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Phase1c Medicine > Gastroeneterology > Flashcards

Gastroeneterology Flashcards

1
Q

What is the secondary prophylaxis of Hepatic encephalopathy?

A

Lactulose and rifaximin

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2
Q

What is the first-line management for hepatic encephalopathy?

A

Lactulose

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3
Q

What are the features of autoimmune hepatitis?

A

Present with signs of chronic liver disease

Acute hepatitis: Fever, jaundice

Amenorrhoea

ANA/SMA/LKM1 antibodies, raised IgG levels

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4
Q

What is the management of autoimmune hepatitis?

A

Steroids

Immunosuppressants - Azathioprine

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5
Q

What autoantibodies are associated with type autoimmune hepatitis?

A

Anti-nuclear (ANA)

Anti-smooth muscle (SMA)

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6
Q

What screening investigation is performed in haemochromatosis?

A

Transferrin saturation

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7
Q

What is the presentation of haemochromatosis?

A

Bronze tint of the skin
Chondrocalcinosis of the finger joints
Raised glucose
Liver disease

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8
Q

Which gene is associated with haemochromatosis?

A

HFE gene

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9
Q

What is the typical iron study profile in a patient with haemochromatosis?

A

Transferrin saturation raised
Raised ferritin
Low TIBC

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10
Q

What is the first-line management of haemochromatosis?

A

Venesection is the first-line management

Desferrioxamine is second line

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11
Q

Which criteria is used in the diagnosis of IBS?

A

Rome criteria

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12
Q

What is the presentation of IBS?

A 
altered stool passage (straining, urgency, incomplete evacuation)
abdominal bloating (more common in women than men), distension, tension or hardness
symptoms made worse by eating
passage of mucus
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13
Q

What is the Rome IV diagnostic criteria for IBS?

A

Recurrent abdominal pain for >3 months with 2 of the following:

1) Related to defecation
2) Associated with a change in frequency of the stool
3) Associated with a change in form (appearance)

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14
Q

What medication is used to induce remission in Crohn’s disease?

A

Prednisolone

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15
Q

What are the presenting features of oesophageal varices?

A

Usually a large volume of fresh blood. Swallowed blood may cause melena. Often associated with haemodynamic compromise. May stop spontaneously but re-bleeds are common until appropriately managed.

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16
Q

What are the presenting features of a Mallory-Weiss tear?

A

Typically brisk small to moderate volume of bright red blood following a bout of repeated vomiting. Malena rare. Usually ceases spontaneously.

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17
Q

What is the management of variceal bleeding?

A

terlipressin and prophylactic antibiotics should be given to patients at presentation (i.e. before endoscopy)
band ligation should be used for oesophageal varices and injections of N-butyl-2-cyanoacrylate for patients with gastric varices
transjugular intrahepatic portosystemic shunts (TIPS) should be offered if bleeding from varices is not controlled with the above measures

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18
Q

What is Peutz-Jeghers Syndrome?

A

Numerous hamartomatous polyps in the GI tract

Pigmented freckles on he lips, face, palms and soles

Intestinal obstruction

GI bleeding

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19
Q

What is the investigation of choice for suspected perianal fistulae in Crohn’s?

A

MRI pelvis

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20
Q

What is administered to induce remission in a severe acute exacerbation of UC?

A

Intravenous corticosteroids

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21
Q

Per the Truelove and Witt’s criteria how many bowel motions is associated with severe UC?

A

> 6 bowel motions a day with blood and fever

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22
Q

What drug is used to maintain remission in UC?

A

Methotrexate

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23
Q

What is administered to induce remission in moderate-mild flares of UC?

A

Oral corticosteroid

Oral or topical Sulfalazine

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24
Q

Melanosis coli is associated with what?

A

Associated with laxative abuse (Senna)

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25
Q

What is the presentation of melanosis coli on histology?

A

Disorder of pigmentation of the bowel wall, histology demonstrates pigment-laden macrophages

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26
Q

What complication of UC is associated with cholestasis?

A

Primary sclerosing cholangitis

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27
Q

Isoniazid therapy can cause what type of vitamin deficiency?

A

B6 deficiency causing peripheral neuropathy

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28
Q

What is the first-line investigation of Budd-Chiari syndrome?

A

Ultrasound with Doppler flow studies

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29
Q

What is GORD?

A

Gastro-oesophageal reflux disease is defined as the inflammation of the oesophageal lining due to the reflux of gastric contents into the oesophagus and oral cavity.

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30
Q

What is the pathophysiology of GORD?

A
  • Increased frequency of transient lower oesophageal sphincter relaxation.
  • Decreased resting LOS pressure
  • Reduced saliva production (Xerostomia) – disturbs pH clearance leading to increased irritation of mucosal oesophageal lining.
  • Abnormal peristalsis  Reduced volume clearance.
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31
Q

What is the definition of a sliding hiatal hernia?

A

In a sliding hiatal hernia, the stomach is distended through the diaphragm superiorly, increasing gastric acid reflux into the distal oesophagus and gastroesophageal junction.

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32
Q

What is the definition of a rolling hiatus hernia?

A

In a rolling hiatus hernia, the gastroesophageal junction is intact, the herniated portion of the stomach is alongside the oesophagus.
• Surgical emergency because the stomach can become ischaemic.
• Barium swallow shows barium in the fundus of the stomach superior to the diaphragm.

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33
Q

What is the presentation fo GORD?

A

Heart-burn - Post-prandial burning sensation in the chest

Aggravated by:

  • Lying supine
  • Bending
  • Large meals
  • Drinking alcohol

Waterbrash
Aspiration
Dysphagia

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34
Q

What is waterbrash?

A

Regurgitation of an excessive accumulation of saliva from the lower part of the oesophagus

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35
Q

What are the symptoms of aspiration pneumonia?

A

Hoarseness, laryngitis, nocturnal cough, and wheee

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36
Q

What are the investigations for GORD?

A

Clinical diagnosis

OGD & biopsy

24-48 ambulatory pH monitoring

Oesophageal manometry

Barium swallow

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37
Q

What is the first-line management for GORD?

A

20mg PPI (Omeprazole) for initial course of 8 weeks

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38
Q

What are the surgical management for GORD?

A
  • Dilatation peptic strictures

* Laparoscopic Nissen’s fundoplication.

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39
Q

What lifestyle changes are made for GORD?

A 
o	Weight loss
o	Elevating head of bed
o	Avoiding provoking factors
o	Smoking cessations
o	Lower fat meals and avoiding large meals in the evening.
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40
Q

What are the two types of oesophageal cancer?

A

Adenocarcinoma

Squamous cell carcinoma

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41
Q

What cell type is implicated in adenocarcinoma?

A

Columnar glandular epithelium

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42
Q

Which type of oesophageal cancer is more prevalent in developing countries?

A

Squamous cell carcinoma

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43
Q

Which type of oesophageal cancer is more prevalent in the Western world?

A

Adenocarcinoma

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44
Q

What are the risk factors for squamous cell carcinoma?

A 
Alcohol 
Tumour 
Plummer-Vinson syndrome  
Achalasia
Scleroderma 
Coeliac disease 
Nutritional deficiencies
 Dietary toxins (e.g., nitrosamines – cured meats, pickles)
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45
Q

What are the risk factors for adenocarcinoma?

A

GORD

Barrett’s oesophagus

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46
Q

What is the most common presenting complaint for oesophageal cancer?

A

Dysphagia

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47
Q

How does dysphagia present in oesophageal cancer?

A

Dysphagia for solids progressing to liquids.

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48
Q

What is the presentation for oesophageal cancer?

A

Odynophagia- Pain on swallowing

Weight loss

Hoarseness - Upper oesophageal tumous can impinge the recurrent laryngeal nerve

Dysphagia

Regurtiation

Cough

Fatigue

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49
Q

What are the metastatic signs in oesophageal cancer?

A

Supraclavicular lymphadenopathy
Hepatomegaly
Hoarseness
Signs of broncopulmonary involvement

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50
Q

What is the first-line investigation for Oesophageal cancer?

A

OGD with biopsy

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51
Q

What is the most common site of squamous cell carcinomas within the oesophagus?

A

Upper two-thirds of the oesophagus

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52
Q

What is the most common site of adenocarcinomas within the oesophagus?

A

Lower 1/3 of oesophagus

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53
Q

What is the preferred modality for regional staging of oesophageal cancer?

A

Endoscopic ultrasound

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54
Q

What radiological modality is used to stage oesophageal cancer?

A

CT chest and abdomen

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55
Q

What is the definitive management for stage 0 or initial stage oesophageal cancers?

A

Endoscopic resection w/wo mucosal ablation (radiofrequency)

Oesophagectomy

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56
Q

What type of oesophagectomy is performed in the management of oesopahgeal cancer?

A

Ivor-Lewis type oesophagectomy

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57
Q

Define acute cholangitis?

A

Acute cholangitis is an infection of the biliary tree

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58
Q

What is the aetiology of acute cholangitis?

A

Due to obstruction of the gallbladder or bile duct due to gall stones

  • ERCP
  • Tumours
  • Bile duct strictures or stenosis
  • Parasitic infection
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59
Q

What type of bacteria is associated with ascending cholangitis?

A

Enteric bacteria - E.coli, Klebsiella, Entercoccous

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60
Q

What is the presentation of ascending cholangitis?

A

Charcot’s triad of symptoms

  • RUQ pain and tenderness
  • Jaundice
  • Fever with rigors

Pruritus
Pale stools

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61
Q

What is Charcot’s triad?

A

RUQ pain and tenderness
Jaundice
Fever

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62
Q

What is Reynold’s Pentad?

A 
Mental confusion
Septic shock-hypotension
-RUQ pain 
-Jaundice
-Fever
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63
Q

What is the first-line diagnostic investigation for ascending cholangitis?

A

Abdominal ultrasound - stones and dilatation of the common bile duct

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64
Q

What blood test findings are seen in ascending cholangitis?

A

Raised inflammatory markers - CRP/ESR

-LFTs - Hyperbillurubinaemia, raised serum transaminases, and alkaline phosphatase

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65
Q

What is the first-line management for ascending cholangitis?

A

Intravenous broad-spectrum antibiotics + rehydration using saline bolus fluid

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66
Q

What is the definitive management for ascending cholangitis?

A

Endoscopic retrograde cholangiopancreatography (ERCP) after 24-48 hours to relieve any obstruction

Cholecystectomy is there are underlying gallstones

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67
Q

What is acute cholecystitis?

A

Inflammation of the gallbladder predominantly due to an impacted gallstone obstruction within the cystic duct or gallbladder neck

-Bile stasis and mucous production can result in gallbladder distension

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68
Q

What is the presentation of acute cholecystitis?

A 
Constant RUQ pain 
Tenderness in RUQ
Palpable mass
Fever
Nausea
Right shoulder tip pain 
Localised peritonism

Guarding
Rebound tenderness
Murphy’s sign positive

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69
Q

What is Murphy’s sign positive?

A

Right hypochondrial tenderness worsens on inspiration.

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70
Q

What is the gold-standard investigation for acute cholecystitis?

A

Abdominal ultrasound of the biliary tree

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71
Q

What does an abdominal ultrasound reveal in acute cholecystitis?

A
  • Pericholecystic fluid
  • Distended gallbladder
  • Thickened gallbladder wall (>3mm)
  • Gallstones
  • Positive sonographic Murphy’s Sign
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72
Q

What does an FBC reveal in acute cholecystitis?

A

Neutrophilia

And moderate leucocytosis

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73
Q

Deranged LFTs in acute cholecystitis may suggest what?

A

Deranged LFTs may indicate Mirizzi syndrome - a gallstone impacted in the distal cystic duct causing extrinsic compression of the common bile duct

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74
Q

What is the definitive management for acute cholecystitis?

A

Cholecystectomy

+ Conservative management - ABx

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75
Q

What is the presentation of biliary colic?

A

colicky right upper quadrant abdominal pain
worse postprandially, worse after fatty foods
the pain may radiate to the right shoulder/interscapular region
nausea and vomiting are common
in contrast to other gallstone-related conditions, in biliary colic there is no fever and liver function tests/inflammatory markers are normal

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76
Q

Where does biliary colic pain radiate to?

A

Right scapula

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77
Q

What can exacerbate biliary colic pain?

A

Precipitated by a fatty meal

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78
Q

What are the main risk factors for biliary colic?

A

Fat: obesity is thought to be a risk factor due to enhanced cholesterol synthesis and secretion
Female: gallstones are 2-3 times more common in women. Oestrogen increases activity of HMG-CoA reductase
Fertile: pregnancy is a risk factor
Forty

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79
Q

What is the pathophysiology of biliary colic?

A

occur due to ↑ cholesterol, ↓ bile salts and biliary stasis

the pain occurs due to the gallbladder contracting against a stone lodged in the cystic duct

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80
Q

What is the gold-standard investigation for biliary colic?

A

Abdominal ultrasound

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81
Q

What is the definitive management for biliary colic?

A

Elective laparoscopic cholecystectomy

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82
Q

What is cirrhosis?

A

A condition in which the liver responds to hepatocyte injury/death by replacing damaged hepatic parenchyma with fibrous tissue and nodules.

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83
Q

What are the risk factors for cirrhosis?

A
  • Chronic alcohol use
  • Hepatitis C infection
  • Chronic hepatitis B infection
  • Autoimmune hepatitis
  • Hereditary haemochromatosis
  • Wilson disease
  • Alpha 1-anittrypsin deficiency
  • Intravenous drug use
  • Other: Unprotected intercourse, obesity, and blood transfusion.
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84
Q

What is the presentation of cirrhosis?

A

Abdominal distension due to ascites in portal hypertension

Jaundice and pruritus - Decompensated cirrhosis secondary to reduced hepatic excretion of conjugated BR.

Haematemesis and melaena

• Hand and nail features: Leukonychia, palmar erythema, and spider naevi.

  • Leukonychia (white nails) – Secondary to hypoalbuminemia
  • Polished nails – Secondary to excessive scratching in pruritus
  • Palmar erythema – Redness of thenar and hypothenar eminences,
  • Spider naevi – Blanch on pressure and spider-like branches fill from a central arteriole.
  • Bruising, finger clubbing and cholesterol deposits in palmar creases in primary biliary cholangitis.
  • Dupuytren contracture in alcohol-related liver disease

• Facial features:

  • Spider naevi – Blanch on pressure and spider-like branches fill from a central arteriole.
  • Telangiectasia – Red focal lesions resulting from irreversible dilatation of small blood vessels in the skin.
  • Bruising, rhinophyma, parotid gland swelling
  • Red tongue in alcohol-related liver disease.
  • Seborrheic dermatitis, jaundiced sclera and xanthelasma.

• Abdominal features

  • Caput medusa – Collateral circulation of the abdominal wall around the umbilicus.
  • Bruising
  • Hepatomegaly
  • Splenomegaly
  • Abdominal distension – Particularly in the flanks with shifting dullness and fluid thrill secondary to ascites.
  • Hepatic bruit – Present with a vascular hepatoma
  • Loss of secondary sexual hair and testicular atrophy in men.
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85
Q

What facial features are seen in decompensated cirrhosis?

A
  • Spider naevi – Blanch on pressure and spider-like branches fill from a central arteriole.
  • Telangiectasia – Red focal lesions resulting from irreversible dilatation of small blood vessels in the skin.
  • Bruising, rhinophyma, parotid gland swelling
  • Red tongue in alcohol-related liver disease.
  • Seborrheic dermatitis, jaundiced sclera and xanthelasma.
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86
Q

What abdominal features are seen in decompensated cirrhosis?

A
  • Caput medusa – Collateral circulation of the abdominal wall around the umbilicus.
  • Bruising
  • Hepatomegaly
  • Splenomegaly
  • Abdominal distension – Particularly in the flanks with shifting dullness and fluid thrill secondary to ascites.
  • Hepatic bruit – Present with a vascular hepatoma
  • Loss of secondary sexual hair and testicular atrophy in men.
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87
Q

What hand and nail features are seen in decompensated cirrhosis?

A

• Hand and nail features: Leukonychia, palmar erythema, and spider naevi.

  • Leukonychia (white nails) – Secondary to hypoalbuminemia
  • Polished nails – Secondary to excessive scratching in pruritus
  • Palmar erythema – Redness of thenar and hypothenar eminences,
  • Spider naevi – Blanch on pressure and spider-like branches fill from a central arteriole.
  • Bruising, finger clubbing and cholesterol deposits in palmar creases in primary biliary cholangitis.
  • Dupuytren contracture in alcohol-related liver disease.
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88
Q

What is hepatic fetor?

A

Sweet putrid smell of the breath

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89
Q

What are the LFT findings in cirrhosis?

A

AST and ALT levels increase with hepatocellular damage

  • Raised BR
  • GGT elevated
  • Reduced albumin
  • Reduced serum sodium
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90
Q

What is the definitive investigation for cirrhosis?

A

Liver biopsy

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91
Q

What does a liver biopsy reveal in cirrhosis?

A

Most specific and sensitive test for diagnosis of cirrhosis.
- Result: Architectural distortion of the liver parenchyma with formation of regenerative nodules.

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92
Q

What are the coagulation study findings in decompensated liver cirrhosis?

A

Prolonged prothrombin time
Reduced platelet count - Thrombocytopenia
INR

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93
Q

What should be performed if ascites is present?

A

Peritoneal tap for microscopy and culture to identify for spontaneous bacterial peritonitis.

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94
Q

What investigation is performed in NAFLD?

A

Transient elastrography

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95
Q

What scoring criteria is used in liver disease to assess the severity of cirrhosis?

A

Child-Pugh Score?

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96
Q

What parameters are assessed in the Child-pugh score?

A 
Bilirubin (umol/l)
Albumin (g/l)
Prothrombin time (seconds prolonged)
Encephalopathy
Ascites
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97
Q

What is SBP?

A

• Spontaneous bacterial peritonitis (SBP) – An ascitic tap with neutrophils >250mm3 indicates SBP. Patients with a low ascitic albumin are especially at risk  Treated with prophylactic antibiotics.

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98
Q

Why do oesophageal varices occur?

A

Portal hypertension leads to dilatation of oesophageal veins. The veins are susceptible to rupture (fatal in patients with coagulopathy).

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99
Q

What bile-acid sequestrants are used to manage pruritus?

A

Cholestyramine

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100
Q

What is the management of ascites?

A

Fluid restriction and low-salt diet

Consider Spironolactone and furosmide

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101
Q

What is the prophylactic management for recurrent episodes of hepatic encephalopathy?

A

Lactulose and rifaximin

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102
Q

What is the definitive treatment for liver cirrhosis?

A

Liver transplant

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103
Q

What scoring system is used to assess the survival benefit of a liver transplant?

A

MELD

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104
Q

Which disease is associated with a secondary cause of achalasia?

A

Chagas disease

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105
Q

What is achalasia?

A

Failure of the LOS to relax resulting in apersistalsis - Degeneration of the myenteric plexus to produce NO and VIP

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106
Q

What is the presentation of achalasia?

A

Dysphagia of both solids and liquids

Regurgitation due to food trapped in the oesophagus

Gradual weight loss -Due to lack of food ingestion

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107
Q

What is the gold-standard investigations for achalasia?

A

High resolution oesophageal manometry - Incomplete relaxation and Aperistalsis at the LOS

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108
Q

What are the other investigations performed in achalasia?

A

Upper GI Endoscopy - Retained food debris with dilated wall

Barium swallow - Birds beak appearance

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109
Q

What is seen in a barium swallow for achalasia?

A

Birds beak appearance

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110
Q

What is the management for achalasia?

A

Heller’s cardiomyotomy

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111
Q

What are the risk factors for GORD?

A 
Hiatus hernia
Obesity
Gastric acid hypersecretion
Alcohol
Smoking
Pregnancy
LOS tone reducing drugs (TCAs)
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112
Q

What are the main presenting features of GORD?

A 
Post-prandial pain
Acid regurgitation - bitter
Waterbrash
Odynophagia
Chronic cough or nocturnal asthma
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113
Q

What is the gold-standard investigation for GORD?

A

Resolution of symptoms after 8 week PPI trial

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114
Q

What is the surgical management for GORD?

A

Nissen fundoplication

Magnetic bead banding

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115
Q

What are the risk factors for PUD?

A 
H.pylori
NSAIDs - Reduced bicarbonate production 
Smoking
Increased/decreased gastric emptying 
Gastric specific ulcers - Cushing (Vagus) and Curling ulcers
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116
Q

What are the two types of peptic ulcers?

A

Duodenal ulcers

Gastric uclers

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117
Q

What enteroendocrine hormone is secreted in Zollinger Ellison Syndrome?

A

Gastrin

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118
Q

What is the PUD presentation?

A

Epigastric pain (pointing sign)

Directly after meal = gastric ulcer

N&V

Mild weight loss

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119
Q

What are the complications of PUD?

A

Haemorrhage
Perforation
Obstruction

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120
Q

What is the gold-standard investigation for PUD?

A

Upper GI endoscopy - reveal ulcerations

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121
Q

What investigations are performed for PUD?

A

Upper GI Endoscopy (Gold)

-H pylori tests - Urea breath test and stool antigen test (test after 6-8 weeks9

Serum fasting gastrin level

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122
Q

What lifestyle changes are recommended in PUD?

A

Smoking cessation

Reducing alcohol intake

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123
Q

What medical therapy is indicated in H.pylori positive PUD?

A

Triple therapy
PPI , amoxicillin, clarithromycin 7 day eradication therapy

-Consider metronidazole if contraindicated

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124
Q

What is the management of H.pylori negative PUD?

A

Offer 4-8 weeks of PPI therapy

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125
Q

Define gastritis?

A

Histological presence of mucosal inflammation

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126
Q

What are the two types of hernias?

A 
Hiatus hernias
Sliding hernias (80%)
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127
Q

Define hiatus hernia?

A

Protrusion of abdominal contents into the thorax - usually stomach

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128
Q

What is the most common hiatus hernia?

A

Sliding hernia

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129
Q

What are the risk factors for hiatus hernias?

A

Obesity

Increasing intra-abdominal pressure

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130
Q

What are the presentation of hiatus hernia?

A

Asymptomatic
GORD symptoms (Worse when lying flat)
Palpitations or hiccups indicate pericardial irritation

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131
Q

What is the gold standard investigation for hiatus hernia?

A

Upper GI endoscopy

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132
Q

What does a CXR reveal in hiatus hernia?

A

Retrocardiac bubble

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133
Q

What is the surgical management for hiatus hernia?

A

Fundoplication

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134
Q

What is the aetiology o Barret’s oesophagus?

A

Metaplasia of normal stratified squamous epithelium to columnar epithelium

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135
Q

What is the gold standard investigation for Barrett’s oesophagus?

A

Upper GI endoscopy with biopsy (Revealing columnar epithelium)

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136
Q

What is the management of non-dysplastic Barrett’s oesophagus?

A

Maximise PPI therapy and surveillance every 2 years

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137
Q

What is the management for low-grade dysplasia?

A

Monitor every 6 months to assess growth

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138
Q

What is the definitive management for high-grade dysplasia?

A

Therapeutic intervention - radiofrequency ablation or endoscopic mucosal resection for nodular growths.

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139
Q

Smoking increases what type of oesophageal carcinoma?

A

Squamous cell carcinoma

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140
Q

What is the presentation of oesophageal cancer?

A

Dysphagia - first solids progressing to liquids
Rapid weight loss
Hoarseness

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141
Q

What is the gold standard investigation for oesophageal cancer?

A

Upper GI Endoscopy with biopsy

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142
Q

Define gastric cancer

A

Neoplasm originating in any portion of the stomach (Adenocarcinoma)

Intestinal - H.pylori associated
diffuse - E-cadherin associated

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143
Q

What are intestinal gastric cancers associated with?

A

H.pylori

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144
Q

What are the main risk factors for gastric cancers?

A

Pernicious anaemia
H pylori
Nitrosamines

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145
Q

What is the presentation of gastric cancer?

A

Vague epigastric abdominal pain
Weight loss common
Lymphadenopathy (Left supraclavicular- Virchow’s node)
Sister mary joseph nodule

Krukhenberg tumour- ovaries

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146
Q

What is the gold standard investigation for gastric cancer?

A

Upper GI endoscopy with biopsy

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147
Q

What does a biopsy reveal in gastric cancer?

A

Signet ring cells

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148
Q

Define Mallory-Weiss Tear

A

Longitudinal lacerations in the mucosa and submucosa near the GOS
Self-limiting

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149
Q

What are the risk factors for a Mallory-Weiss tear?

A

Persistent retching, coughing, vomiting, or straining found in alcoholics and bulimics

(Increase in intra-abdominal pressure)

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150
Q

What is the presentation of Mallory-Weiss tear?

A 
Haematemesis is the most common
Light-headed/dizziness
Postural hypotension
Dysphagia 
Melanea
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151
Q

What is the gold standard investigation in a MW tear?

A

Upper GI Endoscopy

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152
Q

What happens to the serum urea in an upper GI bleed?

A

Serum urea increases (Breakdown of erythrocytes)

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153
Q

What risk assessment scores are associated in upper GI bleeds?

A

Rockall Score

Glasgow-Blatchford score

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154
Q

What is the first-line management of a Mallory-Weiss tear?

A

Endoscopy inject adrenaline or conduct band ligation to stop bleeding

Anti-secretory therapy (PPI) before endoscopy. - seems to reduce re-bleed
Anti-emetics to prevent recurrence

Second line - sengstaken-Blakemore tube

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155
Q

What biochemical marker is raised in an acute upper GI bleed?

A

Urea - may be seen due to the protein meal of blood

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156
Q

What is the Glasgow-Blatchford score?

A

the Glasgow-Blatchford score at first assessment

helps clinicians decide whether patient patients can be managed as outpatients or not

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157
Q

What is the Rockall score?

A

he Rockall score is used after endoscopy
provides a percentage risk of rebleeding and mortality
includes age, features of shock, co-morbidities, aetiology of bleeding and endoscopic stigmata of recent haemorrhage

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158
Q

What is the first-line management of varcieal bleeding after resuscitation with FFP and fluids?

A

Terlipressin and prophylactic Abx

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159
Q

What is the endoscopic therapy for oesophageal varices?

A

Endoscopic variceal band ligation SUPERIOR&raquo_space; to endoscopic sclerotherapy

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160
Q

What is the management of oesophageal varices if band ligation is unsuccessful?

A

Insertion of Sengstaken-Blakemore tube

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161
Q

What is the prophylactic treatment for variceal haemorrhage?

A

Propanolol - reduced rebleeding

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162
Q

What is the most common type of colonic cancer?

A

Adenocarcinoma

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163
Q

What do colonic cancers arise from?

A

Dysplastic adenomatous polyps

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164
Q

What genes are implicated in colonic cancer?

A

HNPCC (Lynch Syndrome)
FAP
Peutz-Jeghers syndrome

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165
Q

What is HNPCC?

A

Hereditary non-polyposis colorectal cancer

Fhx of bowel cancer at a young age
Symptomatic 30 yo’s

Colonoscopy - tumour without polyps (Not FAP)

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166
Q

what is Petuz-Jeghers syndroms?

A

Peutz-Jeghers syndrome is an autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.

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167
Q

What are the UK cancer screening programmes?

A

Breast
Cervical
Bowel

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168
Q

What are the clinical features for Peutz-Jeghers syndrome?

A

Features
hamartomatous polyps in GI tract (mainly small bowel)
pigmented lesions on lips, oral mucosa, face, palms and soles
intestinal obstruction e.g. intussusception
gastrointestinal bleeding

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169
Q

What gene is associated with FAP?

A

APC gene

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170
Q

What is the management for FAP?

A

Annual screening sigmoidoscopy

Polyps found = Resectional surgery

Resection and pouch Vs subtotal colectomy and IRA

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171
Q

What biochemical screening test is available for colorectal cancer?

A

Faecal Immunochemical Test (FIT) tests

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172
Q

What is the FIT test?

A

Type of faecal occult blood test which uses antibodies that specifically recognise human haemoglobin

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173
Q

What is the age threshold to be invited for a flexible sigmoidoscopy screening for bowel cancer?

A

Age 55 years

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174
Q

What are the main risk factors for colorectal cancer?

A

Increasing age
Obesity
IBD (UC)

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175
Q

What is the presentation of colonic cancer?

A

Change in bowel habits

Rectal bleeding (Mixed in the stool and not bright red)

Weight loss
- FLAWs

Tenesmus

Anaemia symptoms

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176
Q

What are the indications for a 2WW for colonic cancer?

A

NICE updated their referral guidelines in 2015. The following patients should be referred urgently (i.e. within 2 weeks) to colorectal services for investigation:
patients >= 40 years with unexplained weight loss AND abdominal pain
patients >= 50 years with unexplained rectal bleeding
patients >= 60 years with iron deficiency anaemia OR change in bowel habit
tests show occult blood in their faeces (see below)

An urgent referral (within 2 weeks) should be ‘considered’ if:
there is a rectal or abdominal mass
there is an unexplained anal mass or anal ulceration
patients < 50 years with rectal bleeding AND any of the following unexplained symptoms/findings:
abdominal pain
change in bowel habit
weight loss
iron deficiency anaemia

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177
Q

A male >55 with FLAWs and altered bowel habits is associated with what

A

Colorectal cancer

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178
Q

What may tenesmus suggest?

A

A rectal mass

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179
Q

What is the most common cause of iron deficiency in men over 60?

A

Colorectal cancer

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180
Q

What does an FBC reveal in colorectal cancer?

A

Iron deficiency anaemia

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181
Q

What examination features are associated with colonic cancer?

A

Anaemia features
Palpable mass (Late)
Distension/ascites (late)
Lymphadenopathy (late)

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182
Q

How is colorectal cancer staged?

A

CT chest/abdomen/pelvis

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183
Q

What is the management of colonic cancer within the Caecal, ascending or proximal transverse colon?

A

Right hemicolectomy with ileocolic anastomosis

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184
Q

What is the surgical management for a colonic cancer residing within the Distal transverse, descending colon?

A

Left hemicolectomy with colo-colon anastomosis

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185
Q

What is the surgical management for sigmoid colon cancer?

A

High anterior resection

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186
Q

What is the surgical management for an anal verge colonic cancer?

A

Abdomino-perineal excision of rectum

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187
Q

What is the diagnostic investigation for colonic cancer?

A

Colonoscopy and biopsy

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188
Q

What does a double-contrast barium enema reveal in colonic cancer?

A

Apple core lesion - cancer causing strictures

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189
Q

What cancer marker is associated with colonic cancer?

A

Carcinoembryonic antigen

-Used to monitor for recurrence in patients post-operatively to assess response to treatment

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190
Q

What is the first-line Investigation for suspected colonic cancer?

A

2WW referral

W LFTs and FBC & DRE

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191
Q

What criteria is used to stage colonic cancer?

A

Duke’s staging + TNM classification

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192
Q

Apple core lesions (on a barium contrast double enema) are associated with what pathology?

A

Colonic cancer

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193
Q

What is Duke A staging in colonic cancer?

A

Tumour confined to the mucosa

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194
Q

What is Duke’s B staging in colonic cancer?

A

Tumour invading the bowel wall

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195
Q

What is Duke C staging in colonic cancer?

A

Lymph node metastases

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196
Q

What is the definitive treatment for colorectal cancer?

A

Surgical excision + adjuvant or neoadjuvant chemo/radiotherapy

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197
Q

What are the common metastasis for colorectal cancer?

A

Liver
Lung
Bone
Brain

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198
Q

What is the most common site for colorectal cancer?

A

Rectal -40%

Sigmoid - 30%

199
Q

What is Crohn’s disease?

A

Transmural inflammation of the GI tract affecting any part of the mouth to anus
Skips lesions

200
Q

Where does Crohn’s disease most commonly affect?

A

Terminal ileum and perianal areas

201
Q

What type of inflammation is associated with Crohn’s disease?

A

Non-caseating granuloma formation

202
Q

What are the clinical features of Crohn’s disease?

A

presentation may be non-specific symptoms such as weight loss and lethargy
diarrhoea: the most prominent symptom in adults. Crohn’s colitis may cause bloody diarrhoea
abdominal pain: the most prominent symptom in children
perianal disease: e.g. Skin tags or ulcers
extra-intestinal features are more common in patients with colitis or perianal disease

203
Q

What are the risk factors for Crohn’s disease?

A 
FHx 
Cigarette smoking
Oral contraceptive pill
Diet high in refined sugars 
?NSAIDs
?not breastfed
204
Q

Describe the epidemiology of Crohn’s disease

A

Ashkenazi Jews
Bimodal peak:
15-40
60-80

205
Q

Describe the abdominal pain in Crohn’s disease

A

Crampy or constant right lower quadrant and periumbilical pain (terminal ileum)

206
Q

Describe the diarrhoea of Crohn’s disease

A

Mucous
Blood
Pus
Nocturnal

207
Q

What peri-anal lesions are associated with CD?

A

Skin tags
Fistulae
Abscesses

208
Q

What extra-intestinal manifestations are associated with CD?

A

Arthropathy (Joint pain)
Skin lesions
-Erythema nodosum
-Pyoderma gangrenosum

Ocular symptoms
-Uveitis, Episcerltiis

209
Q

What skin manifestations are associated with CD?

A

Erythema nodosum

Pyoderma gangrenosum

210
Q

What is erythema nodsum?

A

Swollen fat under the skin causing bumps and patches that look red or darker than the surrounding skin

211
Q

What is pyoderma gangrenosum?

A

Characterised by small red/purple bumps or blisters (Papules or nodules) eventually eroding to painful ulcers - rapid progression

212
Q

What ocular symptoms are associated with CD?

A

Uveitis

Episcleritis

213
Q

Where does pyoderma gangrenosum typically affect?

A

Affects the legs

214
Q

What may be found during an oral exam in a patient with CD?

A

Aphthous ulcers

215
Q

What is the most common site for abdominal tenderness in CD?

A

Terminal ileum

216
Q

What inflammatory markers are raised in CD?

A

ESR
CRP
Faecal calprotectin

217
Q

What is a high risk complication of Crohns?

A

Anaemia of chronic disease

218
Q

What type of diarrhoea is associated w Crohns?

A

Secretory diarrhoea due depletion of bile salt reabsorption

-Steatthorrhoea and increased gallstone formation

219
Q

What vitamin deficiency may be associated with CD?

A

ADEK (Fat-soluble vitamins)

220
Q

Severe ileal disease/resection can lead to what malabsorption?

A

B12 malabsorption

221
Q

A plain AXR reveals what in Crohn’s?

A

Bowel dilation

222
Q

What is revealed by a CT in Crohn’s?

A

Bowel wall thickening

Skip lesions

223
Q

A bowel series X-ray with barium enema reveals what specific findings in Crohn’s disease?

A

Rose thorn ulcers - Deep ulcerations

String sign of Kantor - Fibrosis and strictures

224
Q

String sign of Kantor reveals what in Crohn’s disease?

A

Fibrosis and strictures

225
Q

What do rose thorn ulcers represent in Crohn’s disease?

A

Deep penetrating linear ulcers or fissuring seen within the stenosed terminal ileum

226
Q

What is the confirmative test for Crohn’s disease?

A

Colonoscopy and biopsy (Histological evidence)

227
Q

What is seen on colonoscopy in Crohn’s?

A

Ulcers
Cobblestone appearance
Skip lesions

228
Q

What does String Sign of Kantor represent?

A

Oedema fibrosis with ulcerated mucosa - resembling fraying of string

229
Q

How do you induce remission of Crohn’s disease?

A

Oral or IV steroids
-Prednisolone
Budenoside

230
Q

What is the maintenance therapy for Crohn’s disease?

A

Immunomodulators -
Azathioprine
Mercaptopurine
Methotrexate

231
Q

What are the biological therapies administered for Crohn’s?

A

Adalimumab
Infliximab
Vedolizumab

232
Q

What is the mechanism of Infliximab?

A

TNF-a inhibitors

233
Q

What is the worst complication for Crohn’s disease?

A

Obstruction - stricturing

Management with Hartmann’s operation or colectomy

234
Q

What are the adjuncts in management for Crohn’s disease?

A

Nutritional therapy
Perianal disease mX
Smoking cessation

235
Q

What are the indications for surgical management in Crohn’s?

A

For severe remissions/presentations
Refractory disease
Obstructed Pts

236
Q

What is the first-line immunomodulator in the management of Crohn’s?

A

Azathioprine

237
Q

What is the first-line biological therapy for Crohn’s?

A

Infliximab

238
Q

What adjunctive therapy can be given for cramp relief in Crohn’s?

A

Anti-spasmotics

239
Q

What is the definition of UC?

A

Continuous and uniform inflammation of the large bowel (originating from the rectum)

240
Q

Where does UC begin?

A

Rectum - extending proximally

241
Q

What gene is associated with UC?

A

HLA-B27

Also associated with Ankylosing spondylitis

242
Q

Which colonic layer is affected by UC?

243
Q

What are the risk factors for ulcerative colitis?

A

FHx
HLA-B27
Non-smoking (Smoking is protective in UC)

244
Q

What is the presentation of ulcerative colitis?

A 
Bloody diarrhoea
Rectal bleeding + mucous
Abdominal pain + cramps
Tenesmus
Weight loss
245
Q

What are extra-intestinal manifestations of UC?

A 
Peripheral arthritis
Ankylosing spondylitis
Erythema nodosum
Pyoderma gangrenosum
Episcleritis> Uveitis
246
Q

What examination findings may be seen in UC?

A

Anaemia signs - pallor
DRE - gross or occult blood comes out
Abdominal tenderness

247
Q

Which liver pathology is highly associated with ulcerative colitis?

A

Primary sclerosing cholangitis

248
Q

What blood investigations are to be performed in UC?

A

FBC - Anaemia
LFTs - PSC
CRP/ESR - Inflammation
pANCA

249
Q

What autoantibody is positive in UC?

250
Q

What is a severe complication of UC?

A

Toxic megacolon

251
Q

What stool sample protein indicates inflammation in UC?

A

Faecal calprotectin

252
Q

What signs may be seen in a plain AXR in UC?

A 
Dilated bowel (>6cm = toxic megacolon)
Thumbprinting
253
Q

What is thumbprinting?

A

A radiographic sign of large bowel thickening - caused by oedema related to an infective or inflammatory process (colitis)

Haustra become thickened at regular intervals appearing like thumprints projecting into the aerated lumen

254
Q

What type of bowel enema is used in UC?

A

Double-contrast bowel enema

255
Q

What sign is revealed in a double-contrast bowel enema in UC?

A

Lead-pipe appearance

256
Q

What is the diagnostic investigation for UC?

A

Colonoscopy and Biopsy

257
Q

What colonoscopy findings are seen in UC?

A

Continuous, erythema, bleeding, ulcers

258
Q

What histological findings are associated with UC?

A

crypt abscess

Depletion of goblet cell mucin

259
Q

What is used to induce remission in UC?

A

Topical or oral Mesalazine (5-ASA)

and oral steroids - Oral beclamethasone

260
Q

What is the normal maximum diameter of the small bowel?

A

35MM

Valvuae conniventes extend all the way across

261
Q

What is the maximum normal diameter of the large bowel?

A

55mm

Haustra extend about a third of the way across

262
Q

What is the first-line immunosuppressants in UC?

A

Methotrexate, Mercaptopurine, azathioprine

263
Q

What is the main biologic involved in UC?

A

Infliximab

Ciclosporin

264
Q

What is the definitive cure of UC?

A

Total colectomy

265
Q

What are the three main complications of UC?

A

Colonic adenocarcinoma
Toxic megacolon
Psc

266
Q

Which dietary peptide is associated with coeliac disease?

A

Gliadin

Found in Wheat, rye and Barley

267
Q

What does Coeliac disease result in?

A

Villous atrophy
Hypertrophy of intestinal crypts

Increased lymphocytes in the epithelium and lamina propria

268
Q

What are the risk factors for coeliac disease?

A

FHx
IgA deficiency
T1DM
Autoimmune thyroid disease

F>M
Western countries

269
Q

What is the presentation of coeliac disease?

A

Diarrhoea (Chronic/intermittent)
Bloating
Abdominal pain and discomfort

Extra-intestinal

  • Fatigue
  • weight loss
  • Dermatitis herpetiformis (elbows)
270
Q

What dermatological manifestation is associated with coeliac disease?

A 
Dermatitis herpetiformis (elbows)
Bilateral itchy vesicles and plaques
271
Q

Where does dermatitis herpetiformis affect?

A

Extensor surfaces, face, scalp, necl

272
Q

What are the endoscopic findings in coeliac disease?

A

Loss of folds
Visible fissures
Nodular appearance

Absent villi

273
Q

What is the first-line investigation for coeliac disease?

A

Immunoglobulin A tissue transgutaminase (IgA tTG)
-Elevated titre

Do Serum IgA to screen for IgA deficiency
-Consider IgG ttG

274
Q

What is the diagnostic investigation for coeliac disease?

A

Duodenal biopsy and endoscopy

275
Q

What does an endoscopy reveal in coeliac diseae?

A

Villous atrophy

Crypt hyperplasia

276
Q

What autoantibodies are associated with coeliac disease?

A

IgA ttg

Endomysial antibody

277
Q

What is the management for coeliac disease?

A

Gluten-free diet
-Vitamin + mineral supplements

Refractory - refer to specialist

278
Q

What is the definition of IBS?

A

Chronic condition characterised by recurrent abdominal pain associated with bowel dysfunction

279
Q

What are the three types of IBS?

A

IBS with diarrhoea - IBSD
IBS with constipation - IBS C
IBS mixed type - IBSM

280
Q

What are the risk factors for IBS?

A

History of Physical/Sexual Abuse
PTSD
PMHx: Acute bacterial gastroenteritis
FHx

281
Q

What is the epidemiology of IBS?

A

Females > M (2:1)

<50 Years.

282
Q

What is the presentation of IBS?

A

Abdominal cramping in the lower/mid abdomen

Alteration of stool consistency (diarrhoea/constipation)

Defecation relieves abdominal pain/discomfort

283
Q

What investigations would you perform to exclude IBS?

A 
Anti-tTG (coeliac) 
Fecal calprotectin, lactoferrin (IBD) 
Serrum CRP  (IBD) 
Colonoscopy (IBD)
FBC (anemia – consider CRC) 
FOB test (CRC)
284
Q

What lifestyle management is available for IBS?

A 
Fibre 
Avoid: caffeine, lactose, fructose. 
Stress management
Education + Reassurance 
\+ Probiotics ?
285
Q

What is the medical therapy for IBS?

A

Laxatives (IBS-C)
Antispasmotics (cramps)
Antidiarrhoeals (IBS-D)

286
Q

Define haemorrhoids

A

Vascular rich tissue cushions located within the anal canal

287
Q

What is the aetiology of haemorrhoids?

A

Prolonged/ repetitive straining causes disruption of the tissues and results in elongation/dilation of the haemorrhoidal tissues.

288
Q

What are the two types of haemorrhoids defined by the location to the dentate line?

A

External and internal

289
Q

What is the dentate line?

A

The line between the simple columnar epithelium of the rectum and the stratified epithelium of the anal canal

290
Q

What are grade 1 haemorrhoids?

A

No prolapse

Just prominent blood vessels, only bleeds

291
Q

What are grade 2 haemorrhoids?

A

Prolapse upon bearing down but spontaneously reduce

292
Q

What are grade 3 haemorrhoids?

A

Prolapse upon bearing down and requires manual reduction

293
Q

What are grade 4 haemorrhoids?

A

Permanent prolapse and cannot be manually reduced

294
Q

What does prolapse mean in relation to haemorrhoids?

A

Protrusion beyond the anal opening

295
Q

What are the risk factors for haemorrhoids?

A

Constipation
Pregnancy
Space occupying pelvic lesions

296
Q

What is the presentation of haemorrhoids?

A

Painless bleeding associated with defecation
(Bright red)

Anal pruritus (itching)
Palpable mass felt
297
Q

Describe the bleeding with haemorrhoids

A

bright red associated with defecation

Painless

298
Q

What is the 1st-line and diagnostic investigations for haemorrhoids?

A

Anoscopic examination

Visualise haemorrhoids and confirms diagnosis

299
Q

What is the conservative management of haemorrhoids?

A

Constipation advice

Lifestyle discourage straining

300
Q

What is the management of grade 1 haemorrhoids?

A

Topical corticosteroids (Alleviates pruritus)

301
Q

What is the management of grade 2 and 3 haemorrhoids?

A

Rubber band ligation

302
Q

What is the definitive management for grade 4 haemorrhoids?

A

Surgical haemorrhoidectomy

303
Q

How does rubber band ligation work?

A

Helps to stop blood flowing to the haemorrhoid - haemorrhoid dries up and falls off on their own (1-2 weeks)

304
Q

What is a haemorrhoidectomy?

A

First line treatment for grade 4 internal haemorrhoids.
Under General anesthesia
Only takes ~20 mins
Surgeon excises or uses a stapler to remove haemorrhoids

305
Q

What is a complication of a haemorrhoid?

A

Thrombosed haemorrhoid

306
Q

What is the presentation of thrombosed haemorrhoids?

A

Significant pain and a tender lump

OE: Purplish, oedematous subcutaneous perianal mass

307
Q

What is the management of a thrombosed haemorrhoid?

A

Within 72 hours - consider for excision

Managed with stool softners, ice packs, and analgesia

308
Q

Define rectal prolapse

A

Rectum slides out of the anal canal

309
Q

What is the cause of rectal prolapse?

A

Caused by long-term straining and anything causing weakness of pelvic floor muscles

310
Q

What are the three types of rectal prolapse?

A

Internal
Mucosal - the mucosa drops out
External - Entire rectum drops out

311
Q

What are the risk factors for rectal prolapse?

A

Chronic constipation + straining

Weakened pelvic floor muscles

  • Natural birth
  • trauma

obesity

312
Q

What is the presentation of rectal prolapse?

A

Painless protruding mass following defecation

Mucoid discharge

incontinence

313
Q

What is the first-line dan diagnostic investigation for rectal prolapse?

A

Clinical diagnosis
OE: Visualise
Ask the patient to strain to elicit prolapse

314
Q

What is the mx for rectal prolapse?

A

DeLormes procedure

315
Q

What is an anal fissure?

A

A split in the mucosal lining of the distal anal canal characterised by pain on defecation and rectal bleeding

316
Q

What is the pathophysiology of anal fissures?

A

Hard stools tear the anal skin at the dentate line

Poor blood supply can be a cause

317
Q

What are the risk factors for anal fissures?

A

Hard stool
Pregnancy
Opiates

318
Q

What is the presentation of anal fissures?

A

Pain on defecation

Tearing sensation on defecation

Fresh blood on toilet paper

319
Q

What is the first line diagnostic investigation for anal fissures?

A

Clinical diagnosis

EUAs

320
Q

What is the first line management of anal fissures?

A

Manage constipation
High fibre diet

Adequate fluid intake

Sitz baths

Topical GTN

Topical dilitiazem

321
Q

What topical management is applied for analgesia in anal fissures?

A

Topical GTN

322
Q

What is the management for persistent fissures?

A

Botox and surgical sphincterectomy

323
Q

How does topical GTN work?

A

Relaxes the muscles around the anus to relive the pain

324
Q

What is an anal fistula?

A

A connection between the last part of the bowel and the skin around the anus

325
Q

What is the aetiology of anal fistula?

A

Clogged anal glands and anal abscesses
Crohn’s disease
Radiation (cancer)
Trauma

326
Q

What is the presentation of an anal fistula?

A

Frequent anal abscesses
Pain and swelling around the anus
Bloody / Foul smelling drainage (pus)
“in underwear”

327
Q

What is the investigation of anal fistula?

A

Opening the skin around the anus
Not always visible
Anoscope/rectoscope

328
Q

What is the surgical management of an anal fistula?

A

Fistulotomy

Seton - surgical thread that is left in the fistula - allows it to drain and helps it heal.

329
Q

What is an anal abscess?

A

An infection of the soft tissues and collection of puss around the anus

330
Q

What are the risk factors for anal abscesses?

A

RISK FACTORS:
Anal fistula
Crohn’s disease
Constipation

331
Q

What is the presentation of anal abscess?

A

Perianal pain
Not related to defecation
Perianal swelling and tenderness

332
Q

What is the first line investigation for anal abscess?

A

Clinical diagnosis

Visualise the abscess

333
Q

What sit he definitive management for anal abscess?

A

Surgical drainage of the abscess

334
Q

What is a pilonidal sinus?

A

Caused by the forceful insertion of hairs into the skin of the natal cleft in the sacrococcygeal area. Promotes inflammation and causes a sinus.

335
Q

What is the presentation of pilondial sinus?

A

SACROCOCCYGEAL:
Discharge – offensive, staining underwear
Pain – worst on sitting down
Swelling

336
Q

What is the management of a pilonidal sinus?

A

Surgical treatment - excision + sinus

Hair removal - laser

337
Q

What are the things to note in a stoma?

A

Location (Right - ileostomy, left - colostomy)

Number of lumens 2 = loop
1- end

Flush or spouted

Comment on stoma bag
-Solid/liquid
Colour
Blood mucous
Inspect surrounding skin
338
Q

How is unconjugated bilirurbin transported within the blood?

A

Associated with albumin

339
Q

What is the definition of jaundice?

A

Increased bilirubin concentration in the blood

340
Q

What are the breakdown products of haemoglobin?

A

Unconjugated bilirubin and iron

341
Q

Which enzyme is responsible for conjugating bilirubin?

342
Q

Where is conjugated bilirubin excreted into within the GI tract?

343
Q

How is bilirubin secreted into the stools?

A

Stercobillin

344
Q

How is conjugated bilirubin secreted into the urine?

A

Urobilinogen

345
Q

What are the two common causes of pre-hepatic jaundice?

A

Haemolysis/Gilbert’s

346
Q

What is raised in pre-hepatic jaundice?

A

Unconjugated bilirubin

347
Q

Which enzymes are elevated in hepatic causes of jaudnice?

348
Q

What are the common hepatocellular causes of jaundice?

A

Hepatitis
Viral, alcoholic, autoimmune, drug
Cirrhosis

349
Q

What are the common causes of obstructive jaundice?

A 
Liver mass
Gallstone
PBC/PSC
Pancreattic cancer
Cholangiocarcinoma/Cancer
Drug (ileus)
350
Q

Which liver enzyme is elevated in obstructive jaundice?

351
Q

what is the characteristic presentation of obstructive jaundice?

A

Dark urine (Conjugated bilirubin going into the urine)

Pale stools (lack fo stercobiliin)
Pruritus (Bile salts into circulation)
352
Q

Why is pruritus a presentation in obstructive jaundice?

A

Bile salts produced in the liver cannot enter the duodenum therefore leak into the circulation

-Excoriations result from this

353
Q

What are the markers of the function of the liver?

A

INR
Prothrombin time
Albumin level
Platelet count

354
Q

What is the presentation of hepatitis?

A 
RUQ pain
Jaundice
hepatomegaly
Joint pain 
Nausea
Fatigue
Dark urine
355
Q

What are the three stages of alcoholic liver disease?

A

Steatosis (fatty)
Alcoholic hepatitis (inflammation)
Cirrhosis

356
Q

What is the irreversible stage of alcoholic liver disease?

357
Q

What are the symptoms of alcoholic hepatitis?

A

After long term alcohol use, but sometimes after binge

Nausea, anorexia, weight loss, hepatomegaly

Severe: fever, jaundice, tachycardia, tender hepatomegaly, bruising, encephalopathy, ascites

358
Q

What FBC signs are seen in alcoholic hepatitis?

A

Macrocytic anaemia

359
Q

What are the LFT results in alcoholic hepatitis?

A

AST:ALT ratio >2
Raised Bilirubin
Raised GGT
Decreased albumin

Increased prothrombin time

360
Q

Which liver enzyme is raised in alcoholic hepatitis?

A

AST:ALT >2

361
Q

What is a sensitive marker of significant liver damage?

A

Prothrombin time (Prolonged)

362
Q

What radiological investigation is performed for alcoholic hepatitis?

A

Hepatitic ultrasound

363
Q

What does a liver biopsy reveal in alcoholic hepatitis?

A

Ballooning

Mallory bodies indicates hepatitis

364
Q

What is the management indicated in alcohol abstinence?

A

Chlordiazepoxide

365
Q

What is the management of Wernicke’s Encephalopathy?

A

Thiamine-Pabrinex

366
Q

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

A 
Truncal obesity 
Insulin resistance/diabetes
Hyperlipidasemia
Hypertension 
Metabolic syndrome
Short bowel syndrome
TPN
Signs of insulin resistance
367
Q

What LFTs are seen in NAFLD?

A

AST:ALT elevated <1
GGT/ALP
Check glucose (raised)

368
Q

What is the management of NAFLD?

A

Diet and exercise; controlling RFs (e.g., statins for hypercholesterolaemia, good blood sugar control for diabetics with metformin/thiazolidinediones)

369
Q

How is hepatitis A&E transmitted?

A

Faeco-oral spread (sex/comntaminedwater)

370
Q

What is ht management of viral hepatitis A and E?

A

Supportive

Avoid alcohol/excess paracetamol

371
Q

Which HepA antibody is raised in acute Hep A infection?

A

Anti-HAV IgM - raised for 6 weeks

372
Q

Which HepA antibody is raised in chronic infections?

A

Anti-HAV IgG

373
Q

which hepatitis infection is more likely to become chronic?

A

Hepatitis C

374
Q

What are the risks associated with viral hepatitis C?

A

cirrhosis/hepatocellular carcinoma

375
Q

What is the management of acute hepatitis C infections?

A

Antiviral- sofosbuvir, ledipasvir

376
Q

What is the management of acute hepatitis B?

A

Supportive management

377
Q

What is the management of chronic hepatitis B infection?

A

Anti-viral therapy treatment suppresses HB DNA replication

peginterferon-a-2a OR tenofovir

378
Q

Which antibody is raised in HepB vaccinted individuals?

379
Q

Which antibody is raised in past infections of Hepatitis B?

A

Anti-HBc (IgG positive)

380
Q

Which antibodies are raised in an acute infection of hepatitis B?

A

IgM Anti-HBc

HBsAg

381
Q

Which antibodies are raised in a chronic infection of hepatitis B?

A

HBsAg

IgG positive Anti-HBc

382
Q

How is hepatitis B transmitted?

A

Children more likely to be carriers/chronic

Sexually transmitted, IVDU, vertical

383
Q

How is hepatitis C transmitted?

A

Blood product spread (IVDU/transfusioN)

384
Q

What are the symptoms of an acute HepA infection?

A 
Nausea
Vomiting + Diarrhoea
Fever
Jaundice 
RUQ abdominal pain
385
Q

Which hepatitis is transmitted predominantly by contaminated blood products?

A

Hepatitis C

386
Q

What LFTs are associated with viral hepatitis?

A

AST/ALT (in 1000s)

Viral serology

387
Q

What LFTs are associated with drug-induced hepatitis?

A

AST/ALT (In 1000s)

Serum paracetamol concentration

388
Q

What is the management of a paracetamol overdose?

A

N-acetyl cysteine

389
Q

Which autoantibodies are associated with autoimmune hepatitis?

390
Q

What is the aetiology of cirrhosis?

A

Normal liver is replaced with fibrosis and nodules of regenerating hepatocytes can be stable or decompensated

391
Q

What is the diagnostic investigation for liver cirrhosis?

A

Transient elastrography

392
Q

What are the common causes of liver cirrhosis?

A 
Alcohol misuse
Viral hepatitis (B/C)
Autoimmune hepatitis
Haemcrhomatosis
NASH
Chronic billiary disease
393
Q

What is the peripheral stigmata of chronic liver disease?

A 
Clubbing
Spider naevi
Dupuytren's contracture
Palmar erythem
Gynaecomastia
Bruising
394
Q

What is the definition of portal hypertension?

A

Increased pressure in the portal vein due to cirrhosis

395
Q

What are the signs of portal hypertension?

A

Distended veins (varices)
-Caput medusae and oesophageal varices
Ascites
Splenomegaly

396
Q

What is the management of cirrhosis?

A

Treat cause + avoid hepatotoxic drugs (alcohol, sedative,opiates, NSAIDs)

Monitor risk of complications (MELD score, 6-month USS, endoscopy upon diagnosis and every 3 years).

397
Q

What is. the management of hepatic encephalopathy?

A

Oral lactulose
Oral rifaximin
phosphate enema

398
Q

What gut product is implicated encephalopathy?

399
Q

What should be restricted in hepatic encephalopahty?

A

Short-term protein restriction

400
Q

What is the management of ascites?

A

Sodium restriction
Diuretics - furosemide and spironolactone

Large volume paracentesis

401
Q

What diuretics are used in the managemetn of ascites?

A

Furosemide and spironolactone

402
Q

What ABx are used in the treatment of SBP?

A

Cefuroxime

Metronidazole

403
Q

What neutrophil count is diagnostic of SBP?

A

> 250 neutrophils

404
Q

How is SBP diagnosed?

A

Paracentesis (Needle aspiration of the ascitic fluid)

Ascitic tap

405
Q

What is the primary prophylaxis of varices?

A

Propranolol (Non-selective beta blocker)

406
Q

What is the management of

ruptured oesophageal varices?

A

ABCDE assessment, IV/fluids and blood transfusion/resuscitation

Terlipressin and ABx

Endoscopic varcieal ligation immediately after resuscitation

407
Q

What is the secondary prophylaxis of varices?

A

Non-selective beta blocker (to replace terlipressin after 2-5 days)

TIPS procedure when EVL and beta-blocker fails to prevent

408
Q

Which drug is associated with drug-induced cholestasis?

A

Co-amoxiclav
Nitrofurantoin
OCP

409
Q

What is the characteristic sign of pancreatic cancer?

A

Painless palpable gallbladder (Courvoisier’s law) and jaundice

410
Q

What is the definitive management of biliary colic?

A

Analgesia+ elective lap chole

411
Q

What is the initial management of acute cholecystitis?

A

Clear fluids only
Analgesics
Fluid resus
Broad IV Abx

412
Q

What is the definitive management of acute cholecystitis?

A

Lap chole (within 1 week)

413
Q

What are the two investigations indicated for the diagnosis of acute cholangitis?

A

USS liver and biliary tree ERCP

414
Q

What is the definitive management for ascending cholangitis?

A

Analgesia + ERCP+lap chole

415
Q

What is the major component of gallstones?

A

Cholesterol

416
Q

What are the components of pigment stones?

A

Calcium bilirubinate

417
Q

What are the risk factors for gallstones?

A 
Fair
Fat
Fertile
Female
Forty
OCC, Crohn's
418
Q

Where do most pancreatic cancers arise from?

A

Head of the pancreas

419
Q

What is a common cause of pancreatic cancers?

420
Q

What are the risk factors for pancreatic cancer?

A 
Age>60
Smoking
Obesity
T2DM
Chronic pancreatitis
421
Q

What are the signs and symptoms of pancreatic cancer?

A 
FLAWs
Steatorrhoea
Loss of endocrine function - diabetes
Painless jaundice
Trosseau sign (Migratory thrombophlebitis)
422
Q

What is trousseau sign in pancreatic cancer?

A

Migratory thrombophelbitis

423
Q

What is Courvoisier’s law?

A

In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

424
Q

What tumour marker is associated with pancreatic cancer?

425
Q

What is the diagnostic investigation for pancreatic cancer?

A

Biopsy via ERCP or EUS

426
Q

What does a high-resolution CT scan reveal in pancreatic cancer?

A

Double duct sign

427
Q

What is the first line radiological sign for pancreatic cancer?

A

Abdominal ultrasound

428
Q

What is the definitive management for pancreatic cancer?

A

Whipple’s resection + adjuvant chemo- pancreaticoduodenectomy only is resectable

429
Q

What does double duct sign suggest?

A

Pancreatic cancer

430
Q

What is cholangiocarcinoma?

A

Cancer arising in the bile ducts either intrahepatic or extrahepatic

431
Q

What does Sister-Mary Joseph Nodule represent?

A

Periumbilical lymphadenopathy

432
Q

What does a Virchow’s node represent?

A

supraclavicular lymphadenopathy

433
Q

what is the presentation of cholangiocarcinoma?

A

Jaundice (painless)
Palpable gallbladder
Pruritus
Pale stool, dark urine

434
Q

Which tumour markers are raised in a cholangiocarcinoma?

435
Q

What. is the gold standard investigation for cholangiocarcinoma?

A

ERCP with biopsy

436
Q

What is the initial radiological investigation for cholangiocarcinoma?

A

Abdominal USS

437
Q

What is the management of cholangiocarcinoma?

A

Removal of bile duct – small and localised tumour
Partial hepatectomy – intrahepatic
Whipple’s procedure – for distal bile duct tumours

438
Q

Which biological therapy is indicated for hepatocellular carcinoma?

439
Q

What is the first-line investigation for pancreatic cancer?

A

CT abdomen

440
Q

Which antibodies are associated with autoimmune hepatitis?

A

ANA
ASMA
Anti-LKM

441
Q

Which autoantibodies are associated with Type 1 AIH?

A

Antinuclear antibodies

442
Q

Which autoantibodies are associated with Type 2 AIH?

A

Antibodies to liver/kidney microsomes

443
Q

What is the presentation of autoimmune hepatitis?

A 
Fatigue/malaise
Anorexia
Abdominal discomfort
Hepatomegaly 
Jaundice
Amenrrhoea
Epistaxis
Stigmata of chronic liver disease

Pruritus, arthralgia, nausea, fever and spider angiomata

444
Q

What LFTs are seen in AIH?

A

Raised AST, ALT, GGT, ALP and BR

Low Albumin

445
Q

What does an FBC reveal in AIH?

A

Low Hb, platelets, and WCC (Hypersplenism)

Hypergammaglobulinemia

446
Q

What is the diagnostic investigation for autoimmune hepatitis?

A

Liver biopsy

447
Q

What does a liver biopsy reveal in autoimmune heaptitis?

A

Portal mononuclear and plasma cell infiltrate

448
Q

What is the acute management for autoimmune hepatitis?

A

High-dose corticosteroids (prednisolone) followed by maintenance treatment with gradual reduction in dose

449
Q

What is the maintenance management for autoimmune hepatitis?

A

Azathioprine or 6-mercaptopurine (steroid-sparing agents) with frequent LFT and FBC monitoring.

450
Q

What should be monitored prior to initiating azathioprine or 6-MP?

A

TPMT1 activity

451
Q

What is the definitive treatment for severe autoimmune hepatitis?

A

Liver transplantation

452
Q

What are the prodromal period symptoms for acute hepatitis A?

A

Fever
Malaise
Nausea and vomiting

453
Q

What are the hepatitis symptoms associated with acute hepatitis A?

A

Jaundice - 2 weeks after infection

Hepatomegaly + RUQ pain

Clay coloured stools

Pruritus

Dark urine

454
Q

What is elevated in fulminant hepatitis?

A

Raised serum creatinine

455
Q

What is the LFT picture in acute hepatitis A?

A

Raised AST, ALT, ALP and BR

456
Q

What HepA antibodies are positive during an acute illness?

A

IgM Anti-HAV

Elevated for a period of 3-5 months

457
Q

What HepA antibodies indicate recovery phase?

A

Anti-HAV IgG

458
Q

What is the management for acute HepA?

A

Supportive care - bed rest and symptomatic treatment

  • Antipyretics
  • Anti-emetics
  • Cholestryamine for severe pruritus
459
Q

How is HepB transmitted?

A

Sexual contact, blood, and vertical transmission (from mother to baby).

460
Q

What are the prodrome symptoms for HepB?

A
  • Malaise
  • Headache
  • Anorexia
  • Nausea and vomiting
  • Diarrhoea
  • RUQ pain
  • Serum-sickness type illness (e.g., fever, arthralgia, polyarthritis, urticaria, maculopapular rash).
461
Q

What HepB antibodies are associated with HepB acute?

A
  • HBsAg Positive

* IgM anti-HBcAg

462
Q

What HBV antibodies are associated with chronic HepB?

A
  • HBsAg positive

* IgG anti-HBcAg

463
Q

What HBV Antibodies indicate a cleared HbV infection?

A
  • Anti-HBsAg antibody positive

* IgG anti-HBcAg

464
Q

What is the management for chronic HBV?

A

Entecavir
Tenofovir
Interferon Alpha

465
Q

What is the transmission for HepC?

A

Transmission: Parenteral
• Sexual transmission
• Vertical transmission (Mother to child)

N.B: Transmission is through percutaneous exposure to infected blood – Injection of illicit drugs or transfusion of contaminated blood products.

466
Q

What is the ratio of AST/ALT associated with alcoholic liver disease?

467
Q

What electrolyte abnormality is associated with alcoholic hepatitis?

A

Hyponatremia

468
Q

Define acute pancreatitis

A

Defined as the acute inflammatory process of the pancreas.
• Mild: Minimal organ dysfunction and uneventful recovery (80%)
• Severe: Organ failure and/or local complications  Necrosis, abscesses, and pseudocysts (20%),

469
Q

What are the common causes of pancreatitis?

A
  • Idiopathic
  • Gallstones
  • Ethanol- Alcohol causes 80% of cases
  • Trauma
  • Steroids
  • Mumps/HIV/Coxsackievirus (infection) and Malignancy (pancreatic)
  • Autoimmune
  • Scorpion Venom
  • Hypercalcemia/hyperPTH/hyperlipidaemia/hypothermia (metabolic disorder)
  • ERCP and emboli
  • Drugs (Sodium valproate, steroids, thiazides, and azathioprine)
470
Q

What is the pain presentation for pancreatitis?

A

Epigastric pain radiating to the back

Relieved by sitting forward or lying in the foetal position

Aggravated by movement

Associated with anorexia, nausea and vomiting

471
Q

What are the signs of acute pancreatitis?

A 
Epigastric tenderness
Fever
Shock (tachycardia, tachypnoea)
Decreased bowel sounds (Ileus)
Jaundice
Tetany
472
Q

What are the signs of severe haemorrhagic pancreatitis?

A

Cullen’s sign
Grey-turner sign
Fox’s sign
Chvosteks sign

473
Q

What does Cullen’s sign represent?

A

Periumbillical bruising

474
Q

What does Grey-turner sign represent?

A

Flank bruising

475
Q

What is third spacing in acute pancreatitis?

A

Third-space fluid sequestration in pancreatitis is a result of release of inflammatory mediators, vasoactive mediators, and tissues  Vascular injury and increased capillary permeability

  • Extravasation of fluid into third space.
  • ARDs, pleural effusions, and AKI due to hypovolaemia.
476
Q

What is the first-line diagnostic investigation for acute pancreatitis?

A

Serum amylase (3x upper limit of normal)

-Does not correlate to disease severity

477
Q

What are the other causes of elevated amylase?

A

Perforated duodenal ulcers, cholecystitis
Ectopic pregnancy
Mesenteric infarction

478
Q

Which enzyme marker is a more accurate indicator for acute pancreatitis?

A

Raised serum lipase

479
Q

What is the LFT picture for gallstone pancreatitis?

A

ALP> 150 u/L

480
Q

Which blood markers are raised in acute pancreatitis?

A

CRP
WCC
Glucose - Reduced endocrine function
U&Es

481
Q

Which electrolyte is low in acute pancreatitis?

482
Q

What does an ABG reveal in acute pancreatitis?

A

Hypoxia

Metabolic acidosis

483
Q

What radiological investigations are indicated in the diagnosis of acute pancreatitis?

A

Abdominal ultrasound

  • Identifies gallstones
  • Evidence of biliary dilatation
484
Q

What does an AXR reveal in acute pancreatitis?

A

Sentinel loop sign - dilated proximal bowel loops adjacent to pancreas (Secondary localised inflammation)

485
Q

What scoring criteria is used to assess the severity of acute pancreatitis?

A

Modified Glasgow Imrie score combined with CRP >210 mg/L

486
Q

What are the parameters associated with a modified Glasgow imrie score?

A 
pO2 <8kPa
Age >55
WCC >15
Calcium <2
Urea >16
LDH OR AST >600 >200
Albumin >32
Glucose >10

a score of >= 3 –> Severe disease

487
Q

What is the acute management for acute pancreatitis?

A
  • Fluid & electrolyte resuscitation (Balanced crystalloid)
  • Urinary catheter and NG tube if vomiting (Enteral > parenteral – Reduced infective complications).
  • Analgesia
  • Blood sugar control
488
Q

What type of feed is recommended in acute pancereatitis?

A

Enteral feed

489
Q

What is the definitive management for gallstone pancreatitis?

A

ERCP and Sphincterotomy

Cholecystectomy early

490
Q

What is the most common form of pancreatic cancer?

A

Ductal carcinoma (Exocrine portion of the pancreas)

491
Q

Which antibiotics are the leading cause of Pseudomembranous colitis?

A

Clindamycin and cephalosporins

492
Q

Which score is used to assess the risk of an upper GI rebleed after endoscopy?

A

Rockall score

493
Q

Which HepB antibody suggests ongoing infection?

Phase1c Medicine (11 decks)

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