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MD3002 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are the 2 units in the medulla which control vomiting?

A
  1. Vomiting centre

2. Chemoreceptor Trigger Zone, CTZ

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2
Q

What do the vital centres of the medulla oblongata regulate?

A
  • Respiratory rhythm
  • Heart rate
  • BP
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3
Q

What do the non-vital centres of the medulla oblongata regulate?

A
  • Cough
  • Sneeze
  • Swallowing
  • Vomiting
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4
Q

Where is the Chemoreceptor Trigger Zone specifically located?

A

Area postrema in the floor of the 4th ventricle

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5
Q

What stimuli activate the CTZ (chemorecptor trigger zone)?

A
  • Chemical stimuli
  • Site of action of drugs inhibit/ stimulate emesis
  • Vestibular apparatus
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6
Q

What are the 3 different types of vomiting?

A
  1. Projectile vomiting- gastric outlet / upper GI obstruction
  2. Haematemesis- fresh/altered blood ie. oesophageal varies, bleeding gastric ulcer
  3. Early-morning- pregnancy, alcohol, metabolic disorders (uraemia)
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7
Q

What are the different triggers of nausea/vomiting?

A
  • Stimulation of sensory nerve endings in stomach & duodenum
  • Stimulation of vagal sensory endings in pharynx
  • Drugs/endogenous emetic substances
  • Disturbances of vestibular apparatus
  • Various stimuli of sensory nerves of heart & viscera
  • Rise in intracranial pressure
  • Nauseating smells, repulsive sights, emotional factors
  • Endocrine factors
  • Migraine
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8
Q

What is emesis?

A

Vomiting

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9
Q

Describe Antihistamines?

A
  • H1 histamine receptor antagonists
  • Useful in numerous causes of n/v, including motion sickness & vestibular disorders
  • Side-effects vary ie. drowsiness & antimuscarinic
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10
Q

Give 3 examples of Antihistamines?

A
  1. Cinnarizine
  2. Cyclizine
  3. Promethazine
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11
Q

Describe Antimuscarinics?

A
  • Muscarinic receptor antagonists
  • Blockade of muscarinic receptor-mediated impulses from labyrinth & visceral afferents
  • Useful in motion sickness
  • Side-effects constipation, transient bradycardia, dry mouth
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12
Q

Give an example of a Antimuscarinic?

A

Hyoscine hydrobromide

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13
Q

Describe Dopamine Antagonists?

A
  • Act centrally as dopamine antagonists on CTZ

- Active against CTZ-triggered vomiting but not stomach-induced

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14
Q

Give 3 examples of Dopamine Antagonists?

A
  1. Phenothiazines
  2. Domperidone
  3. Metoclopramide
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15
Q

Describe 5HT3 Antagonists?

A
  • Block 5HT3 receptors in GI tract & in the CNS

- Particularly useful in managing n/v in patients receiving cytotoxic & postoperative n/v

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16
Q

Give 4 examples of 5HT3 Antagonists?

A
  1. Dolasetron
  2. Granisetron
  3. Ondansetron
  4. Palonosetron
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17
Q

Describe Neurokinin 1 receptor antagonists?

A

Adjunct to dexamethasone & a 5HT3 antagonist in preventing n/v associated with chemotherapy

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18
Q

Give 2 examples of Neurokinin 1 receptor antagonists?

A
  1. Aprepitant

2. Fosaprepitant

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19
Q

Describe Synthetic Cannabinoids?

A
  • n/v caused by chemo unresponsive to conventional anti-emetics
  • Side-effects of drowsiness/dizziness
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20
Q

Give an example of a synthetic cannabinoid?

A

Nabilone

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21
Q

Describe Steroids?

A
  • Alone to treat vomiting associated with cancer chemotherapy
  • In conjunction with other antiemetics
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22
Q

Give 2 examples of other Neuroleptics?

A
  1. Haloperidol

2. Levomepromazine

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23
Q

Give 2 examples of Bulk Laxatives?

A
  1. Ispaghula husk

2. Methylcellulose

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24
Q

Give 6 examples of Stimulant Laxatives?

A
  1. Bisacodyl
  2. Dantron
  3. Docusate sodium
  4. Glycerol
  5. Senna
  6. Sodium picosulfate
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25
Q

Give 2 examples of Softener Laxatives?

A
  1. Arachis oil

2. Liquid paraffin

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26
Q

Give 4 examples of Osmotic Laxatives?

A
  1. Lactulose
  2. Macrogols
  3. Magnesium salts
  4. Rectal phosphates
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27
Q

Give 1 example of Peripheral opioid receptor antagonist?

A

Methylnaltrexone bromide

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28
Q

What are the 4 approaches for treatment of acute diarrhoea?

A
  1. Maintenance of fluid & electrolyte balance
  2. Antimotility drug
  3. Antispasmodics
  4. Occasionally antibacterial agent is indicated
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29
Q

Give 4 examples of Antimotility agents?

A
  1. Codeine
  2. Co-phenotrope
  3. Loperamide (imodium)
  4. Morphine
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30
Q

Give an example of a Adsorbents?

A

Kaolin

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31
Q

What are adsorbents NOT used for?

A

ACUTE diarrhoea

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32
Q

Give 3 examples of bulk forming drugs?

A
  1. Ispaghula
  2. Methylcellulose
  3. Sterculia
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33
Q

What 5 things does Bile contain?

A
  1. Bile salts
  2. Bilirubin
  3. Cholesterol
  4. Lecithin
  5. Plasma electrolytes
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34
Q

What is the treatment to dissolve gallstones?

A

Ursodeoxycholic acid

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35
Q

What is the treatment for biliary colic & acute cholecystitis?

A
  • Opioid ie. Morphine/Pethidine parenterally

- &/or diclofenac (NSAID) by suppository

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36
Q

Describe Colestyramine & its uses?

A
  • Anion-exchange resin
  • Forms insoluble complex with bile acids in intestine
  • Relieves pruritus associated with partial biliary obstruction & primary biliary cirrhosis
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37
Q

What diseases can Colestyramine be used in?

A
  • Hypercholesterolaemia

- Crohn’s disease

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38
Q

Name 2 benign (5%) tumours of the oesophagus?

A
  1. Mesenchymal Tumours

2. Squamous papillomas

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39
Q

Name 2 Malignant tumours of the oesophagus?

A
  1. Squamous cell carcinoma (90%)

2. Adenocarcinoma

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40
Q

Name 2 benign tumours of the stomach?

A
  1. Polyps

2. Mesenchymal

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41
Q

Name 4 Malignant tumours of the stomach?

A
  1. Carcinoma
  2. Lymphoma
  3. Carcinoid
  4. Mesenchymal
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42
Q

What is the most common benign tumour of the oesophagus?

A

Leiomyomas (smooth muscle)

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43
Q

What are the 4 factors associated with Squamous cell carcinoma?

A
  1. DIETARY- deficiency of vitamins (A,C,riboflavin), fungal contamination of foodstuff, high content of nitrates/nitrosamines
  2. LIFESTYLE- hot drinks/food, alcohol & tobacco
  3. OESOPHAGEAL DISORDERS- long-standing oesophagitis & Achalasia
  4. GENETIC PREDISPOSITION
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44
Q

What is the incidence (in %) of Squamous cell carcinoma in the 3 different parts of the oesophagus?

A
  • 50% in middle 1/3
  • 30% in lower 1/3
  • 20% in upper 1/3
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45
Q

What does squamous cell carcinoma look like?

A

Small gray-white, plaque-like thickenings that become tumourous masses

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46
Q

What are the 3 patterns of squamous cell carcinoma in the oesophagus?

A
  1. Protruded polypoid exophytic (60%)
  2. Flat, diffuse, infiltrative (15%)
  3. Excavated, ulcerated (25%)
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47
Q

What are the histological changes in squamous cell carcinoma?

A
  • Pleomorphism
  • Hyperchromatism
  • Mitotic figures
  • Atypia
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48
Q

What are the clinical features of squamous cell carcinoma of the oesophagus?

A
  • Dysphagia
  • Extreme weight loss
  • Haemorrhage & sepsis
  • Cancerous tracheoesophageal fistula
  • Metastases to lymph nodes (cervical, mediastinal, paratracheal etc)
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49
Q

What is the prognosis for a patient with squamous cell carcinoma in the oesophagus?

A

5% overall five-year survival

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50
Q

Describe Adenocarcinoma of the oesophagus?

A
  • Lower 1/3
  • Arise from Barrett mucosa (10%)
  • Tobacco & obesity
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51
Q

What does adenocarcinoma of the oesophagus look like?

A
  • Flat/raised patches or nodular masses

- May be infiltrative/deeply ulcerated

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52
Q

Describe the histology of adenocarcinoma of the oesophagus?

A

Mucin-producing glandular tumours

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53
Q

What are the clinical features of adenocarcinoma of the oesophagus?

A
  • Dysphagia
  • Progressive weight loss
  • Bleeding
  • Chest pain
  • Vomiting
  • Heartburn
  • Regurgitation
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54
Q

What is the prognosis of a patient with adenocarcinoma in the oesophagus?

A

20% overall five-year survival

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55
Q

What are benign polyps in the stomach?

A

Nodule/mass that projects above the level of the surrounding mucosa, usually in the antrum

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56
Q

Describe Non-neoplastic (90%) polyps of the stomach?

A
  • Small & sessile (without stalk)
  • Hyperplastic epithelium
  • Cystically dilated glandular tissue
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57
Q

Describe neoplastic- adenomas (5-10%) of the stomach?

A
  • Proliferative dysplastic epithelium
  • Malignant
  • Sessile / pedunculated (stalk)
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58
Q

What are the 3 factors associated with gastric carcinomas in the stomach?

A
  1. ENVIRONMENTAL- H. pylori infection, diet, socioeconomic status, smoking
  2. HOST- chronic gastritis, gastric adenomas, Barrett oesophagus
  3. GENETIC FACTORS- blood group A, family history, hereditary nonpolyposis colon cancer syndrome, familial gastric carcinoma syndrome
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59
Q

How common are the different locations for gastric carcinomas?

A
  • Pylorus & antrum (50-60%)
  • Cardia (25%)
  • Remainder in body & fundus
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60
Q

What are the 3 different macroscopic growth patterns of gastric carcinomas?

A
  1. Exophytic
  2. Flat/depressed –> Linitis plastica
  3. Excavated
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61
Q

What is the morphology of Linitis plastica growth pattern?

A
  • “Leather bottle”
  • Diffuse infiltrative gastric carcinoma
  • Mucosal erosion
  • Markedly thickened gastric wall
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62
Q

What are the 3 different types of adenocarcinomas according to the Lauren Classification?

A
  1. Intestinal type
  2. Diffuse type
  3. Mixed type
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63
Q

Describe the Intestinal type adenocarcinoma according to the Lauren Classification?

A
  • Neoplastic intestinal glands resembling those of colonic adenocarcinoma
  • Cell contain apical mucin vacuoles, abundant mucin may be present in gland lumens
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64
Q

Describe the Diffuse type adenocarcinoma according to the Lauren Classification?

A
  • Gastric-type mucous cells, generally don’t form glands, rather permeate the mucosa & wall as scattered individual cells/small clusters in “infiltrative” growth pattern
  • Mucin expands malignant cells & pushes the nucleus to periphery, creating “signet ring”
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65
Q

Describe the spread of gastric carcinomas?

A
  • Supraclavicular (Virchow) node
  • Duodenum, pancreas, retroperitoneum
  • Metastases to Liver/lungs
  • Metastases to ovaries called Krukenberg tumour
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66
Q

What are the clinical features of gastric carcinomas?

A
  • Asymptomatic until late
  • Weight loss
  • Abdominal pain
  • Anorexia
  • Vomiting
  • Altered bowel habits
  • Dysphagia
  • Anaemic symptoms
  • Haemorrhage
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67
Q

What is the prognosis of a patient with gastric carcinoma?

A
  • Early: 90-95% five-year survival

- Advanced: <15% five-year survival

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68
Q

What % of gastric malignancies does gastric lymphoma make up?

A

5%

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69
Q

What cell is involved in gastric lymphoma?

A

B cell lymphoma of mucousa associated lymphoid tissue (MALT)

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70
Q

What are gastric lymphomas associated with?

A

> 80% associated with chronic gastritis & H. pylori infection

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71
Q

What is the prognosis of a patient with gastric lymphoma?

A

50% five-year survival

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72
Q

What is the morphology of gastric lymphoma?

A
  • Commonly occurs in mucosa/superficial submucosa
  • Lymphocytic infiltrate of the lamina propria surrounds gastric glands & massively infiltrated with atypical lymphocytes & undergoing destruction
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73
Q

What is the functional unit of the liver?

A

Liver lobule

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74
Q

What is the liver lobule composed of?

A
  • Hepatocytes arranged in plates
  • Bloodstream
  • Bile canaliculi
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75
Q

What lies within the vascular spaces (sinusoids) of the liver?

A

Kupffer cells (phagocytic macrophages)

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76
Q

What are the 4 functions of the liver?

A
  1. METABOLIC- carbohydrates, hormones, lipids, drugs & proteins
  2. STORAGE- glycogen, vitamins, iron
  3. PROTECTIVE- detoxification & elimination of toxic compounds, Kupffer cells ingest bacteria & foreign material from blood
  4. BILE- formed in biliary canaliculi, emulsifies fats & route for waste removal
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77
Q

What are the 7 different classifications of liver disease?

A
  1. Infection
  2. Toxic/drug induced
  3. Autoimmune
  4. Biliary tract obstruction
  5. Vascular
  6. Metabolic
  7. Neoplastic
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78
Q

What is Cholestasis?

A

Failure to produce or excrete bile

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79
Q

What is Intrahepatic cholestasis?

A

Problems in secretion of bile by hepatocytes due to damage

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80
Q

What is Extrahepatic?

A

Problems with flow of bile out of the liver due to obstruction

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81
Q

What happens do your urine and stool in Cholestasis & Jaundice?

A
  • Darkened urine

- Lighter stool

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82
Q

What leads to Jaundice?

A
  • Accumulation of (conjugated) bilirubin in the blood

- Excessive haemolysis

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83
Q

What is the definition of Acute Hepatic Failure?

A

Development of severe hepatic dysfunction within 21wks of onset of disease

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84
Q

What is the definition of Chronic Hepatic Failure?

A

Progressive decline in liver function with established disease

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85
Q

What are the 3 possible causes of Acute Hepatitis liver disease?

A
  1. Poisoning (paracetamol)
  2. Infection (Hepatitis A-C)
  3. Inadequate perfusion
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86
Q

What are the 3 possible outcomes for patients with Acute Hepatitis liver disease?

A
  1. Resolution (majority)
  2. Progression to acute hepatic failure
  3. Progression to chronic hepatic damage
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87
Q

What are the 3 common causes of Chronic Liver disease?

A
  1. Alcoholic fatty liver
  2. Chronic active hepatitis
  3. Primary biliary cirrhosis
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88
Q

What are the 3 unusual causes of Chronic Liver disease?

A
  1. alpha-1 AT deficiency
  2. Wilson’s disease
  3. Haemochromatosis
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89
Q

What are the consequences of Chronic Liver disease?

A
  • Cirrhosis
  • Portal hypertension
  • Ascites
  • Renal failure
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90
Q

What is Cirrhosis?

A

Irreversible shrinkage of the liver & fibrosis

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91
Q

What are ascites?

A

Accumulation of fluid in the peritoneal cavity

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92
Q

What are the consequences of Liver Failure?

A
  • Inadequate synthesis of albumin
  • Inadequate synthesis of clotting factors
  • Inability to eliminate bilirubin
  • Inability to eliminate nitrogenous waste
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93
Q

What are signs of liver failure?

A
  • Oedema
  • Bruising
  • Ascites
  • Encephelopathy
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94
Q

What is the definition of Hepatic encephalopathy?

A

Poorly defined neuro-pschiatric disorder that occurs when products normally metabolised by the liver accumulate in the systemic circulation ie. ammonia

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95
Q

What are the current liver function tests?

A
  • Aminotranferases: ALT & ASL for liver cell damage
  • Bilirubin: for cholestasis
  • ALP & γ-GT: for biliary epithelial damage & obstruction
  • Albumin: for synthetic function
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96
Q

When would low albumin be found?

A
  • Post-surgical/ITU due to redistribution
  • Significant malnutrition
  • Nephrotic syndrome
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97
Q

What is Bilirubin?

A

Pigment formed in liver by breakdown of haemoglobin & excreted in bile

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98
Q

Describe the differences between unconjugated & conjugated bilirubin?

A
  • Unconjugated taken up by liver & conjugated

- Conjugated excreted in bile

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99
Q

What is Urobilinogen?

A

Small amounts of bilirubin reabsorbed & excreted in urine

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100
Q

What is the net result of all the different types of cholestasis?

A

Accumulation of bilirubin in circulation = Jaundice

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101
Q

What are sensitive, non-specific enzymes of acute damage to hepatocytes that we can test?

A

AST & ALT

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102
Q

When is γ-GT (enzyme) raised?

A

Cholestasis, alcohol & drugs (phenytoin)

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103
Q

Where else can you find ALT enzyme?

A
  • Cardiac muscle

- Erythrocytes

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104
Q

Where else can you find ALP enzyme?

A
  • Bone
  • Gut
  • Placenta
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105
Q

Where else can you find γ-GT enzyme?

A
  • Bone
  • Biliary tract
  • Pancreas
  • Kidney
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106
Q

Other than liver disease what other things can cause Bilirubin to increase?

A
  • Haemolysis

- Gilberts syndrome

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107
Q

Other than liver disease what other things can cause ALP enzyme to increase?

A
  • Pregnancy

- Adolescence

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108
Q

Other than liver disease what other things can cause AST enzyme to increase?

A
  • Skeletal muscle disorders

- MI

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109
Q

What are the advantages of current LFTs?

A
  • Cheap
  • Widely available
  • Interpretable
  • Direct subsequent investigation (imaging)
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110
Q

What are the disadvantages of current LFTs?

A
  • In newly discovered diseases LFTs have no diagnostic value
  • Little prognostic value in liver transplantation
  • Little value for evaluating therapeutic success
  • Do not assess liver “function”
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111
Q

What is the aetiology of liver disease?

A
  • α-1 antitrypsin deficiency
  • α-fetoprotein tumour marker
  • Caeruloplasmin/copper studies
  • Hepatitis serology
  • Iron studies
  • Autoantibodies
  • Radiology
  • Liver biopsy
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112
Q

Where is the spleen situated in relation to the ribs?

A

Left 9-11 ribs posteriorly

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113
Q

What are the 3 function of the spleen?

A
  1. Mechanical filtration of red blood cells
  2. Active immune response through humeral & cell mediated pathways
  3. Haematopoesis until 5th month of gestation
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114
Q

What vessels does the Gastrosplenic ligament carry?

A

Left gastro-epiploic & short gastric branches of splenic artery (& veins)

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115
Q

What vessels does the Lienorenal (Splenorenal) ligament carry?

A

Splenic artery & vein

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116
Q

What can rib fractures of ribs 9-11 cause?

A

Rupture to the spleen, causing intraperitoneal haemorrhage

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117
Q

Why do you need to be careful when surgically performing splenectomy?

A

Avoid injuring the tail of pancreas when ligating splenic vessels

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118
Q

Describe the splenic artery?

A
  • Largest branch of coeliac artery
  • Along upper border of pancreas
  • Divides into 6 branches which enter spleen at its hilum
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119
Q

Describe the splenic vein?

A
  • Leaves hilum & runs behind tail & body of pancreas

- Behind neck of pancreas, joins superior mesenteric vein to form portal vein (L1)

120
Q

Describe the lymph drainage of the spleen?

A
  • From hilum & pass through the few lymph nodes along course of splenic artery
  • Drain into coeliac nodes
121
Q

Describe the nerve supply of the spleen?

A

Coeliac plexus (foregut T5-9)

122
Q

What does the portal vein drain?

A
  • Lower 1/3 of the oesophagus to halfway down the anal canal
  • Spleen, pancreas & gallbladder
123
Q

What 2 things mix in the sinusoids of the liver?

A

Portal venous blood & oxygenated blood from hepatic artery

124
Q

What union froms the portal vein?

A

Splenic & Superior Mesenteric veins

125
Q

What does the left gastric vein drain?

A

Lower oesophagus & left end of the lesser curve of stomach

126
Q

Where does the left gastric vein drain to?

A

Directly to portal vein

127
Q

What does the inferior mesenteric vein join to form?

A

Joins splenic vein behind pancreas, then joining with portal vein

128
Q

Where does the cystic vein usually drain into?

A

Portal vein, may drain into liver

129
Q

Where does the right gastric vein drain into?

A

Right end of lesser curve of stomach directly to portal vein

130
Q

What are the 4 sites of porto-systemic anastomosis?

A
  1. Lower 1/3 of oesophagus (left gastric vein & oesophageal veins draining into azygos veins)
  2. 1/2 down anal canal (superior rectal veins & middle & inferior rectal veins)
  3. Para-umbilical veins (left branch of portal vein & superficial veins of anterior abdo wall)
  4. Retroperitoneal ascending colon, descending, pancreas & liver portal tributaries anastamose with renal lumbar & phrenic veins
131
Q

What do the para-umbilical veins drain into?

A

Falciform ligament & accompany the ligament theres

132
Q

What are the 3 suprahepatic causes of portal blockage?

A
  1. Cardiac disease
  2. Hepatic vein thrombosis
  3. IVC thrombosis
133
Q

What is the normal portal venous pressure?

A

5-10mmHg

134
Q

What is the hepatic cause of portal blockage?

A

Cirrhosis (alcohol, hepatitis)

135
Q

What is the 2 infra-hepatic causes of portal blockage?

A
  1. Portal vein thrombosis

2. Splenic vein thrombosis

136
Q

What structures lie anterior to the Abdominal Aorta?

A
  • Pancreas
  • Splenic vein
  • Left renal vein
  • Duodenum
  • Root of mesentery & coils of small bowel
  • Lumbar veins
137
Q

What structures lie on the right of the Abdominal Aorta?

A
  • Cisterna chyli
  • Thoracic duct
  • Azygos vein
  • IVC
138
Q

What are the 3 unpaired, anterior/visceral branches of the Abdominal aorta?

A
  1. Coeliac trunk (T12)
  2. Superior mesenteric artery (L1)
  3. Inferior mesenteric artery (L3)
139
Q

What are the 3 paired visceral branches of the abdominal aorta?

A
  1. Middle suprarenal arteries
  2. Renal arteries (L1)
  3. Testicular/ovarian arteries (L2)
140
Q

What are the 3 posterior diaphragm/body wall branches of the abdominal aorta?

A
  1. Inferior phrenic arteries
  2. Lumbar arteries
  3. Median sacral artery
141
Q

What separates the IVC from the portal vein?

A

Entrance into lesser sac

142
Q

What are the 4 Tributaries of the IVC?

A
  1. 2 or 3 anterior visceral tributaries: hepatic veins
  2. 3 lateral visceral tributaries: right suprarenal vein, both renal veins, right gonadal vein
  3. 5 lateral abdominal wall tributaries: inferior phrenic vein & 4 lumbar veins
  4. 3 veins of origin: 2 common iliac & median sacral vein
143
Q

What are the primary imaging tools for the GI tract?

A
  • X-ray
  • CT
  • Ultrasound scan
144
Q

What are the secondary imaging tools for the GI tract?

A
  • MRI

- Fluoroscopy

145
Q

What is the overall sensitivity of X-ray in GI tract imaging?

A

30%

146
Q

What are the pros of X-ray in GI tract imaging?

A
  • Widely available
  • Easy
  • Excludes bowel obstruction/perforation
147
Q

What are the pros of Ultrasound in GI tract imaging?

A
  • Easy, safe
  • Clear visualization of solid organs, free fluid, aorta, pelvis
  • Correlate imaging with tenderness
148
Q

What are the pros of CT in GI tract imaging?

A
  • Explosion
  • Quick
  • Accurate
  • Allows better planning of surgery/intervention
149
Q

What are the pros & cons of MRI in GI tract imaging?

A
  • No radiation
  • Good soft tissue delineation esp pelvis
  • Long examination times
  • Contraindications/claustrophobia
150
Q

Describe the signs/symptoms of Acute Appendicitis?

A
  • Periumbilical pain, nausea & vomiting
  • Localised in right iliac fossa
  • Challenging diagnosis
151
Q

What imaging techniques would you use to diagnose Acute Appendicitis?

A

Ultrasound scan 1st then CT if this is inconclusive (no x-ray)

152
Q

What increases incidence of Acute Diverticulitis?

A

Increase in age

153
Q

What can be the complications of Acute Diverticulitis?

A
  • Abscess
  • Obstruction
  • Perforation
  • Fistulae
154
Q

What are Colo-vesical fistula?

A

Communications between the lumen of the colon and that of the bladder

155
Q

What imaging techniques would you use to diagnose Acute Diverticulitis?

A
  • Plain x-ray (exclude obstruction/perforation)

- CT

156
Q

What is Acute Cholecystitis?

A

Inflammation of the gallbladder

157
Q

What is Acute Cholecystitis almost always secondary to?

A

Gallstones

158
Q

What 3 things is diagnosis of Acute Cholecystitis based on?

A
  1. One local sign of inflammation (Right umbilical pain etc.)
  2. One sign of inflammation (fever, WCC, CRP)
  3. Confirmatory imaging
159
Q

When would you use MRI for diagnosing Acute Cholecystitis?

A

If biliary tree is dilated

160
Q

What can an Ultrasound scan of Acute Cholecystitis show?

A
  • Gallstones
  • Gallbladder wall thickening
  • Local fluid
161
Q

What does MRCP stand for?

A

MR cholangiopancreatography

162
Q

What is Emphysematous cholecystitis?

A

Air in gallbladder

163
Q

What are the common causes for small bowel obstruction?

A
  • Adhesions
  • Cancer
  • Herniae
  • Gallstone ileus
164
Q

What are the symptoms/signs of small bowel obstruction?

A
  • Vomiting, pain, distension

- Increased bowel sounds, tenderness, palpable loops

165
Q

Are adhesions seen in a CT scan of small bowel obstruction?

A

NO

166
Q

What are the causes of large bowel obstruction?

A
  • Colorectal cancer (60%)
  • Volvulus (15%)
  • Diverticulitis (10%)
167
Q

What are the common causes of perforation?

A
  • Perforated ulcer

- Diverticular

168
Q

What are the less common causes of perforation?

A
  • Secondary to cancer

- Secondary to ischaemia

169
Q

What % of bowel blood flow defines bowel ischaemia?

A

<10%

170
Q

What are the causes for bowel ischaemia?

A
  • Arterial occlusion (60-70%)
  • Venous occlusion (5-10%)
  • Non-occlusive hypoperfusion (20-30%)
171
Q

What is the role of plain film?

A

Obstruction & Perforation

172
Q

What is the role of Ultrasound scan?

A

Right umbilical quadrant/ right iliac fossa pain

173
Q

What is the role of CT scan?

A

Primary imaging technique for acute abdominal pain EXCEPT for acute cholecystitis/appendicitis

174
Q

What does the liver synthesise?

A
  • Albumin
  • Clotting factors
  • Complement
  • α-1-antitrypsin
  • Thrombopoietin
175
Q

What does the liver produce?

A

Bile through conjugation of bilirubin

176
Q

What does the liver breakdown?

A
  • Drugs
  • Insulin
  • Ammonia
177
Q

What does the Kupffer cells in the liver do?

A

Phagocytose old blood cells, bacteria & foreign materials from the bloodstream/gut

178
Q

What is Jaundice?

A
  • Yellowing of skin & mucosal surfaces, intense itch

- Bilirubin >40μmol/L

179
Q

What is Prehepatic Jaundice?

A

Haemolysis –> release of bilirubin from RBC’s

180
Q

What is Intrahepatic Jaundice?

A

Liver disease –> excess bilirubin in liver & bloodstream

181
Q

What is Post-hepatic Jaundice?

A

Obstruction of bile outflow –> dark urine & pale stools

182
Q

What zone in a hepatocyte will be effected worse with toxins?

A

Zone 3 next to the central vein

183
Q

What 3 things can Alcoholic liver injury cause?

A
  1. Steatosis
  2. Cirrhosis
  3. Acute hepatitis with Mallory’s hyaline
184
Q

What is Steatosis?

A

Fat deposition due to liver breaking down toxins instead of fats

185
Q

What happens during the inflammatory reaction in Alcoholic liver injury?

A

Acetaldehyde binds to hepatocytes causing damage –> fibrosis

186
Q

What is Mallory hyaline?

A

In damaged hepatocytes, you get aggregates of damaged hyaline protein which causes the cell to die

187
Q

What 2 things leads to cirrhosis?

A

Fibrosis (collagen) + Regeneration –> Cirrhosis

188
Q

What are the 3 morphological classifications of Cirrhosis?

A
  1. Micronodular (<3mm)
  2. Macronodular (>3mm)
  3. Mixed
189
Q

What are complications of cirrhosis?

A
  • Liver failure
  • Hepatic encephalopathy (ammonia)
  • Hyperoestrogenism
  • Low clotting factors (bleeding)
  • Portal hypertension
  • Azygous Vein shunting
  • Hepatocellular carcinoma
190
Q

What are signs of hyperoestrogenism?

A
  • Palmar erythema

- Gynaecomastia

191
Q

What drug overdose can cause injury to liver cells (hepatocellular)?

A

Paracetamol overdose

192
Q

What drug can cause injury to bile production/secretion cells (cholestatic)?

A

Methyl testosterone

193
Q

Describe Acute Biliary Obstruction?

A
  • Usually due to gallstones
  • Colicky pain & jaundice
  • Can cause cholangitis
194
Q

How long does hepatitis have to last before it is classed as chronic?

A

> 6 months

195
Q

What are the 4 possible causes of Chronic Hepatitis?

A
  1. Viral
  2. Alcohol
  3. Drugs
  4. Autoimmune
196
Q

What are the 3 steps for classification of Chronic Hepatitis?

A
  1. Type- aetiology
  2. Grade- degree of inflammation
  3. Stage- degree of fibrosis
197
Q

When does autoimmune hepatits usually present and in which gender is it more common?

A
  • Mid to late teens

- Females

198
Q

What is Interface Hepatitis?

A
  • Hepatocytes around portal triad become damaged

- Because antibodies & cells are getting in there, triad becomes necrotic and swollen –> fibrosis

199
Q

Describe Chronic Hepatitis?

A
  • Plasma cells & swollen hepatocytes
  • Fibrosis
  • Patients may benefit from steriods
200
Q

What are the stages of Primary Biliary Cirrhosis?

A
  • Autoimmune destruction of bile duct epithelium
  • Proliferation of small bile ducts
  • Architectural disturbance
  • Cirrhosis
201
Q

What are the signs and symptoms of Primary Biliary Cirrhosis?

A
  • Jaundice, pruritis, xanthelasmata

- Raised ALP + IgM, AMA

202
Q

What is Haemochromatosis?

A

Iron deposition in liver causing alteration of architecture –> fibrosis –> cirrhosis

203
Q

What is the gene associated with Haemochromatosis?

A

HFE gene

204
Q

What are secondary causes of Haemochromotosis?

A

Regular blood transfusions/iron supplements

205
Q

What is the usual treatment of Haemochromotosis?

A

Regular venesection (give blood) to test iron & ferritin levels

206
Q

Describe what α-1-antitrypsin Deficiency is and what can happen?

A
  • Autosomal recessive disorder
  • Proteins build up in hepatocytes as hyaline
  • Lead to cirrhosis
  • Associated with emphysema
207
Q

What does NASH/NAFLD stand for?

A

Non-alcoholic steatohepatitis/Non-alcoholic fatty liver disease

208
Q

What is NASH/NAFLD associated with?

A

Metabolic Syndrome (DM II, hypertension, decreased HDL cholesterol, increased triglycerides)

209
Q

Describe Wilson’s disease?

A
  • Autosomal recessive disorder

- Failure of liver to excrete copper in bile –> cirrhosis due to build up

210
Q

Other than liver cirrhosis what other things can Wilson’s disease cause?

A
  • Neurological dysfunction by copper build up in brain
  • Kayser-Fleischer rings
  • Low caeruloplasmin
211
Q

What is a Hamartoma?

A

Benign enlarged pocket of normal cells growing from an organ

212
Q

Give examples of 2 benign liver tumours?

A
  • Adenoma

- Haemangioma

213
Q

Give examples of 2 primary malignant liver tumours?

A
  • Hepatocellular carcinoma

- Cholangiocarcinoma

214
Q

What is the aetiology of Hepatocellular Carcinoma?

A
  • Aflatoxins (fungal origin)
  • Hepatits B & C viruses
  • Cirrhosis
215
Q

What problems can arise in the Biliary system?

A
  • Atresia
  • Choledocal cysts
  • Gallstones (cholelithiasis)
  • Cholangiocarcinoma
  • Obstruction
216
Q

Where does Cholangiocarcinoma arise from?

A

Arises from bile duct epithelium anywhere in the biliary system

217
Q

What disease is Cholangiocarcinoma associated with?

A

Ulcerative Colitis

218
Q

What does Cholangiocarcinoma cause?

A
  • Obstructive jaundice
  • Itch
  • Weight loss
  • Lethargy
219
Q

What can Cholangiocarcinoma lead to?

A

Rupture of common bile duct/gallbladder - prognosis poor!

220
Q

What are the risk factors for Gallstones?

A
  • Female, Fair, Fat, Forty, Fertile

- Diabetes mellitus

221
Q

What can gallstones cause?

A
  • Cholecystitis
  • Obstructive jaundice
  • Cholangiocarcinoma
  • Pancreatitis
  • Cholangitis
222
Q

Describe Acute Cholecystitis?

A
  • Due to gallstones
  • Initially sterile then becomes infected
  • Lead to abscess/rupture
  • RUQ pain (biliary colic), fever, nausea, vomiting
223
Q

Describe Chronic Cholecystitis?

A
  • Invariably related to gallstones

- Chronic inflammation with wall thickening

224
Q

What are sign for Annular Pancreas as birth?

A
  • Polyhydramnios
  • Low birth weight
  • Poor feeding
225
Q

What are the metabolic consequences of acute Pancreatitis?

A
  • Decreased calcium
  • Descreased albumin
  • Increased glucose
226
Q

How do you diagnose Acute Pancreatitis?

A

High serum amylase

227
Q

What does chronic pancreatitis cause?

A
  • Fibrosis of pancreas which may lead to diabetes mellitus

- Reduced production of enzymes

228
Q

What can cause Pancreatitis?

A

” I GET SMASHED”

  • Idiopathic
  • Gallstones
  • Ethanol
  • Trauma
  • Scorpion poisoning
  • Mumps
  • Autoimmune
  • Steroids
  • Hypothermia
  • ERCP
  • Drugs
229
Q

Describe Pancreatic Carcinoma?

A
  • Adenocarcinoma
  • Smoking & diabetes mellitus
  • Painless, progressive jaundice
  • Weight loss
230
Q

What are the 5 types of IBD?

A
  1. Ulcerative Colitis
  2. Crohn’s disease
  3. Indeterminate colitis
  4. Pseudomembranous colitis
  5. Diverticulitis
231
Q

Who is prone to getting Ulcerative Coltitis?

A
  • Adolescence & early adulthood
  • Female > Male
  • Non-smokers
232
Q

Describe Ulcerative Colitis?

A
  • Relapsing/remitting course
  • Inflammatory change in colon
  • Rectum –> Variable length of colon
  • Continuous, circumferential, superficial mucosal inflammation
233
Q

What is PANcolitis?

A

When ulcerative colitis is over the entire colon

234
Q

What can Ulcerative colitis cause?

A
  • Iron-deficiency anaemia
  • Raised inflammatory markers (CRP)
  • Dehydration
  • Damage cells leading to dysplasia –> colonic carcinoma
235
Q

What does Ulcerative colitis look like macroscopically?

A

Multiple Pseudopolyps and ulcers along the mucosa of the colon

236
Q

What does Ulcerative colitis look is microscopically?

A
  • Inflamed mucosal layer
  • Crypts shortened/Atrophic
  • Crypt abscess
  • Broad based ulcer eroding into superficial submucosa
  • Plasma/neutrophils
237
Q

Who is prone to getting Crohn’s disease?

A
  • Adolescence & early adulthood
  • Female > Male
  • Smokers
238
Q

Describe Crohn’s disease?

A
  • Relapsing/remitting course
  • Inflammatory change anywhere in GI tract
  • Discreet, focal ulceration
  • “Skip lesions”
  • Terminal ileitis
239
Q

What can Crohn’s disease cause?

A
  • Anaemia: absorption/blood loss
  • Raised inflammatory markers (CRP)
  • Dehydration
240
Q

What does Crohn’s disease look like macroscopically?

A
  • Long streaks of linear ulceration
  • Cobble stone appearance
  • Fat wrap around entire circumference of the bowel
  • Narrow lumen
  • Fistulas (colon-bladder, colon-penis etc)
  • Thickened/fibrotic mesentery
241
Q

What does Crohn’s disease look like microscopically?

A
  • Crypts are shortened/Atrophic
  • +/- Crypt abscesses
  • Atrophic villi
  • Granulomas, Neutrophils/Lymphocytes
242
Q

Why does fat wrap around bowel in Crohn’s disease?

A

Body is trying to contain the inflammation of the bowel wall by wrapping fat

243
Q

What are some extra intestinal manifestations of IBD’s?

A
  • Inflammatory arthropathies
  • Erythema nudism (Crohn’s)
  • Pyoderma gangrenosum
  • Primary sclerosing cholangitis (UC)
  • Iritis/Uveitis
  • Aphthous stomatitis
244
Q

What are the symptoms/signs of Ulcerative Colitis?

A
  • Abdominal pain
  • Bloody, mucoid diarrhoea
  • Weight loss
  • Lethargy
  • Fever
  • Tenesmus
245
Q

What are the symptoms/signs of Crohn’s disease?

A
  • Abdominal pain after eating
  • Watery diarrhoea
  • Weight loss
  • Lethargy
  • Fever
  • +/- Tenesmus
246
Q

What infection can lead to Pseudomembranous Colitis?

A

C. difficile infection

247
Q

What causes Diverticulitis?

A

Increased pressure, particularly within sigmoid colon, cause the mucosa to herniate out

248
Q

What does Adenoma of the small intestine usually affect?

A

Enlarges Ampulla of Vater & turns it into a velvety surface

249
Q

Describe the appearance of Adenocarcinoma of the small intestine?

A
  • Napkin-ring encircling pattern

- Polypoid exophytic masses

250
Q

What are the signs/symptoms of Adenocarcinoma of the small intestine?

A
  • Obstruction
  • Cramping pain
  • Nausea
  • Vomiting
  • Weight loss
251
Q

What can Adenocarcinoma of the small intestine cause?

A

Obstructive Jaundice

252
Q

Give 2 examples of benign non-neoplastic polyps of the colon & rectum?

A
  1. Hyperplastic (90%)

2. Hamartomatous

253
Q

Give 3 examples of benign neoplastic (adenoma) of the colon & rectum?

A
  1. Tubular (most common)
  2. Villous
  3. Tubulovillous
254
Q

Where are 1/2 of Hyperplastic polyps found?

A

Rectosigmoid colon

255
Q

What is the histology of Hyperplastic polyps?

A
  • Well-formed glands & crypts
  • Lined by non-neoplastic epithelial cells
  • Most of which show differentiation into mature goblet or absorptive cells
  • No malignant potential
256
Q

What are Juvenile Hamartomatous polyps?

A

Malformations of the mucosal epithelium & lamina propria in children <5

257
Q

What is the histology of Juvenile Hamartomatous polyps?

A
  • Abundant cystically dilated glands
  • Inflammation is common
  • Surfaces may be congested/ulcerated
  • No malignant potential
258
Q

What is Peutz-Jeghers polyps?

A
  • Autosomal dominant syndrome due to mutation of STK11 gene located on chromosome 19
  • Mucosal epithelium, lamina propria and muscular mucosa
259
Q

What is the cause of neoplastic polyps- adenomas?

A

Arise as the result of epithelial proliferative dysplasia

260
Q

What can Adenomas be a precursor for?

A

Invasive colorectal adenocarcinomas

261
Q

What is the morphology of Tubular Adenomas?

A
  • SMALL are smooth-contoured & sessile

- LARGE are coarsely lobulated & have slender stalks, raspberry-like

262
Q

What is the Histology of Tubular Adenomas?

A
  • Stalk is composed of fibromuscular tissue & prominent blood vessels
  • Presence of dysplastic epithelium which may show mucin vacuoles
  • Degree of dysplasia is low-grade
  • Carcinomatous invasion into submucosal stalk of polyp constitutes invasive adenocarcinoma
263
Q

What does Villous Adenomas look like?

A

Velvety or cauliflower-like masses projecting 1 to 3cm above the surrounding normal mucosa

264
Q

What happens when invasive carcinoma occurs (40%) in a Villous Adenoma?

A

No stalk as a buffer zone so invasion is directly into the wall of the colon

265
Q

What are the clinical features of Colorectal Tubular & Tubulovillous adenomas?

A

Asymptomatic & many discovered during evaluation of anaemia or random bleeding

266
Q

What are the clinical features of Villous Adenomas?

A

Symptomatic & often discovered because of obvious rectal bleeding

267
Q

When is Endoscopic removal of a pedunculated adenoma is regarded as adequate?

A
  1. The adenocarcinoma is superficial & does not approved the margin of excision across the base of the stalk
  2. There is no vascular or lymphatic invasion
  3. Carcinoma is not poorly differentiated
268
Q

Can invasive adenocarcinoma arising in a sessile polyp be resected by polypectomy?

A

NO

269
Q

98% of all cancers in the large intestine are __________?

A

Adenocarcinomas

270
Q

What are the 5 dietary risk factors for Colorectal cancer?

A
  1. Excess dietary caloric intake
  2. Low vegetable fibre
  3. High refined carbohydrates
  4. Intake of red meat
  5. Decreased intake of protective micronutrients
271
Q

Describe the morphology of tumours in the proximal colon?

A
  • Polypoid, exophytic masses
  • Obstruction is uncommon
  • Penetrate the bowel wall as subserosal & serial white, from masses
272
Q

Describe the morphology of tumours in the distal colon?

A
  • Annular, encircling lesions
  • Margins are heaped up, firm & mid-region ulcerated
  • Lumen narrowed, proximal bowel may be distended
  • Penetrate the bowel wall as subserosal & serial white, firm masses
273
Q

What is the histology for Colorectal cancer?

A
  • Range from tall, columnar cells resembling adenomatous lesions to undifferentiated anaplastic masses
  • May produce mucin
  • Invasive tumour incites a strong desmoplastic stroma response
274
Q

What are the clinical features of caecum & right colonic cancer?

A
  • Fatigue
  • Weakness
  • Iron-deficiency anaemia
275
Q

What are the clinical features of left-sided lesions?

A
  • Occult bleeding
  • Changes in bowel habit
  • Crampy left lower quadrant discomfort
276
Q

What is iron-deficiency anaemia in an older male seen as?

A

GI cancer until proven otherwise

277
Q

All colorectal tumours spread to what 3 things?

A
  1. Adjacent structures
  2. Metastasis through lymphatics, blood vessels
  3. Regional lymph nodes, liver, lungs, bones, serosal membrane of peritoneal cavity, brain & others
278
Q

What is Dukes’ Stage for Cancer?

A

A) Confined to submucosa or muscle layer (90+%)
B) Spread through muscle layer, no lymph nodes (70%)
C) Involving lymph nodes (35%)

279
Q

What does the aggressive behaviour of carcinoid tumour correlates with?

A
  • Site of origin
  • Depth of local penetration
  • Size of tumour
  • Histological features of necrosis & mitosis
280
Q

What is the morphology of carcinoid tumours?

A
  • Usually solitary lesion
  • Appendix most common
  • Small intestine, rectum, stomach, colon
  • Intramural or submucosal masses that create small polypoid or plateau-like elevations <3cm
  • Solid, yellow-tan appearance on transection
281
Q

What is the histology of carcinoid tumours?

A
  • Neoplastic cells may form discrete islands, trabeculae, stands, glands or undifferentiated sheets
  • Tumour cells have pink granular cytoplasm & round to oval stippled nucleus
  • Tumour cells contain membrane-bound secretory granules
282
Q

What are the clinical features of Carcinoid tumours?

A
  • Rarely produce local symptoms
  • Cutaneous flushes & apparent cyanosis
  • Diarrhoea, cramps, nausea, vomiting
  • Cough, wheezing, dyspnoea
283
Q

What carcinoid tumours do NOT metastasise?

A

Appendiceal & Rectal Carcinoids

284
Q

What is the overall % five-year survival rate for carcinoids?

A

90%

285
Q

How does Gastrointestinal Lymphoma present?

A

Exhibit no evidence of liver, spleen, mediastinal lymph node or bone marrow involvement at the time of diagnosis

286
Q

What does MALT stand for?

A

Mucosa-associated lymphoid tissue

287
Q

What does IPSID stand for?

A

Immunoproliferative small-intestinal disease

288
Q

Give an example of a B-cell lymphoma?

A

Burkitt lymphoma

289
Q

Describe T-cell lymphomas?

A
  • Associated with long-standing malabsorption syndrome

- Prognosis poor

290
Q

Give 3 examples of Mesenchymal Tumours?

A
  1. Lipomas
  2. Leiomyomas
  3. Leiomyosarcomas
291
Q

Describe Lipomas?

A

Well-demarcated, firm nodules <4cm arising within the submucosa or muscular propria

292
Q

Describe Leiomyosarcomas?

A

Large, bulky, intramural masses that eventually fungate & ulcerate into lumen or project subserosally into abdominal space

293
Q

Describe the 3 zones of the anal canal?

A
  1. Upper (covered with rectal mucosa)
  2. Middle (partially covered with transitional mucosa)
  3. Lower (covered by stratified squamous mucosa
294
Q

What are the commonest benign neoplasm of the anus?

A

Warts (condyloma acuminata)

295
Q

What are 4 malignant carcinomas of the anal canal?

A
  1. Basaloid pattern
  2. Squamous cell carcinoma
  3. Adenocarcinoma
  4. Malignant melanoma (very rare)
296
Q

What is Basaloid pattern carcinoma of the anal canal?

A

Immature proliferative cells derived from the basal layer of stratified squamous epithelium

297
Q

What is squamous cell carcinoma of the anal canal closely associated with?

A

Chronic HPV infection

MD3002 (15 decks)

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