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IBD and Liver Disease > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What LFTs measure

A 
Bilirubin
Alkaline phosphatase
Alanine transaminase
Gamma GT
Aspartate transaminase
Albumin
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2
Q

What are signs of hepatitis

A

Raised transaminases

Raised ALT, AST

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3
Q

What are signs of cholestasis

A

Raised alkaline phosphatase
Raised GGT
Can come from obstruction in the large or small bile ducts

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4
Q

Causes of abnormal liver enzymes

A

Alcohol, medications, non-alcoholic fatty liver disease, space occupying lesion, viral hep, haemochromatosis

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5
Q

Investigations for liver disease

A

FBC, INR, U+E/LFTs, Lipids, imaging, immunology, virology, chemistry

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6
Q

What are causes of cirrhosis

A

Alcohol, chronic viral hep, hemochromatosis, non alcoholic steatohepatitis, primary biliary cirrhosis, autoimmune hep

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7
Q

What are causes of primary sclerosing cholangitis

A

Alpha-1 antitrypsin deficiency
Wilson’s disease
Drug induced

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8
Q

What are features of haemochromatosis

A

Iron overload, autosomal recessive

Cirrhosis, skin pigmentation, diabetes, cardiomyopathy, arthritis, pituitary failure

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9
Q

How to diagnose haemochromatosis

A

Raised ferritin over 1000
Test for HFE gene, liver biopsy + hepatic iron estimation.
Hepatic iron index > 1.9 is diagnostic of haemochromatosis

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10
Q

What is primary biliary cholangitis

A

Intrahepatic obstruction

Causes itching, tiredness, primarily in middle aged females

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11
Q

How to diagnose primary biliary cholangitis

A

Raised IgM, positive anti-mitochondrial antibody

Liver biospy: bile duct damage, granulomatous cholangitis

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12
Q

What is the treatment for primary biliary cholangitis

A

Ursodeoxycholic acid, obeticholic acid

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13
Q

What is the diagnosis for autoimmune hepatitis

A

Raised IgG, positive anti-nuclear antibody, positive smooth muscle antibody, positive liver kidney microsomal antibody
Liver biopsy: interface hep, plasma cell infiltrates

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14
Q

What is the treatment for autoimmune hep

A

Prednisolone, azathiprine

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15
Q

What is alpha-1 antitrypsin deficiency associated with

A

Chronic obstructive pulmonary idsease. PAS positive globules

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16
Q

What is Wilson’s disease

A

Autosomal recessive, disorder of copper metabolism.

Caeruloplasmin synthesis defective, reduced biliary copper excretion

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17
Q

What are clinical features of Wilson’s disease

A

Liver cirrhosis, acute liver failure, neruopyschiatric disorders, Kayser-Fleischer rings

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18
Q

How to diagnose Wilson’s disease

A

Low serum caeruloplasmin, reduced serum copper, high urinary copper excretion, Kayser-Fleisher rings
Liver cooper over 250micrograms/g

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19
Q

What is the treatment for Wilson’s disase

A

Penicillamine, transplantation

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20
Q

What are non-invasive markers of cirrhosis

A 
Physical: tissue elastography
Biochemical: 
Enhanced liver fibrosis score
FIB-4
NAFLD fibrosis score
Fibrotest
AST to platelet ratio
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21
Q

What is NAFLD

A

Non-alcoholic fatty liver disease: steatosis in liver. Can progress to non-alcoholic steatohepatitis, a state in which steatosis is combined with inflammation and fibrosis

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22
Q

What is coeliac disease

A

Chronic systemic, immune mediated disorder in genetically predisposed px

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23
Q

What are clinical presentations of coeliac disease

A

Non specific GI symptoms, malabsorption (diarrhoea, nutritional deficiencies - with consequences including anaemia, osteoporosis)
Dermatitis herpetiformis
Muscle weakness, paraesthesia and ataxia
Amenorrhoea, infertility

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24
Q

What are genetic markers of coeliac disease

A

HLA DQ2 or DQ8

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25
Q

What is the gold standard of coeliac disease diagnosis

A

OGD and duodenal biopsies - can see increased intraepithelial lymphocytes, crypt hyperplasia and villous atrophy

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26
Q

What is the treatment for upper GI bleed

A 
Stop offending drugs
Blood transfusion
Correct clotting (aim INR <1.5). FP/vit k/beriplex
Platelet transufion if <50
Consider abx
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27
Q

What is the specific treatment for non-variceal upper GI bleed

A

PPI - pantoprazole infusion 80mg IV stat

28
Q

What is the specific treatment for variceal upper GI bleed

A

Terlipressin (causes vasoconstriction)
2mg IV
Abx (co-amoxiclav)

29
Q

What does a Blatchford Score over 6 indicate in a GI bleed

A

Over 50% risk of need an intervention

30
Q

When is an OGD needed for an upper GI bleed

A 
Severe bleed (Blatchford over 6 or ongoing haemodynamic instability) - Urgent OGB once resuscitated with protected airway
Give 250mg IV erthyromycin 30mins before
31
Q

What are endoscopic techniques to stop upper GI bleeding

A

Haemo spray (coagulates on surface of ulcer), put bands around ulcer, injection of adrenaline

32
Q

What is the treatment for peptic ulcer

A

Check and eradicate H. pylori
Omeprazole 40mg OD/BD 8 weeks
Repeat scope in 6-8 weeks if gastric ulcer

33
Q

What is the treatment for varcies

A

Propranolo or carvedilol

Endoscopic banding every 2-4 weeks

34
Q

What are varices due to

A

Portal hypertension commonly due to CLD

35
Q

What is a Mallory Weiss tear

A

GOD laceration secondary to retching

36
Q

What causes peptic ulcers

A

H. pylori, NSAIDS or hypersecretory (Gastrinoma)

Need to stop smoking

37
Q

What is the treatment for H pylori

A

7 day triple therapy - PPI, amoxicillin, metronidazole

38
Q

What is the most common gastric malignancy

A

Adenocarcinoma. RF - H, pylori, smoking, preserved food, genetics

39
Q

What is the most common oesophageal malignancy

A

Frequently SCC, but adeno also common

RF - Barrett’s, achalasia, betel nuts

40
Q

What is angiodysplasia

A

Small vascular malformation in the gut. Secondary to mucosal ischaemia or low grade obstruction of mucosal veins. Possible link with AV disease - Heyde’s synrome (GI bleed from angiodysplsia in the presence of aortic stenosis)

41
Q

What is oesophagitis secondary to?

A

Reflux. LA grading system A-D

42
Q

What is UC

A

Inflammatory disorder affecting the mucosa of the large colon

43
Q

What is the pathophysiology of UC

A

Exaggerated mucosal T cell response to host microbiota and/or external stimulae in context of genetically receptive host

44
Q

What are the symptoms of UC

A 
Rectal bleeding
Diarrhoea
Urgency
Intermittent attacks of abdo pain
Blood mucoid stools
Fever
Prescence of p-ANCA
45
Q

How to diagnose UC

A 
Blood tests:
Raised CRP/ESR
Anaemia
Low albumin
Faecal calprotectin
Endoscopy - gold standrad
46
Q

What is the treatment for UC

A

Steroids - prednisolone
Aminosalicylates - Mesavant, Octasa
Immunosuppressants - azathioprine, methotrexate
Biologics: anti-TNF - infliximab, adalimumab, gloimumab
anti-integrin - vedolizumab

47
Q

What are the severe Truelove and Witts criteria for admission

A 
Motions per day over 6
Rectal bleeding
37.8C on 2 of 4 days
Pulse rate over 90
Haemoglobin less than 10.5
ESR over 30

Admit if they meet 2 or more severe criteria

48
Q

What is Crohn’s disease

A

Chronic inflammatory trans-mural inflammation

49
Q

What is the pathophysiology of Crohn’s

A

Exaggerated T cell inflammatory response to environmental factors in the presence of genetically suscpetible host

50
Q

What is the the disease distribution of Crohn’s

A

Ileo-colonic, ileal, colonic, perianal, upper GI

51
Q

What are the symptoms of Crohn’s

A

Diarrhoea, rectal bleeding, abdo pain, weight loss, perianal abscesses, oral ulceration

52
Q

What are the signs of Crohn’s

A

Cachexia, scars, stomas, parenteral nutrition

53
Q

What is the diagnosis for Crohn’s

A

Blood test - anemia, low B12, folate, ferritin, low albumin
Faecal calprtectin
Endoscopy and histology
Imaging - MRI small bowel, MRI pelvis and small bowel USS

54
Q

What is the treatment for Crohn’s

A

Steroids - perdnisolone, budesonide
Abx - ciprofloxacin, metronidazole
Immunosuppressants - azaothioprine, mercaptopurine, methotrexate
Biologics - infliximab, adalimumab, golimumab, vedolizumab
Modulen - anti-inflammatory properties

55
Q

What are surgical options for Crohn’s

A 
Up to 70% will have surgery in their lifetime
Examination under anaesthetic
Stricturoplasty
Colectomy
Diverting colostomy
56
Q

Which IBD is smoking protecting for?

A

UC

57
Q

What is the pathophysiology of prehepatic jaundice

A

Increased breakdown of red cell leads to increased serum bilirubin. Unconjugated bilirubin isn’t water soluble so can’t be excreted in the urine/ Intestinal bacteria convert some of the extra bilirubin into urobilinogen, some of which is reabsorbed and is excreted by the kidneys - hence urinary urobilinogen is increased

58
Q

What is pathophysiology of hepatic jaundice

A

Disorders of uptake, conjugation or secretion of bilirubin

Usually divided into conjugated or unconjugated bilirubinaemia

59
Q

What are causes of pre-hepatic jaundice

A

Congenital red cell issues (sickle cell disease, G6PD deficiency, thalassemia)
Autoimmune haemolytic anemia
Drugs (penicillin, sulphasalzine)
Infections (malaria)
Mechanical (metallic valve prostheses, DIC)
Transfusion reactions

60
Q

What are conjugated hepatic causes of jaundice

A 
Cirrhosis
Malignancy
Viral hep
Drugs (for hepatitis and cholestasis)
Enzymes (dubin johnson syndrome, rotor syndrome)
61
Q

What are unconjugated hepatic causes of jaundice

A

GIlbert’s syndrome

Crigler Najar syndrome

62
Q

What are post hepatic causes of jaundice

A

Biliary tree obstruction (gallstone, pancreatitis, cholangiocarcinoma, post-operative stricture)
Primary biliary cirrhosis
Primary sclerosing cholangitis (80% of PSC have UC)

63
Q

What are features of chronic liver disease

A 
Ascites
Hands: clubbing, Dupuytren's contracture, palmar erythema
Spider naevi
Gynaecomastia
Portal hypertension: splenomegaly and caput medusae
Encephalopathy
Cachexia
Abdominal masses
Lymphadenopathy
64
Q

What is toxic megacolon

A

In extreme UC, there is involvement of the nerve plexus in the muscularis layer resulting in decrease in the motility of the colon and increase in its size over a period of time g

65
Q

What is the earliest lesion in Crohn’s

A

Aphthous ulcer - may fuse together to form serpentine ulcer

66
Q

What is the screening test for Cronh’s

A

Presence of ASCA

IBD and Liver Disease (1 decks)

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