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MED4 ACP > GI Pathology > Flashcards

GI Pathology Flashcards

1
Q

How to differentiate between mechanical & functional oesophageal obstruction clinically?

A

Onset, difficulty initiating, type of food easier to swallow, associated symptoms

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2
Q

Intramural mechanical oesophageal obstruction (3)

A

atresia, stricture, webs / rings

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3
Q

Where does oesophageal atresia most likely occur?

A

near tracheal bifurcation

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4
Q

Which is the most common type of tracheoesophageal fistula?

A

type III

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5
Q

Presentations of oesophageal atresia

A

regurgitation, severe fluid / electrolyte imbalance, aspiration pneumonia

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6
Q

Causes of oesophageal stricture (4)

A

Benign: GERD, injury, idiopathic
Malignant: CA oesophagus

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7
Q

Histology of benign oesophageal stricture

A

fibrosis, atrophy of muscularis propria

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8
Q

Histology of oesophageal webs / rings

A

fibrovascular connective tissue covered by epithelium

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9
Q

Plummer-Vinson syndrome (epidemiology, presentations, complication)

A

female >40y
Presentations: IDA + dysphagia + oesophageal web
Complication: OA oesophagus (SCC)

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10
Q

Oesophageal motility disorders & their barium swallow signs (3)

A

achalasia (bird’s beak), diffuse oesophageal spasm (corkscrew), hypercontractile oesophagus (nutcracker)

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11
Q

Triad of achalasia

A

aperistalsis + ↑ resting LES tone + poor relaxation of LES during swallowing

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12
Q

Aetiology (1+2) & pathogenesis of achalasia

A

Primary or Secondary (Chagas disease, Allgrove syndrome)
Pathogenesis: destruction of inhibitory neurons in myenteric plexus

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13
Q

Complications of achalasia (4)

A

infection, lower oesophageal diverticulum, aspiration pneumonia, OA oesophagus (SCC)

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14
Q

Types of functional oesophageal obstruction (3)

A

oesophageal motility disorders (EDM), neurological disorders, connective tissue diseases

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15
Q

Pathogenesis of oesophageal variceal bleeding

A

portal hypertension –> backflow of portal blood –> dilation of submucosal venous plexus in distal oesophagus –> esophageal varices rupture –> massive haematemesis

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16
Q

Oesophageal lacerations (2) & pathogenesis

A

Mallory-Weiss syndrome (excessive alcohol intake –> retching), Boerhaave syndrome (failed relaxation of glottis while vomiting –> ↑ intraluminal pressure –> perforation)

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17
Q

MC infectious oesophagitis

A

Candida oesophagitis

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18
Q

MC oesophagitis

A

Reflux oesophagitis

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19
Q

Normal protective mechanisms of oesophagus against reflux (7)

A

oesophageal peristalsis, LES, angle of his, diaphragm, pressure difference, gastric rugae, gastric emptying

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20
Q

Presentations of GERD

A

heart burn, regurgitation, dysphagia

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21
Q

Histology of reflux oesophagitis

A

eosinophilic infiltration, intercellular oedema, elongation of stromal papillae

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22
Q

Complications of GERD (3)

A

minor UGIB, stricture, Barrett oesophagus

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23
Q

Diagnosis of eosinophilic oesophagitis (2)

A

OGD: feline oesophagus
Histology: large amount of eosinophils

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24
Q

What is Barrett oesophagus?

A

metaplastic change of distal squamous epithelium into columnar epithelium

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25
Q

Diagnosis of Barrett oesophagus

A

OGD: proximal migration of squamocolumnar junction, salmon-coloured mucosa [1cm above OGJ]
Histology: goblet cells, columnar cells

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26
Q

CA oesophagus epidemiology

A

60~70y male

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27
Q

Presentations of CA oesophagus (10)

A
  • painless progressive dysphagia
  • odynophagia
  • regurgitation
  • ## UGIB
  • hoarseness of voice
  • Horner’s syndrome
  • ## respiratory symptoms
  • metastasis (e.g. Virchow’s node)
  • HHM (hypercalcemia)
  • constitutional symptoms
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28
Q

Is prognosis of CA oesophagus good?

A

poor

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29
Q

OA oesophagus: compare SCC & ADC

A

SCC (90%) [middle 1/3] associated with intake
ADC (10%) [distal 1/3] associated with reflux

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30
Q

Risk factors for oesophageal SCC

A

Lifestyle: smoking, alcohol, hot drink
Oesophageal disorders: achalasia, Plummer-Vinson syndrome
Genetic: tylosis

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31
Q

Erosion vs ulcer

A

Erosion = loss of epithelium
Ulcer = loss of mucosa +/- deeper tissues

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32
Q

Pathogenesis of peptic ulcer disease

A

imbalance of mucosal defence and attack –> (chronic) gastritis –> PUD

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33
Q

Risk factors for peptic ulcer disease

A

Infection: H. pylori
Drugs: NSAIDs, steroid, chemotherapy
Lifestyle: smoking, alcohol, caffeine, stress
Severe stress: Curling ulcer, Cushing ulcer
Iatrogenic: NG tube, OGD
Others: Zollinger Ellison syndrome, pernicious anaemia

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34
Q

Where is PUD caused by pernicious anaemia most commonly found in?

A

gastric body

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35
Q

Pathogenesis of gastritis from pernicious anaemia

A

antibodies to parietal cells –> loss of H/K ATPase –> loss of gastric acid –> ↑ gastrin

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36
Q

Curling ulcer (most common location & pathogenesis)

A

[proximal duodenum] burn –> ↓ plasma vol. –> ischaemia & necrosis of gastric mucosa

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37
Q

Cushing ulcer (most common location & pathogenesis)

A

[stomach, duodenum, oesophagus] intracranial disease –> direct stimulation of vagal nerve –> ↑ gastric acid secretion

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38
Q

MC location for duodenal ulcer

A

D1

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39
Q

MC location for gastric ulcer

A

lesser curvature

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40
Q

Differentiate presentations between duodenal and gastric ulcers

A

DU: pain relieved after eating
GU: pain exacerbated after eating

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41
Q

Differentiate biopsy needs between duodenal and gastric ulcers

A

DU: antrum only
GU: antrum and ulcer edge, need rescope

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42
Q

Gross morphology of PUD

A
  • sharply punched out, slightly elevated around edges
  • clean base
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43
Q

Histology of PUD

A

necrotic debris, inflammation, granulation tissue, fibrosis

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44
Q

Histology of pernicious anaemia

A

G cell hyperplasia, mucosal atrophy

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45
Q

Which is the most common gastric polyp?

A

hyperplastic polyps

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46
Q

Which gastric polyp is associated with PPI use?

A

Fundic gland polyps

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47
Q

Types of gastric polyps (4)

A

hyperplastic, fundic gland, inflammatory, adenomatous

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48
Q

Types of gastric neoplasm and percentages

A

adenocarcinoma (90%), lymphoma (5%), GIST (2%), carcinoid tumour, metastasis

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49
Q

Risk factors for gastric adenocarcinoma

A

Lifestyle: smoking, alcohol, smoked food, nitrosamines
Pre-existing conditions: adenoma, H. pylori infection, pernicious anaemia
Genetics: hereditary diffuse gastric cancer, HNPCC, FAP, P-J syndrome

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50
Q

Gene mutation for hereditary diffuse gastric cancer

A

E-cadherin

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51
Q

Classification of gastric adenocarcionoma

A

Borrmann (endoscopic), Lauren (histologic)

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52
Q

Borrmann classification (4 types)

A

Type 1 (polypoid), Type 2 (fungating / ulcerative), Type 3 (ulcerative infiltrative), Type 4 (diffuse infiltrative)

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53
Q

Which is the most common gastric adenocarcinoma according to Borrmann classification?

A

Type 3

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54
Q

Lauren classification (types)

A

intestinal type, diffuse type, mixed type

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55
Q

Gastric adenocarcinoma: intestinal type vs diffuse type (prevalence, HER2, prognosis, risk factors, histology)

A
  • intestinal type is more common, more HER2 amplification, better prognosis
  • risk factors: intestinal type (all except FHx), diffuse type (HDGC)
  • histology: intestinal type (well-differentiated, cohesive cells), diffuse type (poorly-differentiated, discohesive cells, Signet ring cells)
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56
Q

Signet ring cells

A

Diffuse type gastric adenocarcinoma

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57
Q

Transcoelomic metastasis to ovaries from stomach

A

Krukenberg tumour

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58
Q

Early vs Advanced gastric cancer

A

EGC: limited to mucosa / submucosa (T1) (95% 5-year OS)
AGC: infiltrative into muscularis propria (>= T2) (50% 5-year OS)

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59
Q

Treatment for gastric lymphoma

A

H. pylori eradication therapy

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60
Q

Classification of gastric lymphoma (2)

A

Low grade: MALToma
High grade: Diffuse large B cell lymphoma

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61
Q

GIST location

A

stomach (50%) > small bowel > large bowel

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62
Q

Origin cells of GIST

A

intestinal cell of Cajal

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63
Q

Genetic mutations for GIST

A

c-KIT (95%), PDGFRA

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64
Q

Gross morphology of GIST

A

dumbbell shaped mass with homogenous pink surface

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65
Q

Histology for GIST

A

spindle cells with elongated nuclei, c-KIT mutation on IHC

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66
Q

Prognosis model for GIST (parameters, levels)

A

AFIP model
Parameters: location, size, mitotic index
Levels: low, moderate, high

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67
Q

Management for GIST

A

surgical resection, TKI: imatinib

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68
Q

Types of non-neoplastic intestinal polyps (3)

A

hyperplastic, inflammatory, hamartomatous

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69
Q

Most common intestinal polyps

A

hyperplastic polyps

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70
Q

MC site for hyperplastic polyps

A

sigmoid colon

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71
Q

What are inflammatory polyps and the association?

A

mucosal overgrowth secondary to chronic recurrent mucosal injury & regeneration
(Association: IBD, solitary rectal ulcer)

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72
Q

What is hamartomatous polyps?

A

disorganised overgrowth of tissue indigenous to the site

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73
Q

Types of hamartomatous polyps (4)

A
  1. Juvenile polyps
  2. Peutz-Jeghers syndrome
  3. Cowden syndrome
  4. Cronkhite-Canada syndrome
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74
Q

Where is juvenile polyps mostly found?

A

rectum

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75
Q

Genes for juvenile polyposis syndrome (2)

A

SMAD4, DPC4 (AD)

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76
Q

Histology for juvenile polyps

A

cystically dilated glands, inflamed oedematous stroma

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77
Q

Gene for Peutz-Jeghers syndrome

A

STK11 (AD)

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78
Q

Sites for Peutz-Jeghers syndrome

A

small intestine > colon > stomach

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79
Q

Presentations of Peutz-Jeghers syndrome

A

hamartomatous polyps, mucocutaneous hyperpigentation

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80
Q

Histology of Peutz-Jeghers syndrome

A

Christmas tree appearance / smooth muscle cores

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81
Q

Gene for Cowden syndrome

A

PTEN (AD)

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82
Q

Which cancers are associated with Cowden syndrome? (4)

A

Thyroid cancer, Skin lesions, Breast cancer, CRC

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83
Q

Adenoma classification by architecture (prevalence, malignant potential, features)

A

Tubular (most prevalent), Villous (most possibly malignant, secrete mucus), Tubulovillous (cauliflower like)

84
Q

Definition of advanced adenoma (3)

A

size >1cm, villous / mixed type, or HG dysplasia

85
Q

Compare sessile serrated adenoma and traditional adenoma

A

Sessile: more common, commonly at R. colon, sessile
Traditional: less common, commonly at L. colon, sessile or pedunculated

86
Q

Diagnosis of serrated polyposis syndrome

A

(1) serrated polyps proximal to sigmoid colon + FHx, or (2) >5 serrated polyps proximal to sigmoid colon & >10mm, or (3) >20 serrated polyps

87
Q

Gene for familial adenomatous polyposis

88
Q

Presentations of FAP (which side more common?)

A

> 100 adenomas (MC L. side), multiple gastric fundic gland polyps

89
Q

Genes for attenuated FAP (2)

A

APC or MYH

90
Q

What is Gardner syndrome?

A

FAP + SOD (sebaceous cysts, osteomas, desmoid tumour)

91
Q

What is Turcot syndrome?

A

FAP + CNS tumours

92
Q

Genes for Lynch syndrome (5)

A

DNA mismatch repair genes (AD)
MLH1, MSH2, MSH6, MLH3, PMS6

93
Q

What cancers are associated with Lynch syndrome? (7)

A

stomach, colorectal, pancreas, urinary tract, prostate, ovary, uterus

94
Q

Diagnostic criteria for Lynch syndrome

A

Amsterdam II criteria:
- >= 3 relatives with CRC or Lynch-associated cancers
- >= 2 successive generations
- >= 1 tumour diagnosed before 50y

94
Q

Genetic workup for Lynch syndrome

A

PCR for microsatellite instability –> IHC for MMR

94
Q

Risk factors for CRC

A

Non-modifiable: male >50y, IBD (UC), FAP, Lynch syndrome
Modifiable: diet, obesity, smoking, alcohol

95
Q

Protective factor for CRC

A

prolonged aspirin / NSAID use

96
Q

Compare R sided and L sided CRC

A

R sided: present later, tend to bleed, IDA
L sided: present earlier, tend to obstruct, change in bowel habits

97
Q

Which tumour marker is used to detect recurrence of CRC?

98
Q

Which genetic biomarkers should be tested for CRC and their significance in management?

A

EGFR (anti-EGFR MAb available), KRAS & NRAS (no response to anti-EGFR MAb)

99
Q

Cell origin of carcinoid tumour

A

APUD cells (e.g. enterochromaffin cells)

100
Q

Distribution of carcinoid tumour

A

GIT (75%) and lungs (25%)

101
Q

Grading of carcinoid tumour

A

Ki-67 index

102
Q

Associated malignancy with juvenile polyposis syndrome (4)

A

stomach, pancreas, small bowel, large bowel

103
Q

Associated malignancy with Peutz-Jeghers syndrome (4)

A

breast, gonadal, pancreas, lung

104
Q

Associated malignancy with FAP (4)

A

stomach, gallbladder, thyroid, adrenal

105
Q

Staging methods for CRC (2)

A

TNM, modified Duke’s staging

106
Q

Staining for neuroendocrine tumours (2)

A

chromogranin, synaptophysin

107
Q

Aetiology of ischemic bowel disease: acute (5), chronic (1)

A

acute: embolism, thrombosis, hernia, volvulus, hypoperfusion; chronic: atherosclerosis

108
Q

Compare between ischemic bowel disease embolism and arterial thrombosis

A

embolism: MC, more distal, less extensive; arterial thrombosis: more proximal, more extensive

109
Q

MC site of mesenteric embolism

110
Q

2 phases of ischemic bowel disease

A

hypoxic injury phase –> reperfusion injury phase

111
Q

Which sections of bowel are prone to ischemic damages? (2)

A

splenic flexure, rectosigmoid junction

112
Q

Explain damages caused during reperfusion injury phase of ischemic bowel disease (2)

A

oxygen supply increases –> ROS increases; increase leukocytes & complements –> increase inflammation

113
Q

What is angiodysplasia?

A

abnormal dilated submucosal arteriovenous malformations

114
Q

Pathogenesis of angiodysplasia

A

ageing, peristaltic contraction –> intermittent obstruction of submucosal veins –> loss of pre-capillary spincter competence –> blood bypass capillaries => AVM

115
Q

Presentations of angiodysplasia

A

painless LGIB

116
Q

What is haemorrhoid?

A

variceal dilations of anal / perianal venous plexuses

117
Q

Risk factors for haemorrhoids

A

ageing, sitting on toilet for long, intra-abdominal pressure (constipation, ascites, pregnancy), portal hypertension

118
Q

Compare two types of haemorrhoid

A

External: below dentate line, squamous epithelium, somatic innervation, pain after defecation & perianal swelling;

Internal: above dentate line, columnar epithelium, autonomic innervation, painless fresh PRB & anal itching

119
Q

Grading for internal haemorrhoids

A

1: no prolapse, 2: reduced spontaneously, 3: reduced manually, 4: cannot be reduced

120
Q

Compare between UC and CD (incidence, risk factor, site, pattern (3), complications (2), histology (4), CRC risk, management)

A

Incidence: UC more common
Risk factor: smoking protective; smoking indicative
Site: rectum back up; whole GIT esp terminal ileum
Pattern: (continuous lesion; skip lesion) (no fissures; cobblestone appearance) (pseudopolyps if severe; serositis)
Complications: (toxic megacolon; stricture) (IDA; macrocytic anaemia)
Histology: (mural; transmural) (neutrophils; lymphocytes) (minimal fibrosis; fibrosis) (no granuloma; granuloma)
CRC risk: UC higher
Management: total Colectomy; palliative

121
Q

Pathogenesis of IBD

A

transepithelial flux of luminal bacterial components activate immune responses

122
Q

Extracolonic manifestations of IBD

A

aphthous ulcer, pyoderma gangrenosum, iritis, erythema nodosum, sclerosing cholangitis, arthritis, clubbing

123
Q

Compare true and false diverticulum

A

True: outpounchings of all layers from a tubular structure; False: herniation of mucosa & submucosa

124
Q

Pathogenesis of diverticulosis

A

bowel weaking with ageing + increase intraluminal pressure (e.g. constipation)

125
Q

MC site of diverticulum

A

sigmoid colon, and weakest point where vasa recta enter

126
Q

MC cause of LGIB

A

diverticular bleeding

127
Q

Complications of diverticulosis (4)

A

diverticulitis, perforation & peritonitis, fistula, intestinal obstruction

128
Q

Pathogenesis of solitary rectal ulcer

A

impaired relaxation of anorectal sphincter + sharp angle at anterior rectal shelf –> recurrent abrasion of overlying mucosa –> ulceration

129
Q

Aetiology of increased bilirubin (3+4, 3, 1+2+1)

A

Pre-hepatic: haemolytic anaemia, ineffective erythropoiesis, resorption of internal bleeding, physiological jaundice of the newborn, Gilbert syndrome, Crigler-Najjar syndrome, drugs; Intra-hepatic: hepatic diseases, Dubin-Johnson syndrome, drugs; Post-hepatic: gallstone, cholangitis, cholangioCA, extra-mural compression

130
Q

What is Gilbert syndrome?

A

UGT1A1 mutation –> reduce conjugation

131
Q

What is Crigler-Najjar syndrome?

A

severe form of Gilbert syndrome

132
Q

What is Dubin-Johnson syndrome?

A

defect in transport protein –> cannot excrete bilirubin from hepatocytes (so increase conjugated bilirubin)

133
Q

Explain hyperammonaemia in chronic liver disease (3)

A

decreased functional hepatocytes for urea cycle,
portosystemic shunt –> toxins cannot be cleared,
variceal bleeding –> resorption of bleeding –> increase protein

134
Q

Pathogenesis hepatic encephalopathy

A

build up of nitrogenous waste (e.g. ammonia) –> pass to brain –> metabolized to glutamine –> osmotic effect –> cerebral oedema

135
Q

Aetiology of portal hypertension (1+3+3)

A

Pre-hepatic: portal vein thrombosis / stenosis; Hepatic: cirrhosis, schistosoma, chronic granulomatous disease; Post-hepatic: Budd-Chiari syndrome, IVC thrombosis, RHF

136
Q

Pathogenesis of hepatorenal syndrome

A

vasodilators make blood shunts into splanchnic cirulation & hypoproteinaemia –> reduce ECV –> stimulate RAAS and sympathetic nervous system –> reduce renal arterial supply –> renal failure

137
Q

Acute liver failure definition

A

severe liver injury with onset of encephalopathy within 6 months of first onset of symptoms

138
Q

MC cause of acute liver failure

A

viral hepatitis

139
Q

MC cause of fulminant liver failure

A

drug-induced hepatitis

140
Q

What is cirrhosis?

A

diffuse transformation of liver into regenerative nodules separated by fibrous septa

141
Q

MC causes of cirrhosis (3)

A

HBV, HCV, alcoholic liver disease

142
Q

Pathogenesis of portal hypertension caused by cirrhosis

A

intrahepatic vasoconstriction + mechanical obstruction –> increase vascular resistance; abnormal intrahepatic angiogenesis + splanchnic vasodilation –> increase portal blood flow

143
Q

Classifications of regenerative nodules

A

macronodular (>=3mm, viral hepatitis), micronodular (<3mm, alcholic liver disease, hemochromatosis)

144
Q

Score for assessing cirrhosis severity & predicting 2-year survival (levels, parameters)

A

Child-Pugh score
Levels: A, B, C
Parameters:
- Albumin
- Bilirubin
- Clotting profile
- Distended abdomen (ascites)
- Encephalopathy

145
Q

Score for determining priority for liver transplant (parameters)

A

MELD score
Parameters: bilirubin, INR, creatinine

146
Q

Pathology of viral hepatitis (5)

A

vascular event [acute], inflammatory cells (lymphocytes), necroinflammatory activity (lobular in acute and portal in chronic), fibrosis [chronic], ground-glass hepatocytes [HBV]

147
Q

Grading and staging of viral hepatitis

A
  • Grade (by necroinflammatory activity)
  • Stage (by degree of fibrosis)
    • portal fibrosis –> periportal fibrosis –> bridging fibrosis –> cirrhosis
148
Q

Stages of alcoholic liver disease

A

alcoholic fatty liver –> alcoholic hepatitis –> alcoholic cirrhosis

149
Q

Enzymes involved in the metabolism of alcohol (2)

A

alcohol dehydrogenase, aldehyde dehydrogenase

150
Q

Standard of alcohol intake (in cans of beer per day)

A

M: >1 = significant, >5 = excessive
F cut half

151
Q

Questionnaire to assess alcoholic addiction

A

CAGE questionnaire
(Cut down need, Annoyed, Guilt, Eye-opener)

152
Q

Risk factors for non-alcoholic fatty liver disease (5)

A

obesity, hyperglycaemia, hypertension, hypertriglyceridaemia, low HDL

153
Q

Pathology of ALD / NAFLD (5)

A

Macrovesicular steatosis,
Balloning degernation,
Mallory-Denk bodies,
lobular-based necroinflammatory activity,
perivenular & perisinusoidal fibrosis (chicken wire fence)

154
Q

PBC vs PSC

A

PBC: female, intrahepatic, granulomatous, AMA
PSC: male, both extra and intra-hepatic, fibrosis, p-ANCA

155
Q

MRCP finding of PSC

A

“beads on string” of bile ducts

156
Q

Gene for Wilson disease

A

ATP7B (AR)

157
Q

Pathogenesis of Wilson disease

A

cannot incorporate copper into ceruloplasmin –> impaired biliary secretion of Cu

158
Q

Presentations of Wilson disease (3)

A

[liver] chronic hepatits
[basal ganglia] Parkinsonism, mild behavioural changes, psychosis
[Eye] Kayser-Fleischer rings, Sunflower cataract

159
Q

Biochemical tests for Wilson disease

A

↓ serum ceruloplasmin
↑ urinary Cu
↑ hepatic Cu

160
Q

Pathology of Wilson disease (4)

A
  • copper deposition in hepatocytes
  • periportal Mallory-Denk bodies
  • periportal glycogenated nuclei
  • non-zonal, patchy steatosis
161
Q

Aetiology for haemochromatosis (5)

A
  • Hereditary
  • Blood disorders
  • Repetitive transfusion
  • Inflammatory syndromes
  • Various CLDs
162
Q

Genes for haemochromatosis (3)

A

HFE, TFR2, FPN (AR)

163
Q

Pathogenesis of haemochromatosis

A

excessive intestinal absorption of dietary iron

164
Q

Biochemical tests for haemochromatosis (3)

A

↑ transferrin saturation, ↑ serum ferritin, ↑ hepatic iron index

165
Q

Pathology of haemochromatosis

A

siderosis, fibrosis (portal –> periportal –> bridging –> micronodular cirrhosis)

166
Q

Gene (hereditary pattern) for A1AT deficiency and pathogenesis

A

PiZZ (AR)
retention of misfolded A1AT

167
Q

Presentations of A1AT deficiency (2)

A

chronic hepatitis, panacinar emphysema

168
Q

Pathology of A1AT deficiency

A

cytoplasmic globular inclusion, fibrosis (–> micronodular cirrhosis)

169
Q

Reye’s syndrome: cause and pathology

A

aspirin use in children, diffuse microvesicular steatosis

170
Q

Pathology of paracetamol intoxication

A

pan-acinar necrosis

171
Q

Tumour markers for liver cancer (3)

A

AFP, CEA, CA19.9

172
Q

Benign liver neoplasm (3)

A

Haemangioma (MC), Focal nodular hyperplasia, Hepatocellular adenoma

173
Q

MC liver tumour

A

liver metastasis

174
Q

Risk factors for HCC

A

cirrhosis & its causes, HBV, smoking, alcohol, obesity, DM, aflatoxin

175
Q

Imaging for HCC

A
  • USG HBP
  • Triphasic CT liver scan (gold standard)
  • MRI liver with contrast
176
Q

Triphasic CT liver scan: results for HCC

A

hyperdense arterial phase, washout portovenous phase, hypodense delayed phase

177
Q

MC paediatric liver tumour

A

Hepatoblastoma

178
Q

Pathological pattern of hepatoblastoma (2)

A
  • epithelial (foetal, embryonal…)
  • mesenchymal
179
Q

What is Allgrove syndrome?

A

Achalasia + Addison’s disease + Alacrima (AR)

180
Q

Punched-out ulcer at oesophagus, Cowdry nuclear inclusions

A

HSV oesophagitis

181
Q

Shallow ulcer at oesophagus, nuclear & cytoplasmic inclusions

A

CMV oesophagitis

182
Q

Gray pseudomembrane at oesophagus, with hyphae

A

Candida oesophagitis

183
Q

MC site of angiodysplasia

184
Q

Describe biliary colic

A

RUQ dull constant pain, precipitated by fatty meal, aggravated by breathing, radiation to scapula and R. shoulder, associated with n/v

185
Q

Pathogenesis of acute calculous cholecystitis

A

prolonged gallstone impaction at Hartmann’s pouch / cystic duct –> stagnant bile & bile concentration –> chemical inflammation –> continuous pressure building up –> venous congestion & ischaemia –> secondary bacterial inflammation

186
Q

Murphy’s sign

A

inspiratory arrest during palpation of RUQ –> indicate acute cholecystitis

187
Q

Chronic cholecystitis pathology

A

hyperaemic & eroded mucosa, stones

Rokytansky-Aschoff sinuses, lymphoid aggregates, hypertrophic smooth muscles

188
Q

Aetiology of acute cholecystitis

A

stone, ischaemia

189
Q

Aetiology of acute cholangitis

A

biliary obstruction (stones, benign stricture, malignancy)
post-ERCP
biliary stent in-situ

190
Q

Charcot’s triad & Reynold’s pentad

A

fever + biliary colic + jaundice
+ hypotension + confusion

191
Q

What is recurrent pyogenic cholangitis? What are the aetiologies?

A

recurrent syndrome of bacterial cholangitis in association with intrahepatic pigmented stones & biliary obstruction

Clonorchis sinensis infection, malnutrition (low protein diet –> enzyme deficiency –> breakdown of conjugated bilirubin)

192
Q

Klatskin tumour

A

cholangiocarcinoma at CHD bifurcation

193
Q

Risk factors for cholangiocarcinoma

A
  • DM, obesity
  • PSC, RPC, parasitic infestation, choledochal cyst
  • chronic hepatitis, haemochromatosis
  • Lynch syndrome
  • thorotrast
194
Q

Pathogenesis of acute pancreatitis

A

duodeno-pancreatic reflux –> release of pancreatic enzymes –> autodigestion of pancreas –> relesae of inflammatory mediators & cytokines

195
Q

Aetiology of acute pancreatitis

A

(GAME ID)
gallstone, alcoholism, metabolic (hyperTG, hyperCa), ERCP, idiopathic, drugs

196
Q

Why could acute pancreatitis lead to transient hypoCa?

A

lysis of fat cells –> release of fatty acids –> fat saponification

197
Q

Signs for retroperitoneal haemorrhage

A

Cullen’s sign (periumbilical), Grey Turner’s sign (frank)

198
Q

Complications of acute pancreatitis

A
  • ## retroperitoneal haemorrhage
  • pancreatic fluid collections
  • pancreatic pseudo-aneurysm
  • splenic vein thrombosis
  • pancreatic exocrine insufficiency (steatorrhoea & malnutrition)
  • ## pancreatic endocrine insufficiency (DM)
  • haemodynamic instability, electrolyte imbalance, sepsis, multiple organ failure
199
Q

Prognostic score for acute pancreatitis

A

Ranson’s score

200
Q

Aetiology of chronic pancreatitis

A

alcoholism, idiopathic, autoimmune, obstruction

201
Q

Risk factors for pancreatic carcinoma

A
  • smoking, drinking, obesity
  • DM, chronic pancreatitis
  • FHx
  • hereditary (e.g. Lynch)
202
Q

Tumour marker for pancreatic carcinoma

203
Q

Presentations of haemochromatosis (5)

A

Liver: cirrhosis, hepatomegaly, HCC
Heart: dilated cardiomyopathy, arrhythmia
Skin: bronze pigmentation
Endocrine: DM, hypogonadism, hypothyroidism
Joint: arthritis

204
Q

Pathophysiology basis of ascites by cirrhosis (3)

A

hypoproteniaemia –> ↓ oncotic pressure
portal hypertension –> ↑ hydrostatic pressure

↓ effective circulating volume –> activating RAAS and sympathetic nervous system –> ↑ Na and water reabsorption –> worsen ascites

205
Q

Anti-EGFR Mab for CRC

A

Cetuximab, Panitumumab

西妥昔，帕尼吐滿

MED4 ACP (13 decks)

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