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

what is the progression of alcoholic liver disease?

A

alcohol related fatty liver –> alcoholic hepatitis –> cirrhosis

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

what questionnaires are used in alcohol dependence?

A

CAGE and AUDIT questionnaires

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

what are the complications of alcohol dependence?

A

alcoholic liver disease, cirrhosis, dependence and withdrawal, Wernicke’s, Korsakoff’s, pancreatitis, cardiomyopathy

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

what are the signs of liver disease?

A

jaundice, hepatomegaly, spider naevi, palmar erythema, asterixis, caput medusae, gynaecomastia, bruising, ascites

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

what investigations should be done for alcohol dependence and liver disease?

A

bloods - FBC shows increased MCV, LFTs - high AST, ALT and GGT, clotting and U&Es
endoscopy
CT/MRI
liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the management of alcoholic liver disease?

A

detoxification, abstinence, nutritional support with protein and thiamine, steroids, manage complications, liver transplant

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

what is the progression of alcohol withdrawal?

A

in 6-12 hours - sweating, headache, tremor, craving, anxiety
12-24h - hallucinating
24-48h - seizures
24-72h - delirium tremens

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

what is the pathophysiology of DT?

A

GABA underfunction and glutamate overfunction - excitability due to adrenergic activity - confusion, agitation, delusions, hallucinations

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

what are the signs of DT?

A

tachycardia, HTN, tremor, hyperthermia, ataxia, arrhythmia

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

how is DT managed?

A

benzodiazepines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how is alcohol withdrawal managed?

A

chlordiazepoxide, diazepam, pabrinex, thiamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is liver cirrhosis?

A

chronic inflammation and damage to the liver cells resulting in scar tissue and nodules - resistance and portal HTN

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

what are the causes of cirrhosis?

A

alcoholic liver disease, hep B or C, NAFLD etc

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

what are the tests for cirrhosis?

A

bloods, enhanced liver fibrosis test for NAFLD, USS, fibroscan, endoscopy, CT, MRI, biopsy and Child Pugh score

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

what is the management for cirrhosis?

A

USS every 6m and AFP, endoscopy every 3m, high protein, low sodium diet, MELD score, liver transplant and manage complications

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

what are the complications of liver cirrhosis?

A

malnutrition (regular meals), low sodium and high protein, portal HTN and varices (propanolol, shunt, elastic band ligations, sclerosant injection, resuscitation with vasopressin analogues, vit K and FFP, ABx, endoscopy), ascites (transudative - anti-aldosterone diuretics, paracentesis, ABx, TIPS, transplantation), bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy

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

how is spontaneous bacterial peritonitis managed?

A

ascitic culture and give IV cephalosporin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are some causes of hepatitis?

A

viral, autoimmune, drug, NAFLD, alcohol

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

what is the presentation of hepatitis?

A

abdominal pain, fatigue, jaundice, pruritis, fever, muscle and joint aches, nausea and vomiting, increased AST/ALT and increased bilirubin

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

what is hep A?

A

RNA virus transmitted through faecal oral route, gives nausea, vomiting, jaundice, cholestasis, pale stools, dark urine, hepatomegaly. It is self limiting in 1-3m - manage with analgesia, vaccination and notify PHE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is hep B?

A

DNA virus, transmitted via direct contact and vertical transmission, self limiting or chronic
HBcAB is a previous infection and HBsAg is current
give vaccination, screen for other BBVs, refer, notify PHE, stop smoking and alcohol, education, treat complications, liver transplant if required

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

what is hep C?

A

RNA virus - direct contact
liver cirrhosis and HCC are complications
screen for antibodies and RNA
manage complications, refer, notify PHE, educate, stop drinking and smoking, antivirals for 8-12 weeks and liver transplant

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

what is hep D?

A

RNA virus - only if Hep B is also present
mild and self limiting and rare to progress
no vaccine but inform PHE

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

what is hep E?

A

RNA virus, faecal oral route
mild, self limiting, rare progression, no vaccine
notifiable

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

what is autoimmune hepatitis?

A

T1 - adults - fatigue and liver disease symptoms - ANA and anti-actin, antiSLA and LP
T2 - young - high AST, ALT and jaundice - antiLKMI or LCI
liver biopsy, prednisolone, azathioprine, transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the pathophysiology of PSC?

A

intra and extrahepatic ducts become strictured and fibrosed - obstruction of bile flow out - inflammation, fibrosis and cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the presentation of PSC?

A

jaundice, hepatomegaly, deranged LFTs, chronic RUQ pain, p-ANCA, ANA, aCL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how is PSC diagnosed?

A

MRCP - see lesions and strictures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the complications of PSC?

A

acute bacterial cholangitis, cholangiocarcinoma, cirrhosis, CRC, liver failure, fat soluble vitamin deficiencies, biliary strictures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the management of PSC?

A

liver transplant, ERCP for stenting and dilating, colestyramine, monitor complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what happens in PBC?

A

immune system attacks bile ducts resulting in cholestasis, fibrosis, cirrhosis and LF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the presentation of PBC?

A

fatigue, pruritus, GI disturbance, abdo pain, jaundice, pale stools, xanthoma, xanthelasma, liver failure signs, cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is associated with PBC?

A

middle aged women, other autoimmune conditions and rheumatoid conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the diagnosis of PBC?

A

LFTs (increased ALP and bilirubin later), autoantibodies (anti-mitochondrial, ANA), increased ESR and IgM, liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is the management for PBC?

A

ursodeoxycholic acid to reduce cholesterol absorption, colestyramine, liver transplant and immunosupression

36
Q

what is the progression of PBC?

A

advanced LD and portal HTN resulting in fatigue, steatorrhoea, pruritus, distal renal tubular acidosis, HCC, hypothyroidism

37
Q

what is NAFLD?

A

forms part of metabolic syndrome - increased risk of MI and stroke - fat deposits in liver cells so decreased function, hepatitis and cirrhosis

38
Q

what are the staged of NAFLD?

A

NAFLD, NASH, fibrosis, cirrhosis

39
Q

what are the autoantibodies in NAFLD?

A

ANA, SMA, AMA, LKM-1

40
Q

what are the risk factors for NAFLD?

A

obesity, poor diet, low activity, T2DM, increased cholesterol, middle age, smoking, HTN

41
Q

what are the investigations for NAFLD?

A

LFTs, USS, hep B and C serology, autoantibodies, caeruloplasmin, alpha 1 AT, ferritin and transferrin saturation, enhanced liver fibrosis test (7.7+), NAFLD fibrosis score, fibroscan

42
Q

what is the management of NAFLD?

A

weight loss, exercise, stop smoking, control diabetes, BP, cholesterol, avoid alcohol, ?vit A/pioglitazone

43
Q

what is Wilson’s disease?

A

excessive accumulation of copper in body and tissues due to mutation in protein on C13 - AR inheritance

44
Q

what are the features of Wilsons?

A

hepatic problems - cirrhosis and hepatitis, neuro - dysarthria, dystonia, parkinsonism, psychiatric - depression and psychosis, KF rings, haemolytic anaemia, renal tubular damage, acidosis and osteopenia

45
Q

how is Wilsons diagnosed and treated?

A

serum caeruloplasmin decrease, liver biopsy, 24h urinary copper assay and MRI brain (non specific changes)
copper chelation with penicilliname or trientene

46
Q

what is haemochromatosis?

A

iron storage disorder - increased total body iron and tissue iron - HFR gene of C6 is mutated and usually AR inheritance

47
Q

what is the presentation of haemochromatosis?

A

chronic tiredness, joint pain, pigmentation, hair loss, erectile dysfunction, amenorrhoea, cognitive sx

48
Q

what is the diagnosis and treatment of haemochromatosis?

A

serum ferritin increase, transferrin saturation increase, genetic testing, liver biopsy with Peri’s stain, CT abdomen, MRI - manage with venesection, monitor serum ferritin, avoid alcohol, genetic counselling, monitor and treat complications

49
Q

what are the complications of haemochromatosis?

A

T1DM, cirrhosis, iron deposits in pituitary and gonads, cardiomyopathy, HCC, hypothyroidism, chondrocalcinosis, pseudogout

50
Q

what is alpha 1 antitrypsin deficiency?

A

abnormality in gene for protease inhibitors, elastase secreted by neutrophils - digests connective tissue and is usually inhibited by A1AT - AR inheritance

51
Q

what are the complications of A1AT deficiency?

A

liver- mutant A1AT gets trapped in liver, accumulates, causes damage - cirrhosis and HCC
lungs - A1AT deficiency - excess protease, attack CT - bronchiectasis and emphysema (COPD)

52
Q

how is A1AT deficiency diagnosed?

A

serum A1AT decrease, liver biopsy - cirrhosis, CT thorax and genetic testing

53
Q

what is the management of A1AT deficiency?

A

stop smoking, symptomatic, organ transplant, monitor for complications

54
Q

what is the pathophysiology of GORD?

A

stomach acid refluxes and irritates the oesophageal lining due to it being squamous cells not columnar - metaplasia of these is Barrett’s (pre-malignant to adenocarcinoma)

55
Q

what is the presentation of GORD?

A

dyspepsia, heart burn, acid regurgitation, retrosternal and epigastric pain, bloating, nocturnal cough, hoarse voice

56
Q

what are the red flags for GORD?

A

dysphagia, age>55, weight loss, upper abdo pain and reflux, N+V, treatment resistance, decreased Hb, increased platelets

57
Q

what is the diagnosis for H Pylori?

A

urea breath test, stool antigen test, rapid urease test
eradication therapy = 2xABx and PPI for 7 days

58
Q

what is the management of GORD?

A

lifestyle, acid neutralisation with rennie or gaviscon, PPI, ranitidine, laparoscopic fundoplication

59
Q

how is Barrett’s treated?

A

PPI, photodynamic therapy, laser or cryotherapy

60
Q

what is the most common liver cancer?

A

HCC

61
Q

what are the risk factors for liver cancer?

A

viral hep B and C, alcohol, NAFLD, CLD, PSC

62
Q

what is the presentation of liver cancer?

A

weight loss, abdo pain, anorexia, N+V, jaundice, pruritus

63
Q

what are the investigations for liver cancer?

A

AFP (HCC), Ca19.9 (chca), USS, CT, MRI, ERCP

64
Q

what is the management for HCC and CHCa?

A

HCC - poor prognosis, resection and kinase inhibitors
CHCa - poor prognosis - resection and ERCP stent

65
Q

what is IBD?

A

UC and Crohn’s
inflammation of walls of GIT with periods of exacerbation and remission

66
Q

what is the presentation and characteristics of IBD?

A

diarrhoea, abdo pain, passing blood, weight loss
UC - continuous, colon and rectum, superficial mucosa, smoking protective, excrete blood and mucus
Crohns - no blood or mucus, entire GIT with skin lesions, terminal ileum is worst, transmural, smoking is RF

67
Q

how do you test for IBD?

A

bloods - anaemia, infection, thyroid, kidney, liver, CRP,
faecal calprotectin
endoscopy
USS, MRI, CT

68
Q

what is the management for Crohn’s?

A

induction - steroids (IV hydrocortisone or oral pred)
maintenance - azathioprine, mercaptopurine, methotrexate, infliximab
surgery- resection

69
Q

what is the management of UC?

A

induction - mild or moderate - corticosteroid or aminosalicylate
severe - IV corticosteroid or ciclosporin
maintenance - aminosalicylate, azathioprine, mercaptopurine
surgery - panproctocolectomy, ileostomy

70
Q

what is a peptic ulcer?

A

ulceration of the mucosa of the stomach or duodenum more commonly
breakdown of the protective layer and increased stomach acid from drugs, H Pylori, stress, alcohol, smoking, caffeine, spicy foods

71
Q

what is the presentation of peptic ulcers?

A

epigastric pain worse with eating if gastric or better if duodenum, N+V, coffee ground vomit and haematemesis, melana, iron deficiency anaemia, bleeding

72
Q

what is the management and some complications of peptic ulcer?

A

endoscopy and rapid urease test, biopsy, PPI and monitor
bleeding, perforation, acute abdomen, peritonitis, scarring, strictures, pyloric stenosis

73
Q

what is an upper GI bleed?

A

bleeding from the oesophagus, stomach or duodenum from varices, MW tears, ulcers, cancers etc

74
Q

what is the presentation of a GI bleed?

A

haematemesis, coffee ground vomit, haemodynamic instability, epigastric pain, dyspepsia, jaundice

75
Q

what are the scores used in upper GI bleed?

A

Rockall score if had an endoscopy - risk of rebleeding and mortality
Glasgow Blatchford score - risk of having a bleed

76
Q

what is the management of upper GI bleed?

A

A-E
bleeds - FBC, U&Es, INR, LFTs, XM
access with 2 large bore cannula
transfuse - FFP, and prothrombin if on warfarin
endoscopy and stop drugs such as NSAIDs and anticoagulants
OGD - banding and cauterisation
terlipressin and prophylactic ABx if OV

77
Q

what is IBS?

A

functional bowel disorder - abnormal functioning in otherwise normal bowel

78
Q

what is the presentation of IBS?

A

diarrhoea, constipation, fluctuation of bowel movements, abdo pain, bloating, worse after eating, improved by bowel movements

79
Q

what is the criteria for IBS?

A

normal FBC, ESR, CRP, negative faecal calprotectin, negative coeliac screen, r/o cancer
abdo pain relieved by bowel movement and associated with change in habit plus two of PR mucus, bloating, worse after eating, abnormal habits

80
Q

how is IBS managed?

A

fluids, regular small meals, decreased processed foods, alcohol and caffeine, probiotics, loperamide, laxatives, antispasmodics, amitriptyline, SSRIs, CBT

81
Q

what is coeliac disease?

A

exposure to gluten causes autoimmune reaction - inflammation with autoantibodies, that target epithelial cells (antiTTG and EMA)

82
Q

what are the biopsy results for coeliac?

A

crypt cell hypertrophy and villous atrophy

83
Q

what is the presentation of coeliac?

A

FTT, weight loss, diarrhoea, fatigue, mouth ulcers, anaemia, dermatitis herpetiformis, peripheral neurology, cerebellar ataxia, epilepsy

84
Q

what genes are associated with coeliac?

A

HLA-DQ2 and 8

85
Q

how is coeliac diagnosed?

A

whilst on gluten diet
total IgA to r/o deficiency
antiTTG and antiEMA
biopsy

86
Q

what are the complications and associations of coeliac disease?

A

complications - vitamin deficiency, anaemia, osteoporosis, ulcerative jejunitis, EATL of intestine, NHL, small bowel adenocarcinoma
associations - T1DM, thyroid disease, autoimmune hepatitis, PBC, PSC

87
Q

what is the management of coeliac?

A

life long gluten free diet, treat complications and monitor autoantibodies

Finals (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions