Block 15 Flashcards

(159 cards)

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
Causes of abnormal motility diarrhoea
Diabetes Post vagotomy Hyperthyroid
26
Causes of gallstones
``` Chronic haemolytic Inflammation Infection Rapid weight reduction Stasis e.g. Pregnancy, spinal cord injuries Lithogenic bile ```
27
What are the complications of gall stones?
Most are silent In gall bladder or cystic duct - acute/chronic cholecystitis - empyema - perforations
28
What stimulates gut motility?
Stretch ACh Parasympathetics
29
Define inanition
Exhaustion caused by lack of nourishment
30
Define anorexia
Lack or loss of appetite for food
31
Define cachexia
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.
32
Describe the control of appetite
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
33
Name some methods to stop bacteria crossing the epithelial lining of the gut
Mechanical - tight junctions, longitudinal flow of fluid Chemical - low pH, enzymes (pepsin)' antibacterial peptides released from panneth cells, mucus Biological - commensal bacterial flora
34
Causes of acute pancreatitis
``` Gallstones Alcohol Trauma, surgery, ERCP Viral infections e.g. Mumps Hypothermia Ischaemia Drugs Rare - hyperparathyroidism, hyperlipidaemia ```
35
Signs and symptoms of pancreatitis
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
36
What would you expect to find on investigation of acute pancreatitis?
Raised serum amylase Glucose intolerance Hypocalcaemia Raised CRP, WBC
37
Causes of chronic pancreatitis?
``` Alcohol, most common in males Biliary tract disease Hypercalcaemia Hyperlipidaemia Cystic fibrosis Idiopathic ```
38
Describe the mucosal immune system
MALT (mucosal associated lymphoid tissue) 3/4 of all lymphocytes are found in MALT
39
What are the effector cells formed from CD4+ cells?
TH1 TH2 TH17
40
What are the regulatory cells formed from CD4+ cells?
TR1 TH3 CD26
41
What substances are released from TH1 cells?
IFN gamma
42
Outline GALT
Gut associated lymphoid tissue - Peyers patches - Isolated lymphoid follicles - Mesenteric lymph nodes
43
What is the dominant antibody in the mucosal immune system?
IgA 2 Y shaped antibodies connected end to end Joined by a J chain
44
How are antigens detected by the gut immune system?
- 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
45
What is the function of IgA in the immune system?
``` Binds to mucus Neutralises pathogens and toxins Prevents adherence of micro organisms Neutralise LPS and toxins Can't activate complement - no inflammation ```
46
What are the 2 different types of malnutrition?
Protein-energy metabolism Physiological well, anorexia, suppression of appetite Neglect Specific malnutrition Nutrient deficiency
47
What are the causes of bacterial overgrowth of the GI tract?
Jejunal diverticulosis Obstruction Motility disorders Blind loop syndrome
48
What are the features of coeliac disease?
``` Gluten enteropathy Immune mediated Subtotal villous atrophy Crypt hyperplasia Intraepithelial lymphocytes Deficiency - iron, folate, vitamin D ```
49
What do you test in the blood for coeliac disease?
Anti-tissue tranglutaminase
50
What is the incidence of ulcerative colitis and Crohns?
UC - 11/ 100 000 | Crohn's - 7/ 100 000
51
What is the concordance in monozygotic twins for ulcerative colitis and Crohn's?
UC - 8% | Crohn's - 67%
52
What are the presdisposing factors for GI infections?
``` Age - extremes of age Immunodeficiency - HIV Achlorhydria - absence of gastric acid Inoculum size Pathogen virulence factors ```
53
What are the 4 antibiotic causes of C.diff infection?
4 C's Cephalosporin Co-amoxiclav Clindamycin Clarithromycin
54
What are the features of non-inflammatory GI bacterial infections?
``` No invasion of mucosa Enterotoxins Mucosal adherence Proximal small bowel Vibrio cholerae, enterotoxogenic E. Coli ```
55
What are the features of inflammatory GI bacterial infections?
Invasion of mucosa Colon Campylobacter, salmonella, shigella
56
What are the features of penetrating GI bacterial infections?
Induced phagocytosis Distal small bowel Salmonella typhi, listeria monocytogenes
57
What are the consequences of bacterial overgrowth syndrome?
``` Malabsorption Steatorrhoea Diarrhoea Macrocytic anaemia Deficiency of fat soluble vitamins >10^5 bacteria per ml ```
58
What are the methods for disease control?
``` Surveillence - notifiable under public health act Epidemiology Education Environmental change Immunisation Law ```
59
What are the methods for disease prevention?
``` Public education Staff training Food inspector Equipments well maintained Good raw materials - farm to fork ```
60
Define outbreak
When 2 or more people contract the same infection from a common source
61
What is the blood supply to the liver?
Coeliac trunk - common hepatic - hepatic artery proper Hepatic artery proper - 20% volume, 80% oxygen Hepatic portal vein - 80% volume, 20% oxygen
62
Anatomy of the liver?
``` 4 lobes: right, left, caudate, quadrate Falciform ligament (anterior) Anterior and posterior ligament Triangular ligaments Ligamentum venosum (superior) Ligamentum teres (inferior) ```
63
What are the functions of the liver?
``` Storages of glycogen Gluconeogenesis Protein synthesis Catabolism of amino acids Lipoprotein synthesis Detoxification of nitrogenous molecules Drug metabolism Bilirubin conjugation ```
64
Describe the hepatic lobule
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
Hepatitis A virus
ssRNA Faecal - oral transmission Incubation 2-4 weeks Never causes chronic disease
66
What are the risk factors for hep A infection?
``` Personal contact Travel to high risk areas Male homosexuality Intravenous drug use Certain occupation (sewage workers) ```
67
What are the clinical features of a hep A infection?
``` 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
Hepatitis B virus
dsDNA Paenteral, sexual, perinatal spread Incubation 1-4 months Chronic frequency 10%
69
What are the clinical syndromes that can be caused by hep B virus?
Acute hepatitis with recovery and clearance of virus Fulminant hepatitis Non progressive chronic hepatits Progressive chronic disease ending in cirrhosis Asymptomatic carrier state
70
How common are each of the consequences of hep B infection?
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
Hepatitis C virus
ssRNA Transmission - parenteral, intranasal Incubation - 7-8weeks Chronic frequency - 80%
72
How common are each of the consequences of hep C infection?
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
What are the risk factors for progression from hep C to cirrhosis?
Male over 40 Alcohol Asian
74
What are the medical consequences of alcohol?
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
What are the psychiatric consequences of alcohol?
Alcohol dependence syndrome Suicidal ideation Depression Anxiety
76
What are the causes of pancreatitis?
``` Idiopathic Gall stones Ethanol (alcohol) Trauma Steroid Mumps/malignancy Autoimmune Scorpion bite Hyperlipidaemia/ Hypothermia ERCP Drugs ```
77
What genes are linked with pancreatitis?
PRSS1 trypsinogen gene | SPINK1 - pancreatic secretory trypsin inhibitor (prevents water digestion)
78
How does pancreatitis occur?
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
What happens in pancreatitis?
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
What is the incidence of pancreatitis?
10-20 per 100,000
81
What are the clinical features of pancreatitis?
``` 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
Define chronic pancreatitis
Inflammation of the pancreas with irreversible destruction of exocrine parenchyma, fibrosis and in the late stages destruction of endocrine parenchyma
83
What are the causes of chronic pancreatitis?
Long term alcohol abuse Long standing obstruction of pancreatic duct Hereditary pancreatitis
84
What happens in chronic pancreatitis?
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
What are the clinical features of chronic pancreatitis?
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
What is peritonitis?
Occurs when bacteria from GI lumen are released into abdo cavity Usually E.Coli, streptococci, S. aureus or enterococci
87
What are the clinical features of peritonitis?
``` Acute abdo pain Abdo tenderness Abdominal guarding Exacerbated by moving peritoneum Rebound tenderness Fever Sinus tachycardia ```
88
What are the features of peritonitis?
Dull peritoneal surfaces Turbid fluid accumulation Volume of fluid can vary Dense collection of neutrophils
89
What are the clinical features of severe hepatic dysfunction?
``` Jaundice and cholestasis Hyperammonaemia Palmar erythema Hypogonadism Weight loss Hypoalbuminaemia Hypoglycaemia Spider angiomas Gynaecomastia Muscle wasting ```
90
What are the main primary disease of the liver?
Viral hepatitis Alcoholic liver disease Non alcoholic fatty liver disease Hepatocellular carcinoma
91
What is hepatic encephalopathy?
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
What is cirrhosis?
Diffuse process characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules
93
What processed are central to the pathogenesis of cirrhosis?
Death of hepatocytes Extracellular matrix deposition Vascular reorganisation
94
Pathogenesis of cirrhosis?
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
What are the clinical features of cirrhosis?
``` Can be clinically silent Non specific symptoms Anorexia Weight loss Weakness Incipient or overt hepatic failure Complications related to portal hypertension ```
96
What are the causes of cirrhosis?
``` Hep B and C Alcoholic and non alcoholic steatohepatitis Autoimmune Biliary disease metabolic conditions (haemochromatosis) ```
97
What is portal hypertension?
Increased resistance to portal blood flow which can develop from prehepatic, intrahepatic or posthepatic causes
98
What is the pathogenesis of portal hypertension?
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
What are the clinical consequences of portal hypertension?
``` Ascites Hepatic encephalopathy Spider angioma Oesophageal varices Splenomegaly Periumbilical caput medusa Testicular atrophy Haemmorhoids ```
100
What is a portosystemic shunt?
With rises in portal venous pressure, shunts develop where systemic and portal circulations share capillary beds
101
Where are common locations to get portosystemic shunts?
Veins around rectum - haemmorhoids Cardioesophageal junction - varices Retroperitoneum Falciform ligament of liver
102
What are the 3 liver alterations in fatty liver disease?
Steatosis Hepatitis Fibrosis
103
What are the microscopic changes in fatty liver disease?
``` hepatocyte ballooning Mallory-Denk bodies neutrophil infiltration central vein sclerosis chicken wire fence pattern - fibrosis ```
104
What does hepatocellular steatosis result from?
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
What are the causes of alcoholic hepatitis?
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
What are the clinical features of hepatocellular steatosis?
Hepatomegaly | mild elevation of serum bilirubin and alkaline phosphatase
107
What are the clinical features of alcoholic hepatitis?
``` Acute onset after bout of heavy drinking Malaise Fever Anorexia Weight loss Upper abdominal discomfort Tender hepatomegaly ```
108
What are the investigation findings in alcoholic hepatitis?
Hyperbilirubinaemia Increased alkaline phosphatase Increased neutrophilic leukocytes Increased serum ALT and aspartate aminotransferase
109
What is non alcoholic fatty liver disease commonly associated with?
``` Insulin resistance Metabolic syndrome Type 2 diabetes Obesity Dyslipidaemia Hypertension ```
110
What happens in non alcoholic fatty liver disease?
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
Describe Wilsons disease
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
What are the different tests included in the LFTs?
``` Bilirubin Albumin Transferases - ALT (alanine aminotransferase) - AST (aspartate aminotransferase) Gamma gutamyltransferase GGT Alkaline phosphatase ALP ```
113
What LFT changes would you expect in obstructive disease?
Increased ALP Increased GGT Small increase in AST and ALT
114
What LFT changes would you expect to see with intra-hepatic damage?
Increased AST Increased ALT Small increase in ALP and GGT
115
In what condition would you expect ALT to be greater than AST?
Chronic liver disease
116
In what condition would you expect AST to be greater than ALT?
Cirrhosis
117
What would cause an increase in GGT and ALP?
Cholestasis
118
What would cause an increase in GGT with normal ALP?
Alcohol
119
Outline drug metabolism
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
Describe phase 1 reactions
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
Describe phase 2 reactions
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
Describe first pass metabolism
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
Example of drugs that undergo first pass metabolism
``` Aspirin Metoprolol Morphine Propranolol Salbutamol Verapamil Lidocaine Levadopa GNT ```
124
What are the characteristics of preheaptic jaundice?
``` 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
What are the causes of prehepatic jaundice?
``` Sickle cell anaemia Thalassaemia Spherocytosis Incompatible blood transfusion Malaria Haemolytic anaemia ```
126
What are the characteristics of hepatic jaundice?
``` Increase in conjugated or unconjugated bilirubin Decreased faecal urobilinogen Increased urinary urobilinogen Pale stool Dark urine Increased ALT and AST ```
127
What are the causes of hepatic jaundice?
``` Gilberts Cirrhosis Viral hepatitis Alcoholic hepatitis Autoimmune hepatitis Drug induced hepatits ```
128
What are the characteristics of post hepatic jaundice?
``` Increased conjugated bilirubin Bilirubin in urine Decreased faecal urobilinogen No urobilinogen in urine Pale stools Dark urine Increased ALP, ALT, AST ```
129
What are the causes of post hepatic jaundice?
``` Gall stones Gall bladder carcinoma Pancreatic carcinoma Primary sclerosing cholangitis Pancreatitis Bile duct strictures ```
130
Epidemiology of bowel cancer
3rd most common UK cancer 2nd most common cause of cancer death 47/ 100 000 Higher in men than women
131
What are the risk factors for bowel cancer?
``` 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
Presentation of left sided colon cancer
``` colicky pain rectal bleeding bowel obstruction tenesemus mass in left iliac fossa early change in bowel habit ```
133
Presentation of right sided colon cancer
``` weight loss anaemia occult bleeding mass in right iliac fossa more advanced on presentation ```
134
What is the prognosis (5 year survival rate) for bowel cancer?
Stage 1 = T1/2 M0 N0 = 75% Stage 2 = nodal involvement = 60% Stage 3 = T3/4 - 50% Stage 4 = M1 6%
135
Describe hyperplastic polyps
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
Describe hamartomatous polyps
Occur sporadically Disorganised tumour like growths with mature cells Increased risk of developing colorectal cancer Pedunculated smooth surfaced red lesions <3cm in diameter
137
Describe adenomas in the colon
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
Outline FAP
``` 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
Describe hereditary nonpolyposis colorectal cancer
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
Outline the pathogenesis of adenocarcinoma
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
Describe the morphology of adenocarcinoma
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
What methods are used to view the GI tract?
``` Barium swallow/meal/follow through Barium enema Colonoscopy Endoscopy Abdominal ultrasound CT scan MRI ```
143
What should you think about when choosing a method of GI imaging?
``` Availability Patient tolerance Cost Risk of complications Most likely to answer clinical question ```
144
What are the single and double contrast used in barium radiology?
Single - lumen distended with barium Double - mucosa coated with barium and lumen distended with air
145
What are the limitations of barium swallow/meal?
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
What are the requirements for barium enema?
2 days starvation Strong laxative Barium into colon via rectal tube Colon distended with air or CO2
147
What are the benefits of double contrast barium enema?
Safe with low complication rate Well tolerated Complete examination Able to detect intrinsic and extrinsic disease
148
What are the limitations of DCBE?
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
What are the benefits of endoscopy?
Direct inspection of mucosa Detects early pathology Allows for biopsy or therapeutic procedure Identifies conditions not seen at DCBE
150
What are the limitations of endoscopy (gastric)?
``` 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
What are the common causes of upper GI bleeding?
``` 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
What are the common causes of lower GI bleeding?
``` Anal fissures Angiodysplasia Colitis Colonic carcinoma Colonic polyps Diverticular disease IBD Internal haemorrhoids ```
153
What is the Rockall score and what does it take into account?
Used to determine risk for endoscopy Age Shock Co-morbidity Predicts mortality
154
Describe fluid absorption in the gut
80% in small intestine | 80% of remaining 20% removed in large intestine
155
Describe the process of defaecation
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
Anatomy of the adrenal glands
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
What is the blood supply to the adrenal glands?
``` Superior suprarenal (from inferior phrenic artery) Middle suprarenal (abdominal aorta) Inferior suprarenal (renal arteries) ```
158
What is secreted from each area of the adrenal cortex?
Zona glomerulosa - mineralocorticoids (aldosterone) Zona fasciculata - glucocorticoids (cortisol) Zona reticularis - gonadocorticoids (androgens)
159
Describe the adrenal medulla?
Chromaffin cells in clusters around blood vessels | Produce adrenaline and NA