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Gastro Flashcards

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1
Q

What might LFT for alcoholic liver disease show?

A

AST is normally more raised than ALT. So AST:ALT normally >2 and >3 strongly suggestive of alcoholic cause

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2
Q

How to group the cause of ascites?

A

Those with serum-ascites albumin gradient <11 or >11g/L

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3
Q

What do the two SAAG gradings of ascites mean?

A

more than 11 - indicates portal hypertension so liver disorders most common cause, right heart failure as well
less than 11 - hypoalbuminaemia ie nephrotic syndrome, malnutriton, also malignancy infectios

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4
Q

Management of ascites?

A

reducing dietary sodium, fluid restriction, spironolactone and loop diuretics, drainage if tense, TIPS, prophylactic antibiotics

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5
Q

What might be given as prophylaxis for variceal bleed?

A

beta blockers - carvedilol

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6
Q

What would ascitic fluid analysis show in spontaneous bacterial peritonitis?

A

a white cell count greater than 250mm3

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7
Q

Treatment for alcohol withdrawal?

A

Benzodiazepines eg chlordiazepoxide first line but lorazepam may be preferable in patients with hepatic failure

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8
Q

What is alcoholic hepatitis?

A

a clinical syndrome of recent jaundice, +/- ascites with ongoing alcohol abuse

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9
Q

What is gold standard investigation for alcoholic hepatitis?

A

liver biopsy

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10
Q

What might be raised on FBC of someone with AH?

A

platelets and white cell count

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11
Q

What is the Maddreys discriminant function?

A

a score to predict severity for AH and if steroids need to be used

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12
Q

What is included in Maddrey’s Discriminant Function?

A

prothrombin time and serum bilirubin

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13
Q

What does a positive HbsAg mean?

A

Active infection

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13
Q

What is NASH?

A

when there are features of alcoholic hepatitis on biopsy but absence of history of alcohol excess

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14
Q

What does a postive HbcAb IgG mean?

A

IgG is a past exposure, IgM would mean acute infection

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15
Q

Tumour marker for hepatocellular carcinoma?

A

AFP

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16
Q

Investigating hepatitis C infection?

A

First step is serology for anti-HCV antibodies, pos suggests either current or past infection. If this is then pos an HCV RNA PCR should be performed to confirm active infection

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17
Q

Management of acute HBV?

A

Mainly supportive as risk of progression to chronic is only 5%, the criteria to be treated include ascites, encephalopathy, symptoms for over 4 weeks

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18
Q

HCC screening for people with hep B?

A

6 monthly if at high risk

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19
Q

What gene is normally affected in hereditary haemochromatosis and what is inheritance pattern?

A

HFE gene, autosomal recessive (90% of cases, white populations only)

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20
Q

What can cause secondary haemochromatosis?

A

frequent blood transfusions, iron supplementation, diseases of erythropoiesis

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21
Q

Symptoms of haemochromatosis?

A

fatigue, arthralgia, impaired sexual function, abdo pain, skin hyperpigmentation, diabetes, cardiac disease

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22
Q

Blood test results in someone with haemochromatosis?

A

serum ferritin raised, transferrin saturation raises, raised AST and ALT but normally not more than 2x normal, normal FBC

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23
Q

Treatment for haemochromatosis?

A

venesection (removing blood from patient to stimulate haematopoiesis) and iron chelation for stage 2,3 or 4 patients for who venesection is contraindicated

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24
What gene is defective in Wilson's disease?
ATP7B gene on chromosome 13
25
Clinical features of Wilson's disease?
symptom onset between 10-25 years of age. Liver disease and neurological disease, also kayser-fleischer rings
26
What will you see in investigations for Wilson's disease?
reduced serum caeruloplasmin, reduced serum copper and increased 24 hour urinary copper excretion
27
Treatment for Wilson's disease?
copper chelaters - penicillamine, liver transplantation
28
What kind of drug is sorafenib and when is it used?
a multikinase inhibitor, used in palliative care of HCC
29
Deficiency of what can put at greater risk of HCC?
alpha-1 antitrypsin deficienct
30
Haplotypes involved in coeliac disease?
HLA- DQ 2 or HLA DQ-8
31
Most widely used screening test for coeliac disease?
anti-tissue transglutaminase antibodies (tTG) but will give false negs in patients with IgA deficiency so total serum IgA should be measured too
32
Histological changes on duodenal biopsy of coeliac?
villous atrophy, crypt hyperplasia, increased intraepithelial lymphocytes
33
Patients with HNPCC, what is the next most common cancer after colorectal?
endometrial
34
What is familial adenomatous polyposis?
autosomal dominant condition leads to hundreds of polyps by age 30-40 due to mutation on APC gene (go on to develop carcinoma)
35
What category of people don't need to be offered a FIT test before urgent referal?
People with rectal mass, unexplained anal mass or unexplained anal ulceration
36
What should be done for staging in newly diagnosed colorectal cancer patient?
carinoembryonic antigen, CT chest abdo pelvis, entire colon should be looked at with colonscopy, patients with tumours below peritoneal reflection should have mesorectum evaluated with MRI
37
type of resection for Caecal, ascending or proximal transverse colon?
right hemicolectomy
38
Type of resection for distal transverse, descending colon?
left hemicolectomy
39
Type of resection for sigmoid colon tumor?
High anterior resection
40
Type of resection for cancers of anal verge?
Abdomino-perineal excision of rectum
41
What is Hartmann's procedure?
resection of sigmoid colon with an end colostomy. In emergency where bowel has perforated
42
Most common presentation of colonic diverticular bleeding?
sudden rectal bleeding, without associated pain (diverticulitis would be painful)
43
Main risk factor for gastric cancer?
Helicobacter pylori infection
44
Who should urgent GI endoscopy be offfered to for suspected gastric cancer?
people with dysphagia or people over 55 with weight loss and any of upper abdo pain, reflux, dyspepsia
45
Management of GORD?
Lifestyle changes, patients without any red flag symptoms should be given a four week PPI course. If inadequate response offer H2 receptor antagonists to reduce stomach acid
46
Which GORD patients are eligible for laparoscopic fundoplication?
patients with confirmed GORD on endoscopy that respond to PPI but dont want to continue it long term or cant tolerate acid suppression therapy
47
In Barrett;s oesophagus what are the cell changes that take place?
normal stratified squamous epithelium is replaced by columnar epithelium
48
Management of dyspepsia in general practice?
if no red flag symptoms, test for H.Pylori if pos eradication therapy if neg 2 week empirical treatment with PPI
49
differences in symptoms between duodenal and gastric ulcer?
duodenal - pain is relieved by food, gastric ulcer weight loss more likely. Gastric more likely to be malignant too
50
If H pylori leads to increased acid secretion is it more likely to cause DU OR GU?
duodenal ulcer
51
What do you need to do after H.pylori eradication therapy?
confirm eradication 6-8 weeks after treaatment
52
Which oesophageal cancer is more aggressive?
squamous cell whereas adenocarcinoma is more common and less aggressive
53
Where does squamous cell oesophageal cancer normally spread to vs adenocarcinoma?
squamous cell - bone, brain, liver, lungs adeno - liver lymph nodes
54
If tumour is in proximal gastric region wht type of gastrectomy?
total gastrectomy
55
Indications for cholecystectomy?
if gallstone pancreatitis or cholecystitis. If biliary colic then can have discussion and do clinical assessment to see if its necessary
56
Which hepatitis viruses are associated with faecal-oral route and poor food hygeine?
hep a and hep e
57
What patient group get hepatitis D?
Patients with hep B as hep D requites HBV to replicate
58
Liver enzymes in ischaemic hepatitis?
AST and ALT in the thousands, ALP not such a big increase. LDH levels also rise dramatically
59
What differentials should be considered whenever transminases are in the thousands?
ischaemic hepatitis, acute viral hepatitis, paracetamol toxicity
60
Lab findings in autoimmune hepatitis?
raised ALT, AST, raised serum immunglobulins particularly IgG, ANA and anti-SMA antibodies
61
management of autoimmune hepatitis?
corticosteroids firstline, azathioprine and mecophenolate mofetil can be added
62
What kind of IBD involves transmural inflammation? (full thickness)
Crohn's
63
Histology of someone with Crohn's?
non-caseating granulomas, transmural inflammation, lymphoid aggregates, crypt architectural abnormalities, cryptitis or crypt abscesses
64
Medical management to induce remission in Crohn's?
glucocorticoids first-line eg budesonide. Then 5-ASA drugs eg mesalazine, then azatioprine, infliximab, methotrexate
65
medical management to maintain remission in Crohn's
azathioprine or mercaptopurine is used first-line
66
Test to distinguish between IBS and IBD?
Faecal calprotectin
67
Histology findings in microscopic colitis?
in lymphocytic colitis, increased no of intraepithelial and lamina propria lymphocytes. Collaegnous the same but with a thickened collagenous band
68
Treatment for microscopic colitis?
anti-diarrhoeal drugs such as loperamide may relieve symptoms, budesonide corticosteroid for remission
69
Which IBD is primary sclerosing cholangitis more common?
Ulcerative colitis
70
medical management of UC?
aminosalicylates (5-ASAS) first line eg mesalamine, sulfasalazine.. coritcosteroids can be used to managed flares but should be tapered
71
What gene mutations are associated with increased susceptibility Crohn's?
NOD2/ CARD15
72
What vaccine should patients with coeliac disease receive?
pneumococcal vaccine, due to functional hyposplenism. Also influenza vaccine on individual basis
73
What medication is most associated with developing C.Diff?
clindamycin
74
How do proton pump inhibitors work?
they cause irreversible blockade of H+/K+ ATPase of the gastric parietal cell
75
Adverse effects of proton pump inhibitors?
hyponatremia, hypmagnasaemia, osteoporosis, increased risk of C.diff infections
76
Investigation of choice in patients with severe colitis?
flexibily sigmoidoscopy (colonscopy should be avoided due to risk of perforation)
77
Hallmark presentation of pancreatic cancer?
painless jaundice, pale stools, dark urine and cholestatic liver function test results
78
Life threatening C.Diff treatment?
ORAL vancomycin and IV metronidazole
79
What is Peutz-Jeghers syndrome?
An autosomal dominant condition characterised by numerous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles
80
Best blood test for measuring acute liver failure?
prothrombin time (as liver enzymes will remain in normal limits for extended period) and prothrombin has shorter half life than albumin providing more current info
81
What drugs should be held in C. Diff infections?
meds that are anti-motility and anti-peristaltic as they can predispose to toxic megacolon eg opiods
82
If ongoing h pylri symptoms despite first line therapy what medical management?
continue the PPI, amoxicillin, but switch clarithromycin for metronidazole
83
Diagnosis of famililial adenomatous polyposis, what is the appropriate management?
Prophylactic colectomy
84
How to treat recurrence of C.Difficile within 12 weeks?
Oral fidaxomicin
85
What is primary biliary cholangitis?
autoimmune liver disease that is strongly associated with other autoimune conditions such as Sjogren's syndrome. Often in middle aged women, anti-micochondrial antibodies
85
First line for primary biliary cholangitis
ursodeoxycholic acid
86
What is Gilbert's syndrome?
autosomal recessive condition of defective bilirubin conjugation. Might only see jaundice during fasting or illness and no treatment required

Year 3 (14 decks)

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