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Finals > Gastroenterology and General Surgery > Flashcards

Gastroenterology and General Surgery Flashcards

1
Q

Give the stages of alcoholic liver disease

A
  1. Alcoholic fatty liver disease
  2. Alcoholic hepatitis
  3. Cirrhosis
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2
Q

Give the recommended weekly maximum number of units of alcohol

A

14

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3
Q

Describe the CAGE questionnaire

A

Cut down - have you ever thought you should cut down on your drinking?

Annoyed - do you ever get annoyed at others commenting on your drinking?

Guilty - do you ever feel guilty about your drinking?

Eye opener - do you ever drink in the morning to help you get through the day?

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4
Q

What questionnaires can be used to screen for harmful alcohol consumption?

A

CAGE

AUDIT (>8 suggests harmful use)

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5
Q

Give the serious complications of alcohol consumption

A

Cirrhosis

Wernicke-Korsakoff syndrome

Pancreatitis

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6
Q

Give the presentation of alcoholic liver disease

A
  1. Jaundice
  2. Hepatomegaly
  3. Spider naevi
  4. Asterixis (liver flap)
  5. Palmar erythema
  6. Bruising
  7. Ascites
  8. Caput medusae
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7
Q

Give the investigations for alcoholic liver disease

A

FBC - raised MCV
LFT - raised ALT, ALP, gamma-GT, bilirubin. Decreased albumin
Clotting - elevated PT
USS - increased echogenicity
Endoscopy - to treat oesophageal varices
CT/MRI - to assess for cancer
Biopsy - definitive diagnosis

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8
Q

Give the management of alcoholic liver disease

A
  1. Permanent alcohol abstinence
  2. Thiamine (IV pabrinex)
  3. Steroids - aid short term outcome
  4. Liver transplant
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9
Q

Describe the stages of alcohol withdrawal

A

6-12 hours: tremor, sweating, headache, cravings and anxiety

12-24 hours: hallucinations

24-48 hours: seizures

24-72 hours: delirium tremens

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10
Q

Describe the pathophysiology of delirium tremens

A

Excess excitability of neurones due to removal of previous constant inhibitor (alcohol) which they had adapted to

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11
Q

Give the presentation of delirium tremens

A
  1. Acute confusion/agitation
  2. Delusions/hallucinations
  3. Tremor
  4. Tachycardia/hypertension
  5. Ataxia (difficulty with co-ordinated movement)
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12
Q

Give the management of delirium tremens

A
  1. Chlordiazepoxide (benzodiazepine)
  2. IV parbrinex
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13
Q

Describe the pathophysiology of Wernicke-Korsakoff syndrome

A

Alcohol excess causes thiamine (vit B1) deficiency

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14
Q

Describe the presentation of Wernicke’s encephalopathy

A
  1. Confusion
  2. Oculomotor disturbance
  3. Ataxia
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15
Q

Describe the presentation of Korsakoff syndrome

A
  1. Memory impairment
  2. Behavioural changes

Irreversible - patients require round-the-clock care

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16
Q

Describe the pathophysiology of liver cirrhosis

A

Chronic inflammation results in the replacement of normal hepatic tissue with scar tissue (fibrosis), which disrupts blood flow through the liver and causes portal hypertension.

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17
Q

Give the causes of liver cirrhosis

A
  1. Alcoholic liver disease
  2. NAFLD
  3. Hepatitis B & C
  4. Haemochromatosis
  5. Wilson’s disease
  6. Cystic fibrosis
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18
Q

Give the presentation of liver cirrhosis

A
  1. Jaundice
  2. Hepatosplenomegaly
  3. Spider naevi
  4. Palmar erythema
  5. Bruising
  6. Asterixis
  7. Caput medusae
  8. Ascites
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19
Q

Give the investigations for liver cirrhosis

A
  1. Enhanced liver fibrosis blood test - 1st line
  2. USS
  3. Fibroscan
  4. Liver biopsy
  5. Deranged LFTs
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20
Q

Give the complications of liver cirrhosis

A
  1. Malnutrition
  2. Oesophageal varices
  3. Hepatic encephalopathy
  4. Hepatocellular carcinoma
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21
Q

Describe the presentation of oesophageal varices

A
  1. Asymptomatic
  2. Bleeding - patients may bleed out very quickly!
    a) Haematemesis
    b) Meleana
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22
Q

Give the management of oesophageal varices

A
  1. Propranolol - reduced portal hypertension
  2. Elastic band ligation
  3. Sengstaken-Blakemore tube - compresses oesophageal bleeding
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23
Q

Describe the management of ascites

A
  1. Low-sodium diet
  2. Spironolactone
  3. Paracentesis
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24
Q

Describe spontaneous bacterial peritonitis

A

Infection of the ascitic fluid resulting in generalised infective peritonitis.

Commonly caused by E. coli or klebsiella pneumoniae

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25
Describe the management of spontaneous bacterial peritonitis
1. Culture of ascitic fluid 2. IV cefotaxime
26
Describe the pathophysiology of hepatic encephalopathy
Build-up of toxins which affect the brain - most commonly ammonia
27
Describe the presentation of hepatic encephalopathy
1. Confusion 2. Reduced consciousness
28
Give the management of hepatic encephalopathy
1. Laxatives (i.e. lactulose) - promote ammonia excretion 2. Antibiotics (i.e. rifaximin) - reduces the number of ammonia-producing bacteria 3. Nutritional support
29
Describe the pathophysiology of NAFLD
Deposition of lipids within hepatocytes, which interfere with the normal functioning of the liver - potentially resulting in hepatitis and cirrhosis.
30
Give the management of small intestine bacterial overgrowth syndrome
Rifaximin
31
Describe the stages of NADLD
1. NAFLD 2. Non-alcoholic steato-hepatitis 3. Fibrosis 4. Cirrhosis
32
Give the risk factors for NAFLD
1. Obesity 2. T2DM 3. High cholesterol 4. Older age 5. Smoking 6. HTN
33
Describe the components of a liver screen
If abnormal LFTs with no identifiable cause, do a liver screen: 1. USS liver 2. Hepatitis B & C serology 3. Autoantibodies (e.g. ANA) 4. Immunoglobulins (for autoimmune hepatitis) 5. Caeruloplasmin 6. Alpha-1-antitrypsin 7. Ferritin and transferrin
34
Give the managemnt of NAFLD
1. Weight loss 2. Exercise 3. Avoid alcohol 4. Stop smoking
35
Describe hepatitis
Inflammation of the liver - which can lead to large areas of necrosis and liver failure
36
Describe the causes of hepatitis
1. Alcohol 2. NAFLD 3. Viral 4. Autoimmune 5. Drug induced 9e.g. paracetamol overdose)
37
Give the presentation of hepatitis
1. Abdominal pain 2. Fatigue 3. Pruritus 4. Fever (if viral) 5. N+V 6. Muscle pain 7. Jaundice
38
Describe the presentation of Hepatitis A
Cholestasis: 1. Dark urine 2. Pale stool
39
Describe the management of Hepatitis A
1. Resolves spontaneously in 1-3 months 2. Basic analgesia 3. Vaccination
40
Describe the pathophysiology of Hepatitis B
DNA virus conducted via blood or bodily fluids, or via vertical transmission from mother to fetus
41
Describe the viral markers for Hepatitis B
HBsAg - signifies active infection Anti-HBc - signifies previous infection Anti-HBs - signifies immunity Viral load - to assess extent of infection
42
What pattern of viral markers would be seen in acute/chronic Hepatitis B infection?
+ve HBsAg Chronic Hep B have symptoms for >6 months
43
What pattern of viral markers would be seen in previous Hepatitis B infection?
+ve HBcAg
44
What pattern of viral markers would be seen in previous Hepatitis B infection if now a carrier?
+ve Anti-HBc +ve HBsAg
45
What pattern of viral markers would be seen in previous Hepatitis B vaccination?
+Anti-HBs
46
Give the management of Hepatitis B
Most recover within 2 months, but 10% become chronic carriers 1. Screen for other blood-borne or sexually transmitted infections 2. Notify public health 3. Fibroscan - for cirrhosis 4. Antivirals 5. Liver transplant
47
Give the management of Hepatitis C
1. Notify public health 2. Stop smoking and drinking alcohol 3. USS and fibroscan 4. Direct acting antivirals 5. Liver transplant
48
Give the risks of hepatitis C
Hepatocellular carcinoma Cirrhosis
49
Describe hepatitis D
Can only exist alongside hepatitis B, but increases it's severity
50
Describe hepatitis E
Very mild, self-limiting illness which requires no treatment. If immunocompromised may progress to hepatitis and liver failure.
51
Describe autoimmune hepatitis
Type 1: seen in adults, associated with ANA, anti-actin and anti-SLA Type 2: see in children, associated with anti-LKM, anti-LC Diagnose with biopsy Manage with prednisolone and azathioprine
52
Describe haemochromatosis
Iron storage disorder resulting in excess total iron with resultant deposition in tissues.
53
Describe the inheritance pattern seen in haemochromatosis
Autosomal recessive
54
Describe the presentation of haemochromatosis
1. Age >40 2. Chronic tiredness 3. Joint pain 4. Hair loss 5. Erectile dysfunction 6. Amenorrhoea 7. Memory/mood disturbance 8. Bronze skin pigmentation
55
Describe the diagnosis of haemochromatosis
1. Serum ferritin and transferrin raised 2. Genetic testing 3. Liver biopsy using Perl's stain 4. CT/MRI
56
Describe the complications of haemochromatosis
1. T1DM 2. Liver cirrhosis 3. Hypothyroidism 4. Cardiomyopathy 5. Hepatocellular carcinoma 6. Pseudogout
57
Give the management of haemochromatosis
1. Venesection. (decreases total iron) 2. Monitor serum ferritin 3. Avoid alcohol
58
Describe Wilson's disease
Excessive accumulation of copper as a result of the mutation in the 'Wilson disease protein'
59
Describe the inheritance pattern seen in Wilson's disease
Autosomal recessive
60
Describe the presentation of Wilson's disease
Hepatic: hepatitis and cirrhosis CNS: dysarthria, dystonia, Parkinsonism Psychiatric: depression, psychosis Kayser-Fleischer rings Haemolytic anaemia Osteopenia Renal tubular acidosis
61
Describe the diagnosis of Wilson's disease
Serum caeruloplasmin - the protein which carries copper in the blood, would be low Liver biopsy Serum copper
62
Give the management of Wilson's disease
Copper chelation therapy: 1. Penicillamine 2. Trientene Risk of developing psychosis secondary to Wilson's
63
Give the pathophysiology of alpha-1 antitrypsin deficiency
Alpha-1 antitrypsin normally inhibits elastase (produced by neutrophils) which breaks down elastic tissues. Due to a genetic mutation there is insufficient alpha-1 antitrypsin which results in reduced inhibition of elastase, causing liver cirrhosis, bronchiectasis and emphysema.
64
Describe the diagnosis of alpha-1 antitrypsin deficiency
1. Serum alpha-1 antitrypsin - reduced 2. Liver biopsy 3. CT thorax (for pulmonary complications)
65
Describe the management of alpha-1 antitrypsin deficiency
1. Stop smoking (rapidly accelerates emphysema) 2. Symptomatic management 3. Organ transplantation 4. Monitor for complications (incl. HCC)
66
Give the pathophysiology of pellagra
Vitamin B3 (niacin) deficiency
67
Give the presentation of pellagra
Pellagra: Dermatitis, diarrhoea, dementia/delusions, leading to death
68
Give 1 side effect of sulfasalazine
Heinz body anaemia
69
Describe the pathophysiology of primary biliary cirrhosis
Autoimmune disorder affecting the small bile ducts within the liver resulting in obstruction, as well as fibrosis, cirrhosis and liver failure due to the back-pressure of bile.
70
Describe the presentation of primary biliary cirrhosis
1. Xanthelasma - cholesterol deposits within the skin 2. Pruritus 3. Jaundice 4. Pale stools 5. GI disturbance and abdo pain
71
Describe the investigations for primary biliary cirrhosis
LFTs - raised ALP, ALT and bilirubin Autoantibodies - e.g. AMA, ANA ESR - raised IgM - raised Liver biopsy
72
Give the management of primary biliary cirrhosis
1. Ursodeoxycholic acid 2. Colestyramine 3. Steroids (for immunosuppression) 4. Liver transplant
73
Describe the pathophysiology of primary sclerosing cholangitis
Where the intra/extra-hepatic ducts become strictured and fibrotic, causing an obstruction to the outflow of bile
74
Give the risk factors for primary sclerosing cholangitis
1. UC 2. FHx 3. Male 4. Age 30-40 Infection can trigger in those who are predisposed
75
Give the presentation of primary sclerosing cholangitis
1. Jaundice 2. Chronic RUQ pain 3. Pruritus 4. Fatigue 5. Hepatomegaly
76
Give the investigations for primary sclerosing cholangitis
pANCA, ANA, aCL autoantibodies positive Raised ALP and bilirubin GOLD STANDARD: MRCP (magnetic resonance cholangiopancreatography)
77
Give the management of primary sclerosing cholangitis
1. Liver transplant 2. ERCP (endoscopic retrograde cholangiopancreatography) 3. Colestyramine - helps with pruritus
78
Give the two types of liver cancer
1. Hepatocellular carcinoma 2. Cholangiocarcinoma
79
Give the risk factors for hepatocellular carcinoma
1. Viral hepatitis 2. Alcohol 3. NAFLD
80
Give the risk factors for cholangiocarcinoma
1. Primary sclerosing cholangitis 2. Parasitic infection (liver flukes)
81
Give the presentation of hepatocellular carcinoma
1. Non-specific Sx, e.g. weight loss, abdo pain, anorexia, pruritus 2. Liver dysfunction
82
Give the investigations for hepatocellular carcinoma
1. Alpha-fetoprotein - tumour marker 2. Liver USS 3. CT/MRI (for diagnosis or staging)
83
Give the management of hepatocellular carcinoma
1. Surgical resection 2. Liver transplant possible 3. Sorafenib
84
Describe the pathophysiology of GORD
Stomach acid regurgitates through the lower oesophageal sphincter and irritates the oesophageal epithelium
85
Give the presentation of GORD
1. Heartburn (retrosternal/epigastric pain) 2. Acid regurgitation 3. Hoarse voice 4. Nocturnal cough
86
Give the referral indications for endoscopy in GORD
1. Dysphagia 2. Age >55 3. Weight loss
87
Give the management of GORD
1. Lifestyle advice (lose weight, smaller and lighter meals) 2. Gaviscon & Rennie etc. 3. PPI 4. Ranitidine (as ALTERNATIVE to PPI if not tolerated) - e.g. H2 receptor antagonist
88
Describe the H. pylori bacterium
Gram -ve aerobic bacterium
89
Give the investigations for H. pylori
1. Urea breath test (no PPI for 2 weeks prior) - best for testing following eradication therapy 2. Stool antigen test
90
Give the management of H. pylori
Triple therapy: 1. PPI 2. Amoxicillin 3. Clarithromycin
91
Describe the pathophysiology of Barretts oesophagus
Constant reflux results in metaplasia - conversion of oesophageal squamous epithelium to columnar epithelium. Considered pre-malignant
92
Give the presentation of Barretts oesophagus
1. Improvement in GORD symptoms
93
Give the management of Barretts oesophagus
1. Major risk factor for oesophageal adenocarcinoma - regular endoscopy to identify early 2. PPI 3. Ablation treatment - destroys the epithelium so it is replaced with normal cells
94
Describe the pathophysiology of peptic ulcers
Ulceration of the gastric or duodenal mucosa, commonly caused by NSAIDs, steroids and H. pylori
95
Give the presentation of peptic ulcers
1. Epigastric discomfort/pain 2. N+V 3. Dyspepsia 4. Haematemesis ("coffee-ground" appearance) 5. Iron deficiency anaemia
96
Give the impact of eating on gastric/duodenal ulcers
Gastric: pain worsens Duodenal: pain improves
97
Give the management of peptic ulcers
Triple therapy (PPI + amoxicillin + clarithromycin) - if no H. pylori then PPI only
98
Give the diagnosis of peptic ulcer disease
Endoscopy (+ H. pylori testing)
99
Give the complications of peptic ulcer disease
1. Bleeding - may be life threatening 2. Perforation - may present with acute abdomen and peritonitis
100
Describe the boundaries of the upper GI tract
Mouth -> ligament of Treitz (in duodenum)
101
Give the causes of upper GI bleed
1. Oesophageal varices 2. Mallory-Weiss tear 3. Ulcers 4. Cancer
102
Give the presentation of an upper GI bleed
1. Haematemesis 2. Meleana 3. Haemodynamic instability
103
Give the management of an upper GI bleed
ABATED: A- ABCDE B- bloods (coagulation, crossmatch) A- access T- transfuse E- endoscopy D- drugs (stop anticoagulant and NSAID) Oesophagogastroduodenoscopy - provides interventions to stop bleeding
104
What features are seen in Crohn's but not UC
NESTS: N- no blood or mucus E- entire GI tract S- skip lesions T- transmural (full-thickness) S- smoking is a risk factor Anal strictures and fistulas are seen
105
Give the management of infected strictures/fistulas in Crohn's
Metronidazole
106
Give the features seen in UC but not Crohn's
CLOSEUP: C- continuous inflammation L- limited to colon and rectum O- only superficial mucosa affected S- smoking is protective E- excrete blood and mucus U- use aminosalicylates (e.g. mesalazine/sulfasalazine) P- primary sclerosing cholangitis Drainpipe colon on AXR
107
Give the presentation of IBD
1. Diarrhoea 2. Weight loss 3. Abdominal pain 4. Passing blood
108
Give the diagnostic investigations for IBD
1. Endoscopy with biopsy 2. Faecal calprotectin 3. CRP
109
Give the management of Crohn's for inducing remission
1st line: oral prednisolone/IV hydrocortisone 2nd line: steroids PLUS azathioprine/methotrexate/infliximab
110
Give the management of Crohn's for maintaining remission
1st line: azathioprine 2nd line: methotrexate/infliximab
111
Give the surgical management of Crohn's
Resection of distal ileum if affected in isolation
112
Give the management of UC for inducing remission
1st line: aminosalicylate (e.g. mesalazine) 2nd line: prednisolone If severe disease: 1st line: IV hydrocortisone 2nd line: IV ciclosporin
113
Give the management of UC for maintaining remission
1. Aminosalicylate (e.g. mesalazine) 2. Azathioprine
114
Give the surgical management of UC
Panproctocolectomy (removal of colon and rectum with permanent ileostomy)
115
Give the pathophysiology of IBS
Functional bowel disorder with no discernable organic cause i.e. abnormal functioning of an otherwise normal bowel
116
Give the presentation of IBS
1. Diarrhoea/constipation 2. Fluctuating bowel habit 3. Abdo pain/bloating/PR mucus Sx worst after eating and improved by opening bowels
117
Give the investigations for IBS
1. Faecal calprotectin - to exclude IBD 2. Anti-TTG - to exclude coeliac 3. Normal blood results otherwise
118
Give the management of IBS
1. Low FODMAP diet 2. Probiotic supplements 3. General healthy diet and exercise 4. Loperamide - for diarrhoea 5. Laxatives - for constipation (but avoid lactulose) 6. Hyoscine butylbromide - for cramps Can also give amitryptiline, SSRI or CBT
119
Give the pathophysiology of coeliac disease
Autoimmune condition in which exposure to gluten causes an autoimmune reaction resulting in inflammation of the small bowel
120
Give the antibodies involved in coeliac disease
1. Anti-TTG 2. Anti-EMA
121
Give the histological changes seen in coeliac disease
1. Villous atrophy 2. Crypt hyperplasia These lead to malabsorption
122
Give the presentation of coeliac disease
1. Anaemia - secondary to B12/iron/folate deficiency 2. Dermatitis herpetiformis - itchy blistering rash typically on the abdomen 3. Weight loss 4. Diarrhoea 5. Fatigue 6. Mouth ulcers 7. Failure to thrive in young children
123
Give the management of coeliac disease
Gluten-free diet
124
Give the investigations for coeliac disease
1. Anti-TTG + Anti-EMA + Total IgA (must compare to total IgA as in general IgA deficiency the other antibodies will also be reduced) 2. Endoscopy and intestinal biopsy Tests must be conducted while patient on a gluten-containing diet
125
Give the presentation of peritonitis
1. Guarding 2. Rigidity 3. Rebound tenderness 4. Percussion tenderness 5. Abdo pain on coughing
126
Give the three types of peritonitis
1. Localised - caused by underlying organ inflammation 2. Generalised - rupture of abdominal organ causes widespread inflammation 3. Spontaneous bacterial peritonitis - infection of ascites in a patient with liver disease
127
Give the pathophysiology of appendicitis
Pathogens become trapped in appendix due to obstruction, leading to inflammation, gangrene and rupture. If rupture occurs, faeces and infective material are released into the peritoneal cavity, causing a generalised peritonitis.
128
Give the presentation of appendicitis
1. Anorexia (not eating) 2. Abdo pain (initially central, then shifting to RIF) 3. N+V 4. Low-grade fever 5. Guarding 6. Rebiund tenderness 7. Percussion tenderness
129
Describe Rovsing's sign
Palpation of LIF causes pain in RIF Seen in appendicitis
130
Describe the location of McBurney's point
1/3 distance from ASIS to umbilicus Tenderness at this point suggests appendicitis
131
Give the diagnosis of appendicitis
Clinical picture alongside raised inflammatory markers USS and urine b-hCG - excludes ectopic pregnancy CT - excludes other causes if they are more likely
132
Give the management of appendicitis
Appendicectomy
133
Give the management of peritonitis
1. ABCDE 2. Nil by mouth (in case surgery needed) 3. NG tube (if bowel obstruction or vomiting) 4. IV fluids 5. IV Abx (e.g. tazocin in sepsis) 6. Analgesia 7. Blood crossmatch
134
Which oesophageal malignancy does Barrett's oesophagus increase the risk of?
Adenocarcinoma
135
Which oesophageal malignancy does achalasia increase the risk of?
Squamous cell carcinoma
136
Give 1 risk factor for C. diff infection
PPIs
137
Give the first line therapy for C. diff
Oral vancomycin
138
Give a histological sign of gastric adenocarcinoma
Signet ring cells

Finals (11 decks)

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