Brainscape's Knowledge GenomeTM

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


See full index

Zero to Finals > Gastroenterology > Flashcards

Gastroenterology Flashcards

1
Q

State the three stepwise process of progression of alcoholic liver disease?

A
  1. alcohol related fatty liver
    - drinking –> fat build up
    - can be reversed in two weeks
  2. alcoholic hepatitis
    - inflammation of liver sites
  3. cirrhosis
    - scar tissue replaces healthy liver tissue
    - irreversible
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the recommended alcohol consumption?

A
  • men and women
  • no more than 14 units per week
  • spread over 3 or more days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The CAGE question can be used to quickly screen for harmful alcohol use:

A

C – CUT DOWN? Ever thought you should?

A – ANNOYED? Do you get annoyed at others commenting on your drinking?

G – GUILTY? Ever feel guilty about drinking?

E – EYE OPENER? Ever drink in the morning to help your hangover/nerves?

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

State 6 complications of alcohol

A
  1. Alcoholic liver disease
  2. Cirrhosis
  3. alcohol dependence and withdrawal
  4. Wernicke-korsakoff syndrome
  5. pancreatitis
  6. alcoholic cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are signs of liver disease?

9

A
  • jaundice
  • hepatomegaly
  • spider naevi
  • palmar erythema
  • gynaecomastia
  • bruising
  • ascites
  • caput medusae
  • asterixis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What investigations might you do for an alcoholic liver disease patient?

A

BLOODs

  1. FBC - raised MCV?
  2. LFTs - raised ALT and AST, Gamma-GTT, low albumin, elevated bilirubin in cirrhosis
  3. Clotting - increased prothrombin time, due to reduced synthetic function of liver
  4. U&Es - deranged? hepatorenal syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What might an USS of a patient with alcoholic liver disease show?

A
  • increased echogenecity

- showing fatty changes

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

Complications of liver cirrhosis?

A
  • portal hypertension
  • varices
  • ascites
  • hepatic encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

stages of alcohol withdrawal

A

6 - 12hrs : tremor, sweating, headache, craving and anxiety

12 - 24hrs : hallucinations

24 - 48hrs : seizures

**48 - 72hrs : **delerium tremens

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

What is Delirium tremens?

A
  • medical emergency

- associated with alcohol withdrawal

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

what receptors do alcohol stimulate in the brain?

A
  • GABA receptors

- GABA receptors have relaxing effect on brain

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

Which receptors do alcohol inhibit?

A
  • glutamate receptors

- inhibit electrical acitivity of the brain

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

what occurs to the GABA system with chronic alcohol use?

A
  • GABA system becomes down-regulated

- Glutamate system becomes up regulated

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

How might alcohol withdrawal be managed?

A
  • score patient on their withdrawal symptoms: CIWA-Ar tool
  • Chlordiazepoxide (benzodiazapine)
  • IV high dose B vitamins, followed by lower oral thiamine dose
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does alcohol excess affect thiamine (vitamin B1)

A
  • leads to thiamine deficiency
  • leads to Wernicke’s encephalopathy
  • then Korsakoffs syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe three features of Wernicke’s encephalopathy?

A
  1. confusion
  2. oculomotor disturbances
  3. ataxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe features of Korsakoff’s syndrome?

A
  1. memory impairment (retrograde and anterograde)

2. behavioural changes

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

Fibrosis of the liver can lead to..

A
  • affects structure and blood flow through liver
  • causes increased resistance in the vessels
  • portal hypertension
  • caput medusae?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

List 4 most common causes of liver cirrhosis?

A
  1. Alcoholic liver disease
  2. non-alcoholic fatty liver disease
  3. hepatitis B
  4. hepatitis C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Rarer causes of liver cirrhosis?

A

Autoimmune hepatitis

Primary biliary cirrhosis

Haemochromatosis

Wilsons Disease

Alpha-1 antitrypsin deficiency

Cystic fibrosis

Drugs (e.g. amiodarone, methotrexate, sodium valproate)

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

Asterixis is a sign of:

A

decompensated liver disease

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

A Cirrhosis ultrasound may show?

A
  1. nodularity of liver surface
  2. corkscrew appearance to arteries with increased flow as they compensate for reduced portal flow
  3. enlarged portal vein with reduced flow
  4. ascites
  5. splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what scan is used to check the elasticity of the liver by sending high frequency sound waves into the liver?

A

fibroscan

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

What scoring system is used for liver Cirrhosis?

A

Child-Pugh score

features:

  • bilirubin
  • albumin
  • INR
  • ascites
  • encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

portal vein is derived from the…

A

superior mesenteric vein and the splenic vein

delivers blood to liver

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

portal hypertension is:

A
  • liver cirrhosis increases resistance of blood flow in the liver
  • back pressure causes vessels to become swollen at tortuous
  • at anastomoses sites
  • known as varices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

four common sites of varices?

A
  1. gastro-oesophageal junction
  2. ileocaecal junction
  3. rectum
  4. anterior abdominal wall via the umbilical vein (caput medusae)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

three ways to treat stable varices?

A
  • propranolol to reduce portal hypertension
  • elastic band ligation of varices
  • injection of sclerosant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is a trans jugular intra-hepatic Porto-systemic shunt (TIPS)

A
  • interventional radiologist inserts wire into jugular vein
  • down vena cava
  • via hepatic vein into liver
  • makes connection
  • through hepatic vein and portal vein tissue
  • puts stent in place
  • allows blood to flow directly from portal vein to hepatic vein, relieving the pressure in portal system and varices
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Management of bleeding oesophageal varices?

A
  1. RESUSCITATION
  2. urgent endoscopy
  3. sengstaken-blakemore tube
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Management of bleeding oesophageal varices?

Describe the process of resuscitation?

A
  1. vasopressin analogue (causes v.constriction and slow bleeding in varices)
  2. vitamin K to correct coagulopathy and fresh frozen full of clotting factor plasma
  3. prophylactic broad spectrum antibiotics
  4. intubation and ICU consideration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is a sengstaken-blakemore tube?

A
  • inflatable tube

- inserted into oesophagus to tamponade the bleeding varices

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

Cirrhosis causes what type of ascites?

A
  • transudative

- low protein content

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

management of ascites?

A
  • low sodium diet
  • aldosterone antagonist diruetics (spironolactone)
  • paracentesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is spontaneous bacterial peritonitis?

A
  • infection developing in ascitic fluid and peritoneal lining
  • without clear cause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

most common organisms causing spontaneous bacterial peritonitis?

A
  • E.coli
  • klebsiella pneumoniae
  • gram positive cocci
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

presentation of patient with spontaneous bacterial peritonitis?

A
  • fever
  • abdominal pain
  • deranged bloods
  • ileus
  • hypotenion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what is an ileus?

A

complete or partial non mechanical blockage of small and/or large intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

management of spontaneous bacterial peritonits?

A
  • take an ascitic culture prior to giving antibiotics
  • usually treated with IV cephalosporin
  • such as cefotaxime
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is hepatorenal syndrome?

A
  • occurs in liver cirrhosis
  • hypertension in portal system leads to dilation of portal blood vessels
  • loss of blood volume in other areas of circulation, like kidneys
  • hypotension in kidneys
  • activation of RAAS
  • renal v.constriction
  • this with reduced circulation volume leads to starvation of blood to the kidneys
  • leads to rapid deteriorating kidney function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

fatality of hepatorenal syndrome

A
  • fatal within a week

- unless liver transplant is performed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

give an example of a toxin that builds up causing hepatic encephalopathy?

A
  • ammonia
  • produced from intesitnal gut bacteria
  • laxatives can help clear ammonia from gut before it is absorbed.
  • antibiotics can reduce the amount of ammonia producing bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

management of patient with hepatic encephalopathy?

A
  1. laxatives (lactulose) to promote excretion of ammonia
  2. antibiotics (rifaximin)

rifaximin is useful as it is poorly absorbed and so stays in the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

stages of NAFLD

A
  1. non alcoholic fatty liver disease: fat deposits
  2. non alcoholic steatohepatitis
  3. fibrosis
  4. cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

patients with liver fibrosis as a result of NAFLD may be treated with

A

vitamin E

or

pioglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Most common viral hepatitis world wide

A

hep A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hep A is what type of virus

A

RNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Hep A presents with what symptoms

A
  • nausea
  • vomiting
  • anorexia
  • jaundice
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

management of Hep A

A
  • basic analgesia

- should resolve within 1-3 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Hep B is what type of virus

A

DNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How is Hep B transmitted

A
  • direct contact with blood or bodily fluids
  • IVDU
  • vertical transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Hep A transmitted via

A

faecal oral route

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe recovery time for hep A?

A

usually within 2 months

10% patients become chronic hep B carriers

virus DNA integrated into their own DNA

54
Q

Surface antigen (HBsAg) indicates

A

active infection

55
Q

Surface antigen (HBsAg) indicates

A
  • marker of viral replication

- high infectivity

56
Q

Core antibodies (HBcAb)

A
  • past or current infection
57
Q

Surface antibody (HBsAb)

A
  • implies vaccination or past or current infection
58
Q

Hepatitis B virus DNA (HBV DNA)

A

this is a direct count of the viral load

59
Q

Hep C is what type of virus

A

RNA virus

60
Q

How is hep C spread

A

blood and bodily fluids

no vaccine available

curable via direct actng antiviral medications

61
Q

Hepatitis D is what type of virus

A

RNA virus

can only survive in patients who also have hep B infection

62
Q

Hepatitis E is what type of virus

A

RNA virus

63
Q

Hep E transmitted via

A

faecal oral route

usually produced mild illness

no vaccination

64
Q

type 1 autoimmune hepatitis

A
  • occurs in adults

- less acute than type 2

65
Q

Type 1 autoimmune hepatitis autoantibodies

A
  • anti-nuclear antibodies
  • anti-smooth muscle antibodies
  • anti-soluble liver antigen
66
Q

Type 2 autoimmune hepatitis autoantibodies

A
  • anti-liver kidney microsomes-1

- anti-liver cytosol antigen type 1

67
Q

treatment of autoimmune hepatitis

A
  • high dose steroids (prednisolone)

- azathioprine

68
Q

Haemochromatosis is…

A
  • iron storage disorder

- results in excessive total body iron

69
Q

mutations in what gene on chromosome 6 are linked to haemochromatosis?

A
  • human haemochromatosis protein (HFE) gene
70
Q

describe some symptoms of haemochromatosis?

A
  • chronic tiredness
  • joint pain
  • pigmentation
  • hair loss
  • erectile dysfunction
  • amenorrhoea
  • memory and mood disturbance
71
Q

management of haemochromatosis?

A
  • monitor serum ferritin
  • venesection (removing blood to decrease total iron)
  • avoid alcohol
  • genetic counselling
72
Q

Wilson’s disease

A

excessive accumulation of copper in body and tissues

caused by mutation in wilsons disease protein on chromosome 13

autosoma recessive

73
Q

describe the three main ranges of symptoms of patients with Wilson’s disease?

A
  • hepatic problems
  • neurological problems
  • psychiatric problems
74
Q

neurologic symptoms in Wilsons disease

A
  • dysarthria (speech difficulties)
  • dystonia
  • copper deposition in basal ganglia leads to parkinsonism
75
Q

parkinsonism characterised by what three signs

A
  • tremor
  • bradykinesia
  • rigidity
76
Q

initial investigation of choice for Wilson’s disease

A

serum caeruloplasmin

low [serum caeruloplasmin] characteristic of Wilson’s

77
Q

management of Wilsons disease

A

Copper chelation using:

  • penicillamine
  • trientene
78
Q

briefly summarise the pathophys of alpha 1 antitrypsin deficiency

A
  • neutrophils secrete elastase
  • elastase enzyme digests connective tissues
  • liver produces A1T1 inhibits elastase
  • offers protection
79
Q

two main organs affected by alpha-1-antitrypsin deficiency are

A
  1. Liver : cirrhosis

2. Lungs : bronchiectasis and emphysema in lungs

80
Q

why does bronchiectasis and emphysema occur over time in lungs of patients with A1T1 deficiency ?

A
  • lack of a1t1
  • excess of protease enzymes
  • attack connective tissue lining of lung
81
Q

management for a1t1 deficiency

A
  • smoking cessation to decelerate emphysema
  • symptomatic management
  • organ transplant
82
Q

primary biliary cirrhosis is a condition where..

A
  • immune system attacks

- small bile ducts within the liver

83
Q

presentation of primary biliary cirrhosis?

A
  • fatigue
  • pruritis
  • GI disturbance and abdominal pain
  • jaundice
  • pale stools
  • xanthoma
  • signs of cirrhosis and failure (e.g. ascites, splenomegaly and spider naevi)
84
Q

what is primary biliary cirrhosis associated with?

A
  • other autoimmune diseases (thyroid, coeliac)

- rheumatoid conditions (e.g. systematic sclerosis, sjogrens and rheumatoid arthritis)

85
Q

which autoantibodies are specific to primary biliary cirrhosis?

A
  • anti-mitochondrial antibodies (most specific to PBC)

- anti-nuclear antibodies (present in 35% of patients)

86
Q

treatment of primary biliary cirrhosis?

A
  • ursodeoxycholic acid (reduces intestinal absorption of cholesterol)
  • cholestyramine
  • liver transplant in end stage liver disease
  • immunosuppresion?
87
Q

what is primary sclerosing cholangitis?

A
  • where intrahepatic or extrahepatic ducts become strictured and fibrotic
  • sclerosis: stiffening and hardening
  • cholangitis : inflammation of bile ducts
88
Q

5 key features of presentation of patient with primary sclerosing cholangitis?

A
  1. jaundice
  2. chronic RUQ pain
  3. pruritus
  4. fatigue
  5. hepatomegaly
89
Q

gold standard investigation for diagnosis of primary sclerosing cholangitis?

A

MRCP

magnetic resonance cholangiopancreatography

MRI : liver , bile ducts, pancreas

90
Q

management of primary sclerosing cholangitis?

A

Liver transplant?

  • ERCP to dilate and stent any structures
  • ursodeoxycholic acid
  • cholestryamine (bile acid sequestrate)
91
Q

primary sclerosing cholangitis is heavily associated with

A

ulcerative colitis

92
Q

what are the two types of primary liver cancer?

A

primary liver cancer originates in the liver

two main types: hepatocellular carcinoma, cholangiocarcinoma

93
Q

secondary liver cancer is…

A
  • cancer that originates outside the liver and metastasises to the liver
94
Q

main risk factors for hepatocellular carcinoma is liver cirrhosis due to:

A
  • viral hepatitis B and C
  • alcohol
  • NAFLD
  • chronic liver disease

Liver cancer often remains asymptomatic for a long time and then presents late making prognosis poor.

95
Q

what is a tumour marker for hepatocellular carcinoma?

A
  • alpha-fetoprotein
96
Q

what is a tumour marker for cholangiocarcinoma?

A
  • CA19-9
97
Q

treatment of hepatocellular carcinoma?

A
  • poor prognosis unless diagnosed early
  • kinase inhibitors inhibiting proliferation of cancer cells
  • HCC resistant to chemo
98
Q

treatment of cholangiocarcinoma?

A
  • very poor prognosis unless diagnosed very early
  • ERCP . can be used to place stent in bile duct
  • allows drainage of bile and usually improves symptoms
99
Q

what is an haemangioma

A

benign tumour of liver

often find incidentally

100
Q

what is a focal nodular hyperplasia

A
  • benign liver tumour made of fibrotic tissue
101
Q

most common causes of acute liver failure?

A
  • acute viral hepatitis

- paracetamol overdose

102
Q

symptoms of GORD

A

dyspepsia: indigestion

  • heartburn
  • acid regurgitation
  • retrosternal or epigastric pain
  • bloating
  • nocturnal cough
  • hoarse voice
103
Q

what are key red flag features which would indicate two week wait referral for endoscopy?

A
  • dysphagia
  • aged > 55
  • weight loss
  • upper abdominal pain / reflux
  • treatment resistant dyspepsia
  • nausea and vomiting
  • low haemoglobin
  • raised platelet count
104
Q

management of GORD

A

Lifestyle advice

acid neutralising medication

PPI

ranitidine

surgery for laparoscopic fundoplication

105
Q

what is ranitidine ?

A
  • alternative to PPIs
  • H2 receptor antagonist (antihistamine)
  • reduces stomach acid
106
Q

describe the process of laparoscopic fundoplication?

A
  • tying funds of stomach
  • around lower oesophagus
  • to narrow the lower oesophageal sphincter
107
Q

What class of bacteria is Heliobacter Pylori

A

gram negative

108
Q

Tests for H.pylori

A
  1. urea breath test
  2. stool antigen test
  3. rapid urease test (involves biopsy during endoscopy)
109
Q

Eradication regime for H.Pylori

A

triple therapy

with PPI and two antibiotics (e.g. amoxicillin and clarithromycin)

110
Q

Barretts oesophagus

A

metaplasia from squamous to columnar epithelium

111
Q

treatment for Barretts oesophagus

A

PPI

ablation treatment
- during endoscopy

112
Q

eating typically worsens the pain of what ulcers

A

gastric ulcers

113
Q

management of peptic ulcers

A
  • endoscopy
  • urease test to check for H.pylori
  • high dose PPI
114
Q

State some causes of upper GI bleed

A
  • oesophageal varices
  • mallory-weiss tear
  • ulcers of stomach or duodenum
  • cancers of stomach or duodenum
115
Q

presentation of upper GI bleed

A
  • haematemesis
  • ‘coffee ground’ vomit
  • Melaena
  • low BP, haemodynamic instability, t.cardia, shock=
116
Q

management for upper GI bleed

A

ABCDE

Bloods

Access (2 large bore cannula)

Transfuse

Endoscopy within 24hrs

Drugs

ABATED

117
Q

definitive treatment for upper GI bleed

A

oesophagogastroduodenoscopy

banding of varices, or cauterisation

118
Q

features of Crohn’s disease

A

NESTS

N - no blood or mucus

E - entire GI tract

S - skip lesions on endoscopy

T - terminal ileum, transmural

S - smoking risk factor

119
Q

Ulcerative colitis features

A

CLOSE UP

C - continuous inflammation

L - limited to colon and rectum

O - only superficial mucosa

S - smoking is protective

E - excrete blood and mucus

U - use aminosalicylates

120
Q

marker of bowel inflammation?

A

faecal calprotectin

121
Q

management of Crohn’s

A

first line: steroids (oral prednisolone, or IV hydrocortisone)

consider adding immunosuppressant: azathioprine

122
Q

management of mild moderate ulcerative colitis

A

first line: amino salicylate (e.g. mesalazine)

second line: corticosteroids (e.g. prednisolone)

123
Q

management of severe ulcerative colitis

A

first line: IV corticosteroids (e.g. hydrocortisone)

second line: IV ciclosporin

124
Q

criteria for diagnosis of irritable bowel syndrome?

A
  • Normal FBC, ESR and CRP blood tests
  • faecal calprotectin negative to exclude IBD
  • negative coeliac disease serology (anti-TTG antibodies)
125
Q

management of irritable bowel syndrome?

A
  • fluids
  • regular small meals
  • reduced processed foods
  • limit caffeine and alcohol
  • low ‘FODMAP’
  • probiotics?
126
Q

first line medication for irritable bowel syndrome?

A
  • loperamide for diarrhoea
  • laxative for constipation , avoid lactulose
  • antispasmodics for cramps e.g. hyoscine butylbromide
127
Q

second line medication for irritable bowel syndrome?

A

tricyclic antidepressants

i.e. amitriptyline

128
Q

what is coeliac disease?

A
  • autoimmune
  • exposure to gluten causes inflammation in small bowel
  • auto-antibodies created in response to gluten
129
Q

two antibodies in coeliacs disease

A

anti-TTG

anti-EMA

130
Q

describe what occurs to the small bowel in coeliacs disease?

A
  • villous atrophy
  • crypt hypertrophy
  • malabsorption of nutrients
131
Q

what is the rash that occurs in some coeliac patients?

A

dermatitis herpetiformis

- itchy, blistering rash

132
Q

genetic associations in coeliac disease

A

HLA-DQ2

HLA-DQ8

Zero to Finals (5 decks)

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