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GI pathology > GI pathology > Flashcards

GI pathology Flashcards

1
Q

Oesophageal reflux description and pathology

A

Reflux of gastric acid into oesophagus
Gastric acid refluxes into oesophagus causing thickening of squamous epithelium cells and eventually ulceration.
Can be caused by part of srtomach herniating through oesophageal sphincter

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2
Q

Oesophageal reflux risk factors

A

poorly functioning oesophageal sphincter, drugs such as medicine for asthma, high blood pressure, obesity, smoking

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3
Q

Oesophageal reflux symptoms

A

bloating, nausea, heart burn, dysphagia, chronic sore throat

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4
Q

Oesophageal reflux treatment and complications

A

Antacids
“Barrett’s oesophagus,
Healing by fibrosis”

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5
Q

Oesophageal cancer description/pathology

A

Squamous cell or adenocarcinoma cancer in oesophagus.

Abnormal cell proliferation in oesophagus

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6
Q

Oesophageal cancer risk factors

A

“Squamous: smoking and alcohol

Adenocarcinoma: obesity and Barrett’s oesophagus”

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7
Q

Oesophageal cancer symptoms

A

dysphagia, coughing, hoarseness, chest pain, worsening heartburn

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8
Q

Oesophageal cancer investigations/ local effects

A

endoscopy, bloogs (FBC, glucose, CRP)

local effects include: obstruction, ulceration, perforation

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9
Q

Oesophageal cancer treatment

A

surgery, chemotherapy, radiotherapy

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10
Q

Gastritis description/ pathology

A

Inflammation of the stomach

3 different causes: Autoimmue, Bacterial (helicobacter pylori) and Chemical

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11
Q

Gastritis symptoms/ treatment

A

Nausea, abdominal bloating, heartburn, burning or gnawing feeling in stomach between meals and at night, loss of appetite, bloating
T:antacids

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12
Q

Peptic ulceration description/ pathology

A

ulcers that develop in lining of stomach

imbalance between acid secretion and mucosal barrier

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13
Q

Peptic ulceration symptoms/investigations

A

S:heartburn, acid reflux, abdominal pain, burping, nausea or vomiting
I:endoscopy, bloods

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14
Q

Stomach cancer description/ pathology/risk factors

A

D:Cancer that develops in the lining of the stomach
P:Develops through phases of intestinal metaplasia and dysplasia.
Is an adencarcinoma
RF:Can be a consequnce of h.pylori infection

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15
Q

Stomach cancer symptons

A

dysphagia, abdominal pain, heartburn, blood in stools, weightloss, tiredness, nausea/vomiting, bloadted

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16
Q

Stomach investigations

A

Endoscopy, endoscopic ultrasound,barium meal Xray

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17
Q

Stomach cancer treatment

A

gastrectomy, oesophagogastrectomy, chemotherapy, radiotherapy

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18
Q

Peritonitis description

A

Inflammation of peritoneum

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19
Q

Peritonitis pathology

A 
"Bacterial infection spread by:
Perforation of GI/ biliary tract,
Female genital tract,
Penetration of abdominal wall,
Haematogenous spread"
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20
Q

Peritonitis risk factors

A

Peritoneal dialysis, appendicitis, history of peritonitis

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21
Q

Peritonitis symptoms

A

Abdominal pain, bloatinf, fever, nause/vomiting, loss of appetite, diarrhoea,low urine output, inability to pass stool or gas, fatigue

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22
Q

Peritonitis investigations and treatment

A

I:Peritoneal fluid analysis, blood tests
T:Antibiotics, though may need surgery to remove the infected tissue

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23
Q

Intestinal obstruction description/pathology

A

D;Obstruction within, on or surrounding the intestinal tubes

P:Tumour, hernia, clot

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24
Q

Intestinal obstruction symptoms

A

Pain, vomiting, distension, constipation, borborgmi (strange bowel sounds), early sanity, weight loss, gastric splash, dehydration, metabolic alkalosis

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25
Q

Intestinal obstruction investigations

A

Urine test, FBC, U+E, LFT, ultrasound, CT, laproscopy, laparotomy

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26
Q

Intestinal obstruction treatment

A

Restore circulatinf fluid volume, oxygenation, antibiotics, pain relief

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27
Q

Dyspepsia description and pathology

A

D:”dys=bad
pepsia=digestion”
P:Upper Gi problems (peptic ulcer, gastritis, gastric cancer), hepatic problesm, gallstobes,pancreatic disease, Lower GI (IBS, colonic cancer), coeliac disease, drugs, psychological, metabolic problmes (diabtetes, high Ca), cardiac problems

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28
Q

Dyspepsia risk factors

A 
"Drug history (NSAIDs, steroids, bisphosphonates, Ca antagonits, nitrates, theophyllines)
Lifestyle choices (alcohol, diet, smoking, exercise)"
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29
Q

Dyspepsia symptoms

A

Upper abdominal discomfort, retrosternal pain, anorexia, nausea, vomitinf, bloating, fullness, early satiety and heartburn

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30
Q

Dyspepsia signs

A 
"Anorexia
Loss of weight
Anaemia (iron deficiency)
Recent onset >55 years or persistent despite treatment
Melaena/haematemesis or Mass
Swallowing problems

All signs for reference for endoscopy”

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31
Q

Dyspesia investigations

A

“Bloods (FBC, ferritin, LFTs, UandEs, Calcium, glucose, coeliac serology/serum IgA)
Endoscopy
Test for helicobacter pylori “

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32
Q

Dyspesia treatment

A

antacids

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33
Q

Helicobacter pylori infection description and pathology

A

D:Bacterial infection in digestive tract
P:H.pylori invades in antrum- more likely to get ulcers in duodenum and small bowel, if invades higher up more likely to get gastric cancer

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34
Q

H.pylori infection symptoms

A

Upper abdominal discomfort, retrosternal pain, anorexia, nausea, vomitinf, bloating, fullness, early satiety and heartburn

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35
Q

H.pylori infection investigations

A

Serology (increase IgG), urea breath test, stool antigen test, endoscopy

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36
Q

H.pylori infection treatment

A

“antibiotics, PPI,
eradication therapy- triple therapy for 7 days:
Clarithromycin 500mg
Amoxycillin 1g bd (tetracycline if allergic to penicillin)
PPI eg omeprazole 20mg”

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37
Q

Peptic ulceration treatment

A

If caused by H.pylori- eradication therapy (read h.pylori infection), antacid or H2 receptor antagonist, stopping bad drugs

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38
Q

Causes of acute liver disease

A

Hepatitis (viruses, alcohol, drugs) or bile duct obstruction

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39
Q

What is pre-hepatic jaundice

A

When there is increased release of bilirubin from rbc

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40
Q

Hepatic causes of jaundice

A

Cholestasis and intrahepatic bile duct obstruction

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41
Q

What is cholestasis?

A

Accumulation of bile within hepatocytes or bile canaliculi

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42
Q

Causes of intra-hepatic duct obstruction?

A

Primary biliary cholangitis, primary sclerosing cholangitiis, tumours of liver

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43
Q

Post-hepatic causes of jaundice

A

Cholelithiasis, gallbladder diseases, extra-hepatic duct obstruction

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44
Q

Types of stool analysis?

A

stool culture, faecal calprotectin (increased inflammatory condition), faecal elastase (pancreatic insufficiency/malabsorption

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45
Q

What is the endoscopic retrograde cholangio-pancreatography used to view?

A

Used to visulaise ampulla, biliary system and pancreatic ducts

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46
Q

What is enteroscopy used to visulaise

A

Used to visualise small intestine

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47
Q

What pathways are interrupted by alcohol?

A

glucose-6-phosphate to glucose, acetyl CoA into citric acid cycle, this causes decreased glucose concentration and increased ketone concentration, there is also an increase build up in fatty acids

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48
Q

Labs performed to assess liver damage from alcohol?

A

aspartate amino transferase > alanine amino transferase, raised gamma glutamyl transferase, macrocytosis (creates large rbc), thrombocytopenia (low platlets)- alcohol affects bone marrow

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49
Q

2 ways of measuring alcoholic hepatitis levels?

A

Glasgow hepatitis score, Maddreys discriment function

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50
Q

What are gallstones made up of?

A

A mix of cholesterol and pigment

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51
Q

Risk factors for cholesterol gallstones

A

Obesity, iteal disease, cirrhosis, CF, DM, TPN, heart transplant, delayed GB emptying, clofibrate, long-term low-fat diet

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52
Q

Risk factors for pigment gallstones

A

haemplytic anaemia, bile infection (e.coli, bacteroides)

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53
Q

Causes of congenital biliary tract disease

A

Biliary atresia, choledochal cysts

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54
Q

Causes of benign billary stricture

A

latrogenic, gallstone related, inflammatory causes: pyogenic, parasitic, PSC, pancreatitis, HIV

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55
Q

What does odynophagia mean?

A

pain with swallowing

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56
Q

Name some investigations for oesophageal disease

A

oesphago-gastro-duodenoscopy, upper Gi endoscopy, contrast radiology, oesophageal pH and manometry

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57
Q

3 readings from glasgow criteria score that would result in pancreatitis to be described as severe

A

White cell count >15x10(9)/l, blood glucose >10mmol/l, blood urea >16mmol/l, serum albumin <32g/l, serum calcium <2.0mmol/l, arterial PO2 <7.5kPa

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58
Q

What is hyperamylasaemia and what condition can it be a complication of?

A

Increases serum amylase levels and can be caused by a complication of acute pancreatitis known as pseudocyst

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59
Q

Causes of chronic pancreatitis

A

“O-A-TIGER:
Obstruction of MPD (tumour, sphincter of Oddi dysfunction, pancreatic divisum, duodenal obstruction, trauma, stricture)
Autoimmune
Toxin (ethanol, smoking, drugs)
Idiopathic
Genetic
ENvironmental (tropical chronic pancreatitis)
Recurrent injuries (biliary, hyperlipidaemia, hypercalcemia) “

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60
Q

Name the 3 different approaches to oesophagectomy

A

Ivor Lewis, trans-hiatal, left-thoraco-abdominal

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61
Q

What are the ALARM symptoms?

A 
Anaemia
Loss of weight 
Anorexia
Recent onset of progressive symptoms 
Masses or melaena/ haematemesis
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62
Q

4 main functions of the small intestine?

A

digestion, endocrine and neuronal control, absorption, barrier functions

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63
Q

What is steatorrhoea a result of?

A

fat malabsorption

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64
Q

what are characteristics of steatorrhoea?

A

high fat content, less dense, floats, pale, foul smelling, leaves oily marks on toilet

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65
Q

What is dermatitis herpetiformis?

A

cutaneous manifestation of coeliac disease due to IgA deposit in skin, causes blisgering itch on scalp, shoulder, elbows and knees

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66
Q

Causes for finger clubbing

A

coeliac disease, crohns

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67
Q

What is the gold standard diagnosis of Coeliac?

A

distal duodenal biopsy

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68
Q

Wich conditions is coeliac associated with

A

dermatitis herpetiformins, IDDM, autoimmune thyroid,autoimmune hepatitis, primary biliary cirrhosis, autoimmune gastritis, sjogren syndrome, downs syndrome

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69
Q

What is refractory coeliac disease

A

ongoing symptoms of coeliac disease despite gluten free diet

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70
Q

2 main causes of malabsorption

A

inflammation (eg coeliac disease, crohns) and infection (eg tropical sprue, HIV, giardia lamblia)

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71
Q

Small bowel overgrowth can occur in conditions in which what functions are affected?

A

motility, gut structure, immunity

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72
Q

Difference between structural and functional GI disorders?

A

structual has detectable pathology (macroscopic (cancer) or microscopic (colitis)) and functional has no detectable pathology but is related to gut function

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73
Q

What is non-ulcer dyspsia?

A

dyspeptic type pain with no ulcer

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74
Q

How is vomiting stimulated?

A

via sympathetic and vagal components via vomiting centre or chemoreceptor trigger zone: receptor for opiates, digioxin, chemotherapy, uraemia

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75
Q

What is the likely cause of vomiting if immediately after food?

A

psychogenic

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76
Q

What is the likely cause of vomiting if 1 hour or more after food?

A

pyloric obstruction, motility disorder (diabetes, post gastrectomy)

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77
Q

What is the likely cause of vomiting if 12 hours after food?

A

Obstruction eg tumour

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78
Q

Functional causes of vomiting

A

drugs, pregnancy, migraine, cyclical vomiting syndrome, alcohol

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79
Q

2 main functional diseases of lower GI tract?

A

Irritable bowel syndrome and slow transit constipation

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80
Q

Organic causes of constipation

A

strictures, tumours, diverticular disease, procitis, anal fissure

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81
Q

Functional causes of constipation

A

megacolon, idiopathic constipation, depression, psychosis, instutionalised patients

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82
Q

Systemic causes of constipation

A

diabetes mellitus, hypothyroidism, hypercalcaemia

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83
Q

Neurogenic causes of constipation

A

autonomic neuropathies, parkinson’s disease, strokes, multipe sclerosis, spina bifida

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84
Q

What is the ROME III diagnostic criteria for IBS?

A

recurrent abdominal pain/ discomfort for >3 days/month in the past 3 months, associated with 2 or more: improvement with defaecation, onset associated with change in stool frequency, onset associated with change in stool form

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85
Q

What is the NICE diagnostic criteria for IBS?

A

abdominal pain/ discomfort relieved by defaecation or associated with altered sith still frequency/ form, plus 2 or more of: altered stool passage, abdominal bloating/ distension, symptoms worse by eating, passage of mucus

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86
Q

What is calprotectin and what is it a sign of if present in blood?

A

Calprotectin released by inflamed gut mucosa and is a sign of IBD

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87
Q

Severe attack of ulcerative colitis clinical features

A

stool frequency >6 stools/day with blood, fever, tachycardia, raised ESR, anaemia, albumin <30g/l, leucocytosis/thrombocytosis

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88
Q

Calprotectin levels

A

<50=normal
50-200=equivocal
>200=elevated

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89
Q

Name the differences between crohn’s and ulcerative colitis in histology

A

CD= granulomas and less crypt abscesses than UC

UC has depleted goblet cells

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90
Q

Extra-intestinal manifestations from IBD

A

eyes: uveitis, episcleritis, conjunctivitis
joints: sacrolitis, monoarticular arthritis, ankylosing spondylitis, renal calculi
liver and biliary tress: fatty change, pericholangitis, sclerosing cholangitis, gallstones
skin: pyoderma gangrenosum, erythem nodosum, vasculitis

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91
Q

Name the aminosalicylates

A

Aminosalicylates (mesalazine: acrylic resin (asacol, ipocol, mesren, salofalk) or ethylcellulose microgranules (pentasa))(pro-drugs (balsalazide,olzalazine, sulfasalazine))

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92
Q

Types of steroids used in IBD

A

prednisolone, budenoside

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93
Q

Types of thiopurines used for IBD

A

Azathioprine or 6-Mercaptopurine, these drugs keep inflammation under control

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94
Q

Side effects of thiopurines

A

Leucopenia, hepatoxicity (blood monitoring required), pancreatitis

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95
Q

Immunosuppressants used for IBD

A

ciclosporin, mycophenolate, tacrolimus

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96
Q

Anti-TNFalpha antibodies used in IBD

A

infliximab (8 weekly IV infusion)

adulimumab (2 weekly SC injections)

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97
Q

alpha4b7 integrin blockers

A

vedolizumab (8 weekly IV infusions)

98
Q

IL12/IL23 blockers

A

ustekinumab

99
Q

What antibiotic is used in IBD for crohn’s peri-anal disease and small bowel bacterial over growth

A

metronidazole

100
Q

Define upper and lower GI bleed

A

Upper GI bleed: bleeding from oesophagus, stomach or duodenum, proximal to liigament of trietz
Lower GI bleed: bleeding distal to duodenum, distal to ligament of trietz

101
Q

Upper GI bleed signs

A

haematemesis, melaena, elevated urea, dyspepsia, reflux, epigastric pain, NSAID use

102
Q

Lower GI bleed signs

A

fresh blood/clots, magenta stools, normal urea, typically painless, more common in advanced age

103
Q

Causes of upper GI bleed in the oesophagus

A

oesophageal ulcer, oesophagitis, oesophageal varices, Mallory Weiss Tear, oesophageal malignancy

104
Q

Causes of upper GI bleed in the stomach

A

gastric ulcer, gastritis, gastric varices, portal hypertensive gastropathy, gastric malignancy, angiodysplasia

105
Q

Causes of upper GI bleed in the duodenum

A

duodenal ulcer, duodenitis, angiodysplasia

106
Q

Causes of oesophagitis

A

reflux oesophagitis, hiatus hernia, alcohol, bisphosphonates, systemic illness

107
Q

What is diuelafoy?

A

When a submucosal arteriolar vessel erodes through mucosa, normally in gastric fundus, causing upper GI bleed

108
Q

What is angiodysplasia?

A

A vascular malformation that occurs anywhere in the GI tract, causing upper GI bleeding

109
Q

Colonic causes of lower GI bleed

A

diverticular disease, haemorrhoids, vascular malformations (angiodysplasia), neoplasia, ischaemic colitis, radiation enteropathy/proctitis, IBD

110
Q

What is angiodysplasia treated with?

A

argon phototherapy, transexamic acid, thalidomide

111
Q

What is colonic neoplasia?

A

colonic polyps or carcinoma

112
Q

Investigations for acute lower GI bleed

A

flexible sigmoidscopy, colonoscopy, CT angiography

113
Q

Acute lower GI bleeding small bowel cause

A

meckel’s diverticulum, small bowel angiodysplasia, small bowel tumour/ GIST, small bowel ulceration, anteroentero fistulation

114
Q

Small bowel investigations

A

CT angiogram, meckel’s scan, capsule endoscopy, double balloon enteroscopy

115
Q

Define shock

A

Circulatory collapse resulting in inadequate tissue oxygen deliverly leading to global hypofusion and tissue hypoxia

116
Q

Signs of shock

A

tachypnoea, tachycardia, anxiety or confusion, cool clammy skin, oliguria (low urine output), hypotension

117
Q

What is the Rockhall score used for

A

Designed to predict death and re-bleeding, uses inital assessment and endoscopic findings

118
Q

What is Glasgow Blatchford score used to determine?

A

Used to decide who did not require endoscopy

119
Q

What to do when bleeding is uncontrolled at endoscopy

A

sengstaken-blakemore tube transjugular intrahepatic porto-systemic shunt

120
Q

Define haematemesis

A

vomiting of blood due to active haemorrhage from the oesophagus, stomach or duodenum

121
Q

Define coffee ground vomit

A

brown vomit, poor correlation with significant GI bleeding in isolation often reflection of systemic illness

122
Q

Define melaena

A

black tar-like loose stools per rectum

123
Q

Define magenta stools

A

red-purple stools, normally from right colon or distal small bowel

124
Q

define haematochezia

A

Passage of fresh or altered blood per rectum, may be from upper GI (fast transit) or lower GI

125
Q

Define dyspepsia

A

Epigastric discomfort, that can be exacerbating by eating

126
Q

What is the myenteric plexus made of?

A

Meissener’s plexus is at the base of the submucosa,

Auerbach plexus is between the inner circular and outer longitudinal layers of the muscularis propria

127
Q

Describe idiopathic inflammatory bowel disease

A

Chronic inflammatory conditions resulting from inappropriate and persistent activation of the mucosal immune system driven by the presence of normal intraluminal flora

128
Q

what does pANCA stand for

A

perinuclear antineutrophillic cytoplasmic antibody, found +ve in 75% of UC patients and in 11% of CD patients

129
Q

What is backwash ileitis

A

When the ileus is involved in ulcerative colitis

130
Q

What happens to the mesentery surrounding the colon in crohn’s disease

A

thickened, oedematous and fibrotic

131
Q

What does acute occlusion of one of the 3 major abdominal supply vessels leads to (coeliac, inferioir and superior mesenteric arteries)

A

infarction

132
Q

What does gradual occlusion of one of the 3 major abdominal supply vessels leads to (coeliac, inferioir and superior mesenteric arteries)

A

anastomotic circulation

133
Q

Causes for arterial thrombosis, which predispositions for ischaemia

A

severe atherosclerosis, systemic vasculitis, dissecting aneurysm, hypercoagulate state, oral contraceptive

134
Q

Causes for arterial embolism, which predispositions for ischaemia

A

cardiac vegetations, acute atheroembolism, cholesterol embolism

135
Q

Causes for non-occlusive ischaemia

A

cardiac failure, shock/dehydration, vasoconstrictive drugs

136
Q

histology findings for acute ischaemia

A

oedema, interstitial haemorrhages, sloughing necrosis of mucosa-ghost outlines, bacteria gangrene and perforation

137
Q

main histological types of colorectal polyps

A

tubular, villous, indeterminate tubulovillous

138
Q

Carcinoma sequence: molecular aspects

A

there is activation of oncogene (k-ras, c-myc), loss of tumour suppressor gene (APC, p53, DCC) and defective DNA repair pathway genes (microsatellite instability)

139
Q

What is used to stage colorectal cancer?

A

Dukes staging system

140
Q

What is the aim of population screening for colorectal cancer?

A

detect pre-malignant adenomas/ early cancers in the general population

141
Q

Investigations carried out to screen population for colorectal cancer

A

faecal occult blood test, faecal immunochemical test, flexible sigmoidoscopy, colonoscopy, CT colonography

142
Q

What classes people as high risk for colorectal cancer?

A

if they have heritable conditions (Familial adenomatous polyposis or hereditary non-polyposis colorectal cancer), IBD, familial risk, previous adenomas/ colorectal cancer

143
Q

WHat does FAP stand for?

A

familial adenomatous polyposis

144
Q

What is FAP?

A

FAP is an autosomal dominant condition, which results in multiple adenomas throughout the colon, caused by mutations of the APC gene on chromosome 5

145
Q

How is FAP treated?

A

screening- annual colonoscopy

prophylatic proctocolectomy between 16-25 years

146
Q

What does HNPCC stand for?

A

hereditary non-polyposis colorectal cancer

147
Q

WHat is HNPCC?

A

an autosomal dominant condition, caused by a mutation in the DNA mismatch repair genes (MLH1 and MSH2),tumours have a molecular characteristic called microsatellite instability, in which there are frequenct mutations in short repeated DNA sequences

148
Q

Liver failure description and pathology

A

P:Acute: hepatitis (viruses, alcohol, drugs) causes inflammation of liver and cell damage and death to hepatocytes, bile duct obstruction
D:Complication of acute or chronic liver injury

149
Q

Liver failure risk factors

A

Hept A, B, C, jaundice, Cirrhosis, liver disease, alcoholic liver disease, any disease of liver (see below)

150
Q

Liver failure description

A

Loss of appetite, loss of sex drive, jaundice, fatugue and feeling weak, nausea, vomiting, itchy skin

151
Q

Jaundice description

A

Increasing circulating bilirubin, causing yellowing of skin and eyes

152
Q

Jaundice pathology

A

Pre-hepatic:Increased release of haemoglobin from redcells (haemolysis)

Hepatic: Cholestasis, intra-hepatic bile duct obstruction

Post-hepatic: Cholelithiasis, disease of gallbladder, extra-hepatic duct obstruction

153
Q

Jaundice risk factors

A

Gallstones, alcoholic liver disease, pancreatitis, hepatitis, sickle cell disease

154
Q

Jaundice signs

A

Yellowing os skin and whites of eyes

155
Q

Intrahepaatic bile duct obstruction description

A

Obstruction of intra-hepatic bile duct

156
Q

Intrahepaatic bile duct obstruction pathology

A

Primary biliary cholagitis- organ specific auto-immune disease, causes granulomatous inflammation of bile ducts, there is loss of intra-hepatic bile ducts

Primary sclerosing cholangitis- chronic inflammation and fibrous obliteration of bile ducts, there is loss of intra-hepatic bile ducts

tumours of liver: hepatocellular carcinoma, intra-hepatic bile ducts, metastatic

157
Q

Intraheptaic bile duct risj factors

A

Gallstones, inflammation of bile ducts, trauma, cysts, enlarged lymph nide, pancreatitis, injury to gallbladder, obesity, chronic pancreatitis, sickle cell anaemia

158
Q

Intrahepatic bile duct symptoms, signs

A

Sy:Nausea, vomiting, weight loss, fever, itching, pain in upper right side of the abdomen

Si:light-coloured stools, dark urine, jaundice

159
Q

Intrahepatic bile duct obstruction investigations

A

Anti-mitochondrial auto-antibodies in serum , raised serum alkaline phosphatase

CBC, LFT, Ultrasound, biliary radionuclide scan, cholangiography, MRI, endoscopicretrograde cholangiopacreatography, magentic resonance cholangiopancreatography

160
Q

Intrahepatic bile duct obstruction treatment

A

Treating underlying cause, cholecystectomy, endoscopic retrograde cholangiopancreatography

161
Q

Cirrhosis description

A

End stage chronic liver disease, liver looks very nodular and scarred

162
Q

Cirrhosis pathology?

A

Normal liver structure is replaced by nodules of hepatocytes and fibrous tissue

163
Q

Cirrhosis risk factors

A

Alcohol, hepatitis B,C, immune mediated liver disease (auto-immune hepatitis, primary biliary cholangitis), primary haemochromatosis,Wilson’s disease, obestiy, cryptogenic

164
Q

Cirrhosis symptoms + signs

A

Fatigue, loss of appetite, weight loss, muscle wasting, nausea/vomiting, tenderness or pain around liver area, itchy skin

Jaundice, vomiting blood, dark tarry stools, oedema, abdominal ascites

165
Q

Cirrhosis investigations

A

Magnetic resonace elastography

166
Q

Cirrhosis treatment

A

Changing lifestyle, diet and easing symptoms: diuretics, high blood pressure tablets, creams for itching

167
Q

Cirrhosis complications

A

Altered liver function, abnormal blood flow, increased risk of hepatocellular carcinoma

168
Q

Hepatocellular carcinoma description and risk factors

A

D:Malignant tumour of heaptocytes

RF:Chronic alcohol consumption, hept B, C, Wilson’s disease, primary biliary cirrhosis, non-alcoholic fatty liver disease

169
Q

Hepatocellular carcinoma symptoms and signs

A

Abdominal pain or tenderness, easy bruising or bleeding, ascites

Distened abdomen, yellow skin and eyes, weight loss, pale, chalky bowel movements and dark urine

170
Q

Liver cancer investigations

A

Bloods: AFP, ultrasound, CT, MRI, liver biopsy, endoscopy, laproscopry

171
Q

Liver cancer treatment

A

Chemotherapy, radiotherapy, transplant, hepatectomy

172
Q

Cholangiocarcinoma description and risk factors

A

D: Malignant tumour of bile duct epithelium

RF:Primary sclerosing cholangitis, congenital liver malformations

173
Q

Cholangiocarcinoma symptoms and signs

A

Abdominal pain, loss of appetite, weight loss, itching, nausea/vomiting

Jaundice, greasy stools, dark urine

174
Q

Metastatic cancer in liver syptoms and signs

A

Abdominal pain, vomiting/nausea, weight loss, decreased appetite

Distened abdomen, yellow skin and eyes, weight loss, pale, chalky bowel movements and dark urine

175
Q

Acute cholecystitis description and risk factors

A

acute inflammation of gallbladder

RF:Gallstones, tumour

176
Q

Acute cholecystitis symptoms and signs

A

Pain (typically after a meal), nausea, chills, abdominal bloating, vomiting

Jaundice, clay-coloured stools

177
Q

Acute/ chronic cholecystitis investigations

A

ultrasound, hepatobiliary scintigraphy, cholangiography, CT scans, bloods:LFT, CBC

178
Q

Acute/ chronic cholecystitis treatment

A

Cholecystectomy

179
Q

Chronic cholecystitis description

A

Chronic inflammation and fibrosis of gall bladder

180
Q

Chronic cholecystitis risk factors

A

genetic predisposition, obestity, diabetes, tumours in liver, pancreas or gallbladder, pregnancy

181
Q

Chronic cholecystitis symptoms and signs

A

severe sharp or dull abdominal pains, abdominal cramping and bloating, pain that spreads to back or below right shoulder pain, fever, chills, nausea, vomiting, itching

loose, light coloured stools, jaundice

182
Q

Describe marasmus malnutrition

A

Undernourished causing a child’s weight to be significantly low for their age

183
Q

Describe Kwashiorkor malnutrition

A

Oedema malnutrition, caused by lack of protein in the diet.

184
Q

Describe the term malnutrition

A

A state of nutrition in which a deficiency or excess of energy, protein and other nutrients, causes measurable adverse effects on tissue/ body form, body function and clinical outcome

185
Q

Name the different BMI classes

A

25 overweight

>30 obese

186
Q

3 different causes for undernutrition

A

appetite failure
access failure
intestinal failure

187
Q

4 types of drugs used for IBD

A

aminosalicylates, corticosteroids, immunosuppressants, biologics

188
Q

How do antacids and alginates work?

A

antacids: neutralise gastric acid,
alginates: form a viscous gel that floats on stomach contents and reduces reflux

189
Q

What conditions are acid suppression drugs used for?

A

indigestion, peptic ulcer disease, gastrointestinal refux disease

190
Q

How do H2 receptor antagonists work?

A

BLock histamine receptor and thereby reduce acid secretion

191
Q

Hpw do proton pump inhibitors work?

A

They block proton pump and therby reduce acid secretion, they can cause GI upset and predisposition to c.difficile infection, hypomagnesaemia, B12 deficiency

192
Q

What do prokinetic agents do and how?

A

Prokinetic agents increase gut motility and gastric emptying using the parasympathetic nervous system control of smooth muscle and sphincter tone

193
Q

Name 2 prokinetic agents?

A

Metoclopramide, domperidone

194
Q

What are the 3 mechanisms of anti-spasmodics?

A

anti-cholinergic muscarinic antagonists (inhibits smooth muscle constriction in the gut wall, producing muscle relaxation and reduction of spasm), direct smooth muscle relaxants and Ca-channel blockers reduce calcium which is required for smooth muscle contraction

195
Q

What are the 4 types of laxatives?

A

bulk (isphagula), osmotic (lactulose), stimulant (senna) and softeners (arachis oil)

196
Q

What drug is used to treat gallstones and primary biliary cirrhosis

A

ursodeoxycholic acid

197
Q

How does low albumin levels affect distribution of drugs

A

causes decreased binding and increased free drug concentration

198
Q

How is drug metabolism affecting by liver disease?

A

Liver enzymes are inhibited or induced, there is increased gut bacteria which metabolise drugs

199
Q

How does liver disease affect excretion of drugs?

A

there is increased toxicity if there is hepatobiliary disease

200
Q

Name the 2 types of hepatotoxicity

A 
intrinsic hepatotoxicity (type A adr)
and
idiosyncratic hepatotoxicity (type B ADR)
201
Q

What is the Child-Pugh classification for?

A

classification used to assess the prognosis of chronic liver disease and cirrhosis

202
Q

What is tested for in LFTs?

A

bilirubin, aminotransferases, alkaline phosphatase, gamma GT, albumin, prothrombin time and creatinine

203
Q

Why would alkaline phosphatase be elevated?

A

alkaline phosphatase is an enzyme present in the bile duct that is elevated when there is obstruction of liver infiltration

204
Q

What does prothrombin tome tell us?

A

tells degree of liver dysfunction and is used to calculate scores to decide stage of liver disease, and who gets a liver transplant

205
Q

when is jaundice detectable?

A

When total plasma bilirubin levels exceed 34umol/L

206
Q

What is refeeding syndrome?

A

when you starve your body it is called adapted starvation, causing your body to shut down, if you then eat there is an increase in insulin release which causes extracellular ions to rush into cells causing electrolyte disturbance and death

207
Q

The criteria for people at high risk of refeeding problems?

A

One of the following: BMI<16 kg/m2, weight loss >15% within 3-6 months, little or no nutritional intake for more than 10 days, low levels of K, P or Mg prior to feeding

Or

Two of the following:
BMI<18.5kg/m2, unintentional weight loss >10% in last 3-6 months, little/no nutritional intake for more than 5 days, history of alcohol abuse or drugs (insulin, chemotherapy, antacids, diuretics)

208
Q

Diagnosis of ascites

A

Diagnostic paracentesis

209
Q

Ascities fluid analysis

A

routine: cell count, protein, albumin
optional: culture, glucose, LDH, amylase, gram stain

210
Q

Serum-ascites albumin gradient

A

> 1.1g/dl = portal hypertension, CHF, constrictive pericarditis, BUdd Chiarri, myxedema, massive liver metastases

<1.1g/dl = malignancy, TB, chylous ascites, pancreatic, biliary ascites, nephrotic syndrome, serositis

211
Q

Treatment options for ascites?

A

diuretics, large volume paracentesis, TIPs, aquaretics, liver transplant

212
Q

What environmental factors affect the types of microbes found?

A

transit time, oxygen, pH

213
Q

What does bacterial fermentation of fibre produce?

A

releases additional phytochemicals, maintains slightly acidic pH, increased commensal bacterial population and pH improves resistance to pathogen, essential supply of short chain FAs.

214
Q

3 main short chain fatty acids produced from non-digested charbohydrate

A

Butyrate, propionate, acetate

215
Q

Function of butyrate

A

epithelial cell growth and regeneration

216
Q

Function of propionate

A

guconeogenesis in the liver, satiety signalling

217
Q

Function of acetate

A

transported in blood to peripheral tissues, lipogenesis

218
Q

How does indigenous microbiota defend against pathogens?

A

barrier effect, active competitive exclusion, pH inhibition, mucus layer

219
Q

What do the IgM anti-HBC, igG anti-HBc and anti-HBe antobodies indicate

A

igM anti-HBc= acute infection
IgG anti HBc= chronic infection/exposure
Anti-HBe= inactive virus

220
Q

Treatment for HBV

A

pegylated interferon and oral antiviral drugs

221
Q

5 antiviral drugs

A

lamivudine, adeforvir, entecavir, telbivudine, tenofovir

222
Q

Treatment of Hepatitis C

A

peglFNalpha and ribavirin

223
Q

What is NAFLD score used for and what are teh components?

A

NAFLD score used to stage and for best treatment of NAFLD.

High risk if >45year old, has diabetes, BMI>30, AST:ALT>1, platlet count <150, albumin <34

224
Q

Treatment for Non-alcoholic fatty liver disease

A

diet, exercise, weight loss, insulin sensitizers (metoformin, piofglitazone), glucagon-like peptide-1 analogues eg Liraglutide, farnesoid X nuclear receptor ligand eg Obeticholic acid, vitamin E and weight reduction surgeries

225
Q

Autoimmune liver disease

A

autoimmune hepatitis, primary biliary cholangitis, primary sclerosing cholangitis

226
Q

How do you treat autoimmune hepatitis?

A

steroids and azathioprine

227
Q

How would you treat primary biliary cholangitis

A

ursodeoxycholic acid

228
Q

Primary sclerosing cholangitis antibody positive and treatment

A

lpANCA positive and treat with liver transplant and biliary stents

229
Q

WHat supplies the ascending colon?

A

ileocal and right colic arteries from superioir mesenteric artery

230
Q

What supplies the transverse colon

A

middle colic artery from the SMA

231
Q

What supplies the descending colon and sigmoid

A

left colic and sigmoid arteries from IMA.

they anastamose with marginal artery

232
Q

What supplies the rectum with blood

A

Superior rectal from IMA to proximal rectal supply
middle rectal from the internal iliac artery and the inferior rectal arterysupply the midpart and distal part of the rectum

233
Q

What are the names of the lymph node groups that drain the large colon?

A

epicolic, paracolic, intermediate, central lymph nodes

234
Q

Early, general complications of colonic resection

A

infection, haemorrhage, DVT, chest infection

235
Q

Early, specific complications of colonic resection

A

anastomotic leakage, intra-abdominal abscess, damage to surrounding structures

236
Q

Late complications of colnic resection

A

tumour recurrence, hernia formation and adhesion formation causing obstruction

237
Q

Dysbiosis meaning

A

Microbial imbalance

can result in disease

238
Q

What is a probiotic?

A

Live microorganism which when in adequate amounts confer a health benefit on host (added live bacteria)

239
Q

What is a prebiotic?

A

Substrate that is selectively utilized by host microorganism conferring a healht benefit (food for resident bacteria

240
Q

Health benefits of prebiotics?

A

improved gut function, managemtne t of IBD, reduce risk of colon cancer, increase Ca absorption and bone health

GI pathology (2 decks)

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