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Gastro Flashcards

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1
Q

acute intermittent prophyria pathophysiology and triggers

A

auto dom
porphobilinogen deaminase deficiency
PBGD on chromo 11
latent in most heterozygotes
block in haem synthesis at PBGD reaction stage
> increased ALA and PBG synthesis
> increased urinary excretion of porphyrin precursors and porphyrins

precipitating factors:
- ALAS1 induction
- P450 enzymes
- alcohol
- barbiturates, sulfonamides, enzyme inducers (carbamaz, phenytoin, OCP, rifampicin)
- fluctuations in female sex hormones
- infections
- starvation

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2
Q

manifestations of acute intermittent porphyria

A
  • autonomic neuropathy
    > abdo pain, constipation, vomiting, tachyc, HTN, postural hypot, peripheral neuropathies
  • dark/red urine
  • bulbar paresis > resp failure
  • cerebellar signs
  • hypothalamic dysfunction > SIADH
  • hyponatraemia (SIADH, GI and renal loss)
  • confusion, agitation, disorientation, hallucinations
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3
Q

managing acute intermittent porphyria

A

IV fluids
IV haemin
alternatively 300g dextrose IV

prophylaxis:
non cyclic- haem arginate IV once or twice weekly (risk of iron overload)
cyclic attacks in women- preventative GnRH

liver transplant

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4
Q

complications of acute intermittent porphyria

A

HTN
CKD
hepatocellular ca

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5
Q

types of acute pancreatitis

A

mild- no complications or organ dysfunction
mod- local complications and/or organ dysfunction that resolves within 48h
severe- persistent organ dysfunction leading to local complications (necrosis, abscess, pseudocysts), potentially fatal

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6
Q

causes of pancreatitis

A

Gallstones
Ethanol
Trauma
Steroids
Mumps, coxsackie B
Autoimmune
Scorpion sting
Hyperlipidaemia, hypercalcaemia, hypertriglyceridaemia,
ERCP
Drugs (azathioprine, OCP, steroids, antiretrovirals, fibrates, thiazides)

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7
Q

pathophysiology of pancreatitis

A

intrapancreatic activation of enzymes due to outflow obstruction or acinar cell injury
> autodigestion of parenchyma
> inflammatory cells go to parenchyma and release cytokines
> inflammation

enzymes also cause vascular injury
> vasodilatation and increased permeability
> third space loss
> hypotension, tachyc, shock, multi organ dysfunction

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8
Q

acute vs chronic pancreatitis investigation findings

A

acute:
raised amylase 3x, lipase (lipase remains raised longer)
sentinel loops of adynamic bowel next to pancreas on AXR
CT may confirm inflammation if amylase/lipase levels are not raised

chronic:
speckled calcification on XR, CT
irregular dilatation and stricturing of pancreatic ducts on ERCP, MRCP
endoscopic USS
PABA testing (exocrine function)
faecal elastase (exocrine insufficiency)
OGTT

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9
Q

surgical management of gallstone pancreatitis

A

consider early ERCP for decompression
cholecystectomy during same admission or within 2/52 of discharge once acute symptoms have settled

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10
Q

poor prognostic factors of acute pancreatitis

A

age > 55
WCC > 15
urea > 16
pO2 < 8
calcium < 2
albumin < 32
glucose > 10
LDH 600
AST 200

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11
Q

pathophysiology of alcoholic fatty liver disease

A

alcoholic dehydrogenase concerts alcohol to acetaldehyde to acetic acid to CO2 + H20

> reduces NAD to NAD + H
increases NADH : NAD ratio
increases fatty acid synthesis decreased fatty acid oxidation

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12
Q

pathophysiology of alcoholic hepatitis

A

acetaldehyde binds to macromolecules in hepatocytes
> immune system detects complexes
> neutrophil infiltration
> hepatocyte necrosis and inflammation

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13
Q

dilutional anaemia blood test

A

reduced haematocrit

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14
Q

SAAG and portal hypertension

A

serum albumin minus ascitic albumin
> 1.1 g/L suggests portal HTN

increased SAAG:
cirrhosis, alcoholic hepatitis, schisto, budd chiari, portal v obstruction, cardiac disease, SBP

low or normal SAAG:
nephrotic syndrome, protein losing enteropathy, peritoneal carcinomatosis, TB peritonitis, pancreatic duct leak, biliary ascites

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15
Q

autoimmune hepatitis genetics and environmental triggers

A

HLADR3 and HLADR4 (type 1)
HLA DQB1 and HLA DRB (type 2)

viruses, nitrofurantoin, diclofenac, atorvastatin

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16
Q

type 1 and type 2 autoimmune hepatitis

A

1: most common
antiSMA and ANA
increased IgG
good response to immunosuppression

2: often in children
commonly > cirrhosis
less treatable
ALKM-1, ALC-1
ANA and aSMA neg

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17
Q

autoimmune hepatitis histopathology

A

piecemeal necrosis
mononuclear infiltration of portal and periportal areas
may see fibrosis

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18
Q

pharmacalogical management of autoimmune hepatitis

A

for mod/severe inflammation (serum AST 5x upper limit, serum globulins 2x upper limit normal, necrosis on biopsy)

4/52 prednisolone
alternatively budesonide
steroid + immunosuppressant e.g. azathioprine

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19
Q

budd chiari vs veno-occlusive disease

A

both cause hepatic venous outflow obstruction

BC: any level from small hepatic veins to junction of IVC and RA
VOD: occlusion of terminal hepatic venules and sinusoids

BC associated w/ myeloprolfierative disorders, hypercoagulable disorders, behcet, SLE, sjogrens, mixed CTD, IBD, sarcoid, pregnancy and post portum
secondary BC: external compression or invasion by abscess, tumour or trauma

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20
Q

causes of venous occlusive disease

A

haematopoietic cell transplant
ctx e.g. oxaliplatin
pyrrolizidine alkaloids jamaican bush tea
high dose rtx to liver
post liver transplant

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21
Q

preventing veno-occlusive disorder

A

given ursodeoxycholic acid or heparin to patients undergoing haematopoietic cell transplant

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22
Q

complications of chronic pancreatitis

A

pancreatic duct obstruction
pseudocysts
neuropathic pain
pancreatic ascites, pleural effusion
diabetes
exocrine insufficiency
pancreatic cancer

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23
Q

pancreatic pseudocysts

A

necrotic/haemorrhagic material and enzymes within or near pancreas
no epithelial lining
found on CT
confirmed w/ EUS and FNA
larger cysts > obstruction, vomiting
occur following acute/chronic pancreatitis or trauma

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24
Q

pancreatic divisum

A

congenital
dorsal and ventral ducts do not connect
> dorsal duct drainage is disrupted
asymptomatic or recurrent pancreatitis
dx w/ MRCP or ERCP

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25
cirrhosis pathophysiology
activation of stellate cells > accumulation of collage I and III in parenchyma and Disse space > stellate cells become contractile > increased portal resistance > blood shunted away from liver portal HTN > spleen congestion > hypersplenism and platelet retention
26
coeliac histopathology
loss of brush border villous atrophy crypt hyerplasia
27
coeliac blood tests and biopsy results
IgA-tTG endomysial antibody EMA if IgA-tTG unavailable or weakly positive biopsy: intra-epithelial lymphocytes, villous atrophy, crypt hyperplasia
28
supplementation for coeliac
calcium and vit D for all iron only if deficient
29
HNPCC vs sporadic colorectal ca
younger age of dx more likely to develop in proximal colon rapid transformation from benign to malignant
30
HNPCC non colon associated cancers
endometrial ovarian gastric biliary, urinary, brain, small bowel, pancreas
31
lymphatic spread in colorectal ca
regional nodes > para aortic nodes > thoracic duct supraclavicular nodes in advanced cases upward spread more likely for rectal carcinoma than lateral or downward spread
32
transcoelomic spread of colorectal ca
deposits of malignant nodules throughout peritoneal cavity occurs in 10% after resection spreads to ovaries (Krukenberg tumours)
33
distribution of colorectal tumours
75% in rectum and sigmoid FAP/HNPCC- more right sided 3% w/ primary carcinoma will have another tumour at the time 75% will have an associated benign adenoma 3% of successfully treated cases will get another colorectal tumour within 10 y
34
TNM staging
T0- no evidence of primary tumour Tis- in situ T1- submucosa T2- muscularis mucosa T3- subserosa or non peritonealised pericolic/perirectal tissues T4- directly invades other organs or perforates visceral peritoneum N0- no lymph node mets N1- mets in 1-3 regional nodes N2- mets in 4 regional nodes M1- distant mets
35
dukes staging
A- bowel wall B- through wall but no nodes C- nodes involved D- distant mets
36
right vs left colon ca
Right: proliferative, soft, friable change in bowel habit, PR blood abdo pain and perforation more likely to be asymptomatic Left: annular and constricting change in bowel habit, constipation obstruction, colic, perforation more overt bleeding and mucus PR 25-30% present as obstruction or perforation rectal: bleeding usually presenting complaint tenesmus, palpable prolapsing mass symptoms worse in morning altered bowel habit
37
colorectal ca adjuvant ctx
indicated in TNM III, maybe TNM II 6/12 5-FU + folinic acid (FUFA) or 1/52 5-FU by continuous infusion not indicated for TNM stage I
38
colorectal ca pre op
staging CT colonoscopy or barium enema MRI or endorectal US for local involvement 2 day of liquid only diet + picosulfate to reduce bowel lumen bacteria metro and cephalosporin prophylaxis
39
curative intent surgery for unobstructed colorectal ca
right sided, non obstructed: right hemicolectomy and primary anastamosis, sparing middle colic arteries transverse or splenic, non obstructed: extended right hemi, take middle colic arteries sigmoid or middle/upper rectum: anterior resection, take inferior mesenteric artery and sigmoid and superior rectal branches low rectal and anorectal: abdominoperineal excision and end colostomy, taking inferior mesenteric artery some may be done as transanal excision
40
3 stage approach for obstructed colorectal ca
1- primary decompression w/ proximal loop colostomy 2- resection of tumour at later date, leaving the colostomy to protect anastomosis 3- closure of colostomy
41
hartmann's procedure
primary resection with end colostomy relieves obstruction and resects tumour avoids complications of anastamosis under suboptimal conditions reversal has high complication rate
42
options for obstructed colorectal ca
primary resection and anastomosis hartmanns 3 stage approach
43
anastamotic leak
typically 7-10 days post op higher risk in low anastamoses
44
most common site of perforation
caecum
45
Rome IV criteria
constipation less than three times per week
46
drug causes of constipation
iron and calcium NSAIDs antimuscarinics (procyclidine, oxybutynin) TCAs clozapine, quetiapine carbamazepine, gabapentin, phenytoin antihistamines (hydroxyzine) antispasmodics (hyoscine) CCB diuretics
47
metabolic causes of constipation
hypercalcaemia uraemia hypermagnesaemia hyperkalaemia
48
extra intestinal manifestations of crohns
pauci articular arthritis erythema nodosum aphthous mouth ulcers episcleritis osteopenia, osteoporosis, osteomalacia sacroiliitis, spondylitis polyarticular arthritis pyoderma gangrenosum, psoriasis uveitis
49
crohns vs UC
crohns: ulcers neutrophil infiltrates fistulae B12 and iron def UC: crypt abscesses inflammatory cell infiltrates iron def
50
managing crohns
- pred to induce remission - thiopurines or MTX as adjunct for acute exacerbations and for maintaining remission after complete macroscopic resection - biologics next line to induce/maintain remission - aminosalicylates if steroids not tolerated
51
congenital vs acquired diverticulosis
congenital involve all layers of colon wall acquired involve areas of mucosa that herniate through muscular wall
52
most common location of diverticular disease
sigmoid and descending colon right sided more common in Asian patients
53
benign vs malignant stricture
smooth walled no mucosal disruption no apple core appearances tend to be longer
54
drugs causing DILI
paracetamol halothane NSAIDs isoniazid penicillins, cephalosporins sulfonamides ketoconazole thiazoladinedione ezetimibe kava root
55
antidepressants for IBS abdo pain
TCA e.g. amitripyline 2nd line fluoxetine or citalopram
56
gallstones risk factors
progesterone, oestrogen (female, OCP, HRT, parity) clofibrate crohn's, short bowel syndrome age haemolysis diet diabetes NAFLD obesity
57
gallstones composition
70-90% are cholesterol and bile pigment 10% pure cholesterol pure pigment stones are rare (except in chronic haemolysis) pigment- bilirubin and calcium salts
58
what causes pale stools and dark urine in obstructed jaundice?
pale stools- lack of stercobilinogen dark urine- increased conjugated bilirubin
59
LFTs in gallbladder disease
ALP raised- ALP lines biliary tree GGT raised- reflects acute liver damage as bile backs up into liver ALT and AST will rise with ongoing obstruction due to damage to hepatocytes amylase/lipase raised in pancreatitis
60
investigating gall stones
abdo USS MRCP next line EUS if non invasive investigations fail to demonstrate cause ERCP not used for diagnosis of obstructive jaundice
61
indications for cholecystectomy
acute cholecystitis (within 1/52) symptomatic GB stones symptomatic or asymptomatic CBD stones (also requires clearance of bile duct) gallstone pancreatitis once acute symptoms settle
62
cholecystitis vs cholangitis
fever and RUQ pain cholangitis- also jaundice
63
gastric ca risk factors
japanese h pylori hypochlorydia (pernicious anaemia, chronic atrophic gastritis, partial gastrectomy) FHx inc FAP male, age salt, nitrates, processed diet polyps 50% of gastric cancers are in cardia usually adenocarcinoma from glandular epithelium
64
2WW referral criteria for suspected gastric ca
- abdo mass consistent w/ stomach ca - dysphagia or > 55y with weight loss and epigastric pain/reflux
65
gastric ca treatment
HER2 testing for metastatic adenocarcinoma > trastuzumab triple therapy for h pylori PPIs for ulcers adjuvant chemo for adv disease
66
Lauren classification of gastric ca
diffuse- poorly differentiated, faster rate of mets intestinal- well differentiated, slow growing, M>F
67
GIST tumours
GI stromal submucosal, malignant potential stain with CD117
68
abx for entamoeba histolytica
metronidazole then diloxanide
69
abz for campylobacter
erythromycin
70
abx for shigella and salmonella
not usually indicated give cipro if immunocompromised or bloody diarrhoea trimethroprim can also be used for salmonella
71
what protease inhibitor is particularly likely to cause diarrhoea?
lopinavir
72
CMV colitis microscopy
owl eye sign from inclusion bodies in colonic mucosa
73
managing oral and oesophageal candidiasis in HIV
fluconazole 100-200mg 14/7
74
CMV colitis treatment
ganciclovir
75
microsporidium treatment
albendazole
76
cyclospora/isospora treatment
cotrimoxazole
77
salmonella/shigella dysentry treatment in HIV
azithromycin
78
TB length of treatment
RIPE for 2 months continue isoniazid and rifampicin for another 4 months 9 month regime if pyrazinamide has to be stopped
79
what drugs can cause GORD?
TCAs nitrates CCBs anticholinergics
80
indications for endoscopy for GORD
- > 55y w/ ALARM symptoms Anaemia Loss of weight Anorexia Recent onset progressive symptoms Melaena or haematemesis - dysphagia - treatment refractory symptoms
81
Gilbert syndrome genetics
UGT 1A1 auto recessive
82
Gilbert syndrome triggers of jaundice
fasting/dieting surgery heavy exertion dehydration alcohol infection lack of sleep
83
gilbert syndrome pathophysiology
reduction in UDP glucoronyl transferase > reduction in conjugation of bilirubin > increased unconjugated bilirubin
84
causes of raised conjugated bilurbin
gallstones steatohepatitis EBV, CMV paracetamol, alcoholic hepatitis, erythromycin, oestrogens, corticosteroids Wilsons, haematochromatosis PBC, PSC, autoimmune hepatitis cholangiocarcinoma, renal ca, mets TB, lymphoma, amyloid, sarcoid infiltration
85
risks with gilbert syndrome
increased risk of drug toxicity from gemfibrozil and/or statin may have higher risk of paracetamol OD toxicity
86
location of anal vascular cushions
3, 7, 11 o'clock consists of rectal mucosa, arterioles, venules and their anastamoses
87
haemorrhoids degrees
1st- confined to anal canal. do not prolapse 2nd- prolapse on straining or defecating. spontaneously reduce 3rd- may prolapse spontaneously or on defecation. must be digitally reduced 4th- irreducible
88
HELLP syndrome treatment
IV Mg sulfate IV dexa control bp replace blood products deliver baby
89
LDH and AST in HELLP
both raised LDH to AST ratio < 22
90
hepatic encephalopathy poor prognostic factors
worsening acidosis rising PTT falling GCS
91
precipitants of hepatic encephalopathy
alcohol, drugs GI haemorrhage infections constipation
92
HCC risk factors
hep B and C alcohol haemochromatosis cirrhosis long term OCP alfatoxin from Asperfillus flavus smoking
93
cholangiocarcinoma risk factors
PSC choledochal cyst liver flukes caroli disease (dilatation of intrahepatic bile ducts) smoking
94
risk factors for carcinoma of gallbladder
UC PSC gall stones gallbladder polyps smoking
95
signs of cholangiocarcinoma
obstructive jaundice, pale stools RUQ pain swinging pyrexia
96
haemochromatosis genetics
auto rec HFE mutation- C282Y, H63D
97
jaundice referral criteria
2WW if over 40y obstructive LFTs > upper GI hepatic LFTs > gastro suspected ALD > gastro
98
visceral leischmaniasis
bangladesh, india, NE africa, brazil parasite transmitted by sandflies incubation 10 days to several years fever, weight loss, hepatosplenomegaly ix- biopsy lesions tx: liposomal amphoteracin B
99
liver transplant contraindications
poor cardiac reserve comorbidities incl HIV, severe respiratory disease failure to abstain from alcohol
100
liver transplant immunosuppression
tacrolimus or ciclosporin (calcineurin inhibitors) 6 weeks steroids azathioprine
101
managing flushing from NETs
somatostatin analogues antihistamines ondansetron 5HT3 antag
102
NAFLD liver function tests
3/12 or more persistently raised LFTs ALT up to 3x upper limit normal ALT > AST
103
management of oesophageal tumours depending on stage/grade
T1 adenocarcinoma: endoscopic mucosal resection T1b adenocarcinoma: radical resection T1bN0 squamous: definitive chemoradio or surgical resection
104
pancreatic cancer inherited cancer syndrome
hereditary pancreatitis peutz jeghers familial atypical multiple mole melanoma familial breast ca HNPCC
105
chemo for pancreatic ca
folfirinox gemcitabine +/- capectitabine
106
parasite causing anaemia
hookworm
107
katamaya fever
acute schisto 4-8 weeks post infection fever, urticaria, diarrhoea, hepatosplenomegaly, wheeze and cough
108
how does h pylori cause ulceration?
increases release of acid production in duodenum decreases release of acid in stomach to cause atrophic gastritis and gastric ulcers and increased risk of gastric ca duodenal ulcers are more common than gastric
109
endoscopy testing for h pylori
antral biopsy w/ haematoxylin/eosin or Giema stain urease CLO testing
110
peutz jeghers genetics
auto dom STK11 tumour suppression gene on chromo 19
111
porphyria cutanea tarda clinical features
hypopigmentation, scarring blistering and crusted skin lesions on backs of hands and other sun exposed areas hypertrichosis dark or red urine on standing
112
PCT triggers
iron overload end stage CKD myelofibrosis
113
testing for porphyria cutanea tarda
blood, urine faeces collected in dark container > elevated porphyrins mildly elevated ALT, AST iron overload
114
PCT management
avoid sunlight, ETOHXS, smoking, oestrogens fortnightly phleb consider low dose hydroxychloroquine if ferritin < 600 liver imagine and AFP levels due to increased risk of HCC
115
causes of portal hypertension
cirrhosis portal v thrombosis (congenital, pancreatitis, tumour) budd chiari (tumour, haematological, COCP) intrahepatic tumours constrictive pericarditis RHF splenic vein thrombosis
116
cause of varices
portal HTN > collateral vessels enlarge
117
complications of pregnancy related liver disease
cholestasis: intrauterine foetal demise, preterm delivery meconium amniotic fluid neonatal resp distress fatty liver: maternal liver failure severe coagulopthy foetal demise
118
pregnancy related liver disease risk factors
cholestasis: age < 35y previous or family history multiple gestation hep c fatty liver: previous or family history multiple gestations foetus male sex pre eclampsia or HELLP BMI < 20
119
fatty liver of pregnancy vs cholestasis
LFTs 3x normal (cholestasis less than 2x) elevated bili and ammonia low glucose elevated creat, urea proteinuria elevated PTT, INR, APTT low platelets and fibrinogen
120
stages of PBC
1. destruction of interlobular ducts 2. small duct proliferation 3. fibrosis 4. cirrhosis
121
PBC and PSC treatment
cholestyramine for pruritus obeticholic acid +/- ursodeoxycholic acid liver transplant (end stage liver disease, intractable pruritus) recurrence is rare in PBC but 30% likely in PSC after transplant
122
features of SIBO
steatorrhoea (bile acids are deconjugated by bacteria) megaloblastic anaemia (b12 is used by bacteria) raised folate (synthesised by bacteria) def of fat soluble vitamins
123
124
UC treatment
aminosalicylate corticosteroids for acute phase calcineurin inhib for acute phase thiopurines or MTX to maintain remission second line to aminosalicylates biologics third line
125
hepatitis virus types
hep A- RNA hep B- DNA hep C- RNA hep D- incomplete hep E- RNA also EBV, CMV, HSV, yellow fever, rubella
126
hep B immunisation
anti HBs without anti HBc
127
whipples disease treatment
14/7 ceft or benpen then a year of trimethoprim or sulfamethoxazole
128
high vs low SAAG
high: cirrhosis, alc hep, schisto, fulminant liver failure, budd chiari, portal v obstruction, cardiac disease and SBP secondary to cirrhosis low or normal: nephrotic syndrome, protein losing enteropathy, peritoneal carcinomatosis, TB peritonitis, pancreatic duct leak, biliary

MRCP 2 (12 decks)

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