path Flashcards
(182 cards)
1
Q
MI 30m-12h microscopic
A
necrosis - karyolysis
RBCs
wavy myocytes
hypereosinophilia
2
Q
macroscopic 30m-12h
A
nothing
3
Q
12-24h whats happening
A
necrosis, start of acute inflammation
4
Q
12-24h microscopic
A
contraction band necrosis, some neutrophils
5
Q
12-24h macroscopic
A
mottled haemorrhagic
6
Q
1-3 days whats happening
A
acute inflammation, troponin peak
7
Q
1-3 days microscopic
A
neutrophils
8
Q
1-3 days macroscopic
A
yellowing of walls - puss
9
Q
3-7 days whats happening
A
end of acute inflam, start of early granulation
10
Q
3-7 days microscopic
A
macrophages, vessels of granulation
11
Q
3-7 days macroscopic
A
central yellowing, red rim
12
Q
1-8 weeks whats happening
A
early to late granulation tissue, start of collagen
13
Q
1-8 weeks microscopic
A
initially high cellularity, high vascularity, increasing collagen, fibroblasts
14
Q
1-8 weeks macroscopic
A
white grey translucence
15
Q
> 8 weeks whats happening
A
fibrosis and scar
16
Q
> 8 weeks microscopic
A
fibroblasts, collagen
17
Q
> 8 weeks macroscopic
A
white
18
Q
what are complications of 30-12h and >8 weeks
A
arrhythmia and CF
19
Q
complications 12-24h
A
arrythmia and pericarditis
20
Q
complications 1-3 days and 3-7 days
A
mural thrombus, arrhythmia, rupture
21
Q
complications 1-8 weeks
A
mural thrombus, aneurysm, arrhythmia
22
Q
what type of nucleus do smooth msucle cells have
A
cigar shaped
23
Q
what are nexus junctions
A
same as gap junctions but in heart (part of intercalated disk)
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
25
what do nuclei of granulation tissue vessels look like
puffed up
26
fibrinous exudate
plasma and protein exudate - typical reaction of pericardium or pleura on inflammation
27
dressler's syndrome
presence of pericarditis after MI
28
purulent/suppprative exudate
exudate from blood vessels rich in neutrophils
29
fibrinous exudate
exudate from blood vessels rich in protein (fibrin) (fibrin looks like fairy floss)
30
serous exudate
fluid/plasma exudate from blood vessels rich in plasma
31
difference between lobar and bronchopneumonia
lobar - throughout a lobe, spreads through alveoli
| broncho - patchy, spreads through airways
32
microscopic features of asthma
- goblet cell hyperplasia/hypertrophy
- smooth muscle cell hypertrophy
- bright red eosinophils, bilobed
thickened BM - fibrosis
- lots of lymphocytes
33
what microscopically tells you asthma and not chronic bronchitis
presence of eosinophils and smooth muscle
34
microscopic features of proximal tubules
- big cells - far apart nuclei
| brush border with microvilli
35
how do you tell difference between distal and proximal tubules
distal tubules - nuclei closer together (smaller cells), not as eosinophilic, no brush border
36
microscopic appearance of collecting duct
cuboidal
37
microscopic features of pylonephritis
neutrophils in tubules, nutrophils in interstitium
normal glom
dilated capillaries
38
microscopic features of ATN
necrotic/karyolysis of tubule cells
casts of tubular cells
normal glom
39
microscopic features of benign nephrosclerosis
- glomerulosclerosis
- tubule atrophy - no real tubule lumen
- interstitial fibrosis - space between tubules (shouldnt be any space)
- mononuclear chronic infiltration in interstitium
- arteriosclerosis
- hyaline arteriolosclerosis
40
how can you tell difference between ATN and renal infarct
renal infarct - tubules AND glom are dead
41
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)
hydronephrosis - urine backed up in kidney due to blockage of calyces by calculi
dull visceral pain bc pain in kidney
42
what is polycystic kidney disease
diffuse cysts throughout kidney, genetic, linked to cilia immotility in prox tubule
43
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
polycystic kidney disease
44
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
glomerulosclerosis
45
tissue oxygen delivery equation
tissue O delivery = CO x Hb x %satn X 1.34 ml/min
46
initiation of secondary haemostasis
extrinsic pathway
47
amplification of secondary haemostasis
intrinsic pathway
48
measure of extrinsic pathway
PT
49
measure of intrinsic pathway
APTT
50
what do you measure of warfarin checking
PT
51
what do you measure for heparin checking
APTT
52
what is PT meausre of
extrinsic pathway, warfarin
53
what is APTT measure of
intrinsic pathway, heparin
54
2 components of hyaline arteriolosclerosis
smooth muscle cells produce too much Ecm
| proteins from blood leak into damaged endothelium into wall of vessel
55
3 sequelae of hyaline arteriolosclerosis
1. cerebral haemorrhage
2. benign nephrosclerosis
3. hypertensive retinopathy
56
3 sequelae of atherosclerosis
1. embolic event
2. chronic ischeamia
3. aneurysm
57
type of calcification in atherosclerosis
dystrophic calcification
58
what is metastatic calcification
serum Ca and P too high adn start to precipitate out of solution
59
what is dissection
weakening in intima of blood vessel results in tear and blood between intima and media
60
squelae of dissection
rupture into pericardium - cardiac tamponade
rupture into thorax - exanguination
track to coronary arteries - MI
track to carotid arteries - stroke
61
what is T wave inversion indicative of
hypertrophy
62
when is AF v bad bc patients need atrial kick
in diastolic dysfunction
63
when does LV remodelling occur
post MI
64
what is LV remodelling
increased volume, more spherical, hypertrophy, interstitial fibrosis
65
what stimulates cardiac remodelling
angiogensin, symp on B1Rs
66
what is hypertrophic cardiomyopathy
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
67
what is dilated cardiomyopathy
idopathic, most common cardiomyopathy
68
what does normal endothelium produce thats anticoagulant
thrombomodulin, protein C and S
69
what is arterial thrombus associated with pathologically
endothelial dysfunction
70
virchow's triad
abnormal endothelium
abnormal blood flow
abnormal coagulation
71
4 things that can happen to thrombus
1. dissolution
2. organisation - granulation tissue
3. propogation
4. embolus
72
7 Ps of ischaemia
pale, pulseless, purple, painful, paralysed, paraesthetic, perishingly cold
73
what is tissue factor also known as
thromboplastin
74
how is fibrinolysis activated
protein C inactivates inhibitor of tPA, converts plasminogen to plasmin, breaks down clot
75
microscopic features of cardiac hypertrophy
enlarged rectangular nuclei, bi-nucleated, increased connective tissue
76
how does hypertrophy lead to cardiac failure
impaired perfusion and increased O demand - ischaemia - myocyte death and fibrosis - cardiac failure
77
two consequences of cardiac failure
pulmonary oedema, nutmeg liver
78
where is first area targeted in MI
subendocardium
79
most common cause of MI
acute plaque event from atherosclerosis in coronary arteries
80
symptoms of angina start at __% stenosis
70
81
troponin and CK time to initial elevation adn peak
initial - 6h
| peak - 1-3 days
82
what is a respiratory acinus
resp bronchiole and alveoli
83
what is a respiratory lobule
terminal bronchiole and 3-4 acini
84
define emphysema
abnormal permanent enlargement of air spaces distal to terminal bronchiole, caused by alveolar wall destruction w/out fibrosis
85
define chronic bronchitis
persistent cough productive of sputum for at least 3 months in 2 consecutive years
86
components of chronic bronchitis
chronic irritation causes increase mucous production, mucous gland hypertrophy, increased goblet cells
- inflammation, peribronchial fibrosis, narrowing of airways, +/- metaplasia
87
pink puffer
emphysema - increased breathing so no decreased O
88
blue bloater
chronic bronchitis - tolerates hypoxia, don't increase breathing
89
causes of bronchiectasis
necrotising infection (staph a, flu), CF, cilia disorders
90
what is usual interstitial pneumonitis
fibrosis and inflam that appears to be of different ages - key feature in idiopathic pulmonary fibrosis
91
what is restrictive lung disease
chronic diffuse non-infectious inflammation and fibrosis of inter-alveolar septa
92
what has rusty red sputum
pneumonia
93
dull or stony dull is consolidated lung in pneumonia
dull
94
what is stony dull
pleural effusion
95
what do angry macs release in TB and what they called
epitheloid macs release ROS and MMPs
96
ghon focus
sub-pleural, mid lung
97
ghon complex
lymph node lesion
98
what occurs in primary TB
ghon focus and ghon complex
99
what occurs in secondary TB
granulomatous inflammation and caseous necrosis at apex of lungs
100
describe granulomatous inflammation
epithelioid macrophages surrounding necrosis in some cases, surrounded by lymphs and fibroblasts
may be giant multi-nucleate cells
101
what do you use to 'guess' if likely to be DVT or not
well's DVT score
102
what is pleural rub
rough sound of lung rubbing on pleura - sign of pulmonary infarction from PE
103
buzz words for neoplasia
large nuclei, nuclear pleomorphism, choarse chromatin, prominent nucleoli, hyperchromatic nuclei, mitotic figures, architectural atypia/disorganisation
104
signet ring cells what origin
glandular tissue
105
mucin forming carcinoma
glandular - adenocarcinoma
106
sarcoma suffix indicates
mesenchymal malignant
107
grade
= degree of differentiation
108
stage
= degree of invasion
109
word for undifferentiated tumour
anaplastic
110
what are some oncogene e.g.s
ras, myc
111
what are some TSG e.g.s
p53, RB
112
which type of lung cancer arises more peripherally
adenocarcionma
113
components of nephrotic syndrome
1. oedema
2. proteinuria
3. hypoalbuminaemia
4. hypertriglyceridaemia
114
Some causes of glomerulonephritis
acute post infectious GN, IgA nephropathy, membranous nephropathy
115
glomerulus response to immune complex mediated injury
glom cells proliferate - epithelial, endothelial, mesangial
inflam cells infiltrate - neuts, lymphs, monocytes
BM may proliferate
116
segmental vs global
segmental - part of glom
| global - all of glom
117
diffuse vs focal
diffuse - throughout kidney
| focal - one part
118
what is most common renal cause of ARF
ATN
119
3 types of tubulointerstitial injury
1. ATN
2. acute pyelonephritis
3. acute or chronic tubulointerstitial nephritis
120
what is acute tubulointerstitial nephritis
interstitium and tubules infiltrated by inflam cells, often due to drug allergy
121
top 3 causes of chronic renal failure
diabetes, glomerulonephritis, hypertension
122
does tubular or villous adenoma have higher propensity for malignancy
villous
123
hyperplastic polyp
common and benign, not an adenoma, doesnt transform
124
FAP pathway to cancer
APC Kras mutation DCC deletion P53 deletion
125
lynch inherited disease of what
mutation in DNA repair gene MLH1 or MSH2
126
FAP or lynch more penetrance
FAP 100%
| lynch 70-80%
127
location and type of polyp FAP
pedunculated, on left
128
location and type of polyp lynch
sessile serrated, on RIGHT
129
sessile serrated adenoma frequently have what mutation
BRAF V600E
130
T stages of colon cancer
```
Tis - in situ
T1 - beyond muscularis mucosae
T2 - into muscularis propria
T3 - beyond muscularis propria
T4 - invades other organs or perforates visceral peritoneum
```
131
N stages of colon cancer
N0 - no lymph nodes
N1 - 1-3 nodes
N3 - >/=4
132
where is ALT found
cytosol of hepatocytes
133
where is AST found
cytosol and mitochondria of liver and muscle (and blood cells)
134
is AST or ALT removed faster
AST removed twice as fast
135
how can statins change liver enzyme levels
cause muscle damage causing increase in AST
136
what enzyme levels raised in biliary obstruction
GGT and ALP
137
levels of enzymes higher in intra or extrahepatic biliary obstruction
intrahepatic
138
what liver enzyme raised in alcoholics and why
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
most common cause of raised liver enzymes
obesity
140
definition of acute hepatitis
raised serum transaminase levels for <6 months
141
process of hepatocellular injury in acute hepatitis
- 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
necrosis in acute hepatitis - viral vs paracetamol
viral - necrosis lytic - hepatocytes rupture due to osmotic failure and swelling
paracetamol - coagulative necrosis
143
lobular dissaray in acute viral or toxin hepatitis
viral
144
primary inflammatory cells in acute viral hep
lymphs, plasma cells, macs
145
do you have inflammation in toxin induced acute hepatitis
not really
146
definition of chronic hepatitis
persistent liver injury with raised serum transaminase levels for >6 months
147
how many HCV patients develop cirrhosis
20%
148
how many HCV patients develop chronic disease
80%
149
inflammatory cell infiltrate in acute vs chronic hepatitis
T cells main infiltrate in both!
150
difference between inflammation in acute vs chronic hepatitis
acute - pan-lobular
| chronic - portal tract and periportal inflammation, w injury of periportal hepatocytes (interface hepatitis)
151
what cells contribute to fibrosis in chronic hepatitis
portal fibroblasts and hepatic stellate cells
152
how are stellate cells activated
activated kupfer cells release cytokines that activate stellate cells
153
stages of fibrosis
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
difference between steatosis and steatohepatitis
```
steatosis = fat in hepatocytes
steatohepatitis = fat and hepatocellular injury
```
155
characteristics of steatohepatitis
ballooning, mallory-denk bodies, neutrophils, chicken-wire fibrosis
156
classification of portal hypertension
>8mmHg in portal vein
157
paraneoplastic syndrome of squamous cell carcinoma
hypercalaemia secondary to PTH release
158
paraneoplastic syndrome of small cell carcinoma (lung)
hyponatraemia secondary to SIADH (syndrome of inappropriate anti-diuretic hormone) - too much vasopressin
159
what is dukes a b c d
a - through muscularis mucosa
b - through muscularis propria
c - lymph nodes
d - distant metastases
160
treatment for paracetamol OD
n-acetyl-cysteine
161
if you have right heart failure, where do you get liver congestion and necrosis first
zone 3
162
what colour is a happy kidney macroscopically
brown
163
what would a pylonephritis kidney look like
erythema and pus
164
wedge shaped infarcts in kidney most likely due to
cholesterol emboli (plaque)
165
if you saw thickening of BM of glomerulus without clumps in electron microspopy ?
diabetic nephropathy
166
subepithelial electron dense deposits in kidney
membranous nephropathy
167
what do immune complexes deposited in glomerular BM cause
alter charge (normally neg) and barrier of filtration membrane, allowing protein to pass through
168
what are two causes of interstitial nephritis
1. drug reaction
| 2. infection
169
how do you distinguish interstitial nephritis caused by drug reaction or infection
drug reaction - eosinophilic infiltrate
| infection - lymphocytic infiltrate
170
why lenticulostriate vessels susceptible to damage in hypertension
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
brain lesion macroscopic features:
- if dead patient
- if 1-2 days
- if week
- if >week
dead - nothing
1-2 days - infarct well developed with loss fo grey-white differentiation
if week - gliosis and necrosis
>week - cavitating lesion
172
how could brain infarct lead to death of patient
disruption of BBB in region of infarct - oedema - raised ICP - hermiation and compression of vital structures in brain stem or global cortical ischaemia
173
explain likely pathogenesis of haemorrage post brain infarct
infarction from embolus, lysis of embolus, reperfusion of infarcted area - leaking of necrosed vessels
174
likely cause if multiple cavitating lesions in brain
infective endocarditis of mitral valve
175
symptoms of transtentorial herniation
fixed dilated pupil
176
what proportion of strokes are:
- infarction
- haemorrhage
- subarachnoid
infarction - 75%
h - 20%
subarach - 5%
177
does diabetes cause nephrotic or nephritic syndrome
nephrotic
178
graves gross appearance of thyroid
diffusely enlarged, mahogany red, firm
179
graves microscopy
lymphocytes, papillary crowding, scalloped colloid
180
hashimotos gross thyroid appearance
pale, tan, atrophic thyroid
181
hashimotos thyroid microscophy
germinal centres, hurthle cells, fibrosis
182
what is conn syndrome
aldosterone producing adenoma
