CA2 high yield shits

Question 1

colorectal cancer
a) carcinogenesis
b) gross features
c) histological features
d) clinical presentations
e) complications?
f) prognosis?

Answer 1

carcinogenesis in order: loss of APC, , DNA hypomethylation, KRAS inactivation, loss of 18q, p53 mutation, PRL3 mutation

gross features: fungating, polypoidal or ulcerated appearance. Large tumours predominated in proximal colon. Circumferential growth or apple core lesions more common in distal colon. Carcinomas in proximal colon are polypoid, exophytic mass while those in distal colon are annular, encircling lesions, napkin ring constrictions

histological features: high NC ratio, nuclear membrane irregularity, nuclei hyperchromasia, moderately differentiated -degree of tubule formation, prominent desmoplastic response, abundant intraluminal eosinophilic necrotic debris , extracullular mucin pools in the ‘mucinous’ type of carcinoma

clinical presentations: AAAAFBWOE
altered bowel movements, UNEXPLAINED anemia, asymptomatic (met. to liver, sister joseph nodules where met to umbilical cords), fistulation (pneumaturia due to invasion of bladder), weakness, weight loss, obstruction (vomiting ps could be feculent too, distension, constipation, pain), abdominal pain due to bowel perforation, peritonitis with ascites, pelvic abdominal abscess, extras like abdo pain, organ failure, vascular complications like thrombosis
prognosis
- TNM
T- measure depth of tumour invasion T0= no invasion, T1= invaded submucosa , T2= muscularis propria, T3= invade through muscularis propria to pericolorectal tissues, T4= tumour penetrates to surface of visceral peritoneum
N0= no cancer in nearby LN, N1= 1-3 LN nearby, N2= 4 or more nearby LN
M= distant met or not

Question 2

A) Histology of acute phase of RHD
B) chronic phase of RHD what will happen

C) what valve most affected in IE
D) IVDA pts what valve affected in IE

E) 3 types of IE and their causative organisms

F) complications of IE (local and distal)

G) examples of non-infective endocarditis

Answer 2

A)pancarditis: Aschoff bodies foci of fibrinoid degeneration surrounded by lymophocytes, T lymphocytes, plasma cells, activated macrophages (anitschkow/catepillar cell). Inflammation of valves results in vegetations called verucae

B) Infective endocarditis, thromboembolism, arrhythmias

C) mitral valve, followed by aortic valve
D) tricuspid valve

E) acute IE- staph aureus and HACEK
subacute IE- strep viridans (maybe epidermis)
post IE- strep pyogenes

F)
local complications: suppurative pericarditis, myocardial ring abscess, valve rupture

distant: immune complex mediated (type 3 Hypersensitivity) glomerulonephritis, septic emboli, anemia and splenomegaly

G)
non-bacterial thrombotic endocarditis
libman sacks endocarditis

Question 3

3 types of vegetations on heart valves

Answer 3

1. infective endocarditis
2. rheumatic heart disease (post infective endocarditis)
3. non- bacterial thrombotic endocarditis
4. libman sacks endocarditis (seen in lupus)

Question 4

describe the pathogenesis of acute cholecystitis and its complications

Answer 4

luminal lecithin catalyzed by muscosal phospholipases to form toxic lysolecithin

prostaglandin synthesis causes transmural and mucosal inflammation

exposed mucosal epithelium to direct detergent action of bile salts due to disruption of normal protective glycoprotein mucus layer

distension and increased intraluminal pressure compromise blood flow to mucosa

complications
- empyema/ gangrene with peritonitis and perforation
- septicaemia
- ascending cholangitis
- subdiaphragmatic and pericholecystic abscess