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MOST IMPT Flashcards

1
Q

Transpyloric plane surface markers

A

Lower border of L1
1. Cuts through pylorus of STOMACH
2. Tip of 9th costal cartilage (fundus of GB)
3. Neck of PANCREAS
4. SMA
5. Hilum of KIDNEY
6. Renal arteries (L1/L2)

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1
Q

Sternal angle - RATPLANT?

A

*Rib (2nd)
*Arch of aorta
*Trachea (bifurcation)
*Pulmonary trunk (bifurcation)
Left recurrent laryngeal
Azygos vein (drain to SVC)
Nerves : Cardiac plexus
Thoracic duct (empty into left subclavian vein)

Additionally, lower lobe of left lung starts from T4 posteriorly too

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2
Q

Portal-systemic anastomoses?

A

A : Lower oesophagus
- Sys : Esophageal v
- Port : Left gastric v

B : Rectal
- Sys : Inferior rectal v
- Port : Superior rectal v

C: Umbilicus
- Sys : Epigastric v
- Port : Paraumbilical v

D : Posterior abdominal wall
- Sys : Retroperitoneal v
- Port : Visceral v

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3
Q

Gross & microscopic changes of post-MI?

A

0-12hours : TTC test

12-24hours: pale with blotchy discolouration, brightly eosinophilic, loss of nucleus, intercellular oedema

1-3 days: soft & pale, yellow, neutrophil infiltration

3-10 days: hyperaemic border around yellow area, granulation tissue

6-8 weeks: Fibrous scar

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4
Q

Pathogenesis of atherosclerosis

A
  1. Endothelial injury
    - Increased vascular permeability
    - Monocyte emigration
    - Macrophage activation
    - Smooth muscle recruitment into intima
    - Platelet adhesion
  2. Smooth muscle proliferation
    - cytokines, growth factors, cell synthesise ECM -> Fibrous cap
  3. Foam cells formation
    - lipids enter endothelium
    - fatty streaks
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5
Q

What structure cuts through diaphragm at what level?

A

T8 : vena cava
T10 : oesophagus, vagus nerve
T12 : aortic hiatus [thoracic aorta], thoracic duct, azygos vein

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6
Q

How to differentiate right & left lung?

A

RALS
(right anterior, left superior)
- position of pulmonary artery in relation to bronchus

right - 3 lobes, left - 2 lobes

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7
Q

Relation of epiploic foramen / foramen of Winslow?

A
  1. Anterior: bile duct, hepatic artery & portal vein [portal triad]
  2. Posterior: IVC & diaphragm
  3. Superior: caudate lobe of the liver
  4. Inferior: first part of the duodenum
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8
Q

Relations of lesser sac (omental bursa)?

A
  • anterior : stomach & lesser omentum
  • superior : diaphragm
  • inferior : layers of greater omentum
  • left margin formed by spleen
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9
Q

Relations of pancreas?

A

Head : attached to descending part of duodenum, common BD post

Neck : post -> SMA / splenic v

Body : ant -> stomach. post -> left kidney. forms floor of omental bursa

Tail : hilum of spleen

Uncinate process : ant -> SMA/ SMV

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10
Q

Relations of spleen?

A

Ant : Stomach
Post : (Left) Diaphragm, left lung, T9-11
Inf : Left colic flexure
Medially : Left kidney
+ Hilum : Tail of pancreas

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11
Q

Pathophysiology of GERD

A
  1. Transient LES relaxation
  2. Reflux of gastric contents into esophagus
  3. Squamous epithelial cells secrete inflammatory cytokines in response to acid and bile salts
  4. Inflammatory response damages esophagus
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12
Q

Risk factors of GERD

A

Obese elderly who smokes - old age, high BMI, smoking

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13
Q

Macroscopic appearance of peptic ulcers

A

Round & oval, sharply demarcated, punch-out defect
Mucosal margin may overhang the base slightly
Variable depth
Base is smooth and clean
Scarring and puckering of the wall

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14
Q

Microscopic appearance of peptic ulcers

A

Surface zone of fibrinopurulent exudate
Zone of granulation tissue
Zone of dense scar tissue
Acidophilic layer of necrotic tissue
Interruption of muscularis propria
Endarteritis obliterans (obliteration of lumen of the vessels)

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15
Q

Squamous cell carcinoma vs adenocarcinoma of esophagus

A

SCC - middle 1/3. A/w older men from China/africa
Adenocarcinoma - lower 1/3. A/w Barrett oesophagus

16
Q

Risk factors of squamous cell carcinoma of oral cavity

A
  1. Elderly male, 50-70 y/o
  2. Smoke, alcohol
  3. Betel nut
    A/w erythroplakia
17
Q

HPV negative vs HPV positive SCC of oral cavity

A

HPV negative : keratinising
HPV positive : non-keratinising, better prognosis

18
Q

Characteristic appearance of Barrett’s

A

Red velvety look on distal oesophagus

19
Q

Pathogenesis of acute gastritis - BBIDEN

A
  1. Bicarbonate reduced
  2. Blood flow reduced
  3. Direct damage to gastric epithelium
  4. Intracranial injuries
  5. Elderly
  6. NSAIDs
20
Q

Main sites of peptic ulcer

A

1st part of duodenum (75%)
lesser curve / antrum of stomach (20%)

21
Q

Histological features of H.pylori associated chronic gastritis

A

Active inflammation (neutrophil, lymphocytes etc)
Regenerative changes (mitosis in epithelium)
Atrophy (loss in glandular structure & specialised cells)
Metaplasia (intestinal type)
Hyperplasia
Dysplasia
Invasive adenocarcinoma

22
Q

How does mucosal barrier protect gastric mucosa from autodigestion?

A
  1. Mucus secretion
  2. HCO3- secretion
  3. Epithelial barrier : Intercellular tight junctions provide barrier to back-diffusion of H+ ions. Complete replacement of foveolar cells every 2-7 days
  4. Rich blood flow provides O2, nutrients & HCO3- to epithelial cells & remove back-diffused acid
23
Q

Complications of PUD

A
  1. Bleeding
  2. Perforation
  3. Obstruction
  4. Gastric adenocarcinoma (rare)
24
Q

What is H.pylori associated with?

A

Chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, gastric MALT lymphoma

25
Q

Complications of chronic ulcerative colitis?

A
  1. Malignancy
  2. Toxic megacolon
26
Q

Complications of Crohn’s disease

A
  1. Perianal Fistula
  2. Fat/vitamin malabsorption
  3. Recurrence after surgery
  4. Malignancy (with colonic involvement)
27
Q

IBD : CD vs UC

A

CD : ileum + colon, skip lesions, deep-knife like ulcers, transmural, granulomas, fistula, fat/vitamin malabsorption
UC : colon, diffuse, superficial broad-based ulcers, mucosal, no granulomas/fistula, toxic megacolon

28
Q

Types of hypertension & EGs

A

Rmb is above 140/90
1. Primary HTN (90-95%)
- idiopathic
- smoking / obesity / diet

  1. Secondary HTN (5-10%) - PAIRS
    Pheochromocytoma
    Atherosclerosis
    Intracranial pressure
    Renal artery stenosis
    Stress-related
  2. Malignant HTN
29
Q

Impt complications of MI

A
  1. Arrhythmias (Earliest)
  2. Rupture of myocardiac wall & haemorrhage into pericardium (haemopericardium) → fatal cardiac tamponade (early)
  3. Papillary muscle rupture, valvular failure [due to hypoperfusion] → cardiogenic shock (early)
  4. Thrombus (due to stasis & turbulent blood flow)→ prediposes to stroke, pulmonary embolism (early)
  5. Aneurysms [secondary to fibrosis] (late)
  6. Progressive HF [secondary to fibrosis] (late)

Others :

  • Sudden cardiac death due to VF
  • Pericarditis - Dressler’s syndrome
30
Q

Adenoma-carcinoma genetic change sequence (colorectal carcinoma)

A

Loss of APC
DNA hypomethylation
KRAS activation
Loss of 18q
Loss of p53
PRL3 amplification

31
Q

Complication of diverticular diseases?

A
  1. Acute inflammation (diverticulitis):
  • Pericolic abscess
  • Pericolic fibrosis and adhesions
  • Colovesicular fistula
  • Strictures (can cause obstruction)
  • Free perforation into the peritoneal cavity
  1. Erosion of blood vessels:
  • Rectal Bleeding (can appear as frank blood in stool or occult)
  • Anaemia
32
Q

What are the 3 histological types of NPC & which type is most common?

A

UDK
1. Undiffierentiated non-keratinising carcinoma [most common!! Over 95%]
2. Differentiated nonkeratinising carcinoma
3. Keratinising SCC

33
Q

What are the normal pH, HCO3- and pCO2 levels?

A

pH = 7.35-7.45
HCO3- =22-28 mEq/L
pCO2 = 35-45mHg

34
Q

Gross feature of H. pylori PUD?

A
  1. Round or oval, sharply demarcated punched-out defect without raised edges.
  2. Mucosal margin may overhang the base slightly
  3. Base of ulcer is smooth and clean
  4. Stellate appearance due to scarring and puckering of the wall
35
Q

Pathogenesis of alcoholic liver disease

A
  1. Steatosis: ↑NADH leads to shunting of normal substrates towards lipid biosynthesis; ↓export of lipoproteins; ↑peripheral catabolism of fat
  2. Dysfunction of mitochondrial and cellular membranes:
    Ethanol → acetaldehyde → induces lipid peroxidation (formation of toxic lipid metabolites & oxidative damage) and acetaldehydeprotein adduct formation
  3. Hypoxia and oxidative stress: CYP450 produces ROS (alcohol is inducer) → enhances conversion of other drugs to toxic metabolites; impaired hepatic metabolism of methionine
    ↓glutathione levels
36
Q

Histological features of alcoholic liver disease

A
  • Centrilobular steatosis (reversible with abstention)
  • Hepatocyte swelling (ballooning degeneration) and necrosis
  • Mallory-Denk bodies
  • Neutrophilic reaction
  • Pericellular/perisinusoidal fibrosis (“Chicken-wire fence” pattern)
  • Cirrhosis (micronodular)

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