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Year 2 - Theme A > Block 15 > Flashcards

Block 15 Flashcards

1
Q

What is ulcerative colitis? (definition)

A

Severe ulcerating inflammatory disease that is limited to the colon and rectum and extends only into the mucosa and submucosa

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2
Q

What are the macroscopic features of Crohn’s disease?

A 
Small and large intestine
Skip lesions
Strictures
Thick walls
Cobblestone
Creeping fat
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3
Q

What are the macroscopic features of ulcerative colitis?

A

Colon only
Diffuse distribution - continuous
No strictures
Thin walls

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4
Q

What are the microscopic features of Crohn’s disease?

A 
Transmural inflammation
Deep, knife like ulcers
Marked lymphoid reaction
Marked serositis
Granuloma
Fistula
Crypt abscesses
Paneth cell metaplasia
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5
Q

What are the microscopic features of ulcerative colitis?

A 
Inflammation limited to mucosa
Marked pseudopolps
Ulcers are superficial with a broad base
No Granulomas
No fistulas
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6
Q

What are the clinical features of chron’s disease?

A

Perianal fistula
Fat/vitamin absorption
Recurrence post op
Intermittent attacks of relatively mild bloody diarrhoea, fever and abdo pain (RLQ)
Periods of active disease with asymptomatic periods in between
Can be triggered by smoking and stress
Fistulae

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7
Q

What are some of the extra-intestinal manifestation of Crohn’s disease?

A

Uveitis
Migratory polyarthritis
Ankylosing spondylitis
Clubbing

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8
Q

What are the clinical features of ulcerative colitis?

A

Relapsing attacks of bloody diarrhoea with stringy mucoid material
Lower abdominal pain
Cramps (relieved by defaecation)
Can be relieved by smoking

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9
Q

What is gastroenteritis?

A

a syndrome characterised by GI symptoms including nausea, diarrhoea, vomiting and abdominal discomfort

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10
Q

Microbiology of E.Coli

A

4 different strains: ETEC, EIEC, EHEC, EPEC

Gram negative baccilus
Facultatively anaerobic

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11
Q

Microbiology of salmonella

A

Gram negative bacilli

Flagellated facultatively anaerobic

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12
Q

How does salmonella cause inflammation and diarrhoea?

A

Penetrates cells
Migrates to lamina propria of ileocecal region
Multiplies in lymphoid follicles – hyperplasia and hypertrophy
Leucocytes confine infection to GI tract
Stimulates cAMP and active fluid secretion
Diarrhoea

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13
Q

Epidemiology of Crohns and ulcerative colitis?

A

Females
Teens / early 20s
Caucasians
Incidence is increasing worldwide

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14
Q

Pathogenesis of inflammatory bowel disease?

A

Combination of defects in host interactions with intestinal microbiota, intestinal epithelial dysfunction and aberrant mucosal immune responses

Bacteria enter bowel (influx of bacterial components due to barrier defect)
Activated dendritic cells to commensals
T helper 1 cells - activate macrophages and secrete TNF gamma
T helper 2 cells - secrete IL13
T helper 17 cells - activate neutrophils

NOD2 gene believed to have a link

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15
Q

Microbiology of campylobacter jejuni

A

Gram negative bacilli

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16
Q

What does bile do?

A

Emulsifies dietary fats
Helps eliminate excess cholesterol, bilirubin and other waste products
Signalling molecules - activate MAPK pathway involved in gut signalling

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17
Q

Microbiology of cholera

A

Comma shaped gram negative
Vibrio cholerae
Need to be ingested in large numbers
Produces a toxin that causes a massive fluid and electrolyte loss with no damage to enterocytes

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18
Q

Microbiology of shigella

A

Gram negative bacilli
Faecal-oral, contaminated food and water
Non motile facultatively anaerobic
Different species, shigella dysentriae causes the most severe form

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19
Q

Rotavirus

A

Double stranded RNA

Causes diarrhoea by damaging transport mechanisms

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20
Q

What are the bacteria responsible for food poisoning?

A 
Salmonella
Norovirus
Campylobacter 
E. Coli
Listeria
Clostridium perfringens
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21
Q

What are the 4 mechanisms of diarrhoea?

A

Osmotic
Secretory
Inflammatory
Abnormal motility

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22
Q

Describe osmotic diarrhoea

A

Fluid enters the bowel if there are large quantities of non-absorbed hypertonic substances in the lumen. It occurs because:

  • patient ingested non absorbable substance
  • patient has generalised malabsorption so high concentrations of solute e.g. Glucose remain in the lumen
  • patient has specific absorptive defect e.g. Disaccharidase deficiency

Diarrhoea stops when you stop eating

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23
Q

Causes of secretory diarrhoea

A 
Enterotoxins (cholera, E. coli, c diff) 
Hormones (VIP)
Bile salts in colon
Fatty acids in colon
Some laxatives
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24
Q

Describe inflammatory diarrhoea

A

Occurs due to damage of the intestinal mucosal cells so loss of fluid and blood. Defective absorption of fluid and electrolytes

Dysentery due to shigella, inflammatory conditions like crohns and ulcerative colitis

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25
Q

Causes of abnormal motility diarrhoea

A

Diabetes
Post vagotomy
Hyperthyroid

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26
Q

Causes of gallstones

A 
Chronic haemolytic
Inflammation
Infection
Rapid weight reduction
Stasis e.g. Pregnancy, spinal cord injuries
Lithogenic bile
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27
Q

What are the complications of gall stones?

A

Most are silent

In gall bladder or cystic duct

  • acute/chronic cholecystitis
  • empyema
  • perforations
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28
Q

What stimulates gut motility?

A

Stretch
ACh
Parasympathetics

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29
Q

Define inanition

A

Exhaustion caused by lack of nourishment

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30
Q

Define anorexia

A

Lack or loss of appetite for food

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31
Q

Define cachexia

A

Wasting syndrome. Loss of weight, muscle atrophy, fatigue, weakness and significant loss of appetite in someone not actively trying to lose weight.

Loss do body mass than can’t be reversed nutritionally.

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32
Q

Describe the control of appetite

A

Hypothalamic arcuate nucleus is where various substances act.

Gherlin is released from the stomach and stimulates hunger. This increases neuropeptide Y which increases appetite and increases body weight

Leptin is released from adipose tissue and stimulates satiety. This decreases neuropeptide Y which decreases appetite and body weight

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33
Q

Name some methods to stop bacteria crossing the epithelial lining of the gut

A

Mechanical - tight junctions, longitudinal flow of fluid
Chemical - low pH, enzymes (pepsin)’ antibacterial peptides released from panneth cells, mucus
Biological - commensal bacterial flora

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34
Q

Causes of acute pancreatitis

A 
Gallstones
Alcohol
Trauma, surgery, ERCP
Viral infections e.g. Mumps
Hypothermia
Ischaemia
Drugs
Rare - hyperparathyroidism, hyperlipidaemia
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35
Q

Signs and symptoms of pancreatitis

A

Acute abdominal pain
Central and severe pain that often radiates to the back
Vomiting
History of alcohol excess, gall stones and certain drugs
Guarding and tenderness in upper abdomen

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36
Q

What would you expect to find on investigation of acute pancreatitis?

A

Raised serum amylase
Glucose intolerance
Hypocalcaemia
Raised CRP, WBC

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37
Q

Causes of chronic pancreatitis?

A 
Alcohol, most common in males
Biliary tract disease
Hypercalcaemia
Hyperlipidaemia
Cystic fibrosis
Idiopathic
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38
Q

Describe the mucosal immune system

A

MALT (mucosal associated lymphoid tissue)

3/4 of all lymphocytes are found in MALT

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39
Q

What are the effector cells formed from CD4+ cells?

A

TH1
TH2
TH17

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40
Q

What are the regulatory cells formed from CD4+ cells?

A

TR1
TH3
CD26

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41
Q

What substances are released from TH1 cells?

A

IFN gamma

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42
Q

Outline GALT

A

Gut associated lymphoid tissue

  • Peyers patches
  • Isolated lymphoid follicles
  • Mesenteric lymph nodes
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43
Q

What is the dominant antibody in the mucosal immune system?

A

IgA

2 Y shaped antibodies connected end to end
Joined by a J chain

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44
Q

How are antigens detected by the gut immune system?

A
  • Antigen presented at mucosal system
  • Need to cross the epithelial barrier to stimulate the immune system
  • Peyers patches are covered in M cells
  • They take up the antigen via endocytosis

OR dendritic cells extend across epithelial layer to get to bacteria

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45
Q

What is the function of IgA in the immune system?

A 
Binds to mucus
Neutralises pathogens and toxins
Prevents adherence of micro organisms
Neutralise LPS and toxins
Can't activate complement - no inflammation
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46
Q

What are the 2 different types of malnutrition?

A

Protein-energy metabolism
Physiological well, anorexia, suppression of appetite
Neglect

Specific malnutrition
Nutrient deficiency

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47
Q

What are the causes of bacterial overgrowth of the GI tract?

A

Jejunal diverticulosis
Obstruction
Motility disorders
Blind loop syndrome

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48
Q

What are the features of coeliac disease?

A 
Gluten enteropathy
Immune mediated
Subtotal villous atrophy
Crypt hyperplasia
Intraepithelial lymphocytes
Deficiency - iron, folate, vitamin D
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49
Q

What do you test in the blood for coeliac disease?

A

Anti-tissue tranglutaminase

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50
Q

What is the incidence of ulcerative colitis and Crohns?

A

UC - 11/ 100 000

Crohn’s - 7/ 100 000

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51
Q

What is the concordance in monozygotic twins for ulcerative colitis and Crohn’s?

A

UC - 8%

Crohn’s - 67%

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52
Q

What are the presdisposing factors for GI infections?

A 
Age - extremes of age
Immunodeficiency - HIV
Achlorhydria - absence of gastric acid
Inoculum size
Pathogen virulence factors
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53
Q

What are the 4 antibiotic causes of C.diff infection?

A

4 C’s

Cephalosporin
Co-amoxiclav
Clindamycin
Clarithromycin

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54
Q

What are the features of non-inflammatory GI bacterial infections?

A 
No invasion of mucosa
Enterotoxins
Mucosal adherence
Proximal small bowel
Vibrio cholerae, enterotoxogenic E. Coli
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55
Q

What are the features of inflammatory GI bacterial infections?

A

Invasion of mucosa
Colon
Campylobacter, salmonella, shigella

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56
Q

What are the features of penetrating GI bacterial infections?

A

Induced phagocytosis
Distal small bowel
Salmonella typhi, listeria monocytogenes

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57
Q

What are the consequences of bacterial overgrowth syndrome?

A 
Malabsorption
Steatorrhoea
Diarrhoea
Macrocytic anaemia
Deficiency of fat soluble vitamins
>10^5 bacteria per ml
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58
Q

What are the methods for disease control?

A 
Surveillence - notifiable under public health act
Epidemiology
Education
Environmental change
Immunisation
Law
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59
Q

What are the methods for disease prevention?

A 
Public education
Staff training
Food inspector
Equipments well maintained
Good raw materials - farm to fork
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60
Q

Define outbreak

A

When 2 or more people contract the same infection from a common source

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61
Q

What is the blood supply to the liver?

A

Coeliac trunk - common hepatic - hepatic artery proper

Hepatic artery proper - 20% volume, 80% oxygen
Hepatic portal vein - 80% volume, 20% oxygen

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62
Q

Anatomy of the liver?

A 
4 lobes: right, left, caudate, quadrate
Falciform ligament (anterior)
Anterior and posterior ligament
Triangular ligaments
Ligamentum venosum (superior)
Ligamentum teres (inferior)
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63
Q

What are the functions of the liver?

A 
Storages of glycogen
Gluconeogenesis
Protein synthesis
Catabolism of amino acids
Lipoprotein synthesis
Detoxification of nitrogenous molecules
Drug metabolism
Bilirubin conjugation
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64
Q

Describe the hepatic lobule

A

Triad - branch of portal vein, branch of hepatic artery, bile duct
Sinusoids surrounding by hepatocytes that drains into central vein
Bile canaliculous drains in opposite direction

65
Q

Hepatitis A virus

A

ssRNA
Faecal - oral transmission
Incubation 2-4 weeks
Never causes chronic disease

66
Q

What are the risk factors for hep A infection?

A 
Personal contact
Travel to high risk areas
Male homosexuality
Intravenous drug use
Certain occupation (sewage workers)
67
Q

What are the clinical features of a hep A infection?

A 
Mild flu like symptoms
Anorexia
Nausea
Fatigue
Malaise
Joint pain
Preceding jaundice
Potentially diarrhoea

Icteric phase - dark urine (appears first), pale stools (not always), jaundice (70-85%), abdominal pain, itch, skin rash, hepatomegaly, splenomegaly, lymphadenopathy

68
Q

Hepatitis B virus

A

dsDNA
Paenteral, sexual, perinatal spread
Incubation 1-4 months
Chronic frequency 10%

69
Q

What are the clinical syndromes that can be caused by hep B virus?

A

Acute hepatitis with recovery and clearance of virus
Fulminant hepatitis
Non progressive chronic hepatits
Progressive chronic disease ending in cirrhosis
Asymptomatic carrier state

70
Q

How common are each of the consequences of hep B infection?

A

60-65% - sub clinical disease (100% recovery)

20-25% - acute hepatitis (99% recovery, 1% fulminant hepatitis –> death)

5-10% - carrier

4% - chronic hepatitis (20-30% cirrhosis, also recovery, hepatocellular carcinoma)

71
Q

Hepatitis C virus

A

ssRNA
Transmission - parenteral, intranasal
Incubation - 7-8weeks
Chronic frequency - 80%

72
Q

How common are each of the consequences of hep C infection?

A

15% resolution

85% chronic hepatitis (80% stable disease, 20% cirrhosis) Of the 20% that get cirrhosis (50% stable cirrhosis, 50% death)

Rare - fulminant hepatitis

73
Q

What are the risk factors for progression from hep C to cirrhosis?

A

Male
over 40
Alcohol
Asian

74
Q

What are the medical consequences of alcohol?

A

Liver: alcoholic hepatitis, cirrhosis, liver cancer
GI: oral cavity cancer, oesophageal neoplasm and varices, pancreatitis
CV: AF, hypertension, stroke, cardiomyopathy
Neuro: loss of consciousness, withdrawal, seizures, subdural haemorrhage, peripheral neuropathy, cerebellar degeneration

75
Q

What are the psychiatric consequences of alcohol?

A

Alcohol dependence syndrome
Suicidal ideation
Depression
Anxiety

76
Q

What are the causes of pancreatitis?

A 
Idiopathic
Gall stones
Ethanol (alcohol)
Trauma
Steroid
Mumps/malignancy
Autoimmune
Scorpion bite
Hyperlipidaemia/ Hypothermia
ERCP
Drugs
77
Q

What genes are linked with pancreatitis?

A

PRSS1 trypsinogen gene

SPINK1 - pancreatic secretory trypsin inhibitor (prevents water digestion)

78
Q

How does pancreatitis occur?

A

Pancreatic duct obstruction, increase in duct pressure, accumulation of enzyme fluid into interstitium

Acinar cell injury causing release of enzymes

Defective intracellular transport - proenzymes inappropriately delivered to intracelluar compartment containing lysosymes

79
Q

What happens in pancreatitis?

A

Microvascular damage and leakage causing oedema
Necrosis of fat by lipolytic enzyme
Acute inflammation
Proteolytic destruction of pancreatic parenchyma
Destruction of blood vessels causing interstitial haemorrhage

80
Q

What is the incidence of pancreatitis?

A

10-20 per 100,000

81
Q

What are the clinical features of pancreatitis?

A 
Abdominal pain - constant and intense 
Often referred to back and occasionally the left shoulder
Severity from mild to incapacitating
Anorexia
Nausea
Vomiting
Elevated amylase and lipase

Medical emergency

82
Q

Define chronic pancreatitis

A

Inflammation of the pancreas with irreversible destruction of exocrine parenchyma, fibrosis and in the late stages destruction of endocrine parenchyma

83
Q

What are the causes of chronic pancreatitis?

A

Long term alcohol abuse
Long standing obstruction of pancreatic duct
Hereditary pancreatitis

84
Q

What happens in chronic pancreatitis?

A

Parenchymal fibrosis
Decreased number and size of acini
Sparing of Langerhans cells
Variable dilation of pancreatic ducts
Chronic inflammatory infiltrate around lobules and ducts
Ductal epithelium = atrophied or hyperplastic or squamous metaplasia

85
Q

What are the clinical features of chronic pancreatitis?

A

Can present in several ways:

  1. Repeated attacks of abdo pain or persistent back and abdo pain
  2. Entirely silent until pancreatic insufficiency and diabetes develop
  3. Recurrent attacks of jaundice
  4. Vague attacks of indigestion

Attacks can be precipitated by alcohol abuse, overeating, opiate use
Mild fever
Weight loss
Hypoalbuminaemic oedema

86
Q

What is peritonitis?

A

Occurs when bacteria from GI lumen are released into abdo cavity

Usually E.Coli, streptococci, S. aureus or enterococci

87
Q

What are the clinical features of peritonitis?

A 
Acute abdo pain
Abdo tenderness
Abdominal guarding
Exacerbated by moving peritoneum 
Rebound tenderness
Fever
Sinus tachycardia
88
Q

What are the features of peritonitis?

A

Dull peritoneal surfaces
Turbid fluid accumulation
Volume of fluid can vary
Dense collection of neutrophils

89
Q

What are the clinical features of severe hepatic dysfunction?

A 
Jaundice and cholestasis
Hyperammonaemia
Palmar erythema
Hypogonadism
Weight loss
Hypoalbuminaemia
Hypoglycaemia
Spider angiomas
Gynaecomastia
Muscle wasting
90
Q

What are the main primary disease of the liver?

A

Viral hepatitis
Alcoholic liver disease
Non alcoholic fatty liver disease
Hepatocellular carcinoma

91
Q

What is hepatic encephalopathy?

A

Can develop with acute or chronic liver disease
Occurs due to severe loss of hepatocellular function and shuntingof blood from portal to systemic circulation around a chronically diseased liver.

Patients show a spectrum of brain dysfunction from subtle abnormalities to coma
Rigidity, hyper relfexia, asterixis (flapping tremor)

92
Q

What is cirrhosis?

A

Diffuse process characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules

93
Q

What processed are central to the pathogenesis of cirrhosis?

A

Death of hepatocytes
Extracellular matrix deposition
Vascular reorganisation

94
Q

Pathogenesis of cirrhosis?

A

Activated stellate cells (myofibroblasts) - release chemokines and growth factor
Produce excess collagen
Dense extracellular matrix
Loss of fenestration in endothelial cells (increases pressure in sinusoids and decreases solute exchange)
Loss of microvilli on hepatocytes (decrease transport capability)
Activated Kupffer cells

95
Q

What are the clinical features of cirrhosis?

A 
Can be clinically silent
Non specific symptoms
Anorexia
Weight loss
Weakness
Incipient or overt hepatic failure
Complications related to portal hypertension
96
Q

What are the causes of cirrhosis?

A 
Hep B and C
Alcoholic and non alcoholic steatohepatitis
Autoimmune
Biliary disease
metabolic conditions (haemochromatosis)
97
Q

What is portal hypertension?

A

Increased resistance to portal blood flow which can develop from prehepatic, intrahepatic or posthepatic causes

98
Q

What is the pathogenesis of portal hypertension?

A

Increase resistnance to flow at level of sinusoids and compression of central veins by perivenular fibrosis and parenchymal nodules
Anastamoses between arterial and portal systems
Increase in portal blood flow from hyperdynamic circulation
Arterial vasodilation in splanchnic circulation

99
Q

What are the clinical consequences of portal hypertension?

A 
Ascites
Hepatic encephalopathy
Spider angioma
Oesophageal varices
Splenomegaly
Periumbilical caput medusa
Testicular atrophy
Haemmorhoids
100
Q

What is a portosystemic shunt?

A

With rises in portal venous pressure, shunts develop where systemic and portal circulations share capillary beds

101
Q

Where are common locations to get portosystemic shunts?

A

Veins around rectum - haemmorhoids
Cardioesophageal junction - varices
Retroperitoneum
Falciform ligament of liver

102
Q

What are the 3 liver alterations in fatty liver disease?

A

Steatosis
Hepatitis
Fibrosis

103
Q

What are the microscopic changes in fatty liver disease?

A 
hepatocyte ballooning
Mallory-Denk bodies
neutrophil infiltration
central vein sclerosis
chicken wire fence pattern - fibrosis
104
Q

What does hepatocellular steatosis result from?

A

Shunting of substrates away from catabolism and toward lipid biosynthesis
Because of excess nicotinamide-adenine dinucleotide from metabolism of ethanol by alcohol dehydrogenase

Impaired assembly and secretion of lipoproteins

Increased peripheral catabolism of fat

105
Q

What are the causes of alcoholic hepatitis?

A

Acetaldehyde (metabolite of ethanol) induces lipid peroxidation which may disrupt cytoskeleton and membrane function

Alcohol affects cytoskeleton organisation, mitochondrial function and decrease membrane fluidity

Reactive oxygen species

Cytokine mediated inflammation - TNF, IL1, IL6, IL8

106
Q

What are the clinical features of hepatocellular steatosis?

A

Hepatomegaly

mild elevation of serum bilirubin and alkaline phosphatase

107
Q

What are the clinical features of alcoholic hepatitis?

A 
Acute onset after bout of heavy drinking
Malaise
Fever
Anorexia
Weight loss
Upper abdominal discomfort
Tender hepatomegaly
108
Q

What are the investigation findings in alcoholic hepatitis?

A

Hyperbilirubinaemia
Increased alkaline phosphatase
Increased neutrophilic leukocytes
Increased serum ALT and aspartate aminotransferase

109
Q

What is non alcoholic fatty liver disease commonly associated with?

A 
Insulin resistance
Metabolic syndrome
Type 2 diabetes
Obesity
Dyslipidaemia
Hypertension
110
Q

What happens in non alcoholic fatty liver disease?

A

Steatosis, steatohepatitis, cirrhosis
Impaired oxidation of fatty acids
Increased synthesis and uptake of fatty acids
Decreased hepatic secretion of VLDL
Increased levels of TNF, IL6 which cause liver damage and inflammation

111
Q

Describe Wilsons disease

A

autosomal recessive
Accumulation of toxic levels of copper in organs and tissues especially in the brain, liver and eye.
Mutations in ATP7B gene on chromosome 13
Without ATP7B copper can’t be passed onto apoceruloplasmin
Can’t be excreted into bile
Copper causes toxic injury
Red cell haemolysis and damage due to deposition
Mimics fatty liver disease - cirrhosis

112
Q

What are the different tests included in the LFTs?

A 
Bilirubin
Albumin
Transferases 
- ALT (alanine aminotransferase)
- AST (aspartate aminotransferase)
Gamma gutamyltransferase GGT
Alkaline phosphatase ALP
113
Q

What LFT changes would you expect in obstructive disease?

A

Increased ALP
Increased GGT

Small increase in AST and ALT

114
Q

What LFT changes would you expect to see with intra-hepatic damage?

A

Increased AST
Increased ALT

Small increase in ALP and GGT

115
Q

In what condition would you expect ALT to be greater than AST?

A

Chronic liver disease

116
Q

In what condition would you expect AST to be greater than ALT?

A

Cirrhosis

117
Q

What would cause an increase in GGT and ALP?

A

Cholestasis

118
Q

What would cause an increase in GGT with normal ALP?

A

Alcohol

119
Q

Outline drug metabolism

A

2 reactions: phase 1 and phase 2, usually in liver

Phase 1 - catabolic and products are often more chemically reactive and can be more toxic than parent drug

Phase 2 - synthetic resulting in inactive produces

120
Q

Describe phase 1 reactions

A

Involve the P450 mono oxygenase system
CYP…

Drug
\+P450 enzyme
\+molecular oxygen
\+NADPH
\+flavoprotein

Addition of an oxygen atom to form a hydroxyl group

Not all phase 1 reactions involve the P450 system

121
Q

Describe phase 2 reactions

A

After phase 1 it is susceptible to conjugation = attachment of substituent groups

Resultant conjugate is almost always inactive

e.g. glucaronyl transfer - UDP glucuronyl transferase

122
Q

Describe first pass metabolism

A

Some drugs are extracted so efficiently by liver or gut wall that the amount reaching the systemic circulation is considerably less than the amount absorbed

Much larger dose required when given orally and is unpredictable

123
Q

Example of drugs that undergo first pass metabolism

A 
Aspirin
Metoprolol
Morphine
Propranolol
Salbutamol
Verapamil
Lidocaine
Levadopa
GNT
124
Q

What are the characteristics of preheaptic jaundice?

A 
Inability to conjugate bilirubin fast
Increased serum unconjugated bilirubin
Decreased or no bilirubin in urine
Increased urobilinogen in urine or faeces
Dark brown faeces

Unconjugated hyperbilirubinaemia

125
Q

What are the causes of prehepatic jaundice?

A 
Sickle cell anaemia
Thalassaemia
Spherocytosis
Incompatible blood transfusion
Malaria
Haemolytic anaemia
126
Q

What are the characteristics of hepatic jaundice?

A 
Increase in conjugated or unconjugated bilirubin
Decreased faecal urobilinogen
Increased urinary urobilinogen
Pale stool
Dark urine
Increased ALT and AST
127
Q

What are the causes of hepatic jaundice?

A 
Gilberts
Cirrhosis
Viral hepatitis
Alcoholic hepatitis
Autoimmune hepatitis
Drug induced hepatits
128
Q

What are the characteristics of post hepatic jaundice?

A 
Increased conjugated bilirubin
Bilirubin in urine
Decreased faecal urobilinogen
No urobilinogen in urine
Pale stools
Dark urine
Increased ALP, ALT, AST
129
Q

What are the causes of post hepatic jaundice?

A 
Gall stones
Gall bladder carcinoma
Pancreatic carcinoma
Primary sclerosing cholangitis
Pancreatitis
Bile duct strictures
130
Q

Epidemiology of bowel cancer

A

3rd most common UK cancer
2nd most common cause of cancer death
47/ 100 000
Higher in men than women

131
Q

What are the risk factors for bowel cancer?

A 
Family history of colorectal cancer under 60y
IBD
Crohns
UC
Polyposis syndromes
Nulliparity
Late age of first pregnancy
Early menopause
Diet: rich in meat and fat, low fibre
Sedentary lifestyle
Smoking
Alcohol
Obesity
Diabetes
132
Q

Presentation of left sided colon cancer

A 
colicky pain
rectal bleeding
bowel obstruction
tenesemus
mass in left iliac fossa
early change in bowel habit
133
Q

Presentation of right sided colon cancer

A 
weight loss
anaemia
occult bleeding
mass in right iliac fossa
more advanced on presentation
134
Q

What is the prognosis (5 year survival rate) for bowel cancer?

A

Stage 1 = T1/2 M0 N0 = 75%
Stage 2 = nodal involvement = 60%
Stage 3 = T3/4 - 50%
Stage 4 = M1 6%

135
Q

Describe hyperplastic polyps

A

Common epithelial proliferations in 60s and 70s
Results from decreased epithelial cell turnover and a pile up of goblet cells
Smooth nodular protrusions
<5mm in left colon

136
Q

Describe hamartomatous polyps

A

Occur sporadically
Disorganised tumour like growths with mature cells
Increased risk of developing colorectal cancer
Pedunculated smooth surfaced red lesions
<3cm in diameter

137
Q

Describe adenomas in the colon

A

Benign polyps that give rise to colorectal adenocarcinomas
Epithelial dysplasia
0.3-10cm can be pedunculated or sessile
Size correlates with risk of malignancy

138
Q

Outline FAP

A 
Familial adenomatous polyposis
Autosomal dominant
Mutations in APC gene
Need at least 100 polyps on endoscopy
Colorectal adenocarcinoma in 100% if untreated by 30
139
Q

Describe hereditary nonpolyposis colorectal cancer

A

HNPCC - familial clustering of cancers at several sites
Colorectal, endometrium, stomach, brain
Occurs at a younger age often in right colon
Mutation in MSH2/1

140
Q

Outline the pathogenesis of adenocarcinoma

A

Combination of genetic and epigenetic abnormalities
Mutations of APC tumour suppressor
APC/beta catenin pathway
Causes transcription of genes which promote proliferation
KRAS (late mutation) - promotes growth
TP53 mutation - 70% of cancers
BAX enhances survival of genetically abnormal clones

141
Q

Describe the morphology of adenocarcinoma

A

Tumours in proximal colon
Rarely cause obstruction
Grow along wall

Tumours in distal colon
Annular lesions, napkin ring contrictions
Luminal narrowing

Tall columnar cells
Dysplastic epithelium

142
Q

What methods are used to view the GI tract?

A 
Barium swallow/meal/follow through
Barium enema
Colonoscopy
Endoscopy
Abdominal ultrasound
CT scan
MRI
143
Q

What should you think about when choosing a method of GI imaging?

A 
Availability
Patient tolerance
Cost
Risk of complications
Most likely to answer clinical question
144
Q

What are the single and double contrast used in barium radiology?

A

Single - lumen distended with barium

Double - mucosa coated with barium and lumen distended with air

145
Q

What are the limitations of barium swallow/meal?

A

Limited senstivity for cancer and inflammation
Miss early lesions
Patients need to be fit and mobile
Need to retain stomach full of gas and barium
Poorly tolerated by elderly

146
Q

What are the requirements for barium enema?

A

2 days starvation
Strong laxative

Barium into colon via rectal tube
Colon distended with air or CO2

147
Q

What are the benefits of double contrast barium enema?

A

Safe with low complication rate
Well tolerated
Complete examination
Able to detect intrinsic and extrinsic disease

148
Q

What are the limitations of DCBE?

A

Patients need to be mobile
Must be able to retain air and barium in colon
Less sensitive than colonoscopy
No scope for obtaining histology

149
Q

What are the benefits of endoscopy?

A

Direct inspection of mucosa
Detects early pathology
Allows for biopsy or therapeutic procedure
Identifies conditions not seen at DCBE

150
Q

What are the limitations of endoscopy (gastric)?

A 
Less good at assessing motility and extrinsic disease
Limited views of pharynx and cervical oesophagus
Significant complication rate 0.1%
Mortality rate 0.03%
Cardiopulmonary problems if sedated
Perforation
Haemorrhage
Transmission of infection
151
Q

What are the common causes of upper GI bleeding?

A 
Duodenal ulcers 20-30%
Gastric or duodenal erosions 20-30%
Varices 15-20%
Gastric ulcer 10-20%
Mallory-Weiss tear 5-10%
Erosive oesophagitis 5-10%
Angioma 5-10%
Arteriovenous malformations <5%
152
Q

What are the common causes of lower GI bleeding?

A 
Anal fissures
Angiodysplasia
Colitis
Colonic carcinoma
Colonic polyps
Diverticular disease
IBD
Internal haemorrhoids
153
Q

What is the Rockall score and what does it take into account?

A

Used to determine risk for endoscopy
Age
Shock
Co-morbidity

Predicts mortality

154
Q

Describe fluid absorption in the gut

A

80% in small intestine

80% of remaining 20% removed in large intestine

155
Q

Describe the process of defaecation

A

Collection of faeces in sigmoid colon and rectum
Pressure on walls of large intestine

Involuntary - large peristaltic wave, distension of walls and opening of internal anal sphincter
Pelvic nerve

Voluntary - delay (reverse peristalsis, open external sphincter)
Pudendal nerve

Open sphincters
Levator ani contracts reducing anal-rectal angle

156
Q

Anatomy of the adrenal glands

A

On top of each kidney
Inner medulla
Outer cortex
Surrounded by perinephric fat, enclosed in renal fasica

Cortex has 3 areas -
Zona glomerulos
Zona fasciculata
Zona reticularis

157
Q

What is the blood supply to the adrenal glands?

A 
Superior suprarenal (from inferior phrenic artery)
Middle suprarenal (abdominal aorta)
Inferior suprarenal (renal arteries)
158
Q

What is secreted from each area of the adrenal cortex?

A

Zona glomerulosa - mineralocorticoids (aldosterone)
Zona fasciculata - glucocorticoids (cortisol)
Zona reticularis - gonadocorticoids (androgens)

159
Q

Describe the adrenal medulla?

A

Chromaffin cells in clusters around blood vessels

Produce adrenaline and NA

Year 2 - Theme A (7 decks)

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