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WEEK 4 Flashcards

1
Q

What is each liver lobe composed of?

A

Hepatocytes (parenchymal cells) arranged in plates, in contact with the bloodstream on one side and bile canaliculi (‘little canals’) on the other
- between the plates are vascular spaces (sinusoids) containing Kupffer cells (phagocytic macrophages)

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2
Q

What are the 4 functions of the liver?

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

What is the classification of liver disease?

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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4
Q

Define (i) cholestasis (ii) Intrahepatic cholestasis (ii) extrahepatic cholestasis.

A

(i) failure to produce or excrete bile
(ii) problems in secretion of bile by hepatocytes due to damage
(iii) Problems with flow of bile out of the liver due to obstruction

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5
Q

Describe jaundice

A

Urine darkens
Stools lighter
- it is a result of accumulation of (conjugated) bilirubin in the blood

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6
Q

Define (i) acute hepatic failure (ii) chronic hepatic failure.

A

(i) Development of severe hepatic dysfunction w/in 24 wks of onset of disease
(ii) progressive decline in liver function with established disease

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7
Q

What are the (i) causes (ii) outcomes of ACUTE HEPATITIS?

A

(i) poisoning (paracetamol), infection (Hep A-C), inadequate perfusion
(ii) Resolution in the majority of cases, or progression to either acute hepatic failure or chronic hepatic damage

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8
Q

What are the (i) common causes (ii) unusual causes of chronic liver disease?

A

(i) alcoholic fatty liver, chronic active hepatitis, primary biliary cirrhosis
(ii) alpha1 AT deficiency, Wilson’s disease, haemochromatosis

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9
Q

What are the consequences of chronic liver disease?

A
  1. CIRRHOSIS - irreversible shrinking of liver and fibrosis
  2. PORTAL HYPERTENSION - increased BP in the portal vein leading to
  3. ASCITES - fluid accumulation in peritoneal cavity
  4. RENAL FAILURE
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10
Q

What are the 4 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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11
Q

What are 4 consequences of liver failure?

A

Oedema - reduced oncotic pressure
Bruising - clotting factors
Ascites
Encephelopathy

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12
Q

What is hepatic encephalopathy?

A

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

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13
Q

What are the current liver function tests? (HINT: there’s 4)

A
  1. Aminotransferases - ALT and AST for liver cell damage
  2. Bilirubin - for cholestasis
  3. ALP and gamma GT for biliary epithelial damage and obstruction
  4. Albumin for synthetic function
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14
Q

What is albumin?

A

Main plasma protein of body
Used as an assessment of liver synthetic function BUT lo albumin also found in e.g.
- post surgical/ITU pts due to redistribution
- significant malnutrition
- nephrotic syndrome

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15
Q

What is bilirubin?

A

Breakdown product of haemoglobin

  • unconjugated bilirubin is taken up by the liver and conjugated so that it can be excreted in bile
  • attacked by bacteria in the colon and excreted in faeces
  • small amounts are reabsorbed and excreted in urine as urobilinogen
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16
Q

What is (i) AST and ALT (ii) ALP (iii) gamma GT?

A

(i) sensitive, non specific markers of acute damage to hepatocytes
(ii) increased in liver disease due to increased synthesis in response to cholestasis
(iii) raised in cholestasis, also affected by ingestion of alcohol and drugs such as phenytoin

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17
Q

What are the limitations of biochemical tests? (HINT: there’s 4)

A

Lack of complete organ specificity
Lack of disease specificity
May be ‘over-sensitive’
‘I have this abnormal result, what do i do with it?’

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18
Q

Apart from the liver, where else is (i) ALT (ii) ALP (iii) gamma GT found in the body?

A

(i) cardiac muscle, erythrocytes
(ii) bone, gut and placenta
(iii) bone, biliary tract, pancreas and kidney

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19
Q

What are the (i) pros and (ii) cons of current LFTs?

A

(i) cheap, widely available, interpretable, direct subsequent investigation e.g. imaging
(ii) Almost 40 yrs old and there are many new diseases for which they have non diagnostic value, little prognostic value in liver transplantation or for evaluating therapeutic success, doesn’t assess liver ‘function’

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20
Q

When the pt is asymptomatic but when the following is raised, what does it suggest could be wrong; (i) Bilirubin (ii) ALP (iii) AST (iv) gamma GT

A

(i) haemolysis, Gilberts syndrome
(ii) physiological .g. pregnancy, adolescence
(iii) skeletal muscle disorders, MI
(Iv) v sensitive to alcohol/drugs

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21
Q

What are the causes of a raised LFT? (HINT: there’s 8)

A
  1. Alpha 1 antitrypsin deficiency
  2. Alpha-fetoprotein - tumour marker
  3. Ceruloplasmin/ cooper studies - Wilson’s disease
  4. Hepatitis serology
  5. Iron studies haemochromatosis
  6. Autoantibodies - chronic active hepatitis, PBC
  7. Radiology - obstruction, hepatomegaly
  8. Liver biopsy
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22
Q

What is Gilbert’s Syndrome?

A

Common auto dominant disorder found in up to 7% of pop

  • caused by intermittent mild jaundice evident during periods of fasting and illness
  • due to a conjugating defect in the liver
  • benign and no treatment required
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23
Q

Where is the spleen located?

A

Against the diaphragm from ribs 9-11 on the left, and posteriorly

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24
Q

What is the mneumonic with odd numbers and the spleen? 1, 3, 5, 7, 9, 11

A 
1 inch thick
3 inches wide
5 inches long
weighs 7oz (200g)
lies between the 9th and 11th ribs
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25
Q

What are the 3 functions of the spleen?

A
  1. Mechanical filtration of RBCs
  2. Active immune response through humeral and cell mediated pathways
  3. Haematopoesis until 5th month of gestation
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26
Q

What does the gastrosplenic ligament carry?

A

The left gastro-epiploic and short gastric branches of the splenic artery and the equivalent veins

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27
Q

What does the lienorenal ligament carry?

A

Splenic artery and vein alongside the tail of the pancreas

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28
Q

What can rib fractures do to the spleen?

A

May rupture and cause considerable intraperitoneal haemorrhage

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29
Q

What care must be taken when removing the spleen?

A

To avoid injuring the tail of the pancreas when ligating the splenic vessels

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30
Q

What is the blood supply of the spleen?

A

SPLENIC ARTERY is largest branch of coeliac trunk, has a tortuous course as it runs along the upper border of the pancreas. It divides into about 6 branches, which enter the spleen at its hilum
SPLENIC VEIN leaves hilum and runs behind tail and body of pancreas. Behind the neck of the pancreas the splenic vein joins the SMV to form the portal vein

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31
Q

What is the lymphatic drainage of the spleen?

A

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

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32
Q

What is the nerve supply of the spleen?

A

Nerves accompany the splenic artery and are derived from the coeliac plexus (foregut T5 - 9)

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33
Q

Summarise the portal venous system.

A

The portal vein drains blood from the lower third of the oesophagus to halfway down the anal canal.

  • drains blood from the spleen, pancreas, and gallbladder
  • enters the liver, 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
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34
Q

What is the origin and pathway of the portal vein?

A

About 5cm long and formed behind neck of pancreas by union of splenic and SMV

  • ascends to right behind 1st part duodenum, and enters the lesser omentum
  • runs up infront of opening into lesser sac to the porta hepatis, where it divides into R and L branches
  • in the free edge of the lesser omentum, the portal vein lies behind the hepatic artery with the bile duct to the right of the artery
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35
Q

Where does the SMV pass with regards to the duodenum?

A

Passes in the root of the mesentery, anterior to the 3rd part of duodenum and uncinate process of pancreas

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36
Q

What does the (i) left gastric (ii) IMV drain?

A

(i) lower oesophagus and left end of lesser curve of stomach directly to the portal vein
(ii) hindgut and joins splenic vein in very variable conditions, behind the pancreas, often joining the portal vein itself

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37
Q

What/where does the (i) cystic (ii) right gastric vein drain?

A

(i) directly to portal vein, but may drain to liver

(ii) drains the right end of the lesser curve of stomach directly to the portal vein

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38
Q

What are the 4 sites of porto-systemic anastomosis?

A
  1. At the lower third of the oesophagus - branches of left gastric anastomose with oesophageal veins draining middle oesophagus (varices)
  2. Halfway down the anal canal - sup rectal veins (portal) anastomose with middle and inf rectal veins (systemic) - piles/haemorrhoids
  3. Para-umbilical veins - connect L branch of portal vein with superficial veins of anterior abdominal wall (systemic) - caput medusae
  4. Veins of the retroperitoneal ascending colon, desc colon, duodenum, pancreas and liver (portal) anastomose with renal lumbar and phrenic veins (systemic)
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39
Q

What happens if the portal vein is blocked?

A

Blood flows or ‘bypasses’ into the systemic circulation, usually causing the anastomotic veins to dilate

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40
Q

What are the (i) supra-hepatic causes (ii) hepatic causes (iii) infra-hepatic causes of portal hypertension

A

(i) cardiac disease, hepatic vein thrombosis, IVC thrombosis
(ii) cirrhosis - alcohol, hepatitis etc
(iii) portal vein thrombosis, splenic vein thrombosis

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41
Q

What is the range for normal portal venous pressure?

A

5 - 10 mmHg

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42
Q

What is the origin and location of the abdominal aorta?

A

Begins at aortic hiatus of diaphragm at T12 in the midline

  • extends to L4 (just inf to umbilicus) where it bifurcates into common iliac arteries - just to left of midline
  • retroperitoneal, lies on vertebral column
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43
Q

What are the relations anteriorly and on the right of the abdominal aorta?

A

ANTERIOR = pancreas, splenic vein, L renal vein, duodenum, root of mesentery plus coils of small bowel, lumbar veins
ON RIGHT = cisterna chyli, thoracic duct, azygous vein, IVC

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44
Q

What are the visceral unpaired, anterior branches of the abdominal aorta? (HINT: there’s 3)

A
  1. Coeliac trunk T12
  2. SMA L1
  3. IMA L3
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45
Q

What are the visceral paired branches of the abdominal aorta? (HINT: there’s 3)

A
  1. Middle suprarenal arteries
  2. Renal arteries (L1)
  3. Testicular/ovarian arteries L2
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46
Q

What are the visceral posterior branches of the abdominal aorta? (HINT: there’s 3)

A
  1. Inferior phrenic arteries (also supply suprarenal)
  2. Lumbar arteries
  3. Median sacral artery
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47
Q

What is the IVC formed by? What is its route in the body?

A

Formed by union of common iliac veins @ L5
- ascends on the right side of aorta, pierces central tendon of diaphragm @ T8 and drains into RA
(entrance into lesser sac separates IVC from portal vein)

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48
Q

What are the 4 tributaries of the IVC?

A
  1. 2 or 3 anterior visceral tributaries: the hepatic veins
  2. 3 lateral visceral tributaries: right suprarenal vein, both renal veins, and right gonadal
  3. 5 lateral abdominal wall tributaries: inferior phrenic vein and 4 lumbar veins
  4. 3 veins of origin: 2 common iliac veins and the median sacral vein
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49
Q

Blunt trauma to the liver could cause damage to what 2 BVs?

A

Hepatic vein and IVC injury

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50
Q

What does the left renal vein receive BEFORE passing posterior to the SMA to drain into the IVC?

A

Left suprarenal and left gonadal veins

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51
Q

What are the (i) primary (ii) secondary imaging tools?

A

(i) x-ray, CT, ultrasound

ii) MRI, fluoroscopy (ba meals

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52
Q

When is MRI used as a second line test?

A
  1. Hepato-biliary
  2. Small Bowel
  3. Pelvis
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53
Q

What are the symptoms of acute appendicitis?

A

Periumbilical pain
Nausea
Vomiting
- localises pain to right iliac fossa

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54
Q

What are the imaging techniques used to diagnose acute appendicitis?

A

No role for x-ray

  • CT and USS are important tools
  • ideally, use USS first then CT is this is inconclusive
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55
Q

What is the correlation between acute diverticulitis and age?

A

Incidence of diverticulosis increases with age

  • 10% of pop under 40
  • 60% pop over 80 years old
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56
Q

What does the clinician need to do with regards to acute diverticulitis?

A
  1. Make diagnosis

2. Complications : abscess, obstruction, perforation, fistulae

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57
Q

What imaging is done to diagnose acute diverticulitis?

A

Pain x-ray - exclude obstruction/perforation

- then CT

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58
Q

What is acute cholecystitis? What is the diagnosis based on?

A

Almost always secondary gallstones
Diagnosis based on
- one local sign of inflammatioin (RUQ pain etc.)
- one sign of inflammation (fever, WCC, CRP)
- confirmatory imaging

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59
Q

What imaging is used to diagnose acute cholecystitis?

A

USS shows gallstones, gall bladder wall thickening or local fluid
CT can be false neg
MRI if biliary tree dilatation

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60
Q

What is emphysematous cholecystitis?

A

Air in the gall bladder wall

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61
Q

What are the treatment options for acute cholecystitis?

A

Medical/conservative
Interventional radiology (percutaneous)
Surgery

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62
Q

What are common small bowel obstructions?

A

Adhesions
Cancer
Herniae
Gallstone ileus

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63
Q

What are the (i) symptoms (ii) signs of small bladder obstruction?

A

(i) vomiting, pain and distension

(ii) increased bowel sounds, tenderness, palpable loops

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64
Q

What is the role of imaging for small bowel obstruction?

A

Site, cause, severity, and detects complications

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65
Q

What imaging is used to detect small bowel obstruction?

A
  1. X-RAY
    - 70% sensitivity 60% sensitivity
    - can miss fluid filled loops
  2. CT
    - v. sensitive and specific (>95%)
    - transition point is key
    - adhesions not seen
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66
Q

What are the causes of large bowel obstruction?

A

Colorectal cancer 60%
Volvulus 15%
Diverticulitis 10%

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67
Q

What does the surgeon want to know when diagnosing large bowel obstruction?

A

Site
Cause
Distant disease

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68
Q

What imaging is used to detect large bowel obstruction?

A
  1. X-RAY
    - may be helpful but may not diagnose underlying cause
  2. CT
    - sens/spec greater than 93%
    - shows underlying mass, state of caecum and if theres any distant disease
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69
Q

What are the (i) common (ii) less common causes of perforation?

A

(i) perforated ulcer
Diverticular
(ii) secondary to cancer or secondary to ischaemia

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70
Q

What imaging is used to diagnose perforation?

A
  1. X-RAY
    - may miss small pockets of gas and doesn’t show the site of origin
  2. CT
    - high sens and spec
    - shows free fluid and often shows clues to site of origin (86%) (distribution of gas, any defect in wall and localised inflam change)
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71
Q

What are the causes of bowel ischaemia?

A

Arterial occlusion 60 - 70%
Venous occlusion 5 - 10%
Non-occlusive hypoperfusion 20 - 30%

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72
Q

What are the symptoms of bowel ischaemia?

A

Severe abdominal pain
Vomiting, diarrhoea, distension inconsistent
Borderline amylase, raised WCC, acidotic

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73
Q

What imaging is used to diagnose bowel ischaemia?

A

BIPHASIC CT

  • both arterial and venous contrast enhancement
  • shows site of occlusion and length of affected bowel
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74
Q

What is the role of (i) x-ray (ii) USS (iii) CT?

A

(i) obstruction or perforation
(ii) RUQ/ right iliac fossa pain
(iii) primary imaging technique for acute abdominal pain EXCEPT for acute cholecystitis/appendicitis

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75
Q

What are the types of (i) benign (ii) malignant tumours of the OESOPHAGUS?

A

(i) Mesenchymal tumours
Squamous papillomas
(ii) squamous cell carcinoma
Adenocarcinoma

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76
Q

What are the types of (i) benign (ii) malignant tumours of the STOMACH?

A

(i) Polyps (neoplastic or adenomas)
Mesenchymal
(ii) carcinoma, lymphoma, carcinoid, mesenchymal

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77
Q

What are the names of benign tumours of the oesophagus?

A 
Leiomyomas***
Fibromas
Lipomas
Haemangiomas
Neurofibromas
Lymphangiomas
Mucosal polyps
Squamous papillomas
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78
Q

What are the 2 most common malignant oesophageal tumours? What are 4 others that are rare?

A

Squamous cell carcinoma (90% of all)
Adenocarcinoma

RARE: carcinoid tumour
malignant melanoma
lymphoma
sarcoma

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79
Q

What is the incidence of squamous cell carcinoma? What is the ratio from males to females?

A

Over age of 50
5x more common in men
no.1 country in world = iran, then central china, south africa and southern brazil

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80
Q

What are the 4 factors associated with squamous cell carcinoma?

A
  1. DIETARY
    - deficiency of vitamins
    - fungal contamination of foodstuffs
    - high content of nitrites/nitrosamines
  2. LIFESTYLE
    - burning hot beverage/food
    - alcohol and tobacco
  3. OESOPHAGEAL DISORDERS - long standing oesophagitis and achalasia
  4. PREDISPOSITION
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81
Q

What is the morphology of SSC?

A

20% in upper third
50% in middle third
30% in lower oesophageal third
- small grey-white, plaque-like thickenings that become tumourous masses

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82
Q

What are the three patterns expressed by SSC?

A
  1. Protruded polypoid exophytic (60%)
  2. Flat, diffuse, infiltrative (15%)
  3. Excavated, ulcerated (25%)
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83
Q

What is the histology of a squamous cell carcinoma of the oesophagus?

A

The squamous epithelium

  • pleomorphism
  • hyperchromatism
  • mitotic figures
  • the degree of atypia (low or high grade dysplasia)
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84
Q

What are the clinical features of squamous cell carcinoma?

A
  1. Dysphagia
  2. Extreme weight loss (cachexia)
  3. Haemorrhage and sepsis
  4. Cancerous tracheoesophageal fistula
  5. Metastases (lymph nodes) - cervical, mediastinal, paratracheal, tracheobronchial, gastric and coeliac
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85
Q

Where do adenocarcinomas arise? What age do they tend to occur? What are the predisposing factors?

A

The lower third of the oesophagus

  • age 40, with a median age of 60
  • tobacco and obesity
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86
Q

What do adenocarcinomas arise from?

A

Arises from the Barret mucosa (10%)

- intestinal metaplasia caused by gastric reflux

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87
Q

What is the morphology of adenocarcinoma?

A

Flat or raised patches or nodular masses

  • may be infiltrative or deeply ulcerative
  • mucin producing glandular tumours
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88
Q

What are the clinical features of adenocarcinomas?

A
  1. Dysphagia
  2. Progressive weight loss
  3. Bleeding
  4. Chest pain
  5. Vomiting
  6. Heartburn
  7. Regurgitation
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89
Q

Name and describe the types of benign tumours of the stomach.

A

POLYPS = nodule or mass that projects above the level of the surrounding mucosa (usually in antrum)
- NON NEOPLASTIC (90%) most are small and sessile, hyperplastic surface epithelium and cystically dilated glandular tissue
- NEOPLASTIC - adenomas (5-10%) contain proliferative dysplastic epitheilum with malignant potential, sessile or pedunculated
LEIOMYOMAS and SCHWANNOMAS = rare

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90
Q

How common are gastric carcinomas? Where is it most common?

A

90-95% of malignant tumours of stomach and 2nd most common GI tract tumour in world
high in Japan

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91
Q

What are the factors associated with gastric carcinoma?

A 
ENVIRONMENTAL
- infection by h.pylori
- diet
- low socioeconomic status
- cigarette smoking
GENETIC FACTORS
- slightly increased risk with blood group A
- family history 
- hereditary nonpolyposis colon cancer syndrome
- familial gastric carcinoma syndrome
HOST
- chronic gastritis
- gastric adenomas
- barrett oesophagus
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92
Q

Where do gastric carcinomas arise?

A

Pylorus and antrum 50-60%
- cardia 25%
- with remainder in body and fundus
(lesser curvature is about 40% and greater is 12%)

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93
Q

What is gastric carcinomas classified on the basis of?

A
  1. Depth of invasion (early and advanced)
  2. Macroscopic growth pattern
  3. Histological appearance
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94
Q

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

A
  1. Exophytic
  2. Flat or depressed -> linitis plastica
  3. Excavated
95
Q

How are adenocarcinomas classified histologically? (HINT: the Lauren classification)

A
  1. INTESTINAL TYPE
    - composed of neoplastic intestinal glands resembling those of colonic adenocarcinoma
    - cells often contain apical mucin vacuoles and abundant mucin may be present in gland lumens
  2. DIFFUSE TYPE
    - composed of gastric type mucous cells which generally don’t form glands, but permeate the mucosa and wall as scattered individual cells or small clusters in an ‘infiltrative; growth pattern
    - mucin formation expands the malignant cells and pushes nucleus to periphery creating a ‘signet ring’
  3. MIXED TYPE
96
Q

How do gastric carcinomas spread?

A

All gastric carcinomas eventually penetrate the wall and spread to regional and more distant lymph nodes

  • supraclavicular (virchow) node
  • local invasion into duodenum, pancreas and retroperitoneum
  • metastases to liver and lungs
  • metastases to ovaries (Krukenberg tumour)
97
Q

What are the clinical features of gastric carcinoma?

A

Asymptomatic until it is too late

- weight loss, abdo pain, anorexia, vomiting, altered bowel habits, dysphagia, anaemic symptoms, haemorrhage

98
Q

What is gastric lymphoma?

A

5% of gastric malignancies

  • B cell lymphomas of mucosa associated lymphoid tissue
  • more than 80% are associated with chronic gastritis and H. pylori infection
99
Q

What is the morphology of gastric lymphoma?

A

Commonly occurs in mucosa or superficial submucosa
- lymphocytic infiltrate of the lamina propria surrounds gastric glands massively infiltrated with atypical lymphocytes and undergoing destruction

100
Q

What are the 2 separate units (both in the medulla) that are the central neural regulation of vomiting?

A
  1. The vomiting centre

2. The chemoreceptor trigger zone (CTZ)

101
Q

What do the (i) vital (ii) non-vital centres of the medulla oblongata regulate?

A

(i) resp rhythm, HR and BP

(ii) cough, sneeze, swallowing and vomiting

102
Q

What is the vomiting centre? What are its inputs and outputs?

A

A collection of multiple sensory, motor and control nuclei

  • receive nerve impulses from both vagal and sympathetic afferent nerve fibres
  • motor impulses are transmitted from the vomiting centre
103
Q

What are the stimuli that are caused during motion sickness?

A

Vestibular labyrinth - vestibular nuceli (brain stem) - cerebellum - CTZ - vomiting centre - vomit

104
Q

Where is the CTZ located? What is its function?

A

Is in the area postrema in the floor of the 4th ventricle

  • is sensitive to chemical stimuli and is the site of action of drugs which stimulate or inhibit vomiting
  • also concerned with the mediation of motion sickess
105
Q

Define (i) nausea (ii) retching (iii) vomiting.

A

(i) feeling of wanting to vomit, is associated with autonomic effects (salivation, pallor, sweating), often symptom before vomiting
(ii) strong involuntary effort to vomit that is unproductive
(iii) expulsion of gastric contents through the mouth

106
Q

What factors can trigger nausea/vomiting? (NOTE: there’s 9 so list as many as poss!)

A
  1. Stimulation of sensory nerve endings in stomach and duodenum
  2. Stimulation of vagal sensory endings in pharynx
  3. Drugs or endogenous emetic substances
  4. Disturbances of vestibular apparatus
  5. Various stimuli of sensory nerves of the heart and viscera
  6. Raise in intracranial pressure
  7. Nauseating smells, repulsive sights, emotional factors
  8. Endocrine factors
  9. Migraine
107
Q

What are 3 types of vomiting? Describe them.

A
  1. PROJECTILE VOMITING
    - suggestive of gastric outlet or upper GI obstruction
  2. HAEMATEMESIS
    - vomiting fresh or altered blood (oesophageal varices, bleeding gastric ulcer)
  3. EARLY MORNING
    - pregnancy, alcohol dependence, some metabolic disorders (uraemia)
108
Q

What are the 8 types of anti-emetic?

A
  1. Antihistamines
  2. Antimuscarinics
  3. Dopamine antagonists
  4. 5HT(3) antagonists
  5. Neurokinin 1 receptor antagonists
  6. Synthetic cannabinoids
  7. Steroids
  8. Other neuroleptics
109
Q

Describe what antihistamines are, what they are used for, their side effects and name 3 examples.

A

H1 histamine receptor antags that are useful in numeroud N/V cases (motion sickness and vestibular disorders)
- side ffects vary e.g. drowsiness and antimuscarinic effects
Ex - Cinnarizine, cyclizine, promethazine

110
Q

Describe what antimuscarinics are, what they are used for, their side effects and name an example.

A

Block muscarinic receptor-mediated impulses from the labyrinth and from visceral afferents
- used in motion sickness as a patch or tablets
- side effects = constipation, transient bradycardia and dry mouth
Ex - Hyoscine hydrobromide

111
Q

What is the MoA of dopamine antagonists? Give examples.

A

Active against CTZ triggered vomiting but NOT stomach induced vomiting

  1. The PHENOTHIAZINES and related drugs (also classed as neuroleptics/antipsychotics)
    - chloropromazine, perphenazine, prochlorperazine, trifluoperazine
  2. DOMPERIDONE
  3. METOCLOPRAMIDE
112
Q

What is the MoA of 5HT(3) antagonists? When are they used? Give 4 named examples.

A

Block 5HT(3) receptors in GI tract and CNS
- useful in managing N/V in pts receiving cytotoxics and post op N/V
E.g. Dolasetron, Granisetron, Ondansetron, Palonosetron

113
Q

When are Neurokinin 1 receptor antagonists used? Name 2 examples.

A

As an adjunct to dexamethasone and a 5HT(3) antag in preventing N/V from chemotherapy
Ex - Aprepitant, Fosaprepitant

114
Q

Name a synthetic cannabinoid, give its use and common side effect(s).

A

NABILONE

- used for N/V from chemo that’s unresponsive to conventional anti-emetics

115
Q

Name a steroid and state what it is used to treat with regards to emesis.

A

DEXAMETHASONE

- can be used alone to treat vomiting associated with cancer chemo, or in conjunction with other antiemetics

116
Q

Name 2 other neuroleptics.

A

Haloperidol

Levomepromazine

117
Q

What are the 5 types of laxatives? Give examples for each.

A
  1. Bulk-forming laxatives
    - ispaghula husk, methylcellulose
  2. Stimulant laxatives
    - bisacodyl, dantron, docusate sodium, glycerol, senna, sodium picosulfate
  3. Faecal softeners
    - arachis oil, liquid paraffin
  4. Osmotic laxatives
    - lactulose, macrogols, Mg salts, rectal phosphates
  5. Peripheral opioid-receptor antagonists
    - mathylnaltrexone bromide
118
Q

What are 3 of the ways/methods that laxatives work by?

A
  1. Bulk-fibre provides increased volume and promotes peristalsis by distension
  2. Some laxatives soften stool by coating and breaking up particles
  3. Liquid mixes with stool to soften
119
Q

What 2 things does diarrhoea involve?

A

Increased motility of GI tract

Decrease in absorption of fluid and therefore a loss of electrolyte

120
Q

What are the 4 approaches for the treatment of ACUTE diarrhoea?

A
  1. maintenance of fluid and electrolyte balance e.g. oral rehydration preparation
  2. Antimotility drugs
  3. Antispasmodics e.g. hyoscine butylbromide (buscopan), mebeverine
  4. Occasionally antibacterial agent is indicated e.g. systemic bacterial infection, campylobacter enteritis, shigellosis and salmonellosis
121
Q

What 3 things are used to treat CHRONIC diarrhoea?

A
  1. ANTIMOTILITY AGENTS
    - codeine, co-phenotrope, loperamide (imodium) and morphine
  2. ADSORBENTS
    - kaolin, light
  3. BULK FORMING DRUGS
    - useful in controlling diarrhoea associated with diverticular disease
    - ispaghula, methylcellulose, sterculia
122
Q

What 5 things does bile contain?

A 
Bile salts
Bilirubin
Cholesterol
Lecithin
Plasma electrolytes
123
Q

What are the majority of gallbladder stones in the UK?

A

Cholesterol stones

124
Q

What medication is used to treat gallstones?

A

Ursodeoxycholic acid

- if mild symptoms and not amenable to other treatment

125
Q

How is biliary colic and acute cholecystitis treated?

A

Biliary colic is very painful and may require an opioid (morphine or pethidine) parenterally and/or diclofenac (NSAID) by suppository

  • these routes are chosen as overcomes difficulties in absorption caused by vomiting
  • pain that continues for over 24 hrs or accompanied by fever usually necessitates hospital admission
126
Q

What is cholestyramine? What is its MoA? When is it used?

A

An anion-exchange resin

  • forms an insoluble complex with bile acids in intestine
  • relieves pruritis (skin itching) associated with partial biliary obstruction and primary biliary cirrhosis
  • can also be used in some cases of diarrhoea (Crohn’s related) and in hypercholesterolaemia
127
Q

What 3 vessels make up the portal triad?

A

Bile duct (common)
Hepatic artery
Hepatic portal vein

128
Q

What 3 functions does the liver have?

A
  1. SYNTHESISES albumin, clotting factors, complement, alpha 1 antitrypsin and thrombopoetin
  2. PRODUCES bile through conjugation of bilirubin
  3. BREAKS DOWN drugs insulin and ammonia
129
Q

What is the function of Kupffer cells?

A

They phagocytose old blood cells, bacteria and foreign materials from bloodstream/gut

130
Q

What value of bilirubin suggests you are jaundiced?

A

Greater than 40 micromol/L

131
Q

What is the difference between conjugated and unconjugated bile?

A 
UNCONJUGATED = water insoluble
CONJUGATED = water soluble (can be excreted in urine) therefore pt will have dark urine
132
Q

Define (i) prehaptic (ii) intrahepatic (iii) post hepatic (obstructive) jaundice.

A

(i) haemolysis resulting in release of bilirubin from RBCs therefore build up of bilirubin
(ii) liver disease resulting in excess bilirubin in liver and bloodstream
(iii) Obstruction of bile flow out of liver - pts have dark urine and pale stools

133
Q

What are the 4 main causes of acute liver injury?

A
  1. Viral infections
  2. Alcohol (most common cause)
  3. Adverse drug reactions
  4. Biliary obstruction (gallstones)
134
Q

What symptoms/signs do acute liver injury pts have? What signs/symptoms suggest the pt has then gone into liver failure?

A

Jaundice, malaise
Raised serum bilirubin and transaminases
Liver failure = decreased albumin, ascites, bruising, encephalopathy

135
Q

What liver zone is closest to the blood supply? Why is this significant?

A

They are the most oxygenated and healthy hepatocytes

- these are hit first by toxic drugs e.g. alcohol

136
Q

In alcoholic liver injury - what type of hepatocyte necrosis do you get?

A

Zone 3 - which is closest to the central vein

137
Q

What 3 diseases can arise as a result of alcoholic liver injury?

A
  1. Steatosis
  2. Cirrhosis
  3. Acute hepatitis with Mallory’s hyaline
138
Q

What is steatosis?

A

Fat deposition - metabolism altered

You get a build up of Mallory’s hyaline - a build up due to hepatocyte damage

139
Q

How does inflammation arise in alcoholic liver injury? What does this result in?

A

Acetaldehyde binds to hepatocytes causing damage

- eventually start to produce collagen therefore fibrosis

140
Q

What is cirrhosis?

A

Fibrosis (collagen) + regeneration

141
Q

What are the 5 causes of cirrhosis?

A
  1. Alcohol
  2. Hep B and C viruses
  3. Iron overload
  4. Autoimmune liver disease
  5. Gallstones
142
Q

How is cirrhosis classified morphologically?

A

MICRONODULAR - nodnules less than 3mm
MACRONODULAR - nodules greater than 3mm
MIXED

143
Q

What are the complications of cirrhosis (HINT: there’s 3)

A
  1. LIVER FAILURE
    - hepatic encephalopathy (ammonia), build up of steroid hormones => hyperoestrogenism (palmar erythema and gynaecomatia), bleeding
  2. PORTAL HYPERTENSION
    - increased hepatic vascular resistance, AV shunting - oesophageal varices, haemorrhoids, caput medusae
  3. HEPATOCELLULAR CARCINOMA
144
Q

What are the two ways drugs can injure the liver?

A
  1. Injury to liver cells (hepatocellular) e.g. paracetamol overdose
  2. Injury to bile production/secretion cells (cholestatic) e.g. methyl testosterone
145
Q

What is acute biliary obstruction due to? What does it cause? How can it become complicated?

A

Usually due to gallstones

  • causes colicky pain and jaundice
  • can be complicated by infection of blocked CBD (cystic bile duct) = cholangitis
146
Q

Define chronic hepatitis.

A

Any inflammation of the liver lasting more than 6 months

- sustained elevation of transaminases (require liver biopsy to classify cause)

147
Q

What are the 4 causes of chronic hepatitis?

A

Viral
Alcohol (most common)
Drugs
Autoimmune

148
Q

How is chronic hepatitis classified?

A
  1. TYPE - aetiology
  2. GRADE - degree of inflammation
  3. STAGE - degree of fibrosis
149
Q

What is autoimmune chronic active hepatitis?

A

Females more than mores and usually presents in mid to late teens
Get:
- interface hepatitis
- plasma cells and swollen hepatocytes
- fibrosis
- ANA, AMA, raised serum IgG and transaminases, anti-LKM

150
Q

What may autoimmune chronic active hepatitis pts benefit from?

151
Q

Who does primary biliary cirrhosis tend to affect?

A

Females more than males at about 40-50 years old

152
Q

What are the stages of primary biliary cirrhosis? (HINT there’s 4)

A
  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
153
Q

What are the symptoms/signs of primary biliary cirrhosis?

A

Jaundice, pruritis, xanthelasmata

- raised ALP (alkaline phosphatatse) and IgM, AMA (anti mitochondrial antibodies)

154
Q

What is haemochromatosis?

A

Men more likely than women, inherited caused by faulty gene

  • iron deposition in the liver that causes alteration of architecture causing fibrosis and in turn cirrhosis
  • autosomal recessive: HFE gene (primary haemochromatosis)
155
Q

How is haemochromatosis diagnosed?

A

Venesection is done regularly

- need to test iron and ferritin levels beforehand

156
Q

What is alpha-1-antitrypsin deficiency?

A

Autosomal recessive disorder where you end up with low levels of alpha-1-antitrypsin

  • proteins build up in hepatocytes as hyaline
  • can lead to cirrhosis
  • it is also associated with emphysema
157
Q

What is NASH/NAFLD? What is it associated with?

A

Non-alcoholic steatohepatitis/ Non-alcoholic fatty liver disease
Associated with Metabolic Syndrome (DM II, hypertension, decreased HDL cholesterol, increased triglycerides)
- get fat deposition in hepatocytes than can lead to cirrhosis

158
Q

What is Wilson’s Disease?

A

Autosomal recessive disorder that is the failure of the liver to excrete copper in bile resulting in the build up of copper in the liver leading to cirrhosis

159
Q

Why do those with Wilson’s disease tend to have neurological disease?

A

Copper also deposits in brain tissue

160
Q

What will blood tests for Wilson’s disease show?

A

Low caeruloplasmin

161
Q

What are the types of (i) Devleopmental/hamartomas (ii) benign (iii) maliganant liver tumours?

A

(i) cysts or hamartomas
(ii) incidental finding
Adenoma, haemangioma
Liver cysts
(iii) Metastases are v. common (espec in colon)
Primary (hepatoceullar carcinoma and cholangiocarcinoma)

162
Q

What is hepatocellular carcinoma? When does it arise? What is its aetiology?

A 
Often multifocal
- arises in cirrhotic lover
AETIOLOGY
- aflatoxins - fungal toxin
- Hep B and C
- cirrhosis
163
Q

What are the congenital malformations of the biliary system? What 4 other things can be seen in the biliary system?

A

CONGENITAL = atresia and choledocal cysts

Gallstones, cholecystitis, cholangiocarcinoma, obstruction

164
Q

Where does cholangiocarcinoma? What is it associated with? What does it cause? What can it lead to?

A

Arises form bile duct epithelium anywhere in biliary system

  • associated with ulcerative collitis
  • causes obstructive jaundice, itch, weight loss, lethargy
  • can lead to rupture of common bile duct/gall bladder
165
Q

What are the 6 risk factors for gallstones (HINT: the 5 F’s)

A 
Females
Fair
Fat
Forty
Fertile
Diabetes mellitus
166
Q

What can gallstones cause?

A 
Cholecystitis 
Obstructive jaundice
Cholangitis
Pancreatitis
Cholangiocarcinoma
167
Q

What is acute cholecystitis? What are the symptoms of cholecytitis?

A

Usually caused by gallstones
- is intiially sterile then becomes infected and may lead to abscess/rupture
SYMPTOMS = RUQ pain (biliary colic), fever, nausea, vomiting

168
Q

What is chronic cholecystitis?

A

Invariably related to gallstones

- chronic inflammation with wall thickening

169
Q

What is an annular pancreas? What does it cause?

A

Pancreas wraps around 2nd part of pancreas causing obstruction
- polyhydraminos, low birth weight, poor feeding

170
Q

What does acute pancreatitis cause?

A

Catastrophic metabolic consequences

- decreased calcium, decreased albumin and increased glucose

171
Q

Why is pancreatitis a medical emergency? How is it diagnosed?

A

Have massive fluid losses into retroperitoneal space causing shock

  • high mortality rates
  • diagnosed by high serum amylase
172
Q

What are the 7 causes of acute pancreatitis?

A 
Alcohol
Shock
Hypothermia
Mumps
Trauma
Scorpion bites
Gallstones
173
Q

What is chronic pancreatitis? What does it cause? What do pts require?

A

Multiple episodes of acute

  • causes fibrosis of pancreas that may lead to diabetes mellitus
  • reduced production of enzymes which can require supplements
174
Q

What is pancreatic carcinoma? What is it associated with? How does it present? WHEN is it operable?

A

An adenocarcinoma associated with smoking and diabetes mellitus

  • presents with painless, progressive jaundice, also causes weight loss
  • may be operable if small and close to ampulla
175
Q

What is the aetiology of IBD?

A

Multifactorial
Genetic factors
Autoimmune/immune dysfunction
Environmental factors (internal and external)

176
Q

What are the 5 types of IBD?

A 
Ulcerative colitis
Crohn's disease
- indeterminate colitis
- pseudomembranous colitis
- diverticulitis
177
Q

Who does ulcerative colitis tend to affect?

A

Females more than males

  • adolescents and early adulthood (median age 30)
  • non smokers
178
Q

What is ulcerative colitis characterised by?

A

Inflammatory change in colon

- almost always affects rectum and then a variable length of colon proximally

179
Q

If your entire colon is involved in ulcerative colitis what it it called?

A

PANcolitis

180
Q

What re the 3 features of UC?

A

Contiguous
Circumferential
Superficial inflammation

181
Q

What are the symptoms of UC?

A 
Abdo pain
Mucous/bloody diarrhoea
Lethargy
Weight loss
Dehydrated
Feeling of needing to pass stool but can't
182
Q

What can UC pts present with?

A

Iron deficiency anaemia
Raised inflammatory markers
Dehydrated

183
Q

What is the histological appearance of a pts colon with UC?

A

Inflamed mucosal layer
Crypt abscesses
Broad based ulcers eroding into superficial mucosa
Goblet cell loss

184
Q

Who does Crohn’s disease tend to affect?

A

Females more than males

  • adolescence and early adulthood (median age 30)
  • smokers
185
Q

Where does Crohn’s disease tend to affect the GIT?

A

Characterised by an inflammatory change anywhere in GI tract

  • small intestine alone 40%
  • small intestine AND colon 30%
  • colon alone 30%
186
Q

What are the symptoms of Crohn’s?

A 
Abdominal pain
Weight loss
Lethargy
Dehydration
Diarrhoea (less blood than UC)
187
Q

Where will you initially see inflammation in those with Crohn’s?

A

The ileum

‘terminal ileitis’

188
Q

What can Crohn’s pts present with?

A

Anaemia - absorption/blood loss
Raised inflammatory markers
Dehydration

189
Q

What features are seen histologically in a Crohn’s pt?

A

Increased no. inflammatory cells
Granulomas (collection of histiocytes)
Thin fissuring ulcers that can go quite deep (through muscle)
Fat wrapping
Thickened bowel wall as inflammation leading to fibrosis throughout bowel wall

190
Q

What are those with Crohn’s more likely to have compared with UC pts?

191
Q

What are the extraintestinal manifestations of both Crohn’s and UC pts? (HINT: there’s 6)

A 
Inflammatory arthropathies
Erythema nodosum (Crohn's)
Pyoderma gangrenosum
Primary sclerosing cholangitis
Iritis/uveitis
Aphthous stomatitis
192
Q

What is pseudomembranous colitis caused by? What does it look like? How is it treated/managed?

A

C. diff can lead to it

  • acute inflammatory reaction of bowel
  • classic eruption type lesion
  • to improve - treat c.diff
193
Q

What causes diverticulitis? Where do they tend to occur?

A

Increased pressure within sigmoid colon causes mucosa to herniate out
- they can occur anywhere but tend to be sigmoid colon

194
Q

What is the difference with congenital diverticulitis?

A

They always take muscle with them (congenial)

195
Q

What is diverticulosis/diverticular disease?

A

Diverticulosis/diverticular disease is not inflamed

196
Q

What is a small intestine benign tumour? What age group does it affect? What structure does it affect? Does it have malignant potential?

A

An adenoma

  • 30 to 60 year old pt with occult blood loss
  • usually affects ampulla of Vater (enlarged and exhibits a velvety surface)
  • Yes, it has potential to become an adenocarcinoma
197
Q

What is a type of small intestine malignant tumour? Where does it occur? What does it cause? What symptoms arise?

A

ADENOCARCINOMA

  • in duodenum usually 40 - 70 year olds
  • napkin ring encircling pattern and polypoid exophytic masses
  • causes intestinal obstruction, cramping pain, nausea, vomiting and weight loss
  • may cause obstructive jaundice
198
Q

What does non neoplastic mean?

A

No new growth of cells

- just abnormal growth of current cells

199
Q

What are the types of (i) non neoplastic (ii) neoplastic (adenoma) benign tumours of colon and rectum?

A

(i) Hyperplastic (90%)
Hamartomatous
(ii) Tubular, Villous and Tubulovillous

200
Q

Where are hyperplastic polyps found? What do they look like macroscopically and histologically? Do they have any malignant potential?

A

1/2 are found in rectosigmoid colon
Nipple like, hemispheric, smooth, moist protrusions of the mucosa
Histologically: well formed glands and crypts, lined by non-neoplastic epithelial cells - most of which show differentiation into mature goblet or absorptive cells
NO malignant potential

201
Q

What are the 2 types of Hamartomatous polyps?

A

Juvenile polyps

Peutz-Jeghers polyps

202
Q

What does juvenile polyps do to the body? Who do they affect? What do they look like histologically? Do they have any malignant potential?

A

Malformations of the mucosal epithelium and lamina propria
- affects children under 5
- 80% of them occur in rectum
Histologically: abundant cystically dilated glands, inflammation common and surface may be congested or ulcerated
NO malignant potential

203
Q

Where are Peutz-Jeghers polyps found in body? What do they involve? Do they have any malignant potential?

A

Stomach 25%, colon 30% and small bowel

  • involve the mucosal epithelium, lamina propria and muscularis mucosa
  • don’t have malignant potential but increased risk of getting malignancies elsewhere
204
Q

How are adenomas classified?

A
  1. TUBULAR ADENOMAS 75%
    - small pedunculated lesions
  2. VILLOUS ADENOMAS 1-10%
    - large neoplasms that are usually sessile
  3. TUBULOVILLOUS ADENOMA 5-15%
    - combination of the both
205
Q

What are adenomas precursors for? What is the risk correlated with?

A 
For invasive colorectal adenocarcinoma
Risk is correlated with:
- polyp size
- hitological architecture
- severity of epitheliual dysplasia
206
Q

What are adenomas precursors for? What is the risk correlated with?

A 
For invasive colorectal adenocarcinomas
Risk is correlated with:
- polyp size (rare in tubular and high risk in sessile)
- histological architecture
- severity of epithelial dysplasia
207
Q

What is the morphology of tubular adenomas (i) macroscopically (ii) histologically?

A

(i) 90% in colon, or stomach or SI
- small tubular adenomas are smooth contoured and sessile whereas large ones tend to be coarsely lobulated and have slender stalks raspberry-like
(ii) stalk is composed of fibromuscular tissue and prominent BVs. Presence of dysplastic epithelium, which lines glands as a tall, hyperchromatic, disordered epithelium which may show mucin vacuoles. Degree of dysplasia is low-grade but high grade may be present. Carcinomatous invasion into submucosal stalk of polyp constitutes invasive carcinoma

208
Q

Where do villous adenomas commonly occur? What is their appearance macroscopically?

A

Commonly in rectum and rectosigmoid

  • sessile
  • velvety of cauliflower like masses projecting 1-3cm above surrounding normal mucosa
209
Q

What is the histology of villous adenomas?

A

Frond like villiform extenstions of mucosa
Covered by dysplastic, sometimes very disorderly columnar epithelium. All degrees of dysplasia may be encountered. When invasive carcinoma occurs, there’s no stalk as a buffer zone so the invasion is directly into the wall of the colon

210
Q

What are the clinical features of tubular, villous and tubulovillous adenomas?

A

Colorectal tubular and tubulovillous adenomas may be asymptomatic but many are discovered during evaluation of anaemia or occult bleeding
Villous adenomas are more symptomatic and often discovered because of obvious rectal bleeding

211
Q

Endoscopic removal of a pedunculated (tubular) adenoma is regarded as an adequate if…..? (HINT: there’s 3 things)

A
  1. The adenocarcinoma is superficial and doesn’t 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
212
Q

What is FAP syndrome?

A

FAMILIAL ADENOMATOUS POLYPOSIS

  • Mutations of adenomatous polyposis coli gene
  • pts develop 500 - 2500 colonic adenomas that carpet the mucosal surface
  • vast majority of polyps are tubular adenomas
  • have a 100% risk of developing adenocarcinoma before age of 30
213
Q

What type of cancer is the most common in the large intestine?

A

Adenocarcinomas

214
Q

What are the dietary factors that can increase chances of getting an adenocarcinoma? (HINT: there’s 5)

A
  1. Excess dietary caloric intake relative to requirements
  2. Low content of vegetable fibre
  3. High content of refined carbs
  4. Intake of red meat
  5. Decreased intake of protective micronutrients
215
Q

Where are the common sites adenocarcinomas tend to arise?

A 
Rectosigmoid colon 55%
Caecum/Ascending colon 22%
Transverse colon 11%
Descending colon 6%
Other sites 6%
216
Q

What is the morphology of tumours in the (i) proximal colon (ii) distal colon?

A

(i) polypoid, exophytic masses. Obstruction uncommon. Penetrate bowel wall as subserosal and serosal white firm masses
(ii) annular circuling lesions, napkin-ring constrictions. Margins are heaped up, beaded, and firm, and mid region is ulcerated. Lumen markedly narrowed and bowel may be distended. They penetrate bowel wall as subserosal and serosal white, firm masses

217
Q

When using barium enema, what classic shape is seen with an adenocarcinoma?

A

Apple core lesion

218
Q

What is the histology of adenocarcinomas?

A

May range from tall, columnar cells resembling their counterparts in adenomatous lesions to undifferentiated, anaplastic masses. May produce mucin and invasive tumour incites a strong desmoplastic stromal response

219
Q

What are the clinical features of adenocarcinomas?

A

Asymptomatic for years
If affecting caecum and right colonic - fatigue, weakness and iron deficiency anaemia
Left sided lesions - occult bleeding, changes in bowel habit, or crampy left lower quadrant discomfort
Systemic manifestations such as weakness, malaise and weight loss signify more extensive disease

220
Q

What does iron deficiency anaemia in an older man mean?

A

GI cancer unless proven otherwise

221
Q

Where do colorectal tumours spread to?

A

Direct extension into adjacent structure
OR
Metastasis through lymphatics and BVs

222
Q

Describe the Dukes’ staging system.

A

A) confined to the submucosa or muscle layer - 5y survival = 90%
B) spread through muscle layer, not yet lymph node involvement - 5y survival = 70%
C) involving lymph nodes - 5y survival = 35%

223
Q

Where are carcinoid tumours derived from? Is there any difference between benign and malignant? What does the aggressive behaviour correlate with?

A

Derived from endocrine cells
- only 2% of colorectal malignancies but almost 1/2 of small intestine malignant tumours
- no reliable histological difference between benign and malignant
Aggressive behaviour:
- site of origin
- depth of local penetration
- size of tumour
- histological features of necrosis and mitosis

224
Q

Where is the most common site(s) of carcinoid tumours?

A

Appendix = most common

- small intestine (ileum), rectum, stomach and colon

225
Q

What does carcinoid tumours look like on transection?

A

Solid, yellow-tan appearance

226
Q

What is the histology of carcinoid tumours?

A

Neoplastic cells may form discrete islands, trabeculae, strands, glands or undifferentiated sheets
Tumour cells are monotonously similar, having a scant, pink glandular cytoplasm and a round to oval stippled nucleus.
By electron microscopy tumour cells contain membrane-bound secretory granules with dense-core granules in cytoplasm

227
Q

What are the clinical features of carcinoid tumours?

A

Rarely produce local symptoms

  • caused by angulation or obstruction of SI
  • some neoplasms associated with a distinct carcinoid syndrome
228
Q

What is carcinoid syndrome? What are the symptoms?

A

From excess of serotonin, 5-HT

  • cutaneous flushes and apparent cyanosis
  • diarrhoea, cramps, nausea, vomiting
  • cough, wheezing, dyspnoea
229
Q

What is the 5y survival rate for carcinoids?

230
Q

Define GI lymphoma.

A

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

231
Q

What is the difference between B cell lymphomas and T cell lymphomas?

A

B cell have a long survival rate

T cell have a small survival rate and prognosis is poor

232
Q

What are the 3 types of mesenchymal tumours?

A

LIPOMAS - well-demarcated, firm nodules less than 4cm arising w/in submucosa or muscularis propria
LEIOMYOMAS
MEIOMYOSARCOMASS - large, bulky, intramural masses that eventually fungate and ulcerate into lumen or project subserosally into abdominal space

233
Q

What are the types of malignant (carcinomas) tumours of anal canal? (HINT: there’s 4)

A

BASALOID PATTERN
- immature proliferative cells derived from basal layer of strat. squamous epithelium
SQUAMOUS CELL CARCINOMA - closely associated with chronic HPV infection
ADENOCARCINOMA - extension of rectal adenocarcinoma
MALIGNANT MELANOMA (v. rare)

MD3002 (14 decks)

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