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GI And Liver > Pathology > Flashcards

Pathology Flashcards

1
Q

What is GORD?

A

This is retrosternal and epigrastric pain as a result of chronic regurgitation of stomach acid into the bottom of the oesophagus

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2
Q

name 5 risk factors for GORD

A 
pregnancy
obesity
smoking
excessive coffee intake
hiatus hernia
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3
Q

name 3 complications of GORD

A

barrettes oesophagus
peptic stricture
adenocarcinoma

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4
Q

what is the presentation of GORD

A 
heart burn
regurgitation
dysphagia
sore throat
anorexia
water brash- excessive salivation
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5
Q

name 5 exacerbating factors of GORD

A 
alcohol
lying down
bending forwards
stooping
hot drinks
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6
Q

what is the morphological change which occurs in GORD to become barretts oesophagus

A

squamous metaplasia to columnar in the lower 3rd of the oesophagus. white squamous epithelial cells are replaced by pink columnar epithelial cells

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7
Q

what are the red flag features of GORD?

A

age of onset >55 with a high risk feature; more than 2 1st degree relatives with upper GI cancer
onset of symptoms

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8
Q

how many biopsies need to be taken of the oesophageal dysplasia to grade the severity?

A

4 biopsies

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9
Q

what is the treatment for GORD?

A

lifestyle changes: weight loss, reduce alcohol intake, dont drink hot drinks, dont eat a heavy meal before bed
medications: Proton pump inhibitors- omeprazole
prokinetics- metocloperamide- aids gastric emptying
nissen fundoplication: surgery where the fundus of the stomach is wrapped around the lower oesophageal sphincter to increase oesophageal tone

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10
Q

what is the treatment for barretts oesophagus if the metaplasia is dysplastic? (ie is showing pre-malignant changes)

A

oesophagealectomy- segmental or total

endoscopic therapy- radiofrequencty ablation/mucosal resection

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11
Q

what is mallory weiss tear?

A

haematemesis caused by a linear oesophageal tear, usually caused by vomitting

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12
Q

name 4 causes of mallory weiss tear except alcohol

A
  1. vomitting
  2. drugs- aspirin ingestion
  3. hiatus hernia
  4. hyperemesis gravidarum (excessive nausea and vomitting seen in pregnancy occasionally)
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13
Q

how might mallory weiss tear present?

A

dizziness and light headed due to blood loss
melaena- black stools
haemoptysis- coughing up blood

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14
Q

how is the treatment of mallory weiss tear determined?

A

Rockall score of re-bleed; determines the likely hood of a patient to bleed again according to their age, co-morbidities, diagnosis, initial bleed extent and shock.

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15
Q

what is the treatment for mallory weiss tear?

A

restore anaemia
endoscopic thermal treatment for active bleeds
epinephrine binds all adrenergic receptors- vasoconstriction- reduce bleeding
check clotting factors

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16
Q

name 3 pre-hepatic causes of oesophageal varices

A
  1. obstruction
  2. portal vein thrombosis
  3. increased portal blood flow
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17
Q

name 3 hepatic and post hepatic causes of oesophageal varices

A

hepatic: idiopathic portal hypertension, cirrhosis of the liver, chronic hepatitis
post-hepatic: budd-chiari syndrome, constricted pericarditis, compression of the portal vein due to neoplasm

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18
Q

name 3 risk factors for oesophageal varices

A
  1. alcohol abuse
  2. cirrhosis
  3. increased portal pressure
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19
Q

what is the treatment for oesophageal varices?

A
  1. beta blockers- propranolol to reduce BP
  2. endoscopic banding lifation
  3. transjugular intrahepatic portosystemic shunting- takes the pressure off the vessels
  4. terlipressin- vasopressin analogue- vasoconstriction; can be given IV in acute bleed.
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20
Q

how does alchalasia present?

A

dysphagia with SOLIDS AND LIQUIDS from onset
regurgitation of food from dilated oesophagus- particularly common at night; may result in aspiration pneumonia
spontaneous chest pain
weight loss/malnutrition

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21
Q

how do you diagnose alchalasia?

A

barium swallow- to show dilated oesophagus and smooth tapering down- like a birds beak!
CXR: wide mediastinum, double right heart border due to dilated oesophagus
endoscopy to exclude malignancy

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22
Q

define a peptic ulcer

A

a breach in the superficial epithelial cells penetrating down into the muscularis mucosa

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23
Q

name 2 causes of peptic ulcer disease other than H.pylori

A
  1. NSAIDS

2. Zollinger-Ellison syndrome (gastrin secreting tumour in the antrum causing hyperacidity)

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24
Q

name 3 differentiating symptoms of a gastic ulcer and a duodenal ulcer?

A

gastric ulcers present with burning epigastric pain worse AFTER eating, no pain at night, wight loss and bleeding can result in haematemesis or melaena
Duodenal ulcers present with pain when HUNGRY and EMPTY, relieved by EATING, pain waking up at night, no weight loss, bleeding only results in melaena

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25
Q

buzz word for peptic ulcer disease

A

gnawing/burning pain

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26
Q

name 4 complications of peptic ulcers

A
  1. penetration- eroding adjacent organs; pancreas or liver
  2. haemorrhage- of stomach contents
  3. perforation- into a blood vessel
  4. gastric mucosa associated lymphoid tissue
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27
Q

what is the treatment for H.plori infection ?

A

triple therapy: omeprazole, amoxicillin and clarithromycin

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28
Q

how do the antibiotics amoxicillin and clarithromycin work on bacteria?

A

amoxicillin inhibits cell wall synthesis

clarithromycin inhibits protein synthesis in the ribosomes

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29
Q

name 3 causes of gastroentereitis

A

ABC
autoimmune- crohns disease
bacteria- H.pylori, e.coli
C- chemical; biliary reflux and NSAIDS

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30
Q

how do NSAIDS cause mucosal damage?

A

NSAIDS inhibit the action of COX enzymes, therefore preventing the synthesis of prostaglandins- depletion of mucosal barrier- increasing the damage to the stomach wall.

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31
Q

what is the treatment for gastroenteritis?

A
  1. treat the cause
  2. proton pump inhibitors- omeprazol
  3. histamine 2 antagnoists: cimetidine
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32
Q

name the cell which produces histamine and where are they found?

A

neuroendocrine cells, found in the fundus and body

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33
Q

where are parietal cells found and what do they secrete?

A

found in the fundus and body

secrete intrinsic factor and HCL

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34
Q

name 5 symptoms of gastritis

A
  1. abdominal pain
  2. abdominal bloating
  3. nausea/vomiting
  4. indigestion
  5. percinous aneamia
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35
Q

define dyspepsia

A

No definition- it is a condition made up of the following symptoms:
post-prandial fullness
early satiation
epigastric pain for 4 weeks or more

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36
Q

name 5 causes of malabsorbtion

A
  1. coeliac disease
  2. extensive surgical resection- eg in crohns
  3. lactose intollerance
  4. pancreatic insufficiency- eg in CF
  5. primary bile malabsorbtion
    others include: bacterial overgrowth, whipples disease, blind loop syndrome
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37
Q

what is abetalipoproteinaemia?

A

a rare autosomal disease with a mutation in the MTP gene. MTP normally transcribes for a transport protein which enables lipid transport across the cell membrane. Therefore the mutation results in the malaborbtion of lipids and lipid soluble vitamins- A,K,E,D

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38
Q

name the fat soluble vitamins

A

A,K E,D

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39
Q

what is the major consequence of primary bile malabsorption?

A

you are unable to absorb bile in the ileum, thus you are unable to absorb any fat soluble substances as bile is required for the emulsification of fats.

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40
Q

name 5 symptoms of malabsorbtion

A 
steatorrhoea
palor
diarrhoea
weight loss
lethargy
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41
Q

what are the signs of anaemia

A 
anaemia
bleeding disorders
oedema
metabolic bone disease
neurological features
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42
Q

what is coeliac disease?

A

t cell mediated autoimmune destruction of the small bowl causing villous atrophy and malabsorption, potentially initiated the bodies over-reaction to the toxic protien gliadin in dietary gluten

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43
Q

what HLA groups are coeliac disease associated with?

A

HLA: DQ2 & DQ8

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44
Q

what is the protein in gluten which is supposedly the causative agent for the autoimmune response?

A

Gliadin

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45
Q

what are the symptoms of coealiac disease?

A 
diarrhoea
steatorrhoea
nausea and vomitting
abdominal pain and bloating
apthous ulcers
weight loss
iron deficiency anaemia
osteomalacia
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46
Q

what is the diagnosis for coeliac disease?

A

the patient must be on a gluten diet and there will be presence of:
autoantibodies- IgA tTG (tissue transglutimase) and EMA (anti-endomysial antibody)
duodenal biopsy showing intra-epithelial lymphocytes, proliferation of the crypts of Lieberkuhn, villous atrophy and hypoplasia of the small bowel architecture. Marsh staging of villous atrophy
FBC,
LFT
HLA typing

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47
Q

what autoantibody is present most cases of coeliac disease

A

IgA tTG (tissue transglutimase)

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48
Q

what is the treatment for coeliac disease?

A

lifelong gluten free diet

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49
Q

name 5 extra-GI features of inflammatory bowel disease

A 
Uveitis
seronegative spondyloarthropathies
erythema nodosum
DVT
autoimmune haemolytic anaemia
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50
Q

name 3 differentiating features between tropical sprue and coeliac disease

A
  1. vilous atrophy in tropical sprue is incomplete whereas in coeliac disease it is complete
  2. tropical sprue is caused by an infection whereas coeliac is an autoimmune reaction
  3. tropical sprue does not improve with a gluten free diet, however can be treated with antibiotics- tetracycline, whereas coeliac disease only improves with a gluten free diet.
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51
Q

define tropical sprue

A

malabsorbtion of at least 2 different substances after other causes have been excluded- ie the malabsorption is not secondary to a bacterial/ viral/protzoal infection

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52
Q

what are the key morphological features seen in tropical sprue JEJUNAL biopsy?

A

increased inflammatory cells in the lamina propria

partial villous atrophy

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53
Q

what is the causative agent of Whippels disease?

A

tropheryma whippelii

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54
Q

how does whippels disease present?

A

weight loss, lymphadenopathy, joint pain pigmentation and malabsorption

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55
Q

define diarrhoea

A

an increase in frequency of defecation and fluidity of the volume of the faeces that is normal for the patient

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56
Q

what are the pharamceutical treatments available for IBD (inflammatory bowel disease)?

A

5 aminosalicyclates- Mesalazine
steroids: azothioprine
TNF alpha antibody- infliximab

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57
Q

what are the extra-intestinal manifestations of IBD?

A

joint complications, uveitis, erythema nodosum, sclerosing cholangitis

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58
Q

what mutation is crohns disease associated with which may be a protective feature from UC?

A

NOD2 mutation expressed in epithelial cell, dendritic cells and paneth cells (secrete defensins)

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59
Q

name 4 factors which increase your risk of crohns

A
  1. smoking
  2. NSAIDS
  3. high sugar diet
  4. altered cell mediated immunity
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60
Q

what are the main symptoms of crohns disease?

A

weight loss
abdominal pain (may be colicky)
diarrhoea ±blood in stools
other features: malaise, lethargy, anorexia, steatorrhoea if in small bowel disease

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61
Q

signs of crohns disease

A

dehydration, clubbing, abdominal tenderness, anaemia signs of systemic involvement- uveitis, erythema nodosum, joint complications

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62
Q

name 5 complications of crohns disease

A 
obstruction
perforation
malabsorbtion
fistula formation- ulcers may proliferate through the endothelial lining and produce abnormal connections between adjacent bowel segments
neoplasia
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63
Q

what is the treatment for induction to remission in crohns disease

A

methotrexate/prednisolone- corticosteroids

anti-TNF alpha; infliximab

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64
Q

what is the treatment for maintenance in crohns disease

A

5-aminosalicylic acid- Mesalazine
azothioprine- steroid sparing immunosuppressant
Anti-TNF alpha- infliximab
elimination diet

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65
Q

when is surgery indicated in crohns disease?

A
  1. obstructed bowel
  2. perforated bowel
  3. failure to respond to therapy
  4. local complications- fistula/abscess
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66
Q

what investigation procedure would you use to distinguish between crohns and UC and why?

A

endoscopy- can take biopsies to show changes in mucosal layer.
can see crypt abscesses, granulomas, apthous ulcers, mucosal islands, skip lesions more clearly

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67
Q

name 5 complications of ulcerative colitis

A
  1. increased risk of bowel cancer
  2. increased risk of ankylosing spondylitis
  3. fatty change in the liver
  4. inflammation of the bile ducts
  5. subcutaneous inflammation of the skin- erythema nodosum
    toxic megacolon!!!!
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68
Q

what is gastroenteritis?

A

inflammation of the GI tract that involves both the stomach and the small intestine

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69
Q

name 5 causes of non infectious diarrhoea

A
  1. idiopathic
  2. malignancy
  3. increased alcohol consumption
  4. laxitive use
  5. anatomical abnormality
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70
Q

name the 3 types of diarrhoea

A
  1. osmotic- a non absorbable substance enters the bowel and draws up excessive water- increasing the motility of the bowel and increasing the volume of fluidity and frequency in the faeces
  2. secretory- excessive secretion of mucus and fluids
  3. motility- food is not properly mixed and digestion is impaired- motility of the gut increases
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71
Q

name 2 causes of osmotic diarrhoea

A

pancreatic enzyme deficiency

ingestion of non absorbable sugar and lactase

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72
Q

what does obsitpation mean?

A

failure to pass stools or gas

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73
Q

what is a fistula

A

an abnormal connection between an organ, vessel, intestine or another structure

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74
Q

name a causative agent of acute and chronic diarrhoea

A
  1. acute= e.coli

2. chronic= giardia lambia parasite

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75
Q

name 4 ways in which e.coli avoids destruction by the host

A
  1. produces a biofilm to protect itself from phagocytosis
  2. produces a shigella like toxin which destroys RBC’s
  3. has adhesion molecules to adhere to endothelial cells
  4. invades and spreads between cells disrupting their cell structure
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76
Q

What are the 3 most common causes of travellers diarrhoea?

A

e.coli
salmonella
campylobacter pylori

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77
Q

how do you treat parasitic infections such as giardia lambia?

A

metranidazole

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78
Q

define travellers diarrhoea

A 
3 or more informed stools in the past 24 hours whilst travelling away from home with one of the following:
fever
nausea
vomiting
abdominal cramps
dysentry (mucus and blood in faeces)
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79
Q

what are the toxins produced by Clostridium difficile which would be detected on ELISA and in the stools which isuseful for diagnosis?

A

toxin A and B

they cause depolymerisation of actin and cytoskeleton rearrangement

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80
Q

what do you do when you suspect a C.diff infection? SIGHT?

A 
S- suspect C.dif
I- isolate patient
G- gloves and apron
H- hand washing
T- test stool for toxinsss
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81
Q

what is the classification of diarrhoea

A

Bristol stool form scale

scale from 1-7 becoming increasingly watery and fluid like

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82
Q

what are the signs of severe dehydration?

A 
sunken eyes
reduced skin turgor
coma/reduced consciousness
rapid pulse
cyanosis
cold limbs
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83
Q

name 3 causes of small bowel obstruction (SHAN)

A

Small bowel

  1. adhesions
  2. neoplasia
  3. hernias
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84
Q

name 3 causes of large bowel obstruction (MSSD)

A

Malignancy
Strictures
sigmoid colon volvulus
Diverticular disease

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85
Q

what are the differences seen on XRAY with obstructions in the small bowel and large bowel when dilated with gas?

A

small bowel: centrally placed, and transverse lines are present
Large bowel: peripherally places and Haustra are present

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86
Q

if there was an obstruction in one patient in thier small bowel and in the large bowel of another patient, which one would present with constipation first and why?

A

the person with the large bowel obstruction, because the small bowel obstruction may present with profuse vomiting first

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87
Q

what would you see on examination of someone with intestinal obstruction

A

hyper-resonant bowels/ increased bowel sounds
large mass obstructing the bowel lumen
tachycardia
dehydration

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88
Q

what is the initial management of bowel obstruction

A

resuscutation with IV fluids
decompression
surgery may be required

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89
Q

where are the 3 most common places for the bowel to be obstructed?

A

iliocaecal junction
gastro-oesophageal spincter
pyloric-duodenal junction

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90
Q

name 3 causes of intraluminal obstruction

A
  1. neural dysfunction: hirshprungs disease- abscence of myenteric plexus reducing parasympathetic innervation of the GI tract
  2. malignancy
  3. inflammation- crohns disease
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91
Q

name 5 causes of extraluminal obstruction

A
  1. adhesions- most commonly due to silicon gloves
  2. volvulus (the bowel turns on itself)
  3. peritoneal tumours- exerting pressure on the bowel wall obstructing the lumen from the outside inwards
  4. strangulation- lack of blood supply
  5. intusuceptions- bowel fold overlap one another like a telescope
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92
Q

what is the function of the cells of cajal?

A

these are involved in stimulating spontaneous electrical waves for contraction along the GI tract

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93
Q

what are the functions of the parasympthetic nervous system and sympathetic nervous systems in the GI tract?

A

parasympathetic NS: stimulates digestion and the submucosal (Meisseners plexus) to secrete mucus
sympathetic NS: inhibits digestion

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94
Q

what is the function of auebachs plexus?

A

it controls smooth muscle contraction and peristalsis

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95
Q

what is a hernia

A

an abnormal protrusion of the lining of a cavity wall with or without its contents through a natural orifice or a weakened area

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96
Q

how do you evaluate the severity of Ulcerative collitis?

A

True Love and Witts criteria

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97
Q

apart from a gluten free diet, what else would you give to a coeliac patient and why?

A

pneumococcal vaccination because they are commonly hyposplenic- their spleen doesn’t work very well, and thus they are not efficient at destroying encapsulated bacteria

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98
Q

name 3 causes of paralytic ileus

A
  1. trauma
  2. drugs
  3. hirsprungs disease
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99
Q

what are the differences between a indirect and direct inguinal hernia?

A

indirect inguinal hernia goes through the deep inguinal ring, lateral to the inferior epigastric artery.
direct inguinal hernia goes posterior to the inguinal canal medial to the inferior epigastric artery

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100
Q

how would gastric outlet obstruction present?

A

nausea, vomiting, satiety, dehydration, malnutrition

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101
Q

how do you treat an inguinal hernia?

A

watch and wait
abdominal mesh repair- to strengthen the abdominal wall and prevent herniation from occuring again
key hole surgery to remove the hernia if it is causing obstruction and close off the orifice

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102
Q

what are haemorrhoids? (piles)

A

this is bleeding from the perianal cushions- there are 3 all which contribute to anal closure, there is no sensory fibres above the dentate line- hence they are not painful until they protude and thrombose/block venous return from the anal sphincter.

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103
Q

what investigations would you do for a patient presenting with bright red rectal bleeding on paper or stools?

A
  1. PR examination
  2. abdominal examination to rul out DD
  3. protoscopy in males
  4. sigmoidoscopy if high risk- over age of 50 and if the pathology is thought to be higher up
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104
Q

what is the treatment for haemorrhoids?

A

pain relief- NOT NSAIDS- paracetamol
cryotherapy- freeze off protruding haemorrhoids
band ligation- close off blood supply causing them to necrose and be extreted with the stools

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105
Q

how does a pilnoidal sinus present?

A

fouls smelling discharge , pain and swelling around the anus and natal cleft

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106
Q

how might you investigate an intestinal obstruction?

A

FBC
abdominal Xray
barium enema
CT

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107
Q

what is acute colonic pseudo-obstruction?

A

short onset, malfunctioning of the colon presenting with complaints mimicing a mechanical obstruction but without a mechanical cause

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108
Q

how does a paitient with an acute pseudo obstruction present?

A

rapid and progressive abdominal distention, pain,

Xray shows a gas filled large bowel- may become a toxic megacolon

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109
Q

what is sepsis?

A

2 features of SIRS with a confined suspected infection

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110
Q

what are the features of SIRS? (severe inflammatory response syndrome)

A 
at least 2 of the following:
HR>90
temperature >38
PaCO2 90bpm
WCC>12,000 or 20 breaths per minute
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111
Q

what is a pilnoidal sinus and how does it present?

A

this is a small sinus which develops at the top of the cleft of the buttock. Hair follicles may obstruct it causing it to become inflamed and infected.
Presentation- pain, difficulty sitting or lying down, swelling and foul smelling discharge

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112
Q

how do you treat a pilonoidal sinus?

A

NSAIDS for pain relief
antibiotics to clear infection
surgery to remove sinus if it does not heal or clear

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113
Q

what is charcots triad and what is it associated with?

A

RUQ pain
fever
jaundice
associated with acute cholangitis

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114
Q

what is acute cholangitis and acute cholecystisis?

A

acute cholangitis= infection of the bile DUCTS- due to retrograde ascent of gut bacteria up the common bile duct/ hepatic portal vein into the biliary tree
acute cholcystitis= infection of the gall bladder commonly due to a gall stone obstructing the outflow tract

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115
Q

name 2 organisms commonly causing acute cholangitis

A

e.coli

klepsiella spp

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116
Q

how would you investigate acute cholangitis?

A

transabdominal USS
magnetic resonance cholangiography
endoscopic retrograde CT

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117
Q

apart from giving broad spec antibiotic, how else would you treat acute cholangitis?

A

IV fluids
correct coagulopathy
endoscopic billiary drainage
take sample for culture- alter for narrow spectrum antibiotics

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118
Q

name a causative agent for each of the following liver abscesses
pyogenic
amoebic
fungal

A

e.coli or k.pneumonia= pyogenic (puss forming abscess)
amoebic abscess: E. histolica (entamoebae histolica)
Fungal: Candida

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119
Q

how would you treat a liver abscess?

A

depends on the causative agent
usually broad spec antibiotic- gentamicin
drain puss surgically

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120
Q

what is a diverticulum?

A

an outpouching of the bowel usually at sites of entry of perforating arteries

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121
Q

what is the difference between a diverticulosis and diverticulitis

A 
diverticulosis= there are several outpouchings of the bowel 
diverticulitis= there is an infection in the diverticula in the bowel
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122
Q

what is the difference between true and false diverticulum?

A

false diverticulum are composed of mucosa

true diverticular consist of all layers of parent viscus

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123
Q

what are the symptoms of diverticular disease

A

95% are asymptomatic
fever
abdominal pain especially in the Left illiac fossa
tender palpable mass
diarrhoea/constipation- altered bowel habit

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124
Q

what investigations would you do for diverticular disease?

A 
PR exam- may reveal a pelvic abscess or colorectal cancer
sigmoidoscopy
barium enema
colonoscopy
FBC
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125
Q

what are the treatments for diverticular disease?

A

well balanced diet
amoxicillin for infections
hospital admission if severe- IV fluids and GI rest

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126
Q

name 3 complications of diverticular disease

A
  1. perforation of the ileus (most common)- peritonitis
  2. rupture of an infected diverticula- sepsis
  3. haemorrhage through a blood vessel- usually sudden and painless
    fistulae formation
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127
Q

what is a fistula?

A

an abnormal connection between 2 epithelialized surfaces

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128
Q

how does acute diverticulitis present and how would you treat it?

A

sudden onset, severe left iliac fossa pain, fever and constipation.
Elevated ESR, CRP USS shows thickened bowel and large pericollections
treatment: IV fluids and nutrition for bowel rest- admit to hospital
co-amoxiclav and metronidazole

129
Q

why is the peritoneum such a good place for bacterial growth?

A

because it has a high fat content and a large blood supply!!!

130
Q

name 3 causes of peritonitis

A

trauma
ruptured abscess/diverticula
on dialysis
spontaneous due to displacement of bacteria from the GI tract to the ascitic fluid

131
Q

how would you treat peritonitis?

A

drain ascites- take sample and culture
antibiotics for infective organism
hydration and electrolyte replacement
control infection source- ensure organ function is maintained

132
Q

what is the blood supply to the midgut?

A

superior mesenteric artery- extits aorta at L2

133
Q

what is the blood supply to the hindgut and what level does it exit the aorta>

A

inferior mesenteric artery, exits the aorta at L3

134
Q

what are the main branches of the inferior mesenteric artery?

A

left colic
sigmoid branch
superior rectal branch

135
Q

where is ischemia of the bowel most likely to occur?

A

at the caecum and splenic flexure

136
Q

what is the marginal artery of drummond?

A

this is the site of anastamosis along the transverse colon between the superior and inferior mesenteric arteries.

137
Q

what level does the superior rectal artery begin at?

A

L3

138
Q

how does ischaemic collitis usually present?

A

sudden abdominal pain, red faeces ± diarrhoea

139
Q

name 4 predisposing factors to ischaemic collitis

A
  1. contraceptive pill
  2. patients on nicorandil (vasodilator for angina)
  3. thrombophilia patients- high coagulopathy
  4. small vasuculitis patients
140
Q

what are the complications of ischaemic colitis?

A
  1. bowel perforation
  2. intestinal gangrene
  3. sepsis
141
Q

how would you infestigate ischaemic colitis

A
  1. flexible sigmoidoscopy/colonoscopy
  2. blood
  3. AXR
  4. CT scan
142
Q

what might you seen on an abdominal XRAY with ischaemic colitis

A

thumb printing at splenic flexure

distended abdomen

143
Q

name 3 causes of mesenteric ischaemia (broad)

A
  1. outflow obstruction (venous)
  2. arterial inflow occlusion- atheroma, thrombosis, emboli
  3. infarction without occlusion
144
Q

how does mesenteric ischaemia present?

A

sudden abdominal pain and vomitting, distended abdomen. tender, abscent bowel sounds, hypotensive

145
Q

how would you treat mesenteric ischaemia?

A

bowel resection surgically- to remove ischaemic sections* patients may end up with short-bowel syndrome

146
Q

what is the main cause of chronic mesenteric ischaemia common in elderly?

A

atheromatous occlusion/ cholesterol emboli

147
Q

define irritable bowel syndrome

A

a collection of abdominal symptoms for which no organic cause is found.

148
Q

what are the guidlines to diagnose IBS?

A

at least 3 days per month of recurrent abdominal pain and one of the following for 6 months or more:
improvements on defecation
change in bowel habit
change in stool appearance

149
Q

name 4 symptoms of IBS and 3 extra-abdomial features

A

symptoms: change in bowel frequency, abdominal distention, abdominal pain worse after food, nausea, incomplete evacuation.
extra-abdominal feature: back pain, hyper-mobile joints and poorsleeping.

150
Q

what are the 3 types of IBS?

A

mixed IBS- both loose and watery or hard and firm for more than 25% of the bowel movements
diarrhoea dominant: watery and loose stools >25% of bowel movement
constipation dominant: hard and firm stools for >25% of bowel movements

151
Q

treatments for IBS

A 
high fibre diet
psychological therapy
treatment of dyspepsic symptoms
codeine phophate for severe diarrhoea
laxitives : 5HT4 receptor antagonist
elimination diet to explore dietary triggers
pro-biotics?
152
Q

name 8 causes of acute pancreatitis “GET SMASHED”

A 
Gall stones
Ethanol
Trauma
Steroids
Mumps
Autoimmune (PAN)
Scorpion venom
Hypothermia/hyperlipidaemia
ERCP (endoscopic retrograde choliangiopancreatography)
Drugs
153
Q

what is Cullens sign and Grey turners sign?

A

Cullens sign: periumbilical bruising- shown in acute pancretitis
Grey turners sign: bruising on the flanks from blood vessel autodigestion and retroperitoneal haemorrhage

154
Q

what causes cullens sign and grey turners sign?

A

autodigestion of blood vessels and retroperitoneal haemorrhage

155
Q

how might acute pancreatitis present>

A 
acute onset severe epigastric/central abdominal pain
vomitting and nausea
fever
jaundice
tachycardia
shock
cullens sign- periumbilical bruising
grey turners sign- flank bruising, radiating to the back; may be releived by sitting forwards
156
Q

how do you predict the severity of acute pancreatitis?

A 
modified glasgow score
Age>55
PaO2 10
etc
requires >8 for ITU
take signs at onset and 48 hours later
157
Q

what will you see on AXRAY in acute pancreatitis?

A

no psoas shadow- due to retroperitoneal fluid increase

senitel loop of the proximal jejunum from the ileus due to air filled in the space

158
Q

what investigations would you do for acute pancreatitis?

A
  1. ABG
  2. FBC- serum amylase raised, serum lipase raised ( more specific for pancreatitis)
  3. AXR
    4LVF
  4. CT to assess severity- modified glasgow score
    6 US if gallstones suspected
    ERCP if LFT worsen
159
Q

name 3 early complications of acute pancreatitis

A
  1. shock
  2. ARDS
  3. renal failure
160
Q

name 3 late complications of acute pancreatitis

A
  1. pancreatic necrosis
  2. bleeding of splenic artery
  3. thrombosis of splenic artery
161
Q

what are the symptoms and signs of chronic pancreatitis?

A
  1. intermittend abdominal pain
  2. bloating
  3. steatorrhoea
  4. weight loss
  5. brittle diabetes
162
Q

name 3 causes of chronic pancreatitis

A
  1. alcohol
  2. cystic fibrosis
  3. haemachromatosis
163
Q

what are the 3 clinical signs of appendicitis?

A
  1. Psoas sign: pain on extension of the right hip
  2. Rovsings sign: palpation of the left lower quadrant emits pain in the right lower quadrant
  3. Cope’s sign: pain during internal rotation of a flexed hip
    rebous tenderness around McBurneys point!
164
Q

how does appendicitis present?

A

generalised abdominal pain followed by localisation to the right iliac fossa
nausea
fever
occasional diarrhoea

165
Q

what are the signs seen in appenditis?

A

psoas sign, rovsings sign, obturator sign, may be a palpable mass in the right iliac fossa
guarding of the abdomen

166
Q

how do you treat appendicitis?

A

appendilectomy

metrondiazole and cefuroxime

167
Q

name 3 differential diagnosis of appendicitis

A
  1. ectopic pregnancy
  2. cholecystitis
  3. perforated ulcer
168
Q

name 3 complications of appendicitis

A
  1. rupture of the appendix
    2, appendix mass
  2. appendix abscess
169
Q

what criteria are supposed to be used but are rarely used in assessing appendicitis?

A

alvarado score- assesses the patients need for surgery (score more than 7)

170
Q

what is the arterial supply to the foregut?

A

coeliac artery

171
Q

what is the somatic referral from the foregut, midgut and hindgut?

A

epigastrum=foregut
perimbilical=midgut
suprapubic= hindgut

172
Q

what makes up the foregut?

A

the proximal to 2/3rds of the duodenum

173
Q

commonly occurs in FAT, FERTILE AND FEMALES

A

biliary colic

174
Q

what are the 2 types of gall stone?

A

cholesterol stones

calcium bilirubinate

175
Q

what features are seen in biliary colic?

A

severe constant epigastric pain with a crescendo character
nasuea and vomiting
if rigors and fever present it is suggestive of a secondary complication

176
Q

in biliary colic what would be seen in the FBC?

A

elevates serum bilirubin, alkaline phosphatase and aminotransferase

177
Q

how would you manage biliary colic surgically?

A

shock wave tithotripsy

cholecystectomy

178
Q

name 3 complications which could arise from biliary colic

A
  1. pancreatitis
  2. acute cholangitis
  3. acute cholecystitis
179
Q

name 4 hepatotoxic drugs

A
  1. pyrazinamide- TB drug
  2. azothioprine
  3. paracetamol
  4. tetracycline
180
Q

what is the treatment for a paracetamol overdose?

A

n-acetyl-cystine, a precursor of glutathione which conjugates with paracetamol to increase the bodies ability to excrete it

181
Q

what complications may arise from a paracetamol overdose apart from liver failure?

A

renal failure
fluid and electrolyte misbalance
hypoglycaemia
hepatic encephalopathy

182
Q

give 3 non infective causes of hepatitis

A
  1. drugs
  2. alcohol
  3. trauma
  4. autoimmune disease
183
Q

name 3 causes of hepatitis which are not hepatitis viruses

A
  1. EBV
  2. CMV
  3. yellow fever
184
Q

which hepatitis virus is a DNA virus?

A

Hep B- the rest are RNA

185
Q

what is the commonest cause of liver failure in the UK?

A

alcoholic liver injury

186
Q

what 3 things does alcohol do in the liver which results in liver failure?

A
  1. diverts cellular metabolism away from essentials to digest alcohol
  2. acetyaldehyde the main product of alcohol metabolism binds to liver cell proteins- hepatocyte damage
  3. stimulates the synthesis of collagen- fibrosis and cirrhosis of the liver
187
Q

Name 5 general signs of viral hepatitis

A

fever, mailase, upper abdominal dyscomfort, jaundice, hepatomegaly spider naevi

188
Q

what is leukonychia?

A

white nails or milk spots on nails seen in alcoholic liver disease

189
Q

what is ascities?

A

accumulation of fluid within the peritoneal cavity

190
Q

name 5 causes of ascities

A
  1. malignancy
  2. pancreatitis.
  3. nephrotic syndrome
  4. liver cirrhosis
  5. HF
191
Q

which type of hepatitis virus would you be particularly worried about with pregnant women and how would you diagnose it?

A

HVE
ELISA testing for anti-HEV, IgG and IgM
PCR serum or stool for HEV antigens
has a higher incidence of progression to liver failure in pregnant women

192
Q

who can be infected by HDV?

A

people already infected with HBV

193
Q

how would you diagnose HDV??

A

IgM anti-delta antibodies in a patient with chronic liver disease who is HBsAg positive

194
Q

what does ELISA stand for?

A

enzyme linked immunosorbent assay testing

195
Q

name 4 conditions HCV is associated with

A

cirrhosis
autoimmune thyroid disease
lymphoma
glomerulonephritis

196
Q

how is cirrhosis histologically diagnosed?

A
  1. loss of normal hepatic architecture
  2. bridging fibrosis activated by the stellate cells in the space of Disse
  3. nodular regeneration- nodules vary in size
197
Q

which blood investigations would be useful for investigating cirrhosis

A

albumin
prothrombin- clotting studies
LFT’s: high alanine aminotransferase, high aspartate aminotransferase.
levels of alpha-feto protien; strongly associated with hepatocellular carcinoma

198
Q

what is primary biliary cirrhosis?

A

interlobular ducts are damaged by chronic granulomatous inflammation- progressive cholestasis, cirrhosis and portal hypertension. Potentially caused by autoimmune destruction of hepatocytes in response to an environmental trigger.

199
Q

what is the difference between haemoptysis and haematemesis?

A 
haematemesis= upper GI bleed- Vomitting up blood
Haemoptysis= coughing up bleed due to pathology of the respiratory tract
200
Q

name 3 contraindications for liver transplant

A

active sepsis outside the hepatobilliary tree
malignancy outside the liver
liver metastases
patient is not psychologically committed

201
Q

name 4 complications of liver cirrhosis

A

portal hypertension
ascites
porto-systemic encephalopathy
renal failure

202
Q

which vessels fuse to form the portal vein

A

superior mesenteric and splenic veins (inferior mesenteric fuses with the splenic)

203
Q

name 3 causes of portal hypertension

A
  1. pre-hepatic: due to blockage of portal vein- eg thrombosis
  2. intra-hepatic: distortion of liver architecture in cirrhosis/ schistosomiasis/sarcoidosis
  3. post-hepatic: venous blockage outside the liver- budd chiari syndrome
204
Q

what is the component of faeces which makes it brown?

A

stercobilin

205
Q

why are signs jaundice in infants much more dangerous than in adults?

A

infants have not yet fully developed their blood brain barrier- bilirubin can enter the brain tissue and accumulate damaging the brain tissue

206
Q

name 5 causes of chronic liver disease

A 
Hepatitis B
primary hepatocarcinoma
trauma
primary autoimmune destruction
haemochromotosis
budd-chiari syndrome
207
Q

what is budd chiari syndrome?

A

hepatic vein occlusion by thrombosis or a tumour, therefore reducing blood flow from the liver back to the IVC

208
Q

give 5 presenting features of portal hypertension

A
  1. splenomegaly
  2. haematemesis
  3. malaena
  4. asities
  5. heptatic encephalopathy
209
Q

name 2 factors which makes gastro-oesophageal variceal bleeding more likely?

A

portal hypertension

large varices

210
Q

how should you manage an acute variceal bleed?

A 
resucitate with fluids and plasma expanders or transfusion to restore plasma volume
injection sclerotherapy 
variceal banding
vasoconstriction therapy
ballon tamponade
211
Q

how do you prevent variceal re-bleed?

A

transjugular intrahepatic portocaval shunt
beta blockers to reduce BP
variceal banding

212
Q

what is primary biliary cirrhosis?

A

damage to the interlobar hepatic ducts by autoimmune chronic granulomatous inflammation. It results in cholestasis, cirrhosis and portal hypertension

213
Q

what antibody is found in 98% of patients with primary biliary cirrhosis?

A

ANA

214
Q

how do you treat PBC?

A

prednisolone± azothioprine
liver transplant if liver failure results or if there is no response to treatment
ursodeozycholic acid- improves bilirubin and aminotransferase levels

215
Q

name 3 conditions PBC is associated with?

A

Keratoconjunctivitis sicca
thyroid disease
rheumatoid arthritis

216
Q

name 5 clinical features of PBC

A
  1. pruitus
  2. jaundice
  3. yellow deposits on the eyelids
  4. hepatomegaly
  5. fatigue
217
Q

what is shown on liver biopsy with PBC?

A

granulomas around the bile ducts

218
Q

give 3 differential diagnosis for PBC

A

autoimmune cholangitis
extrahepatic biliary obstruction
gall stones

219
Q

what is a postive Murphy’s sign and what is it seen in?

A

this is when the right upper quadrant it palpated, the patient is asked to breath deeply. A patient suffering with acute cholecystitis (inflammation of teh gall bladder) will feel pain when they breath in because the gall bladder touches the pressure from the palpation. The patient will “catch their breath” in inhalation.

220
Q

name 10 signs of liver disease

A
  1. hepatomegaly
  2. jaundice
  3. pruritus
  4. ascites
  5. bruising/bleeding
  6. encephalopathy
  7. dark urine
  8. pale stools
  9. spider naevi
  10. steatorrhoea
221
Q

what is fulminant liver failure?

A

a clinical condition resulting from massive necrosis of liver cells leading to severe liver function impairment

222
Q

name 3 common drugs that could cause liver failure

A
  1. paracetamol
  2. tetracycline
  3. azothioprine
223
Q

name 4 complications of liver failure

A
  1. hepatic encephalitis
  2. hypoglycaemia
  3. ascites
  4. infection
224
Q

what are the 3 stages of alcoholic liver disease?

A
  1. fatty change
  2. alcoholic hepatitis
  3. alcoholic cirrhosis
225
Q

name a complication specific to cirrhosis

A

hepatocellular cacinoma

226
Q

what histological changes are seen with each degree of alcoholic liver disease?

A

stage 1: mostly in zone 3 cells become swollen with fat, collagen can be laid down around central hepatic veins
stage 2: leukocytes cell infiltrates causing hepatocyte necrosis (zone 3). Mallory bodies (hyaline cartilage) may be present
stage 3: massive loss of hepatocyte cells and fibrin deposition- micronodules within the sinusoids

227
Q

what is jaundice?

A

yellowing of the skin, sclera and mucosa due to increaseds plasma bilirubin>35mmol/L

228
Q

what is the inheritance pattern of haemochromatosis

A

autosomal recessive

229
Q

why is haemachromatosis sometimes referred to as Bronze diabetes?

A

it commonly presents with hyperglycaemia and bronzed skin pigmentation

230
Q

what histological stain could be used to identigy excess iron

A

h&E

231
Q

name 2 ways of treating haemochromatosis

A

filter the blood via venesection regularly

desferrioxamine

232
Q

what is desferrioxamine and what is it used for?

A

it is an iron chelating agent, it is used to reduce the amount of iron in the blood by reducing its absorbtion. Used in haemochromatosis

233
Q

what is the difference between haemosiderosis and haemochromatosis?

A 
Haemosiderosis= excess Fe with normal architecture of the liver
Haemochromatosis= excess Fe with subsequent cirrhosis
234
Q

what investigations would you do for haemachromatosis?

A

FBC: shows elevated ferritin, serum iron,
Genetic testing
liver biopsy: bronze stained hepatocytes with Perl stain, cirrhosis and duct proliferation

235
Q

what is the characteristic feature seen in Wilsons disease in the iris?

A

Kaysers Fleischers rings

236
Q

what is the pathophysiology and genetic inheritance of Wilsons disease?

A

autosomal recessive condition with a mutation in the copper transporter ATPase on chromosome 13. The gene mutation prevents copper from being excreted in the bile, hence it accumulates, most commonly in the liver and basal ganglia

237
Q

what signs do you see in Wilsons disease?

A

tremor, involuntary movements, eventually dementia

Kayser fleisher rings in the iris

238
Q

what would you see in the serum for wilsons disease?

A

low concentration of serum caeruloplasmin (a copper containing protein)

239
Q

how would you treat wilsons disease?

A

life long penicillamine

240
Q

name 3 side effects of the treatment for Wilsons disease

A
  1. nausea
  2. rash
  3. reduced WCC
241
Q

what symptoms might you get with ascites?

A

nausea
suppressed appetite
increased dysopnea- fluid pressure on the diaphragm
abdominal pain

242
Q

what are the signs of ascities

A

weight gain
gross abdominal distention
signs of underlying condition

243
Q

what treatment would you give for ascities?

A
  1. diuretics- spironalactone
  2. fluid restriction
  3. surgical ascities tap
    treat the cause
244
Q

what might you see on Xray in a patient with a sigmoid volvulus and who is it more likely to occur in?

A

inverted U loop of the bowel

more common in the elderly co-morbid and constipated patient

245
Q

how might a volvulus of the stomach present?

A

triad of gastro-oesophageal obstruction symptoms:
epigastric abdominal pain
vomiting then retching

246
Q

what might you find in the serum from an autoimmune hepatitis patient?

A

Anti SMC antibodies
Anti- LKM1 (anti-liver/kidney microsomal type 1) antibodies
ANA

247
Q

what is primary biliary cirrhosis?

A

inflammation of the biliary ducts in the liver, due to granuloma formation- potentially an autoimmune condition triggered by an environmental cause

248
Q

what investigations would you do for primary biliary cirrhosis?

A

FBC: low albumin and reduced prothrombin time
ANTIMITOCHONDRIAL ANTIBODIES
LFT: elevated AST, ALT, alkaline phosphate
biopsy: granuloma formation around the bile ducts- cirrhosis

249
Q

what is the treatment for primary biliary cirrhosis

A

treatment is not very sucessful
ursodeoxycholic acid for cholestasis
colestyramine for the itch

250
Q

name 2 diseases associated with primary biliary cirrhosis

A

RA

autoimmune thyroid disease

251
Q

what is the difference between primary biliary cirrhosis and primary biliary sclerosis?>

A

primary biliarry cirrhosis= inflammation of the intrahepatic bile ducts due to granuloma formation and Anti Mitochondrial antibodies
Primary biliary sclerosis= progressive inflammation of the intra and extrahepatic bile ducts- fibrosis and strictures due to ANCA antibodies; eventually end stage liver failure.

252
Q

describe the differences seen on biopsy in primary biliary cirrhosis and primary biliary sclerosis

A

primary biliary cirrhosis= granulomas around the interlobular bile ducts
primary biliary sclerosis= onion ring like appearance due to periductal oedema and irregular lesions with lymphocyte infiltration.

253
Q

how do you assess the severity of ulcerative colitis?

A

True Love and Witts criteria

254
Q

name 5 causes of liver cirrhosis

A
  1. chronic alcohol abuse
  2. alpha-1 antitrypsin deficiency
  3. Wilsons disease
  4. HBV infection
  5. HIV infection
255
Q

give 5 signs of cirrhosis

A
  1. clubbing
  2. jaundice- yellowing of the sclera around the eyes, pale faeces, dark urine
  3. hypoalbuminaemia
  4. hepatomegaly
  5. ascites
256
Q

what score would you use to grade the severity of liver cirrhosis

A

Child-Pugh grading; a point based system for levels of bilirubin, albumin, prothrombin time, encephalitis and ascites. If the score >8 there is an increased risk of variceal bleeding

257
Q

give 3 treatment options (broad) for cirrhosis

A
  1. avoid NSAIDS
  2. colestryamine for itch
  3. Ursodeoxycholic acid
258
Q

define portal hypertension

A

a pressure gradient in the portal system of 10mmHg or more

259
Q

give 3 broad causes of portal hypertension

A
  1. pre-hepatic; splenic vein thrombosis
  2. intrahepatic: cirrhosis
  3. post-hepatic; Budd-chiari syndrome
260
Q

name 4 symptoms of portal hypertension

A
  1. jaundice
  2. splenomegaly
  3. dilated veins on the anterior abdominal wall
  4. ascities
261
Q

name 3 signs of a hyperdynamic circulation

A
  1. bounding pulse
  2. warm peripheries
  3. low BP
262
Q

why is the caudate lobe often unaffected by portal hypertension?

A

because it has an alternative blood supply (from a branch off the inferior vena cava, not from the hepatic portal vein)

263
Q

how might budd-chiari syndrome present?

A

acute abdominal pain, hepatomegaly and ascities, liver failure

264
Q

name 4 causes of budd-chiari syndrome

A
  1. hypercoagulable states- pregnancy, thrombophilia
  2. radiotherapy
  3. liver tumour
  4. HCV infection
265
Q

what is the standard treatment for Budd- Chiari syndrome?

A

trans-jugular-intrahepatic porto-systemic shunt
long term anticoagulation
liver transplant

266
Q

define hyperacute liver failure

A

encephalopathy wihtin 7d onset of jaundice

267
Q

give 5 causes of liver failure (not including infection)

A
  1. Budd-chiari syndrome
  2. autoimmune hepatitis
  3. alpha-1-antitrypsin deficiency
  4. Wilsons syndrome
  5. Haemachromotosis
268
Q

name 4 complications of liver failure

A
  1. ascites
  2. encephalitis
  3. increased risk of infection
  4. hypoglycaemia
269
Q

what is the criteria for liver transplant? Kings College london

A

prothrombin time >100 or 3/5 of the following
drug induced liver failure
age 40
>1 week onset between jaundice and encephalitis
bilirubin >300mmol/L
PT>50

270
Q

where do 95% of liver tumours metastasise from?

A
  1. lung
  2. breast
  3. colon
  4. stomach
271
Q

how would a hepatocellular carcinoma usually present?

A

weight loss, fever mailaire, RUQ pain

Jaundice presents late unless cholangioma

272
Q

give 4 signs of a liver tumour

A
  1. hepatomegaly
  2. terry’s nails (white proximal but distal 1/3rd is reddened)
  3. clubbing
  4. hyperdynamic circulation
273
Q

what tumour marker would you use expect to be elevated in the blood with hepatocellular carcinoma?

A

alpha fetoprotein elevates in 80% of HCC

274
Q

where are squamous cell tumour of the oesophagus commonly found?

A

middle 1/3rd of the oesophagus

275
Q

name 4 risk factors for developing a squamous cell tumour of the oesophagus

A
  1. smoking
  2. excessive alcohol consumption
  3. corrosive strictures
  4. achalasia
276
Q

name 4 risk factors for developing adenocarinoma os the oesophagus

A
  1. long standing GORD
  2. Barretts oesophagus
  3. tobaccos smoking
  4. breast cancer treated with radiotherapy
277
Q

which virus may be associated with adenocarinoma of the oesophagus?

A

HPV

278
Q

name the treatment options for adenocarcionma of the oesphagus

A
  1. non-expandable metal stent- to aid swallowing if obstructed by tumour
  2. oesophageal resection- need to remove 5cm above and below the cancer for survival- can be done key hole pulling the oesphagus up through the chest, or ivor lewis pulling the oesophagus down through the abdomen
    10% survival at 5 yrs
279
Q

why do you not use chemotherapy to treat an adenocaricoma of the stomach?

A

it is not effective- chemo is only affective against squamous cell carcinomas of the oesophagus

280
Q

what autosomal dominant condition characterised by thickened palms and soles and white patches in the mouth is associated with oesophageal cancer?

A

Tylosis

281
Q

what muscle cancer can also be found in the oesophagus and mouth in patients with AIDS?

A

Kaposi’s sarcoma

282
Q

what is the survival rate of oesophageal tumours at 5 years?

A

10% at 5 years

283
Q

how might an oesophageal carinoma present?

A

progressive and unrelenting dysphagia, weight loss, lymphadenopathy, coughing and aspiration into the lungs

284
Q

name 4 risk factors for gastric adenocarinoma

A
  1. H.pylori infection
  2. constant use of NSAIDS
  3. family history
  4. tobacco smpoking
    percinous anaemia is another
285
Q

how is gastric cancer defined?

A

carcinoma confined to the mucosa or submucosa

286
Q

what are the 2 main types of gastric adenocarcinoma

A
  1. intestinal- well formed glandular structures

2. diffuse- poorly cohesive cells that infiltrate into the gastric wall

287
Q

what are the symptoms of stomach cancer?

A

50% are asymptomatic in early disease. late disease; epigastric pain, nausea, anorexia, weight loss, vomiting, anaemia

288
Q

name 3 signs of stomach cancer

A
  1. palpable epigastric mass
  2. weight loss
  3. Virchows node (enlarged lymph node in the left supraclavicular fossa(
289
Q

name 2 other types of stomach cancer

A

primary gastric lymphoma

gastric polyps

290
Q

name 4 red flag symptoms for gastric cancer

A 
weight loss
recurrent vomitting
dyphagia
early satiety
family history of cancer
291
Q

how might a small intestine tumour present?

A 
abdominal pain
weight loss
symptoms of anaemia
diarrhoea
palpable mass
292
Q

which types of cancers might be found in the small intestine

A

adenocarcinoma- duodenum and jejenum

lymphoma- jejenum

293
Q

which cell type do carcinoid tumour arise from?

A

enterochromaffin cells

294
Q

where are carcinoid tumours most commonly found?

A

in the appendix and terminal ileum

295
Q

when does carcinoid syndrome occur and which hormones are involved?

A

when there is metastases to the liver. Hormones: 5HT, histamine, prostaglandins

296
Q

how might carcinoid syndrome present?

A

blue-ish red flushing, hepatomegaly, abdominal pain, watery diarrhoea

297
Q

what is the pharmacological treatment for carcinoid tumours?

A

octreotide- resembles somatostatine and inhibits the secretion of many hormones produced

298
Q

how might cholangiosarcoma present?

A

jaundice, RUQ pain, weight loss,abnormal LFT’s, generalised pruritus

299
Q

name 2 risk factors for cholangiosarcoma

A

primary biliary sclerosis

choledochal cysts

300
Q

what investigations would you do for suspected cholangiosarcoma?

A

Magenetic resonance choliangiopancreatography
USS of the gall bladder
FBC: see elevated bilirubin levels

301
Q

name 3 different types of eating disorder

A
  1. anorexia nervosa
  2. bulimia nervosa
  3. binge eating disorder
302
Q

what is binge eating disorder?

A

episodes of binge eating characterised by eating in a discrete period of time

303
Q

give 5 features of binge eating disorder

A
  1. lack of control of eating
  2. eating alone
  3. eating very rapidly
  4. eating large amounts of food when not hungry
  5. feeling uncomfortably full
304
Q

give 4 characteristics of anorexia nervosa

A
  1. intense fear of gaining weight
  2. self evaluation based on body image
  3. denial of seriousness of low body weight
  4. restricted intake of food leading to a significantly low body weight
305
Q

give 3 charaacteristics of night eating syndrome?

A

eating >25% of daily calories after the evening meal
lack of morning appetite
difficulty falling alseep

306
Q

how might you as a doctor approach a person with an eating disorder

A
  1. identify the risks of the disorder with the patient
  2. explore the pros and cons of the disorder with the patient
  3. try to identify the cause of the disorder
  4. try to establish a goal/target for improvement - need to get the patient to accept their disorder first
  5. food diary
  6. refer for interpersonal/cognitive/behavioural therapy counselling
  7. get the family/close friends involved with helping making the change
  8. weekly telephone calls
307
Q

how might alpha-1-antitrypsin deficiency present?

A

dysopnoea, cough, wheeze jaundice, fatigued, hepatomegaly

308
Q

what tumour markers might you look for in pancreatic carcinoma?

A

CA 19-9

309
Q

which gene mutation is associated with alpha-1-antitrypsin mutation

A

SERPINA1 gene on chromosome 14

310
Q

how would you test for alpha-1-antitrypsin deficiency?

A

serum levels of alpha-1 antitrypsin

311
Q

what is the most likely benign lesion of the colon to undergo malignant transition?

A

Villous adenoma

312
Q

patient presents with severe RUQ pain after a heavy meal, on a background of intermittent RUQ discomfort

A

choledocholithiasis

313
Q

a patient presents with progressive jaundice, 10kg weight loss, palpable liver edge but no massess and an extremely high alkaline phosphate; what is the likely cause?

A

metastases to the liver

314
Q

a patient presents with progressive painless jaundice and general malaise. There is a slight epigastric mass, PR examination shows soft pale stools. what is the likely cause?

A

carcinoma at the head of the pancreas

315
Q

name 3 complications of a hernia

A
  1. obstruction of the hernia
  2. strangulation of the hernia
  3. irreducible hernia- impossible return of the hernia contents to the bowel
316
Q

how might a paralytic ileus present?

A

painless distention, vomiting, absent minimal bowel sounds

317
Q

define ascites

A

chronic accumulation of serous fluid within the abdominal cavity

318
Q

what is the stages of ascities?

A

stage 1- detectable only after careful examination
stage 2- easily detectable but only a small volume
stage 3- obvious but not tense asites
stage 4- tense ascites

319
Q

what is the treatment of ascities?

A

treat the underlying cause
diuretics; spironolactone
salt and fluid restrictions
shunts- portosystemic shunts in liver cirrhosis, pertoneovenous shunts

GI And Liver (3 decks)

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