Gastrointestinal Flashcards

1
Q

What is the acute abdomen?

A

A sudden, severe onset of acute abdominal pain lasting less than 24 hours

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2
Q

What signs may indicate peritonitis?

A

Guarding or rigidity
Rebound tenderness
Absent bowel sounds

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3
Q

What is a complication of peritonitis?

A

Spontaneous bacterial peritonitis - spontaneous infection of the ascites in cirrhotic liver disease

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4
Q

What is the difference between localised and generalised peritonitis?

A

Localised - due to underlying organ inflammation such as appendicitis
Generalised - due to perforation such as peptic ulcer or ruptured appendix

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5
Q

What is the foregut border and supply?

A

Mouth to the major duodenal papilla

Coeliac axis - T12

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6
Q

What is the midgut border and supply?

A

Major duodenal papailla to 2/3 along the transverse colon

Superior mesenteric artery - L1

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7
Q

What is the hindgut border and supply?

A

Left 1/3 along the transverse colon to the upper anal canal

Inferior mesenteric - L3

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8
Q

What is a hernia?

A

Protrusion of a viscus or part of a viscus through a defect in the abdominal wall

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9
Q

What is the process of a hernia becoming strangulated?

A

Bowel through narrow neck may cause swelling and so an interrupted blood supply.
Capillary pressure increases - leaks into hernial cavity - increases the pressure - increased swelling and pressure - venous outflow reduced - stasis of blood - thrombosis - greater pressure - swelling - necrosis and death of bowel

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10
Q

What is a Richter’s hernia?

A

Strangulation of the bowel without obstruction.
One wall of the bowel is protruding through the weakness in the abdominal wall. Bowel contents can still pass through but the bowel can still become ischaemic and die

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11
Q

What are the borders of the inguinal cavity?

A

Roof - M - Transversus abdominis muscles and internal oblique muscle
Anterior - A - External and internal oblique aponeurosis
Lower - L - lacunar ligament and inguinal ligament
Posterior - T - Conjoint tendon and transveralis fascia

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12
Q

What are the types of oesophageal cancers and their associations?

A

Squamous - Can affect anywhere in the oesophagus, but more common in upper and middle 1/3 - associated with smoking and drinking, HPV, achalasia
Adenocarcinoma - Affects lower 1/3. GORD and obesity

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13
Q

What antibiotics might you give early in acute peritonitis?

A

IV metronidazole 500mg + Cefuroxime 750mg

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14
Q

What are the causes of upper GI perforations?

A
INVITED 
Infections - H.pylori
Neoplasm - Gastric carcinoma
Vascular - inflammatory or AI
Iatrogenic - ERCP or OGD
Traumatic - stab wound 
Endocrine - Zollinger Ellison syndrome 
Drugs - NSAIDs
Chemicals - batteries
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15
Q

What organisms are commonly involved in intra-abdominal abscesses?

A

Anaerobes, E.coli, klebsiella, enterococcus

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16
Q

What is the definitive management for an intra-abdominal abscess?

A

IV antibiotics if septic - Amox + met + gent
Radiologically guided US or CT drainage
Open surgical drainage if ^ not possible or safe

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17
Q

What are the first line antibiotics in spontaneous bacterial peritonitis?

A

IV Tazobactam with piperacillin 4.5g/8h

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18
Q

What triad may be seen in cholangitis? (Inflammation of the biliary tree)

A

Charcot’s triad - Jaundice, RUQ pain, fever

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19
Q

What pentad may indicate Acute suppurative Cholangitis?

A

Reynold’s - Jaundice, Fever, RUQ pain, hypotension, confusion

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20
Q

What is Mirizzis syndrome?

A

Obstructive jaundice
Caused by extrinsic compression of an extra hepatic biliary duct from one or more calculi in the cystic duct or GB. Can present with biliary duct dilation and can mimic e.g. cholangiocarcinoma

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21
Q

What type of pancreatic cancer is most common?

A

Adenocarcinoma of the head of the pancreas

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22
Q

What tumour marker indicates pancreatic cancer?

A

CA19-9

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23
Q

What might cause raised amylase?

A
Acute pancreatitis
Ectopic pregnancy
Bowel perforation
Mesenteric ischaemia
DKA
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24
Q

What scale can be used to assess acute pancreatitis?

A
PANCREAS Glasgow scale/Imrie scale
PaO2 < 60
Age > 55
Neutrophils (WCC >15)
Calcium < 2
uRea > 16
Enzymes (LDH > 600 or ALT/AST >200)
Albumin < 32
Sugar > 10
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25
Q

What are some local complications of acute pancreatitis?

A
Pancreatic pseudocyst
Pancreatic necrosis 
Pancreatic abscess
Infected pancreatic necrosis
Gastric outlet obstruction
Haemorrhage 
Portal vein thrombosis
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26
Q

What are some distant complications of acute pancreatitis?

A
Hypotension/ shock
Renal failure, liver failure, multi organ failure
Infection
Respiratory failure 
Ileus
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27
Q

What structural changes occur in chronic pancreatitis?

A

Calcification, fibrosis and atrophy

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28
Q

What are some complications of chronic pancreatitis?

A

Ascites, Pancreatic pseudocysts, pancreatic cancer, diabetes

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29
Q

What are some causes of upper GI bleeding?

A
Mallory-Weiss tear 
Oesophgeal varices
Stomach or duodenal ulcer
Stomach or duodenal cancer
Gastritis 
GORD
Angiodysplasia
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30
Q

What score establishes the risk of having an upper GI bleed?

A

Glasgow-blatchford scale

Drop in Hb, rise in urea, Bp, HR, syncope, meleana

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31
Q

How would you manage an upper GI bleed?

A

ABATED
A-E assessment and immediate fluid resuscitation
Bloods - FBC, Xmatch, LFTs, U&Es (Urea), CRP, INR, clotting
Access - 2 large bore cannula - for fluids, give O2
Transfuse when Hb <7-8g/dL (FFP/platlets/prothrombin complex concentrate)
Endoscopy (adrenaline injection/banding of varies/ heater probe/ sengstaken tube/ surgery)
Drugs - STOP NSAIDs and anticoagulants

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32
Q

What is first line management in acute variceal bleeding?

A

Resus - IV fluids, transfuse <7g/dL
*Antibiotics (Ceftriaxone or Ciprofloxacin) + Terlipressin (Vasoactive drug) EARLY
Endoscopic banding 1st line for varices
TIPS or sengstaken tube for uncontrolled bleeding

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33
Q

Dysphagia can be split into 2 main causes, what are they?

A

Oesophageal - inability to pass food or liquid down the oesophagus
Oropharyngeal - Difficulty initiating swallowing - coughing on swallowing, nasal regurgitation, choking

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34
Q

What are the possible causes of inability to pass solid food only down the oesophagus?

A

Mechanical obstruction -
Progressive? (>50? weight loss?) – Carcinoma. (Heart burn?) - peptic stricture
Inermittent? - lower oesophageal ring dysfunction

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35
Q

What are the possible causes of inability to pass solid and liquids down the oesophagus?

A

Neuromuscular disorder -
Intermittent - Diffuse oesophageal spasm
Progressive - (reflux sx?) - Scleroderma. Achalasia

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36
Q

What are the possible causes of dysphasia where there is trouble initiating swallowing?

A

Neuro - Bulbar plasy
Muscular - Myasthenia gravis, muscular dystrophy
Structural - Thyromegaly

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37
Q

What may be the problem in a patient presenting with dysphagia who has a neck bulge and gurgling noise occurs on drinking?

A

Pharyngeal pouch

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38
Q

What causes corkscrew appearance on a barium swallow?

A

Diffuse oesophageal spams - intermittent - both solids and liquids
Usually with chest pain
Multifocal high amplitude contractions possibly due to dysfunction of the inhibitory neurones.

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39
Q

What might cause a patient to present with odynophagia, dysphagia, mouth thrush and white spots on endoscopy?

A

Oesophageal candidiasis - in immunocompromised patients due to candid albicans.
Tx - Fluconazole 50mg for 7-14 days

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40
Q

What is Achalasia?

A

Motility disorder due to progressive destruction of the ganglion cells in the myenteric plexus.
Failure of the lower oesophageal sphincter to relax and progressive failure of smooth muscle contraction

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41
Q

What investigations might you do in suspected achalasia?

A

Endoscopy
*Oesophgeal Manometry - Absence of peristalsis, Higher lower oesophageal resting tone and failure of the lower sphincter to relax.
Barium swallow - Bird beak appearance.

Tx - Ca channel blockers or nitrates or Laproscopic hellers myotomy or balloon dilation

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42
Q

What is a pharyngeal pouch?

A

Zenker’s diverticulum
Uncoordinated swallowing movement cause herniation through the cricopharyngeal muscle
Chronic cough, neck lump, gurgling, hoarse voice, halitosis, aspiration, regurgitation

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43
Q

What are some ALARMing symptoms in peptic ulcer disease?

A
Iron deficiency Anaemia
Loss of weight
Anorexia 
Recent onset/progressive symptoms
Melaena and coffee ground vomit - haematemesis 
Dysphagia
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44
Q

What triple therapy is used in H.pylori?

A

PPi + amoxicillin + Clarithromycin or metronidazole 7 days PO

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45
Q

Give some features of diffuse gastric cancer?

A

Mainly affects cardia. Associated with GORD
Individuals malignant cells with mucin vacuoles (signet ring cells)
Can invade extensively but not seen well endoscopically - Linitis plastica
Mets to ovaries - Krunkenberg tumour, Mets to umbilicus - sister Mary Jospeh nodule, mets to stomach - Virchows node, mets to pouch of douglas - Blumer’s shelf

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46
Q

Where does coeliac disease affect?

A

Small bowel - particularly the jejunum

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47
Q

What is the genetic link to coeliac disease?

A

HLA-DQ2/8

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48
Q

What antibodies are found in coeliac and what must you test before checking for these?

A

Anti-TTG - Anti-tissue transglutaminase
Anti-EMA - Anti-endomysial antibody
These will rise if the disease is active and may disappear with effective treatment
Check for an IgA deficiency

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49
Q

What are some complications of untreated coeliac disease?

A
Vitamin deficiency 
Anaemia 
Osteoporosis
Enteropathy associated T cell lymphoma of the intestines
NHL
Small bowel adenocarcinoma
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50
Q

What diseases are associated with coeliac?

A
Dermatitis herpitiformis (itchy blistering skin rash typically on the abdomen)
T1DM
IgA deficiency
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51
Q

What are some signs of GI malabsorption?

A
Anaemia (low Fe, B12 or folate)
Bleeding disorders (Low Vitamin K - Longer INR)
Metabolic bone disease (low Vitamin D)
Neuropathy (low Ca)
Oedema (low protein)
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52
Q

What is refractory coeliac disease?

A

Recurrent malabsorptive symptoms and villous atrophy despite being on a strict gluten free diet for at least 6-12 months in the absence of another cause of non-responsive treated coeliac disease and overt malignancy
Can try steroids - Azathioprine

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53
Q

What are some features of intestinal type gastric cancer?

A

Due to H.pylori
Distal stomach affected - body and antrum
Pangastritis can lead to it/ atrophic gastritis
Ulcerated growth

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54
Q

A complication of a gastrectomy is dumping syndrome, what is this?

A

Sudden and large passage of hypertonic gastric fluid into the small bowel causing large intraluminal fluid shifts causing nausea, diarrhoea, hypovolaemia and intestinal distention,

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55
Q

What liver function test may indicate excess alcohol?

A

AST:ALT ratio >1.5

56
Q

What are some characteristic features of alcoholic hepatitis and what scoring system can be used?

A

Hepatomegaly ± fever ± leucocytosis ± hepatic bruit

Glasgow Alcoholic hepatitis score - age, WCC, urea, PT/INR, bilirubin

57
Q

What is non-alcoholic fatty liver disease?

A

A metabolic syndrome with problems with processing and storing energy increasing the likelihood of heart disease, stroke and diabetes
Can progress to hepatitis and cirrhosis

58
Q

What investigations might you do in suspected NAFLD?

A
US of liver 
Hepatitis B and C serology
Alpha 1 antitrypsin levels 
Immunology/autoantibodies (anti-mitochondiral in PBC, Anti-smooth muscle in AI hepatitis, Anti-nuclear in SLE)
Ferritin and transferritin levels (HH)
59
Q

What is acute on chronic liver failure?

A

When a patient with chronic liver disease such as cirrhosis has an acute decompensation due to a varity of causes such as:
Infection - SBP, pneumonia, skin infection
Hepatotoxic insult - alcohol, hepatitis, drugs
Hypoglycaemia or electrolyte disturbance

60
Q

What are some features of acute decompensation in acute on chronic liver disease?

A

Encephalopathy, ascites, oedema, jaundice, fever

61
Q

What is hepatic encephalopathy?

A

A neuropsychiatric disorder affecting cognitive function in acute-on-chronic liver disease

62
Q

What clinical signs may indicate hepatic encephalopathy and what is the treatment?

A

Asterixis, altered conscious level
Type ! - anxiety, lack of awareness and shortened attention span
Type II - ataxia, lethargy, subtle personality changes, inappropriate behaviour
Type III - gross disorientation, confusion, seizures
Type IV - Completely unresponsive, coma

Give Lactulose (10-15ml) - binds ammonia to stool

63
Q

In acute alcohol withdrawal when might symptoms first show?

A

~ 8 hours after withdrawal

Shaking, sweating, tremor, anxiety, N&V

64
Q

When do symptoms start to peak in acute alcohol withdrawal and what might they be? (think of severe Sx)

A

24-72 hours after withdrawal

Delirium tremens, hallucinations, seizures- tonic clonic

65
Q

What is a serious possible complication of acute alcohol withdrawal?

A

Delirium tremens - usually 3-4 days after withdrawal. Sudden onset confusion -
Agitation, tremor, confusion, hallucinations
altered cognition and vital signs *
Respiratory alkalosis, wernicke-korsakoff psychosis

Tx - Benzodiazepines, IV fluids, Antipsychotics

66
Q

What syndrome occurs in acute thiamine deficiency?

A

Wernicke-korsakoff syndrome: Triad -
Ophthalmoplegia, ataxia (cerebellar), confusion
Diagnosis: Reduced Red cell transketolase activity

Give IV thiamine

67
Q

What is the tumour marker for hepatocellular cancer?

A

Alpha fetoprotein

68
Q

What scoring systems can be used to asses severity in cirrhosis?

LFTs often normal in cirrhosis

A

Childs-turcotte-pugh score for severity- Encephalopathy, bilirubin, ascites, albumin, PT
MELD - Gives a % 3 month mortality- used every 6months for patients with compensated cirrhosis

69
Q

How might you diagnoses spontaneous bacterial peritonitis?

A

Ascitic diagnostic tap
Cell count: WCC > 500/cm3 ± Neutrophils >250/cm3
Albumin: serum ascitic albumin gradient = serum albumin - ascitic albumin g/L
HIGH SAAG = liver cause - portal hypertension
Low SAAG = malignancy, trauma, infection

70
Q

What is fulminant hepatic failure?

A

A potentially reversible severe liver injury with the onset of hepatic encephalopathy within 8 weeks of the appearance of the first symptom with no history of pre-existing liver disease

71
Q

What is the difference between hyperacute, acute and sub-acute liver failure?

A

Hyperacute is Hepatic encephalopathy within 7 days of jaundice
Acute is HE within 8-28 days of jaundice
Sub acute is HE within 29-84 days of jaundice

72
Q

What is the definition of acute liver failure and the criteria?

A

Potentially reversible severe liver injury, with an onset of HE within 8 weeks of the first symptoms in the absence of pre-exisitng liver disease.
INR >/= 1.5
Neurocognitive disturbance with any degree of hepatic encephalopathy
No pre-exisitng liver disease
Disease course = 26 weeks

73
Q

What are the grades of hepatic encephalopathy?

A

Grade 1 - Drowsy but coherent: mood changes
Grade 2 - Drowsy, confused at times, inappropriate behaviour
Grade 3 - Very drowsy, stuporous but rousable, or restless and screaming
Grade 4 - Comatose - barely rousable

74
Q

What do you give in a paracetamol overdose?

A

N-acetylcysteine

75
Q

In acute liver failure, what treatment can you give for a prolonged PT?

A

IV vitamin K 10mg ONCE

76
Q

In acute liver failure what could you give for cerebral oedema?

A

Mannitol 100ml 20%

ICP monitoring

77
Q

What treatment could you give if Wilsons disease was causing acute liver failure?

A

Penicillamine and IV vit E

78
Q

Where might you get Hepatitis A and what is the management?

A

Travel related. Faecal oral route. Shed via biliary tree into gut. Usually always acute.
Can cause Acute liver failure.
Tx - Maintain hydration, avoid alcohol, self-limiting
Vaccine - inactivated virus

79
Q

What is special about Hepatitis E?

A

Can cause neurological symptoms - Guillain barre syndrome, ataxia, myopathy
Tx - Ribavirin

80
Q

Hepatitis B is diagnosed if sAg or DNA is detectable for it, what does HBV DNA mean/indicate?

A

Viral load count

81
Q

How would you manage chronic Hep B infection (HBaAg or HBV DNA detected >6months)

A

Suppress viral replication and prevent further liver damage
Immune-modulatory - Interferon
Suppress viral replication - Tenofovir or Entecavir

82
Q

What is special about Hepatitis D?

A

Requires Hepatitis B to survive and replicate

Tx - Peg IFN

83
Q

How can you distinguish Hep C?

A

Extra-hepatic manifestation such as fatigue, depression, diabetes, neuropathy, CVD, cancer
Tx- Direct acting antivirals PO 8-12wks (Ribavirin + Peg IFN)

84
Q

What is IBS?

A

A mixed group of abdominal symptoms in which no organic cause can be found.

85
Q

What is the diagnostic criteria for IBS?

A

Abdominal pain/ discomfort
Relieved by defecation or associated with an altered bowel frequency to altered stool
AND >/=2 of:
Urgency, abdominal bloating, incomplete evacuation, mucous PR, worsening of Sx after food

86
Q

What is an adenomatous polyp?

A

A true neoplastic polyp formed by excessive growth of the colorectal epithelium

87
Q

What is Familial adenomatous polyposis?

A

AD mutation in APC gene on chromosome 5

Characterised by thousands of adenomatous polyps in the colorectum and increased formation in the stomach and duodenum.

88
Q

What is hereditary non-polyposis colorectal cancer?

A

AD mutation in the mismatch repair gene (MMR) which predisposes to increased genetic defects to acquire in the polyps.
Increased risk of other cancers: Ovarian, stomach, hepatobiliary, brain, upper urinary tract

89
Q

What is feacal calprotectin?

A

Calcium binding protein, predominantly derived from neutrophils

90
Q

What is Crohns disease?

A

A chronic transmural granulomatous inflammatory disease affecting the entire gut, from mouth to anus.
Most common site - ileum and colon

91
Q

What can help distinguish between crohns and UC?

A

Anti-saccharomyces cerevisae antibodies (ASCA)

92
Q

What biological agents can be used in Crohns?

A

Anti-TNF - adalimumab, Infliximab
Anti-integrins - alpha4beta7 Vedolizumab
Anti-IL12/23 - Ustekinumab

93
Q

What score can be used in the endoscopic findings of Crohns?

A

Rutgeerts

94
Q

What is first line in Crohns disease?

A

Steroids - PO 20-40mg Prednisolone or IV hydrocortisone

2nd line - PO 2-2.5mg/kg Azathioprine or 6-mercaptopurine

95
Q

What drugs are used in the remission of Crohns?

A

Azathioprine or 6-mercaptopurine

2nd line - biologics

96
Q

What is the most common type of colorectal cancer?

A

Adenocarcinoma of rectum

Usually on the LEFT

97
Q

What staging is used in colorectal carcinoma?

A
Dukes staging
A- confined to the mucosa
B - infiltrated the muscular wall
C- local lymph node spread
D - distant mets
98
Q

What is the most common site of diverticulitis?

A

Sigmoid colon

LIF pain

99
Q

What might AF and abdominal pain indicate?

A

Mesenteric ischaemia

100
Q

What is the most common cause of SBO and LBO?

A

SBO - adhesions

LBO - cancer

101
Q

What is rigler’s triad?

A

For gall stone ileus, in the remnant of the vitelline intestinal duct, 20cm from terminal ileum
Pneumobilia
Radiolucent gall stones
SBO

102
Q

What is the triad seen in serotonin syndrome?

A
Autonomic instability (HTN, excessive sweating, mydriasis, hyperthermia, tachycardia)
Mental status change (anxiety, confusion, coma)
Neuromuscular features (clonus, hypertonicity, hyperreflexia)
103
Q

Kings criteria is used in paracetoamol overdose to determine the need for a liver transplant. Explain the criteria.

A

pH < 7.3 or lactate > 3mmol/L following resus OR

AKI/ Creatinine >300 + INR > 6.5/ PT>100s + grade 3/4 encephalopathy

104
Q

Describe paracetamol metabolism in a paracetamol overdose.

A

In an overdose the enzymes used to metabolism paracetamol become saturated and so it is metabolised a different way and becomes NAPQI.
NAPQI is a toxic metabolite but is inactivated by glutathione. When Glutathione becomes saturated NAPQI is free in its toxic form and causes necrosis.
N-acetyl-cycteine works to restore glutathione

105
Q

What could you give in a methanol or ethylene glycol overdose?

A

Ethanol

Competitively blocks the formation of toxic metabolites by having a higher affinity for alcohol dehydrogenase

106
Q

What could you give in a beta blocker overdose?

A

High dose Insulin therapy

107
Q

What could you give in a calcium channel blockers overdose?

A

6g IV Calcium gluconate over 5-10min or in severe overdose high dose insulin therapy

108
Q

What could you give in a benzodiazepine overdose?

A

Flumazenil

109
Q

What could you give in a TCA overdose?

A

Hyperosmolar sodium bicardonate
(used in drugs that impair fast acting Na channels)

for any drug ingestion <1 hr - activated charcoal

110
Q

What could you give in a digoxin overdose?

A

Digi bind

111
Q

What is Riglers sign?

A

Double wall sign - Due to there being intraluminal and extraluminal free gas

112
Q

What signs might present on AXR in a patient with UC?

A

Thumb printing in an acute presentation due to mucosal thickening and oedema of the haustra
Lead pipe colon in chronic presentation, loss of normal haustra
Toxic megacolon, life threatening dilation without obstruction and systemic response

113
Q

What is a key finding that would indicate an intra-abdominal abscess?

A

Swinging fever** - usually over 38.5 degrees occurring twice a day, followed by tachycardia

114
Q

What are some causes of chronic gastritis?

A

ABC
Autoimmune - Pernicious anaemia
Bacteria - H.pylori - High IL-8 - pangastritis or low IL-8-antra-predominant gastritis
Chemical - NSAIDs, bile reflux, ethanol, oral iron

115
Q

Adenocarcinoma is the most common type of gastric carcinoma, what are the classifications of gastric cancer?

A

Diffuse - associated with GORD, affects cardia
Intestinal - associated with H.pyloir. Affects antrum and body. Associated with Pangastritis as there are high levels of IL-8, hypochloridia, atrophic gastritis, intestinal metaplasia, dysplasia and then cancer

116
Q

What is cholangitis?

A

Infection of the biliary tree (CBD), due to outflow obstruction and infection.
(stone, stricture, post-ERCP, cholangiocarcinoma)
Ecoli, enterococcus, klebsiella

117
Q

What does it mean for acute pancreatitis to be mild moderate or severe?

A

Mild - no organ failure to local or systemic complciations
Moderate - organ failure lasting less than 48 hours ± local or systemic complications without persistent organ failure
Severe - single or multi organ failure

118
Q

What triad is seen in wernickes encephalopathy?

A

Opthalmoplegia, ataxia, cognitive impairment

119
Q

What are some causes of cirrhosis?

A

Drugs - methotrexate, amiodarone
Alcohol - Alcoholic hepatitis, alcoholic fatty liver
Metabolic - Non-alcoholic fatty lover disease or Non-alcoholic steatohepatits
Inherited - HH, Wilson’s, alpha1 antitrypsin def
AI - AI hepatitis, PBC, primary sclerosing cholangitis
Infection - Hep B or C

120
Q

Before you do an ascitic tap what do you need to know and where do you perform the tap?

A

INR < 1.5, Platelets > 50

3-5cm under umbilicus or 5cm superiomedially from ASIS

121
Q

Explain how you would interpret serum albumin ascites gradient?

A

If its hight, ie more serum albumin - Traunduate - due to portal hypertension - cirrhosis, hepatic failure, portal vein thrombosis, alcoholic hepatitis
If low, ie more ascitic albumin - exudate - infection or malignancy - TB, malignancy, pancreatitis, nephrotic syndrome, bowel obstruction

122
Q

What is primary sclerosing cholangitis?

A

AI liver disease. Causes Cholestasis due to progressive fibrosis of the intra and extra hepatic ducts.
Can eventually cause cirrhosis or cholangiocarcinoma
LFTs show obstructive picture with raised ALP
May be ANCA +ve
Associated with IBD - UC

123
Q

How might you differentiate PBC and PSC?

A

PBC - Interlobular bile ducts destroyed. 10F>M, 50-60y, anti-mitochondrial antibodies
PSC - Intra and extra hepatic ducts, 2M>F, 30-40y, ANCA, IBD

124
Q

List some anatomical features of crohns and UC.

A

UC - Loss of haustra, perudopolyps
Crohns - Fat wrapping, cobble stoning, thick walls, strictures (can cause obstruction in a virgin abdomen), ulcers, fissures

125
Q

What are some clinical signs of cirrhosis ?

A

Caput medusa, spider naevi, palmer erythema, SBP, splenomegaly, bruising, gynaecosmatsia, malnourished, asterixis

126
Q

What is decompensated liver cirrhosis?

A

Acute deterioration in liver function in patients with cirrhosis.
Jaundice, ascites, hepatic encephalopathy, sepsis, renal impairment, GI bleeding

127
Q

What are some precipitants of decompensation in cirrhosis?

A

GI bleeding, constipation, dehydration, infection/sepsis, Alcoholic hepatitis, HCC, acute portal vein thrombosis, drugs (alcohol, NSAIDs, opiates), ischaemic liver injury

Complete BASL bundle within 6 hours of admission

128
Q

In the BASL bundle for decompensated cirrhosis what might you give if there is a Hx of alcohol excess?

A

IV Pabinex
Fixed dose and symptoms triggered tx
Use LORAZEPAM instead of diazepam - slower onset but rapid elimination of metabolites not impaired in liver disease

129
Q

How would you manage a patient if the ascitic tap had >250cells/mm3 PMN?

A

IV antibiotics according to protocol
IV amoxicillin + Temocillin
or if penicillin allergic - IV Ciprofloxacin + Vancomycin
IV albumin - 100ml 20% albumin

Long term prophylaxis if indicated - Co-trimoxazole, Rifaxamin***

130
Q

In decompensated cirrhosis they use the BASL bundle, what are the 7 areas looked at?

A
  1. Investigations
  2. Alcohol - Pabrinex, lorazepam
  3. Infections - SBP? albumin and Abs
  4. AKI - fluid resus, stop nephrtoxins
  5. GI bleeding - terlipressin + Abx, IV Vit K? FF? plts? transfusion?
  6. Encephalopathy - Lactulose
  7. Other - VTE prophylaxis
131
Q

What drug can be given in patients who have had an episode of HE to prolong remission and reduce hospital admission?

A

Rifaximin

Decreases production and absorption of ammonia

132
Q

What are the grades of HE?

A
Cerebral oedema
Spikes in HTN
Deconjugated eye movements 
Papilloedema 
If not treated -- Decerebrate posturing and brainstem coning
133
Q

What is the criteria for a liver transplant in acute liver failure?

A

Paracetamol OD with pH <7.3
Grade 3/4 encephalopathy AND PT > 100s

Or ALL 3 of
PT > 100s, Cr >300microM, grase 3-4 HE

134
Q

What drugs can cause hypotension with bradycardia syndrome?

A

BB, Ca channels, digoxin

135
Q

What test would you do in a 18year old male with suspected appendicitis?

A

CT abdo/pelvis - are the suitable for conservative management - IV antibiotics
Laparoscopy
(US would not move you forward - in females as looking at gynae pathology too)