GI Pathology Flashcards

(207 cards)

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
Diagnosis of Barrett oesophagus
OGD: proximal migration of squamocolumnar junction, salmon-coloured mucosa [1cm above OGJ] Histology: goblet cells, columnar cells
26
CA oesophagus epidemiology
60~70y male
27
Presentations of CA oesophagus (10)
- painless progressive dysphagia - odynophagia - regurgitation - UGIB --- - hoarseness of voice - Horner's syndrome - respiratory symptoms --- - metastasis (e.g. Virchow's node) - HHM (hypercalcemia) - constitutional symptoms
28
Is prognosis of CA oesophagus good?
poor
29
OA oesophagus: compare SCC & ADC
SCC (90%) [middle 1/3] associated with intake ADC (10%) [distal 1/3] associated with reflux
30
Risk factors for oesophageal SCC
Lifestyle: smoking, alcohol, hot drink Oesophageal disorders: achalasia, Plummer-Vinson syndrome Genetic: tylosis
31
Erosion vs ulcer
Erosion = loss of epithelium Ulcer = loss of mucosa +/- deeper tissues
32
Pathogenesis of peptic ulcer disease
imbalance of mucosal defence and attack --> (chronic) gastritis --> PUD
33
Risk factors for peptic ulcer disease
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
34
Where is PUD caused by pernicious anaemia most commonly found in?
gastric body
35
Pathogenesis of gastritis from pernicious anaemia
antibodies to parietal cells --> loss of H/K ATPase --> loss of gastric acid --> ↑ gastrin
36
Curling ulcer (most common location & pathogenesis)
[proximal duodenum] burn --> ↓ plasma vol. --> ischaemia & necrosis of gastric mucosa
37
Cushing ulcer (most common location & pathogenesis)
[stomach, duodenum, oesophagus] intracranial disease --> direct stimulation of vagal nerve --> ↑ gastric acid secretion
38
MC location for duodenal ulcer
D1
39
MC location for gastric ulcer
lesser curvature
40
Differentiate presentations between duodenal and gastric ulcers
DU: pain relieved after eating GU: pain exacerbated after eating
41
Differentiate biopsy needs between duodenal and gastric ulcers
DU: antrum only GU: antrum and ulcer edge, need rescope
42
Gross morphology of PUD
- sharply punched out, slightly elevated around edges - clean base
43
Histology of PUD
necrotic debris, inflammation, granulation tissue, fibrosis
44
Histology of pernicious anaemia
G cell hyperplasia, mucosal atrophy
45
Which is the most common gastric polyp?
hyperplastic polyps
46
Which gastric polyp is associated with PPI use?
Fundic gland polyps
47
Types of gastric polyps (4)
hyperplastic, fundic gland, inflammatory, adenomatous
48
Types of gastric neoplasm and percentages
adenocarcinoma (90%), lymphoma (5%), GIST (2%), carcinoid tumour, metastasis
49
Risk factors for gastric adenocarcinoma
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
50
Gene mutation for hereditary diffuse gastric cancer
E-cadherin
51
Classification of gastric adenocarcionoma
Borrmann (endoscopic), Lauren (histologic)
52
Borrmann classification (4 types)
Type 1 (polypoid), Type 2 (fungating / ulcerative), Type 3 (ulcerative infiltrative), Type 4 (diffuse infiltrative)
53
Which is the most common gastric adenocarcinoma according to Borrmann classification?
Type 3
54
Lauren classification (types)
intestinal type, diffuse type, mixed type
55
Gastric adenocarcinoma: intestinal type vs diffuse type (prevalence, HER2, prognosis, risk factors, histology)
- 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)
56
Signet ring cells
Diffuse type gastric adenocarcinoma
57
Transcoelomic metastasis to ovaries from stomach
Krukenberg tumour
58
Early vs Advanced gastric cancer
EGC: limited to mucosa / submucosa (T1) (95% 5-year OS) AGC: infiltrative into muscularis propria (>= T2) (50% 5-year OS)
59
Treatment for gastric lymphoma
H. pylori eradication therapy
60
Classification of gastric lymphoma (2)
Low grade: MALToma High grade: Diffuse large B cell lymphoma
61
GIST location
stomach (50%) > small bowel > large bowel
62
Origin cells of GIST
intestinal cell of Cajal
63
Genetic mutations for GIST
c-KIT (95%), PDGFRA
64
Gross morphology of GIST
dumbbell shaped mass with homogenous pink surface
65
Histology for GIST
spindle cells with elongated nuclei, c-KIT mutation on IHC
66
Prognosis model for GIST (parameters, levels)
AFIP model Parameters: location, size, mitotic index Levels: low, moderate, high
67
Management for GIST
surgical resection, TKI: imatinib
68
Types of non-neoplastic intestinal polyps (3)
hyperplastic, inflammatory, hamartomatous
69
Most common intestinal polyps
hyperplastic polyps
70
MC site for hyperplastic polyps
sigmoid colon
71
What are inflammatory polyps and the association?
mucosal overgrowth secondary to chronic recurrent mucosal injury & regeneration (Association: IBD, solitary rectal ulcer)
72
What is hamartomatous polyps?
disorganised overgrowth of tissue indigenous to the site
73
Types of hamartomatous polyps (4)
1. Juvenile polyps 2. Peutz-Jeghers syndrome 3. Cowden syndrome 4. Cronkhite-Canada syndrome
74
Where is juvenile polyps mostly found?
rectum
75
Genes for juvenile polyposis syndrome (2)
SMAD4, DPC4 (AD)
76
Histology for juvenile polyps
cystically dilated glands, inflamed oedematous stroma
77
Gene for Peutz-Jeghers syndrome
STK11 (AD)
78
Sites for Peutz-Jeghers syndrome
small intestine > colon > stomach
79
Presentations of Peutz-Jeghers syndrome
hamartomatous polyps, mucocutaneous hyperpigentation
80
Histology of Peutz-Jeghers syndrome
Christmas tree appearance / smooth muscle cores
81
Gene for Cowden syndrome
PTEN (AD)
82
Which cancers are associated with Cowden syndrome? (4)
Thyroid cancer, Skin lesions, Breast cancer, CRC
83
Adenoma classification by architecture (prevalence, malignant potential, features)
Tubular (most prevalent), Villous (most possibly malignant, secrete mucus), Tubulovillous (cauliflower like)
84
Definition of advanced adenoma (3)
size >1cm, villous / mixed type, or HG dysplasia
85
Compare sessile serrated adenoma and traditional adenoma
Sessile: more common, commonly at R. colon, sessile Traditional: less common, commonly at L. colon, sessile or pedunculated
86
Diagnosis of serrated polyposis syndrome
(1) serrated polyps proximal to sigmoid colon + FHx, or (2) >5 serrated polyps proximal to sigmoid colon & >10mm, or (3) >20 serrated polyps
87
Gene for familial adenomatous polyposis
APC (AD)
88
Presentations of FAP (which side more common?)
>100 adenomas (MC L. side), multiple gastric fundic gland polyps
89
Genes for attenuated FAP (2)
APC or MYH
90
What is Gardner syndrome?
FAP + SOD (sebaceous cysts, osteomas, desmoid tumour)
91
What is Turcot syndrome?
FAP + CNS tumours
92
Genes for Lynch syndrome (5)
DNA mismatch repair genes (AD) MLH1, MSH2, MSH6, MLH3, PMS6
93
What cancers are associated with Lynch syndrome? (7)
stomach, colorectal, pancreas, urinary tract, prostate, ovary, uterus
94
Diagnostic criteria for Lynch syndrome
Amsterdam II criteria: - >= 3 relatives with CRC or Lynch-associated cancers - >= 2 successive generations - >= 1 tumour diagnosed before 50y
94
Genetic workup for Lynch syndrome
PCR for microsatellite instability --> IHC for MMR
94
Risk factors for CRC
Non-modifiable: male >50y, IBD (UC), FAP, Lynch syndrome Modifiable: diet, obesity, smoking, alcohol
95
Protective factor for CRC
prolonged aspirin / NSAID use
96
Compare R sided and L sided CRC
R sided: present later, tend to bleed, IDA L sided: present earlier, tend to obstruct, change in bowel habits
97
Which tumour marker is used to detect recurrence of CRC?
CEA
98
Which genetic biomarkers should be tested for CRC and their significance in management?
EGFR (anti-EGFR MAb available), KRAS & NRAS (no response to anti-EGFR MAb)
99
Cell origin of carcinoid tumour
APUD cells (e.g. enterochromaffin cells)
100
Distribution of carcinoid tumour
GIT (75%) and lungs (25%)
101
Grading of carcinoid tumour
Ki-67 index
102
Associated malignancy with juvenile polyposis syndrome (4)
stomach, pancreas, small bowel, large bowel
103
Associated malignancy with Peutz-Jeghers syndrome (4)
breast, gonadal, pancreas, lung
104
Associated malignancy with FAP (4)
stomach, gallbladder, thyroid, adrenal
105
Staging methods for CRC (2)
TNM, modified Duke's staging
106
Staining for neuroendocrine tumours (2)
chromogranin, synaptophysin
107
Aetiology of ischemic bowel disease: acute (5), chronic (1)
acute: embolism, thrombosis, hernia, volvulus, hypoperfusion; chronic: atherosclerosis
108
Compare between ischemic bowel disease embolism and arterial thrombosis
embolism: MC, more distal, less extensive; arterial thrombosis: more proximal, more extensive
109
MC site of mesenteric embolism
SMA
110
2 phases of ischemic bowel disease
hypoxic injury phase --> reperfusion injury phase
111
Which sections of bowel are prone to ischemic damages? (2)
splenic flexure, rectosigmoid junction
112
Explain damages caused during reperfusion injury phase of ischemic bowel disease (2)
oxygen supply increases --> ROS increases; increase leukocytes & complements --> increase inflammation
113
What is angiodysplasia?
abnormal dilated submucosal arteriovenous malformations
114
Pathogenesis of angiodysplasia
ageing, peristaltic contraction --> intermittent obstruction of submucosal veins --> loss of pre-capillary spincter competence --> blood bypass capillaries => AVM
115
Presentations of angiodysplasia
painless LGIB
116
What is haemorrhoid?
variceal dilations of anal / perianal venous plexuses
117
Risk factors for haemorrhoids
ageing, sitting on toilet for long, intra-abdominal pressure (constipation, ascites, pregnancy), portal hypertension
118
Compare two types of haemorrhoid
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
Grading for internal haemorrhoids
1: no prolapse, 2: reduced spontaneously, 3: reduced manually, 4: cannot be reduced
120
Compare between UC and CD (incidence, risk factor, site, pattern (3), complications (2), histology (4), CRC risk, management)
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
Pathogenesis of IBD
transepithelial flux of luminal bacterial components activate immune responses
122
Extracolonic manifestations of IBD
aphthous ulcer, pyoderma gangrenosum, iritis, erythema nodosum, sclerosing cholangitis, arthritis, clubbing
123
Compare true and false diverticulum
True: outpounchings of all layers from a tubular structure; False: herniation of mucosa & submucosa
124
Pathogenesis of diverticulosis
bowel weaking with ageing + increase intraluminal pressure (e.g. constipation)
125
MC site of diverticulum
sigmoid colon, and weakest point where vasa recta enter
126
MC cause of LGIB
diverticular bleeding
127
Complications of diverticulosis (4)
diverticulitis, perforation & peritonitis, fistula, intestinal obstruction
128
Pathogenesis of solitary rectal ulcer
impaired relaxation of anorectal sphincter + sharp angle at anterior rectal shelf --> recurrent abrasion of overlying mucosa --> ulceration
129
Aetiology of increased bilirubin (3+4, 3, 1+2+1)
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
What is Gilbert syndrome?
UGT1A1 mutation --> reduce conjugation
131
What is Crigler-Najjar syndrome?
severe form of Gilbert syndrome
132
What is Dubin-Johnson syndrome?
defect in transport protein --> cannot excrete bilirubin from hepatocytes (so increase conjugated bilirubin)
133
Explain hyperammonaemia in chronic liver disease (3)
decreased functional hepatocytes for urea cycle, portosystemic shunt --> toxins cannot be cleared, variceal bleeding --> resorption of bleeding --> increase protein
134
Pathogenesis hepatic encephalopathy
build up of nitrogenous waste (e.g. ammonia) --> pass to brain --> metabolized to glutamine --> osmotic effect --> cerebral oedema
135
Aetiology of portal hypertension (1+3+3)
Pre-hepatic: portal vein thrombosis / stenosis; Hepatic: cirrhosis, schistosoma, chronic granulomatous disease; Post-hepatic: Budd-Chiari syndrome, IVC thrombosis, RHF
136
Pathogenesis of hepatorenal syndrome
vasodilators make blood shunts into splanchnic cirulation & hypoproteinaemia --> reduce ECV --> stimulate RAAS and sympathetic nervous system --> reduce renal arterial supply --> renal failure
137
Acute liver failure definition
severe liver injury with onset of encephalopathy within 6 months of first onset of symptoms
138
MC cause of acute liver failure
viral hepatitis
139
MC cause of fulminant liver failure
drug-induced hepatitis
140
What is cirrhosis?
diffuse transformation of liver into regenerative nodules separated by fibrous septa
141
MC causes of cirrhosis (3)
HBV, HCV, alcoholic liver disease
142
Pathogenesis of portal hypertension caused by cirrhosis
intrahepatic vasoconstriction + mechanical obstruction --> increase vascular resistance; abnormal intrahepatic angiogenesis + splanchnic vasodilation --> increase portal blood flow
143
Classifications of regenerative nodules
macronodular (>=3mm, viral hepatitis), micronodular (<3mm, alcholic liver disease, hemochromatosis)
144
Score for assessing cirrhosis severity & predicting 2-year survival (levels, parameters)
Child-Pugh score Levels: A, B, C Parameters: - Albumin - Bilirubin - Clotting profile - Distended abdomen (ascites) - Encephalopathy
145
Score for determining priority for liver transplant (parameters)
MELD score Parameters: bilirubin, INR, creatinine
146
Pathology of viral hepatitis (5)
vascular event [acute], inflammatory cells (lymphocytes), necroinflammatory activity (lobular in acute and portal in chronic), fibrosis [chronic], ground-glass hepatocytes [HBV]
147
Grading and staging of viral hepatitis
- Grade (by necroinflammatory activity) - Stage (by degree of fibrosis) - portal fibrosis --> periportal fibrosis --> bridging fibrosis --> cirrhosis
148
Stages of alcoholic liver disease
alcoholic fatty liver --> alcoholic hepatitis --> alcoholic cirrhosis
149
Enzymes involved in the metabolism of alcohol (2)
alcohol dehydrogenase, aldehyde dehydrogenase
150
Standard of alcohol intake (in cans of beer per day)
M: >1 = significant, >5 = excessive F cut half
151
Questionnaire to assess alcoholic addiction
CAGE questionnaire (Cut down need, Annoyed, Guilt, Eye-opener)
152
Risk factors for non-alcoholic fatty liver disease (5)
obesity, hyperglycaemia, hypertension, hypertriglyceridaemia, low HDL
153
Pathology of ALD / NAFLD (5)
Macrovesicular steatosis, Balloning degernation, Mallory-Denk bodies, lobular-based necroinflammatory activity, perivenular & perisinusoidal fibrosis (chicken wire fence)
154
PBC vs PSC
PBC: female, intrahepatic, granulomatous, AMA PSC: male, both extra and intra-hepatic, fibrosis, p-ANCA
155
MRCP finding of PSC
"beads on string" of bile ducts
156
Gene for Wilson disease
ATP7B (AR)
157
Pathogenesis of Wilson disease
cannot incorporate copper into ceruloplasmin --> impaired biliary secretion of Cu
158
Presentations of Wilson disease (3)
[liver] chronic hepatits [basal ganglia] Parkinsonism, mild behavioural changes, psychosis [Eye] Kayser-Fleischer rings, Sunflower cataract
159
Biochemical tests for Wilson disease
↓ serum ceruloplasmin ↑ urinary Cu ↑ hepatic Cu
160
Pathology of Wilson disease (4)
- copper deposition in hepatocytes - periportal Mallory-Denk bodies - periportal glycogenated nuclei - non-zonal, patchy steatosis
161
Aetiology for haemochromatosis (5)
- Hereditary - Blood disorders - Repetitive transfusion - Inflammatory syndromes - Various CLDs
162
Genes for haemochromatosis (3)
HFE, TFR2, FPN (AR)
163
Pathogenesis of haemochromatosis
excessive intestinal absorption of dietary iron
164
Biochemical tests for haemochromatosis (3)
↑ transferrin saturation, ↑ serum ferritin, ↑ hepatic iron index
165
Pathology of haemochromatosis
siderosis, fibrosis (portal --> periportal --> bridging --> micronodular cirrhosis)
166
Gene (hereditary pattern) for A1AT deficiency and pathogenesis
PiZZ (AR) retention of misfolded A1AT
167
Presentations of A1AT deficiency (2)
chronic hepatitis, panacinar emphysema
168
Pathology of A1AT deficiency
cytoplasmic globular inclusion, fibrosis (--> micronodular cirrhosis)
169
Reye's syndrome: cause and pathology
aspirin use in children, diffuse microvesicular steatosis
170
Pathology of paracetamol intoxication
pan-acinar necrosis
171
Tumour markers for liver cancer (3)
AFP, CEA, CA19.9
172
Benign liver neoplasm (3)
Haemangioma (MC), Focal nodular hyperplasia, Hepatocellular adenoma
173
MC liver tumour
liver metastasis
174
Risk factors for HCC
cirrhosis & its causes, HBV, smoking, alcohol, obesity, DM, aflatoxin
175
Imaging for HCC
- USG HBP - Triphasic CT liver scan (gold standard) - MRI liver with contrast
176
Triphasic CT liver scan: results for HCC
hyperdense arterial phase, washout portovenous phase, hypodense delayed phase
177
MC paediatric liver tumour
Hepatoblastoma
178
Pathological pattern of hepatoblastoma (2)
- epithelial (foetal, embryonal...) - mesenchymal
179
What is Allgrove syndrome?
Achalasia + Addison's disease + Alacrima (AR)
180
Punched-out ulcer at oesophagus, Cowdry nuclear inclusions
HSV oesophagitis
181
Shallow ulcer at oesophagus, nuclear & cytoplasmic inclusions
CMV oesophagitis
182
Gray pseudomembrane at oesophagus, with hyphae
Candida oesophagitis
183
MC site of angiodysplasia
R. colon
184
Describe biliary colic
RUQ dull constant pain, precipitated by fatty meal, aggravated by breathing, radiation to scapula and R. shoulder, associated with n/v
185
Pathogenesis of acute calculous cholecystitis
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
Murphy's sign
inspiratory arrest during palpation of RUQ --> indicate acute cholecystitis
187
Chronic cholecystitis pathology
hyperaemic & eroded mucosa, stones Rokytansky-Aschoff sinuses, lymphoid aggregates, hypertrophic smooth muscles
188
Aetiology of acute cholecystitis
stone, ischaemia
189
Aetiology of acute cholangitis
biliary obstruction (stones, benign stricture, malignancy) post-ERCP biliary stent in-situ
190
Charcot's triad & Reynold's pentad
fever + biliary colic + jaundice + hypotension + confusion
191
What is recurrent pyogenic cholangitis? What are the aetiologies?
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
Klatskin tumour
cholangiocarcinoma at CHD bifurcation
193
Risk factors for cholangiocarcinoma
- DM, obesity - PSC, RPC, parasitic infestation, choledochal cyst - chronic hepatitis, haemochromatosis - Lynch syndrome - thorotrast
194
Pathogenesis of acute pancreatitis
duodeno-pancreatic reflux --> release of pancreatic enzymes --> autodigestion of pancreas --> relesae of inflammatory mediators & cytokines
195
Aetiology of acute pancreatitis
(GAME ID) gallstone, alcoholism, metabolic (hyperTG, hyperCa), ERCP, idiopathic, drugs
196
Why could acute pancreatitis lead to transient hypoCa?
lysis of fat cells --> release of fatty acids --> fat saponification
197
Signs for retroperitoneal haemorrhage
Cullen's sign (periumbilical), Grey Turner's sign (frank)
198
Complications of acute pancreatitis
- 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
Prognostic score for acute pancreatitis
Ranson's score
200
Aetiology of chronic pancreatitis
alcoholism, idiopathic, autoimmune, obstruction
201
Risk factors for pancreatic carcinoma
- smoking, drinking, obesity - DM, chronic pancreatitis - FHx - hereditary (e.g. Lynch)
202
Tumour marker for pancreatic carcinoma
CA19.9
203
Presentations of haemochromatosis (5)
Liver: cirrhosis, hepatomegaly, HCC Heart: dilated cardiomyopathy, arrhythmia Skin: bronze pigmentation Endocrine: DM, hypogonadism, hypothyroidism Joint: arthritis
204
Pathophysiology basis of ascites by cirrhosis (3)
hypoproteniaemia --> ↓ oncotic pressure portal hypertension --> ↑ hydrostatic pressure ↓ effective circulating volume --> activating RAAS and sympathetic nervous system --> ↑ Na and water reabsorption --> worsen ascites
205
Anti-EGFR Mab for CRC
Cetuximab, Panitumumab 西妥昔,帕尼吐滿