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Gastroenterology Flashcards

1
Q

Describe the progression of alcoholic liver disease

A

Alcohol-related fatty liver: reversible in 2 weeks

Alcoholic hepatitis: if mild, reversible with abstinence

Cirrhosis: liver made of scar tissue, irreversible, very poor prognosis if continue drinking

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2
Q

What are the CAGE questions

A

Cut down (ever thought you should)

Annoyed (if others comment on drinking)

Guilty

Eye-opener (drink in morning to help hangovers)

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3
Q

What are the AUDIT questions

A

Alcohol use disorders identification test

Developed by WHO

Screen for harmful alcohol use

> 8 = harmful

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4
Q

What are the complications of alcohol consumption

A

Alcoholic liver disease

Cirrhosis

Hepatocellular carcinoma

Alcohol dependence and withdrawal

Wernicke-Korsakoff syndrome

Pancreatitis

Alcoholic cardiomyopathy

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5
Q

What are the signs of liver disease

A

Jaundice

Hepatomegaly

Spider naevi

Palmar erythema

Gynaecomastia

Bruising

Ascites

Caput medusae

Flapping tremor

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6
Q

What investigations are needed for alcoholic liver disease

A

FBC, LFTs, clotting, U&Es

Ultrasound (fibroscan assesses elasticity of liver)

Endoscopy (oesophageal varices)

CT/MRI

Liver biopsy

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7
Q

What abnormalities would be seen in LFTs in alcoholic liver disease

A

High ALT and AST

High gamma-GT

High ALP later in disease

Low albumin

High bilirubin

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8
Q

What is the management for alcoholic liver disease

A

Permanently stop drinking

Consider detoxification regime

Nutritional support (thiamine, high protein)

Steroids

Treat complications of cirrhosis

Refer for liver transplant in severe disease (abstain for 3 months first)

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9
Q

Explain the timeframe of alcohol withdrawal

A

6 - 12 hrs: tremors, sweating, headaches, cravings, anxiety

12 - 24 hrs: hallucinations

24 - 48 hrs: seizures

24 - 72 hrs: delirium tremens

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10
Q

What is delirium tremens

A

Medical emergency

Due to alcohol withdrawal

Extreme excitability of brain, excess adrenergic activity

Presentation: acute confusion, severe agitation, delusions, hallucinations, tremors, tachycardia, hypertension, hyperthermia, ataxia, arrhythmias

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11
Q

How is alcohol withdrawal managed

A

High dose IV vitamin B

Then regular low dose thiamine

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12
Q

What is liver cirrhosis

A

Due to chronic inflammation of liver cells

Liver cells replaced by scar tissue

Nodules of scar form within liver

Increased resistance in vessels leading to liver (portal hypertension)

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13
Q

What are the common causes of liver cirrhosis

A

Alcoholic liver disease

Non-alcoholic fatty liver disease

Hepatitis B

Hepatitis C

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14
Q

What are the signs of liver cirrhosis

A

Jaundice

Hepatomegaly

Splenomegaly

Spider naevi

Palmar erythema

Gynaecomastia

Testicular atrophy

Bruising

Ascites

Caput medusae

Flapping tremor

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15
Q

What investigations are needed for liver cirrhosis

A

LFTs, clotting

Enhanced liver fibrosis blood test

Ultrasound (corkscrew arteries, enlarged portal veins, ascites, splenomegaly)

Fibroscan (if at risk, test every 2 years)

Endoscopy (oesophageal varices)

CT/MRI

Liver biopsy

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16
Q

What is the Child-Pugh score

A

Assesses progression of cirrhosis

Takes into account: bilirubin, albumin, INR, ascites, encephalopathy

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17
Q

What is the MELD score

A

Use every 6 months in patients with compensated cirrhosis

Gives estimated 3 month mortality

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18
Q

What is the management for liver cirrhosis

A

Ultrasound and aFP every 6 months

Endoscopy every 3 years

High protein, low sodium diet

MELD score every 6 months

Consider liver transplant

Manage complications

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19
Q

What are the complications of liver cirrhosis

A

Malnutrition

Portal hypertension

Varices and variceal bleeds

Ascites

Spontaneous bacterial peritonitis

Hepato-renal syndrome

Hepatic encephalopathy

Hepatocellular carcinoma

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20
Q

What are the stages of non-alcoholic fatty liver disease

A

Non-alcoholic fatty liver disease

Non-alcoholic steatohepatitis

Fibrosis

Cirrhosis

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21
Q

What are the risk factors for non-alcoholic fatty liver disease

A

Obesity

Poor diet

Low activity levels

Type 2 diabetes

High cholesterol

Middle age or above

Smoking

Hypertension

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22
Q

What are the investigations for non-alcoholic fatty liver disease

A

Non-invasive liver screen: ultrasound, hep B and C serology, autoantibodies, immunoglobulins, alpha 1 antitrypsin levels, ferritin and transferrin saturation

Enhanced liver fibrosis blood test: first line for fibrosis, based on markers, gives severity of fibrosis

NAFLD fibrosis score: based on age, BMI, liver enzymes, platelets, albumin, diabetes

Fibroscan: elasticity of liver

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23
Q

What is the management for non-alcoholic fatty liver disease

A

Weight loss

Exercise

Smoking cessation

Control co-morbidities

Avoid alcohol

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24
Q

What are the different types of hepatitis

A

Alcoholic

Non-alcoholic fatty liver disease

Viral

Autoimmune

Drug induced

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25
Q

How might hepatitis present

A

Abdominal pain

Fatigue

Pruritis

Muscle and joint aches

Nausea and vomiting

Jaundice

Fever

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26
Q

How are LFTs deranged in hepatitis

A

AST and ALT high

Bilirubin high

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27
Q

Give an overview of hepatitis A

A

RNA virus

Faecal-oral route

Presentation: nausea vomiting, anorexia, jaundice, cholestasis, hepatomegaly

Resolves in 1-3 months

Management: basic analgesia

Vaccine available

Notifiable disease

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28
Q

Give an overview of hepatitis B

A

DNA virus

Direct contact with blood/bodily fluids, vertical transmission

Most recover in 2 months, 10% become chronic

Use viral markers to test

Vaccine available

Management: low threshold for screening, screen for other blood-borne infections and STIs, notify public health, smoking cessation, stop alcohol, test for complications, antiviral medication, liver transplant

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29
Q

Give an overview of hepatitis C

A

RNA virus

Spreads through bodily fluids

No vaccine

Curable through 8-12 weeks of direct antivirals

3/4 become chronic

Antibody testing for screening, RNA testing for diagnosis

Management: low threshold for screening, screen for other blood-borne infections and STIs, notify public health, stop smoking, stop drinking alcohol, educate, inform risky contacts, test for complications, liver transplant

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30
Q

Give an overview of hepatitis D

A

RNA virus

Only found alongside hep B

Notifiable disease

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31
Q

Give an overview of hepatitis E

A

RNA virus

Faecal-oral transmission

Normally clears within a few months

No treatment required

Rarely progresses to chronic hepatitis/liver failure

No vaccine

Notifiable disease

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32
Q

Give an overview of autoimmune hepatitis

A

Genetic predisposition, viral infection triggers

Type 1 in adults: autoantibodies - ANA, anti-actin, anti-SLA/LP

Type 2 in children: autoantibodies - anti-LKM1, anti-LC1

Diagnosis - liver biopsy

Treatment: high dose prednisolone, immunosuppressants

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33
Q

What is haemochromatosis

A

Iron storage disorder

Excessive total body iron

Iron depletion in tissues

Autosomal recessive

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34
Q

What are the symptoms of haemochromatosis

A

Presents in > 40s (finally become symptomatic)

Chronic tiredness

Joint pains

Pigmentation

Hair loss

Erectile dysfunction

Amenorrhoea

Memory and mood issues

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35
Q

How is haemochromatosis diagnosed

A

Serum ferritin levels

Transferrin saturation
Liver biopsy (iron in parenchymal cells)

CT abdomen

MRI (iron deposits in liver)

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36
Q

What is the management for haemochromatosis

A

Venesection

Monitor serum ferritin

Avoid alcohol

Genetic counselling

Monitor compliance

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37
Q

What are the complications of haemochromatosis

A

Type 1 diabetes (iron affects pancreas)

Liver cirrhosis

Endocrine and sexual problems

Cardiomegaly

Hepatocellular carcinoma

Hypothyroidism

Arthritis

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38
Q

What is Wilson’s disease

A

Excessive accumulation of copper

Autosomal recessive

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39
Q

What are the clinical features of Wilson’s disease

A

Chronic hepatitis

Cirrhosis

Neurological problems

Psychiatric problems

Kayser-Fleischer rings in cornea

Haemolytic anaemia

Renal tubular acidosis

Osteopenia

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40
Q

How is Wilson’s disease diagnosed

A

Serum caeruloplasmin (low)

Liver biopsy (gold standard)

24-hour urine copper assay

MRI brain (non-specific changes)

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41
Q

What is the management for Wilson’s disease

A

Copper chelation (penicillamine, trientine)

42
Q

What is alpha 1 antitrypsin deficiency

A

Autosomal recessive

Inhibition of neutrophil elastase enzyme

Live: cirrhosis, hepatocellular carcinoma

Lungs: bronchiectasis, emphysema

43
Q

How is alpha 1 antitrypsin deficiency diagnosed

A

Low serum alpha 1 antitrypsin

Liver biopsy

Genetic testing

High resolution CT thorax

44
Q

What is the management for alpha 1 antitrypsin deficiency

A

Smoking cessation

Symptomatic management

Organ transplant

Monitor for hepatocellular carcinoma

45
Q

What is primary biliary cirrhosis

A

Immune system attacks small bile duct of liver

Initially affects intralobar ducts (Canal of Hering)

Obstruction to outflow of bile, causing cholestasis

Ultimately get: fibrosis, cirrhosis, liver failure

F>M

46
Q

How might primary biliary cirrhosis present

A

Fatigue

Itching

Jaundice

Xanthelasma

GI disturbance

Pale stools

Signs of cirrhosis and liver failure (ascites, splenomegaly, spider naevi)

47
Q

How is primary biliary cirrhosis diagnosed

A

LFTs (ALP high initially, then bilirubin raised)

Autoantibodies (anti-mitrochondrial, anti-nuclear)

High ESR

High IgM

Liver biopsy

48
Q

What is the management for primary biliary cirrhosis

A

Ursodeoxycholic acid (reduces intestinal absorption of cholesterol)

Colestyramine (bile acid sequestrant)

Liver transplant

Immunosuppression

49
Q

What are the complications of primary biliary cirrhosis

A

Advanced liver cirrhosis

Portal hypertension

Symptomatic pruritus

Fatigue

Steatorrhoea

Distal renal tubular acidosis

Hypothyroidism

Osteoporosis

Hepatocellular carcinoma

50
Q

What is primary sclerosing cholangitis

A

Intrahepatic/extrahepatic ducts become strictured and fibrosed

Obstruction to outflow of bile

Eventually leads to hepatitis, fibrosis, cirrhosis

Associated with ulcerative colitis

51
Q

What are the risk factors for primary sclerosing cholangitis

A

M>F

30 - 40

Ulcerative colitis

Family history

52
Q

How might primary sclerosing cholangitis present

A

Jaundice

Chronic right upper quadrant pain

Pruritus

Fatigue

Hepatomegaly

53
Q

What are the investigations for primary sclerosing cholangitis

A

LFTs (ALP very deranges, bilirubin high)

Autoantibodies (p-ANCA, ANA, aCL)

54
Q

How is primary sclerosing cholangitis diagnosed

A

Magnetic resonance cholangiopancreatography (MRCP)

55
Q

What is the management for primary sclerosing cholangitis

A

ERCP (dilate and stent strictures)

Ursodeoxycholic acid (slow disease progression)

Cholestyramine (bile sequestrant)

Liver transplant

56
Q

What are the complications of primary sclerosing cholangitis

A

Acute bacterial cholangitis

Cholangiocarcinoma

Colorectal cancer

Cirrhosis

Liver failure

Biliary strictures

Fat soluble vitamin deficiency

57
Q

What are the 2 main types of liver cancer

A

Hepatocellular carcinoma

Cholangiocarcinoma

58
Q

What are haemangiomas/focal nodular hyperplasias

A

Benign tumours of liver

59
Q

What are the risk factors for liver cancer

A

Hepatocellular carcinoma: cirrhosis

Cholangiocarcinoma: primary sclerosing cholangitis

60
Q

How might liver cancer present

A

Weight loss

Abdominal pain

Anorexia

Nausea and vomiting

Jaundice

Pruritus

Painless jaundice (cholangiocarcinoma)

61
Q

What are the investigations for liver cancer

A

Alpha-fetoprotein (hepatocellular carcinoma)

Ca19-9 (cholangiocarcinoma)

Liver ultrasound

CT/MRI for staging

ERCP (biopsy)

62
Q

What is the management for hepatocellular carcinoma

A

Poor prognosis unless picked up very early

Resection

Liver transplant

Kinase inhibitors (sorafenib, regorafenib, lenvatinib)

Usually resistant to chemotherapy and radiotherapy

63
Q

What is the management for cholangiocarcinoma

A

Poor prognosis unless picked up very early

Resection

ERCP (stenting)

Usually resistant to chemotherapy and radiotherapy

64
Q

Which patients would be unsuitable for a liver transplant

A

Significant co-morbidities

Excessive weight loss and malnutrition

Active hep B/C

End stage HIV

Active alcohol use

65
Q

What is involved in post liver transplant care

A

Lifelong immunosuppressants

Avoid alcohol

Avoid smoking

Monitor for disease recurrence

Monitor for cancer

Monitor for rejection (abnormal LFTs, fatigue, fevers, jaundice)

66
Q

What is GORD

A

Stomach acid refluxes through lower oesophageal sphincter and irritates lining of oesophagus

Oesophagus - squamous cell carcinoma

Stomach - columnar epithelium

67
Q

How might GORD present

A

Heartburn

Acid regurgitation

Retrosternal/epigastric pain

Bloating

Nocturnal cough

Hoarse voice

68
Q

What would be red flags in GORD

A

Dysphagia (2ww)

Age (>55 2ww)

Weight loss

Upper abdominal pain

Reflux

Treatment-resistant dyspepsia

Nausea and vomiting

Low Hb

Raised platelets

69
Q

What is the management for GORD

A

Lifestyle advice (weight loss, smaller meals, stay upright)

Acid-neutralising medications: gaviscon, rennie

PPIs: omeprazole, lansoprazole

Ranitidine: H2 receptor antagonist

Surgery (laparoscopic fundoplication - tie fundus around lower oesophagus)

70
Q

Give an overview of H pylori

A

Gram negative aerobic

Causes gastritis and ulcers

Produces ammonia (neutralises stomach acid, damages epithelial cells)

Testing: 2 weeks without PPI, urea breath test, stool antigen test

Eradication: PPI + 2 antibiotics (7 days)

71
Q

What is Barrett’s oesophagus

A

Metaplasia of lower oesophageal epithelium

Can develop into adenocarcinoma

Treat with PPIs and ablation

72
Q

Where can peptic ulcers be found

A

Stomach

Duodenum

73
Q

What can cause peptic ulcers

A

Medications (steroids, NSAIDs)

H pylori

Stress

Alcohol

Smoking

Spicy food

74
Q

How does eating relate to peptic ulcers

A

Worsens pain in gastric ulcers

Improves pain in duodenal ulcers

75
Q

How might peptic ulcers present

A

Epigastric pain

Nausea and vomiting

Dyspepsia

Haematemesis

Melena

Iron deficiency anaemia

76
Q

What is the management for peptic ulcers

A

Endoscopy (rapid urease test, biopsy)

High dose PPI

77
Q

What are the complications of peptic ulcers

A

Bleeding from ulcer

Perforation (acute abdomen, peritonitis)

Scarring and strictures (pyloric stenosis)

78
Q

What are the causes of upper GI bleeds

A

Oesophageal varices

Mallory-Weiss tears

Peptic ulcers

Cancer in upper GI tract

79
Q

How might upper GI bleeds present

A

Haematemesis

Coffee ground vomit

Melaena

Haemodynamic instability

Symptoms of underlying pathology (epigastric pain in peptic ulcers, jaundice in liver disease)

80
Q

Explain the Glasgow-Blatchford score

A

> 0 = high risk of upper GI bleed

Drop in Hb

Rise in urea

Blood pressure

Heart rate

Melaena

Syncope

81
Q

What is the Rockall score

A

Risk of rebleeding and mortality after endoscopy

Age

Features of shock

Co-morbidities

Cause of bleeding

Endoscopic stigmata of recent haemorrhage

82
Q

What is the management for upper GI bleeds

A

ABATED

ABCDE

Bloods (Hb, U&Rs, coag, liver screen, crossmatch)

Access (2 large bore canulae)

Transfuse

Endoscopy (urgent, within 24 hrs)

Drugs (stop anticoagulants and NSAIDs)

Definitive management: oesophagogastroduodenoscopy (banding, cauterisation)

83
Q

What are the features of Crohn’s disease

A

Crow’s NEST

No blood/mucus

Entire GI tract

Skip lesions on endoscopy

Terminal ileum most affected, transmural (full thickness)

Smoking is a risk factor

84
Q

What are the features of ulcerative colitis

A

UC CLOSEUP

Continuous inflammation

Limited to colon and rectum

Only superficial mucosa affected

Smoking is protective

Excrete blood and mucus

Use aminosalicylates

Primary sclerosing cholangitis

85
Q

How might inflammatory bowel disease present

A

Diarrhoea

Abdominal pain

Passing blood

Weight loss

86
Q

What are the investigations for inflammatory bowel disease

A

Routine bloods

Faecal calprotectin

Stool culture

Endoscopy with biopsy

Ultrasound/CT/MRI (look for complications)

87
Q

What are acute admissions of IBD at high risk of

A

VTE

Need prophylactic heparin

88
Q

What is the management for Crohn’s disease

A

Induce remission: steroids, immunosuppressants (azathioprine, methotrexate, infliximab)

Maintain remission: use some combination of same drugs

Surgery: only if affecting distal ileum

89
Q

What is the management for ulcerative colitis

A

Induce remission: aminosalicylate, corticosteroids, IV corticosteroids

Maintain remission: aminosalicylate, azathioprine

Surgery: remove colon and rectum, left with permanent ileostomy

90
Q

What is irritable bowel syndrome

A

Functional bowel disorder

Diagnosis of exclusion

91
Q

What are the symptoms of irritable bowel syndrome

A

Diarrhoea

Constipation

Fluctuating bowel habits

Abdominal pain

Bloating

Worse after eating

Improved by opening bowels

92
Q

What is the NICE diagnostic criteria for irritable bowel syndrome

A

Excluded other pathologies

Abdominal pain and discomfort plus to of: abnormal stool, bloating, worse after eating, PR mucus

93
Q

What is the management for irritable bowel syndrome

A

Diet and exercise advise

First line: loperamide (diarrhoea), laxatives (constipation, but avoid lactulose), antispasmodics (cramps)

Second line: tricyclic antidepressants

Third line: SSRI

CBT

94
Q

What is coeliac disease

A

Autoimmune condition

Exposure to gluten causes inflammation of small bowel

Especially jejunum

Get atrophy of intestinal villi

Malabsorption of nutrients

Genetic associations: HLA-DQ2, HLA-DQ8

95
Q

Which antibodies are associated with coeliac disease

A

Anti-tissue transglutaminase (anti-TTG)

Anti-endomysial (anti-EMA)

96
Q

How might coeliac disease present

A

Failure to thrive (children)

Diarrhoea

Fatigue

Weight loss

Mouth ulcers

Anaemia

Dermatitis herpetiformis

Neurological symptoms (peripheral neuropathy, cerebral ataxia, epilepsy)

97
Q

How is coeliac disease diagnosed

A

Investigate while still eating gluten

Check total IgA

Check antibodies (anti-TTG, anti-EMA)

Endoscopy (crypt hypertrophy, villous atrophy)

98
Q

Which conditions are associated with coeliac disease

A

Type 1 diabetes

Thyroid disease

Autoimmune hepatitis

Primary biliary cirrhosis

Primary sclerosing cholangitis

99
Q

What is the treatment for coeliac disease

A

Lifelong gluten-free diet

100
Q

What are the complications of coeliac disease

A

Vitamin deficiency

Anaemia

Osteoporosis

Ulcerative colitis

Lymphoma of intestines

Small bowel adenocarcinoma

Neurological complications (gluten ataxia, neuropathy)

101
Q

What does a liver screen include

A

Hep B and C serology

Iron studies (ferritin and transferrin saturation)

Autoantibodies (AMA, SMA)

Immunoglobulins

Ceruloplasmin (if >30)

Alpha 1 antitrypsin

Coeliac serology

Thyroid function tests

Lipids

Glucose

Medicine (9 decks)

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