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Year 1 Body Systems > Clinical GI > Flashcards

Clinical GI Flashcards

1
Q

What are the 3 common causes of liver disease in the UK?

A

1) Viral hepatitis
2) Alcohol consumption
3) Non-alcoholic fatty liver disease (NAFLD)

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2
Q

What is viral hepatitis and what 3 common pathogens can it be caused by?

A

Inflammation of the liver
Can be acute or chronic
Can be caused by Hep A, B or C

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3
Q

What is the transmission route of Hep A?

A

Faecal - oral route

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4
Q

What is the duration and treatment of Hep A?

A

Most common infective agent
Short duration infection
No treatment is required - virus clears completely from body after infection - patients dont become carriers

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5
Q

What are the symptoms of Hep A? 2

A

1) Nausea and anorexia

2) Jaundice 1-2 weeks after symptoms noticed

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6
Q

For which hepatitis infections is a vaccination available?

A

Hep A and B

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7
Q

What are the symptoms of Hep C infection?

A

Asymptomatic often chronic infection

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8
Q

How is hep C transmitted?

A

Largely by blood / blood products

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9
Q

What are the symptoms of Hep B infection? 5

A

1) Nausea and anorexia
2) Jaundice
3) Fever
4) Rashes
5) Polyarthritis (pain and swelling in joints)

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10
Q

What is the commonest route of infection for Hep B?

A

Vertical

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11
Q

What is the treatment for Hep B infection and is it successful?

A

Treatment involves treating symptoms
48 weeks course pegylated interferon injections, or long term oral antiviral agents (Tenofavir)
Up to 10% continue to carry the virus and develop chronic infection which may lead to liver damage causing fibrosis and ultimately cirrhosis
There is also an increased risk of hepatocellular cancer

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12
Q

What is non-alcoholic fatty liver disease?

A

Accumulation of triglycerides in hepatocytes which is not related to alcohol intake

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13
Q

What are the risk factors for non-alcoholic fatty liver disease? 5

A

1) Obesity
2) Hypertension
3) Insulin resistance
4) Type 2 DM
5) Hyperlipidaemia
NB. patients may be completely asymptomatic til have advanced liver disease such as cirrhosis

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14
Q

How can non-alcoholic fatty liver disease lead to cirrhosis?

A

Fat accumulation can be associated with inflammation (non alcoholic steatohepatitis) which may develop into fibrosis and cirrhosis

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15
Q

Liver disease can lead to portal hypertension, what are the symptoms of this?

A

Oesophageal and gastric varices, frequentlly asymptomatic and no pain is felt but they can burst and internal bleeding can lead to death

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16
Q

What is alcoholic liver disease?

A

Accumulation of triglycerides in hepatocytes which affects hepatocyte function
Metabolism of alcohol causes an increase in fatty acid synthesis and a decrease in fatty acid metabolism resulting in accumulation of triglycerides in liver

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17
Q

What is alcoholic hepatitis and how can it often present?

A

Inflammation due to fat accumulation in the liver which can develop after even a few weeks
This can present with jaundice and carries significant mortality
More long term use can lead to fibrosis and eventually cirrhosis

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18
Q

What are the common symptoms of alcoholic liver disease? 5

A

1) Jaundice (extra hepatic jaundice - cholestatic jaundice - obstruction by cirrhotic tissue, also intra hepatic jaundice due to failing liver)
2) Steatorrhoea (Pancreatitis = complication of cirrhosis, lack of lipase and thus fatty stools)
3) Puritis (due to build up of bilirubin and bile products in the skin - elicit a mild inflammatory response)
4) Bruising - decreased synthesis of clotting factors - poor absorption of fat soluble vitamin Vit K)
5) Low blood glucose (liver can no longer store glycogen and alcohol metabolism leads to increased NADH inhibiting gluconeogenesis)

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19
Q

What 4 drugs are used to treat alcohol dependence and what are there general mechanisms?

A

1) Chlordiaepoxide - cross tolerence with alcohol, helps reduce withdrawal symptoms
2) Disulphirum - inhibits alcohol dehydrogenase - makes feel ill if drink
3) Naltrexane - opioid re-uptake inhibitor, reduces cravings for alcohol
4) Acamprosate - Binds NMDA receptors in the brain suppressing alcohol cravings

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20
Q

What do LFT’s look like in liver disease?
(Albumin
total bilirubin
alkaline phosphatase
alkaline transaminase and aspartate transaminase
gamma glutamyl transferase)

A

Albumin - decreased - not made in diseased liver
Total bilirubin - increased - lack of conjugation and lack of excretion
Alkaline phosphatase - increased - found in bile duct cells, get bile duct damage secondary to scarring
Alkaline transaminase, aspartate transaminase - Normally found in hepatocytes, released when cells damaged (if history of long term damage, this will not be raised as cells have already been damaged - not many left to rupture)
Gamma-glutamyl transferase - induced by alcohol, early indicator of liver damage

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21
Q

Other than liver function tests, what other tests can be carried out to investigate alcoholic liver disease?

A

1) Liver biopsy
2) CT scan
3) MRI

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22
Q

Where along the GI tract can Crohn’s disease occur?

A

Anywhere from mouth to anus

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23
Q

Where along the GI tract can ulcerative colitis occur?

A

Colorectum

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24
Q

What is the disease distribution of Crohn’s disease?

A

Patchy - skip lesions

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25
Q

What is the disease distribution of ulcerative colitis?

A

Continuous

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26
Q

What are the 4 histological findings in Crohn’s disease?

A

1) Transmural inflammtion (all the way across wall)
2) Granulomas
3) Gland preservation
4) Aphthous ulceration

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27
Q

What are the 4 histological findings in ulcerative colitis?

A

1) Mucosal or sub mucosal inflammtion
2) Loss of goblet cells
3) Gland destruction
4) Crypt abscess formation

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28
Q

What are the 2 complications of Crohn’s disease?

A

1) Fistula

2) Stricturing

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29
Q

What are the 2 complications of Ulcerative colitis?

A

1) Colonic dilatation

2) Toxic megacolon

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30
Q

Does smoking improve or worsen Crohn’s disease?

A

Worsen

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31
Q

Does smoking improve or worsen ulcerative colitis?

A

Improve

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32
Q

Can Crohn’s or ulcerative colitis be cured with surgery?

A

Crohns - No

Ulcerative colitis - yes

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33
Q

What are the symptoms of inflammatory bowel disease? 9

A

1) Diarrhoea
2) Rectal bleeding
3) Passage of mucous par rectum
4) Faecal urgency and incontinence
5) Abdominal pain
6) Weight loss
7) Fatigue and lethargy
8) Mouth ulcers
9) Perianal pain/ discharge

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34
Q

What are the clinical signs of IBD? 7

A

1) Abdominal tenderness
2) Abdominal mass on palpation
3) Anaemia
4) Anal fissure
5) Fistulae
6) Perianal abscesses
7) Mouth ulcers

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35
Q

What are the 6 kind of extra-intestinal signs and symptoms of IBD?

A

1) Musculoskeletal (arthritis, ankylosing spondilitis, osteoporosis)
2) Hepatobiliary (primary sclerosing cholangitis - stricturing of bile ducts causing blockage)
3) Vascular (vasculitis, venous thromboembolism)
4) Dermatological (mouth ulcers and leg rashes)
5) Ocular (inflammation of components of the eye)
6) Renal (kidney stones, glomerulonephritis, tubulo-interstitial nephritis)

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36
Q

What is the treatment of Crohn’s disease to induce remission?

A

Short term anti-inflammatory treatment - corticosteroids

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37
Q

What is the treatment of Crohn’s disease to maintain remission?

A

1) Immunosuppressants
2) Amino-salicylates - for disease in colon
3) Methotrexate - anti inflammatory and immunosuppressant
4) Antibiotics

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38
Q

What is the treatment of Crohn’s disease in resistant cases where remission cant be maintained?

A

Biological therapy - TNF-alpha antibodies

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39
Q

What is gout?

A

Type of arthritis where crystals of sodium urate form inside and outside of joints, due to consumption of excess purine bases

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40
Q

What is an overweight and obese BMI?

A 
>25kg/m2 = overweight
>30kg/m2 = obese
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41
Q

Above what blood glucose would someone be considered to have impaired glucose tolerence?

A

> 6.1mmol/L

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42
Q

What risks are associated with obesity? 7

A

1) Hypertension
2) Stroke
3) Type 2 DM
4) MI
5) Cancer eg. colon
6) Osteoarthritis
7) Psychological problems

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43
Q

In weight loss what is the advised target for people trying to lose weight?

A

Try to lose 10% of their body weight

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44
Q

Why is waist circumference measured in obesity?

A

Waist circumference is a measure of adipose tissue, intra adbominal fat is particularly bad, its a good indicator of obesity

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45
Q

What is BMR and how is it calculated?

A

Basic metabollic rate

BMR/day = 8.3 x (weight in kg) + 846kcal

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46
Q

What is a PAR and what does it tell you?

A

Physical activity

Tells you how many more calories you would be burning carrying out that activity compared to BMR

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47
Q

What are the 5 presenting features of diabetes?

A

1) Polyuria and polydipsia (thirst)
Osmotic diuresis and osmotic activation of hypothalamus
2) Weight loss and fatigue
Impaired glucose utilisation (lose it in the urine)
3) Pruritis vulvae and balanitis
Vaginal Candidiasis
4) Hunger
Lack of insulin preventing hypothalamic glucose uptake
5) Blurred vision
Altered activity due to uptake of glucose into lens

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48
Q

What is the difference in treatment for Type 1 and Type 2 DM?

A

Type 1 - Insulin (matched to the size of meals)

Type 2 - Diet, exercise (Weight loss), oral hypoglycemics, insulin later

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49
Q

What is latent autoimmune diabetes in adults?

A

Type 1 DM (Peak age 12)

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50
Q

What is maturity onset DM of the young?

A

Type 2 DM (Peak age 60)

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51
Q

What is gestational diabetes?

A

Diabetes that occurs during pregnancy (pregnancy is the ultimate stress test), often is relieved after pregnancy but there is a greater chance of developing Type 2 DM later in life

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52
Q

What 3 things could diabetes be secondary to?

A

1) Pancreatic destruction (CF, pancreatitis)
2) Acromegaly (over production growth hormone)
3) Cushing’s syndrome

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53
Q

What are the 3 clinical features of Type 1 diabetes that if 2 are recognised are an indication for immediate insulin treatment at any age?

A

1) Weight loss
2) Moderate or large ketones in urine
3) Short history (weeks) of severe symptoms

54
Q

What are the 3 aims of treatment in Type 1 DM?

A

1) Relief of symptoms
2) Prevention of ketoacidosis
3) Prevention of microvascular and macrovascular complications

55
Q

What are the microvascular complications of DM and how can they be monitored?

A

1) Retinopathy - regular eye tests
2) Neuropathy - regular foot examination
3) Nephropathy - Urine test for microalbumin and blood test for kidney function (U&E’s)

56
Q

30% of people with DM in the UK develop diabetic nephropathy, what is the major increased risk when they develop this?

A

CV mortality (from 2x healthy population to 30x healthy population)

57
Q

In hypoglycaemia below what level is cognition affected?

A

3mmol/L - prolonged reaction time
2mmol/L - abnormal ECG and confusion
1mmol/L - coma and seizures

58
Q

What 2 hormones are released by the body to protect against hypoglycaemia?

A

1) Adrenaline
2) Glucagon
Both increase hepatic glucose output

59
Q

What are the signs and symptoms of hypoglycaemia?

A

Autonomic - tremor, anxiety, tachycardia, sweating, pallor, nausea
Neuroglycopenic - confusion, drowsiness, lethargy, lack of concentration, slurrred speech, aggression, coma

60
Q

Why is it important to monitor insulin and blood glucose closely?

A

Need tight glucose control, not so low as to cause hypoglycaemia and not so high as to lead to complications

61
Q

What is the prevelance of Type 2 DM?

A

15-20% prevelance in developing countries

62
Q

What is the pathophysiology of Type DM?

A

Sedentary lifestyle and a genetic predisposition lead to insulin resistance so an increased hepatic glucose output and decreased uptake of glucose into liver and muscle - this leads to hyperglycaemia which causes compensatory insulin secretion byt the B cells of the pancreas - as diabetes progresses the insulin response becomes impaired due to pancreatic exhaustion

63
Q

What are the 3 macrovascular complications of Type 2 DM and why do they occur?

A

1) MI
2) Stroke
3) Peripheral vascular disease (atherosclerosis)
Occur because:
1) Altered lipid metabolism so high circulating levels of Chylomicrons and VLDL
2) Glycation of LDL and LDL receptor - lower uptake of LDL, LDL infiltrate endothelium and are oxidised and taken up by macrophages - this increases formation of atherosclerosis
3) Glycation of blood proteins - gives less flexibility, more danger of stasis

64
Q

At diagnosis of Type 2 DM by how many years is life expectancy reduced?

A

10

65
Q

What is the treatment in Type 2 diabetes?

A

Weight loss and exercise if substantial will reverse hyperglycaemia
Management usually consists of BP control, blood glucose and lipid control

66
Q

What is the mode of action of the oral anti-diabetic agents:

1) GLP-1 analogues
2) DPP-4 inhibitors
3) Sulphonylureas
4) Pioglitazone
5) Gliflozins
6) a-gluocosidase inhibitors
7) Metformin

A

1) GLP-1 analogues - mimic GLP-1 , a GI incretin hormone that increases insulin secretion and inhibits glucagon secretion
2) DPP-4 inhibitors - block the DPP-4 enzyme which inactivates GLP-1
3) Sulphonylureas - stimulate pancreatic insulin secretion
4) Pioglitazone - increase insulin sensitivity of adipose, muscle and liver tissue
5) Gliflozins - increase glucose excretion by kidneys
6) a-glucosidase inhibitors - slow digestion and absorption of carbs (competitive inhibition of enzyme that breaks down carbs)
7) Metformin (Biguanide) - Suppress hepatic glucose output and increase insulin sensitivity

67
Q

What is HbA1C and what does it indicate?

A

Glycosylated Hb and indicates blood glucose levels over the past 3 months - want HbA1C to be as low as possible

68
Q

What are the 3 points of the Ramzi’s diabetic triangle?

A

1) Improve glucose levels
2) Avoid hypoglycaemia
3) Limit glucose variability

69
Q

In which type of diabetes are ketones found?

A

Type 1

70
Q

What is functional dyspepsia?

A

Dyspepsia without structural cause for symptoms (ie. an ulcer) when investigated with endoscopy

71
Q

What are the 2 main cause of peptic ulceration?

A

1) H.pylori infection

2) NSAIDs

72
Q

Why can the use of NSAIDs lead to peptic ulceration?

A

They block the COX enzyme which catalyses the production of prostaglandins from arachidonic acid
Prostaglandins inhibit gastric acid secretion in the stomach

73
Q

What is peptic ulceration and why may an ulcer bleed?

A

Occurs when there is a break in the epithelial cells which penetrates to the muscularis mucosa in either the stomach or duodenum, they have a fibrous base caused by inflammation - bleed when the ulcer reaches blood vessels and erodes them

74
Q

What are the signs and symptoms of peptic ulceration (not bleeding)? 5

A

1) Epigastric pain (may come on after eating, may be relieved by antacids, eating or drinking milk)
2) Epigastric tenderness
3) Nausea
4) Anorexia
5) Weight loss

75
Q

What are the clinical signs and symptoms of a bleeding peptic ulcer? 6

A

1) Haematemesis - vomiting bright red blood
2) Coffee ground vomiting - vomiting older blood
3) Melena - black tarry stools
4) Rectal bleeding
5) Tachychardia and hypotension due to anaemia
6) Raised blood urea - from digestion of large amounts of blood protein

76
Q

Which COX enzyme is responsible for the effects on the gastric mucosa?

A

COX 2

77
Q

What is the difference between the COX 1 and COX 2 enzymes?

A

COX 1 - consitutively acts in many tissues, responsible for the inflammatory response
COX 2 - induced by cytokines in areas of inflammation, responsible for the effects on the gastric mucosa

78
Q

What is the pathogenic process of H. pylori?

A

Common infection related to poor hygiene
H.pylori increases the release of gastrin
H.pylori releases exotoxins and secretory enzymes (mucinase, protease and lipase) which cause gastric mucosal injury

79
Q

How is H pylori adapted to grow in the stomach?

A

Releases urease which catalyses the conversion of urea to NH3 and CO2 which neutralises the gastric acid in its local environment allowing it to survive

80
Q

What are the 3 possible complications of peptic ulcers, how are they identified and how are they treated?

A

1) Perforation - CXR shows air under diaphragm, treated with surgery
2) Gastric outlet obstruction (pyloric stenosis) - projectile vomiting and a distended stomach - treated with surgery
3) Bleeding - treated with endoscopy, cortirising the exposed vessels and injecting the base of the vessel with adrenaline to cause vasoconstriction

81
Q

What is the difference between dyspepsia with alarm symptoms and uncomplicated dyspepsia? (6 alarm symptoms)

A

Dyspepsia with or without red flag features including:

1) Weight loss
2) Dysphagia/odynophagia (painful swallowing)
3) Persistent vomiting
4) Haematamesis or melena
5) Palpable epigastric mass
6) Family history of gastric cancer
7) Onset > 45-55 years

82
Q

What are the 3 potential causes of dyspepsia?

A

1) Gastro-oesophageal reflux disease
2) Peptic ulcer
3) Gastric cancer

83
Q

Which patients with dyspepsia are offered endoscopy (6 alarm symptoms)?

A

Older patients or patients with alarm features including:

1) Weight loss
2) Dysphagia
3) Haematemesis or melena
4) Palpable epigastric mass
5) Family history of gastric cancer
6) Vomiting

84
Q

What are the 3 non invasive and the 2 invasive methods for diagnosing H pylori?

A 
NON INVASIVE 
1) Carbon-urea breath test
2) H.pylori serology
3) H.pylori stool Ag
INVASIVE (done at endoscopy)
1) Rapid urease test
2) Histological examination of biopsy specimens
85
Q

What is the treatment of H pylori infection?

A

PPI combined with 2 Abx eg. amoxicillin, clarithromycin, metronidazole
Could also give a H2 antagonist (Ranitidine, Famotidine) which also reduces gastric acid secretion

86
Q

Why should patients diagnosed with H pylori infection stop smoking?

A

It slows mucosal healing

87
Q

What is the role of PPIs in the treatment of H pylori infection?

A

Blocking acid secretion speeds up ulcer healing and alleviates symptoms rapidly

88
Q

How should peptic ulceration from the use of NSAIDs be prevented?

A

All patients prescribed an NSAID should be prescribed empirical PPI

89
Q

What are the 2 broad principal causes of malabsorption and their sub sections?

A

IMPAIRED DIGESTION (this could be intraluminal or terminal digestion)
- Pancreatic insufficiency (CF/chronic pancreatitis)
- Lack of bile (liver disease/biliary obstruction)
- Lack of intestinal enzymes (eg. lactase/sucrase - lactose intolerence)
IMPAIRED ABSORPTION
- Damage to absorbative surface (Crohns/UC)
- Decreases in absorbative surface area (intestinal resection)
- Inherited defects (eg. SGLT -1 mutation)

90
Q

What are the 4 mechanisms causing diarrhoea?

A

1) Osmotic
2) Secretory
3) Inflammatory
4) Abnormal motility

91
Q

What kind of diarrhoea occurs in lactose intolerence?

A

Osmotic - failure to digest lactose results in osmotically active susbtances in the lumen of the gut

92
Q

Why does abdominal distension, flatulence and acidic stools occur in lactose intolerence?

A

Bacteria in the gut ferment the undigested lactose to monsaccharides, then a variety of metabolites in the gut (lactic acid - acidic stools) producing gases (H2, CO2, CH3) causing abdominal distension and flatulence

93
Q

What kind of diarrhoea occurs in Cholera infection?

A

Secretory

94
Q

How does the cholera toxin cause secretory diarrhoea?

A

1) Cholera toxin irreversible activates Gs raising intracellular cAMP
2) cAMP opens CFTR channels allowing Cl- ions to enter the lumen
3) Na+ and K+ ions flow out to maintain electrical neutrality
4) Water follows creating vastly increased secretion

95
Q

What kind of diarrhoea occurs in coeliac disease?

A

Osmotic

96
Q

Coeliac disease is an autoimmune disease triggered by which substance?

A

Gliadin, an intermediate metabollite in the digestion of gluten

97
Q

What Ag is coeliac disease associated with?

A

Human leucocyte MHC antigens DQ2 and DQ8

98
Q

What is the principal reason for malabsorption in coeliac disease?

A

Decreased surface area for absorption

99
Q

What changes occur to the small intestine in coeliac disease?

A

Atrophy of the microvilli and crypt hyperplasia
Mucosal thickness remains constant but the ultrastructure resembles that of the colon rather than the SI - flattened surface and consequent reduction in surface area

100
Q

What is the treatment for coeliac disease?

A

Remove sources of gluten from the diet

101
Q

What is meconium ilieus?

A

Meconium (first stool of child containing mostly bile) is too thick to pass through the SI, secretory mechanisms are inadequate due to the absence of CFTR - water absorption is dominant

102
Q

What kind of diarrhoea occurs in CF and why?

A

Osmotic - thickened mucous blocks pancreatic duct, lack of digestive enzymes - osmotically active substances in lumen - osmotic diarrhoea

103
Q

What are the 11 signs and symptoms of CF?

A

1) No meconium stool within the first 24 hours of life (meconium ileus)
2) Steatorrhoea
3) Salty skin
4) Persistent respiratory infections
5) Weight loss
6) Clubbing
7) Diarrhoea - osmotic
8) Easy fatigue
9) Delayed growth
10) Coughing and wheezing
11) Splenomegaly

104
Q

What is the net secretion of water in faeces?

A

0.1L

9L secreted, 8.9L reabsorbed

105
Q

How is a diagnosis of coeliac disease made? 3

A

1) Clinical history
2) Serological test - endomysial EMA and tissue transglutaminase - tTG Ab
3) Duodenal biopsy via upper GI endoscopy - see scalloping of surface in coeliac disease

106
Q

What is cholestatic liver disease?

A

Cholestasis is the impairment of bile formation or bile flow

107
Q

What is primary sclerosing cholangitis and what does it ultimately lead to?

A

Inflammation/fibrotic process affecting intra/extra hepatic bile ducts which leads to bile duct strictures
Ultimately leads to cirrhosis and liver failure (only proven treatment is liver transplant)

108
Q

What are the clinical signs and symptoms of cholestatic liver disease or primary sclerosing cholangitis? 3

A

1) Jaundice
2) Puritis
3) Steatorrhoea

109
Q

What is chronic pancreatitis?

A

Irreversible glandular destruction and alturation of anatomy/function of the pancreas due to chronic inflammation

110
Q

What are the 5 possible causes of chronic pancreatitis?

A

1) Alcohol (>70%)
2) Familial
3) Congenital (pancreas divisum)
4) Autoimmune
5) Genetic (CFTR, SPINK1, PRSS1)

111
Q

What are the 2 symptoms of chronic pancreatitis?

A

1) Epigastric pain often radiating to the back which is exacerbated by alcohol or food
2) Weight loss

112
Q

What are the 6 complications of chronic pancreatitis?

A

1) Exocrine insufficiency - fat malabsorption, steatorrhoea, fat soluble Vit D deficiency
2) Endocrine insufficiency - diabetes (40-70% of patients)
3) Pancreatic duct strictures
4) Jaundice, infection, haemorrhage, rupture
5) Portal hypertension
6) Increased risk of cancer

113
Q

What 4 investigations would be carried out in a patient with suspected chronic pancreatitis?

A

1) Faecal elastase 1 (produced by pancreas and passed out in faeces largely unaltered)
2) Plain abdominal X ray
3) Ultrasound/CT
4) MRCP vs. ERCP (ways of looking at ducts and evidence of strictures)

114
Q

What is the management of chronic pancreatitis?

A

1) Remove precipitant (eg. alcohol)
2) Pain control
3) Treat diabetes (often need insulin)
4) Pancreatic enzyme supplements ( creon - lipase, protease, amylase)
5) Vitamin supplementation
6) Endoscopic stenting of strictures, surgery

115
Q

What are the consequences of intestinal resection?

A

Ileal resection - bile acid malapsorption, B12 deficiency

Short bowel syndrome - electrolyte and fluid depletion

116
Q

What is the largest independent risk factor for Crohn’s disease or UC?

A

Family history

117
Q

NOD2 and IL-23 are involved in what GI disorders?

A

NOD2 - Crohn’s - intracellular processing of Ag

IL-23 - Crohn’s and UC - regulator of chronic inflammation

118
Q

How is IBD diagnosed, what basic tests, endoscopy tests and radiology is carried out?

A

Basic tests - anaemia (malapsorption), markers of inflammation (CRP, Calprotectin)
Endoscopy tests - sigmoidoscopy, colonoscopy, gastroscopy with biosies
Radiology - barium studies /CT/MRI scans

119
Q

When do we operate on IBD?

A

EMERGENCY - bowel perforation, bowel obstruction, toxic dilatation, absesses, severe bleeding
ELECTIVE - cancer, failed medical treatment, patient choice

120
Q

What 4 different surgeries can be carried out on a patient with UC?

A

1) Proctocolectomy - remove whole colon with ileostomy (stoma from ileum)
2) Ileal pouch - so faeces still come out anus, following closure of loop ileostomy
3) Ileocecal resection - terminal ileum and cecum removed, small intestine joined to colon
4) Colectomy with ileorectal anastamoses

121
Q

What treatment may be given after surgery in the case of an ileal pouch, ileocecal resection and colectomy with ileorectal anastamoses?

A

Probiotic therapy

122
Q

In which intercostal space does the upper border of the liver lie?

A

5th

123
Q

What are the 8 functions of the liver?

A

1) Bile production
2) Cholesterol synthesis
3) Blood protein synthesis (albumin)
4) Carbohydrate metabolism
5) Drug excretion
6) Ammonia metabolism
7) Bilirubin excretion
8) Fatty acid metabolism

124
Q

Where does the hepatitis A virus replicate and what kind of virus is it?

A

RNA virus replicates in the hepatocytes

Leads to hepatocyte necrosis and lymphocyte inflitration

125
Q

What are the clinical features of Hep A infection?

A

1) Jaundice
2) Lymphadenopathy
3) Hepatomegaly
4) Splenomegaly
5) Rash
6) Arthralgia

126
Q

What is chronic liver disease?

A

A permanent and usually progressive pathological change throughout the liver
Lobular architecture becomes deranged
Fibrosis and nodular regeneration - cirrhosis
Variety of causes

127
Q

What 7 things can cause cirrhosis?

A

1) Hep B
2) Hep C
3) Alcohol
4) Non alcoholic fatty liver disease
5) Primary biliary cirrhosis
6) Primary sclerosing cholangitis
7) Autoimmune liver disease

128
Q

What are the 4 morphological results of liver cirrhosis?

A

1) Hepatocytes damaged and function poorly
2) Sinusoidal/cannalicular pathways distrubed
3) Disrupted intra hepatic biliary drainage
4) Disturbed vascular perfusion

129
Q

What are the 9 clinical effects of cirrhosis?

A

1) Jaundice
2) Ascites (accumulation fluid in peritoneal cavity)
3) Bleeding tendency
4) Portal hypertension
5) Encephalopathy (function of brain affected)
6) Splenomegaly
7) Renal failure
8) Endocrine abnormalities
9) Hepatocellular carcinoma

130
Q

What are the clinical effects of biliary obstruction? 8

A

1) Jaundice
2) Dark urine
3) Pale stools
4) Itching
5) Steatorrhoea
6) Weight loss
7) Vitamin deficiencies (ADEK)
8) Pain

131
Q

What 4 things - the deadly quartet - make up metabolic syndrome?

A

1) Abdominal obesity
2) Hypertension
3) DM
4) Dyslipidaemia

132
Q

What is the difference between steatosis and steatohepatitis?

A

Steatosis precedes steatohepatitis
Steatosis - fat droplet accumulation in the liver
Steatohepatitis - inflammation of liver due to fat droplet accumulation

Year 1 Body Systems (17 decks)

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