

mesenchymal malignant

107
Q

grade

A

= degree of differentiation

108
Q

stage

A

= degree of invasion

109
Q

word for undifferentiated tumour

A

anaplastic

110
Q

what are some oncogene e.g.s

A

ras, myc

111
Q

what are some TSG e.g.s

A

p53, RB

112
Q

which type of lung cancer arises more peripherally

A

adenocarcionma

113
Q

components of nephrotic syndrome

A
  1. oedema
  2. proteinuria
  3. hypoalbuminaemia
  4. hypertriglyceridaemia
114
Q

Some causes of glomerulonephritis

A

acute post infectious GN, IgA nephropathy, membranous nephropathy

115
Q

glomerulus response to immune complex mediated injury

A

glom cells proliferate - epithelial, endothelial, mesangial
inflam cells infiltrate - neuts, lymphs, monocytes
BM may proliferate

116
Q

segmental vs global

A

segmental - part of glom

global - all of glom

117
Q

diffuse vs focal

A

diffuse - throughout kidney

focal - one part

118
Q

what is most common renal cause of ARF

A

ATN

119
Q

3 types of tubulointerstitial injury

A
  1. ATN
  2. acute pyelonephritis
  3. acute or chronic tubulointerstitial nephritis
120
Q

what is acute tubulointerstitial nephritis

A

interstitium and tubules infiltrated by inflam cells, often due to drug allergy

121
Q

top 3 causes of chronic renal failure

A

diabetes, glomerulonephritis, hypertension

122
Q

does tubular or villous adenoma have higher propensity for malignancy

A

villous

123
Q

hyperplastic polyp

A

common and benign, not an adenoma, doesnt transform

124
Q

FAP pathway to cancer

A

APC Kras mutation DCC deletion P53 deletion

125
Q

lynch inherited disease of what

A

mutation in DNA repair gene MLH1 or MSH2

126
Q

FAP or lynch more penetrance

A

FAP 100%

lynch 70-80%

127
Q

location and type of polyp FAP

A

pedunculated, on left

128
Q

location and type of polyp lynch

A

sessile serrated, on RIGHT

129
Q

sessile serrated adenoma frequently have what mutation

A

BRAF V600E

130
Q

T stages of colon cancer

A 
Tis - in situ 
T1 - beyond muscularis mucosae
T2 - into muscularis propria 
T3 - beyond muscularis propria
T4 - invades other organs or perforates visceral peritoneum
131
Q

N stages of colon cancer

A

N0 - no lymph nodes
N1 - 1-3 nodes
N3 - >/=4

132
Q

where is ALT found

A

cytosol of hepatocytes

133
Q

where is AST found

A

cytosol and mitochondria of liver and muscle (and blood cells)

134
Q

is AST or ALT removed faster

A

AST removed twice as fast

135
Q

how can statins change liver enzyme levels

A

cause muscle damage causing increase in AST

136
Q

what enzyme levels raised in biliary obstruction

A

GGT and ALP

137
Q

levels of enzymes higher in intra or extrahepatic biliary obstruction

A

intrahepatic

138
Q

what liver enzyme raised in alcoholics and why

A

GGT, bc metabolism of alcohol causes decrease in NAD+ and increase in NADH so need another redox system so increase GGT to increase glutathione levels

139
Q

most common cause of raised liver enzymes

A

obesity

140
Q

definition of acute hepatitis

A

raised serum transaminase levels for <6 months

141
Q

process of hepatocellular injury in acute hepatitis

A
  • zonal necrosis - zone 3 around central veins
  • extends to bridging necrosis - from central vein to portal tract in zone 3
  • then multi-acinar necrosis throughout acinars
142
Q

necrosis in acute hepatitis - viral vs paracetamol

A

viral - necrosis lytic - hepatocytes rupture due to osmotic failure and swelling

paracetamol - coagulative necrosis

143
Q

lobular dissaray in acute viral or toxin hepatitis

A

viral

144
Q

primary inflammatory cells in acute viral hep

A

lymphs, plasma cells, macs

145
Q

do you have inflammation in toxin induced acute hepatitis

A

not really

146
Q

definition of chronic hepatitis

A

persistent liver injury with raised serum transaminase levels for >6 months

147
Q

how many HCV patients develop cirrhosis

A

20%

148
Q

how many HCV patients develop chronic disease

A

80%

149
Q

inflammatory cell infiltrate in acute vs chronic hepatitis

A

T cells main infiltrate in both!

150
Q

difference between inflammation in acute vs chronic hepatitis

A

acute - pan-lobular

chronic - portal tract and periportal inflammation, w injury of periportal hepatocytes (interface hepatitis)

151
Q

what cells contribute to fibrosis in chronic hepatitis

A

portal fibroblasts and hepatic stellate cells

152
Q

how are stellate cells activated

A

activated kupfer cells release cytokines that activate stellate cells

153
Q

stages of fibrosis

A

stage 1 - enlarged portal tracts with surrounding fibrosis, no septa
stage 2 - septa but not much linking between portal tracts
stage 3 - portal to portal bridging
stage 4- cirrhosis

154
Q

difference between steatosis and steatohepatitis

A 
steatosis = fat in hepatocytes 
steatohepatitis = fat and hepatocellular injury
155
Q

characteristics of steatohepatitis

A

ballooning, mallory-denk bodies, neutrophils, chicken-wire fibrosis

156
Q

classification of portal hypertension

A

> 8mmHg in portal vein

157
Q

paraneoplastic syndrome of squamous cell carcinoma

A

hypercalaemia secondary to PTH release

158
Q

paraneoplastic syndrome of small cell carcinoma (lung)

A

hyponatraemia secondary to SIADH (syndrome of inappropriate anti-diuretic hormone) - too much vasopressin

159
Q

what is dukes a b c d

A

a - through muscularis mucosa
b - through muscularis propria
c - lymph nodes
d - distant metastases

160
Q

treatment for paracetamol OD

A

n-acetyl-cysteine

161
Q

if you have right heart failure, where do you get liver congestion and necrosis first

A

zone 3

162
Q

what colour is a happy kidney macroscopically

A

brown

163
Q

what would a pylonephritis kidney look like

A

erythema and pus

164
Q

wedge shaped infarcts in kidney most likely due to

A

cholesterol emboli (plaque)

165
Q

if you saw thickening of BM of glomerulus without clumps in electron microspopy ?

A

diabetic nephropathy

166
Q

subepithelial electron dense deposits in kidney

A

membranous nephropathy

167
Q

what do immune complexes deposited in glomerular BM cause

A

alter charge (normally neg) and barrier of filtration membrane, allowing protein to pass through

168
Q

what are two causes of interstitial nephritis

A
  1. drug reaction

2. infection

169
Q

how do you distinguish interstitial nephritis caused by drug reaction or infection

A

drug reaction - eosinophilic infiltrate

infection - lymphocytic infiltrate

170
Q

why lenticulostriate vessels susceptible to damage in hypertension

A

they are v small arteries coming directly off medium sized ones, in hypertension they’re exposed to unusually high pressures for vessels of their size

171
Q

brain lesion macroscopic features:

  • if dead patient
  • if 1-2 days
  • if week
  • if >week
A

dead - nothing
1-2 days - infarct well developed with loss fo grey-white differentiation
if week - gliosis and necrosis
>week - cavitating lesion

172
Q

how could brain infarct lead to death of patient

A

disruption of BBB in region of infarct - oedema - raised ICP - hermiation and compression of vital structures in brain stem or global cortical ischaemia

173
Q

explain likely pathogenesis of haemorrage post brain infarct

A

infarction from embolus, lysis of embolus, reperfusion of infarcted area - leaking of necrosed vessels

174
Q

likely cause if multiple cavitating lesions in brain

A

infective endocarditis of mitral valve

175
Q

symptoms of transtentorial herniation

A

fixed dilated pupil

176
Q

what proportion of strokes are:

  • infarction
  • haemorrhage
  • subarachnoid
A

infarction - 75%
h - 20%
subarach - 5%

177
Q

does diabetes cause nephrotic or nephritic syndrome

A

nephrotic

178
Q

graves gross appearance of thyroid

A

diffusely enlarged, mahogany red, firm

179
Q

graves microscopy

A

lymphocytes, papillary crowding, scalloped colloid

180
Q

hashimotos gross thyroid appearance

A

pale, tan, atrophic thyroid

181
Q

hashimotos thyroid microscophy

A

germinal centres, hurthle cells, fibrosis

182
Q

what is conn syndrome

A

aldosterone producing adenoma

exam revision (15 decks)

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