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MD3002 Weeks 1-6 > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are the two units of vomiting neural control?

A

Central neural regulation of vomiting is controlled by 2
separate units both in the medulla:
1) The Vomiting centre
2) The Chemoreceptor Trigger Zone, CTZ

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2
Q

List the types of drugs which may be used to modify the emetic response and gut motility

A
  • Antihistamines
  • Antimuscarinics
  • Dopamine antagonists
  • 5HT3 antagonists
  • Neurokinin 1 receptor antagonists
  • Synthetic cannabinoids
  • Steroids
  • Other neuroleptics
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3
Q

Vestibular labyrinth –> ______ ____ (____ ____) –> cerebellum –> ____ –> vomiting centre —> vomit

A

Vestibular labyrinth –> Vestibular nuclei (brain stem) —->cerebellum –> CTZ –> vomiting centre —> vomit

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4
Q

Vestibular labyrinth –> ______ ____ (____ ____) –> cerebellum –> ____ –> vomiting centre —> vomit

A

Vestibular labyrinth –> Vestibular nuclei (brain stem) —->cerebellum –> CTZ –> vomiting centre —> vomit

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5
Q

What is the difference between nausea, retching and vomiting?

A

Nausea: Feeling of wanting to vomit

  • Associated with autonomic effects: salivation / pallor / sweating
  • Often prodrome of vomiting

Retching: Strong involuntary effort to vomit, Unproductive

Vomiting: Expulsion of gastric contents through the mouth

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6
Q

Triggers for vomiting/nausea

A
  • Stimulation of the sensory nerve endings in the stomach and duodenum.
  • Stimulation of the vagal sensory endings in the pharynx.
  • Drugs or endogenous emetic substances.
  • Disturbances of the vestibular apparatus.
  • Various stimuli of the sensory nerves of the heart and viscera.
  • A rise in intracranial pressure.
  • Nauseating smells, repulsive sights, emotional factors.
  • Endocrine factors
  • Migraine
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7
Q

3 types of vomiting and the difference between them?

A
  1. Projectile vomiting
    Suggestive of gastric outlet or upper GI obstruction
  2. Haematemesis
    Vomiting fresh or altered blood (“coffee- grounds”) e.g. oesophageal varices, bleeding gastric ulcer
  3. Early-morning
    e. g. pregnancy, alcohol dependence, some metabolic disorders (uraemia)
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8
Q

How do antihistamines act as anti-emetics? Name 3 examples. Side effects?

A

• H1 histamine receptor antagonists
• Useful in numerous causes of N/V; including
motion sickness + vestibular disorders
• Side-effect profiles vary e.g. drowsiness and antimuscarinic effects

Examples:

  1. Cinnarizine
  2. Cyclizine
  3. Promethazine
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9
Q

How do antimuscarinics act as anti-emetics? Name an example. Side effects?

A

Muscarinic receptor antagonists
Mechanism: Blockade of muscarinic receptor-mediated impulses from the labyrinth and from visceral afferents
Example: Hyoscine hydrobromide
Side effects: Constipation, transient bradycardia, dry mouth

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10
Q

How do dopamine antagonists act as anti-emetics? Name 3 examples

A 
Mechanism: Act centrally as dopamine antagonists on the CTZ. Active against CTZ-triggered vomiting but not stomach-induced vomiting.
Examples:
1. Phenothiazines e.g. chloropromazine
2. Domperidone
3. Metoclopramide
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11
Q

How do 5HT3 antagonists act as anti-emetics? Name 4 examples

A

Block 5HT3 receptors in GIT and in the CNS. Particularly useful in managing N/V in patients receiving cytotoxic and postoperative N/V

Examples:

  1. Dolasetron
  2. Granisetron
  3. Ondansetron
  4. Palonosetron
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12
Q

How do neurokinin 1 receptor antagonists act as an anti-emetic? 2 examples?

A

Adjunct to dexamethasone and a 5HT3 antagonist in preventing N/V associated with chemotherapy

Examples: Aprepitant, fosaprepitant

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13
Q

How do synthetic cannabinoids act as anti-emetics? Name an example

A

Used for N/V caused by chemo unresponsive to conventional anti-emetics
Side effects: Drowsiness/ dizziness

Example: Nabilone

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14
Q

Use of steroids as anti-emetics? Example?

A

Used alone, to treat vomiting associated with cancer chemotherapy or in conjunction with other antiemetics
Example: Dexamethasone

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15
Q

Name 2 other neuroleptics used to treat emesis?

A

Haloperidol

Levomepromazine

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16
Q

Before prescribing laxatives, what 3 steps must be taken?

A
  1. Ensure the problem is constipation
  2. Check the patient’s “norm”
  3. Try to reverse the cause, including diet.lifestyle changes
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17
Q

What are the 5 types of laxatives?

A
  1. Bulk-forming laxatives
  2. Stimulant laxatives
  3. Faecal softeners
  4. Osmotic laxatives
  5. Peripheral opioid-receptor antagonists
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18
Q

How do laxatives work?

A

Bulk fibre provides increased volume and promotes peristalsis by distension
Some laxatives soften stool by coating and breaking up particles
Liquid mixes with stool to soften

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19
Q

Name examples of the following types of laxatives:
Bulk (2)
Stimulate (6)
Softener (2)
Osmotic (4)
Peripheral opioid receptor antagonist (1)

A

Bulk: Ispaghula husk, methylcellulose
Stimulant: bisacodyl, dantron, docusate sodium, glycerol, senna, sodium picosulfate
Softener: arachis oil, liquid paraffin
Osmotic: lactulose, macrogols, magnesium salts, rectal phosphates
Peripheral opioid receptor antagonist: methylnaltrexone bromide

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20
Q

What two properties of diarrhoea lead to loss of electrolytes?

A

Increase in the motility of the GIT

Decrease in the absorption of fluid

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21
Q

4 approaches to treating ACUTE diarrhoea?

A
  1. Maintenance of fluid and electrolyte balance e.g. oral rehydration preparation
  2. Antimotilty drugs
  3. Antispasmodics e..g. hyoscine hutylbromide (buscopan), mebeverine
  4. Antibacterial agent is indicated e.g. systemic bacterial infection, campylobacter enteritis, shigellosis and salmonellosis
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22
Q

What 3 agents are used to treat chronic diarrhoea?

Name at least 2 examples for each

A

Antimotility agents:

  • Codeine
  • Co-phenotrope
  • Loperamide (Imodium)
  • Morphine

Adsorbents:

  • *Not for acute diarrhoea**
  • Kaolin
  • Light

Bulk forming drugs:

  • Useful in controlling diarrhoea associated with diverticular disease
  • Ispaghula
  • Methycellulose
  • Sterculia
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23
Q

5 components of bile?

A 
Bile salts
Bilirubin
Cholesterol
Lecithin
Plasma electrolytes
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24
Q

Which hormone stimulates gallbladder emptying?

A

Cholecystokinin (CCK)

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25
Q

Treatment of gallstones?

A
  1. Lap Chole

2. Ursodeoxycholic acid to dissolve gallstones

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26
Q

Treatment of biliary colic and acute cholecystitis?

A

Biliary colic:

  • V painful so may require morphine / pethidine (opioids) or diclofenac (NSAID) by suppository
  • Parenteral/rectal route chosen as overcomes difficulties in absorption caused by vomiting

If pain continues for 24hrs+ or accompanied by fever = HOSPITAL ADMISSION

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27
Q

Bile acid sequestrates:
Main example?
Mechanism?
Uses?

A

Main example: Colestyramine (an anion-exchange resin)
Mechanism: Froms an insoluble complex with bile acids in the intestine
Uses:
- Relives pruritus associated with partial biliary obstruction and primary biliary cirrhosis
-Diarrhoea episodes e.g. Crohn’s disease cirrhosis
-Hypercholesterolaemia

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28
Q

What is Cholestyramine and it’s uses?

A

A bile acid sequestrant.
It works by helping the body remove bile acids, which can lower cholesterol levels in the blood. The medicine is also used to relieve itching that’s caused by a bile duct blockage.

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29
Q

What is the classification for benign and malignant tumours of the oesophagus

A

Benign:

  • Mesenchymal e.g. Leiomyomas (Smooth muscle)
  • Squamous papillomas

Malignant:

  • Squamous cell carcinoma
  • Adenocarcinoma
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30
Q

What is the classification of benign and malignant tumours of the stomach

A

Benign:

  • Polyps: Non-neoplastic, adenomas
  • Mesenchymal

Malignant:

  • Carcinoma (epithelial cells)
  • Lymphoma
  • Carcinoid
  • Mesenchymal
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31
Q 
Sqaumous cell carcinoma:
Incidence?
Associated factors?
Morphology? (Location, structure and patterns)
Clinical features?
Prognosis
A

SSC
Incidence:
->50
-More males

Associated factors:

  • Diet: Vitamin deficiency, fungal contamination of foods, high content of nitrites/nitrosamines
  • Lifestyle: Hot food/drinks, alcohol, tobacco
  • Oesophageal disorders: Long standing oesophagitis and achalasia
  • Genetic predisposition

Morphology:

  • Location: Mainly in middle 1/3 of oesophagus
  • Small, gray/white, plaque-like thickenings that become tumours masses
  • Three patterns:
    1. Protruded polypoid exophytic
    2. Flat, diffuse, infiltrative,
    3. Exacavated, ulcerated

Clinical features:

  • Dysphagia
  • Extreme weight loss
  • Haemorrhage and sepsis
  • Metastases to lymph nodes
  • Cancerous TEF

Prognosis: 5% overall five-year survival

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32
Q 
Adenocarcinoma:
Where does it occur?
Incidence?
Associations?
Morphology?
Histology?
Clinical features?
Prognosis?
A

In lower 1/3 of oesophagus

Incidence: Age 40

Associations:

  • Arise from Barrett Mucosa (intestinal metaplasia caused by gastric reflux)
  • Tobacco and obesity

Morphology:

  • Flat/ raised patches or nodular masses
  • May be infiltrative or deeply ulcerative

Histology:
Mucin producing glandular tumours

Clinical features:
• Dysphagia
• Progressiveweightloss
• Bleeding
• Chestpain
• Vomiting
• Heartburn
• Regurgitation

Prognosis: 20% overall five year survival

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33
Q

How is TNM staging of tumours broken down?

A

Tis carcinoma in situ
T1 invasion of submucosa
T2 invasion of muscularis propria T3 invasion of adventitia
T4 invasion of adjacent structures

N0 no node spread
N1 regional node metastases

M0 no distant spread
M1 distant metastases

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34
Q

What is a polyp?

A

Module or mass that projects above the level of the surrounding mucosa, usually at the Antrum

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35
Q

What is the most common malignant tumour of the stomach?

A

Gastric carcinoma

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36
Q

What are the environmental, host and genetic factors of gastric carcinomas?

A

Environmental:

  • Infection ny H pylori
  • Diet
  • Low socioeconomic status
  • Cigarette smoking

Host:

  • Chronic gastritis
  • Gastric adenomas
  • Barrett oesophagus

Genetic:

  • Increased risk with blood group A
  • Family history
  • Hereditary non-polyposis
  • Familial gastric carcinoma syndrome
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37
Q 
Gastric carcinoma:
Location?
Classification?
Macroscopic growth factors?
Morphology?
Clinical features?
Prognosis?
A

Location:
-Pylorus and Antrum **

Classification on the basis of:

  1. Depth of invasion
  2. Macroscopic growth pattern
  3. Histological subtype

Macroscopic growth patterns:

  • Exophytic
  • Flat or depressed –> Linitis plastica
  • Excavated

Morphology:

  • All carcinomas eventually spread to regional and more distant lymph nodes.
  • ->Supraclavicular node
  • ->Local invasion to duodenum, pancreas and retroperitoneum
  • Metastases to the liver and lungs are common
  • Metastases to the liver and lungs
  • Metastases to the ovaries called Krukenberg tumour
Clinical features:
• Asymptomatic until late
• Weight loss
• Abdominal pain
• Anorexia
• Vomiting
• Altered bowel habits
• Dysphagia
• Anaemic symptoms
• Haemorrhage

Prognosis: 90-95% for early gastric cancer. Less than 15% for advanced

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38
Q

What is the histopathology of intestinal, diffuse and mixed type gastric adenocarcinomas?

[LAUREN CLASSIFICATION]

A

Intestinal type:

  • Composed of neoplastic intestinal glands resembling those of colonic adenocarcinoma
  • Cells often contain apical mucin vacuoles

Diffuse type:

  • Composed of gastric-type mucous cells which permeate the mucosa and wall as scattered individual cells or small clusters in a n “infiltrative” growth pattern
  • Mucin formation expands the malignant cells and pushes the nucleus to the periphery, creating a “signet ring”

Mixed type

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39
Q 
Gastric lymphoma:
What are they?
Associations?
Prognosis?
Morphology?
A

What are they?
B cell lymphomas of mucosa-associated lymphoid tissue (MALT lymphomas)

Associations: Chronic gastritis and H. pylori infection

Prognosis: 50% five year survival

Morphology:

  • Occurs in mucosa and superficial submucosa
  • Lymphocytic infiltrate of the lamina propria surrounds gastric glands massively infiltrated with atypical lymphocytes and undergoing destruction
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40
Q

Functions of the liver?

A

METABOLIC: Breakdown down carbohydrates, hormones, lipids, drugs and proteins
STORAGE: Glycogen, vitamins, iron
PROTECTIVE: Detoxification and elimination of toxin compounds, kupffer cells ingest bacteria and other foreign material from blood
BILE: Produced and excreted. Formed in biliary canaliculi, emulsifies fats and provides route for waste removal

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41
Q

What two vessels supply the liver and what do they supply it with?

A

Hepatic artery= Oxygenated blood

Portal vein - Nutrient rick blood

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42
Q

What is the functional unit of the liver and where is it composed of?

A

Liver lobule:

  • Hexagonal in shape
  • Hepatocytes arranged in plates
  • In contact with bloodstream one one side and bile canaliculi on the other
  • Between the plates are vascular spaces (sinusoids) containing Kupffer cells (phagocytic macrophages)
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43
Q

Classifications of liver disease

VAN MIT

A

Infection- Viral, bacterial, parasitic
Toxic/drug induced
Autoimmune
Biliary tract obstruction- Tumours, gallstones
Vascular
Metabolic : Haemochromatosis, Wilson’s, hereditary hyperbilirubinaemias
Neoplastic

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44
Q

What is cholestasis?
Classifications?
What does it lead to?

A

Failure to produce or excrete bile

  • Intrahepatic = Problems in secretion of bile by hepatocytes due to damage
  • Extrahepatic = Problems with flow of bile out of the liver due to obstruction

Result:

  • Accumulation of bilirubin in the blood leading to JAUNDICE.
  • Urine darkens
  • Stool becomes lighter
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45
Q

Other cause for jaundice apart from cholestasis?

A

Excessive haemolysis, so bilirubin is uncongutated and does not appear in urine

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46
Q

Difference between acute and chronic hepatic failure?

A

Acute: Development of severe hepatic dysfunction within 24wks of onset of disease

Chronic: Progressive decline in liver function with established disease

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47
Q

What are 3 causes of acute hepatitis?

A

Poisoning e.g. from paracetamol
Infection (Hepatitis A-C)
Inadequate perfusion

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48
Q

3 potential outcomes for acute hepatitis?

A

Resolution
Progression to acute hepatic failure
Progression to chronic hepatic damage

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49
Q

3 common and uncommon causes for chronic liver disease?

A

Common:

  • Alcoholic fatty liver
  • Chronic active hepatitis
  • Primary biliary cirrhosis

Unusual causes:

  • Alpha-1 AT deficiency
  • Wilson’s disease
  • Haemochromatosis
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50
Q

6 consequences of chronic liver disease

A
  1. Cirrhosis
  2. Portal hypertension
  3. Ascites
  4. Renal failure
  5. Easy bruising due to lack of production of clotting factors
  6. Oedema as osmotic pressure is reduced
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51
Q

What is cirrhosis?

A

Irreversibile shrinkage of the liver and fibrosis

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52
Q

What is portal hypertension?

Consequences?

A

Increased blood pressure in the portal vein leading to:

  • Haemorrhage of oesophageal / gastric varices
  • Hepatic encephalopathy (detoxifying function bypassed)
  • Hypersplenism
  • Decreased resistance to infections
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53
Q

What is ascites as a consequence of chronic liver disease?

A

Accumulation of fluid in the peritoneal cavity

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54
Q

What are the features 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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55
Q

What is hepatic encephalopathy?

Name an example

A

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

Ammonia: Decreased liver capacity to synthesize urea and glutamine means the ammonia is no longer adequately metabolised and accumulates in the systemic circulation

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56
Q

What 4 Liver Function Tests are done to test if liver disease is present?

A
  1. Aminotransferases: ALT and AST for liver cell damage
  2. Bilirubin- For cholestasis (suggesting bile flow blockage)
  3. ALP and gamma-GT for biliary epithelial damage and obstruction
  4. Albumin for synthetic function
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57
Q

What is albumin?

What’s is its relevance in liver function tests?

A

Albumin is a main plasma protein

Used as an assessment of liver synthetic function but low albumin also found in the following:

  • Post surgical/ITU patients due to redistribution
  • Significant malnutrition
  • Nephrotic syndrome
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58
Q

What is bilirubin?

A

Breakdown product of haemoglobin

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59
Q

What happens to unconjugated bilirubin?

A

Taken up by the liver and then conjugated. This can then be excreted in bile.
It is then attacked by bacteria in the colon and excreted in faeces.
Small amounts are reabsorbed and excreted in urine as urobilinogen

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60
Q

Name 4 of the liver enzymes that are used in Liver Function Tests?

A

AST and ALT
Bilirubin
ALP
gamma-GT

NOT EXCLUSIVELY FOUND IN LIVER TISSUE

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61
Q

What do AST and ALP levels suggest in Liver Function Tests?

A

These are non-specific markers of acute damage to hepatocytes

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62
Q

What does ALP levels suggest in Liver Function Tests?

A

Increase in liver disease due to increased synthesis in response to cholestasis

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63
Q

What does gamma-GT levels suggest in Liver Function Tests?

A

Raised in colestasis, also affected by ingestion of alcohol and drugs such as phenytoin

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64
Q

4 limits of biochemical tests?

A
  1. Lack of complete organ specificity
  2. Lack of disease specificity
  3. May be over sensitive
  4. “I have this abnormal result, what do I do with it?”
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65
Q

Bilirubin abnormal in asymptomatic patient, why?

A

Haemolysis

Gilbert’s syndrome

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66
Q

ALP abnormal in asymptomatic patient, why?

A

Physiological change e.g. pregnancy, adolescence

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67
Q

AST abnormal in asymptomatic patient, why?

A

Skeletal muscle disorders

MI

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68
Q

gamma-GT abnormal in asymptomatic patient, why?

A

Alcohol

Drugs

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69
Q

Pro’s and con’s of LFTs?

A

Pros:

  • Cheap
  • Widely available
  • interpretable
  • Direct subsequent investigation

Cons:

  • Outdated by new diseases
  • Little prognostic value in liver transplantation
  • Little value for evaluating therapeutic success
  • Do not assess liver function
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70
Q

What is the relation of the ribs to the spleen?

A

The spleen lies with ribs 9-11 to the left and posteriorly

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71
Q 
How thick is the spleen?
How long is it?
How wide is it?
Which ribs?
How much does it weigh?

HINT: 1,3,5,7,9,11

A 
1,3,5,7,9,11 
The spleen is: 
1 inch thick; 
3 inches wide;                 	     5 inches long;
weighs 7oz (200g);
lies between the 9th and11th ribs
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72
Q

Functions of the spleen?

A
  1. Mechanical filtration of red blood cells
  2. Active immune response through humeral and cell mediated pathways
  3. Haematopoesis until 5th month of gestation
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73
Q

What organs lie on/into the spleen?

A

Stomach in the gastric area
Left kidney in the renal area
Splenic flexure in the colic area

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74
Q

The spleen is surrounded by peritoneum that was derived from the dorsal mesentery of the ______

A

The spleen is surrounded by peritoneum that was derived from the dorsal mesentery of the stomach

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75
Q

Connections of the spleen?

What vessels are carried in each connection?

A

It is connected to the stomach by the Gastrosplenic ligament
Carries: Left gastro-epiploic and short gastric branches of the splenic artery (and equivalent veins)

It is connected to the posterior abdominal wall, adjacent to the left kidney, by the Lienorenal (Splenorenal) ligament
Carries: Splenic artery and vein alongside the tail of the pancreas

76
Q

Risk of rib 9-11 fracture?

A

Rupture spleen causing intraperitoneal haemorrhage

77
Q

What structure is at risk during removal of the spleen?

A

When removing the spleen, great care must be taken to avoid injuring the tail of the pancreas when ligating the splenic vessels

78
Q

Arterial supply of spleen?

A

The splenic artery is the largest branch of the coeliac artery
[It has a tortuous course as it runs along the upper border of the pancreas]
The artery then divides into about six branches, which enter the spleen at its hilum

79
Q

Venous drainage of spleen?

A

The splenic vein leaves the hilum and runs behind the tail and the body of the pancreas Behind the neck of the pancreas, the splenic vein joins the superior
mesenteric vein to form the portal vein (L1, Transpyloric Plane)

80
Q

Lymph drainage of spleen?

A

The lymph vessels emerge from the hilum and pass through a few lymph
nodes along the course of the splenic artery and then drain into the coeliac
nodes

81
Q

Nerve supply of spleen?

A

The nerves accompany the splenic artery and are derived from the coeliac
plexus (foregut T 5 to 9))

82
Q

5 parts of the pancreas

A 
Uncinate process
Head
Neck
Body
Tail
83
Q

Where does the portal venous system drain?

A

lower 1/3 of oesophagus
Spleen
Pancreas
Gall bladder

84
Q

When the portal vein reaches the liver what does it do?

A

Branches and supplies the sinusoids, from which blood passes into the hepatic veins that join the inferior vena cava
In the sinusoids, the portal venous blood mixes with oxygenated blood from the hepatic artery

85
Q

What vessels unite to form the portal vein?

A

Splenic vein

Superior Mesenteric Vein

86
Q

Where does the left gastric vein drain before it directly drains into the portal vein?

A

Lower oesophagus

Left end of the lesser curve of the stomach

87
Q

What vessel joins the splenic vein and drains the hindgut?

A

The inferior mesenteric vein drains the hindgut and joins the splenic vein in very variable positions behind the pancreas, often joining the portal vein itself

88
Q

Which vessels drain into the portal vein?

A 
Splenic vein ( + IMV)
SMV
Left gastric vein
Right gastric vein
Cystic vein
89
Q

Where does the right gastric vein drain before it directly drains into the portal vein?

A

Drains the right end of the lesser curve of the stomach directly to the portal vein

90
Q

What are the 4 sites of porto-systemic anastomosis?

A
  1. At the lower third of the oesophagus
  2. Halfway down the anal canal
  3. The para-umbilical veins
  4. The veins of the retroperitoneal ascending colon, descending colon, duodenum, pancreas and liver
91
Q

How does the lower third of the oesophagus act as a site of porto-systemic anastomosis?

A

At the lower third of the oesophagus, the oesophageal branches of the left gastric vein (portal tributary) anastomose with the oesophageal veins
draining the middle third of the oesophagus into the azygos veins (Varices)

92
Q

How does halfway down the anal canal act as a site of porto-systemic anastomosis?

A

Halfway down the anal canal, the superior rectal veins (portal tributary)
draining the upper half of the anal canal anastomose with the middle and inferior rectal veins that are systemic tributaries of the internal iliac and internal pudendal veins, respectively (Piles or Haemorrhoids)

93
Q

How does the para-umbilical act as a site of porto-systemic anastomosis?

A

The para-umbilical veins connect the left branch of the portal vein with the
superficial veins of the anterior abdominal wall (systemic tributaries). The
para-umbilical veins travel in the falciform ligament and accompany the ligamentum teres (Caput Medusae)

94
Q

How do veins of the retroperitoneal intestine, pancreas and liver act as a site of porto-systemic anastomosis?

A

The veins of the retroperitoneal ascending colon, descending colon, duodenum, pancreas, and liver (portal tributaries) anastomose with the renal, lumbar, and phrenic veins (systemic tributaries)

95
Q

The portal vein drains blood from the visceral organs to the liver
If this is stopped by a ‘blockage’ blood flows or ‘bypasses’ into the systemic circulation, usually causing the anastomotic veins to dilate.

Supra-hepatic causes?
Hepatic causes?
Infra-hepatic causes?

Consequences?

A

Supra-hepatic causes:
Cardiac disease
Hepatic vein thrombosis
IVC thrombosis

Hepatic causes:
-Cirrhosis (due to alcohol, hepatitis)

Infra-hepatic causes:

  • Portal vein thrombosis
  • Splenic vein thrombosis

Consequences

  • Oesophageal varices
  • Haemorrhoids
  • Caput medusa
96
Q

Visceral branches on the abdominal aorta:
3 unpaired, anterior branches?
3 paired branches to viscera?

A

3 unpaired, anterior branches:

  • Coeliac trunk T12
  • Superior mesenteric artery L1
  • Inferior mesenteric artery L3

3 paired branches to viscera:

  • Middle suprarenal arteries
  • Renal arteries L1
  • Testicular and ovarian arteries (L2)
97
Q

Posterior branches of the abdominal aorta, supplying diaphragm / body wall?

A
  1. Inferior phrenic arteries
  2. Lumbar arteries
  3. Median sacral artery
98
Q

The IVC is formed by the union of which vessels, at which location?

A

It is formed by the union of the common iliac veins behind the right common iliac artery at the level of L5 vertebra

99
Q

What are the tributaries of the IVC?

A
  1. Two or three anterior visceral tributaries: the hepatic veins
  2. Three lateral visceral tributaries: the right suprarenal vein (the left vein drains into the left renal vein), both renal veins, and the right gonadal vein (the left vein drains into the left renal vein)
  3. Five lateral abdominal wall tributaries: the inferior phrenic vein and four lumbar veins
  4. Three veins of origin: two common iliac veins and the median sacral vein
100
Q

What are the primary and secondary GIT imaging tools used?

A

Primary: X-ray, CT and USS

Secondary: MRI, Fluoroscopy (e.g. Barium meals, barium enemas)

101
Q

What types of x-ray are used to examine the GIT?

Excludes what pathology?

A

Types: Spine AXR, Crest CXR

Excludes bowel obstruction perforation

102
Q

The normal portal venous pressure is 5 - 10mm Hg

If elevated above this the term ‘____ _______’
is used

A

The normal portal venous pressure is 5 - 10mm Hg

If elevated above this the term ‘portal hypertension’
is used

103
Q

Which is more accurate, CT or USS?

A

Sensitivity of CT vs USS- 89% vs 70%

CT results in 46%-60% change in management :)

104
Q

Cons of CT scans?

A

Radiation exposure

Renal impairment

105
Q

Pros/ cons of MRI scan?

A

Pros:
No radiation
Good soft tissue delineation esp in pelvis

Con’s:
Long examination time
Not 24/7 in Fife
Contraindications/ claustrophobia

106
Q

Acute appendicitis:
Symptoms?
Localises at?
Scans used?

A

Symptoms: Periumbilical pain, nausea & vomiting

Localises at RIF

USS first, then CT

107
Q 
Acute divericulitis:
Main age group affected by diverticulosis?
1/3+ are misdiagnosed as?
Complications?
Scans used?
A

80yrs +

Misdiagnosis: Appendicitis, colorectal Ca

Complications: Abscess, obstruction, perforation, fistulae

Scans: Plain x-ray, CT

108
Q

Acute cholecystitis:
Normally secondary?
Diagnosis basis?
Scans?

A

Almost always secondary gallstones

Diagnosis based on:
• One local sign of inflammation (RUQ pain etc)
• One sign of inflammation (fever ,WCC, CRP)
• Confirmatory imaging

Scans:
USS: Reveals gallstones, GB wall thickening, local fluid
CT: Can be false -ve
MRI: If biliary tree dilatation

109
Q

What is an MRCP?

A

MR cholangiopancreatography

110
Q

What is Emphysematous cholecystitis?

Treatment options?

A

Air in gallbladder wall.
Common in diabetics

Treatment: Medical, interventional radiology, surgery

111
Q 
Small bowel obstruction:
Common in?
Symptoms?
Signs?
Imaginig defines?
Scans?
A
  • Common – adhesions, cancer, herniae and gallstone ileus
  • Symptoms: vomiting, pain and distension
  • Signs: Increased bowel sounds, tenderness, palpable loops
  • Imaging defines: site, cause, severity and detects complications (eg perforation, ischaemia)

Scans:
X-ray: For initial inspection. Can miss fluid filled loops.
CT: Transition point revealed, key. Adhesions not seen.

112
Q 
Large bowel obstruction:
Causes?
Consistency of clinical presentation?
Surgeon wants to know?
Scan used?
A

Causes:
• Colorectal cancer 60% • Volvulus 15%
• Diverticulitis 10%

Clinical presentation often variable

Surgeon wants to know: Site, cause, distant disease

Scan used:CT
• sens/. Spec >93% 
• Transition point
• Underlying mass • State of caecum
• Distant disease
113
Q

Different forms of perforation in GIT?

A

Perforated ulcer
Diverticular **

(Less common: 2ndary to cancer, ischaemia)

114
Q

Scan used to identify perforation?

A 
CT:
• High sens and spec 
• Shows free fluid
• Will often show clues to site of origin (86%)
-Distribution gas
-Defect in wall
-Localised inflammatory change
115
Q 
Bowel ischaemia:
What % of CO = ishaemia?
Causes?
Signs/symptoms?
Scan chosen?
A

If <10% CO to GI, then ischaemia develops

Cause:
• Arterial occlusion – 60-70%
• Venous occlusion – 5-10%
• Non-occlusive hypoperfusion – 20-30%

S/S:
• Severe abdominal pain
• Vomiting, diarrhoea, distension inconsistent
• Borderline amylase, raised WCC, acidotic

Scan: Biphasic CT
-Shows site of occlusion, length of affected bowel

116
Q

In summary, the following scans are used for:

  • Plain film?
  • USS? Hint: RHS
  • CT?
A

Role of plain film: obstruction orperforation

Role of USS – RUQ/ RIF pain

Role CT – Primary imaging technique for acute abdominal pain except for acute cholecystitis/ appendicitis

117
Q

What two vessels join to form the common bile duct?

A

Cystic duct

Common hepatic duct

118
Q

Portal triad is made up of which structures?

A

Bile duct
Hepatic artery
Hepatic portal vein

119
Q

The liver synthesises, produces and breaks down what?

A

Synthesises: Albumin, clotting factors, complement, alpha-1-antitrypsin, thrombopoietin
Produces: Bile through conjugation of bilirubin
Breaks down: Drugs, insulin, ammonia

120
Q

What do Kupffer cells do?

A

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

121
Q

Jaundice:
What is it?
Can cause?
Classified by conjugation of bilirubin?

A

Jaundice is the yellowing of the skin and mucosal surfaces. When bilirubin levels are >40micromol/L
Can cause intense itch

Unconjugated is water insoluble. Conjugated is water soluble so can be excreted in the urine, leading to dark urine.

122
Q

Classification of jaundice by cause: Prehepatic, intrahepatic and post-hepatic?

STARRED

A

Prehepatic: Haemolysis –> Release for bilirubin from RBCs

Intrahepatic: Liver disease –> Excess bilirubin in liver and bloodstream

Post-hepatic (obstructive): Obstruction of bile outflow –> Dark urine and pale stools

123
Q

Main causes for acute liver injury?

A

Viral infections
Alcohol
Adverse drug reactions
Biliary obstructions

124
Q

Consequences of acute liver injury?

A

Jaundice, malaise
Raised serum bilirubin and transaminases
Liver failure: decrease in albumin, ascites, bruising, encephalopathy

125
Q

Patterns of hepatocyte injury, zones of injury?

A 
Zone 1 (on outskirts): Greatest blood supply so most susceptible but also most reliant 
Zone 3 (inner zone): If injury in this zone then that's when symptoms are experienced as cells cannot regenerate
126
Q

3 forms of liver injury due to alcohol?

A

Steatosis
Cirrhosis
Acute hepatitis with Mallory’s hyaline

127
Q

What is steatosis?

Why does Mallory’s hyaline develop?

A

Fat deposition altered by metabolism

Mallory’s hyaline builds up due to hepatocyte damage

128
Q

What is the process of cirrhosis development due to alcohol?

A
  1. Acetaldehyde binds to hepatocytes causing damage → Inflammatory reaction
  2. Inflammation → fibrosis
  3. Fibrosis (collagen) + Regeneration → Cirrhosis
129
Q

What are the 3 morphological classifications of cirrhosis?

A

Micronodular: Nodules <3mm
Macronodular: Nodules >3mm
Mixed

130
Q

Complications of cirrhosis?

A
  • Liver Failure – hepatic encephalopathy (ammonia), build up of steroid hormones → hyperoestrogenism (palmar erythema and gynaecomastia), bleeding
  • Portal hypertension –↑ hepatic vascular resistance, AV shunting – oesophageal varices, haemorrhoids, caput medusae
  • Hepatocellular carcinoma
131
Q

How does drug induced liver injury vary depending on the drug?

A

Paracetamol= Injury to liver cells (hepatocellular)
overdose

Methyl testosterone= Injury to bile production/secretion cells
(cholestatic)

132
Q

Acute biliary obstruction:
Usually due to?
Causes?
Complication?

A
  • This is usually due to gallstones
  • Causes colicky pain and jaundice
  • Can be complicated by infection of the blocked CBD - cholangitis
133
Q

Main 4 causes of chronic hepatitis?

A

Viral
Alcohol
Drugs
Autoimmune

134
Q

Chronic hepatits, is hepatitis that lasts more than…

A

6 months

With sustained elevation of transaminases which requires liver biopsy to classify cause

135
Q 
Primary biliary cirrhosis:
Females vs males?
Stages?
Presentation?
Test results of ALP + IgM, AMA
A

Females > Males
Stages:
1. Autoimmune destruction of bile duct epithelium: Dense lymphocytic infiltration
2. Proliferation of small bile ducts
3. Architectural disturbance: Portal and bridging fibrosis
4. Cirrhosis

Presentation: Jaundice, pruritus, xanthelasmata

Raised ALP + IgM, AMA

136
Q

What is haemochromatosis

A

Iron deposition in the liver causing alteration of architecture –> Fibrosis –> Cirrhosis

137
Q

Difference between a lobule and acinar view of the liver?

A

Lobule: Blood on outside going inwards
Acinar: Blood supply in between

138
Q

Causes for cirrhosis?

A 
Alcohol
Hep B and C
Iron overload
Gallstones
Cirrhosis
Autoimmune liver disease
139
Q 
Autoimmune chronic active hepatitis:
Gender incidence?
Age incidence?
Feartures?
Treatment
A

Females > Males

Usually presents in mid-late teens

Features:

  • Interface hepatitis
  • Plasma cells and swollen hepatocytes present
  • Fibrosis
  • ANA, SMA, raised IgG and transaminases, Anti-LKM (liver-kidney microsomal)

Treatment: Patients may benefit from steroids

140
Q

Which gene codes for the protein involved in haemochromatosis?

A

HFE (autosomal recessive)

141
Q

Treatment for haemochromatosis?

A

Regular venesection (test iron and ferritin levels)

142
Q

What is alpha-1 antitrypsin deficiency:
Dominance?
Causes?

A

Autosomal recessive disorder
Leads to low levels of alpha-1 -antitrypsin

Leads to protein build up in hepatocytes as hyaline as transport protein is deficient
–>Cirrhosis
(associated with emphysema)

143
Q

What is NASH/NAFLD?
Associated with which metabolic syndrome?
Mechanism?

A

Non-alcoholic steatohepatitis / Non- alcoholic fatty liver disease
Associated with Metabolic Syndrome (DM II, hypertension, ↓HDL cholesterol, ↑ triglycerides
Mechanism: Fat deposition in hepatocytes – can lead to cirrhosis

144
Q 
Wilson's disease:
Dominance?
What is it?
Deposition sites?
Clinical signs?
A

• Autosomal recessive disorder
• Failure of the liver to excrete copper in bile → build up of copper in liver → cirrhosis
• Copper also deposits in brain tissue → neurological dysfunction
Clinical signs: Kayser-Fleischer rings

145
Q

What is hepatocellular carcinoma?
Often arises in….
Aetiology?

A

Malignant liver tumour
Often multifocal

Often arises in cirrhotic liver

Aetiology:

  • Aflatoxin (fungal origin)
  • Hep B and C viruses
  • Cirrhosis
146
Q

6 pathologies of the biliary system?

A
  1. Gallstones (cholelithiasis)
  2. Cholecystitis
  3. Cholangiocarcinoma
  4. Obstruction
    Congenital malformations
  5. Atresia
  6. Cholesocal cysts
147
Q

Cholangiocarcinoma:
Location?
Association?
Causes?

A
  • Arises from bile duct epithelium anywhere in the biliary system (intra- and extra-hepatic)
  • Associated with ulcerative colitis

Causes: obstructive jaundice, itch, weight loss and lethargy
Can lead to rupture of common bile duct or gallbladder – prognosis poor

148
Q

Risk factors for gallstones? F’s*

A

Female, Fair, Fat, Forty, Fertile

Diabetes mellitus

149
Q

Most common gallstones?

A

Cholesterol (yellow), bile pigment (green) , mixed

150
Q

What 6 conditions can gallstones lead to?

A

Cholecystitis, obstructive jaundice, cholangitis, pancreatitis, cholangiocarcinoma

151
Q

Difference between acute and chronic cholecystitis?

A

Acute –
• Usually caused by gallstones
• Initially sterile then becomes infected • May lead to abscess/rupture
• Symptoms – RUQ pain (biliary colic), fever, nausea/vomiting

Chronic –
• Invariably related to gallstones
• Chronic inflammation with wall thickening

152
Q

What is an annular pancreas?

Presents as?

A

At 2nd part of duodenum

Causes obstruction

Presentation: Polyhydramnios, low birth weight, poor feeding

153
Q

Pancreatitis:
Acutely leads to?
Chronic leads to?

A 
Acutely leads to: 
• Causes catastrophic metabolic consequences –
↓ calcium, ↓ albumin, ↑ glucose 
• High serum amylase – diagnostic
• Massive fluid losses → SHOCK 
• High mortality rates

Chronic leads to;
• Multiple episodes of acute
• Causes fibrosis of pancreas – may lead to
diabetes mellitus
• Reduced production of enzymes – require supplements (creon)

154
Q 
Pancreatic carcinoma:
Type of cancer?
Associations?
Presentation?
Clinical sign?
Prognosis?
A
  • Adenocarcinoma
  • Associated with smoking and diabetes mellitus
  • Presents with painless, progressive jaundice
  • Weight loss
  • Poor prognosis
  • May be operable if small and close to ampulla
155
Q

Layer of GIT wall?

A 
Mucosa
Muscularis mucosae
Submucosa
Submucosal plexus
Circular later 
Myenteric plexus
Longitudinal muscle
Serosa
156
Q

Aetiology of IBS?

A 
• Multifactorial
• Genetic factors
• Autoimmune / Immune dysfunction 
• Environmental factors
-External 
-Internal
157
Q

5 main types of IBD?

A
  • Ulcerative Colitis
  • Crohn’s Disease
  • Indeterminate colitis (either Crohn’s or ulcerative)
  • Pseudomembranous Colitis
  • Diverticulitis
158
Q

Ulcerative colitis:
Which part of GIT inflamed?
Characteristics of inflammation?
Consequences?

A

Variable length of colon + rectum inflamed
If entire colon = PANcolitis

Inflammation:

  • Contiguous
  • Circumferential
  • Superficial inflammation

Consequences:

  • Anaemia due to iron deficiency
  • Raised inflammatory markers
  • Dehydration
159
Q

Which is more common in spokers, UC or Crohn’s?

A

Crohns

160
Q

Crohn’s:
Inflammation characteristics?
Signs/Symptoms?
Why does obstruction occur

A 
Inflammation characteristics:
• Characterised by inflammatory change anywherein the GI tract
• Discreet, focal ulceration
• ‘Skip lesions’
• Terminal ileitis

S/S:

  • Anaemia (absorption/ blood loss)
  • Raised inflammatory markers
  • Dehydration

Body trying to contain inflammation so fat wraps around the inflammation. Leading to the lumen being compressed

161
Q

Crohn’s patients more likely to get.. than UC patients?

A

Fistula.

When ulcer permeate through bowel wall. Leading to faeces leakage and infections elsewhere in the body

162
Q

Extraintestinal manifestations of Crohn’s?

A
  • Inflammatory arthropathies
  • Erythema nodosum (Crohn’s)
  • Pyoderma gangrenosum
  • Primary sclerosing cholangitis (UC)
  • Iritis/Uveitis
  • Aphthous stomatitis
163
Q

What is diverticulitis?

A

In diverticular disease, small bulges or pockets (diverticula) develop in the lining of the intestine. Diverticulitis is when these pockets become inflamed or infected.

164
Q

Classification of lower GI tumours:
SI: Benign? Malignant?
Colon & rectum: Benign? Malignant?

A

SI-
Benign: Adenoma, Mesenchymal tumours
Malignant:
Adenocarcinoma & Carcinoid, Lymphomaand Sarcomas

Colon and rectum-
Benign: Non-neoplasticpolyps, Neoplastic-Adenoma
Malignant: Adenocarcinoma(98%), Carcinoid, Anal zone carcinoma, Lymphoma. Leiomyosarcomas

165
Q

Where is usually affected by adenoma (SI benign tumour)?

A

Ampulla of vater, becomes enlarged and exhibits a velvety surface

166
Q

Usual presentation of adenoma of SI benign tumour?

A

30- to 60-year-old patient with occult blood loss.

167
Q

Adenocarcinoma (SI malignant tumours)
Usual presentation?
May result in?
Symptoms?

A

Usual presentation:
– occur in the duodenum, usually in 40- to 70-year-old patients
– napkin-ringencircling pattern
– polypoidexophytic masses

May cause: intestinal obstruction, obstructive jaundice

Symptoms: cramping pain, nausea, vomiting, and weight loss

168
Q

Examples of benign tumours of the colon and rectum?

Non-neoplastic and neoplastic

A

• Non-neoplastic polyps:
– Hyperplastic (90%)
– Hamartomatous

• Neoplastic–Adenoma:
– Tubular
– Villous
– Tubulovillous

169
Q 
Hyperplastic polyps:
What is it's cancerous classification?
Structure?
1/2 found in...
Malignant potential?
Age incidence?
A

Benign tumour of the colon and rectum that is non-neoplastic

Structure: Nipple-like, hemispheric, smooth, moist protrusions of the mucosa

1/2 found in rectosigmoid colon

No malignant potential

Found in 60yrs+

170
Q 
Hamartomatous polyps: Juvenile polyps 
Cancerous classification?
What are they?
Age?
Where are they found?
Malignant potential?
A

Benign tumour of the colon and rectum that is non-neoplastic

What are they?
Malformations of the mucosal epithelium and lamina propria

Age? Less that 5yrs

80% found in rectum

No malignant potential

171
Q 
Hamartomatous polyps: Peutz-jeghers polyps
What is it's classification?
Associated syndrome?
Layers of GIT wall involved?
Malignant potential?
A

Benign tumour of colon and rectum, non-neoplastic
Associated to Peutz-Jeghers autosomal dominant syndrome
Involved the mucosal epithelium, lamina propria, and muscularis mucosa

No malignant potential
• Increased risk of the pancreas, breast, lung, ovary, and uterus carcinoma

172
Q 
Neoplastic polyps (adenomas):
Structure?
Gender and age incidence
Classified into?
Arise as result of...
A

Structure:

  • Small, pedunculate lesions
  • Large neoplasms that are usually sessile

Gender: Equal

Age: Most after 60yrs

Classifications: Tubular adenomas, villous adenomas, tubulovillous adenomas

Arise as a result of epithelial proliferative dysplasia

173
Q

Neoplastic polyps- Adenomas:
Precursor for?
Risk is correlated with?
Impossible/possible to determine clinical significance?

A

denomas are a precursor lesion for invasive colorectal adenocarcinomas

Risk is correlated with:
• Polypsize
• Histological architecture
• Severity of epithelial dysplasia

IMPOSSIBLE from gross inspection of a polyp to determine its clinical significance

174
Q 
Tubular adenomas:
Location?
Shape?
Histology?
Clinical features?
Treatment?
A

Location: Colon

Shape: Small = Smooth-contoured and sessile. Large= Coarsely lobulated and have slender stalks raspberry-like

Histology:

  • Stalk is composed of fibromuscular tissue and prominent blood vessels
  • Dysplastic low grade epithelium
  • Carcinomatousinvasioninto the submucosal stalk of the polyp constitutes invasive adenocarcinoma

Clinical features:

  • May be asymptomatic
  • Evaluation of anaemia or occult bleeding

Treatment: Endoscopic removal of a pedunculate adenoma.
If invasive and sessile polyp further surgery may be required.
BENIGN

175
Q 
Villous adenomas:
Age?
Location?
Shape?
Histology?
Clinical features?
Treatment?
A

Age: Older persons
Location: Rectum and rectosigmoid
Shape: Sessile, up to 10cm

Histology:

  • Frond (1/2 leaf) like villiform extensions of the mucosa
  • Covered by dysplastic columnar epithelium
  • All degrees of dysplasia present
  • When invasive carcinoma occurs, there is no steak as a buffer zone and invasion is directly into the wall of the colon

Clinical features:

  • May be asymptomatic
  • Evaluation of anaemia or occult bleeding
  • More symptomatic than colorectal tubular
  • Overt rectal bleeding

Treatment: Endoscopic removal of a pedunculate adenoma.
If invasive and sessile polyp further surgery may be required.
BENIGN

176
Q

3 conditions to allow tubular and villous adenomas to be removed via endoscope?

A

Must be a pedunculate adenoma

(1) the adenocarcinoma is superficial and does not approach the margin of excision across the base of the stalk
(2) there is no vascular or lymphatic invasion
(3) the carcinoma is not poorly differentiated

177
Q 
Colorectal carcinoma:
Gender?
Age?
Aetiology?
Location?
Histology?
Clinical features?
Classification of lesion?
A

Gender: Rectum, more men. More proximal tumours, equal.

Age: 60-79

Aetiology:
Dietary factors: Excess calorific intake, lowe veg fibre intake, high content of refined carbs, intake of red meat, decreased intake of protective micronutrients

Location? Mainly rectosigmoid colon

Histology?

  • Range from tall, columnar cells to undifferentiated, anapaestic masses
  • May produce mucin

Clinical features?

  • Asymptomatic for years
  • In caecum and right colonic = fatigue, weakness, iron deficiency
  • In left side = occult bleeding, changes in bowel habit, cramps in LLQ
  • Iron deficiency anaemia in an older male means gastrointestinal cancer until proven otherwise
  • Significiant manifestations such as weakness, malaise and weight loss signify more extensive disease
  • All colorectal cancers spread. Mainly to liver, lungs and bones.

Classification of lesion by Duke’s stage:
A = Confined to the submucosa or muscle layer. 90% 5yr survival
B= Spread through the muscle layer, but does not yet involve lymph nodes. 70% 5yr survival
C= Involving lymph nodes. 35% 5yr suvival.

178
Q

In colorectal colon, what is the morphology in the proximal colon?

A

– Polypoid,exophytic masses
– Obstructionis uncommon
– Penetrate the bowel wall as subserosal and serosal white, firm masses

179
Q

In colorectal colon, what is the morphology in the distal colon?

A

– Annular, encircling lesions - napkin-ring constrictions
– Themarginsareclassically heaped up, beaded, and firm, and the mid-region is ulcerated
– Thelumenismarkedly narrowed, and the proximal bowel may be distended
– Penetratethebowelwallas subserosal and serosal white, firm masses

180
Q 
Carcinoid tumours:
Derived from which cells?
Make up _% of colorectal malignancies but almost \_\_%of small intestinal malignant tumours?
Age?
Histological significance?
Most common site?
Clinical features?
Which carcinoma did tumours do not metastasise?
A

Derived from endocrine cells
Make up 2% colorectal malignancies but almost 50% of small intestinal malignant tumours
Age: 60yrs+
Histological features: No reliable difference between benign and malignant
Appendix is the most common site
Clinical features:
-Rarely produces local symptoms
-Caused by obstruction of SI
-Can be associated with a distinctive carcinoid syndrome

Appendiceal and rectal carincinoi do not metastasise. Whereas clean, gastric and colonic will spread to liver once lymph nodes are reached

181
Q

Symptoms of carcinoid syndrome?

A

Due to excess of serotonin

  • ->
  • Cutaneous flushes and apparent cyanosis
  • Diarrhoea, cramps, nausea, vomiting
  • Cough, wheezing and dyspnoea
182
Q

What is gastrointestinal lymphoma?

Different forms of B cell lymphoma?

T cell lymphoma, associated and prognosis?

A

Primary gastrointestinal lymphomas exhibit no evidence of liver, spleen, mediastinal lymph node, or bone marrow involvement at the time of diagnosis

B cell:

  • MALT (mucosa- associated lymphoid tissue) mainly in stomach and SI
  • IPSID (Immunoproliferative small intestinal disease)
  • Burkitt lymphoma

T cell:

  • Associated with long standing malabsorption syndrome
  • Poor prognosis
183
Q

3 forms of lower GIT mesenchymal tumours?

A

Lipomas (within submucosa or muscular is propria)
Leiomyomas
Leiomyosarcomas (intramural that ulcerate into lumen)

184
Q

What are the 3 zones of the anal canal?

A
  • the upper (covered with rectal mucosa)
  • the middle (partially covered with a transitional mucosa)
  • lower (covered by stratified squamous mucosa)
185
Q

What is the commonest benign neoplasm of the anus?

A

Warts

186
Q

4 forms of malignant (carcinomas) of the anal canal?

A
  1. Basaloid pattern
    • immature proliferative cells derived from the basal layer of a stratified squamous epithelium
  2. Squamous cell carcinoma
    • closely associated with chronic HPV infection
  3. Adenocarcinoma
    • extension of rectal adenocarcinoma
  4. Malignant Melanoma (very rare)
187
Q

Which vitamins are fat soluble and which are water soluble

A

Fat Soluble: A, D, E, K

Water soluble: C, B1, B2, Niacin, B6, B5, Biotin, B12, Folic acid

MD3002 Weeks 1-6 (5 decks)

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