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Phase 2a > GI/Liver > Flashcards

GI/Liver Flashcards

1
Q

What are the two major causes of acute pancreatitis?

What is the pneumonic for other causes?

A

BIG TWO: Gallstones + Alcohol

I GET SMASHED - 
Idiopathic, 
Gallstone, 
Ethanol Abuse, 
Trauma, 
Steroids, 
Mumps, 
Autoimmune disease, Scorpion stings, Hyperlipidaemia & Hypercalcaemia, 
ERCP procedure, Drugs
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2
Q

What is the characteristic presentation of acute pancreatitis?
Symptoms?

A

Severe epigastric pain that radiates to the back

Weight loss, nausea/vomiting, shock

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3
Q

2 names of bruising signs in acute pancreatitis?

Why can hypocalcaemia occur?

A

Cullen’s sign (belly button bruise), Grey Turner’s sign (bruising along flank)

Hypocalcaemia (used up by fat necrosis - saponification)

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4
Q

Two major complications of acute pancreatitis?
How is acute pancreatitis managed?
How is it diagnosed? 2 out of 3 of what…

A

DIC & ARDS

Analgeisa, drainage of fluid, antibiotics if needed, rest

2 out of 3 of: Characteristic pain, raised serum amylase & lipase, abdominal CT scan

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5
Q

What is chronic pancreatitis? What is the most common cause?

Name two other causes

A

“Multiple bouts of acute inflammation leading to irreversible damage”

Most common cause: ALCOHOL

Autoimmune pancreatitis & cystic fibrosis

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6
Q

What is the characteristic presentation of chronic pancreatitis?
Signs based off of pancreatic insufficiency?

A

Similar presentation to acute:
Severe abdominal pain, epigastric pain radiating to the back, nausea/vomiting, anorexia
Malabsorption, weight loss, steatorrhoea (greasy + smelly stools), ADEK vitamin deficient

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7
Q

What is a pancreatic pseudocyst? Accounts for how much of pancreatic masses
What are two dangers of a pseudocyst doing?

A

A collection of fluid rich in pancreatic enzymes, blood and necrotic tissue.

Form 75% of all pancreatic masses

Can rupture or form an abscess

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8
Q

What is the cell type in the vast majority of pancreatic carcinoma?
Symptoms of pancreatic carcinoma?

Two signs of pancreatic carcinoma?

A

Epithelial cells lining ducts

Mid-epigastric pain radiates to mid or lower back, worse when lying flat
Nausea, vomiting, fatigue
Weight loss

Trousseau sign of malignancy - blood clots felt as small lumps under skin
Courvoisier sign - Gallbladder is enlarged & palpable & non-tender (unlike gallstones)

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9
Q

Name the risk factors of pancreatic carcinoma

What key antigen and enzymes would be raised in pancreatic carcinoma? Is this diagnostic?

What is a Whipple procedure?

A

Family history (BRCA2), Diabetes, Chronic pancreatitis, Liver cirrhosis, Smoking, Obesity, Red meat, Male, Over 65

CA19-9 antigen is elevated along with serum amylase and serum lipase (NOT DIAGNOSTIC)

A complex surgical operation used to remove the head of the pancreas, first part of the small intestine, the gall bladder and the bile duct

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10
Q

What is biliary atresia?

When would it present and what with?

A

Failure to form or early desturction of extrahepatic biliary tree

Present very early in life (within 3 months) with Jaundice

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11
Q

What is primary sclerosing cholangitis?

Two important GI conditions it is associated with?

A

Inflammation and scarring of the bile ducts both inside and outside the liver

Ulcerative colitis and Crohn’s

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12
Q

What does cholelithiasis mean?
Two types? More common?
Three reasons they occur?

A

Formation of gallstones

Cholesterol (70%) and bilirubin (30%)

  • Supersaturation
  • Decreased phospholipids or bile acids - Crohn’s and Cirrhosis
  • Stasis
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13
Q

Do cholesterol gallstones show up on X-ray?

What are the risk factors for cholesterol gallstones?

A

Generally no

Risk factors: 5 F’s: Female, Fertile, Fat, Fair, Forty

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14
Q

Do bilirubin/pigmented gallstones show up on X-ray?

What are the risk factors for bilirubin/pigmented gallstones? (2)

A

Generally yes

Risk factors:
Extravascular haemolysis, biliary tract infection

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15
Q

When do you treat gallstones?
What is the general symptoms of gallstones?
Two treatment options?

A

Only treat when symptomatic - often asymptomatic

Obstructive jaundice, colicky RUQ pain, nausea & vomiting

Only treated if symptomatic - cholecystectomy or bile acid dissolution therapy

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16
Q

What are the 5 key complications of cholelithiasis?

A

Biliary colic:
Stone lodged causing colicky RUQ pain

Acute & chronic cholecystitis:
Inflammation of the gallbladder wall

Ascending cholangitis:
Bacterial infection of bile ducts

Gallstone ileus:
Rupture and stone enters small bowel

Gallbladder carcinoma:
Increased chance with cholelithiasis

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17
Q

What is a positive Murphy’s sign?
Shows what condition?
Would differentiate from what other complication of gallstones?

A

Placing a hand at costal margic in RUQ - asking the patient to breathe deeply
Causing pain is positive

Acute cholecystitis

Differentiate from asecnding cholangitis

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18
Q

What condition are Rokitansky-Aschoff sinuses associated with?
What is porcelain gallbladder?

A

Chronic cholecystitis

Calcified gall bladder from chronic inflammation

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19
Q

What should be the texture of the liver normally? What does it become in cirrhosis? Why?

A

Should be smooth

Becomes bumpy - due to regenerative nodules from fibrosis

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20
Q

What cells cause fibrosis in the liver? Where do they occupy? Name one other function of these cells

A

Stellate cells
Peri-sinusoidal space
Store vitamin A

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21
Q

Name two main causes of cirrhosis?

3 other causes?

A

CHRONIC ALCOHOL & CHRONIC HEPATITIS

Autoimmune hepatitis
Iron or Copper overload
Other drug-related disease

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22
Q 
Complications of liver disease:
Portal HTN leads to... (ABCDE)
Increased oestrogen leads to (3)
Ammonia leads to?
Skin goes...?
Hand tremors are called...?
A 
Ascites
Bleeding (from varices)
Caput medusae
Diminished liver function - hypoalbuminaemia, coagulation issues
Enlarged spleen

Gynecomastia
Spider angiomata (more than 5)
Palmar erythema

Hepatic encephalopathy

Jaundice

Asterixis

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23
Q

What number defines portal HTN?

A

> 12 mmHg

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24
Q

What is Budd-Chiari syndrome?

A

A thrombus or tumour that obstructs venous flow in the liver towards the IVC

A rare cause of portal HTN

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25
Q

Flow-chart of non-alcoholic fatty liver disease?

Associated with what syndrome? So, link with?

A

Steatosis -> Steatohepatitis -> Fibrosis -> Cirrhosis

Metabolic syndrome, link with insulin resistance

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26
Q

Symptoms of fatty liver disease:
Often?
Significant?

A

Often asymptomatic or non-specific (fatigue and malaise)

Significant damage - hepatomegaly, pain, jaundice, ascities

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27
Q

What does AST and ALT stand for?
Which of them is specific to liver, which is also found in other tissues?
What does GGT and ALP stand for?

A

Alanine transaminase
Aspartate transaminase

ALT: specific to liver
AST: also in heart, skeletal muscle kidney, pancreas etc

Gamma glutamyl transferase
Alkaline phosphatase

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28
Q

Which of ALT and AST is normally higher?

High AST is often common with…

A

Normally ALT

High AST:
Alcoholic liver disease, Non-alcoholic fatty liver disease, cirrhosis

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29
Q

What level of fat is diagnostic for NAFLD?

A

> 5% abnormal fat content

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30
Q

What is alcohol converted into in the liver?
What enzyme?
Why is this a problem with excess conversion?

A

Acetaldehyde

Alcohol dehydrogenase

Requires conversion of NAD+ into NADH which increases fat production leading to steatosis

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31
Q

What is ascites?
3 different causes?
Can investigate by…?

A

Accumulation of fluid in the peritoneal cavity caused an abdominal swelling

Portal HTN (cirrhosis/Budd-Chiari), Heart failure, infections (TB)

Can investigate by taking fluid and testing (neutrophils, protein, cytology, amylase)

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32
Q

3 types of jaundice/icterus?
Brief explanantion?
Colour of urine and stools?

A

Obstructive (extrahepatic) - bile duct obstruction (dark urine, pale stools)

Hepatocellular (intrahepatic) - disease of liver cells
(dark urine, normal stools)

Haemolytic (prehepatic) - increased destruction of RBCs (urine and stools normal)

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33
Q

What DILI stand for?

What are the most common causes for this?

A

Drug Induced Liver Injury (DILI)

Paracetamol 50%, Idiosyncratic 15%
Also: antibiotics, CNS drugs, etc

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34
Q

What is the treatment for a paracetamol overdose?

How does it work?

A

N acetyl cysteine (NAC)

Provides cysteine for glutathione synthesis - which gets conjugated with toxic metabolic of paracetmol

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35
Q 
HAV:
How is it spread?
Acute or chronic?
DNA or RNA?
Envelope?
Classicaly acquired by?
A 
Faeco-oral route
Only acute (< 6 months)
RNA
No envelope
Travelers
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36
Q 
HBV:
How is it spread?
Acute or chronic?
DNA or RNA?
Envelope?
A

Blood, perinatal transmission, sex, IV
Acute (normally) + Chronic
DNA
Does have envelope

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37
Q 
HCV:
How is it spread?
Acute or chronic?
DNA or RNA?
Envelope?
A

Blood, perinatal transmission, sex, IV
Acute + Chronic (normally)
RNA
Does have envelope

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38
Q 
HDV:
How is it spread?
When does it occur (2 possibilities)m
DNA or RNA?
Envelope?
A

Blood, perinatal transmission, sex, IV
Co-infection with HBV or superinfection after HBV
RNA
Does have envelope

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39
Q 
HEV:
How is it spread?
Acute or chronic?
DNA or RNA?
Envelope?
Classicaly acquired from?
A 
Faeco-oral route
Only acute (< 6 months)
RNA
No envelope
Contaminated water or undercooked seafood
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40
Q

What other two viruses can cause hepatitis?

A

EBV and CMV

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41
Q

What is the key marker of infection in hepatitis?

When does it disappear?

A

Hepatitis B surface antigen (HBsAG)

Only disappears if resolved

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42
Q

What does IgM (core) represent in hepatitis?
What does IgG (core) represent in hepatitis?
What does IgG (surface) represent in hepatitis?

A

IgM for HBcAB represents acute stage hepatitis

IgG for HBcAB represents chronic stage hepatitis

IgG for HBsAG represents resolution or immunization

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43
Q

Where will primary hepatocellular tumour normally spread to?
What do secondary liver cancers often come from? (4)
What is more common?

A

Lungs

Colon, Pancreas, Breast, Lung

Secondary is more common

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44
Q

What are common causes of hepatocellular carcinoma:
Most common? - which of these two is more dangerous?
Big category?
How can mouldy food be a problem?

A 
Hep B (more dangerous due to being a DNA virus)
Hep C

Cirrhosis - alcoholic hepatitis, haemochromatosis, PBC, alpha1-antitrypsin deficiency

Aflatoxins due to aspergillus moulds in foods. Affects p53 gene

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45
Q

What is the name of the stool chart?
T1 and T2 = ?
T3 and T4 = ?
T5, T6, T7 = ?

A

BRISTOL Stool Chart
1, 2 = constipation
3, 4 = normal
5, 6, 7 = towards diarrhoea

46
Q

What is gastroenteritis?
Main symptom
Other symptoms?

A

Same as “infective diarrhoea”
MAIN = DIARRHOEA
Other:
vomiting, abdominal pain, fever, fatigue, dehydration

47
Q

Infectious diarrhoea causes:
VIRUS - percent, examples
BACTERIA - percent, examples
PARASITES - percent, example

In hospitals, risk is?

A
  • Viruses (50-60%): Norovirus, Rotavirus, Astrovirus, Adenovirus
  • Bacteria (30-40%): Salmonella (non-typhoidal, typhoidal, paratyphoidal), Campylobacter, E. Coli, Shigella, S. Aureus, C. Difficle, V. Cholerae
  • Parasites (>2%): Giarda, Cryptosporidium

Hospitals - risk of C. diff

48
Q

What are the drugs that frequently cause a C. difficle diarrhoea? (3)
What is the main two treatments?
How is it diagnosed?

A

Cephalosporins, Co-amoxiclav, Clindamycin

Metronidazole, Vancomycin

Using a stool sample - toxin test

49
Q

What population does autoimmune hepatitis normally occur in?

Ratio of female to male?

Association with what two points?

ALT and AST

A

Common in young women

female:male = 4:1

HLA-DR3 and HLA-DR4, and other autoimmune disease

Both elevated, ALT > AST

50
Q

What does PBC stand for?
Very basic pathophysiology?
Much more common in…?

A

Pimrary biliary cholangitis or Primary biliary cirrhosis

Autoimmune attack on bile duct

Much more common in females

51
Q

What is the normal function of alpha-1 antitrypsin?
Therefore what does a deficiency lead to?
Affects which two orgnas?
How does it affect these?

A

A1AT normally inactivates elastase - therefore, lots of elastase breakdown with a deficiency

Lungs - can cause COPD
Liver - cirrhosis and liver failure

52
Q 
Wilson's disease:
What is it? 
What type of defect in what gene?
2 roles of this gene?
4 points that this affects?
A

Excess copper in the body

Autosomal recessive defect in the ATP7B gene

ATP7B enzymes binds Cu to apoceruloplasmin and excretes it into bile as well

Basal Ganglia - movement
Cerebral cortex - dementia
Cornea - Kayser-Fleischer rings
Liver - hepatitis, cirrhosis and liver failure

53
Q

What is haemochromatosis?
Primary and Secondary?
How can it damage tissues?

A

Too much absorption of iron into the blood

Primary - gene mutation
Secondary - frequent blood transfusions

Forms free radicals via the Fenton reaction

54
Q

List the tissues damaged in haemochromatosis and what the damage leads to?

A

Liver - cirrhosis, increased risk of cancer

Pancreas - T1DM and malabsorption

Heart - bronze pigmentation

Pituitary gland - amenorrhea and testicular atrophy

Joints - degenerative joint disease

Skin - Cardiomyopathies

55
Q

Two types of peritonitis?

Basic symptoms?

A

Localised - inflammation of an underlying organ

General - direct irritation of the peritoneum (more serious)

Dull pain that becomes sharp
Pain worse on coughing or moving
Systemic symptoms and generally unwell

56
Q

Causes of peritonitis? (5) Bacteria - (3)

A

A (Appendicitis)

E (Ectopic pregnancy)

I (Infections) -
E. Coli, Enterococci, Streptococci

O (Obstruction)

U (Ulcer)

57
Q

How would oesophageal cancer present?
Would it present early or late?
Specific SSC symptom?

A

Generally presents late

Progressive dysphagia, weight loss, haematemesis, chest pain

SSC: hoarse voice and cough

58
Q

Two types of oesophageal cancer?
Where does each usually occur?
What is more common worldwide? What is more common in the west?

A

ADENOCARCINOMA
Normally lower 1/3rds
Most common type in the west

SQUAMOUS CELL CARCINOMA
Upper 2/3rds
Most common type worldwide

59
Q

Oesophageal cancers:
What is the major risk factor for adenocarcinoma?

What are the risk factors for SSC - principle?
Special syndrome?

A

ADENOCARCINOMA:
GORD causing metaplasia in the oesophagus (Barrett’s)

SSC: (irritation)
Alcohol, tobacco, very hot tea, achalasia (LES can’t relax - food stuck), oesophageal webs

Plummer-Vinson Syndrome:
iron deficiency anaemia, glossitis, (big red tongue)
cheilosis, (side of mouth inflammation)
oesophageal webs/rings

60
Q

How do you differentiate between a benign and malignant ulcer? (3 points)

A

Benign ulcers: small, punched out, no pile up of mucosa at edge

Malignant ulcers: large, irregular, pile up of mucosa at edge

61
Q

Presentation of gastric carcinoma?
Risk factors?
3 rare signs?
What lymph node?

A

Presents late - weight loss, abdominal pain, dyspepsia and early satiety, nausea

Risk factors:
Family history, increases with age, alcohol, obesity, smoking

Acanthosis nigricans (thicken and darkening of skin at axilla
Leser-Trelat sign (brownish spots all over the skin)
Polyarteritis nodosa

Often spreads to left supraclavicular node (Virchow’s node)

62
Q

Two types of gastric adenocarcinoma?

Which is more common?

A

INTESTINAL (more common) - large, irregular ulcer with heaped up margins

DIFFUSE (less common) - undifferentiated, worse prognosis

63
Q

Intestinal gastric carcinoma:
Mainly associated with?
Where does it often occur?
Other risk factors?

A

Mainly associated with H. pylori
Less curvature of antrum

Risk factors: any intestinal metaplsia, nitrosamines (link to Japan), blood type A

64
Q 
Diffuse gastric carcinoma:
Association with what mutation?
Where does it occur in the stomach?
What cells are seen?
What is linitis plastica?
A

CDH1 mutation
Anywhere in stomach
Signet ring cells
Thickening of stomach wall

65
Q

3 other types of gastric cancer, other than adenocarcinoma?

A

Lymphoma in MALT
Carcinoid tumour - G-cell
Leiomyosarcoma - smooth muscle cells

66
Q

What is Mallory-Weiss Syndrome?
What is the cause? Link to…
Main symptom?

A

Bleeding from a tear in the mucosa at the junction of the stomach and the oesophagus

Severe vomiting - often alcohol or bulimia

Painful haematemesis

67
Q

Two complications of GORD?
What are the main risk factors?
What rare 3 conditions could also cause it?

A

Barrett’s oesophagus and oesophageal stenosis

Risk factors:
Obesity, fat-rich diet, caffieine, alcohol, medications

Rare:
Hiatal hernia (stomach slides up through diaphragm)
Sclreoderma (muscle in LES is replaced with connective tissue)
Zollinger-Ellison Syndrome (gastroma which secretes gastrin)

68
Q

Symptoms of GORD? - will worsen when….

3 investigations for diagnosis?
3 points on management?

A

Pyrosis (heartburn), Regurgitation, Stenosis, Chronic cough or hoarseness
WORSE WHEN LYING DOWN

pH monitoring, X-RAY w/ barium, Endoscopy w/ biopsy

Lifestyle changes - losing weight, avoiding certain foods (spice/fat/chocolate/coffee/alchol), keep head elevated during sleep, don’t lie down after a meal
Antacids - neutralise acidity
PPIs (+ H2 receptor blockers if needed)

69
Q

Two types of gastritis?

Two subtypes of… (which of these is more common)

A

Acute and Chronic

Chronic - autoimmune or H. pylori (more common)

70
Q

Risk factors for acute gastritis?
Curling ulcer = ?
Cushing ulcer = ?
3 complications?

A

NSAIDs, shock, chemotherapy, heavy alcohol

Curling = severe burns/trauma
Cushing = increased intracranial pressure (Vagal stimulation)

Superficial inflammation, erosion (loss of epithelium), ulcer (loss of mucosa)

71
Q

Autoimmune chronic gastritis:
Where does it occur? (what cells does it attack?)
Associated with what type of anaemia?
Increases risk of?

A

Often occurs on the body and fundus - attack on gastric parietal cells

Pernicious anaemia - lack of intrinsic factor

Increased risk of gastric adenocarcinoma

72
Q

Chronic H. pylori gastritis:
Where does it usually occur?
Increases risk of 3 things?
Treatment?

A

Antrum is common site

Increased risk of ulceration, gastric adenocarcinoma and MALT lymphoma

Treatment: triple therapy (2 antibiotics and 1 PPI)
Amoxicllin, Metronidazole, Esomeprazole

73
Q

Two types of peptic ulcer disease: which is more common?

A 
proximal duodenum (90%)
distal stomach (10%)
74
Q 
What is the normal cause of a duodenal ulcer? Very rare other cause?
Does it worsen or improve with meals?
What happens to the Brunner glands?
Anterior or posterior usually?
Posterior complications (2)
A

H. pylori - rarely due to ZE syndrome (gastroma)

Improve with meals

Brunner glands will hypertrophy - more mucous for protection

Normally anterior

Acute pancreatitis and gastroduodenal artery affected

75
Q 
What is the normal causes of a gastric ulcer? 
Does it worsen or improve with meals?
Normally benign or malignant?
Where does it usually occur?
Complication due to this position?
A

Usually due to H pylori, but also NSAIDs and bile reflux

Worsens with meals

Normally benign - small, punched out, no pile up

Normally on lesser curvature of antrum

Risk of left gastric artery bleed

76
Q

Normal presentation of peptic ulcer disease?
Main?
3 others
Weight loss vs Weight gain

A

Epigastric pain - aching or burning

Also - bloating, belching, vomiting/nausea

Weight loss: gastric
Weight gain: duodenal

77
Q

Genes related to coeliac disease? Significance of these genes in practice?
What is the main antibody tested for?
What are the other two antibodies?
Note if these come back negative

A

HLA-DQ2 and HLA-DQ8 - high negative predictive value

IgA-tTG
IgA: endomysium & gliadin

Can be IgA deficient - test IgG instead

78
Q

Usual presentation of coeliac disase:
Children & Adults

Association with what dermatological condition?

A

Children: abdominal distension, diarrhoea and failure to thrive

Adults: chronic diarrhoea and bloating with gluten association

DERMATITIS HERPETIFORMIS (IgA deposition)

79
Q 
Pathophysiology of coeliac:
What component of gluten?
First step?
Moves into?
Second step?
Leads to two negative points...
A 
Gliadin
Gliadin is bound to IgA
Moves into lamina propria
Deamidated by tTG
Inflammation - 
B cells form antibodies
Inflammatory cytokines damage endothelium
80
Q

2 main histological changes in coeliac disease?
Where does it occur most?
Can a refractory period occur? Why? (2)

A

Biopsy: flattening of villi, hyperplasia of crypts,

Most prominent in duodenum

Refractory disease may be present despite good dietary control - indication of small bowel carcinoma (rare) or T-cell lymphoma

81
Q

How does IBS present?
Pathological changes?
2 risk factors?

A

Relapsing abdominal pain and change in bowel habits - relieved with defecation

No identifiable pathological changes

Gastroenteritis (norovirus, rotavirus), Stress

82
Q

What is the two points of treatment for IBS?

A

Modify fibre for constipation or diarrhoea

Reduces FODMAPs (apples, cherries, peaches, artificial sweeteners, legumes, green veg)

83
Q

What is the classical presentation of IBD?
Which quadrant in UC vs CD?
Which is more common?
Which is autoimmune, whcih is immune-related?

A

Teen to 30 year old with recurrent bouts of diarrhoea and abdominal pain

UC: rectum - left lower quadrant, AUTOIMMUNE
CD: ileum - right lower quadrant, IMMUNE-RELATED

Ulcerative colitis is more common than Crohn’s disease

84
Q 
Ulcerative colitis:
What layers of GI tract?
Distribution? (2)
Histological hallmark?
Loss of ... ? Called ... on x-ray?
Smoking is ... ?
A

Mucosa (+ submucosa) only (ulcer)

Begins in the rectum and extends proximally up to caecum (continuous)

Crypt abscess - histology hallmark

Loss of haustra (lead pipe)

Smoking is protective

85
Q

Ulcerative colitis:
2 associations?
3 complications?
3 medications?

A

Association: Primary sclerosing cholangitis and p-ANCA (vasculitis links)

Complications: toxic megacolon, dysplasia & carcinoma

Anti-inflammatory drugs - sulfasalazine, mesalazine
Immunosuppressants - corticosteroids
Biologics - infliximab, golimumab, adalimumab

86
Q 
Crohn's disease
What layers of GI tract?
Distribution? (2)
Histological hallmark?
Appearance on endoscopy called?
Smoking is ... ?
Genetic link?
A

Transmural (full thickness)

Anywhere from mouth to anus with skip lesions (most common is terminal ileum & colon)

Granulomas

Cobblestone mucosa

Smoking increases risk of CD

NOD2 gene - family history is important

87
Q

Crohn’s disease:
Any associations?
Complications?
3 medications?

A

AS, sacroiliitis, migratory polyarthritis, erythema nodosum, uveitis

Malabsorption with nutritional deficiency, kidney stones, fistula, carcinoma (if colonic disease is present)

Anti-inflammatory drugs
Antibiotics - control gut bacteria and reduce immune response
Immunosuppressants (corticosteroids - prednisolone)

88
Q

What are the two important points about faecal calprotectin in practice?

A

Correlation with on-going or up-coming flare-ups

High negative predictive value - can exclude IBD

89
Q

What is the most common cause for appendicitis:
Adults?
Children?
Two others?

A

Adult - fecalith (poo stone)
Children - lymphoid hyperplasia

Undigested seeds and pinworm infection

90
Q

How does appendicitis present?
Initally…
Then…
What is it ruptures…

A

Initially:
Periumbilical pain, fever and nausea

Pain will localise to the right lower quadrant at McBurney’s point

Rupture results in peritonitis that presents with guarding and rebound tenderness

91
Q

Two complications of acute appendicitis?

What is the treatment of appendicitis?

A

Rupture
Periappendiceal abscess

Appendectomy and abscess drained if present

92
Q

What are the two types of polyps?
Which can form adenocarcinoma of the colon?
What is removed in colonoscopy?

A

Colonic:
Hyperplastic polyp - benign with no malignant potential

Adenomatous:
Benign - but pre-malignant

Both are removed in colonscopy - can’t distinguish between them

93
Q

What is the technical name of colorectal cancer?
Where is it most common?
Where does it have a worse prognosis?
Link to what heart disease?

A

Adenocarcinoma
More common in the distal colon
Worse prognosis in proximal colon
Link to S. bovis endocarditis

94
Q

Two types of colorectal cancer cells?
What gene mutation?
Appearance?

A

Adenomatous: APC mutation, cells look normal

Serrated: DNA repair gene mutation, saw-tooth appearance

95
Q

What are the two staging systems for colorectal cancer?

Explain one of these?

A

TNM & Duke’s

A: Mucosa only
B: Full layer
C: Full layer and 1 lymph node close to the bowel
D: Metastasis to liver, lungs or bones

96
Q

Risk factors for colorectal cancer:
Three non-modifiable?
Three modifiable?
Two specific disorders?

A

Increasing age & IBD & genetics

Obesity, smoking, lack of fiber

Familial adenomatous polyposis (FAP)
Hereditary non-polyposis (HNPCC) - also leads to ovarian and endometrial cancer

97
Q

Symptoms of cancer:
Initially…
Normal in ascending?
Normal in descending?

A

Initially asymptomatic

Asecnding: pain & weight loss, later diagnosis, anaemia from bleeding

Descending: bowel obstruction, earlier diagnosis, doesn’t bleed as much, makes a ring

98
Q

Colorectal cancer:
Tumour marker? Note on it?
Treatment?

A

Tumour marker CEA - not very specific, need colonoscopy

Surgery & chemotherapy

99
Q

What is the difference between ischaemic colitis and mesenteric ischaemia?
Which is more common?
Where does ischaemic colitis most commonly occur and why?

A

ISCHAEMIC COLITIS = large bowel (colon) - more common
MESENTERIC ISCHAEMIA = small bowel

Splenic flexure - water-shed area

100
Q

What is a volvulus?
3 types and who is most common in?
What is the major complication?

A

“Twisting of intestine and supporting mesentery leading to bowel obstruction”

Sigmoid - common, pregnancy
Caecal - young adults
Midgut - small babies and children

Major complication = infarction

101
Q

Two types of ischaemic GI aetiologies?
Examples?
What layers wil each infarct?

A

OCCLUSIVE: thrombus, thromboembolism, tumour, hernia, volvulus, intussuception
TRANSMURAL infarct

NON-OCCLUSIVE (systemic decrease - hypovolemia, low cardiac output)
MUCOSAL infarct

102
Q

How does ischaemic colitis often present:
Initial:
Infarction:

A

Post-pranidal pain and weight loss

Severe pain and bloody diarrhoea

103
Q

What does SBO stand for?
What are the two main causes?
More or less common than LBO?

A

Small bowel obstruction
Previous surgery - adhesions (60%)
Crohn’s disease (25%)
More common than LBO

104
Q

What does LBO stand for?
What are the two main causes?
More or less common than SBO?

A 
Large bowel obstruction
Colorectal malignancy (90% in west)
Volvulus (more common in Africa)
105
Q

Difference in presentation of LBO vs SBO:
Pain?
Vomiting?

A

Pain:
colicky in SBO
constant in LBO

Vomiting:
earlier in SBO
later in LBO - more faecal like

106
Q

What are diverticula?
Where is it more common globlally?
Having diverticula is called?
Major complication is called?

A

Out-pouches of the intestinal wall

More common in the west

Diverticulosis

Diverticulitis - inflamed

107
Q

Where do diverticula normally occur? Why?

Difference between a true or false/pseudo diverticula? Which of these is more common?

A

Normally occur in colon - specifically the sigmoid colon

Smallest lumen - highest pressure on intestinal wall

True - all layer out-pouched
False - only mucosa and submucosa

108
Q

What are the risk factors for diverticulosis? (4)

A

Low fibre, increased age, obesity, Marfans & Ehlers-Danlos

109
Q

How does diverticulosis normally present?
Two points?
How does diverticulitis present in contrast? (4)

A 
Asymptomatic
Possibly bleeding (haematochezia -fresh), vague abdominal pain

Left lower quadrant pain, tenderness, abdominal distention and fever

110
Q

Two complications of diverticulosis?
Two causes of first?
Two examples of second?

A

DIVERTICULITIS - inflamed diverticula
Erosion of wall from high pressure
Lodged fecalith - often pain left lower quadrant, without bleeding

FISTULA
Colovesicular - bladder
Colovaginal - vagina

Phase 2a (9 decks)

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