Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Finals > Gastro > Flashcards

Gastro Flashcards

1
Q

Younger women with deranged LFTs and signs of liver disease. Differential?

A

Autoimmune hepatitis

Viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is azathioprine safe to use in pregnancy?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Conditions associated with autoimmune hepatitis?

A

Hashimoto’s thyroiditis, RA, Grave’s, IBD, pleurisy, AIHA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Stepwise plan of autoimmune hepatitis

A
  1. Autoimmune profile –> ANA and SMA
  2. Protein electrophoresis –> high titres IgG suggestive
  3. Arrange other bloods –> FBC, LFTs
  4. Consider liver biopsy –> interface hepatitis + plasma cells +++
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Approach for autoimmune hepatitis

A
  1. Watchful waiting –> asymptomatic, pre-cirrhotic
  2. Immunosuppression –> pred 40mg PO, taper and add azathioprine for long term
  3. Liver transplant in severe disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is remission of autoimmune hepatitis monitored?

A

Measuring AST/ALT and IgG levels post-therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is primary biliary cirrhosis?

A

Chronic autoimmune disease characterised by progressive destruction of small intrahepatic bile ducts, resulting in cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Clinical features of PBC?

A

Fatigue + pruritus = earliest

Jaundice = late

Other –> hepatosplenomegaly, facial hyperpigmentation, xanthelasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does PBC cause xanthelasma?

A

Dietary cholesterol metabolised in liver and excreted in bile. In PBC there is fibrosis of the biliary tracts causing cholestasis. Cholesterol accumulates and deposits around the eyes and tendons.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Stepwise plan for PBC?

A
  1. LFTs –> primary cholestatic picture
  2. Autoimmune profile + Ig electrophoresis
  3. Imaging –> exclude extrahepatic obstruction (US / MRI)
  4. Consider biopsy –> if unclear = lymphocytic infiltration with granulomatous changes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Management of PBC?

A
  1. Ursodeoxycholic acid
  2. Symptomatic treatment –> pruritus (cholestyramine), malabsorption (replace fat-soluble vitamins)
  3. Consider liver transplant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is hereditary haemochromatosis?

A

An autosomal recessive genetic disorder characterised by excess iron deposition throughout the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Early features of haemochromatosis

A

Non-specific = fatigue, abdo pain, arthralgia, ED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Late complications of haemochromatosis

A

Endocrine –> diabetes, hypogonadism

Cardiac –> arrhythmias, cardiomyopathy

Hepatic –> hepatomegaly, cirrhosis

MSK –> bronze skin, arthralgia

Neuro –> mood disturbances, memory impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What causes bronzing of skin in hereditary haemochromatosis?

A

Excess haemosiderin deposition + haemosiderin-induced melanocyte activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What mutation causes haemochromatosis?

A

HFE gene on chromosome 6 –> regulates hepcidin

Hepcidin inhibits ferroportins in gut –> increased iron absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How do you manage haemochromatosis?

A
  1. Dietary advice –> low iron, avoid alcohol
  2. Regular venesection –> stimulate bone marrow to produce new RBCs and use up iron
  3. Chelation therapy –> IV desferrioxamine (if CI)
  4. Genetic counselling –> first degree
  5. Liver transplant –> end stage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is hepatocellular carcinoma?

A

The commonest primary cancer arising from liver hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of HCC?

A

Chronic HBV and HCV

Cirrhosis –> ALD, HHC, PBC

Fungal infection –> Aspergillus

Misc –> PSC, androgenic steroids, COCP use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How would you investigate HCC?

A
  1. Imaging –> US for screening, otherwise CT / MRI
  2. Consider liver biopsy
  3. Tumour markers –> alpha-fetoprotein (6 month follow up)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How would you manage HCC?

A

Non-cirrhotic –> hepatic resection

Single nodule <5cm or <3 nodules <3 cm –> liver transplant

Consider RFA

Multinodular, intermediate –> trans-arterial chemoembolisation

Advanced –> chemotherapy (e.g. SORAFENIB)

Palliative care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is the differential for a RIF mass?

A

Crohn’s disease, appendix mass / abscess, caecal carcinoma, ovarian/renal mass, TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Clinical features of Crohn’s?

A

Diarrhoea, often not bloody

Abdo discomfort +/- weight loss

Aphthous ulcers, glossitis, fistulae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some extra-abdominal manifestations of Crohn’s?

A

Derm –> erythema nodosum, pyoderma gangrenosum

Eyes –> anterior uveitis, episcleritis

MSK –> arthritis, AnkSpond

Liver –> gallstones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How would you investigate Crohn’s?

A
  1. Bloods –> FBCs, LFTs, haematinics
  2. Stool testing –> MC&S (exclude infection), faecal calprotectin
  3. Imaging –> AXR +/- erect CXR, MRI pelvis, capsule endoscopy
  4. Endoscopy –> ileocolonoscopy + biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the management of Crohn’s in terms of inducing remission.

A
  1. First line = oral/IV corticosteroids
  2. Consider budesonide or 5-ASA therapy in some situations
  3. Add-on in resistive (2+ exacerbations/year) cases –> azathioprine or 6-MP (or methotrexate if CI)
  4. Consider biologics –> e.g. infliximab, adalimumab
  5. Consider surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the management of Crohn’s in terms of maintaining remission.

A
  1. Stop smoking + lifestyle advice
  2. First-line = azathioprine or 6-MP (never use long-term steroids)
  3. Alternative = MTX
  4. Stricture management –> balloon dilatation via colonoscopy, otherwise surgery
  5. Monitoring –> assess osteopenia/-porosis, colonoscopy surveillance for colorectal Ca if >10 years since symptom onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the management of Crohn’s in terms of managing perianal disease.

A
  1. Consider oral ABx –> e.g. metro / cipro
  2. Consider immunosuppression –> azathioprine +/- infliximab
  3. Consider surgery
29
Q

What are some major features of oesophageal disorders?

A

Dysphagia –> slow progressive + heartburn = peptic stricture; rapid = malignancy; to both liquid and solid progressive = achalasia

Odynophagia –> oesophagitis, e.g. reflux/infection

Substernal discomfort –> reflux of gastric contents into oesophagus, worse when lying

Regurgitation

30
Q

What is the main sign of oesophageal disease?

A

Weight loss due to decreased intake of food

31
Q

Which test is used to assess H. pylori post-eradication therapy?

A

Urea breath test

32
Q

Most common organisms in pyogenic liver abscesses?

A

Children = S. aureus

Adults = E. Coli

33
Q

Management of pyogenic liver abscess?

A

Image-guided drainage + IV antibiotics

Amoxicillin + ciprofloxacin + metronidazole

Allergic –> ciprofloxacin + clindamycin

34
Q

Diagnostic marker of choice for carcinoid syndrome?

A

5-HIAA

35
Q

What is the name of the stain used in biopsy for HHC?

A

Perl’s

36
Q

Typical iron study in patient with HHC

A

Transferrin sat >55% or >50%

Raised ferritin and iron

Low TIBC

37
Q

What markers of iron study are aimed for in venesection for HHC?

A

Transferrin <50%

Ferritin <50

38
Q

Which gastro drug can cause hypomagnesaemia?

A

Omeprazole

39
Q

List some adverse effects of PPIs

A

Hyponatraemia, hypomagnesaemia

Osteoporosis

Microscopic colitis

Inc. risk C. Diff

40
Q

Single most important investigation for patient with severe flare of UC?

A

AXR –> exclude toxic megacolon

41
Q

What is coeliac disease?

A

An autoimmune disorder triggered by gluten consumption, resulting in small bowel inflammation and subsequent malabsorption.

42
Q

Which HLA is coeliac disease associated with?

A

HLA-DQ2

43
Q

What should be assessed before starting therapy with azathioprine or mercaptopurine?

A

Thiopurine methyltransferase (TPMT) activity

44
Q

What constitutes a MILD flare of UC?

A

< 4 stools daily +/- blood

No systemic disturbance

Normal ESR and CRP

45
Q

What constitutes a MODERATE flare of UC?

A

4 - 6 stools a day

Minimal systemic disturbance

46
Q

What constitutes a SEVERE flare of UC?

A

> 6 stools a day

Evidence of systemic disturbance

47
Q

What are some systemic disturbances that can be caused by a severe UC flare?

A

Fever, tachycardia

Acute abdomen

Anaemia

Hypoalbuminaemia

48
Q

Causes of pancreatitis

A

GET SMASHED

Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion venom
Hypercalcaemia, hypothermia
ERCP
Drugs
49
Q

What drugs can cause pancreatitis?

A 
Azathioprine
Mesalazine
Bendroflumethiazide
Furosemide
Steroids
Sodium Valproate
50
Q

Antibodies for autoimmune hepatitis type I?

A

ANA and SMA

51
Q

Antibodies for autoimmune hepatitis type II?

A

anti-LKM1

52
Q

Antibodies for autoimmune hepatitis type III?

A

soluble liver-kidney antigen

53
Q

Melanosis coli

A

Laxative abuse

54
Q

Treatment for Wilson’s disease

A

Penicillamine

55
Q

Wilson’s disease mutation

A

ATP7B gene on Chr 13

56
Q

Clinical presentation of coeliac disease.

A

GI –> malabsorption, unexplained weight loss

Metabolic –> IDA, B12/folate deficiency, hypocalcaemia, faltering growth

Derm –> dermatitis herpetiformis, severe aphthous oral ulcers

Misc –> autoimmune conditions, lymphoma

57
Q

Most common inherited colorectal cancer

A

HNPCC

58
Q

What is SAAG used for?

A

SAAG usually < 11

SAAG > 11 implies portal hypertension

59
Q

What is the most specific and sensitive marker of cirrhosis in chronic liver disease?

A

Thrombocytopenia (< 150)

60
Q

What neutrophil count in ascitic tap is diagnostic of SBP?

A

> 250

61
Q

Management of SBP?

A

IV cefotaxime

62
Q

MoA of loperamide?

A

Loperamide is a μ-opioid receptor agonist which does not have systemic effects as it is not absorbed through the gut

63
Q

Epigastric pain + diarrhoea

A

Zollinger-Ellison syndrome

64
Q

Triad of intestinal angina?

A

Colicky post-prandial abdo pain
Weight loss
Abdominal bruits

65
Q

Most common site of diverticula?

A

Sigmoid colon

66
Q

Unruptured sigmoid volvulus —> Rx?

A

rigid sigmoidoscopy + flatus tube insertion

67
Q

The hepatic portal vein is formed by the union of _ + _ ?

A

Superior mesenteric and splenic veins

68
Q

Tumour marker for cholangiocarcinoma?

A

CA 19-9

69
Q

dyspepsia and over 55?

A

endoscopy

Finals (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions