Gastro

Question 1

Define coeliac disease

Answer 1

A systemic autoimmune disease triggered by dietary gluten peptides found in wheat, rye, barley, and related grains

Atrophy of the intestinal villi, hypertrophy of the crypts and increased numbers of lymphocytes in the epithelium and lamina propria

Leads to GI symptoms and malabsorption

Question 2

Explain the aetiology / risk factors of coeliac disease

Answer 2

Aetiology:
The requirement for DQ2 (95% of coeliac) or DQ8 (the rest) (both MHCII variants) is a major factor in the genetic predisposition to coeliac disease. However, most DQ2- or DQ8-positive people never develop coeliac disease despite daily exposure to dietary gluten.
Hypothesised environmental factors include initial exposure to gluten peptides, GI infection (mimicry) and damage to the intestinal-epithelial barrier leading to abnormal exposure of the mucosa to gluten peptides

• Loss of immune tolerance to peptide antigens derived from prolamins (e.g gliadin, secalin etc.) is central abnormality.
• These peptides are resistant to human proteases, so persist into the small intestine
• They get through to intestinal submucosa in coeliac patients, trigger innate and adaptive immune response
• Innate: stimulate IL-15
• Adaptive: tTG deamidates gliadin, allowing high affinity binding only to DQ2 and DQ8 HLA found on APCs and Th cells.
• This leads to Th1-derived cytotoxic T lymphocytes (–> villous atrophy and crypt hypertrophy) AND Th2 triggers plasma cell maturation and anti-gliadin and anti-tTG Ab production.

Risk factors (strong):
family history of coeliac disease
immunoglobulin A deficiency
type 1 diabetes
autoimmune thyroid disease

Question 3

Summarise the epidemiology of coeliac disease

Recognise the presenting symptoms of coeliac disease

Answer 3

1% of population, can present at any age (peaks childhood and 50-60y/o)

Stinking stools/steatorrhoea;

Diarrhoea;

Abdo pain and bloating;

nausea &

vomiting;

and failure to thrive,

to iron-deficiency anaemia or osteoporosis.

1/3 asymptomatic

RECURRENT MOUTH ULCERS!

Question 4

Recognise the signs of coeliac disease on physical examination

Answer 4

Signs of anaemia

angular stomatitis

weight loss

RASH (intensely itchy)!!!! Dermatitis herpetiformis (vesicular rash, chronic AI skin condition ass with coeliac disease, often on elbows)

Apthous ulcers

Clubbing

Question 5

Identify appropriate investigations for coeliac disease and interpret the results

Answer 5

Bloods: Reduced Hb (causes iron deficiency anaemia), b12, ferritin.

FIRST LINE INVESTIGATION: 
Anti-transglutaminase is single perferred test (but is an IgA Ab, so check IgA levels to exclude subclass deficiency)

Anti-endomysial (95% specific unless patient is IgA deficient) is most specific

Anti-gliadin antibodies

THEN,

DEFINITIVE DIAGNOSTIC: OGD and duodenal biopsy. The classic histological
appearance of bowel affected by coeliac disease is the presence of ‘subtotal villous
atrophy with crypt hyperplasia’.

Where doubt persists, hla dq2 and dq8 genotyping may help.

Question 6

Generate a management plan for coeliac disease

Answer 6

1. Referral to dieticians for gluten free diet advice

Lifelong gluten-free diet—patients become experts. Rice, maize, soya, potatoes, and sugar are ok. Limited consumption of oats (≤50g/d) may be tolerated in patients with mild disease.

Gluten-free biscuits, flour, bread, and pasta are prescribable.

Monitor response by symptoms AND repeat serology! (If coeliac disease is not getting better on a gluten free diet it is nearly always because the patient is not being strict enough about their diet and the TTG is a good way to screen for this without putting them back through the OGD and biopsy.)

2. Referral for gastroscopy and duodenal biopsy
3. Screening of 1st degree relatives!
4. Bone density scan (osteopaenia)

Question 7

Summarise the prognosis for patients with coeliac disease

Answer 7

higher overall mortality than in the general population.

Question 8

Summarise the complications for patients with coeliac disease

Answer 8

higher overall mortality than in the general population.

Anaemia; dermatitis herpetiformis (ohcs);

osteopenia/osteoporosis (lack of absorption of calcium, vit D, vit K)

hyposplenism (offer ‘flu and pneumococcal vaccinations);

gi t-cell lymphoma (rare; suspect if refractory symptoms or ↓weight);

↑risk of malignancy (lymphoma, gastric, oesophageal, colorectal)…Celiac disease (CD) is associated with intestinal lymphoma and other forms of cancer, especially adenocarcinoma of the small intestine, of the pharynx, and of the esophagus.

neuropathies.

Question 9

Define alcoholic hepatitis

Answer 9

Inflammatory liver injury caused by chronic heavy intake of alcohol

Question 10

Explain the aetiology / risk factors of alcoholic hepatitis

what diseases is it part of
(histopathalogical features)

Answer 10

Part of a spectrum of ARLD:
o Alcoholic fatty liver (steatosis)
o Alcoholic hepatitis
o Chronic cirrhosis

Steatosis happens when lack of NAD+ and increased NADH (due to the alcohol metabolism to acetaldehyde) mean there is less fat metabolism and increased fat production in the liver= fatty changes/steatosis. On histology you see the circles of fat.

Alcoholic hepatitis occurs because there is a build up of ROS (due to metabolism of alcohol). The ROS can damage DNA and proteins too. The acetaldehyde can also form adducts with macromolecules like cell membrane, enzymes etc. Acetyaldehyde adducts can be recognised by your immune system, causing neutrophil infiltration. There are mallory bodies on histology, which are located in the cytoplasm and are damaged intermediate filaments

DEFINING HISTO FEATURES FOR ALCO HEP:

• liver cell damage
• inflammation
• fibrosis

ASSOCIATED HISTO FEATURES FOR ALCO HEP:

• fatty change
• mega mitochondria

• Histopathological features of alcohol hepatitis:
o Centrilobular ballooning
o Degeneration and necrosis of hepatocytes
o Steatosis – fatty change
o Neutrophilic inflammation
o Cholestasis – condition in which bile cannot flow from liver to the duodenum
o Mallory-hyaline inclusions (eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments)
o Giant mitochondria

Question 11

Summarise the epidemiology of alcoholic hepatitis

Answer 11

In long-term heavy alcohol consumers, about 90% to 100% develop fatty liver, 20% to 35% develop alcoholic hepatitis, and 8% to 20% develop alcoholic cirrhosis.

The risk of ALD is at least 2 times higher in patients who are overweight

Question 12

Recognise the presenting symptoms/signs of alcoholic hepatitis

Answer 12

General ARLD symptoms:
Fatigue, anorexia, weight loss, jaundice, fever, N&V, RUQ discomfort

In advanced liver disease:
Abdo distension and weight gain (ascites), asterix, leg swelling

on examination:
Signs of portal HTN +
ascites, splenomegaly, venous collateral circulations

Question 13

Identify appropriate investigations for alcoholic hepatitis and interpret the results

Answer 13

Bloods:

1. LFTs: AST, ALT, Alk Phos, bili, protein, albumin, GGT
2. FBC
3. Basic metabolic panel (Na+, K+, Cl-, HCO3-, urea, creatinine)
4. Coagulation profile (PT, INR)

Imaging:

1. Ultrasound should be performed among patients with harmful alcohol use, as it helps diagnose alcoholic fatty liver disease in patients with hepatic steatosis.
2. USS/CT of abdo useful to exclude cholecystitis, biliary obstruction and liver mass
3. Liver biopsy only indicated in patients with atypical presentation to evaluate co-existing liver disease like haemochromatosis, AI hepatitis or if it is very very severe

Question 14

Generate a management plan for acute management of alcoholic hepatitis

Acute management:
-Nutrition, electrolyte, ascites, hepatorenal syndrome?

Answer 14

Acute:

• Thiamine, vit C and other multivitamins (initially parenterallly)
• Monitor and correct K+, Mg2+ and glucose
• Treat encephalopathy with oral lactulose and phosphate enemas
• Treat ascites with spironolactone with or without frusemide (furosemide) or therapeutic paracentesis.
• Glypressin and N-acetylcysteine for hepatorenal syndrome.

Continue nutritional support with eneteral nutrition ASAP (nasogastric tube). Protein restriction only in encephalopathy.

Steroids reduce short term mortality in severe alcogholic hepatitis patients

[SEE ALCOHOL DEPENDENCE FOR LONG TERM MANAGEMENT)

Question 15

Identify the possible complications of alcoholic hepatitis and its management

Answer 15

Hepatic encephalopathy 
Coagulopathy 
GI bleeds
Portal HTN
Hepatorenal failure
HCC 
Sepsis

Question 16

Summarise the prognosis for patients with alcoholic hepatitis

Answer 16

Alcoholic fatty liver (steatosis) usually reverts to normal with alcohol

The 5-year survival rate for people with cirrhosis who stop drinking is about 90%, compared with 70% of those who do not stop drinking. However, for late-stage cirrhosis (e.g., jaundice, ascites, or gastrointestinal bleeding), the survival rate is only 60% for those who stop drinking and 35% for those who do not.abstinence

Question 17

How is alcohol metabolised in the liver

Answer 17

Alcohol is metabolised mainly in the liver, through 2 main pathways: alcohol dehydrogenase and cytochrome P-450 2E1.

Question 18

Why might ALT/AST be normal in advanced liver disease

Answer 18

AST and ALT can be normal either in the absence of significant liver inflammation (a reassuring sign) or in advanced cirrhosis in which there are few viable hepatocytes left to produce the transaminases (a sign of end-stage disease).

Question 19

Which transaminase is usually raised higher in ARLD

Answer 19

AST level is almost always elevated (usually above the ALT level). The classic ratio of AST/ALT >2 is seen in about 70% of cases.

Question 20

The presence of which cell type is prognostic in severe alcoholic hepatitis

Answer 20

The presence of polymorphonuclear cells on liver biopsy may be prognostic for survival of patients with severe alcoholic hepatitis

Question 21

Which drugs are used to treat alcohol withdrawal syndrome

Answer 21

Benzodiazepines are the most commonly used drugs to treat AWS

Long acting protect against seizures and deliurum,

Shorter acting safer in older adults/those with hepatic dysfunction

Question 22

How are liver transplants decided

Answer 22

MELD score

Question 23

…..

Answer 23

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Question 24

……….

Answer 24

……….

Question 25

...........

Answer 25

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Question 26

# Define portal HTN - What is portal vein formed of - Normal pressure in the portal vein, what about in portal HTN - 4 common sites of porto-systemic anastamoses - How to distinguish rectal varices from haemarrhoids

Answer 26

Portal veins formed by joining of the splenic with the superior mesenteric vein Normal pressure is 5–8 mmHg with only a small gradient across the liver to the hepatic vein, in which blood is returned to the heart via the inferior vena cava If pressure rises to 10-12mmHg, the compliant venous system dilates and collaterals form within the systemic venous system. The main sites of collaterals are the gastro-oesophageal junction, rectum, left renal vein, diaphragm, retroperitoneum and the anterior abdominal wall via the umbilical vein. The collaterals at the gastro-oesophageal junction (varices) are superficial and tend to rupture. Rectal varices are found frequently (30%) if looked for and can be differentiated from haemorrhoids, which are lower in the anal canal.

Question 27

Explain aetiology/risk factors of portal HTN

Answer 27

- Liver injury, fibrogenesis and activated myofibroblasts increase resistance to flow, leading to portal HTN. This can happen in pre-cirrhotic and cirrhotic livers. - The hyperdynamic circulation of cirrhosis causes peripheral and splanchnic vasodilation (-->splenomegaly and ascites), and sodium retention (related to ascites) increases plasma volume expansion Causes: Prehepatic: portal vein thrombosis Intrahepatic: Presinusoidal-schistosomiasis/sarcoidosis Sinusoidal- chirrhosis Postsinusoidal- venoocclusive disease, budd-chiari syndrome Posthepatic: Right heart failure, constrictive pericarditis, IVC obstruction

Question 28

Summarise epidemiology of portal HTN

Answer 28

...

Question 29

Recognise presenting symptoms of portal HTN

Answer 29

Patients are often asymptomatic, the only clinical evidence being splenomegaly, although features of chronic liver disease may exist GI haemmorahage may be the initial presenting symptom Those patients with more advanced liver disease often present with ascites, hepatic encephalopathy , jaundice, coagulopathy, or spider angiomata. splenomegaly and dilated abdominal wall veins

Question 30

Recognise the signs of portal HTN on physical examination

Answer 30

caput medusae, splenomegaly, edema of the legs, and gynecomastia

Question 31

Identify appropriate investigations for portal HTN and interpret the results Gold standard investigation

Answer 31

Clinical diagnosis can be made in the setting of end-stage liver disease and in the presence of ascites and/or varices Splenomegaly can result in sequestration of platelets from the systemic circulation, and low platelet counts may be the earliest abnormal laboratory finding. Imaging: Duplex doppler ultrasonography-provides specifics regarding the direction and velocity of portal flow. CT/MRI not that useful. Pressure measurement studies generally not indicated (The gold standard for determining if there is portal hypertension is obtaining a hepatic venous pressure gradient measurement, where a catheter is inserted inside the inferior vena cava, and then inside the portal vein to measure the difference between both pressures.) Endoscopic diagnosis (in patients with acute gastrointestinal hemorrhage after initial resuscitation)

Question 32

Generate a management plan for portal HTN i. Ascites ii. Acute variceal bleed.

Answer 32

Treatment of portal hypertension is aimed at prevention of complications. The main goal of therapy is to decrease portal pressures 1. Ascites. Diuretics (spironolactone and furesomide). Restrict sodium to <2g/day (or restrict fluid if hyponatraemia). Monitor weight. Therapeutic paracentesis with IV human albumin if difficult to control 2. Varices. Medical. Any upper GI bleed: ABC, IV access, fluids, G&S, cross match blood, OGD. For variceal bleed you need to give Abx (CEFTRIAXONE or CIPROFLOXACIN) and TERLIPRESSIN OR VASOPRESSIN OR OCTREOTIDE too. Then, within 12 hrs do OGD (once haemodynamically stable) to perform endoscopic variceal ligation (EVL)= banding. Sclerotherapy 2nd line if EVL not possible A TIPS should then be performed in high risk patients 72hrs after EVL. If it's not performed, the patient should be put on a beta blocker (nadalol/propanalol) after the vasoactive drug has been stopped. Nonsurgical Transjugular Intrahepatic Portal-Systemic Shunt (TIPSS)- radiologic procedure in patients who have had recurrent bleeding despite medical or endoscopic management. Contraindicated in severe liver dysfunction, renal failure and heart failure AT ANY STAGE, IF THE BLEEDING IS UNCONTRLLABLE, USE BALLOON TAMPONADE OR SELF EXPANDING METAL MESH STENT

Question 33

Identify the possible complications of portal HTN and its management

Answer 33

Bleeding varices, ascites, gastropathy, spenomegaly,

Question 34

Summarise the prognosis for patients with portal HTN

Answer 34

Variceal haemorrhages have a 1-year mortality of 40%

Question 35

# Define acute pancreatitis (mild vs severe)

Answer 35

An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems. Mild: Associated with minimal organ dysfunction and uneventful recovery. Severe: Associated with organ failure and/or local complications such as necrosis, abscess or pseudocyst

Question 36

Explain the aetiology / risk factors of acute pancreatitis

Answer 36

Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation. Most common: Gallstones, alcohol (80% cases). Others: Drugs (e.g. steroids, azathioprine, thiazides, valproate), trauma, ERCP or abdominal surgery, infective (e.g. mumps, EBV, CMV, coxsackie B, mycoplasma), hyperlipidaemia, hyperparathyroidism, anatomical (e.g. pancreas divisum, annular pancreas), idiopathic. Or you can use the mnemonic I: idiopathic G: gallstones, genetic - cystic fibrosis E: ethanol (alcohol) T: trauma S: steroids M: mumps (and other infections)/malignancy A: autoimmune S: scorpion stings/spider bites H: hyperlipidaemia/hypercalcaemia/hyperparathyroidism (metabolic disorders) E: ERCP D: drugs (tetracyclines, furosemide, azathioprine, thiazides and many others)

Question 37

Summarise the epidemiology of acute pancreatitis

Answer 37

Common. Annual UK incidence 10/10 000. Peak age is 60 years; in males, alcohol-induced is more common while in females, principal cause is gallstones.

Question 38

Recognise the presenting symptoms of acute pancreatitis

Answer 38

Severe epigastric or abdominal pain (radiating to back, relieved by sitting forward, aggravated by movement). Associated with anorexia, nausea and vomiting. There may be a history of gallstones or alcohol intake.

Question 39

Recognise the signs of acute pancreatitis on physical examination

Answer 39

Epigastric tenderness, fever. Shock, tachycardia, tachypnoea. Reduced bowel sounds (due to ileus, mechanism unclear). If severe and haemorrhagic, Turner's sign (flank bruising) or Cullen's sign (periumbilical bruising).

Question 40

Identify appropriate investigations for acute pancreatitis and interpret the results

Answer 40

Bloods: Increase amylase (usually >3 x normal but does not correlate with severity); FBC (raised WCC), U&Es, raised glucose, raised CRP, reduced Ca2+, LFTs (maybe deranged if gallstone pancreatitis or alcohol), ABG (for hypoxia or metabolic acidosis) USS: for gallstones/biliary dilation, pancreatic inflammation, calcification and free fluid Erect CXR: There may be pleural effusion. Mainly for excluding other causes. AXR: To exclude other causes of acute abdomen. Psoas shadow may be lost. May show a sentinel loop of bowel (localised ileus caused by intra-abdominal inflammation) CT scan: If diagnostic uncertainty or if persisting organ failure, signs of sepsis or deterioration for severe cases. Can be used for staging pancreatitis and detecting complications (e.g. necrosis) MRCP: Can be used instead of CT in patients with renal insufficiency who cannot tolerate IV contrast. Scoring system (Balthazar score): combination of grade of pancreatitis and degree of necrosis.

Question 41

Generate a management plan for acute pancreatitis When operate, when FNA

Answer 41

1. Assessment of severity. Modified glasgow scale combined with CRP (>210mg/L): ``` P- PO2 (<8kPa) A- Age >55 N- WCC (>15*10^9/L) C- Ca2+ <2mmol/L uR- Urea >16mmol/ E- Enzymes (LDH>600) A- Albumin >32g/L S- glucose >10mmol ``` (REMEMBER AMYLASE DOES NOT INDICATE SEVERITY!) 2. Medical: - Fluid and electrolyte rescusitation, urinary catheter and NG tube if vomiting - Analgesia and blood sugar control - Reduced infective complications and mortality with enteral as opposed to parenteral feeding - Prophylactic Abx only reduce mortality if infective pancreatic necrosis develop 3. ERCP and sphincterotomy - For gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct, ideally within 72 h. All patients should undergo definitive management of gallstones during same admission or within 2 weeks. 4. Early detection and treatment of complications - e.g. if persistent symptoms and > 30% pancreatic necrosis or signs of sepsis should undergo image guided fine needle aspiration for culture 5. Surgical: Patient with necrotizing pancreatitis should be managed in a specialist unit. Minimal access or open necresectomy (drainage and debridement of all necrotic tissue).

Question 42

Identify the possible complications of acute pancreatitis and its management What is a pseudocyst

Answer 42

Local: Pancreatic necrosis; pseudocyst (peripancreatic fluid collection persisting >4 weeks); abscess; ascites; psuedoaneurysm or venous thrombosis Systemic: Multiorgan dysdunction, sepsis, renal failure, ARDS, DIC, hypocalcaemia, diabetes Long term: Chronic pancreatitis (with diabetes and malabsorption)

Question 43

Summarise the prognosis for patients with acute pancreatitis

Answer 43

Twenty percent follow severe fulminating course with high mortality (infected pancreatic necrosis associated with 70% mortality), 80% run milder course (but still 5% mortality).

Question 44

Define chronic pancreatitis

Answer 44

Chronic inflammatory disease of the pancreas characterized by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain.

Question 45

Explain the aetiology / risk factors of chronic pancreatitis Pathophysiology. Important cell type?

Answer 45

Alcohol (70%). Idiopathic in 20%. Rare: Recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathryroidism, hypertriglyceridemia. From rapid medicine: Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atropy, ductal dilatation, cyst and stone formation. Pancreatic stellate cells are thought to play a role, converting from quiescent fat storing cells to myofibroblast-like cells forming extracellular matrix, cytokines and growth factors in response to injury. Pain is associated with raised intraductal pressures and inflammation.

Question 46

Summarise the epidemiology of chronic pancreatitis

Answer 46

Annual UK incidence ~ 1/100 000; prevalence ~ 3/100 000. Mean age 40– 50 years in alcohol-associated disease.

Question 47

Recognise the presenting symptoms of chronic pancreatitis

Answer 47

Recurrent, severe epigastric pain, radiating to th eback, relived by sitting forward, can be exacerbated by eating or drinking alcohol. Over many years, weight loss, bloating and pale offensive stools (steatorrhoea).

Question 48

Recognise the signs of chronic pancreatitis on physical examination

Answer 48

Epigastric tenderness. Signs of complications e.g. weight loss, malnutrition

Question 49

Identify appropriate investigations for chronic pancreatitis.

Answer 49

1st investigation: blood glucose and CT scan (pancreatic calcifications, focal or diffuse enlargement of the pancreas, ductal dilation, and/or vascular complications). USS can be done if CT not available but is not as good. Bloods: Glucose (raised may indicate endocrine dysfunction); Amylase and lipase (usually NORMAL); raised immunoglobulins, especially IgG4 in autoimmune pancreatitis USS: percutaneous or endoscopic: can show hyperechoic foci with post acoustic shadowing ERCP or MRCP: Early changes include main duct dilatation and stumping of branches. Late manifestations are duct strictures with alternating dilatation ( chain of lakes appearance). AXR: Pancreatic calcification may be visible. CT scan: Pancreatic cysts, calcification. Tests of pancreatic exocrine function: Faecal elastase.

Question 50

Generate a management plan for chronic pancreatitis

Answer 50

General: - Treatment mainly symptomatic and supportive, e.g. dietary advice, abstinence from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacements, e.g. Creon, analgesia for exacerbations of pain. - Chronic pain management may need specialist input. The sensory nerves to the pancreas transverse the coeliac ganglia and splanchnic nerves, coeliac plexus block (CT or EUS-guided neurolysis) and transthoracic splanchnicectomy offer variable degrees of pain relief. Endoscopic therapy: Sphincterotomy, stone extraction, dilatation or stenting of strictures. Extracorporeal shock-wave lithotripsy is sometimes used for fragmentation of larger pancreatic stones prior to endoscopic removal. Surgical: May be indicated if medical management has failed. Options include lateral pancreaticojejunal drainage (modified Puestow procedure), resection (pancreaticoduodenectomy or Whipple's) or limited resection of the pancreatic head (Beger procedure) or combined opening of the pancreatic duct and excavation of the pancreatic head (Frey procedure).

Question 51

Identify the possible complications of chronic pancreatitis and its management

Answer 51

Local: Pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites, pancreatic carcinoma. Systemic: Diabetes, steatorrhoea, reduced quality of life, chronic pain syndromes and dependence on strong analgesics.

Question 52

Summarise the prognosis for patients with chronic pancreatitis

Answer 52

PROGNOSIS Difficult to predict as pain may improve, stabilize or worsen. Surgery improves symptoms in 60– 70% but results are often not sustained. Life expectancy can be reduced by 10– 20 years.

Question 53

Define Barrett’s oesophagus

Answer 53

Pre-malignant condition Metaplastic change in the eosophagus, from stratified squamous epithelium to simple columnar epithelium (which is usually native to lower GI tract)

Question 54

Explain the aetiology / risk factors of Barrett’s oesophagus 2 types of barretts and which is worse

Answer 54

Chronic acid exposure --> reflux esophagitis (chronic irritation) --> metaplasia Bile acids --> intestinal differentiation --> promotes cancer growth 2 types depending on z line: -If z-line and GEJ coincide then there's intestinal metaplasia at the GEJ. This is associated with H Pylori. Short-segment Barrett's esophagus (< 3 cm of columnar epithelium between Z-line and GEJ) Long-segment Barrett's esophagus (> 3 cm of columnar epithelium between Z-line and GEJ). Higher risk of adenocarcinoma! Risk factors: ``` Bulimia Central obesity Previous chemical damage to esophageal epithelium (e.g. swallowing lye) Smoking Hiatal hernia Angle of His >60 (newborns) Scleroderma! ```

Question 55

Triggers for GORD

Answer 55

Bending down, supine position Habits: smoking and/or alcohol consumption Psychological factors: especially stress

Question 56

Recognise the presenting symptoms of Barrett’s oesophagus

Answer 56

Often asymptomatic, Frequent, prolonged heartburn, dysphagia, haematemesis, epigastric pain, weight loss

Question 57

Recognise the signs of Barrett’s oesophagus on physical examination

Answer 57

Often asymptomatic, Frequent, prolonged heartburn, dysphagia, haematemesis, epigastric pain, weight loss

Question 58

Identify appropriate investigations for Barrett’s oesophagus and interpret the results

Answer 58

OGD + biopsy and histological corroboration using the prague criteria (C&M, look up if time). IHC staining assists. Histologically: Histological appearance of the squamocolumnar junction in a case of Barrett's esophagus. The underlying glandular epithelium contains goblet cells, indicating intestinal metaplasia.

Question 59

Generate a management plan for Barrett’s oesophagus

Answer 59

Medical management with PPIs Endoscopy with 4-quadrant biopsies at every 2cm of the suspicious area. If no dysplasia: repeat endoscopy every 3-5 years If indefinite for dysplasia: repeat endoscopy with biopsies after 3–6 months of optimized PPI therapy If low-grade dysplasia: Endoscopy therapy of the irregularity (Usually including endoscopic mucosal resection and radiofrequency ablation) OR surveillance every 12 months with biopsies every 1cm If high grade dysplasia: Endoscopy therapy of the irregularity (Usually including endoscopic mucosal resection and radiofrequency ablation)

Question 60

Identify the possible complications of Barrett’s oesophagus and its management

Answer 60

Eosophageal adenocarcinoma Annual endoscopic observation for nondysplastic/low-grade lesions Management of acid reflux: Avoid/reduce intake of foods known to worsen refl ux: chocolate, coffee, tea, peppermint, alcohol, fatty/spicy/acidic foods. High dose long term PPIs.

Question 61

Summarise the prognosis for patients with Barrett’s oesophagus

Answer 61

.

Question 62

Define acute cholangitis

Answer 62

Ascending cholangitis, also known as acute cholangitis or simply cholangitis, is inflammation of the bile duct (cholangitis), usually caused by bacteria ascending from its junction with the duodenum (first part of the small intestine). It tends to occur if the bile duct is already partially obstructed by gallstones.

Question 63

Explain the aetiology / risk factors of acute cholangitis Most common causative organism

Answer 63

1. Gallstone blocking flow of bile through the CBD Bile usually flushes out the bacteria going from the gut into the biliary system via the ampulla of vater, but when this flow is obstructed, a bacterial infection can move up the CBD, called ascending cholangitis. Remember the risk factors for gallstones are the 4 Fs: Female, Fertile (aka PREGNANT), Fat (obese) or Forty (age) 2. Strictures= type of abnormal narrowing in a passage in the body. (e.g due to a nearby cancerous growth OR injury from a procedure) Note that the bacteria can colonise distal to the blockage in the CBD, but also migrate beyond the blockage and infect the stagnant bile and surrounding tissue Most common causative organisms= mixture of enteric organisms e.g. E Coli, klebsiella and enterococcus.

Question 64

Summarise the epidemiology of acute cholangitis

Answer 64

..

Question 65

Recognise the symptoms/signs of acute cholangitis on physical examination

Answer 65

Fever, RUQ pain, jaundice* These 3 are called charcot's triad *ONLY if there is high pressure proximal to the obstruction such that the spaces between cells lining the CBD have bigger gaps between them, allowing bile (and bacteria!) to leak into the blood stream Reynolds pentag= Fever, RUQ pain, jaundice, hypotension and confusion

Question 66

Identify appropriate investigations for acute cholangitis and interpret the results

Answer 66

BMJ best practice: 1. USS 2. CT (if USS non diagnostic) 3. MRCP (if USS non diagnostic) Then go to ERCP If high suspicion of acute cholangitis (e.g. charcto traid +ve)--> straight to diagnostic and therapeutic ERCP If acute cholangitis suspected but without charcot triad --> RUQ USS (-->CT/MRI if nondiagnostic-->MRCP if still non-diagnostic but suspicion is high)

Question 67

Generate a management plan for acute cholangitis

Answer 67

Manage symptoms: rehydration and Abx To definitively treat, you need to remove the blockage, e.g. using ERCP to suck out the gallstone + sphincterotomy For larger gall stones, can use shockwave lithrotripsy Percutaneous transhepatic cholangiography (PTC) if ERCP is unsuccessful or unavailable Interval cholecystectomy if gallstones present/concurrent cholecystitis

Question 68

Identify the possible complications of acute cholangitis and its management

Answer 68

Proximal to the obstruction (e.g. gallstone or stricture), there can be openings in the gaps between the cells lining the CBD, allowing bile AND the bacteria to leak out into the bloodstream. --> septic shock (leading to hypotension and confusion due to leaky blood vessels

Question 69

Summarise the prognosis for patients with acute cholangitis

Answer 69

Septic shock

Question 70

Define haemochromatosis

Answer 70

A condition of iron overload- the body absorbs too much iron

Question 71

Explain the aetiology / risk factors of haemochromatosis

Answer 71

Primary (Hereditary haemochromatosis- RECESSIVE): -Gene mutation in the HFE gene causes duodenal cells to bring too much iron into the bloodstream perhaps due to hepcidin deficiency Secondary haemochromatosis -Repeat blood transfusions. The RBCs in the transfusion are broken down after 120 days, but the iron is not It causes damage because iron can undergo the fenton reaction which leads to free radical production. Free radicals cause cellular damage, cell death and tissue fibrosis over many years.

Question 72

Summarise the epidemiology of haemochromatosis Why do men experience early haemochromatosis?

Answer 72

Presents in men age 50 And in women around 10-20 years after the menopause Later in women because they have better opportunity to get rid of iron due to menstrual bleeding But it is NOT a gender specific disease

Question 73

Recognise the presenting symptoms of haemochromatosis

Answer 73

May be asymptomatic Non specific: -Weakness, fatigue, lethargy, abdo pain Later: -Small/large joints pains (most commonly 2nd/3rd metacarpophalangeal joints), degenerative joint disease (involves calcium crystals) - Liver disease symptoms (those with cirrhosis at increased risk of HCC) - DM (type 1 due to destruction of beta islet cells) - Hypogonadism (amenorrhoea in women/testic atrophy in men) due to pituitary dysfunction - Cardiac failure (can lead to arrhythmia) - Skin pigmentation

Question 74

Recognise the signs of haemochromatosis on physical examination

Answer 74

WITH SEVERE iron overload: - Bronze skin (iron deposition and increased melanin production) - Liver: hepatosplenomegaly - Heart: signs of HF/ arrhythmia - Hypogonadism: testic atrophy, loss of hair, gynaecomastia

Question 75

Identify appropriate investigations for haemochromatosis and interpret the results

Answer 75

Iron: High Transferrin saturation: high Total iron binding capacity: low Increased ferritin (usually signals to decrease transferrin production) BIOPSY Brown spots inside cells can represent iron, but htedse can be be confused with a pigment called lipofuscin which is part of normal wear and tear of cells. To confirm it's iron you can use Prussian blue stain, which shows iron as blue.

Question 76

What is iron critical for in the body

Answer 76

o2 transport Oxidative phosphorylation

Question 77

Outline how iron is usually handled in the body

Answer 77

We only absorb about 10% of the iron we ingest per day, because the body has no mechanism to actively excrete iron Fe 2+ and haem can be absorbed across the luminal membrane of the intestinal enterocytes (Fe3+ must be converted to Fe2+ to be absorbed, and this is catalysed by Vit C) Once inside, one of two things can happen to the Fe2+: 1. It can be transferred into the blood stream by ferroportin. After than it is then transferred back to Fe3+ and carried by transferrin 2. It can be transferred back to Fe3+ in the cytosol and bound to apoferritin, which holds the Fe3+, inert. This is useful when there's enough iron in the body, because the apoferritin just gets excreted into the faeces. Hepcidin inhibits ferroportin to reduce iron intake. Iron is stored as ferritin intracellulary in the body

Question 78

Treatment for haemochromatosis

Answer 78

Phlebotomy! Deferoxamine -this drug binds free iron in the blood and allows it to be excreted in the urine

Question 79

T/F acute cholecystits is a risk factor for cholangiocarcinoma

Answer 79

F. Neither cholelithiasis nor cholecystitis is associated with increased risk of cholangiocarcinoma. Risk factors include Primary sclerosing cholangitis, chronic duct inflammation, infections, and ulcerative colitis.

Question 80

T/F acute cholecystitis is a risk factor for gall bladder carcinoma

Answer 80

Acute cholecystitis is not a risk factor for carcinoma of the gallbladder, but multiple stones increase the risk of GBC. It should be noted that the vast majority of patients with cholelithiasis will not develop carcinoma of the gallbladder.

Question 81

T/F acute cholcystitis and high alcohol consumption are risk factors for pancreatic cancer

Answer 81

F. Acute cholecystitis/ alcohol does not increase the risk of pancreatic cancer. Pancreatic cancer risk factors include smoking, a high-fat diet, and chemical exposures. Of note, alcohol consumption is not a demonstrated risk factor.

Question 82

T/F acute cholcystitis is a risk factor hepatocellular carcinoma

Answer 82

T, but while patients who have gallstones or have undergone cholecystectomy may have an increased risk of hepatocellular carcinoma (HCC), the biggest risk factors for HCC are hepatitis B, hepatitis C, and cirrhosis.

Question 83

What is rigler triad

Answer 83

pneumobilia (air in the biliary tract), low small bowel obstruction with distended small bowel loops and an impacted gallstone in the terminal ileum =GALL STONE ILEUS

Question 84

What is gallstone ileus

Answer 84

A mechanical small bowel obstruction secondary to gallstone impaction in the terminal ileum The gallstone passes through a cholecystoduodenal fistula, travels the length of the small bowel, and obstructs proximal to the ileocecal valve. It is an unusual complication of cholecystolithiasis and chronic cholecystitis. Gallstone ileus is an uncommon cause of small bowel obstruction, however, in the elderly, it accounts for up to 25% of non-strangulated bowel obstructions. Females are more frequently affected.

Question 85

Which antibodies are associated with each of the following conditions: - Primary biliary cirrhosis - Primary sclerosing cholangitis Which type of biliary ducts are affected in each case

Answer 85

PBC. Your typical AI conditions. Associated with RA, sjorgen. Sero positive- AMA antibodies. Intrahepatic ducts affected. PSC. Associated with UC. Concentric rings of fibrosis on MCRP. Perinuclear antineutrophil cytoplasmic antibody. Extrahepatic ducts

Question 86

Define achalasia

Answer 86

Eosophageal motility disorder characterised by loss of peristalsis and failure of relaxation of the LOS

Question 87

Explain the aetiology / risk factors of achalasia Which cells are affected? Which infection causes a similar effect?

Answer 87

Degeneration of ganglion cells of the myenteric plexus in the oesophagus due to an unknown cause. Oesophageal infection with Trypanosoma cruzi seen in Central and South America produces a similar disorder (Chagas' disease).

Question 88

Summarise the epidemiology of achalasia

Answer 88

present 25-60 years

Question 89

Recognise the presenting symptoms of achalasia

Answer 89

Insidious onset/gradual progression of: - intermittent dysphagia involving solids and liquids; - difficulty belching; - regurgitation (particularly at night); - heartburn; - chest pain (atypical/cramping, retrosternal); - weight loss.

Question 90

Recognise the signs of achalasia on physical examination

Answer 90

Signs of complications Clubbing

Question 91

Identify appropriate investigations for achalasia and interpret the results

Answer 91

Best test is MANOMETRY: - Elevated resting LOS pressure - Incomplete LOS relaxation - Absence of peristalsis in the distal smooth muscle portion of the oesophagus Barium swallow: - dilated eosophagus which smoothly tapers down to the sphincter (beak-shaped) - tertiary peristalsis waves (multiple, disorganised contractions appear as dilations and constrictions through a portion or the entire length of the oesophagus- not triggered by swallowing) CXR: - widened mediastinum/double right heart border (dilated eosophagus), - air-fluid level in the upper chest (due to stasis in a thoracic oesophagus filled with retained secretions and food) and - absence of the normal gastric air bubble Endoscopy: only to exclude malignancy which can mimic achalasia Serology for antibodies against T. cruzi if chaga's is suggested by epidemiology and symptoms. Blood film might show parasites

Question 92

What causes each of the following types of peristalsis: - primary - secondary - tertiary

Answer 92

- primary: normal! Peristalsis triggered by swallowing, followed by deglutitive inhibition. - secondary: Secondary peristaltic waves occur after swallowing to clear the esophagus of food, reflux, or gas. They are triggered by esophageal distention. - tertiary: caused by esophageal spasm or by achalasia

Question 93

bulky and foul smelling stools?

Answer 93

This is classic description of steatorroeah (doesn't have to be diarroeah like!)

Question 94

What is D-xylose and what is it used for

Answer 94

It is a monosaccharide that is absorbed through small intestines and excreted through the kidneys. It helps to distinguish structural from functional causes of steatorrhoeah (which is due to fat malabsorption). If the level of D-xylose excretion is low, it suggests there is a structural problem with absorption (so the excreted sugar is low as well as the fat would be). E.g. Coeliac and crohn's But if D-xylose is normal then it suggests this is an issue affecting fats only, and thus is a functional problem (e.g. exocrine pancreatic insufficiency leading to lack of lipase and thus lack of absorption of fats, leading to steatorroeah)

Question 95

What will the excretion of D-xylose show in the following conditions: - Coeliac disease - Crohn's - Small intestinal bacterial overgrowth - Pancreatic insufficiency

Answer 95

Coeliac: reduced excretion Crohn's: normal excretion (i don't get why but think this test is old anyway) Pancreatic insufficiency: normal Small intestinal bacterial overgrowth: decreased urinary excretion of D-xylose

Question 96

What is mackler's triad

Answer 96

Boerhaave syndrome is characterized by the Mackler triad (vomiting, chest pain, and subcutaneous emphysema) in just 14% of patients.

Question 97

What does an upturned U shape on abdominal radiograph represent

Answer 97

grossly dilated loop of sigmoid colon, secondary to volvulus.

Question 98

Ischaemic colitis usually involves which part of the colon, and what sign do you get on abdominal radiograph

Answer 98

Ischaemia tends to involve the splenic flexure and is associated with mucosal oedema (“thumbprinting”)

Question 99

Initial management of patient with sigmoid volvulus. What if it recurs?

Answer 99

Passage of a decompressing flatus tube will relieve symptoms and is relatively non-invasive. For some patients this treatment may suffice. Volvulus may be recurrent however, requiring sigmoid colectomy and obtunded patients, or those with associated perforation, may require surgery also.

Question 100

What is the management of caecal volvulus

Answer 100

.These patients usually require a right hemicolectomy.

Question 101

Initial management of patient with sigmoid volvulus. What if it recurs?

Answer 101

Passage of a decompressing flatus tube will relieve symptoms and is relatively non-invasive. For some patients this treatment may suffice. Volvulus may be recurrent however, requiring sigmoid colectomy and obtunded patients, or those with associated perforation, may require surgery also.

Question 102

Sigmoid volvulus is due to twisting of the bowel on what mesentery, what about caecal volvulus

Answer 102

Both lax

Question 103

What is splenic injruy associated with

Answer 103

Rib fractures (40%), left kidney injury (25%) and less commonly diaphragmatic rupture (2%)

Question 104

T/F most splenic lacerations are self limiting

Answer 104

T The majority of splenic lacerations are self limiting and can be managed conservatively avoiding the need for a splenectomy

Question 105

What would an US be used for in an emergency with presumed splenic injury

Answer 105

Just to assess for free air/fluid (not looking at solid organs)

Question 106

What is splenic injruy associated with

Answer 106

Rib fractures (40%), left kidney injury (25%) and less commonly diaphragmatic rupture (2%)

Question 107

T/F most splenic lacerations are self limiting

Answer 107

T The majority of splenic lacerations are self limiting and can be managed conservatively avoiding the need for a splenectomy

Question 108

What vaccines and prophylaxis are to be given following splenectomy

Answer 108

Post-splenectomy, patients are at increased risk of severe bacterial infections in particular: - Pneumococcus, - Meningococcus and - Haemophilus influenzae, all of which can be vaccinated against. Also at risk of malaria, so they should take caution when travelling to affected countries Long term penicillin for prophylaxis (it's controversial but still done)

Question 109

How would you differentiate small bowel obstruction from small bowel ileus on examination

Answer 109

In paralytic ileus, bowel sounds are usually absent on auscultation, whereas a high-pitched tinkling sound would be heard in the early phase of a mechanical bowel obstruction (i.e. bowel sounds increased).

Question 110

Why do you insert a NG tube in ileus/obstruction

Answer 110

Patients will be much more comfortable if you insert a nasogastric tube to decompress the stomach and upper small bowel.

Question 111

What must you consider when giving analgesia for patients with ileus?

Answer 111

The distension of bowel loops found in ileum will cause abdominal pain and therefore the patient is likely to need analgesia, although be aware that opiate analgesia slows the gut and may then contribute to ongoing ileus. Review chart for other drugs that might be contributing.

Question 112

What causes electrolyte abnormalities and dehydration in ileus/mechanical obstruction

Answer 112

Bowel distention leads to third-space volume loss, resulting in dehydration and electrolyte abnormalities. And Vomiting

Question 113

Which electrolytes are particualrly important to correct in ileus

Answer 113

Correct electrolytes in particular K and Mg, aiming for a K of greater than 4 to maximise the chance of the gut getting moving again.

Question 114

What do you need to monitor when giving TPN

Answer 114

1. Daily inspection of line & dressing 2. 4hr temp and observations 3. Blood glucose 4. Daily electrolytes 5. Accurate recording of fluid balance

Question 115

What are the complications of TPN

Answer 115

1. Infection of the central line 2. TPN has high sugar content (sugar derangement can develop in even those w/o diabetes- it also increases the risk of infection if blood sugar high) 3. Fluid balance problems (either becauses losses from NG, fistula, high output stoma etc are not adequately corrected on top of the TPN volume, or because people forget that TPN contains a lot of fluid and then give standard IV fluids in addition) 4. Electrolyytes need to be watched as TPN patients often have difficult fluid balance with high losses and GI fluid contains a lot of electrolytes in particular Na, K and Mg. Additionally electrolytes can be dramatically affected by refeeding syndrome

Question 116

What should TPN patients be given before they begin this form of nutrition and why

Answer 116

Pabrinex Pabrinex contains a mixture of B vitamins and vitamin C. The reason we give it is to make sure that the patient has plenty of thiamine available to them as they start feeding. Thiamine is required to process the food which has been given and if you have been in a state of starvation then thiamine levels will be low with a risk that it could be used up as feeding commences. This results in Wernicke’s encephalopathy which is reversible if thiamine is given rapidly. If it is not identified and thiamine administered then it will rapidly progress to Korsakoff’s Psychosis an irreversible dementia.

Question 117

Why are alcoholics given pabrinex/thiamine

Answer 117

Because they frequently have a very poor quality diet in the community and so can develop Wernicke’s when they are give proper meals in the hospital, it is nothing to do with the withdrawal itself.

Question 118

What is a typical history for bowel ischaemia

Answer 118

Cramping pain and bleeding

Question 119

Megacolon is usually associated with what

Answer 119

It leads to sepsis (fever and high WCC)

Question 120

Air absent vs present in the rectum when querying bowel obstruction?

Answer 120

Air absent in the rectum is consistent with left sided obstruction e.g. sigmoid stricture If air is present in the rectum it makes left sided obstruction unlikely. It is more likely to be pseudo- obstruction, or possibly a low lying lesion in the rectum

Question 121

What is the difference between ileus and pseudoobstruction

Answer 121

Pseudo-obstruction is defined as acute, marked distention of the large bowel. As with ileus, it occurs in the absence of a definable mechanical pathology. Pseudo-obstruction is clearly limited to the colon alone, whereas ileus involves both the small bowel and colon.

Question 122

How is pseudo-obstruction usually managed

Answer 122

Conservatively. Exclusion of a mechanical obstruction is needed in a proportion of patients, either via CT scan or colonscopy. Colonscopic decompression is useful in acute cases Neostigmine treatment is useful in acute cases

Question 123

Which electrolyte imbalance is a cause of pseudo-obstruction

Answer 123

Hypokalaemia

Question 124

Which surgery is assocaited with pseudo-obstruction

Answer 124

There is an association with recent surgery, particularly orthopaedic

Question 125

Differentiate the broad management of ileus vs mechanical obstruction

Answer 125

It is important to differentiate the two, as ileus can often be resolved by conservatively managing the physiological upset that caused it in the first place. In contrast the causes of mechanical obstruction are often surgical, as in our case.

Question 126

If you 'cant get above' a scrotal lump, what does this indicate

Answer 126

You should be able to do so with any such lump that is confined solely to the scrotum. If you can’t, the lump must be originating from the abdomen

Question 127

What is the differentials for a lump that you can't "get above" How do you differentiate the two

Answer 127

It will be either be a hydrocele of the spermatic cord (which transilluminates and is found in babies and infants) or an inguinal hernia.

Question 128

Define hernia

Answer 128

An abnormal protrusion of a viscus from one cavity into another.

Question 129

Outline 2 classic features of hernia

Answer 129

Two classic features of hernias are that they have a cough reflex (owing to transmitted pressure from the abdomen) and that they can be reduced (pushed back) into the abdomen.

Question 130

When will you see a loss of classic features of hernia

Answer 130

If however, the loop of bowel or mesentery passing through them should get stuck, from narrowing of the hernial orifices for example, these two features will not be elicited.

Question 131

How do you differentiate a narrowed hernial orifice from hernia incarceration. How do you differentiate this from infarction (due to strangulation)

Answer 131

Narrowed orifice --> loss of classic features Incarcerated --> hard hernia Infarcted --> The latter is typified by severe tenderness over the hernia and signs and symptoms of peritonitis caused by bacteria and intestinal/colonic material escaping from necrotic bowel.

Question 132

What is hernial incarceration

Answer 132

If the impingement is tight enough, gastrointestinal contents will not be able to pass through any loops of bowel involved, and intestinal obstruction will ensue.

Question 133

What is hernial strangulation

Answer 133

Blood supply to the incarcerated protruding viscus can also be compromised, leading to ischaemia and infarction. This is called strangulation.

Question 134

How do you differentiate large from small bowel in abdominal x ray

Answer 134

A more reliable means of telling small from large bowel is to look at their respective bowel markings; small bowel has valvulae conniventes (bands which go all the way round the bowel circumferentially – see Fig 1) while large bowel has haustra (lines which do not quite go all the way around). Also, large bowel more peripheral and small bowel more central (but not reliable as things are mobile)

Question 135

Main causes of mechanical obstruction (in small and large bowel) and of functional obstruction (ileus)

Answer 135

Mechanical Small bowel: incarcerated hernia and adhesions Large bowel: strictures (e.g. secondary to diverticular disease) and intra-luminal cancers Ileus variety of reasons that interfere with the normal physiology of the bowel, eg. immediately following bowel surgery, during electrolyte disturbances, and sepsis

Question 136

How does bowel obstruction cause shock

Answer 136

Up to 9L are secreted into the GI tract everyday (as wll as whatever fluid has come from food and drinking). The body usually reabsorbs this in the large bowel, so it's easy to understand how bowel obstruction and the accumulation of fluid in the third space can result in severe hypovolaemia and then shock

Question 137

Indirect inguinal hernias are associated with which developmental variation

Answer 137

Indirect inguinal hernias are associated with a patent processus vaginalis, an invagination of the embryonic parietal peritoneum into the scrotum. This results in the formation of the inguinal canal which permits the testes to subsequently enter the scrotum from the abdomen. The processus vaginalis usually close within 18 months of birth, but persists in a significant proportion of individuals into adulthood. In such people, there is a potential pathway by which bowel can gain entry into the scrotum via the inguinal canal, just like the testes did in utero.

Question 138

Differentiate the path of direct and indirect inguinal hernias into the scrotum

Answer 138

Whereas indirect inguinal hernias exit both the deep and superficial inguinal orifices (or ‘rings’) before entering the scrotum, direct hernias exit the abdomen via the superficial ring only. This occurs as a result of weakening of the abdominal muscles that make up the superficial ring, and is unsurprisingly more common in older patients.

Question 139

What are incisional hernias

Answer 139

Muscle weakening can also explain why hernias are also more common at the sites of surgical incisions, ie. surgical scars. These are known as incisional hernias, and can easily be demonstrated on the abdomen, if present, by asking a patient to lift their torso off the examination couch without using their hands (almost as if they are doing a sit-up).

Question 140

What structures in the gut can herniate

Answer 140

In terms of which viscera is involved, anything that is relatively mobile can herniate. This includes the small bowel (by way of the mesentery), transverse and sigmoid colon (by way of their respective mesocolons), omentum, and even the ovaries and fallopian tubes (as result of the mesovarium). Any of theses viscera could become incarcerated and eventually, strangulate within a hernia.

Question 141

T/F toxic megacolon results from obstruction

Answer 141

Not correct. Toxic megacolon is a consequence usually of ulcerative colitis (more rarely crohns disease). It CAUSES an ileus (so reduced bowel sounds)

Question 142

T/F an incompetent ileocaecal valve is actually good in the case of left colonic obstruction

Answer 142

T! A competent ileocaecal valve will stop bowel contents moving from the obstructed colon back into the small intestine so will actually increase risk of colonic perforation

Question 143

What abdominal sign might suggest colonic carcinoma on barium enema

Answer 143

Apple core lesion

Question 144

What imaging modality is best way to investigate colonic carcinoma

Answer 144

In cases of large and small bowel obstruction, especially if no history to suggest adhesions, CT has largely become the technique of choice for further assessment. Air distension of the bowel is not employed (as per colonography) as this may precipitate perforation. CT will identify the cause of obstruction non-invasively in most cases and will also provide staging information etc (liver, lungs, regional nodes). Use contrast enhanced

Question 145

How would you manage small bowel obstruction What are the indications for surgery In what proportion of cases do you think the obstruction resolves spontaneously with conservative management

Answer 145

Standard things first: 1) Assess ABC 2) NBM 3) IV fluids and NG tube to aspirate gastric contents 4) Analgesia Then referral to surgical team, who will probably trial conservative management first: A sensible approach would be: 1) A trial of conservative management, i.e. fl uids and NG aspiration (‘drip and suck’), to see if the obstruction resolves of its own accord. He should be reviewed regularly to ensure he does not deteriorate (e.g. bowel strangulation). 2) Surgery, if: − there are signs of strangulation or peritonism; − after ~48 hours the obstruction has not resolved; or − there is no history of abdominal surgery, making adhesions less likely and more sinister causes more likely (virgin abdomen) In 75% of cases, adhesions resolve spontaneously with conservative management.

Question 146

Differentiate a pancreatic pseudocyst and a pancreatic abscess, both complications of acute pancreatitis

Answer 146

The pseudocyst is defined as a localized collection of pancreatic juices confine to a retroperitoneal area by a fibrous membrane without epithelium; an abscess is a collection of pus and necrotic tissue. A pancreatic abscess would present with pain, and features of sepsis.

Question 147

2 methods of pseudocyst drainage?

Answer 147

The pseundocyst can also be drained percutaneously or through the stomach wall at EUS. A blind attempt at gastroscopy is not generally advocated due to the increased risks.

Question 148

Which blood test is a measure of pancreatic exocrine function

Answer 148

Faecal elastase

Question 149

What is the treatment of pancreatic exocrine insufficiency

Answer 149

Oral enzyme replacement e.g. creon

Question 150

What is the tumour marker for pancreatic carcinoma

Answer 150

(CA19-9)

Question 151

if you suspect pancreatic cancer and feel a mass in the right upper quadrant, what is this likely to represent

Answer 151

Not the tumour itself! The right upper quadrant mass is likely to represent a distended gallbladder (due to biliary obstruction)

Question 152

When is MRCP most useful

Answer 152

MRCP is a useful diagnostic tool only and is best suited for assessment of suspected choledocholithiasis.

Question 153

What is the technique of choice for staging pancreatic carcinoma

Answer 153

CT is the technique of choice for staging pancreatic carcinoma (look for local invasion of duodenum and vessels, enlarged regional nodes and liver metastases).

Question 154

What will be found in malignant vs inflammatory causes of biliary obstruction on ercp

Answer 154

Malignant: shouldered and irregualar Inflammaotry: smooth

Question 155

Risk factors for pancreatic cancer

Answer 155

Cigarette, diabetes

Question 156

What are the complications of ERCP

Answer 156

``` Perforation Aspiration pneumonia Haemorrhage Acute pancreatitis Ascending cholangitis ```

Question 157

What is the best modality for each of the following in the adbomen: - air - calcification

Answer 157

CT for both

Question 158

What is porcelain gallbladder

Answer 158

Calcification in the wall of the gallbladder It is associated with gallstones and chronic inflammation of the gallbladder There is an association with gallbladder carcinoma Surgery is indicated

Question 159

What is emphysematous cholecystits

Answer 159

A type of cholecystitis more common in diabetics Air arises in the wall of the gallbladder due to gallbladder ischaemia and infection with gas-forming organisms (clostridium) Symptoms and signs are initially minor but mortality is high due to sepsis

Question 160

Risk factors for gallstones

Answer 160

'fair, fat, female, fertile and forty' pregnant

Question 161

T/F lap chole has lower complication that open chole

Answer 161

F A Cochrane review comparing the two methods of surgery found no differences in mortality, complications, or operative time. There was however, clear evidence of a shorter stay in hospital with quicker convalescence.

Question 162

Which two organisms can mimic ileo-caecal chrohns disease?

Answer 162

Yersinia and TB!

Question 163

t/f patients with ileocaecal tuberculosis present with pulmonary TB in the vast majority of cases

Answer 163

F.... A chest radiograph should be performed to demonstrate previous or active pulmonary tuberculosis, although half of all patients do not present with a previous history of pulmonary TB.

Question 164

T/F onset of achalasia is usually slower than malignancy What else might help you differentiate

Answer 164

T. benign pathologies e.g. peptic stricture and achalasia tend to have longer histories Achalasia commonly just as bad for liquids as it is for solids

Question 165

What would the best investigations for dysphagia be?

Answer 165

Upper GI endoscopy opy first if you suspect cancer If this is normal then a barium swallow can give important information on oesophageal motility and is better at picking up achalasia.

Question 166

Which investigation is used to confirm achalasia after barium swallow

Answer 166

Manometry is used to confirm the diagnosis of achalasia

Question 167

T/F achalasia is a risk factor for oesophageal carcinoma

Answer 167

T!

Question 168

Progressive dysphasia with aspiration and difficulty swallowing solids and liquids from the atart?

Answer 168

Achalasia /motility disorder

Question 169

What is an infectious cause of dysphagia, and who might present with it

Answer 169

Oesophageal candidiasis generally occurs in patients who are frail and immunosuppressed, particularly those on steroids, including inhaled steroids. It tends to present with odinophagia and dysphagia and oral plaques are usually present.

Question 170

What could be the chest xray findings in achalasia

Answer 170

A chest x-ray may show a dilated oesophagus in achalasia with absence of the gastric air bubble Look on google images for " VCU Department of Radiology Esophageal Dilatation with “Air Esophogram Sign"

Question 171

What would the barium swallow show for achalasia vs malignancy

Answer 171

Achalasia: There is a tight, smooth narrowing of the distal oesophagus Malignancy: irregular stricture (usually happens on a background of GORD)

Question 172

What are the possible interventions for achalasia

Answer 172

Balloon dilation Surgical cardiomyotomy Anti-reflux medication

Question 173

Define volvulus

Answer 173

Colonic volvulus: Rotation of a loop of bowel around the axis of its own mesentery that results in bowel obstruction and potential ischaemia. 65% sigmoid colon, 30% caecum

Question 174

Explain the aetiology / risk factors of volvulus

Answer 174

Anatomical factors: - Long sigmoid mesentery - Mobile caecum - Chronic constipation and debility - Age - Very high residue diet - Tumour - Adhesions - Chagas' disease of the colon Rotation of the segment of bowel results in partial or complete closed loop obstruction. With a 360 degree twist, the veins tot he bowel are compressed and occluded, leading to circulatory impairment and, if not relieved, gangrene and perforation

Question 175

Summarise the epidemiology of volvulus

Answer 175

5-10% of large bowel obstructions, more common in elderly

Question 176

Recognise the presenting symptoms of volvulus

Answer 176

Abdo pain and swelling, absolute constipation and later vomiting May be previous episodes with spontaneous resolution

Question 177

Recognise the signs of volvulus on physical examination

Answer 177

Signs of bowel obstruction: - Distension - Tenderness - Tinkling bowel sounds

Question 178

Identify appropriate investigations for volvulus and interpret the results

Answer 178

Abdominal xray: -Massively dilated loop of bowel, may have a -Coffee bean shape: In caecal valvulus it points towards the lower right quadrant In sigmoid it points to the left. -May be associated with proximally dilated loops of bowel and collapse Water soluble contrast enema: -Demonstrates the site of obstruction. In sigmoid volvulus there is "bird beak" or "ace of spades" deformity with spiral narrowing of the distal bowel at the site CT scan: identifiies mesentery and bowel as well as signs of bowel ischaemia

Question 179

Define ulcerative colitis

Answer 179

Most common type of IBD. Chronic RELAPSING and REMITTING inflammatory bowel disease affecting the LARGE bowel (including the rectum) Flare (new damage has happened) Affects mucosa and submucosa or large intestine ONLY

Question 180

Explain the aetiology / risk factors of ulcerative colitis Which antibody is it associated with? What condition?

Answer 180

Genetic suceptibility + environmental trigger (sulfide producing bacteria?) Autoimmune in origin (stress and diet are secondary meaning they worsen it) T cells destroy the lining of the large instestine leaving ulcers. Associated with increased serum pANCA (antibodies that attach neutrophils), which may result from cross-reactivity with antigens from gut bacteria. UC patients seem to have higher proportion of bacteria that produce sulfides, and high sulfide is correlated with active periods of destruction. Associated with primary sclerosing cholangitis.

Question 181

Summarise the epidemiology of ulcerative colitis ------------------------------------- What is the pattern of ulceration in UC

Answer 181

15% positive family history Young women in teens-30s have high prevalence Caucasions and eastern european jews high prevalence Peak onset 20-40 ------------------------------ Pattern tends to be circumferentiala and continuous (goes all the way around the surface of the lumen, and then it progressively works itway back CONTINUOUSLY from the rectum around the large bowel

Question 182

Recognise the presenting symptoms of ulcerative colitis

Answer 182

Pain in left lower quadrant (correspond to rectum) More severe and frequent bouts of diarrhoea + BLOOD/mucus in stool Did you know: stool frequency is related to severity of disease! Tenesmus and urgency (the destruction of epithelium and mucosa causes bleeding into the stools, and the destruction also means that the colon can't perform its important function of reabsorbing water, leading to diarrhoea)

Question 183

Recognise the signs of ulcerative colitis on physical examination EXTRA-GI manifestations?

Answer 183

- Fe deficiency anaemia, dehydration - Clubbing - Abdo terderness, tachycardia - Blood, mucus and tenderness on PR. Extra GI manifestations (uveitis, renal calculi, arthropathy, sacroiliitis, ankylosing spondylitis, erythema nodosum (BUT MORE COMMON IN CROHNS rash on anterior shin) , pyoderma gangrenosum (on leg, non-infectious painful pustules or nodules become ulcers), oesteoporisis (due to steroid treatment), amyloidosis)

Question 184

Identify appropriate investigations for ulcerative colitis and interpret the results T/F faecal calprotectin is a measure of disease severity in UC When is barium enema/colonoscopy dangerous

Answer 184

Blood: FBC (reduced Hb, increased WCC), increased ESR/CRP. Reduced albumin. LFT Stool: culture as infectious colitis is a differential. FAECAL CALPROTECTIN- marker for disease severity AXR: rule out toxic megacolon Diagnosis requires colonoscopy/flexible sig- take biopsy: severity, histological confirmation, detects dysplasia Barium enema: mucosal ulceration with granular appearance and filling defects (pseudopolyps), featureless narrow colon, loss of haustral pattern (LEAD PIPE/HOSEPIPE APPEARANCE). Radiological imaging: CT scan, MRI barium enema, X-ray COLONOSCOPY AND BARIUM ENEMA DANGEROUS IN ACUTE EXACERBATION

Question 185

Generate a management plan for ulcerative colitis Identify the possible Acute exacerbation?

Answer 185

``` Acute exacerbation: IV rehydration, IV corticosteroids, Abx, bowel rest, pareneteral feeding may be necessary, DVT prophylaxis. Monitor fluid balance and vital signs. -If toxic megacolon develops, low threshold for proctocolectomy and ileostomy as perforation has 30% mortality. ``` Chronic management DEPENDS ON SEVERITY, which is determined by: low Hb, low albumin, increased ESR/CRP, bleeding, fever and diarrhoea frequency (<4/day mild, 4-6 moderate, >6 severe) MILD DISEASE: Anti-inflammatory medications: oral/rectal 5-ASA derivatives (sulfasalazine) +/- rectal steroids MODERATE-SEVERE DISEASE: Anti-inflammatory medications: oral/rectal 5-ASA derivatives (sulfasalazine) + Immunosupressants (corticosteroids, azathioprine, cyclosporin) ``` Biological treatments -Infliximab -Adalimumab -Golimumab (these 3 are all anti-TNFa) ``` SURGICAL (inicated for failure of treatment, presence of complications or prevention of colonic carcinoma): -Proctocolectomy (generally curative) with ileostomy OR ileoanal pouch formation

Question 186

complications of ulcerative colitis and its management

Answer 186

See extra GI manifestations GI complications: - Haemorrhage - Toxic megacolon - Perforation - Colonic carcinoma (extensive disease >10 years of UC) - Gallstones - PSC - Large joint arthritis - Anterior uveitis - Apthous ulceration

Question 187

Summarise the prognosis for patients with ulcerative colitis What are the poor prognostic factors (ABCDEF)

Answer 187

Relapsing and remitting, normal life expectancy Poor prognostic factors: -Albumin (<30g/L), Blood PR, CRP raised, Dilated loops of bowel, Eight or more bowel movements per day, Fever (>38 degrees in first 24hrs)

Question 188

Obturator hernia is associated with which sign

Answer 188

Obturator hernias occur through the obturator canal and they present with inner thigh pain when the hip is internally rotated (Howship- Romberg sign).

Question 189

How does the coughing test distinguish direct and indirect inguinal hernia

Answer 189

When you ask them to cough you place your hand over the midpoint of the inguinal ligament (where the deep ring is). An indirect inguinal hernia enters the inguinal canal through the deep ring. So when they cough, the hernia will not protrude. But a direct hernia enters the inguinal canal through a weakening in the posterior wall of the inguinal canal, medial to the deep ring. So covering over the deep ring will not stop protrusion of direct hernia when intra-abdominal pressure is increased through a cough

Question 190

What is a spigelian hernia

Answer 190

Spigelian hernias occur when abdominal contents herniate through the linea semilunaris, typically occurring inferior and lateral to the umbilicus.

Question 191

What do each of the following signs represent: ``` Psoas sign Rovsing's sign Cope's sign Aaron's sign Murphy's sign ```

Answer 191

Psoas: passive extension of right leg. Pain represents a retrocaecal inflammed appendix Rovsing's: palpation of the LIF causes pain in the RIF. Cope's sign: pain on flexion and internal rotation of the hip and indicates that the appendix lies close to the obturator inernus Aarons sign: referred epigastric pain when pressure is applied over mcburney's point Murphy's sign (cholecystitis): cessation of inspiraton when two fingers are placed below the right costal margin in the MCL and the patient is asked to take a deep breath in.

Question 192

Grade haemorrhoids

Answer 192

Grade 1: no prolapse Grade 2: prolapse on defecation but reduces spontaneously Grade 3: prolapse requires manual reduction Grade 4: remain persistently prolapsed and cannot be reduced

Question 193

Differentiate type 1 and type 2 rectal prolapse

Answer 193

``` Type 1 (incomplete) rectal prolapse occurs when only the rectal mucosa protrudes through the anus. Seein in children and adults, associated with straining, constipation and haemorrhoids ``` ``` type 2 (complete) occurs when all layers of the rectum protrude through the anus, creating a mass which has palpable, concentric muscular rings. Mainly in adults, associated with constipation, advanced age, chronic straining, neurologic conditions like MS, CF in kids ```

Question 194

Symptoms of rectal prolapse

Answer 194

Protrutding anal mass, may need digital replacemnet. Some patients report constipation, but fecal incontinence is more common due to the lax anal tone. Passing mucus or blood PR. Can present as emergency with irreducible or strangulated prolapse

Question 195

2 main causes of rectal prolapse

Answer 195

1 Lax anal tone due to pundendal nerve damage | 2) Prolonged straining

Question 196

When would metronidazole be used

Answer 196

Metronidazole is effective against anaerobes, and, so, is used to treat several GI infections (e.g. C. difficile colitis), pelvic inflammatory disease and aspiration pneumonia.

Question 197

What is the typical presentation of right vs left sided colorectal cancers?

Answer 197

Left-sided colorectal cancer tends to present earlier with a change in bowel habit and PR bleeding, whereas right-sided tends to present later with abdominal pain and symptoms of anaemia (e.g. shortness of breath, fatigue). There is a degree of overlap between these presentations as left- sided colorectal cancers are also associated with symptoms of anaemia.

Question 198

Where is colorectal cancer most commonly found

Answer 198

Colorectal cancer most commonly occurs in the rectum (27%) followed by the sigmoid colon (20%) and caecum (14%).

Question 199

Which tumour marker is most specific for colorectal cancer

Answer 199

Serum carcinoembryonic antigen | CEA – the most specific tumour marker for colorectal cancer

Question 200

Virchow's node is commonly associated with which type of cancer

Answer 200

Don’t get caught out by the enlargement of Virchow’s node (Troisier’s sign) described in this SBA. Although this is most often associated with gastric cancer, it can also be found in other abdominal malignancies.

Question 201

What is the typical presentation of gastric cancer

Answer 201

Gastric cancer is also more | likely to present with dyspepsia, vomiting, early satiety, bloating and melaena.

Question 202

Define appendicitis

Answer 202

Acute inflammation and infection of the vermiform appendix, which is the little closed-ended hollow tube attached to the caecum

Question 203

Explain the aetiology / risk factors of appendicitis What are the specific causes Which is more common in children What then causes pain Which bacteria

Answer 203

Usually, appendicitis occurs because something obstructs the appendix: - Faecalith (hardened faecal matter) - Lymphoid follicle growth (lymphoid hyperplasia)= more common in children - Caecal carcinoma - Undigested material (gum, seeds) - Intestinal parasites (pinworms) The mucosa in the appendix will secrete fluid and mucous, which build up behind the obstruction in the appendix. This increases pressure, making appendix grow in size and it will physically push on the nearby afferent visceral nerve fibers, causing abdominal pain. Along with that, the flora and bacteria in the gut, usually E. coli and Bacteroides fragilis, will multiply in the appendix. This triggers the immune system to recruit white blood cells and pus starts to accumulate, resulting in full-blown inflammation of the appendix. As the pressure keeps growing and the appendix continues to swell up, it will push on and compress nearby small blood vessels causing ischemia and local necrosis. As a result, inflammation extends to the serosa of the appendix, where it begins to spread to the parietal peritoneum, irritating it. The growing colony of bacteria can then invade the wall of the appendix causing more inflammation, and the wall becomes weaker and weaker, to the point where the appendix can rupture.

Question 204

Summarise the epidemiology of appendicitis

Answer 204

Any age, most common 2nd and 3rd decade. One of commonest surgical diagnoses with 7% lifetime risk

Question 205

Recognise the presenting symptoms of appendicitis

Answer 205

Acute appendicitis typically starts with nausea, vomiting, fever and periumbilical abdo pain (due to visceral nerve irritation, due to the enlarged appendix) Within 24-48hrs, the appendix becomes more swollen and inflamed, irritating the abdominal wall, causing the pain to get more severe and migrate to right lower quadrant and causing fever

Question 206

Recognise the signs of appendicitis on physical examination

Answer 206

McBurney's sign (tenderness at McBurney's point- located one-third of the distance from the anterior superior iliac spine to the belly button.) Another sign is Rovsing’s sign, which is palpation of the left lower quadrant and moving along the path of the large intestine towards the right. The obturator sign is when the person flexes the hip and knees to 90 degrees while lying down, and the clinician rotates the hip internally. The psoas sign where the person lies on their left side and the clinician extends the right hip. Since the appendix borders the psoas muscle, when it’s stretched by hip extension, the friction will lead to pain. SIGNS OF PERITONITIS (I.E. RUPTURED APPENDIX) Guarding Then there’s the Blumberg's sign, also known as rebound tenderness, where a deep palpation and quick release causes pain during the release.

Question 207

Identify appropriate investigations for appendicitis and interpret the results

Answer 207

Lab and imaging tests. Increased WCC with NEUTROPHIL DOMINANCE of around 85% Dehydration and electrolye imbalances Urinalysis to rule out genitourinary condition: - slight WCC elevation: rritation of the bladder or ureter by an inflamed appendix - significant WCC elevation: suggests UTI ULTRASOUND IS THE IMAGING OF FIRST CHOICE: - Shows enlarged appendix with diameter of more than 6mm, as well as tenderness over the appendix with compression of the USS probe - If there's an abscess, there might be increased echogenicity of inflamed periappendiceal fat, and may an appendicolith (a calcified deposit within the appendix) A CT scan is done as a follow-up if the ultrasound is inconclusive. MRI is recommended over CT in pregnant women and children who can cooperate, to minimize radiation exposure. CT findings: enlarged appendix, appendiceal wall thickening of more than 2 millimeters, periappendiceal fat stranding, appendiceal wall enhancement, and there may also be evidence of an abscess. CT has 94% sensitivity and 95% specificity so is gold standarf

Question 208

Generate a management plan for appendicitis

Answer 208

Management: -General: IV fluids, broad spectrum antibiotics pre- and perioperatively if signs of sepsis. - Surgical: appendicectomy, open or laproscopic - Post op: Abx may be continued in cases of gangernous or perforated appendix The standard treatment for appendicitis is surgical removal of the appendix, or appendectomy. The goal is to operate early, before appendiceal rupture and peritonitis develop.

Question 209

Identify the possible complications of appendicitis and its management

Answer 209

Inflammatory mass, appendiceal abscess, perforation and peritonitis, rarely portal pyaemia. Management of appendicieal abscess: -Drainage percutaneously (USS/CT guided) or itnraoperatively (with appendicectomy)

Question 210

Summarise the prognosis for patients with appendicitis

Answer 210

Appendicectomy is curative. If untreated, can be life threatening. Diagnosis can be difficult in the very young, elderly and pregnant. Morbidity and mortality in these groups are higher

Question 211

The following atypical presentations suggest which anatomical position of the appendix: Pain in the right flank Pain in the RUQ Plain in the lower abdomen

Answer 211

Pain in the right flank= retrocaecal Pain in the RUQ= long appendix Plain in the lower abdomen=pelvic appendix A pelvic appendix may be associated with urinary frequency or loose stools due to bladder of bowel irritation

Question 212

Summarise the indications for an appendicectomy

Answer 212

1) Acute appendicitis | 2) Interval proceudre following management of an appendix mass with IV antibitoics

Question 213

Which anatomical position can the appendix lie in

Answer 213

Retrocaecal (70%) Pelvic (20%) Subcaecal (2%) Pre- or post-ileal (5%)

Question 214

Identify the possible complications of an appendicectomy

Answer 214

Relatively uncommon, but presence reflects the degree of inflammmation or peritonitis: e.g. ileus, haemorrhage, wound infection, more rarely local abscess or a pelvic abscess, perforation

Question 215

Classic triad of Budd-chiari syndrome

Answer 215

No known cause in 50% of people Remaining 50%- 75% have thrombosis of hepatic vein (primary), 25% have external compression of the hepatic vein (secondary budd-chiari) - Hepatomegaly - Ascites - Abdo pain

Question 216

What is the most sensitive investigation for gall stones?

Answer 216

Abdominal USS!

Question 217

Which drugs cause cholestasis

Answer 217

``` Clavulanic acid Penicillins Oestroges Erythromycin Chlorpromazine ```

Question 218

Explain how the relation of pain to eating can help distinguish gastric from duodenal ulcers?

Answer 218

Duodenal and gastric ulcers tend to be associated with pain. The pain caused by duodenal ulcers is often epigastric and before meals/at night and relieved by eating/milk. Gastric ulcers may cause pain related to meals.

Question 219

Following an OGD successfully diagnosing gastric cancer, what would be done before surgery

Answer 219

Needs staging before surgery can be considered. This is done using a contrast enhanced chest, abdomen and pelvic CT scan. (Note ndoscopic ultrasound has little role in staging gastric cancer, but is used to stage oesophageal cancer for local invasion)

Question 220

What is the most common type of stomach cancer

Answer 220

Adenocarcinoma.

Question 221

What are the risk factors for gastric carcinoma

Answer 221

ncreasing age Male sex Poor socio-economic status Helicobacter pylori A diet involving a high level of salt and preserved foods Smoking Atrophic gastritis, pernicious anaemia, post-gastrectomy, Ménétrier’s disease, adenomatous polyps Familial risk: families with a very high incidence have been identified. There is a 2- to 3-fold increased risk to first-degree relatives of gastric cancer patients. There is a link between E-cadherin gene mutations and some familial gastric cancers. Blood group A Hypogammaglobulinaemia

Question 222

T/F stomach cancers can prosent as an ovarian mass

Answer 222

T. A Krukenberg tumor refers to a malignancy in the ovary that metastasized from a primary site, classically the gastrointestinal tract, although it can arise in other tissues such as the breast. Gastric adenocarcinoma, especially at the pylorus, is the most common source.

Question 223

What are the most common causes of bowel obstruction

Answer 223

SBO: - Intra-abdominal adhesions - Hernias - Crohn's disease - Malignancy - Volvulus LBO: Colon carcinoma Diverticilar disease Volvulus

Question 224

Where are common sites of metastasis for LBO

Answer 224

Pericolic lymph nodes Liver and lung

Question 225

Which side of the colon is more likely to obstruct when it has a tumour there and why

Answer 225

Left sided tumours are more likely to obstruct because the colonic diameter is smaller on the left side and the bowel content more solid.

Question 226

"acute cramping pain and rectal bleeding" with obstruction

Answer 226

Consistent with ischaemia

Question 227

When is a barium enema contraindicated

Answer 227

in patients who are at risk of perforation (can cause peritonitis)

Question 228

Lack of gas in the rectum makes which type of obstruction less likely

Answer 228

Pseudo-obstruction. Lack of gas in the rectum makes true obstruction more likely

Question 229

Which AXR sign suggests ischaemic obstruction

Answer 229

Thumb printing

Question 230

What is the management of a diverticular abscess

Answer 230

If small and walled off: Conservatively in the first instance using rehydration, nil by mouth and broad spectrum intravenous antibiotics. Follow-up CT to ensure abscess resolution – if enlarging consider percutaneous drainage. Interval colonoscopy will be required once acute inflammation has resolved.

Question 231

Faeculent vaginal discharge may suggest which disease? Name other complications.

Answer 231

Diverticular disease is a common cause of fistula, either with small bowel, bladder or vagina and may present with pneumaturia, or faeculent vaginal discharge. It is also a cause of profound rectal haemorrhage.

Question 232

What is the cause of most diverticular disease

Answer 232

Most diverticula are acquired, secondary to low-fibre diet and they may occur throughout the bowel, although most arise in the sigmoid region. Low-fibre diets and constipation are risk factors for the development of diverticulae.

Question 233

Define primary biliary cirrhosis

Answer 233

PBC is a chronic inflammatory liver disease involving progressive destruction of INTRAHEPATIC bile ducts, leading to cholestasis and, ultimately, cirrhosis.

Question 234

Explain the aetiology / risk factors of primary biliary cirrhosis Which antibodies

Answer 234

T cells destroying cholangiocytes lining intrahepatic bile ducts As the cholangiocytes are damaged, the tight junctions are impaired in the ducts, and bile can leak into - blood --> jaundice and hypercholesterolaemia - hepatocytes --> chronic liver disease First you get CHOLANGITIS (inflammation of the bile ducts) which then advances to cirrhosis DISEASE ASSOCIATION: - Autoimmune hepatitis - Sjorgens syndrome Antibodies to mitochondria (anti-mitochondrial antibody, AMA) - 95% have this!

Question 235

Summarise the epidemiology of primary biliary cirrhosis

Answer 235

9:1 female to male ratio! Affecting middle aged women

Question 236

Recognise the presenting symptoms of primary biliary cirrhosis

Answer 236

Can be an incidental finding on blood tests (e.g. raised alk phos and cholesterol). Fatigue, weight loss and pruritis Discomfort in the RUQ rarely May present with complication of liver decompensation: jaundice, ascites, variceal haemorrhage Symptoms of associated conditions: - Dry eyes and mouth (Sjorgens) - Arthritis, raynaud phenomenon (rheumatoid)

Question 237

Recognise the signs of primary biliary cirrhosis on physical examination

Answer 237

Early: might not be signs Late: Jaundice (once lots of the cholangiocytes are destroyed) Xanthomas (cholesterol from the bile can leak into the blood too and then be deposited) Pruritis (before jaundice sets in? But also because of bile salts in bile) Joint pain and arthropathy--> linked to rheumatoid arthritis Skin pigmentation Hepatomegaly Ascites Signs of chronic liver disease (palmar erythema, clubbing, spider naevi)

Question 238

Identify appropriate investigations for primary biliary cirrhosis and interpret the results

Answer 238

BLOOD: - LFTs (raised AlkPhos, GGT, bilirubin can be normal or raised in later stages, transaminases initially normal, then inrease with disease progression and development of cirrhosis) - AMAs - Increased IgM and increased cholesterol typical - TFTs (PBC associated with autoimmune thyroid disease) - Plasma calcium, phosphate USS: exclude biliary obstruction (gall stones and strictures) Liver biopsy: chronic inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepaticyte (repeat liver biopsies whilst on treatment)

Question 239

Complications of PBC

Answer 239

Cirrhosis and associated complications: - Jaundice - Encephalopathy - Ascites - Variceal bleeding - HCC! - Hyperlipidaemia - Malabsorption of fat soluble vitamins

Question 240

What is the use of the erect abdominal radiograph

Answer 240

Abdominal radiographs are generally performed supine- erect films are RARELY undertaken, but can demonstrate air-fluid levels in dilated small bowel So it is done only when there is strong clinical evidence of small bowel obstruction, but supine film is unhelpful

Question 241

What is a respiratory complication of a subphrenic abscess

Answer 241

You can get a reactive pleural effusion in the lobe of the right lung

Question 242

What is the imaging of choice for a subphrenic abscess

Answer 242

Chest x-ray and supine abdo xray Then ultrasound. You can visualise the abscess and then USS can guide percutaneous drainage

Question 243

What type of bacteria are usually the causative organisms of a subphrenic abscess

Answer 243

Causative pathogens tend to be anaerobes or Gram-ves.

Question 244

Does a pleural effusion reactive to a subphrenic abscess require drainage

Answer 244

Pleural effusions are usually reactive and resolve with treatment of abscess – they do not usually need drainage unless impairing respiration.

Question 245

Subphrenic abscess is a complication of which conditions

Answer 245

Perforation of hollow viscus (appendix, colon) Inflammatory process (pancreatitis, cholecystitis) Trauma of internal organs (stab, gunshot) Complication of surgery (splenectomy, cholecystectomy, gastrectomy) Idiopathic Diverticulitis

Question 246

If you are investigating the integrity of an anastomosis in the bowel, what investigation should you use

Answer 246

Contrast enema with WATER-SOLUBLE CONTRAST Water-soluble contrast should be introduced via a Foley catheter Barium contrast is contra-indicated in the presence of suspected bowel perforation – it can cause a medistinitis or peritonitis if it extravasates

Question 247

What is the main cause of anastomotic breakdown. What would need to be done usually in a failed recto-sigmoid anastamosis

Answer 247

Anastomotic breakdown is usually secondary to ischaemia (incidence of 5%) and the bowel usually needs to be defunctioned with preparation of a covering colostomy. The anastomosis may then be repaired at a later date.

Question 248

Define primary sclerosing cholangitis

Answer 248

Chronic cholestatic liver disease characterized by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts. (whereas PBC affects intrahepatic)

Question 249

Explain the aetiology / risk factors of primary sclerosing cholangitis HLA associations? Antibody association, or none significant?

Answer 249

Don't really know ASSOCIATED WITH ULCERATIVE COLLITIS (and Crohn's disease)- 70% of PSC patients have UC. About 5% of patients with UC develop PSC. Thought to be an autoimmune disease due to T cells attacking bile duct cells Associated with: HLA-B8 HLA-DR3 HLA-DRw52a pANCA is a very significant antibody association. As many as 80% of PSC patients have it

Question 250

Summarise the epidemiology of primary sclerosing cholangitis

Answer 250

Usually presents between 25 and 40 years

Question 251

Recognise the presenting symptoms of primary sclerosing cholangitis

Answer 251

May be asymptomatic, diagnosed after persistently raised AlkPhos. May present with intermittent: - Jaundice - Pruritis - RUQ tenderness - Weight loss - Fatigue Hx of ulcerative colitis

Question 252

Recognise the signs of primary sclerosing cholangitis on physical examination

Answer 252

May have no signs or have evidence of jaundice, hepatosplenomegaly, spider naevi, palmar erythema or ascites

Question 253

Identify appropriate investigations for primary sclerosing cholangitis and interpret the results

Answer 253

BLOODS: -LFTs: Raised ALP, GGT, mild raised transaminases. Later, raised bilirubin and reduced albumin SEROLOGY: - Elevated IgM in the serum - Elevated pANCA (70%), raised ASM and ANA (~30%) ERCP: Stricturing and interspersed dilation (beading) of intrahepatic and, occasionally, extrahepatic bile ducts, small diverticula on the common bile duct may be seen. MRCP: Enables non-invasive imaging of the biliary tree. Liver biopsy: Confirms diagnosis and allows staging of disease. HISTOLOGY: -Onion skin appearance of bile ducts, due to concentric rings of fibrosis

Question 254

Complications of PSC

Answer 254

Recurrent cholangitis, biliary cirrhosis, cholangiocarcinoma (bile duct carcinoma,!15% of cases), portal hypertension (encephalopathy, ascites/oedema, variceal bleeding), metabolic bone disease.

Question 255

What do the following AXR signs represent Coffee bean sign Embryo sign

Answer 255

A caecal volvulus produces a gas bubble on AXR that looks like an embryo and, hence, is called ‘embryo sign’. A sigmoid volvulus produces a gas bubble in the shape of a coffee bean – ‘coffee bean sign’.

Question 256

What are the 4 ways of detecting H Pylori infection`

Answer 256

1) Urea breath test 2) Blood antibody test 3) Stool antigen test 4) Rapid urease test/campylobacter like organism (CLO) test

Question 257

Outline the urea breath test

Answer 257

The patient swallows urea labelled with radioactive carbon-14. If CO2, containing the labelled carbon, is detected in the patient’s breath 10-30 minutes later, it suggests that the urea has been cleaved by urease produced by H. pylori.

Question 258

Outlien the CLO test

Answer 258

A biopsy of stomach mucosa is put into a medium containing urea and an indicator. The urease produced by H.pylori hydrolyses urea to ammonia, which changes the pH of the medium and makes the indicator change colour.

Question 259

What are diverticulae

Answer 259

Diverticulae are outpouchings of the mucosa and submucosa that have herniated through the muscularis.

Question 260

What is the cause of rectal bleeding in divertciulitis

Answer 260

They most commonly occur in the sigmoid and descending colon, particularly at the sites of nutrient artery penetration (hence, the rectal bleeding).

Question 261

What does cryptosporidium cause

Answer 261

diarrhoeal illness in immunocompromised patients

Question 262

# Define diverticular disease Define: diverticulosis, divercular disease, diverticulitis. How is it classified

Answer 262

Diverticulosis: The presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel. Diverticular disease: Diverticulosis associated with complications, e.g. haemorrhage, infection, fistulae. Diverticulitis: Acute inflammation and infection of colonic diverticulae. Hinchey classification of acute diverticulitis: Ia: phlegmon, IbandII: localizedabscesses, III: perforation with purulent peritonitis or IV: faecal peritonitis

Question 263

Explain the aetiology / risk factors of diverticular disease What causes diverticulitis

Answer 263

Anywhere in GI tract but most commonly colon. Formed in areas of high pressure, this is why most common in the sigmoid colon (which has the lowest diameter in the colon, and thus the highest pressure) Association with low fibre, thus constipation. Symptoms may be worse when eating red meat May be a secondary cause e.g. connective tissue disorders like Marfan and Ehlers Danlos Often occurs where there is nutrient artery perforating the colon wall, making this part of the muscle weaker. Diverticulitis is an inflamed diverticula, due to erosion from high pressures (more likely) or lodged faecolith (less common). This can lead to bacterial overgrowth, leading to: diverticulitis, perforation, pericolic phlegmon, abscess, ulceration, fistula or stricture (which can lead to obstruction)

Question 264

Summarise the epidemiology of diverticular disease

Answer 264

COMMON! 60% of people living in industrialized countries will develop colonic diverticula, rare <40years. Right-sided diverticula are more common in Asia.

Question 265

Recognise the presenting symptoms of diverticular disease When does bleeding occur. Hx for diverticulosis, diverticulitis and diverticular fistula please.

Answer 265

Diverticulosis- diverticula not infected or inflamed: - Often asymptomatic (80-90%) - Stomach pain - Rectal bleeding (haematochezia) because the vessels are now only protected from the lumen by mucosa (no longer run in the muscle layer, as the mucosa has pouched into the muscle). Often found incidentally Diverticulitis is NOT ASSOCIATED with rectal bleeding (haematochezia) because the blood vessels are scarred from bleeding: - Ass with left lower quadrant pain - Fever Diverticular fistula with the bladder: pneumaturia, faecaluria, recurrent UTI.

Question 266

Recognise the signs of diverticular disease on physical examination

Answer 266

Diverticulitis: tender abdomen + signs of local or generalised peritonitis if perforation has occurred

Question 267

Identify appropriate investigations for diverticular disease and interpret the results Acute setting?

Answer 267

Hb: FBC. High WCC and CRP in diverticulitis. ``` Barium enema (+/- air contrast)- NOT IN THE ACUTE SETTING: -Demonstrates presence of diverticulae with saw-tooth appearance of lumen. Contraindicated with diverticulitis in case there is perforation ``` Flexible sigmoidoscopy & colonoscopy: -Diverticulae can be seen. Other pathology excluded. IN ACUTE SETTING: -CT scan for evidence of diverticular disease and complication

Question 268

Generate a management plan for diverticular disease Asymptomatic? If diverticulitis? Surgical options

Answer 268

Aysymptomatic (diverticulosis) : -No treatment (maybe some more fibre in diet) Symptomatic diverticular disease: - Dietary modification and fibre supplements - Oral Abx Symptomatic diverticulitis (uncomplicated) - Analgesia - Oral Abx therapy - Low residue diet - Swtich to IV Abx if goes on >72hr Symptomatic diverticulitis with acute rectal bleeding - Endoscopic haemostasis, if fails then angiographic embolisation if fails then surgery - Oral Abx - Analgesia Symptomatic diverticulitis unresponsive to IV Abx or with abscess >3cm diameter, perforation, fistulae or obstruction - Radiological drain/surgery - IV Abx - Analgesia Surgery (For patients with severe or diffuse peritonitis): Open: hartmann's procedure (resection and stoma) or one-stage resection and anastomosis (risk of leak and defunctioning stoma though) Laparscopic (more recent): drainage, peritoneal lavage and drain placement

Question 269

Identify the possible complications of diverticular disease and its management

Answer 269

Diverticulitis Pericolic abscess Perforation Faecal peritonitis Colonic obstruction Fistula. The diverticulae may rupture and then form a fistula, e.g. with the bladder. Which can cause faecal matter OR AIR in the urine. Haemorrahge

Question 270

Summarise the prognosis for patients with diverticular disease

Answer 270

Ten to 25% of patients will have one or more episodes of diverticulitis. Of these, 30% will have a second episode.

Question 271

What are the GI causes of clubbing

Answer 271

Inflammatory bowel disease (e.g. ulcerative colitis and Crohn’s disease) is liver cirrhosis, primary biliary cirrhosis, oesophageal leiyomyoma, coeliac disease and achalasia.

Question 272

Define gastritis

Answer 272

Inflammation of the gastric mucosa. Acute: neutrophil invasion Chronic: lymphocyte and plasma cell infiltration

Question 273

Explain the aetiology / risk factors of gastritis What causes acute gastritis

Answer 273

Acute gastritis is an imbalance between mucosal defenses and acidic environment of the stomach Starts with gastric EROSIONS (which penetrate only into the mucosa). These are NOT gastric ulcers (which penetrate into the submucosa and deeper) These can be caused by: - XS alcohol, corticosteroids, meds - NSAIDS - H Pylori infection - Extreme physiological stress (sepsis, shock, trauma) ----------------------- Chronic gastritis is caused by chronic inflammation due to: -H Pylori (most common type of gastritis), affects antrum. CagA is carcinogenic from H Pylori -AI gastritis (type IV hypersensitivity) It is characterised by chronic inflammation leading to gastric atrophy and metaplasia and dysplasia, and gastric adenocarcinoma AI gastritis also associated with increased risk of neuroendocrine tumours

Question 274

Summarise the epidemiology of gastritis

Answer 274

.

Question 275

Recognise the presenting symptoms of gastritis

Answer 275

ACUTE GASTRITIS: Epigastric pain Nausea Vomiting Life threatening upper GI bleed (can cause melaena) --------------------- Symptoms: Asymptomatic sometimes Epigastric pain Nausea Vomiting

Question 276

Identify appropriate investigations for gastritis and interpret the results

Answer 276

``` Diagnosis: Endoscopic biopsy Detection of H pylori using: -Serology -Stool antigen test -Urease breath test ```

Question 277

Generate a management plan for gastritis

Answer 277

Treating the underlying cause (remove NSAIDs) Antacids Antibiotics to eradicate the H Pylori infection: -Triple therapy: PPI + clari + amoxicillin for 2 weeks

Question 278

Identify the possible complications of gastritis and its management

Answer 278

Chronic: Infectious (H Pylori): Peptic ulcers, MALTomas Autoimmune: Pernicious anaemia, iron deficiency anaemia, carcinoid tumour

Question 279

Define peptic ulcer disease

Answer 279

Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin

Question 280

Explain the aetiology / risk factors of peptic ulcer disease and gastritis Where are the gastric ulcers and duodenal ulcers usually located

Answer 280

Imbalance between damaging action of acid and pepsin and mucosal protective mechanism. STRONG CORRELATION with H. PYLORI. RF: - H pylori (95% of duodenal ulcer and 70-80% of gastric ulcer) - NSAID use - Zollinger Ellison (rare) Gastric ulcers usually in gastric antrum Duodenal usually in duodenal bulb

Question 281

Summarise the epidemiology of peptic ulcer disease and gastritis

Answer 281

Common. Annual incidence is about 1–4/1000. More common in males. Duodenal ulcers have a mean age in the thirties, while gastric ulcers have a mean age in the fifties. H. pylori is usually acquired in childhood and the prevalence is roughly equivalent to age in years.

Question 282

Recognise the presenting symptoms of peptic ulcer disease and gastritis

Answer 282

Epigastric abdominal pain, relieved by antacids Variable relationship with food. Worse when eating (or 30 minutes after) --> more likely to be gastric. (may lose weight as they avoid meals) Worse several hours later (actually improves with eating, so may be weight gain??) --> duodenal May present with complications (haematemesis, malaena)

Question 283

Recognise the signs of peptic ulcer disease and gastritis on physical examination

Answer 283

May be none. Epigastric tenderness Signs of complicaations (anaemia, succession splash in pyloric stenosis)

Question 284

Identify appropriate investigations for peptic ulcer disease and gastritis and interpret the results

Answer 284

BLOODS: - Hb (anaemia) - Amylase (exclude pancreatitis) - U&Es - Clotting screen (if GI bleeding) - LFT ENDOSCOPY: - 4 quadrant gastric ulcer biopsies to rule out malignancy - Duodenal ulcer need NOT be biopsies ROCKALL SCORING: -For severity of GI bleed. <3 is good prognosis. >8 have high mortality risk ``` H PYLORI TEST: C-Urea breath test Serology: IgG Ab against H Pylori Stool antigen test Campylobacter like organism test (YELLOW TO RED if present) ``` Histology of biopsy of limited value

Question 285

Generate a management plan for peptic ulcer disease and gastritis ACUTE

Answer 285

ACUTE: -Resuscitation if perforated or bleeding (IV colloids/crystalloids), close monitoring of vital signs, and proceeding endoscopic or surgical treatment. Acute meds: -Patients with upper GI bleeding should be treated with IV PPI at presentation until cause of bleeding confirmed -Patients with active bleeding peptic ulcer should continue IV PPI -Swtich to oral PPI if there is no rebleeding within 24 hrs Acute endoscopy: -Haemostasis by injection sclerotherapy, laser or electrocoagulation Acute surgery: If perforated or ulcer-related bleeding cannot be controlled ``` NON-ACUTE: H. Pylori eradication: Triple therapy for 1-2 weeks 1 PPI and 2 Abx e.g. (clari + amox + omeprazole) or (metronidazole + tetra + omeprazole) ``` IF NOT associtated with H Pylori: -PPIs for at least 8 weeks or H2 antagonists. Stop NSAID use (especially diclofenac, use misoprostol if NSAID use is necessary)

Question 286

Identify the possible complications of peptic ulcer disease and gastritis and its management

Answer 286

Rate of major complication is 1% per year including: 1) Haemorrhage (haematemesis, melaena, iron-deficiency anaemia) 2) perforation (more common in anterior wall of duodenum) 3) obstruction/pyloric stenosis due to scarring, penetration, pancreatitis). 4) Malignant gastric ulcer (gastric MALT lymphoma, gastric adenocarcinoma)

Question 287

Summarise the prognosis for patients with peptic ulcer disease and gastritis

Answer 287

Overall lifetime risk"10%. Generally good as peptic ulcers associated with H. pylori can be cured by eradication.

Question 288

How do NSAIDs affect the gastric musocsa

Answer 288

They block the COX enzyme, which reduces production of prostaglandin E2 Prostaglandin E2 protects gastric mucosa by increasing mucus production and suppressing gastric acid production

Question 289

Outline stress ulcers

Answer 289

Sepsis, shock and trauma can lead to stomach erosions. Specific types: curling's ulcers (secondary to burns) and cushings ulcer (secondary to brain injuries)

Question 290

What might point you towards zollinger ellison with a peptic ulcer

Answer 290

If the ulcer is in the DISTAl duodenum or another atypical place

Question 291

What causes haemorrhage in gastric ulcer and duodenal ulcer

Answer 291

When gastric ulcer in lesser curvature of the stomach erodes into the left gastric artery When duodenal ulcer erodes into posterior wall of duodenum and into the gastroduodenal artery

Question 292

What is the most common cause of iron deficiency anaemia in men <50 vs men >50

Answer 292

under 50: peptic ulcer over 50: colorectal carcinoma

Question 293

How can perforated duodenal ulcer present

Answer 293

Referred pain to shoulder due to irritation of phrenic nerve and pneumoperitonuem (free air under diaphragm)

Question 294

What is zollinger ellison syndrome

Answer 294

Gastrinoma (secretes gastrin --> hyperacidic environment)

Question 295

What medications worse GORD

Answer 295

Drugs that damage the mucosa: NSAIDs, steroids, bisphosphinates, aspirin Drugs that affect eosophageal motility: nitrates, TCAs and anticholinergics

Question 296

Management of GORD

Answer 296

GORD is managed with lifestyle interventions such as stopping smoking, avoiding spicy food, losing weight, having small, regular meals and avoiding eating before bed. Patients are usually started on a once daily PPI and patients who do not respond should be offered twice daily PPIs.

Question 297

Triad of features assocaited with acute mesenteric ischaemia

Answer 297

Severe abdominal pain, normal abdo examination and shock

Question 298

Cause of acute mesenteric ischaemia

Answer 298

This is characterised by vascular compromise of the small bowel due to occlusion of the superior mesenteric artery

Question 299

What is the cause of acute vs chronic mesenteric ischaemia

Answer 299

Acute disease occurs due to arterial thrombosis (e.g. due to atherosclerosis) or embolism (e.g. due to emboli from AF). Other causes of acute mesenteric ischaemia include venous thrombosis (in hypercoagulable states) and non-occlusive disease (e.g. hypotension). Chronic mesenteric ischaemia usually occurs due a combination of a low-flow state, such as heart failure, and atherosclerotic disease.

Question 300

How does chronic mesenteric ischaemia present

Answer 300

It presents with ‘gut claudication’ (poorly localised, colicky, post-prandial abdominal pain), PR bleeding and weight loss.

Question 301

What are the x ray findings associated with severe mesenteric ischaemia

Answer 301

In advanced disease, it may show a gasless abdomen, thickening of the bowel wall and pneumatosis (air within the bowel wall due to necrosis). If the abdominal X-ray in inconclusive, a CT scan should be performed.

Question 302

What is riglers sign and pneumoperitneum and what are they signs of

Answer 302

Rigler'- air present on both sides of the bowel wall, creating the impression of a double wall Pneumoperitoneum (air under the diaphragm) are signs of perforation.

Question 303

T/F constipation can present with diarrhoea

Answer 303

T. Faecal impaction in the distal colon can lead to liquid stools leaking through the little space left in the lumen causing, what is known as, overflow diarrhoea. It can lead to faecal incontinence.

Question 304

What are the cell types in the anus

Answer 304

Dentate line. separates the upper 2/3 from the lower 1/3 of the anus. Upper: mucosa lined by simple columnar epithelium Lower: Anoderm (squamous epithelium)

Question 305

What are haemmarhoids

Answer 305

Now, hemorrhoids are normal vascular structures in the anal canal that act as cushions for the stool as it passes through.

Question 306

What is haemarrhoidal disease

Answer 306

Hemorrhoidal disease is when hemorrhoids get swollen or inflamed; but the term "hemorrhoid" is often used to refer to the disease.

Question 307

Aertiology and risk factors for haemarrhoids

Answer 307

Hemorrhoids are often caused by chronically or recurrently increased abdominal pressure, from a variety of causes. For example, straining during bowel movements, chronic diarrhea or constipation, obesity, pregnancy, and old age.

Question 308

Classify haemarrhoids into 2 typesq

Answer 308

Internal hemorrhoids are ones above the dentate line, and external hemorrhoids are ones below the dentate line.

Question 309

Grade internal haemorrhoids

Answer 309

Internal hemorrhoids are subclassified into four grades based on the degree of prolapse from the anal canal. Grade I hemorrhoids don’t protrude outside the anal canal. Grade II hemorrhoids protrude outside the anus during bowel movement, but they retract spontaneously. Grade III are prolapsed hemorrhoids that don’t retract spontaneously, but they can be pushed back in manually. Finally, grade IV hemorrhoids are prolapsed hemorrhoids that cannot be manually pushed back in.

Question 310

History of haemorrhoids

Answer 310

Internal hemorrhoids usually don’t cause symptoms, but sometimes they get inflamed, causing itching and painless passage of bright red blood with a bowel movement. On the other hand, external hemorrhoids are innervated somatically, and they’re typically painful, especially when associated with thrombosed hemorrhoids, which have no blood flow due to a blood clot in the vein, and swelling in the affected area. Bright red bleeding on toilet paper or dripping into pan after passage of stool. NEVER MIXED WITHIN STOOL. Itching, anal lumps

Question 311

Signs of haemorrhoids - Puruple/blue veins? - Dark pink, glistening masses at the anal margin? - Purplish hue?

Answer 311

A diagnosis is usually made based on a visual and digital exam of the anus (can see grade III and grade IV) Internal hemorrhoids look like bulging purplish-blue veins, and prolapsed internal hemorrhoids appear dark pink, glistening, and are sometimes tender masses at the anal margin. Thrombosed external hemorrhoids are tender and have a purplish hue.

Question 312

Investigations for haemorrhouds

Answer 312

Diagnosis of stage III and IV internal haemmorhoids and external haemorrhoids can be made on examination, but grade I and II internal haemorrhouds can’t be seen or felt, and confirmation requires anoscopy

Question 313

If there are haemrrhoids with changes in bowel habits?

Answer 313

Further testing with flexible sigmoidoscopy or colonoscopy is recommended if signs and symptoms suggest another digestive system disease and in individuals older than 40 years with symptoms of colorectal cancer, like weight loss and change in bowel habit

Question 314

Management of haemorrhoids

Answer 314

Conservative: High fibre diet, fluid intake, topic creams containing LAs, corticosteroids on short term basis Local therapy (for 1st and 2nd degree): - Injection sclerotherapy (5% phenol injected into submucosa above a haemarrhoid) - Banding proximal to haemorrhoid (higher cure, but more painful0 Surgical (3rd and 4th degree, symptomatic): Open haemorrhoidectomy= incision of haemorrhoidal cushions with preservation of skin between the haemorrhoids to avoid stricturing. Stapled haemorrhoidectomy. Post op: laxatives, metronidazole

Question 315

Complications of haemorrhoids What about of slerotherapy and haemorrhoidectomy

Answer 315

Bleeding, prolapse, thrombosis Slcero: prostatitis, perineal sepsis, rarely impotence Haemorhoidectomy: pain, bleeding, incontinence

Question 316

Anal fissure definition and causes T/F the pathology of anal fissure just relates to the skin

Answer 316

Elongated ulcer in anal canal lower part Trauma: constipation tears posterior anal lining. In pregnant women, anterior fissures more common as damaged pelvic floor elaves anterior anal tissues less supported Inflammation: IBDs ------------ Mechanical tear in anal mucosa + sphincter spasm

Question 317

Age for anal fissure

Answer 317

Most common under age of 40. Male=female

Question 318

Hx of anal fissure

Answer 318

Severe burning pain on defaecation, can persist for hours Patients may avoid bowel movements Bright red bleeding per rectum, small amount Itchy

Question 319

Examination of anal fissure

Answer 319

Can see a sentinel pile. DRE may not be possible due to pain Chronic fissures --> firm, indurated ridge

Question 320

Investigations of anal fissure

Answer 320

Diagnosis on history Exclude other things

Question 321

Management of anal fissure

Answer 321

ON PRESENTATION: Conservative: ensure stools soft and easily passed Medical: conservative GTN (but can cause headache), topical dilitiazem RESISTANT: Surgical: Botox/surgical sphincterotomy. Botox more recently 2nd line anal advancement flap

Question 322

Complication of anal fissure

Answer 322

Chronic fissure and chronic pain

Question 323

What is a pilonidal sinus

Answer 323

Abnormal epithelium line tract filled with hair that opens to the skin surface, most commonly into natal cleft

Question 324

Cause of pilonidal sinus

Answer 324

Caused by sheared hairs penetrating the skin and inciting inflammatory reaction, with intermittent negative pressure drawing in more hair

Question 325

Epidemiology of pilonidal sinus

Answer 325

Ass with hirsute individuals. Occupations like hairdressors may develop interdigital pilonidal sinus

Question 326

Hx of pilonidal sinus

Answer 326

Painful natal cleft, esppecially if inflamed/superimposed infection Discharge and swelling

Question 327

Examination of pilonidal sinus

Answer 327

Midline opening or pits seen between buttocks, hair may protrude Tender swelling that may be fluctant/discharge etc. if assocaited infection/abscess

Question 328

Investigation of pilonidal sinus

Answer 328

None needed for diagnosis, If infection raised WCC Glucose (diabetes)

Question 329

Management of acute pilonidal sinus Management of chronic pilonidal sinus

Answer 329

Incision and drainage under LA if small, for evaculation of pus and hair. Cavity irrigated and packed, dressings changed regualry to allow secondary closure. Not usually nececssary for Abx post op Chronic: sinus tract excision under GA with exploration, laying open and removal of tract. Wound closure by primary closure, or left open and healing by secondary intention. Wounds closed primarily heal more quickly, but higher risk of recurrence Karydakis operation: asymmetric excision with lateral closure, flattnes nad lateralises midline cleft Bascom technique

Question 330

Define Perianal abscess Perianal fistula

Answer 330

Abscess: pus collection in perianal region Fistula: abnormal chronically infected tract communicating between perianal skin and either anal canal or rectum

Question 331

Types of perianal abscess

Answer 331

Classified according to location

Question 332

What are the anatomical landmarks for discrubing a low anal vs high anal fistula

Answer 332

low- below puborectalis high- at or above puborectalis pelvirectal- involving levator ani

Question 333

Pepperpot perineum sign?

Answer 333

Multiple perineal fistulae (Crohn's disease)

Question 334

What is perianal fistulae ass with

Answer 334

Crohn's, diabetes, malignancy

Question 335

History in perianal fistulae/absces

Answer 335

Constant throbbing pain in perineum Intermittent discharge (blood stained/mucus) near anal region

Question 336

Perianal fistula/abscess examination

Answer 336

Localised tender perianal swelling or small skin opening with discharge, corresponding to opening of fistula PR an area of induration corresponding to abscess or fistula tract.

Question 337

What is goodsall's rule

Answer 337

Rule of tump to correlate location of internal fistula opening based on location of external fistula opening. If external opening is anterior to anal canal, fistula runs radially and directly into the anal canal If external opening is posterior to the anal canal, the fistula follows a curved path, opening internally in the posterior midline

Question 338

Investigations for perianal fistula/abscess

Answer 338

Clinical examination, under anaesthetic if neccessary Blood: FBC, CRP, ESR, blood cultures if pyrexial Complex fistulae: MRI extremely useful to study tracts, and plan for surgical excision Endoanal ultrasound: used by less useful

Question 339

Management of perianal abscess/fistula

Answer 339

SURGICAL, under anaesthaesia. Open drainage of abscess: incision and drainage. ALL patients should be put on broad spectrum antibiotics with gram -ve cover. E.g. Ampicillin + metronidazole Antibiotics useful if there is surrounding cellulitis

Question 340

Rectal prolapse in a child which investigation

Answer 340

Sweat chloride test- 10% will have CF

Question 341

Investigations for rectal prolapse

Answer 341

Proctosigmoidoscopy, defaecating proctogram or barium enema

Question 342

Management of rectal prolapse Conservative Emergency Chronic

Answer 342

Conservative: bulk laxatives. high fibre diet might be sufficient in kids Emergency: Acute prolapse may be manually reduced after adequate analgesia. Patients nursed with ice packs topically prior to attempted manual reduction to reduce swelling If bowel is gangrenous, excision by rectosigmoidosicopy Incomplete prolapse: -Submucosal sclerotherapy with pnol, bandoing or haemorrhoidectomy Complete prlapse: - Operative repair using laparoscopic, abdominal or perineal approaches. - E.g. ripstein rectopexy is

Question 343

Prognosis of rectal prolapse

Answer 343

Sponatenosusly resolves usually in kids 15% recurrence in adults

Question 344

What are the following surgical procedures used for 1) Hartmann's 2) Left colectomy 3) Abdomino-perineal resection 4) Anterior resection 5) Delorme's procedure

Answer 344

1) Removal of sigmoid (you remove the area, and then create a rectal stump and an end colostomy. You then perform primary anastamosis at a later date (if it's an emergency at the time with inflammation etc.) 2) CaSncer localised to descending colon Remove from 2/3 along transverse colon down to the beginning of the sigmoid. 3) Low lying rectal cancers- removes anus, rectum and part of sigmoid. End colostomy 4) High lying rectal tumour. emoves upper 2/3 of rectum and part of sigmoid colon. Anal sphoncter remains in tact and an anastamosis formed 5) Delorme's- full thickness rectal prolapse

Question 345

Differentiating between anal fissure and haemorrhoids

Answer 345

An anal fissure is a painful tear in the squamous lining of the lower anal canal, which causes pain on defecation and bright red blood streaked on the toilet paper/stools but not mixed in with the stools. Anal fissures often occur in patients with a low fibre diet and poor fluid intake who may be constipated and strain at the stool. Haemorrhoids are enlarged and engorged anal vascular cushions that can bleed. They are very common and usually present with bright red rectal bleeding that is separate to the stool and may drip into the pan after defecation.

Question 346

Peutz-jehger syndrome

Answer 346

Diffuse GI polyp + mucocutanous pigmentation of lip and gum BENIGN but increased risk of cancer

Question 347

Familial polyposis coli Inheritence?

Answer 347

Multiple stomach, small and large bowel adenomas. Autosomal dominant premalignant

Question 348

Gardner's syndrome

Answer 348

Osteomas, soft tissue tumours, sebaceous cysts, congeital hypertrophy of RPE and multiple colonic adenomas.

Question 349

Turcots syndrome

Answer 349

Glioblastomas or medulloblastomas with mutliple clonic adenomas. Premalignant ``` Turcot syndrome is a variant of familial adenomatous polyposis (FAP) that is characterized by extensive polyposis of the GI tract as well as CNS tumors, usually medulloblastoma . ```

Question 350

Cronkhite canadas syndrome

Answer 350

Alopecia, nail atrophy, pigmentation, watery diarrhoea, multiple colnic adnomas, premalignant

Question 351

What is receommended in familial polposis coli

Answer 351

Early subtotal colectomy

Question 352

Aetiology of colorectal cancer

Answer 352

Sequence from epithelial dysplasia to adenoma and then carcinoma. Accumulation of genetic changes, activation of oncogenes (APC, K-ras) and inactication of tumour suppresser genes (p53, DCC)

Question 353

RF for colorectal cancer

Answer 353

Colorectal polyps Previous CRC IBD (particularly UC) Genetic syndromes (FAP, lynch sydrome)

Question 354

Gender specifics of colorectal cancer

Answer 354

Rectal, male>female | Colon female>male

Question 355

History of colorectal cancer

Answer 355

Can be asymptomatic and present with faecal occult bloods. Left sided: change in bowel habit, rectal bleeding or blood/mucus mixed with stools. Right sided: Later presentation, symptoms of anaemia, weight loss and non-sepcifc malaise (more rarely lower abdo pain) Rectal masses: tenesmus

Question 356

What might CRC look like on barium enema

Answer 356

Apple core lesion, for annular tumours

Question 357

Investigations for CRC

Answer 357

Screening: blood (FBC), stool (occult or frank) Endoscopy: sigmoidoscopy and colonoscopy allows visualisation and biopsy. Imaging: barium enema, CT scan, MRI, endorectal ultrasound.

Question 358

State the operation for the following cancers: - Caecal tumour - Transverse colon tumours - Descending colon tumours - Sigmoid tumours - High mid-rectal - Low rectal - Emergency

Answer 358

- Caecal tumour: right hemicolectomy - Transverse colon tumours: extended right hemicolectomy - Descending colon tumours: left hemicolectomy - Sigmoid tumours: anterior resection - High mid-rectal: Anterior resection with total mesorectal excision - Low rectal: Abdominoperineal resection if unable to clear below tumour - Emergency: Hartmann's procedure

Question 359

Chemo and radio for CRC?

Answer 359

Radio: neoadjucant Chemo: FOLFOX (5-FU)

Question 360

Dukes staging

Answer 360

``` A=confined to bowel wall B= breached serosa, no lymph nodes C1=breached serosa, lymph node involved but not apical C2=breached serosa, apical lymph nodes D=distant mets. ```

Question 361

At what portal pressure might anastamoses become congested and dilated

Answer 361

When the portal pressure is > 12 mm Hg, these | anastomoses become congested and dilated, and are prone to bleeding.

Question 362

Organisms commonly involved in SBP

Answer 362

The bacteria most commonly involved are E. coli and Klebsiella pneumoniae

Question 363

Which transaminase is higher in the serum with alcoholic hepatitis. What is the ratio

Answer 363

An AST to ALT ratio (AST:ALT) > 2 is suggestive of liver damage secondary to alcohol abuse. Chronic alcohol consumption also induces a rise in serum GGT.

Question 364

Symptomatic GORD, lower dysphagia and painless regurgitation of food. Likely diagnosis

Answer 364

Hiatus hernia

Question 365

2 types of hiatus hernia

Answer 365

Sliding (80%): Gastro-oesophageal junction (GEJ) slides into the thorax Rolling: GEJ remains in place but a bulge of fundus herniates into the chest alongside the oesophagus

Question 366

Best investigation for hiatus hernia

Answer 366

Barium swallow is the best investigation to confirm the diagnosis

Question 367

What might hiatus hernia show in chest x ray

Answer 367

If the hiatus hernia is very large, a CXR may show a retrocardiac mass with an airfluid level. `

Question 368

Management of hiatus hernia

Answer 368

Management of a hiatus hernia comprises of lifes`tyle changes (e.g. weight loss), treatment of reflux (PPIs) and surgery in refractory cases. Nissen fundoplication is the most commonly used surgical procedure for hiatus hernias.

Question 369

Criteria for acute severe colitis (in UC)

Answer 369

``` Frequency of stool >6 Overtly bloody stool Fever (>37.5) Tachycardia (>90) Anaemia (Hb<105) Raised ESR (>30) ```

Question 370

Management of acutely presenting UC

Answer 370

1st line -->IV steroids 2nd line --> asporin 3rd line --> infliximab (Bone protection also required, so give Adcal D3 with it) Heparin is really important because patients with acute s evere ulcerative colitis are at high risk of thromboembolic events so unless they have significant haemorrhage, the risk of a clot is higher than the risk of bleeding.

Question 371

What is a loop vs end ileostomy

Answer 371

End ileostomy is when everything distal to the stoma is cut out (i.e the whole colon) Loop ileostomy is used when, there is still a colon, but, for example, you are waiting for a wound to heal further round the colon. So you cut the ileum open onto the skin, so that the faecal matter doesn't pass through the colon to allow it to heal first

Question 372

What is the faecal matter like that comes from an ileostomy | How to deal?

Answer 372

Faecal matter will be more liquid in nature High output from this type of stoma can quickly lead to dehydration. Loperamide/ codeine may be needed to control the output

Question 373

What does an ileostomy look like compared to a colostomy

Answer 373

the ileum will form a ‘spout’ at the skin surface (compared to a colostomy which will be flat)

Question 374

Which 3 symptoms are diagnostic of acute cholangitis

Answer 374

The triad of acute pain, fever and jaundice is diagnostic of ascending cholangitis

Question 375

Initial treatment of ascending cholangitis

Answer 375

The initial treatment is intravenous antibiotics and intravenous fluid (often a lot of i.v. fluid is needed for resuscitation). Analgesia may also be required. Especially during these initial investigations the patient is likely to be kept nil by mouth, making IV fluids even more important.

Question 376

T/F a bile duct always dilates after a cholecystecomy anyway

Answer 376

The common bile duct can dilate after cholecystectomy, although not usually much above 7mm in patients of this age. So dilation >7mm might indcate a stone

Question 377

Investigation if you suspect a stone given abdo USS

Answer 377

MRCP is a non-invasive tool which is good at evaluating the biliary tree. The stone may already have passed so ERCP may not be necessary However there can often be a delay in organising an MRCP and many clinicians would proceed with ERCP in a patient with evidence of ascending cholangitis and a dilated CBD

Question 378

What procedure can be done to remove stones, what if it's not possible

Answer 378

ERCP is the technique of choice although if this is not technically possible for some reason then these stones can be reached and stents inserted etc. at PTC performed by interventional radiology. (percutaneous transhepatic cholangiogram and stone retrieval) Open bile duct exploration is a last resort due to a high mortality risk.

Question 379

What is HCC

Answer 379

Primary malignancy of hepatocytes, usually occurring in a cirrhotic liver.

Question 380

Aetiology of HCC

Answer 380

3 main causes 1) Chronic liver damage (e.g. alcoholic liver disease, hepatitis B, hepatitis C, autoimmune disease), . 2) Metabolic disease (e.g. haemochromatosis), and . 3) Aflatoxins (Aspergillus flavus fungal toxin found on stored grains or biological weapons).

Question 381

T/F primary HCC is more common than secondary malignancy of the liver

Answer 381

Common making up 1–2% of all malignancies, but less common than secondary liver malignancies.

Question 382

Hx of HCC

Answer 382

Symptoms of malignancy: Malaise, weight loss, loss of appetite. Symptoms of chronic liver disease: Abdominal distension, jaundice. History of carcinogen exposure: High alcohol intake, Hepatitis B or C, aflatoxins.

Question 383

Examination HCC

Answer 383

Signs of malignancy: Cachexia, lymphadenopathy. Hepatomegaly: Nodular (but may be smooth). Deep palpation may elicit tenderness. There may be bruit heard over the liver. Signs of chronic liver disease: Jaundice, ascite (see Cirrhosis).

Question 384

Investigation of HCC

Answer 384

Blood: raised AFP (high sensitivity). LFT can show biliary obstruction Imaging: - (1st imaging): Abdo USS, but it is not sensitive for tumours <1cm - (superior imaging, but not 1st line) CT (CAP): to define structural lesion and spread - Duplex scan of liver: for large vessel invasion - Liver biopsy (usually NOT required for diagnosis) confirms histology of tumour, but risk of tumour seeding along biopsy tract Staging: -CXR, CT CAP, radionuclide bone scan Screening: AFP and abdominal USS in at-risk individuals

Question 385

What is a HCC in young people with no Hx of liver disease, and what tumour marker can be used

Answer 385

Vitamin B12-binding protein is a marker of fibrolamellar hepatocellular carcinoma

Question 386

What is the management of gastroenteritis

Answer 386

Gastroenteritis is a self-limiting disease that can be managed with bed rest and oral rehydration (to compensate for fluid and electrolyte losses from sweating, diarrhoea and vomiting). Admit if cannot retain oral fluids, has features of shock or is severely dehydrated. Abx prescribed when causative organism identified by stool culture

Question 387

Blistering rash on the elbows?

Answer 387

Dermatitis herpetiformis

Question 388

Differentiate hiatus hernia sliding and rolling

Answer 388

Overall it's herniation of contents of abdominal cavity into the mediastinum through the eosophageal hiatus in the diaphragm. Sliding: GOJ is a above diaphragm Rolling (or paraeosophageal): defect in phreno-eosophageal membrane. GOJ does not move but fundus is lead point of herniation You can get a mixed type (=type III) And type IV is when other abdo contents come through too

Question 389

Aetiology of hiatus hernia

Answer 389

Congenital or acquired. Thinning and increased laxity of the phreno-oesophageal ligament with age Associated with obesity, GORD, chronic eosophagitis

Question 390

Which hiatus hernia is more common

Answer 390

Type 1 (95%) Increase in frequency with age

Question 391

Hx of hiatus hernia

Answer 391

Many asymptomatic. Reflux symptoms of heart burn, indigestion, postprandial fullness and regurg No examination findings unless complications develop

Question 392

Investigation for hiatus herna.

Answer 392

1st line: Upper GI series (i.e. barium x-ray), chest ray (retrosternal cardiac bubble) OGD doesn't rule out. But patients with reflux symptoms should have this to check for eosophagitis or dysplasia CT/MRI when diagnosis not clear Manometry and pH monitoring- double hump configuration seen due to gastric herniation above high pressure zone of the crura.

Question 393

Management of hiatus hernia

Answer 393

Conservative: modification of lifestyle factors (weight loss, avoid late meals) Medical management if there's symptomatic GORD. PPIs Surgical repair if refractory to medical therapy. Laparoscopic hernia reduction, crural repair combined with antireflux fundoplication (Nissen's)

Question 394

Complications of hiatus hernia

Answer 394

Eosophageal: eosophagitis, erosions/ulceration, stricutres, Barrett's Other: rarely, incarceration of para-eosophageal hernia, strangulation or peroration. Can enlarge with time and sometimes progress to where the entire stomach lies in thoracic cavity. Surgery: high recurrence rates in large hiatus hernias. If mesh repair is used, infections, stricturing and veisceral erosions are risks

Question 395

T/F hypoglycaemia is a cause of pancreatitis

Answer 395

F. hyperlipidaemia, hyperglycaemia, hypercaleamia is the H in GET SMASHED!

Question 396

C difficile causes what type of gut inflammation Treatment

Answer 396

The release of toxins by C. difficile leads to extensive inflammation and disruption of the brush border membrane of the colon, resulting in what is known as pseudomembranous colitis. Metronidazole or vancomycin

Question 397

History of a subdiaphragmatic abscess

Answer 397

Upper abdominal pain radiating to the shoulder tip with a swinging fever in the days/weeks following abdominal surgery is suggestive of a subphrenic abscess. These are localised collections of pus, commonly underneath the right or left hemidiaphragm, which usually occur following a breach in the integrity of the peritoneum (e.g. perforated viscus, bowel surgery). Patients may also complain of malaise, weight loss, nausea, hiccups (due to diaphragmatic irritation by the abscess), a dry cough and shoulder tip pain (referred pain) on the affected side. There may be an associated pleural effusion

Question 398

How would a liver abscess present differently to subdiaphragmatic abscess

Answer 398

Liver abscesses can present similarly, but gastrointestinal signs such as hepatomegaly and jaundice will be more prominent, and respiratory symptoms are unlikely.

Question 399

Imaging for suspected subdiaphragmatic abscess

Answer 399

affected side. The patient’s respiratory symptoms are likely to be due to a pleural effusion. Abdominal CT or ultrasound are the preferred imaging modalities for visualising an abscess. FBC can aid diagnosis by showing leukocytosis and a chest X-ray will reveal a raised hemidiaphragm and a pleural effusion.

Question 400

T/F atelectasis can occur as a complication of subphrenic abscess

Answer 400

T

Question 401

How would ascending cholangitis present differently to cholecystitis

Answer 401

``` In cholecytsitis you can get RUQ (as with ascending cholangitis), bit with chole, Signs of jaundice are not typical, as obstruction of the biliary tract is limited to the gallbladder . ```

Question 402

Pruritis in pregnancy?

Answer 402

Intrahepatic cholestasis of pregnancy is a reversible form of cholestasis affecting some pregnant women in their second or third trimesters characterized by hepatic dysfunction and pruritus of the skin caused by elevated bile acids in the bloodstream, causing bile salt deposition in the skin, and secondary skin lesions due to scratching only (no primary lesions).

Question 403

Define Wilson's

Answer 403

Reduced biliary excretion of copper and accumulation of copper in teh liver and brain, cornea and kidneys Hence it is aka hepatolenticular degeneration

Question 404

Which area of the brain does copper accumulate in particuarly in wilsons

Answer 404

Basal ganglia

Question 405

Cause of wilson's

Answer 405

Mutation in gene on chromosome 13 that codes for copper-transporting ATPase in hepatocytes. The mutation inferferes iwth the transport of copper into the INTRACELLULAR compartments for incorporation into caeuruloplasmin (and secretion into the plasma) or excretion in the bile. XS copper damages hepatocyte mitocondria causing cell death and release of FREE copper into the plasma, which is subsequently deposited in other tiddues

Question 406

T/F wilson's can cause liver disease in young children, and neuro disease in young adults

Answer 406

T. Liver disease may present in children (>5 years). Neurological disease usually presents in young adults.

Question 407

Hx of Wilson's disease

Answer 407

Liver: May present with hepatitis, liver failure or cirrhosis. Jaundice, easy bruising, variceal bleeding, encephalopathy. Neurological signs: Dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia. Psych: Conduct disorder, personality change, psychosis

Question 408

Examination of wilson's

Answer 408

Liver: Hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia. Neurological: As above. Eyes:Green or brown Kayser–Fleischer ring at the corneal limbus, sun flower cataract (copper accumulation in the lens, seen with slit lamp).

Question 409

Investigations for wilsons

Answer 409

LFTs (raised AST, ALT and AlkPhos), serum caeruloplasmin and copper (LOW, but may provide false-negatives as caeurloplasmin is an acute phase protein) 24hr urinary copper levels increased Liver biopsy: increased copper content Genetic analysis. No simple genetic test

Question 410

Kayser fleischer involves copper deposition in which layer of the cornea

Answer 410

Descemet's membrane

Question 411

What is the normal copper handling in the body

Answer 411

Normal copper is taken from the gut to the liver via the portal vein. It is taken into hepatocytes. When inside hepatocytes, the copper-transporting ATPase (ATP7B) can move copper into either 1) Vesicles, where it can then be taken into the bile cannuliculi (major route) 2) Bind it to apoceruloplasmin, which is then called caeruloplasmin. This can be excerted by the urine. With the defect in this enzyme, the copper creates free radicals, damaging hepatocytes and then spilling out into the blood to damage other tissues

Question 412

What happens to blood caeruloplasmin in wilsons

Answer 412

IT REDUCES (counterintuitive) This is because you need the ATP7B protein (which isn't produced in wilson's) to actually create caeruloplasmin from apoceruloplasmin. So you won't get caeruloplasmin being produced, the the level in the blood will be low. Apocaeruloplasmin is realtively unstable and doesn't last long in the plasma

Question 413

What haem problem can wilsons cause

Answer 413

Haemolytic anaemia because copper can cause direct damage to circulating RBCs

Question 414

What is the most likely cokmplication of crohns

Answer 414

Perianal fistulae

Question 415

Triple therapy for peptic ulcers involving h pylori?

Answer 415

H. pylori is eradicated using triple therapy: a 1 week treatment regimen consisting of a PPI (e.g. omeprazole) and two antibiotics (most commonly amoxicillin and clarithromycin or clarithromycin and metronidazole) – each drug is taken twice daily.

Question 416

What if triple therapy fails in H pylori

Answer 416

Triple therapy is effective in 80-85% of cases. If this fails second-line therapy involves using a different combination of antibiotics or adding a bismuth compound (quadruple therapy).

Question 417

Pancreatic pseudocysts present with what

Answer 417

They are fluid filled round well demarcated dark circles in the pancreas on abdominal CT

Question 418

What to pancreatic pseudocysts results from

Answer 418

Chronic pancreatitis or pancreatic trauma

Question 419

What HLA is coeliac associated with

Answer 419

HLA-DQ2

Question 420

Black pigmented gall stones?

Answer 420

``` The presence of pigmented stones, which are small darkly colored stones, indicates the presence of chronic hemolysis or cirrhosis . Chronic hemolysis and cirrhosis both create an internal environment of high heme turnover, leading to higher than normal concentrations of unconjugated bilirubin and subsequently crystallized calcium bilirubinate that precipitates from solution and form crystals. ```

Question 421

What stones would you find in someone with small intestine resection

Answer 421

Reuced reabsorption of bile salts. Leads to reduced hepatic bile acid secretion and deranged composition of hepatic bile Saturation of bile and formation of CHOLESTEROL gall stones

Question 422

Diabetes mellitus which type of gallstones

Answer 422

Diabetes mellitus has been shown to be associated with an increased risk of cholesterol gallstones

Question 423

Chronic Abx and gall stones?

Answer 423

``` Chronic antibiotic therapy, such as the use of ceftriaxone , can lead to the increase precipitation of ceftriaxone - calcium complexes. This supersaturation and crystal formation predisposes patients to increased cholesterol ``` gallstones , not pigmented gallstones .

Question 424

What is IBS

Answer 424

A functional bowel disorder defined as recurrent episodes (in the absence of detectable organic pathology) of abdominal pain/discomfort for >6 months of the previous year, associated with two of the following: - Altered stool passage - Abdominal bloating - Symptoms made worse by eating - Passage of mucous

Question 425

Aetiology of IBS

Answer 425

Unknown. Visceral sensory abnormalities, gut motility abnormalities, psychosocial factors (particularly stress), food intolerance (e.g. lactose) are all implicated.

Question 426

Investigations for IBS

Answer 426

Diagnosis mainly from history. Blood: FBC (anaemia), LFTs, ESR, CRP, TFT. Antibodies for coeliac (anti-endomysial or anti-transglutaminase antibodies) Stool examination: Microscopy and culture for parasites, cysts and infection. Ultrasound: To exclude gallstone disease. Hydrogen breath test: To exclude dyspepsia associated with Helicobacter pylori. Endoscopy: Upper GI endoscopy, sigmoidoscopy or colonoscopy if other pathologies suspected.

Question 427

Management of IBS

Answer 427

ALL CASES: lifestyle and dietary modification ``` -Constipation predominant: Add laxatives (lactulose) If there is bloating you can add antispasmodics or SSRI ``` ``` -Diarrhoea predominant: Add antidiarrhoeals (loperamide) If there is bloating you can add antispasmodics or TCA ``` CBT may also be helpful

Question 428

Complication of IBS

Answer 428

Increased risk of colonic diverticulae

Question 429

What are mixed stones made of. What proportions of gall stones do they make up What associations does it have

Answer 429

Contain cholesterol, calcium bilirubinate, phosphate and protein (80%). Associated with older age, female, obesity, parenteral nutrition, drugs (OCP, octreotide), family history, ethnicity (e.g. Pima Indians), interruption of the entero hepatic recirculation of bile salts (e.g. Crohn's disease), terminal ileal resection.

Question 430

What are pure cholesterol stones made of. What proportions of gall stones do they make up What associations does it have

Answer 430

Pure cholesterol stones (10%): Similar associations as mixed stones.

Question 431

What are pigment stones made of. What proportions of gall stones do they make up What associations does it have

Answer 431

Pigment stones (10%): Black stones made of calcium bilirubinate ("bilirubin secondary to haemolytic disorders, cirrhosis), brown stones due to bile duct infestation by liver fluke Clonorchis sinensis. Associated with haemolytic disorders (e.g. sickle cell, thalassemia, hereditary spherocytosis).

Question 432

What % of gall stones are asymptomatic

Answer 432

90%!!!!

Question 433

Biliary colic Hx and examination

Answer 433

Sudden onset, severe right upper quadrant or epigastric pain, constant in nature. May radiate to right scapula, often precipitated by a fatty meal. Can last hours, may be associated nausea and vomiting. Right upper quadrant or epigastric tendernes

Question 434

Acute cholecystitis Hx and examination

Answer 434

Patient systemically unwell, fever, prolonged upper abdominal pain that may be referred to the right shoulder (due to diaphragmatic irritation). Tachycardia, pyrexia, RUQ/epigastric tenderness. Guarding and rebound, Murphys sign.

Question 435

Ascending cholangitis Hx and examination

Answer 435

Classical association between right upper quadrant pain, jaundice and rigors (Charcot’s triad). If combined with hypotension and confusion, it is known as Reynold’s pentad. Pyrexia, RUQ pain and jaundice

Question 436

Investigations for gall stones

Answer 436

FBC, LFTs, lipase and amylase, ABDOMINAL USS Abdominal ultrasound has low sensitivity for choledocholithiasis, but accuracy is better for any accompanying bile duct dilation. Then, MRCP for suspected choledocholithiasis that is not confirmed by abdominal ultrasound.

Question 437

Management of mild biliary colic symptoms

Answer 437

Conservaive, avoidance of fat in diet

Question 438

Management of choledocholithiasis

Answer 438

Admit, IV fluids, analesia, antiemetics and Abx if signs of infection (cholecystitis or cholangitis) If there is evidence of obstruction, urgent biliary drainage by ERCP or percutaneous transhepatic cholangiogram. If symptoms worsen/don't improve, suspect localised abscess or empyema. Drain percutaneously by cholecystostomy and pigtail catheter Elective cholecystectomy if concurrent cholelithiasis or cholecystitis

Question 439

Mangement of cholelithiasis (i.e. stones in gallbladder, but no infection)

Answer 439

Supportive care, analgesics Elective cholecystectomy for: Symptomatic cholelithiasis Asymptomatic cholelithiasis only if at increased risk of gallbladder cancer

Question 440

Management of acute cholecystitis

Answer 440

(cholelithiasis or biliary sludge leading to inflammation of gall bladder wall) Supportive care, analgesics IV antibiotics Cholecystectomy (timing depends on severity)

Question 441

Management of acute cholangitis

Answer 441

Supportive care, analgesics IV antibiotics (Moderate to mild community acquired: cefuroxime. Severe community acquired: meropenem, pip-taz. Healthcare-associated: meropenem, pip-taz SURGICAL: If mild cases, do elective chole within 24-72hrs. If complications (gangrene, perforation) or condition worsens, do emergency lap chole. If there are high risk of surgical complications and/or they're critically ill, do emergency percutaneous biliary drainage (e.g. cholecystostomy), follow up with interval surgery when possible. In severe, high risk cases: delayed elective cholecystectomy (>2 weeks)

Question 442

What is bouveret's syndrome

Answer 442

gallstones causing gastric outlet obstruction

Question 443

What is mirizzi syndrome

Answer 443

common hepatic duct obstruction by an extrinsic compression from an impacted stone in the cystic duct

Question 444

What Abx are used for actue cholangitis

Answer 444

Cephalosporin and metronidazole

Question 445

What is the commenest neurological manifestation of sarcoid

Answer 445

``` Sarcoidosis only rarely presents with neurologic complications. The most common neurological involvement that presents in this clinical situation is facial nerve palsy - either unilateral or bilateral. ```

Question 446

T/F patients should refrain from a gluten-free diet until biopsy

Answer 446

True, kind of. A tTG antibody test will be done on everybody first, then preferably a small bowel biopsy If patients have put themselves onto a gluten free diet before small bowel biopsies were obtained, and feel so much better that they are not able to go back to gluten for the required 6-8 weeks before the biopsies are taken, then they can have HLA genotyping. Same goes for children (anti-tTG and HLA genotyping is enough, so they don't have to have biopsy)

Question 447

What are the complication of coeliac disease

Answer 447

Coeliac disease is associated with lymphocytic colitis Small bowel lymphoma in the context of coeliac disease, although in all the text books, is vanishingly rare and certainly not something that we would screen all newly diagnosed patients for.

Question 448

What should you screen for for newly diagnosed patients with coeliac

Answer 448

osteopenia / osteoporosis is very common in patients who are newly diagnosed with coeliac disease and screening is recommended.

Question 449

Patient with coeliac disease diagnosis but after 6 months diarroea hasn't resolved, still hasn't put on much weight

Answer 449

If coeliac disease is not getting better on a gluten free diet it is nearly always because the patient is not being strict enough about their diet and the TTG is a good way to screen for this without putting them back through the OGD and biopsy. Even trace gluten like on utensils, or using the same toaster, can cause inflammation

Question 450

Progressive dysphagia for food and GORD?

Answer 450

Peptic stricture needs to be excluded, along with oesophageal carcinoma

Question 451

Management for symptomatic, benign peptic stricture

Answer 451

Balloon dilatation is the treatment of choice for symptomatic, benign peptic strictures. Endoscopy and biopsy confirmation of benign disease must be undertaken prior to dilatation. Temporary oesophageal stenting can be considered for patient’s refractory to repeated balloon dilatation.

Question 452

Investigation of eosophageal perforation

Answer 452

CT scan with WATER SOLUBLE oral contrast

Question 453

Which extra-intestinal manifestations of UC are related to the activity of the colitis

Answer 453

``` Pyoderma gangrenosum Erythema nodosum Episcleritis Aphthous ulcers Anterior uveitis Acute arthropathy ```

Question 454

Which extra-intestinal manifestations of UC are NOT related to the activity of the colitis

Answer 454

Sacroiliitis/ank spond | PSC

Question 455

Acute severe UC management

Answer 455

Intravenous hydrocortisone is first-line management for acute severe colitis. Antibiotics would only be started if there was concern about toxic megacolon and risk of perforation or signs of infection which are not apparent in this case.

Question 456

What if you've give IV corticosteroids for acute severe UC and it doesn't work

Answer 456

NICE guidance recommends the use of intravenous ciclosporin for patients who are not responding to intravenous hydrocortisone or where hydrocortisone treatment is not appropriate. TNF-alpha and should only be considered if intravenous ciclosporin is contra-indicated or inappropriate.

Question 457

Contraindications for ciclosporin

Answer 457

Hypertension and renal impairment

Question 458

Best long term management for eosophageal varicies

Answer 458

Non-cardioselective beta blockers Non-cardioselective beta-blokers are the first line treatment of prevention of variceal bleeding. Where a beta-blocker is not tolerated or if there is a singificant contra-indication to their usage, then regular endoscopy with variceal band ligation would be the second-line managment.

Question 459

T/F TIPSS is a prophylactic treatment for variceal bleeding

Answer 459

F.... A TIPSS may also be considered with an acute presentation of variceal bleeding not managed by endscopy but is not used as prophylactic management.

Question 460

T/F pabrinex is best given as a rapid IV bolus in wernicke's

Answer 460

F Wernicke’s encephalopathy is reversible but needs prompt treatment with thiamine (B1) to prevent progression to Korsakoff’s psychosis (permanent loss of short-term memory). IV Pabrinex however needs to be given at a controlled rate as giving too quickly increases the risk of anaphylaxis

Question 461

T/F you should treat wernicke's with glucose infusion

Answer 461

F It may be precipitated by glucose infusion

Question 462

T/F chronic alcoholism is assocaited with chronic kidney disease

Answer 462

F Chronic alcohol intake is not associated with pulmonary fibrosis or chronic kidney disease

Question 463

T/f alcohol is associated with diabetes

Answer 463

F. Pancreatic damage can precipitate diabetes

Question 464

Who are benign liver tumours especially frequent in

Answer 464

Young women

Question 465

What types of bening liver tumours are there. What is most to least common

Answer 465

hepatic hemangioma (most common) > focal nodular hyperplasia (FNH) > hepatocellular adenoma (rare)

Question 466

Epidemiology of hepatic benign tumors

Answer 466

Sex: women to men (∼ 6:1) Age: can appear at any age, but mostly affects young women Most often an incidental finding on imaging tests

Question 467

Cause of liver benign tumour: | Hepatocellular adenoma

Answer 467

oral contraceptives and anabolic steroids

Question 468

Cause of liver benign tumour: | Hepatic haemangioma

Answer 468

possible hormonal component; estrogen therapy associated with increased growth in size

Question 469

Symptoms/clinical findings of benign liver tumours

Answer 469

Usually asymptomatic | Large tumors --> upper abdominal pain, fullness, and nausea

Question 470

Best initial test for liver tumour, further test to reach definitive diagnosis , and if unsure

Answer 470

``` Best initial test: ultrasound Further imaging Contrast-enhanced CT MRI Biopsy: to confirm diagnosis if imaging is inconclusive ```

Question 471

Where are hepatocellular adenomas more commonly located

Answer 471

Right lobe

Question 472

Ultrasound of a suspected liver benign tumour shows a central stellate scar

Answer 472

Focal nodular hyperplasia

Question 473

Histology of a hepatocellular benign tumour: Cavernous vascular spaces of variable size, lined by flat endothelial cells

Answer 473

Hepatic hemangioma

Question 474

Histology of a hepatocellular benign tumour: Enlarged hepatocytes, with small and regular nuclei, cytoplasmic glycogen and lipid deposits Arranged in sheets or 2-cell thick cords Normal hepatic lobular architecture is absent

Answer 474

Hepatocellular adenoma

Question 475

What are the types of liver cysts

Answer 475

Simple cyst (congenital, usually asymptomatic- USS and CT) Congenital polycystic liver (associated with PKD) Hyatid echinococcal cysts

Question 476

What is crohn's

Answer 476

A chronic granulomatous inflammatory bowel disease resulting in destruction of the GI wall anywhere along the GI tract.

Question 477

Aetiology of crohn's

Answer 477

Genetic and environmental factors

Question 478

Hx of crohn's

Answer 478

Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction). Diarrhoea (can be bloody, but typically not/steathorrhoea) Fever, malaise, weight loss Symptoms of complications

Question 479

Exam of crohn'ss

Answer 479

Weight loss, clubbing, signs of anaemia. Aphthous ulceration of the mouth. Perianal skin tags, fistulae and abscesses. Signs of complications (eye disease, joint disease, skin disease).

Question 480

Commmon locations for crohns

Answer 480

CD may involve any or all parts of the entire GI tract from mouth to perianal area, although it is usually seen in the terminal ileal and perianal locations.

Question 481

What is the association between IBD and smoking

Answer 481

Smokers are more than twice as likely to develop Crohn's as non-smokers. This is in contrast to ulcerative colitis, in which smoking reduces the risk of developing the disease by up to 40%.

Question 482

T/F OCC and NSAIDS increase the risk of crohns

Answer 482

Yes

Question 483

Which organism, which casues an acute ileitis, is a differential for crohn's

Answer 483

Yersnia enterocolitica (an alternative differential)

Question 484

Investigations for crohns

Answer 484

BLOOD: FBC (anaemia, leukocytosis) Iron studies (normal, or iron deficient, due to GI bleeding or malabsorption of iron) b12 and folate (normal of low)- b12 deficiency most common in ileocaecal CD/post-ileocaecal resection STOOL MICROSCOPY AND CULTURE (exclude infective colitis) AXR- toxic megacolon Erect CXR- IF RISK OF PERFORATION USS- GI wall thickening/may detect abscesses/fistulas Plain radiography with barium swallow Colonoscopy/ OGD and biopsy

Question 485

Why do a plain radiography with barium swallow in crohn's? What might be found

Answer 485

To detect fistulas or stenoses. Creeping fat- Proliferated mesenteric fat between the intestinal loops is pathognomonic for CD. String sign- fibrotic bits look like string

Question 486

Why do endoscopy in crohns? What might you find

Answer 486

Endoscopy confirms the diagnosis, assesses the extent of the disease, differentiates CD from other diseases (e.g., ulcerative colitis, peptic ulcers, etc.), and may also be used as a therapeutic tool (e.g., dilatation of ducts, intestinal loops). Segmental involvement MACROSCOPIC findings: - Linear ulcers (snail trails) - Other apththous haemorrhagic mucosa defects (pinpoint lesions) - Cobblestone sign - Fissures/fistulas - Ertyhema and transumral inflammation

Question 487

What might you find in crohns histology

Answer 487

Skip lesions (discontinuous inflammation) Hypertrophic lymph nodes Transmural inflammation: Non-caseating granulomas Giant cells Distinct lymphoid aggregates of the lamina propria

Question 488

Management of ACUTE exacerbation of crohns

Answer 488

Fluid resuscitation, IV or oral corticosteroids, 5-ASA analogues (e.g. mesalazine, sulfasalazine) may induce a remission in colonic Crohn's disease Elemental diet may induce remission (more often used in children). Parenteral nutrition may be necessary. Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin). Assess for complications.

Question 489

Conservative management of crohns

Answer 489

Stop smoking, dietician referral. Education and advice (e.g. from inflammatory bowel disease nurse specialists).

Question 490

Long term medical management of crohn's disease

Answer 490

Steroids for acute exacerbation 5-ASA to reduced relapses (mild to moderate disease) Steroid sparing agents for immunosuppression (azathioprine, methotrexate). Reduces relapse Anti-TNF (infliximab). Only for refractory cases

Question 491

Long term surgical managemnet of crohns

Answer 491

Indicated for failure of medical treatment, failure to thrive in children or the presence of complications. This involves resection of affected bowel and stoma formation, although there is a risk of disease recurrence.

Question 492

Complications of crohn's

Answer 492

GI: haemorrhage, bowel strictures, perforation, fistulae (between bowel, bladder, vagina), perianal fistulae and abscess, GI carcinoma (5% risk in 10 years), malabsorption

Question 493

Extraintestinal features of crohns

Answer 493

Uveitis, episcleritis, gallstones, kidney stones, arthropathy, sacroiliitis, ank spond, erythema nodosum, pooferman gangrenosum, amyloid!!!!!

Question 494

Prognosis of crohn's

Answer 494

Chronic relapsing condition. Two-thirds will require surgery at some stage and two-thirds of these >1 surgical procedure.

Question 495

Which type of hernia has the highest rate of incarceration of the small bowel

Answer 495

``` Femoral hernias protrude below the inguinal ligament through the femoral canal . This type of hernia most commonly occurs in women and has the highest rate of incarceration of the small bowel ```

Question 496

What tube is used for short term vs long term enteral nutrition

Answer 496

Short-term: nasogastric tube Long-term (> 2–3 weeks): Gastrostomy tube: gastric feeding tube inserted endoscopically through a small incision through the abdomen into the stomach or Jejunostomy tube: feeding tube inserted through a small incision through the abdomen into the jejunum to bypass the distal small bowel and/or colon

Question 497

Contraindications for parenteral nutrition

Answer 497

``` Enteral nutrition is feasible Serum hyperosmolality Severe hyperglycemia Severe electrolyte abnormalities Volume overload ```

Question 498

What is the route of administration for short and long term parenteral nurtition

Answer 498

arenteral nutrition is required for < 2 weeks: peripheral venous line, or peripherally inserted central catheter Parenteral nutrition is required for > 2 weeks: tunneled central venous catheter or a port

Question 499

Metabolic complications associated with specialised nutritional support

Answer 499

Electrolyte imbalances: hypocalcemia, hypomagnesemia, hypophosphatemia Hyperglycaemia Refeeding syndrome Gallstone disease NAFLD Renal damage Acalculous cholecystits

Question 500

What causes refeeding syndrome

Answer 500

If there has been poor nutrition, then giving someone good nutrition will suddenly increase the insulin This will switch on protein, fat synthesis in the liver and elsewhere, which will use up the already depleted reserves of phosphate, magnesium, and thiamine in chronically malnourished patients. A drop in thiamine levels can cause Wernicke's encephalopathy. Additionally, insulin causes an intracellular shift of potassium, phosphate, and magnesium. The resulting drop in these serum levels can trigger cardiac arrhythmias

Question 501

What is vitamin b1 (thiamine) needed for

Answer 501

Thiamine enables the body to use carbohydrates as energy. It is essential for glucose metabolism, and it plays a key role in nerve, muscle, and heart function

Question 502

Multiple hamartous polyps on the colon of a young person

Answer 502

``` Juvenile polyposis syndrome is a rare, autosomal dominant condition that involves hamartomatous polyps of the GI tract, especially the colorectum. Patients should be regularly screened for colorectal cancer . ```

Question 503

hamatomatous polyps of the GI tract, mucosal hyperpigmentation

Answer 503

``` Peutz-Jeghers syndrome (PJS) is an autosomal dominant syndrome associated with hamatomatous polyps of the GI tract, mucosal hyperpigmentation , and increased risk of cancer` . Though this patient has hamartomatous lesions of the GI tract, he does not have the pigmented macules seen in more than 95% of PJS. ```

Question 504

Cause of acute cholecystits

Answer 504

It develops in up to 10% of patients with symptomatic gallstones. In most cases (90%), it is caused by complete cystic duct obstruction usually due to an impacted gallstone in the gallbladder neck or cystic duct, which leads to inflammation within the gallbladder wall. In 5% of cases, bile inspissation (due to dehydration) or bile stasis (due to trauma or severe systemic illness) can block the cystic duct, causing an acalculous cholecystitis.

Question 505

Investigations for cholecystitis

Answer 505

1. USS (if no sepsis suspected) 2. MRCP 3. Endoscopic ultrasound (CT or MRI of abdomen if septic and you suspect gangrenous cholecystitis/gallbladder perforation)

Question 506

Management of acute cholecystitis

Answer 506

See booklet

Question 507

What are the causes of GI perforation

Answer 507

1. Gastroduodenal: - Ruptured peptic ulcers - Rarely gastric carcinoma 2. Large bowel (most common) : - Diverticulitis and colorectal carcinoma (80%) - Crohn's - Acute appendicitis - Volvulus, UC (Toxic megacolon, trauma, complication of colonoscopy 3. Small bowel: - Trauma, infection (typhoid, TB), Crohn's - Obstruction due to adhesions 4. Eosophagus: - Boorhaeve's - Iatrogenic perforation in OGD (more commonly during dilation of strictures)

Question 508

Signs of GI perforation on examination

Answer 508

Unwell, signs of localised and generalised peritonitis with abdominal rigidity and guarding Reduced/absent bowel sounds Loss of liver dullness due to overlying gas Shock, pyrexia, pallor and dehydration

Question 509

Investigations for GI perforation. First imaging?

Answer 509

Blood: FBC, U&E, LFT, amylase (can be raised in perforation) Erect CXR (gas under diaphragm) AXR can show abnormal gas shadows in tissue..... Riglers sign referes to gfas on either side of the bowel wall. Lateral decubitas film best for intraperitoneal gas though CT very sensitive for free intraperitnoeal gas

Question 510

What is a liver abscess

Answer 510

A pyogenic liver abscess is a rare disease characterized by solitary/multiple collections of pus within the liver. Can be due to bacterial, fungal or parasitic infection

Question 511

What is the cause of a pyogenic liver abscess

Answer 511

Polymicrobial commonly. Escherichia coli, Klebsiella, enterococcus, bacteroides, streptococci, staphylococci

Question 512

Which other organisms can cause liver cysts

Answer 512

Amoebic (amboeba histolytica) Hyatid cyst (tapeworm Echinococcus granulosis)

Question 513

Hx of liver abscesses

Answer 513

Fever, malaise, nausea, anorexia, night sweats, weight loss RUQ or epigastric pain, which may be referred to shoulder (diaphragmatic irritation) Jaundice, diarrhoea, pyrexia of unknown origin. Foreign travel

Question 514

Risk factor for developing a liver abscess

Answer 514

Diabetes

Question 515

Examination of liver absceses

Answer 515

Fever (continuous/spiking), jaundice Tender hepatomegaly, R lobe affected more commmonly than left Dullness to percussion and breath sounds at right base of lung, caused by reactive pleural effusion.

Question 516

Liver abscess with raised eosinophils

Answer 516

Hyatid cyst

Question 517

Investigations of liver abscesses

Answer 517

FBC, LFTs, blood culture,, PT and aPTT IMAGING: USS Gram stain and culture of aspirated abscess fluid CT

Question 518

What are the LFT findings with liver abscess

Answer 518

High Alk Phos, mildly elevated AST/ALT and bili, hypoalbuminaemia

Question 519

Why is clotting profile used in liver abscesses

Answer 519

Indicated to check that blood clotting is within normal limits before aspiration is performed

Question 520

When would you not aspirate a liver abscess

Answer 520

If there is abnormal clotting or if you suspect hyatid

Question 521

What is oesophageal carcinoma

Answer 521

Malignant tumour arising in the oesophageal mucosa. Two major histological types: squamous cell carcinoma and adenocarcinoma

Question 522

What is the cause of squamous cell carcinoma in oesophagus

Answer 522

Alcohol, tobacco, nutritional deficiency, HPV infection, achalasia, Plummer-Vinson syndrome, tylosis, scleroderman, coecliac disease, lye stricture, previous thoracic radiotherapy , dietary nitrosamines

Question 523

What is the cause of adenocarcinoma

Answer 523

GORD, Barrett's oesophagus (intestinal metaplasia of the distal oesophageal mucosa with "0.5–0.7% incidence of adenocarcinoma per year).

Question 524

Where is squamous cell carcinoma vs adenomcarcinoma more common within the oesophagus

Answer 524

Squamous cell carcinomas are more common in the mid-upper oesophagus. Adenocarcinoma usually develops in the lower oesophagus or, increasingly, the gastrooesophageal junction

Question 525

How do oesophageal cancers spread

Answer 525

Spread is typically initially direct (oesophagus has no serosa) and longitudinal via an extensive network of submucosal lymphatics to tracheobronchial, mediastinal, coeliac, gastric or cervical nodes

Question 526

Hx of eosophageal cancer

Answer 526

Early: symptomatic/symptoms of reflux. Later: dysphagia, initially worse for solids, regurgitation, cough or choking after food, pain (odynophagia), weight loss, fatigue, voice hoarseness (may indicate recurrent laryngeal nerve palsy).

Question 527

Examination of oesophageal cancer

Answer 527

No physical signs may be evident, signs of weight loss. With metastatic disease there may be supraclavicular lymphadenopathy, hepatomegaly. Respiratory signs may be due to aspiration or direct tracheobronchial involvement

Question 528

Which investigations would you do for oesophageal cancer 1st test? Staging

Answer 528

1st test: OGD + biopsy OGD is the first test in patients with severe dysphagia, odynophagia, or weight loss. This will differentiate oesophageal cancer from benign causes of dysphagia Staging: CT thorax and abdo

Question 529

What metabolic disturbance might present in oesophageal obstruction

Answer 529

patients may become severely volume-depleted and hypokalaemic because of their inability to swallow fluids and their own potassium-rich saliva.

Question 530

What investigation might be done prior to treatment once a diagnosis of oesophageal cancer is confirmed

Answer 530

Endoscopic ultrasound (EUS) is now a standard pre-treatment test It can identify all the histological layers of the oesophagus and thereby confirm the T-stage with 90% accuracy. It can also identify abnormal or enlarged mediastinal and coeliac axis lymph nodes, and enable cytological examination by fine needle aspiration (FNA). Crucial prior to surgery

Question 531

Where do inguinal hernias appear with respect to the pubic tubercle?

Answer 531

Superior and MEDIAL! (I know it's confusing but this is correct)

Question 532

Why are right sided indirect inguinal hernias more common?

Answer 532

They are more common on the right side in males, because the right testis descends later and there is an increased incidence of failed closure of the processus vaginalis (thus predisposing to hernias)

Question 533

A 35-year-old Indian man presents with a swelling lateral to the femoral artery. On examination it is tender and fluctuant, but cannot be reduced. He also describes a recent history of weight loss and night sweats.

Answer 533

TB. A known complication of intraabdominal TB is abscess formation in the lumbar vertebrae (Pott's disease). Such an abscess may track down the psoas sheath and into the groin, forming a psoas abscess. Psoas abscesses are described as 'cold', as they are painless and not warm to touch.

Question 534

A 35-year-old Indian man presents with a swelling lateral to the femoral artery. On examination it is tender and fluctuant, but cannot be reduced. He also describes a recent history of weight loss and night sweats.

Answer 534

TB. A known complication of intraabdominal TB is abscess formation in the lumbar vertebrae (Pott's disease). Such an abscess may track down the psoas sheath and into the groin, forming a psoas abscess. Psoas abscesses are described as 'cold', as they are painless and not warm to touch.