Gastro Flashcards

1
Q

Define coeliac disease

A

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

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2
Q

Explain the aetiology / risk factors of coeliac disease

A

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
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3
Q

Summarise the epidemiology of coeliac disease

Recognise the presenting symptoms of coeliac disease

A

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!

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4
Q

Recognise the signs of coeliac disease on physical examination

A

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

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5
Q

Identify appropriate investigations for coeliac disease and interpret the results

A

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.

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6
Q

Generate a management plan for coeliac disease

A
  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.)

  1. Referral for gastroscopy and duodenal biopsy
  2. Screening of 1st degree relatives!
  3. Bone density scan (osteopaenia)
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7
Q

Summarise the prognosis for patients with coeliac disease

A

higher overall mortality than in the general population.

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8
Q

Summarise the complications for patients with coeliac disease

A

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.

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9
Q

Define alcoholic hepatitis

A

Inflammatory liver injury caused by chronic heavy intake of alcohol

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10
Q

Explain the aetiology / risk factors of alcoholic hepatitis

what diseases is it part of
(histopathalogical features)

A

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

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11
Q

Summarise the epidemiology of alcoholic hepatitis

A

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

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12
Q

Recognise the presenting symptoms/signs of alcoholic hepatitis

A

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

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13
Q

Identify appropriate investigations for alcoholic hepatitis and interpret the results

A

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
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14
Q

Generate a management plan for acute management of alcoholic hepatitis

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

A

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)

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15
Q

Identify the possible complications of alcoholic hepatitis and its management

A
Hepatic encephalopathy 
Coagulopathy 
GI bleeds
Portal HTN
Hepatorenal failure
HCC 
Sepsis
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16
Q

Summarise the prognosis for patients with alcoholic hepatitis

A

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

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17
Q

How is alcohol metabolised in the liver

A

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

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18
Q

Why might ALT/AST be normal in advanced liver disease

A

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).

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19
Q

Which transaminase is usually raised higher in ARLD

A

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.

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20
Q

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

A

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

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21
Q

Which drugs are used to treat alcohol withdrawal syndrome

A

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

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22
Q

How are liver transplants decided

A

MELD score

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23
Q

…..

A

…………

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24
Q

……….

A

……….

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25
Q

………..

A

……….

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26
Q

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
A

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.

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27
Q

Explain aetiology/risk factors of portal HTN

A
  • 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

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28
Q

Summarise epidemiology of portal HTN

A

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29
Q

Recognise presenting symptoms of portal HTN

A

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

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30
Q

Recognise the signs of portal HTN on physical examination

A

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

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31
Q

Identify appropriate investigations for portal HTN and interpret the results

Gold standard investigation

A

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)

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32
Q

Generate a management plan for portal HTN

i. Ascites
ii. Acute variceal bleed.

A

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

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33
Q

Identify the possible complications of portal HTN and its management

A

Bleeding varices, ascites, gastropathy, spenomegaly,

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34
Q

Summarise the prognosis for patients with portal HTN

A

Variceal haemorrhages have a 1-year mortality of 40%

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35
Q

Define acute pancreatitis

(mild vs severe)

A

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

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36
Q

Explain the aetiology / risk factors of acute pancreatitis

A

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)

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37
Q

Summarise the epidemiology of acute pancreatitis

A

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.

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38
Q

Recognise the presenting symptoms of acute pancreatitis

A

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.

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39
Q

Recognise the signs of acute pancreatitis on physical examination

A

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).

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40
Q

Identify appropriate investigations for acute pancreatitis and interpret the results

A

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.

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41
Q

Generate a management plan for acute pancreatitis

When operate, when FNA

A
  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!)

  1. 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
  2. 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.
  3. 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
  4. Surgical: Patient with necrotizing pancreatitis should be managed in a specialist unit. Minimal access or open necresectomy (drainage and debridement of all necrotic tissue).
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42
Q

Identify the possible complications of acute pancreatitis and its management

What is a pseudocyst

A

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)

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43
Q

Summarise the prognosis for patients with acute pancreatitis

A

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

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44
Q

Define chronic pancreatitis

A

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

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45
Q

Explain the aetiology / risk factors of chronic pancreatitis

Pathophysiology. Important cell type?

A

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.

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46
Q

Summarise the epidemiology of chronic pancreatitis

A

Annual UK incidence ~ 1/100 000; prevalence ~ 3/100 000.

Mean age 40– 50 years in alcohol-associated disease.

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47
Q

Recognise the presenting symptoms of chronic pancreatitis

A

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).

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48
Q

Recognise the signs of chronic pancreatitis on physical examination

A

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

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49
Q

Identify appropriate investigations for chronic pancreatitis.

A

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.

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50
Q

Generate a management plan for chronic pancreatitis

A

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).

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51
Q

Identify the possible complications of chronic pancreatitis and its management

A

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.

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52
Q

Summarise the prognosis for patients with chronic pancreatitis

A

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.

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53
Q

Define Barrett’s oesophagus

A

Pre-malignant condition

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

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54
Q

Explain the aetiology / risk factors of Barrett’s oesophagus

2 types of barretts and which is worse

A

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!
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55
Q

Triggers for GORD

A

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

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56
Q

Recognise the presenting symptoms of Barrett’s oesophagus

A

Often asymptomatic,

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

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57
Q

Recognise the signs of Barrett’s oesophagus on physical examination

A

Often asymptomatic,

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

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58
Q

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

A

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.

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59
Q

Generate a management plan for Barrett’s oesophagus

A

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)

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60
Q

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

A

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.

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61
Q

Summarise the prognosis for patients with Barrett’s oesophagus

A

.

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62
Q

Define acute cholangitis

A

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.

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63
Q

Explain the aetiology / risk factors of acute cholangitis

Most common causative organism

A
  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)

  1. 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.

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64
Q

Summarise the epidemiology of acute cholangitis

A

..

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65
Q

Recognise the symptoms/signs of acute cholangitis on physical examination

A

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

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66
Q

Identify appropriate investigations for acute cholangitis and interpret the results

A

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)

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67
Q

Generate a management plan for acute cholangitis

A

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

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68
Q

Identify the possible complications of acute cholangitis and its management

A

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

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69
Q

Summarise the prognosis for patients with acute cholangitis

A

Septic shock

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70
Q

Define haemochromatosis

A

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

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71
Q

Explain the aetiology / risk factors of haemochromatosis

A

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.

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72
Q

Summarise the epidemiology of haemochromatosis

Why do men experience early haemochromatosis?

A

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

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73
Q

Recognise the presenting symptoms of haemochromatosis

A

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
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74
Q

Recognise the signs of haemochromatosis on physical examination

A

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
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75
Q

Identify appropriate investigations for haemochromatosis and interpret the results

A

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.

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76
Q

What is iron critical for in the body

A

o2 transport

Oxidative phosphorylation

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77
Q

Outline how iron is usually handled in the body

A

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

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78
Q

Treatment for haemochromatosis

A

Phlebotomy!

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

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79
Q

T/F acute cholecystits is a risk factor for cholangiocarcinoma

A

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.

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80
Q

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

A

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.

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81
Q

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

A

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.

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82
Q

T/F acute cholcystitis is a risk factor hepatocellular carcinoma

A

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.

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83
Q

What is rigler triad

A

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

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84
Q

What is gallstone ileus

A

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.

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85
Q

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

A

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

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86
Q

Define achalasia

A

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

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87
Q

Explain the aetiology / risk factors of achalasia

Which cells are affected?

Which infection causes a similar effect?

A

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).

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88
Q

Summarise the epidemiology of achalasia

A

present 25-60 years

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89
Q

Recognise the presenting symptoms of achalasia

A

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.
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90
Q

Recognise the signs of achalasia on physical examination

A

Signs of complications

Clubbing

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91
Q

Identify appropriate investigations for achalasia and interpret the results

A

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

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92
Q

What causes each of the following types of peristalsis:

  • primary
  • secondary
  • tertiary
A
  • 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
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93
Q

bulky and foul smelling stools?

A

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

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94
Q

What is D-xylose and what is it used for

A

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)

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95
Q

What will the excretion of D-xylose show in the following conditions:

  • Coeliac disease
  • Crohn’s
  • Small intestinal bacterial overgrowth
  • Pancreatic insufficiency
A

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

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96
Q

What is mackler’s triad

A

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

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97
Q

What does an upturned U shape on abdominal radiograph represent

A

grossly dilated loop of sigmoid colon, secondary to volvulus.

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98
Q

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

A

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

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99
Q

Initial management of patient with sigmoid volvulus.

What if it recurs?

A

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.

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100
Q

What is the management of caecal volvulus

A

.These patients usually require a right hemicolectomy.

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101
Q

Initial management of patient with sigmoid volvulus.

What if it recurs?

A

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.

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102
Q

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

A

Both lax

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103
Q

What is splenic injruy associated with

A

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

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104
Q

T/F most splenic lacerations are self limiting

A

T

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

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105
Q

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

A

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

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106
Q

What is splenic injruy associated with

A

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

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107
Q

T/F most splenic lacerations are self limiting

A

T

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

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108
Q

What vaccines and prophylaxis are to be given following splenectomy

A

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)

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109
Q

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

A

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).

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110
Q

Why do you insert a NG tube in ileus/obstruction

A

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

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111
Q

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

A

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.

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112
Q

What causes electrolyte abnormalities and dehydration in ileus/mechanical obstruction

A

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

And

Vomiting

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113
Q

Which electrolytes are particualrly important to correct in ileus

A

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.

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114
Q

What do you need to monitor when giving TPN

A
  1. Daily inspection of line & dressing
  2. 4hr temp and observations
  3. Blood glucose
  4. Daily electrolytes
  5. Accurate recording of fluid balance
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115
Q

What are the complications of TPN

A
  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
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116
Q

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

A

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.

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117
Q

Why are alcoholics given pabrinex/thiamine

A

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.

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118
Q

What is a typical history for bowel ischaemia

A

Cramping pain and bleeding

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119
Q

Megacolon is usually associated with what

A

It leads to sepsis (fever and high WCC)

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120
Q

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

A

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

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121
Q

What is the difference between ileus and pseudoobstruction

A

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.

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122
Q

How is pseudo-obstruction usually managed

A

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

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123
Q

Which electrolyte imbalance is a cause of pseudo-obstruction

A

Hypokalaemia

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124
Q

Which surgery is assocaited with pseudo-obstruction

A

There is an association with recent surgery, particularly orthopaedic

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125
Q

Differentiate the broad management of ileus vs mechanical obstruction

A

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.

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126
Q

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

A

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

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127
Q

What is the differentials for a lump that you can’t “get above”

How do you differentiate the two

A

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

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128
Q

Define hernia

A

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

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129
Q

Outline 2 classic features of hernia

A

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.

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130
Q

When will you see a loss of classic features of hernia

A

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.

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131
Q

How do you differentiate a narrowed hernial orifice from hernia incarceration.

How do you differentiate this from infarction (due to strangulation)

A

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.

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132
Q

What is hernial incarceration

A

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.

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133
Q

What is hernial strangulation

A

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

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134
Q

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

A

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)

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135
Q

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

A

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

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136
Q

How does bowel obstruction cause shock

A

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

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137
Q

Indirect inguinal hernias are associated with which developmental variation

A

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.

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138
Q

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

A

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.

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139
Q

What are incisional hernias

A

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).

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140
Q

What structures in the gut can herniate

A

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.

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141
Q

T/F toxic megacolon results from obstruction

A

Not correct.
Toxic megacolon is a consequence usually of ulcerative colitis (more rarely crohns disease).

It CAUSES an ileus (so reduced bowel sounds)

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142
Q

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

A

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

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143
Q

What abdominal sign might suggest colonic carcinoma on barium enema

A

Apple core lesion

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144
Q

What imaging modality is best way to investigate colonic carcinoma

A

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

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145
Q

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

A

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.

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146
Q

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

A

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.

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147
Q

2 methods of pseudocyst drainage?

A

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.

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148
Q

Which blood test is a measure of pancreatic exocrine function

A

Faecal elastase

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149
Q

What is the treatment of pancreatic exocrine insufficiency

A

Oral enzyme replacement e.g. creon

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150
Q

What is the tumour marker for pancreatic carcinoma

A

(CA19-9)

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151
Q

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

A

Not the tumour itself!

The right upper quadrant mass is likely to represent a distended gallbladder (due to biliary obstruction)

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152
Q

When is MRCP most useful

A

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

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153
Q

What is the technique of choice for staging pancreatic carcinoma

A

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

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154
Q

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

A

Malignant: shouldered and irregualar

Inflammaotry: smooth

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155
Q

Risk factors for pancreatic cancer

A

Cigarette, diabetes

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156
Q

What are the complications of ERCP

A
Perforation
Aspiration pneumonia
Haemorrhage
Acute pancreatitis
Ascending cholangitis
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157
Q

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

  • air
  • calcification
A

CT for both

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158
Q

What is porcelain gallbladder

A

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

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159
Q

What is emphysematous cholecystits

A

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

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160
Q

Risk factors for gallstones

A

‘fair, fat, female, fertile and forty’

pregnant

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161
Q

T/F lap chole has lower complication that open chole

A

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.

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162
Q

Which two organisms can mimic ileo-caecal chrohns disease?

A

Yersinia and TB!

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163
Q

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

A

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.

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164
Q

T/F onset of achalasia is usually slower than malignancy

What else might help you differentiate

A

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

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165
Q

What would the best investigations for dysphagia be?

A

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.

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166
Q

Which investigation is used to confirm achalasia after barium swallow

A

Manometry is used to confirm the diagnosis of achalasia

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167
Q

T/F achalasia is a risk factor for oesophageal carcinoma

A

T!

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168
Q

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

A

Achalasia /motility disorder

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169
Q

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

A

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.

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170
Q

What could be the chest xray findings in achalasia

A

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”

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171
Q

What would the barium swallow show for achalasia vs malignancy

A

Achalasia: There is a tight, smooth narrowing of the distal oesophagus

Malignancy: irregular stricture (usually happens on a background of GORD)

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172
Q

What are the possible interventions for achalasia

A

Balloon dilation
Surgical cardiomyotomy
Anti-reflux medication

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173
Q

Define volvulus

A

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

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174
Q

Explain the aetiology / risk factors of volvulus

A

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

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175
Q

Summarise the epidemiology of volvulus

A

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

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176
Q

Recognise the presenting symptoms of volvulus

A

Abdo pain and swelling, absolute constipation and later vomiting

May be previous episodes with spontaneous resolution

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177
Q

Recognise the signs of volvulus on physical examination

A

Signs of bowel obstruction:

  • Distension
  • Tenderness
  • Tinkling bowel sounds
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178
Q

Identify appropriate investigations for volvulus and interpret the results

A

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

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179
Q

Define ulcerative colitis

A

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

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180
Q

Explain the aetiology / risk factors of ulcerative colitis

Which antibody is it associated with? What condition?

A

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.

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181
Q

Summarise the epidemiology of ulcerative colitis

What is the pattern of ulceration in UC

A

15% positive family history

Young women in teens-30s have high prevalence

Caucasions and eastern european jews high prevalence

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

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182
Q

Recognise the presenting symptoms of ulcerative colitis

A

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)

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183
Q

Recognise the signs of ulcerative colitis on physical examination

EXTRA-GI manifestations?

A
  • 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)

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184
Q

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

A

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

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185
Q

Generate a management plan for ulcerative colitis
Identify the possible

Acute exacerbation?

A
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

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186
Q

complications of ulcerative colitis and its management

A

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
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187
Q

Summarise the prognosis for patients with ulcerative colitis

What are the poor prognostic factors (ABCDEF)

A

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)

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188
Q

Obturator hernia is associated with which sign

A

Obturator hernias occur through the obturator canal and

they present with inner thigh pain when the hip is internally rotated (Howship-
Romberg sign).

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189
Q

How does the coughing test distinguish direct and indirect inguinal hernia

A

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

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190
Q

What is a spigelian hernia

A

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

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191
Q

What do each of the following signs represent:

Psoas sign
Rovsing's sign 
Cope's sign
Aaron's sign
Murphy's sign
A

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.

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192
Q

Grade haemorrhoids

A

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

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193
Q

Differentiate type 1 and type 2 rectal prolapse

A
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
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194
Q

Symptoms of rectal prolapse

A

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

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195
Q

2 main causes of rectal prolapse

A

1 Lax anal tone due to pundendal nerve damage

2) Prolonged straining

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196
Q

When would metronidazole be used

A

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.

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197
Q

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

A

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.

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198
Q

Where is colorectal cancer most commonly found

A

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

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199
Q

Which tumour marker is most specific for colorectal cancer

A

Serum carcinoembryonic antigen

CEA – the most specific tumour marker for colorectal cancer

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200
Q

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

A

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.

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201
Q

What is the typical presentation of gastric cancer

A

Gastric cancer is also more

likely to present with dyspepsia, vomiting, early satiety, bloating and melaena.

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202
Q

Define appendicitis

A

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

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203
Q

Explain the aetiology / risk factors of appendicitis

What are the specific causes
Which is more common in children

What then causes pain

Which bacteria

A

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.

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204
Q

Summarise the epidemiology of appendicitis

A

Any age, most common 2nd and 3rd decade.

One of commonest surgical diagnoses with 7% lifetime risk

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205
Q

Recognise the presenting symptoms of appendicitis

A

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

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206
Q

Recognise the signs of appendicitis on physical examination

A

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.

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207
Q

Identify appropriate investigations for appendicitis and interpret the results

A

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

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208
Q

Generate a management plan for appendicitis

A

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.

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209
Q

Identify the possible complications of appendicitis and its management

A

Inflammatory mass, appendiceal abscess, perforation and peritonitis, rarely portal pyaemia.

Management of appendicieal abscess:
-Drainage percutaneously (USS/CT guided) or itnraoperatively (with appendicectomy)

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210
Q

Summarise the prognosis for patients with appendicitis

A

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

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211
Q

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

A

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

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212
Q

Summarise the indications for an appendicectomy

A

1) Acute appendicitis

2) Interval proceudre following management of an appendix mass with IV antibitoics

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213
Q

Which anatomical position can the appendix lie in

A

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

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214
Q

Identify the possible complications of an appendicectomy

A

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

215
Q

Classic triad of Budd-chiari syndrome

A

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
216
Q

What is the most sensitive investigation for gall stones?

A

Abdominal USS!

217
Q

Which drugs cause cholestasis

A
Clavulanic acid 
Penicillins 
Oestroges 
Erythromycin 
Chlorpromazine
218
Q

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

A

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.

219
Q

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

A

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)

220
Q

What is the most common type of stomach cancer

A

Adenocarcinoma.

221
Q

What are the risk factors for gastric carcinoma

A

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

222
Q

T/F stomach cancers can prosent as an ovarian mass

A

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.

223
Q

What are the most common causes of bowel obstruction

A

SBO:

  • Intra-abdominal adhesions
  • Hernias
  • Crohn’s disease
  • Malignancy
  • Volvulus

LBO:
Colon carcinoma
Diverticilar disease
Volvulus

224
Q

Where are common sites of metastasis for LBO

A

Pericolic lymph nodes

Liver and lung

225
Q

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

A

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

226
Q

“acute cramping pain and rectal bleeding” with obstruction

A

Consistent with ischaemia

227
Q

When is a barium enema contraindicated

A

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

228
Q

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

A

Pseudo-obstruction.

Lack of gas in the rectum makes true obstruction more likely

229
Q

Which AXR sign suggests ischaemic obstruction

A

Thumb printing

230
Q

What is the management of a diverticular abscess

A

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.

231
Q

Faeculent vaginal discharge may suggest which disease?

Name other complications.

A

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.

232
Q

What is the cause of most diverticular disease

A

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.

233
Q

Define primary biliary cirrhosis

A

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

234
Q

Explain the aetiology / risk factors of primary biliary cirrhosis

Which antibodies

A

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!

235
Q

Summarise the epidemiology of primary biliary cirrhosis

A

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

236
Q

Recognise the presenting symptoms of primary biliary cirrhosis

A

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)
237
Q

Recognise the signs of primary biliary cirrhosis on physical examination

A

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)

238
Q

Identify appropriate investigations for primary biliary cirrhosis and interpret the results

A

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)

239
Q

Complications of PBC

A

Cirrhosis and associated complications:

  • Jaundice
  • Encephalopathy
  • Ascites
  • Variceal bleeding
  • HCC!
  • Hyperlipidaemia
  • Malabsorption of fat soluble vitamins
240
Q

What is the use of the erect abdominal radiograph

A

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

241
Q

What is a respiratory complication of a subphrenic abscess

A

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

242
Q

What is the imaging of choice for a subphrenic abscess

A

Chest x-ray and supine abdo xray

Then ultrasound. You can visualise the abscess and then USS can guide percutaneous drainage

243
Q

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

A

Causative pathogens tend to be anaerobes or Gram-ves.

244
Q

Does a pleural effusion reactive to a subphrenic abscess require drainage

A

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

245
Q

Subphrenic abscess is a complication of which conditions

A

Perforation of hollow viscus (appendix, colon)

Inflammatory process (pancreatitis, cholecystitis)

Trauma of internal organs (stab, gunshot)

Complication of surgery (splenectomy, cholecystectomy, gastrectomy)

Idiopathic

Diverticulitis

246
Q

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

A

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

247
Q

What is the main cause of anastomotic breakdown.

What would need to be done usually in a failed recto-sigmoid anastamosis

A

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.

248
Q

Define primary sclerosing cholangitis

A

Chronic cholestatic liver disease characterized by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts.

(whereas PBC affects intrahepatic)

249
Q

Explain the aetiology / risk factors of primary sclerosing cholangitis

HLA associations?

Antibody association, or none significant?

A

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

250
Q

Summarise the epidemiology of primary sclerosing cholangitis

A

Usually presents between 25 and 40 years

251
Q

Recognise the presenting symptoms of primary sclerosing cholangitis

A

May be asymptomatic, diagnosed after persistently raised AlkPhos.

May present with intermittent:

  • Jaundice
  • Pruritis
  • RUQ tenderness
  • Weight loss
  • Fatigue

Hx of ulcerative colitis

252
Q

Recognise the signs of primary sclerosing cholangitis on physical examination

A

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

253
Q

Identify appropriate investigations for primary sclerosing cholangitis and interpret the results

A

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

254
Q

Complications of PSC

A

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

255
Q

What do the following AXR signs represent

Coffee bean sign
Embryo sign

A

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’.

256
Q

What are the 4 ways of detecting H Pylori infection`

A

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

257
Q

Outline the urea breath test

A

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.

258
Q

Outlien the CLO test

A

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.

259
Q

What are diverticulae

A

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

260
Q

What is the cause of rectal bleeding in divertciulitis

A

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

261
Q

What does cryptosporidium cause

A

diarrhoeal illness in immunocompromised patients

262
Q

Define diverticular disease

Define: diverticulosis, divercular disease, diverticulitis.

How is it classified

A

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

263
Q

Explain the aetiology / risk factors of diverticular disease

What causes diverticulitis

A

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)

264
Q

Summarise the epidemiology of diverticular disease

A

COMMON!

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

265
Q

Recognise the presenting symptoms of diverticular disease

When does bleeding occur.

Hx for diverticulosis, diverticulitis and diverticular fistula please.

A

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.

266
Q

Recognise the signs of diverticular disease on physical examination

A

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

267
Q

Identify appropriate investigations for diverticular disease and interpret the results

Acute setting?

A

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

268
Q

Generate a management plan for diverticular disease

Asymptomatic?

If diverticulitis?
Surgical options

A

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

269
Q

Identify the possible complications of diverticular disease and its management

A

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

270
Q

Summarise the prognosis for patients with diverticular disease

A

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

271
Q

What are the GI causes of clubbing

A

Inflammatory bowel disease (e.g. ulcerative colitis and Crohn’s disease) is

liver cirrhosis,

primary biliary cirrhosis,

oesophageal leiyomyoma,

coeliac disease and

achalasia.

272
Q

Define gastritis

A

Inflammation of the gastric mucosa.

Acute: neutrophil invasion

Chronic: lymphocyte and plasma cell infiltration

273
Q

Explain the aetiology / risk factors of gastritis

What causes acute gastritis

A

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

274
Q

Summarise the epidemiology of gastritis

A

.

275
Q

Recognise the presenting symptoms of gastritis

A

ACUTE GASTRITIS:
Epigastric pain

Nausea

Vomiting

Life threatening upper GI bleed (can cause melaena)

Symptoms:
Asymptomatic sometimes

Epigastric pain

Nausea

Vomiting

276
Q

Identify appropriate investigations for gastritis and interpret the results

A
Diagnosis: 
Endoscopic biopsy 
Detection of H pylori using: 
-Serology 
-Stool antigen test
-Urease breath test
277
Q

Generate a management plan for gastritis

A

Treating the underlying cause (remove NSAIDs)

Antacids

Antibiotics to eradicate the H Pylori infection:
-Triple therapy: PPI + clari + amoxicillin for 2 weeks

278
Q

Identify the possible complications of gastritis and its management

A

Chronic:

Infectious (H Pylori): Peptic ulcers, MALTomas

Autoimmune: Pernicious anaemia, iron deficiency anaemia, carcinoid tumour

279
Q

Define peptic ulcer disease

A

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

280
Q

Explain the aetiology / risk factors of peptic ulcer disease and gastritis

Where are the gastric ulcers and duodenal ulcers usually located

A

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

281
Q

Summarise the epidemiology of peptic ulcer disease and gastritis

A

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.

282
Q

Recognise the presenting symptoms of peptic ulcer disease and gastritis

A

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)

283
Q

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

A

May be none.

Epigastric tenderness

Signs of complicaations (anaemia, succession splash in pyloric stenosis)

284
Q

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

A

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

285
Q

Generate a management plan for peptic ulcer disease and gastritis

ACUTE

A

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)

286
Q

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

A

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)

287
Q

Summarise the prognosis for patients with peptic ulcer disease and gastritis

A

Overall lifetime risk”10%.

Generally good as peptic ulcers associated with H. pylori can be cured by eradication.

288
Q

How do NSAIDs affect the gastric musocsa

A

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

289
Q

Outline stress ulcers

A

Sepsis, shock and trauma can lead to stomach erosions.

Specific types: curling’s ulcers (secondary to burns) and cushings ulcer (secondary to brain injuries)

290
Q

What might point you towards zollinger ellison with a peptic ulcer

A

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

291
Q

What causes haemorrhage in gastric ulcer and duodenal ulcer

A

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

292
Q

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

A

under 50: peptic ulcer

over 50: colorectal carcinoma

293
Q

How can perforated duodenal ulcer present

A

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

294
Q

What is zollinger ellison syndrome

A

Gastrinoma (secretes gastrin –> hyperacidic environment)

295
Q

What medications worse GORD

A

Drugs that damage the mucosa: NSAIDs, steroids, bisphosphinates, aspirin

Drugs that affect eosophageal motility: nitrates, TCAs and anticholinergics

296
Q

Management of GORD

A

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.

297
Q

Triad of features assocaited with acute mesenteric ischaemia

A

Severe abdominal pain, normal abdo examination and shock

298
Q

Cause of acute mesenteric ischaemia

A

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

299
Q

What is the cause of acute vs chronic mesenteric ischaemia

A

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.

300
Q

How does chronic mesenteric ischaemia present

A

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

301
Q

What are the x ray findings associated with severe mesenteric ischaemia

A

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.

302
Q

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

A

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.

303
Q

T/F constipation can present with diarrhoea

A

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.

304
Q

What are the cell types in the anus

A

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)

305
Q

What are haemmarhoids

A

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

306
Q

What is haemarrhoidal disease

A

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

307
Q

Aertiology and risk factors for haemarrhoids

A

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.

308
Q

Classify haemarrhoids into 2 typesq

A

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

309
Q

Grade internal haemorrhoids

A

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.

310
Q

History of haemorrhoids

A

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

311
Q

Signs of haemorrhoids

  • Puruple/blue veins?
  • Dark pink, glistening masses at the anal margin?
  • Purplish hue?
A

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.

312
Q

Investigations for haemorrhouds

A

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

313
Q

If there are haemrrhoids with changes in bowel habits?

A

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

314
Q

Management of haemorrhoids

A

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

315
Q

Complications of haemorrhoids

What about of slerotherapy and haemorrhoidectomy

A

Bleeding, prolapse, thrombosis

Slcero: prostatitis, perineal sepsis, rarely impotence

Haemorhoidectomy: pain, bleeding, incontinence

316
Q

Anal fissure definition and causes

T/F the pathology of anal fissure just relates to the skin

A

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

317
Q

Age for anal fissure

A

Most common under age of 40.

Male=female

318
Q

Hx of anal fissure

A

Severe burning pain on defaecation, can persist for hours

Patients may avoid bowel movements

Bright red bleeding per rectum, small amount

Itchy

319
Q

Examination of anal fissure

A

Can see a sentinel pile.

DRE may not be possible due to pain

Chronic fissures –> firm, indurated ridge

320
Q

Investigations of anal fissure

A

Diagnosis on history

Exclude other things

321
Q

Management of anal fissure

A

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

322
Q

Complication of anal fissure

A

Chronic fissure and chronic pain

323
Q

What is a pilonidal sinus

A

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

324
Q

Cause of pilonidal sinus

A

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

325
Q

Epidemiology of pilonidal sinus

A

Ass with hirsute individuals.

Occupations like hairdressors may develop interdigital pilonidal sinus

326
Q

Hx of pilonidal sinus

A

Painful natal cleft, esppecially if inflamed/superimposed infection

Discharge and swelling

327
Q

Examination of pilonidal sinus

A

Midline opening or pits seen between buttocks, hair may protrude

Tender swelling that may be fluctant/discharge etc. if assocaited infection/abscess

328
Q

Investigation of pilonidal sinus

A

None needed for diagnosis,

If infection raised WCC

Glucose (diabetes)

329
Q

Management of acute pilonidal sinus

Management of chronic pilonidal sinus

A

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

330
Q

Define
Perianal abscess
Perianal fistula

A

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

331
Q

Types of perianal abscess

A

Classified according to location

332
Q

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

A

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

333
Q

Pepperpot perineum sign?

A

Multiple perineal fistulae (Crohn’s disease)

334
Q

What is perianal fistulae ass with

A

Crohn’s, diabetes, malignancy

335
Q

History in perianal fistulae/absces

A

Constant throbbing pain in perineum

Intermittent discharge (blood stained/mucus) near anal region

336
Q

Perianal fistula/abscess examination

A

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.

337
Q

What is goodsall’s rule

A

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

338
Q

Investigations for perianal fistula/abscess

A

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

339
Q

Management of perianal abscess/fistula

A

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

340
Q

Rectal prolapse in a child which investigation

A

Sweat chloride test- 10% will have CF

341
Q

Investigations for rectal prolapse

A

Proctosigmoidoscopy, defaecating proctogram or barium enema

342
Q

Management of rectal prolapse

Conservative

Emergency

Chronic

A

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
343
Q

Prognosis of rectal prolapse

A

Sponatenosusly resolves usually in kids

15% recurrence in adults

344
Q

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

A

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

345
Q

Differentiating between anal fissure and haemorrhoids

A

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.

346
Q

Peutz-jehger syndrome

A

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

347
Q

Familial polyposis coli

Inheritence?

A

Multiple stomach, small and large bowel adenomas.

Autosomal dominant

premalignant

348
Q

Gardner’s syndrome

A

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

349
Q

Turcots syndrome

A

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
.
350
Q

Cronkhite canadas syndrome

A

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

351
Q

What is receommended in familial polposis coli

A

Early subtotal colectomy

352
Q

Aetiology of colorectal cancer

A

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)

353
Q

RF for colorectal cancer

A

Colorectal polyps

Previous CRC

IBD (particularly UC)

Genetic syndromes (FAP, lynch sydrome)

354
Q

Gender specifics of colorectal cancer

A

Rectal, male>female

Colon female>male

355
Q

History of colorectal cancer

A

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

356
Q

What might CRC look like on barium enema

A

Apple core lesion, for annular tumours

357
Q

Investigations for CRC

A

Screening: blood (FBC), stool (occult or frank)

Endoscopy: sigmoidoscopy and colonoscopy allows visualisation and biopsy.

Imaging: barium enema, CT scan, MRI, endorectal ultrasound.

358
Q

State the operation for the following cancers:

  • Caecal tumour
  • Transverse colon tumours
  • Descending colon tumours
  • Sigmoid tumours
  • High mid-rectal
  • Low rectal
  • Emergency
A
  • 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
359
Q

Chemo and radio for CRC?

A

Radio: neoadjucant

Chemo: FOLFOX (5-FU)

360
Q

Dukes staging

A
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.
361
Q

At what portal pressure might anastamoses become congested and dilated

A

When the portal pressure is > 12 mm Hg, these

anastomoses become congested and dilated, and are prone to bleeding.

362
Q

Organisms commonly involved in SBP

A

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

363
Q

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

A

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.

364
Q

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

A

Hiatus hernia

365
Q

2 types of hiatus hernia

A

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

366
Q

Best investigation for hiatus hernia

A

Barium swallow is the best investigation to confirm the diagnosis

367
Q

What might hiatus hernia show in chest x ray

A

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

368
Q

Management of hiatus hernia

A

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.

369
Q

Criteria for acute severe colitis (in UC)

A
Frequency of stool >6
Overtly bloody stool
Fever (>37.5)
Tachycardia (>90)
Anaemia (Hb<105)
Raised ESR (>30)
370
Q

Management of acutely presenting UC

A

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.

371
Q

What is a loop vs end ileostomy

A

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

372
Q

What is the faecal matter like that comes from an ileostomy

How to deal?

A

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

373
Q

What does an ileostomy look like compared to a colostomy

A

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

374
Q

Which 3 symptoms are diagnostic of acute cholangitis

A

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

375
Q

Initial treatment of ascending cholangitis

A

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.

376
Q

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

A

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

377
Q

Investigation if you suspect a stone given abdo USS

A

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

378
Q

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

A

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.

379
Q

What is HCC

A

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

380
Q

Aetiology of HCC

A

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).

381
Q

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

A

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

382
Q

Hx of HCC

A

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.

383
Q

Examination HCC

A

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).

384
Q

Investigation of HCC

A

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

385
Q

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

A

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

386
Q

What is the management of gastroenteritis

A

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

387
Q

Blistering rash on the elbows?

A

Dermatitis herpetiformis

388
Q

Differentiate hiatus hernia sliding and rolling

A

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

389
Q

Aetiology of hiatus hernia

A

Congenital or acquired.

Thinning and increased laxity of the phreno-oesophageal ligament with age

Associated with obesity, GORD, chronic eosophagitis

390
Q

Which hiatus hernia is more common

A

Type 1 (95%)

Increase in frequency with age

391
Q

Hx of hiatus hernia

A

Many asymptomatic.

Reflux symptoms of heart burn, indigestion, postprandial fullness and regurg

No examination findings unless complications develop

392
Q

Investigation for hiatus herna.

A

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.

393
Q

Management of hiatus hernia

A

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)

394
Q

Complications of hiatus hernia

A

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

395
Q

T/F hypoglycaemia is a cause of pancreatitis

A

F.
hyperlipidaemia, hyperglycaemia, hypercaleamia

is the H in GET SMASHED!

396
Q

C difficile causes what type of gut inflammation

Treatment

A

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

397
Q

History of a subdiaphragmatic abscess

A

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

398
Q

How would a liver abscess present differently to subdiaphragmatic abscess

A

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

399
Q

Imaging for suspected subdiaphragmatic abscess

A

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.

400
Q

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

A

T

401
Q

How would ascending cholangitis present differently to cholecystitis

A
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
.
402
Q

Pruritis in pregnancy?

A

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).

403
Q

Define Wilson’s

A

Reduced biliary excretion of copper and accumulation of copper in teh liver and brain, cornea and kidneys

Hence it is aka hepatolenticular degeneration

404
Q

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

A

Basal ganglia

405
Q

Cause of wilson’s

A

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

406
Q

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

A

T.

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

407
Q

Hx of Wilson’s disease

A

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

408
Q

Examination of wilson’s

A

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).

409
Q

Investigations for wilsons

A

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

410
Q

Kayser fleischer involves copper deposition in which layer of the cornea

A

Descemet’s membrane

411
Q

What is the normal copper handling in the body

A

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

412
Q

What happens to blood caeruloplasmin in wilsons

A

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

413
Q

What haem problem can wilsons cause

A

Haemolytic anaemia because copper can cause direct damage to circulating RBCs

414
Q

What is the most likely cokmplication of crohns

A

Perianal fistulae

415
Q

Triple therapy for peptic ulcers involving h pylori?

A

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.

416
Q

What if triple therapy fails in H pylori

A

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).

417
Q

Pancreatic pseudocysts present with what

A

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

418
Q

What to pancreatic pseudocysts results from

A

Chronic pancreatitis or pancreatic trauma

419
Q

What HLA is coeliac associated with

A

HLA-DQ2

420
Q

Black pigmented gall stones?

A
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.
421
Q

What stones would you find in someone with small intestine resection

A

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

422
Q

Diabetes mellitus which type of gallstones

A

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

gallstones

423
Q

Chronic Abx and gall stones?

A
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
.

424
Q

What is IBS

A

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
425
Q

Aetiology of IBS

A

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

426
Q

Investigations for IBS

A

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.

427
Q

Management of IBS

A

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

428
Q

Complication of IBS

A

Increased risk of colonic diverticulae

429
Q

What are mixed stones made of. What proportions of gall stones do they make up

What associations does it have

A

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.

430
Q

What are pure cholesterol stones made of. What proportions of gall stones do they make up

What associations does it have

A

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

431
Q

What are pigment stones made of. What proportions of gall stones do they make up

What associations does it have

A

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).

432
Q

What % of gall stones are asymptomatic

A

90%!!!!

433
Q

Biliary colic Hx and examination

A

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

434
Q

Acute cholecystitis Hx and examination

A

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.

435
Q

Ascending cholangitis Hx and examination

A

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

436
Q

Investigations for gall stones

A

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.

437
Q

Management of mild biliary colic symptoms

A

Conservaive, avoidance of fat in diet

438
Q

Management of choledocholithiasis

A

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

439
Q

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

A

Supportive care, analgesics

Elective cholecystectomy for:

Symptomatic cholelithiasis
Asymptomatic cholelithiasis only if at increased risk of gallbladder cancer

440
Q

Management of acute cholecystitis

A

(cholelithiasis or biliary sludge leading to inflammation of gall bladder wall)

Supportive care, analgesics
IV antibiotics
Cholecystectomy (timing depends on severity)

441
Q

Management of acute cholangitis

A

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)

442
Q

What is bouveret’s syndrome

A

gallstones causing gastric outlet obstruction

443
Q

What is mirizzi syndrome

A

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

444
Q

What Abx are used for actue cholangitis

A

Cephalosporin and metronidazole

445
Q

What is the commenest neurological manifestation of sarcoid

A
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.
446
Q

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

A

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)

447
Q

What are the complication of coeliac disease

A

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.

448
Q

What should you screen for for newly diagnosed patients with coeliac

A

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

449
Q

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

A

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

450
Q

Progressive dysphagia for food and GORD?

A

Peptic stricture needs to be excluded, along with oesophageal carcinoma

451
Q

Management for symptomatic, benign peptic stricture

A

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.

452
Q

Investigation of eosophageal perforation

A

CT scan with WATER SOLUBLE oral contrast

453
Q

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

A
Pyoderma gangrenosum
Erythema nodosum 
Episcleritis 
Aphthous ulcers 
Anterior uveitis 
Acute arthropathy
454
Q

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

A

Sacroiliitis/ank spond

PSC

455
Q

Acute severe UC management

A

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.

456
Q

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

A

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.

457
Q

Contraindications for ciclosporin

A

Hypertension and renal impairment

458
Q

Best long term management for eosophageal varicies

A

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.

459
Q

T/F TIPSS is a prophylactic treatment for variceal bleeding

A

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.

460
Q

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

A

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

461
Q

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

A

F

It may be precipitated by glucose infusion

462
Q

T/F chronic alcoholism is assocaited with chronic kidney disease

A

F

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

463
Q

T/f alcohol is associated with diabetes

A

F.

Pancreatic damage can precipitate diabetes

464
Q

Who are benign liver tumours especially frequent in

A

Young women

465
Q

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

A

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

466
Q

Epidemiology of hepatic benign tumors

A

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

467
Q

Cause of liver benign tumour:

Hepatocellular adenoma

A

oral contraceptives and anabolic steroids

468
Q

Cause of liver benign tumour:

Hepatic haemangioma

A

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

469
Q

Symptoms/clinical findings of benign liver tumours

A

Usually asymptomatic

Large tumors –> upper abdominal pain, fullness, and nausea

470
Q

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

A
Best initial test: ultrasound
Further imaging 
Contrast-enhanced CT
MRI
Biopsy: to confirm diagnosis if imaging is inconclusive
471
Q

Where are hepatocellular adenomas more commonly located

A

Right lobe

472
Q

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

A

Focal nodular hyperplasia

473
Q

Histology of a hepatocellular benign tumour:

Cavernous vascular spaces of variable size, lined by flat endothelial cells

A

Hepatic hemangioma

474
Q

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

A

Hepatocellular adenoma

475
Q

What are the types of liver cysts

A

Simple cyst (congenital, usually asymptomatic- USS and CT)

Congenital polycystic liver (associated with PKD)

Hyatid echinococcal cysts

476
Q

What is crohn’s

A

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

477
Q

Aetiology of crohn’s

A

Genetic and environmental factors

478
Q

Hx of crohn’s

A

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

479
Q

Exam of crohn’ss

A

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).

480
Q

Commmon locations for crohns

A

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.

481
Q

What is the association between IBD and smoking

A

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%.

482
Q

T/F OCC and NSAIDS increase the risk of crohns

A

Yes

483
Q

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

A

Yersnia enterocolitica (an alternative differential)

484
Q

Investigations for crohns

A

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

485
Q

Why do a plain radiography with barium swallow in crohn’s?

What might be found

A

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

486
Q

Why do endoscopy in crohns? What might you find

A

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
487
Q

What might you find in crohns histology

A

Skip lesions (discontinuous inflammation)

Hypertrophic lymph nodes

Transmural inflammation:
Non-caseating granulomas
Giant cells
Distinct lymphoid aggregates of the lamina propria

488
Q

Management of ACUTE exacerbation of crohns

A

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.

489
Q

Conservative management of crohns

A

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

490
Q

Long term medical management of crohn’s disease

A

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

491
Q

Long term surgical managemnet of crohns

A

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.

492
Q

Complications of crohn’s

A

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

493
Q

Extraintestinal features of crohns

A

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

494
Q

Prognosis of crohn’s

A

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

495
Q

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

A
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
496
Q

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

A

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

497
Q

Contraindications for parenteral nutrition

A
Enteral nutrition is feasible
Serum hyperosmolality
Severe hyperglycemia
Severe electrolyte abnormalities
Volume overload
498
Q

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

A

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

499
Q

Metabolic complications associated with specialised nutritional support

A

Electrolyte imbalances:
hypocalcemia, hypomagnesemia, hypophosphatemia

Hyperglycaemia

Refeeding syndrome

Gallstone disease

NAFLD

Renal damage

Acalculous cholecystits

500
Q

What causes refeeding syndrome

A

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

501
Q

What is vitamin b1 (thiamine) needed for

A

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

502
Q

Multiple hamartous polyps on the colon of a young person

A
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
.
503
Q

hamatomatous
polyps
of the GI tract, mucosal
hyperpigmentation

A
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.
504
Q

Cause of acute cholecystits

A

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.

505
Q

Investigations for cholecystitis

A
  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)

506
Q

Management of acute cholecystitis

A

See booklet

507
Q

What are the causes of GI perforation

A
  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)
508
Q

Signs of GI perforation on examination

A

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

509
Q

Investigations for GI perforation. First imaging?

A

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

510
Q

What is a liver abscess

A

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

511
Q

What is the cause of a pyogenic liver abscess

A

Polymicrobial commonly.

Escherichia coli, Klebsiella, enterococcus, bacteroides, streptococci, staphylococci

512
Q

Which other organisms can cause liver cysts

A

Amoebic (amboeba histolytica)

Hyatid cyst (tapeworm Echinococcus granulosis)

513
Q

Hx of liver abscesses

A

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

514
Q

Risk factor for developing a liver abscess

A

Diabetes

515
Q

Examination of liver absceses

A

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.

516
Q

Liver abscess with raised eosinophils

A

Hyatid cyst

517
Q

Investigations of liver abscesses

A

FBC, LFTs, blood culture,, PT and aPTT

IMAGING:
USS
Gram stain and culture of aspirated abscess fluid
CT

518
Q

What are the LFT findings with liver abscess

A

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

519
Q

Why is clotting profile used in liver abscesses

A

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

520
Q

When would you not aspirate a liver abscess

A

If there is abnormal clotting or if you suspect hyatid

521
Q

What is oesophageal carcinoma

A

Malignant tumour arising in the oesophageal mucosa.

Two major histological types: squamous cell carcinoma and adenocarcinoma

522
Q

What is the cause of squamous cell carcinoma in oesophagus

A

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

523
Q

What is the cause of adenocarcinoma

A

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

524
Q

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

A

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

525
Q

How do oesophageal cancers spread

A

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

526
Q

Hx of eosophageal cancer

A

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).

527
Q

Examination of oesophageal cancer

A

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

528
Q

Which investigations would you do for oesophageal cancer

1st test?

Staging

A

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

529
Q

What metabolic disturbance might present in oesophageal obstruction

A

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

530
Q

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

A

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

531
Q

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

A

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

532
Q

Why are right sided indirect inguinal hernias more common?

A

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)

533
Q

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.

A

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.

534
Q

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.

A

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.