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Gastroenterology Flashcards

1
Q

Name some functions of the liver

A
  • Carbohydrate metabolism (via glucagon)
  • Lipid metabolism
    • Formation of cholesterol
  • Vitamin (A,D,E,K) storage and metabolism
  • Bile production and secretion
  • Protein synthesis - albumin, coagulation factors, plasma proteins
  • Immunity (via Kuppfer cells)
  • Drug metabolism
    • Phase 1 (oxidation/reduction by P450
    • Phase 2 (conjugation)
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2
Q

What is portal hypertension?

A

Pressure in portal vein > 12 mmHg

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3
Q

Name some causes of portal hypertension

A
  • Prehepatic
    • Portal vein thrombosis
    • AV fistula
    • Splenomegaly
  • Hepatic
    • Cirrhosis
    • Chronic hepatitis
    • Chronic pancreatitis
    • Biliary cirrhosis
    • Primary sclerosing cholangitis
  • Post-hepatic
    • IVC obstruction
    • Right heart failure
    • Hepatic vein thrombosis
    • Constrictive pericarditis
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4
Q

Name the portosystemic anastamoses in portal hypertension

A
  • Oesophageal varices (left gastric → azygous)
  • Haemorrhoids (superior rectal → inferior rectal)
  • Caput medusae (umbilical → epigastric
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5
Q

Name some clinical features of portal hypertension

A
  • Portosystemic anastomoses
  • Ascites
  • Splenomegaly (+ thrombocytopenia)
  • Hepatomegaly
  • Liver failure
  • Variceal bleeding (haematemesis
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6
Q

Name some investigations into portal hypertension

A
  • Bloods - FBC, U&E, LFT, clotting
  • Hepatitis screen (A, B, C, D, E, CMV, EPV)
  • Ultrasound/CT (portal vein > 13mm)
  • Transabdominal Doppler Ultrasound
  • Hepatic Venous Pressure Gradient (HVPG)
    • Assesses severity
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7
Q

How is portal hypertension treated?

A
  • Transjugular Intrahepatic Portosystemic Shunting (TIPS) = shunt between portal vein and hepatic vein
  • Prevent bleeding
    • B blockers
    • Nitrates
    • Vasopressin/terlipressin
    • Band ligation of varices
    • Balloon tamponade
  • Treat ascites (paracentesis)
  • Treat hepatic encephalopathy
  • Liver transplant
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8
Q

How is ascites treated?

A
  • Paracentesis
  • Albumin replacement
  • Salt restriction
  • Spironolactone
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9
Q

How is hepatic encephalopathy treated?

A
  • Low protein intake
  • Lactulose (30ml) - excrete ammonia and nitrous toxins
  • Enema
  • Antiobiotics (rifaximin) - decrease concentration of ammonia-producing bacteria in colon
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10
Q

How is ascites treated?

A
  • Paracentesis + albumin replacement IV
  • Salt restricted diet
  • Spironolactone - blocks aldosterone receptor in collecting tubule (counteracts salt-retention function of aldosterone)
  • TIPS
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11
Q

What is cirrhosis?

A

Fibrosis of the liver parenchyma with nodular regeneration and hepatocellular necrosis

  • Micronodular = uniform nodules < 4mm
  • Macronodular = larger nodules, irregularly distributed
  • Mixed
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12
Q

Name some causes of cirrhosis

A
  • Congenital
    • Haemachromatosis
    • Wilsons (copper)
    • A1 anti trypsin deficiency
  • Acquired
    • Excess/chronic alcohol intake
    • Chronic hepatitis
    • Primary biliary cirrhosis
    • Gallstones
    • Hepatic vein obstruction
  • Idiopathic
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13
Q

Name some clinical features of cirrhosis (decompensated)

A
  • Jaundice
  • Spider naevi
  • Ascites
  • Low albumin
  • Clotting disorders
  • Portal hypertension
  • Encephalopathy
  • Gynaecomastia
  • Testicular atrophy
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14
Q

How is cirrhosis investigated?

A
  • Metabolic screen (serum copper)
  • Hepatitis screen (A, B, C, D, E, CMV, EBV)
  • Autoimmune screen
    • AMA (PBC)
    • Anti smooth muscle (hepatitis, PBC)
  • LFTs
  • Abdo ultrasound / CT
  • Liver biopsy
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15
Q

How is cirrhosis managed?

A
  • Alcohol abstinence / addiction programme
  • Weight loss
  • Treat causes
    • Hepatitis B - interferon alpha
    • Hepatitis C - ribavirin
    • Autoimmune - immunosuppression
    • Gallstones - cholecystectomy
  • Transplant
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16
Q

Name the common LFTs. How are they interpreted?

A
  • ALT more specific
  • AST:ALT > 2 = alcoholic liver disease
  • AST:ALT ratio = 1 = viral hepatitis
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17
Q

What are the risk factors for developing hepatocellular carinoma?

A
  • Viral hepatitis
  • Chronic alcoholism
  • Smoking
  • > 70 years
  • Aflatoxin exposure (molds)
  • Family history
  • Contraceptives
  • Androgens
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18
Q

What are clinical features of hepatocellular carcinoma?

A
  • Cirrhosis
  • Dull ache in RUQ
  • Ascites
  • Jaundice
  • Hepatomegaly (irregular and craggy)
  • Systemic
    • Fatigue
    • Weight loss
    • Lethargy
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19
Q

How is hepatocellular carinoma investigated?

A
  • LFTs
  • Alpha fetoprotein (AFP) > 500 ng/ml in 70% of cases
  • Ultrasound
  • Staging CT scan
  • Needle biopsy
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20
Q

What is the management for hepatocellular carinoma?

A
  • Surgical resection (if no cirrhosis)
  • Transplant
  • Image-guided ablation
  • Transarterial chemoembolisation
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21
Q

Which malignancies metastasises to the liver?

A
  • Bowel (portal system)
  • Breast
  • Pancreas
  • Stomach
  • Lung
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22
Q

Name some pre-hepatic causes of jaundice

A

Excessive red cell breakdown

  • Haemolytic anaemia
  • Transfusion reaction
  • Congenital red cell abnormalities
    • Sickle cell
    • Spherocytosis
  • Gilberts Syndrome (familial non-haemolytic anaemia)

Normal urine and stool colour

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23
Q

Name some causes of hepatic jaundice

A

Dysfunction/obstruction in liver

  • Infection = hepatitis, EBV, CMV
  • Drugs = paracetemol overdose, antipsychotics, antibiotics (tetracycline, erythromycin)
  • Alcoholic liver disease
  • CIrrhosis
  • Haemochromatosis
  • Carcinoma

Dark urine

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24
Q

Name some causes of post-hepatic jaundice

A

Biliary obstruction

  • Gallstones
  • Bile duct stones
  • Cholangiocarcinoma
  • Pancreatic cancer (head) - PAINLESS JAUNDICE
  • Strictures (surgery)
  • Pancreatitis
  • Biliary cirrhosis

Dark urine and pale stools (less stercobilinogen in faeces)

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25
Q

How is jaundice investigated?

A
  • Bloods - LFTs, PT, FBC, U&E. clotting
  • Urinanalysis (high urobilinogen = haemolytic anaemia)
  • Hepatitis screen
  • Blood film (haemolysis)
  • Ultrasound scan - liver, gall bladder, bile ducts, pancreas (obstructive)
  • MRCP - visualise biliary tree (T2)
  • Liver biopsy (hepatitis)
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26
Q

What pattern of LFTs would you see in each type of jaundice

A
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27
Q

How is jaundice managed?

A
  • General
    • IV fluids
    • Monitor urine output
    • vit K 10mg (if inc PT)
    • Nutrition
    • Treat infection
  • Anti-histamine (itching)
  • Treat encephalopathy
  • Treat underlying causr
    • Haemolytic anaemia = steroids
    • Gallstones = ERCP, cholecystectomy, stent
    • Liver disease = transplant
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28
Q

Name some complications of jaundice

A
  • Hepatorenal syndrome
  • Deranged coagulation
  • Cholangitis
  • Hepatic encephalopathy
  • Immunosuppresion
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29
Q

What is hepatorenal syndrome?

A

The development of kidney failure in patients with advanced liver disease.

Thought to be caused by systemic vasoconstriction

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30
Q

What are the different types of hiatus hernia?

A
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31
Q

Name some risk factors for developing hiatus hernia

A
  • Age
    • Loss of diaphragmatic tone
    • Increasing intra-abdominal pressures
    • Increased size of oesophageal hiatus
  • Pregnancy
  • Obesity
  • Ascites
  • Female
  • Previous surgery
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32
Q

What are clinical features of hiatus hernia?

A
  • GORD - burning epigastric pain
    • Worse lying flat
  • Vomiting
  • Weight loss
  • Early satiety
  • Bleeding
  • Hiccups
  • Dysphagia
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33
Q

How is hiatus hernia investigated?

A
  • OGD (endoscopy)
  • Barium swallow
  • CT abdo and thorax (exclude malignancy)
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34
Q

How is hiatus hernia managed?

A
  • Conservative
    • Stop smoking
    • Lose weight
    • Reduce alcohol
  • Pharmacological
    • PPI
    • Antacids
    • Mucosal protectants
    • Promotilants (metoclopramide)
  • Surgical (if persistent symptoms, complications or nutritional failure)
    • Curoplasty = hernia reduced from thorax
    • Fundoplication = gastric fundus wrapped around lower oesophagus to strengthen LOS
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35
Q

Name some complications of hiatus hernia

A
  • Volvulus (Borchadt’s triad)
    • Severe epigastric pain
    • Retching (but no vomiting)
    • Inability to pass NG tube
  • Hernia recurrence
  • Bloating (can’t belch)
  • Fundal necrosis
  • Dysphagia
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36
Q

What is a peptic ulcer? Where is it most common?

A

Break in the lining of the GI tract

Most common in lesser curve of stomach and proximal duodenum

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37
Q

Name some causes of peptic ulcers

A
  • H-pylori (gram negative bacillus)
  • Female
  • NSAIDs (inhibit prostaglandin synthesis)
  • High alcohol intake
  • Steroid use
  • Chemotherapy
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38
Q

What are the clinical features of peptic ulcers?

A
  • Epigastric pain
    • Worse with eating if stomach
    • Worse with empty stomach if duodenal
  • Nausea
  • Anorexia
  • Weight loss
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39
Q

How are peptic ulcers investigated?

A
  • Gastroscopy / OGD
    • Histology biopsy
    • Rapid urease ‘CLO’ test (H pylori)
  • H pylori test
    • Carbon-13 breath urea breath test
    • Serum antibodies
    • Stool antigen
  • FBC (anaemia/bleeding)
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40
Q

How are peptic ulcers managed?

A
  • Conservative
    • Stop smoking
    • Weight loss
    • Reduce alcohol intake
    • Avoid NSAIDs
  • PPI (8 weeks) omeprazole
  • Antacids (gaviscon)
  • If H pylori postive = antibiotic regime
  • Surgery (if complications, outlet obstruction or failure of medical therapy)
    • Partial gastrectomy
    • Selective vagotomy
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41
Q

How is H pylori treated?

A

7 day, twice daily course of:

  • PPI (omeprazole 20-40mg)
  • Amoxicillin
  • Clarithromycin or metronidazole

If allergic to penicillin = PPI, clarithromycin and metronidazole

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42
Q

Name some complications of peptic ulcers

A
  • Acute upper GI bleeding
  • Pyloric stenosis
  • Iron deficiency anaemia
  • Perforation
  • Gastric outlet obstruction
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43
Q

What is Zollinger-Ellison syndrome?

A

Hypergastrinaemia causing extensive ulceration. Caused by gastrinoma (intrapancreatic)

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44
Q

Name some risk factors for developing a gastic adenocarcinoma

A
  • > 50
  • Male
  • H pylori
  • Smoking
  • East asian
  • Chronic gastritis
  • Blood group A
  • Excess alcohol
  • High salt diet
  • Family history
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45
Q

What are the clinical features of gastic adenocarcinoma?

A
  • Dyspepsia
  • Dysphagia
  • Nausea and vomiting
  • Melaena
  • Haematemesis
  • Systemic = weight loss, anaemia, lethargy
  • Epigastric mass
  • Virchow’s node
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46
Q

How is gastic adenocarcinoma investigated?

A
  • Bloods
    • CEA (carcinoembryonic antigen) in 50%
    • FBC
    • LFTs
  • OGD / endoscopy
  • Biopsies
  • CT chest-abdo-pelvis (metastases)
  • Staging laparascopy (peritoneal metastases)
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47
Q

How is gastic adenocarcinoma treated?

A
  • Adequate nutrition
  • Peri-op chemotherapy
  • Curative resection (if T1/2, N0/1, P0) = gastrectomy
  • Endoscopic Mucosal Resection if T1
  • Palliatve if T3 or more
    • Chemo
    • Gastrectomy/bypass
    • Stenting
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48
Q

What are the complications of gastic adenocarcinoma?

A
  • Gastric outlet obstruction
  • Iron deficiency anaemia
  • Perforation
  • Malnutrition
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49
Q

What are the risk factors for developing GORD?

A
  • Age
  • Obesity
  • Alcohol
  • SMoking
  • Caffeine
  • Fatty foods
  • Previous surgery
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50
Q

What is GORD? What causes it?

A

Acid from the stomach leaks up into the oesophagus

  • Reduced LOS tone
  • Increased intragastric pressure
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51
Q

What are the clinical features of GORD?

A
  • Dyspepsia / chest pain
    • Burning
    • Retrosternal
    • Worse with lying down, straining, after meals and bending over
  • Excessive belching
  • Odynophagia
  • Chronic cough
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52
Q

What are the red flags of GORD symptoms?

A
  • Dysphagia
  • Weight loss
  • Early satiety
  • Loss of appetite
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53
Q

How is GORD investigated?

A
  • Endoscopy (if red flags, new onset or failure of medical treatment)
  • 24 hour pH monitoring
    • Demeester score > 14.72
  • Oesophogeal manometry (motor function test) via a high-resolution catheter
    • Excludes motility disorder
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54
Q

How is GORD managed?

A
  • Conservative
    • Avoid precipitants (alcohol, caffeine, fatty foods)
    • Weight loss
    • Stop smoking
  • Pharmacological
    • PPI (omeprazole 20mg OD)
    • Antacids (Gaviscon)
    • Metoclopramide 10mg tds (increases gastric and oesophageal emptying)
  • Surgery (if persistent symptoms, complications or avoidance of long term PPI therapy)
    • Laparascopic fundoplication (Nissen’s) = wrap fundus around intra-abdominal oedeophagus
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55
Q

What are the complications of GORD?

A
  • Aspiration pneumonia
  • Barrett’s oesophagus
  • Oesophagitis
  • Stricutres
  • Malignancy
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56
Q

What are the complications of fundoplication surgery?

A

During:

  • Bleeding requiring transfusion
  • Injury to intra-abdominal organs (mainly spleen)

After:

  • Dysphagia
  • Bloating
  • Inability to vomit
  • Dumping syndrome = food moves too quickly from the stomach to the duodenum
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57
Q

What is Barrett’s Oesophagus?

A

Metaplasia of the lower oesophageal epithelial lining from stratified squamous to simple columnar due to chronic acid reflux

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58
Q

How is Barrett’s oesophagus investigated?

A

Biopsy of oesophageal epithelium via endoscopy

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59
Q

How is Barrett’s oesophagus managed?

A
  • Lifestyle advice
    • Stop smoking
    • Weight loss
    • Diet change
  • PPI (omeprazole)
  • Stop NSAIDs/other meds that affect acidity
  • Routine endoscopy
    • GORD = every 2-5 years
    • low grade = every 6 months
    • high grade = every 3 months
  • If premalignant lesion = Endoscopic Mucosal Resection (EMR)
  • If carcinoma = oesophagectomy
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60
Q

What are the types of oesophageal cancer and risk factors for both?

A
  • Squamous cell (middle and upper thirds)
    • Smoking
    • Alcohol
    • Low vit A
    • Chronic achalasia
  • Adenocarcinoma (lower third)
    • Barrett’s
    • GORD
    • High fat diet
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61
Q

What are the clinical features of oesophageal cancer?

A
  • Dysphagia
    • Progressively worsens from solids to liquids
  • Haematemesis
  • Significant weight loss
  • Odonyphagia
  • Productive cough
  • Hoarseness (recurrent laryngeal nerve)
  • Horner’s (sympathetic trunk)
  • Neck swelling (IVC obstruction)
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62
Q

What is the NICE guidance on criteria for urgent endoscopy?

A
  • New onset dysphagia
  • > 55 years with
    • Weight loss
    • Upper abdominal pain
    • Dyspepsia
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63
Q

Name some oesophageal motility disorders

A

Achalasia = failure of smooth muscle/LOS relaxation

Diffuse oesophageal spasm = multi-focal, high amplitude contractions of the oesophagus

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64
Q

How are oesophageal motility disorders investigated?

A
  • Manometry
    • Hypertonicity
    • Failure of relaxation
    • Repetitive, simultaneous, ineffective contractions (DOS)
  • Barium swallow
    • Cork screw (DOS)
    • Bird’s beak (achalasia)
  • OGD to exclude malignancy
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65
Q

How is achalasia managed?

A
  • Conservative - lots of pillows, eat slowly, lots of fluids
  • Botox injection into LOS
  • Endoscopic balloon dilatation
  • Laparascopic Heller’s myotomy
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66
Q

How is diffuse oesophageal spasm managed?

A
  • Smooth muscle relaxants
    • Nitrates
    • CCB
    • Benzodiazepines
  • Pneumatic dilatation (rupture muscle fibres via balloon)
  • Myotomy
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67
Q

Name some causes of acute pancreatitis

A

GET SMASHED

  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion sting
  • Hypercalcaemia
  • ERCP
  • Drugs - azathioprine, NSAIDs, thiazide
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68
Q

How is acute pancreatitis classified?

A
  • Oedematous (70%) = transient fluid collections
  • Severe/necrotising = necrosis with psuedocysts
  • Haemorrhagic (5%)
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69
Q

Name some clinical features of acute pancreatitis

A
  • Sudden onset of severe epigastric pain
    • Radiates to back
  • Nausea and vomiting
  • Fever
  • Dehydration
  • Hypotension
  • Tachycardia
  • Guarding
  • Ecchymosis (retroperitoneal haemorrhage)
    • Left flank (Grey-Turners)
    • Periumbilical (Cullen’s)
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70
Q

How is acute pancreatitis investigated?

A
  • Bloods
    • Amylase (>1000 U) / lipase
    • LFTs (cholestatic)
    • FBC
    • U+E
    • Glucose
  • AXR
  • CT - pancreatic oedema, swelling
  • US - identify gallstones
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71
Q

What AXR signs are present in acute pancreatitis?

A
  • Absent psoas shoadow
  • Sentinel loop sign
  • Colon cut off sign (splenic flexure)
  • Gallstones
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72
Q

Name a criteria for severe pancreatitis

A

Glasgow-Imrie criteria (score >/=3 within 48 hours)

  • PaO2 < 8kPa
  • Age > 55
  • Neutrophils/WCC > 15000
  • Corrected calcium < 2mmol/L
  • uReas > 16 mmol/L
  • Enzymes (AST > 200, LDH > 600)
  • Albumin < 32g/L
  • Sugar/glucose > 10mmol/L
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73
Q

How is acute pancreatitis managed?

A
  • Large calibre IV access - crystalloid fluid up to 1L
  • Catheterise and fluid balance chart
  • Analgesia
  • NG tube if vomiting
  • IV antibiotics (IV imipenem) if severe
  • Cholecystecomy if gallstones
  • ERCP if bileduct stones
  • CT-guided aspiration
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74
Q

Name some causes of chronic pancreatitis

A
  • Chronic alcoholism
  • Idiopathic
  • Cystic fibrosis
  • Recurrent acute pancreatitis
  • Infection (HIV, mumps)
  • Obstruction (stricture/tumour)
  • Autoimmune (SLE, PBC)
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75
Q

Name some clinical features of chronic pancreatitis

A
  • Chronic epigastric pain
    • Radiates to back
    • Worse with food and alcohol
    • Eased when leaning forward
  • Exocrine dysfunction (fat/protein malabsorption)
    • Anorexia
    • Weight loss
    • Steatorrhoea
  • Endocrine failure (loss of B islet cells) = diabetes mellitus
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76
Q

How is chronic pancreatitis managed?

A
  • Analgesia
  • Stop alcohol
  • Diet - antioxidants, carbs, protein, low fat
  • Exocrine enzyme supplements (Creon)
  • Diabetes control (insulin)
  • Surgery (treat cause)
    • Whipple’s (pancreaticoduodenectomy)
    • ERCP if duct stone
    • Sphincterecomy
    • Total pancreatectomy
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77
Q

Name some complications of chronic pancreatitis

A
  • Pseudocyst
  • Steatorrhoea
  • Malabsorption
  • Diabetes
  • Effusions
  • Ascites
  • Malignancy
  • Acute-on-chronic pancreatitis
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78
Q

Name some risk factors for pancreatic cancer

A
  • Smoking
  • Chronic pancreatits
  • Diabetes
  • High fat diet
  • Alcoholism
  • Genetics (MEN-1 syndrome)
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79
Q

What is Courvoisiers law?

A

When jaundice and an enlarged/palpable gall bladder are present, the cause is rarely gallstones and malignancy should be considered

80
Q

What is a pancreatic cysts? What types are there?

A

Collection of fluid within the pancreas

  • Serous cyst = low malignancy risk
  • Mucinous cyst = high malignancy risk
81
Q

What are gallstones?

A

Bile contains cholesterol, phospholipids and bile pigements (from Hb metabolism) and is produced in the liver and stored in the gallbladder. Bile containing excess cholesterol predisposes to stone formation

82
Q

What are the different types of gallstone?

A
  • Cholesterol (excess cholesterol production) 10%
    • Link with poor diet and obesity
  • Pigment (bile salts) 10%
    • Black = hemolytic disease
    • Brown = chronic cholangitis / parasites
  • Mixed 80%
83
Q

Name some risk factors for developing gallstones

A

5 Fs:

  • Fat
  • Female
  • Fertile
  • Forty
  • Family history
  • Pregnancy
  • OCP (oestrogen increases cholesterol into bile)
  • Haemolytic anaemia
84
Q

Name some clinical features of gallstones

A
  • Biliary colic = sudden, dull and colicky pain in RUQ
    • Exacerbated with fatty foods (stimulates duodenum to release CCK which contracts gallbladder)
    • Radiates to epigastrium and/or back
  • Acute cholecystitis = severe, continuous RUQ pain
    • Persistent despite pain relief
    • Inflammation (fever, inc HR, inc WCC)
    • Murphys sign = halt in inspiration due to pain when applying pressure over RUQ)
  • Chronic cholecystitis
  • Mucocele = gallbaldder continues producing mucus and becomes distended
85
Q

How are gallstones investigated?

A
  • Bloods
    • FBC
    • CRP
    • U+E
    • LFTs (inc ALP)
    • Amylase
    • Culture
  • Urinanalysis (+ pregnancy test)
  • Transabdominal ultrasound
  • MRCP
  • Abdominal x-ray
86
Q

How are gallstones managed?

A
  • Analgesia (diclofenac 75mg IM/opioids)
  • Antibiotics if infection
  • Lifestyle changes
    • Low fat diet
    • Weight loss
    • Exercise
  • Cholecystectomy within 6 weeks
    • 1 week if acute cholecystitis
  • Percutaneous cholecystotomy to drain infection
  • Lithotripsy (high risk of recurrence)
87
Q

Name some complications of gallstones

A
  • Empyema
  • Chronic cholecystitis
  • Bouveret’s syndrome = stone impacts to cause duodenal obstruction
    • Due to fistula formation
  • Gallstone ileus (obstruction at terminal ileum)
  • Obstructive jaundice
  • Ascending cholangitis
  • Acute pancreatitis
88
Q

Name some risk factors for cholangiocarcinomas

A
  • Primary sclerosing cholangitis
  • UC
  • Toxins (rubber, aircraft industry)
  • Infective (HIV, hepatitis)
  • Congenital
  • Alcohol
  • DIabetes
89
Q

Name some clinical features of cholangiocarcinomas

A
  • Post-hepatic jaundice
  • Pruritis
  • RUQ pain
  • Early satiety
  • Weight loss
  • Anorexia
  • Malaise
90
Q

How are cholangiocarcinomas investigated?

A
  • Obstructive jaundice markers - (inc bilirubin, ALP, GGT)
  • Tumour markers (CEA, CA19-9)
  • Ultrasound
  • MRCP
  • ERCP - biopsy, brush cytology
  • CT scan - assess local spread
91
Q

How are cholangiocarcinomas managed?

A
  • Surgery (if patient fit enough, no metastases, suitable tumour)
    • Partial hepatectomy (intrahepatic/Klatskin)
    • Whipple’s (distal CBD)
    • Cholecystectomy (gall bladder)
  • Palliative
    • Endoscopic stenting (self expanding metal stents)
    • Surgical bypass
    • Radio/chemotherapy
92
Q

Describe the different types of inguinal hernia

A
  • Direct (20%) = bowel enters inguinal canal ‘directly’ through a weakness in the posterior wall of the canal (Hesselbach’s Triangle)
    • Secondary to abdominal wall laxity
  • Indirect (80%) = bowel enters inguinal canal via the deep inguinal ring due to an incomplete closure of the processus vaginalis (peritoneal outpouching for testicular descent)
93
Q

How can inguinal hernias be differentiated clinically and surgically?

A
  • Clinical = reduce hernia and place pressure over deep inguinal ring (midpoint of inguinal ligament) and ask patient to cough
    • If hernia still protrudes = direct
  • Surgical
    • Indirect = lateral to inferior epigastric artery
    • Direct = medial to inferior epigastric artery
94
Q

What are the risk factors for developing an inguinal hernia?

A
  • Male
  • Older age
  • Obesity
  • Raised intra-abdominal pressure
95
Q

Name some clinical features of an inguinal hernia

A
  • Lump in groin
  • Mild discomfort
    • Worse with standing/activity
  • If irreducible - painful, tender, erythematous
  • If causing obstruction - distension, vomiting, constipation
96
Q

How is an inguinal hernia managed?

A

If symptomatic, irreducible or obstructed:

  • Open repair (for primary unilateral) = Lichenstein technique = removal of hernial sac and reinforcement of posterior wall of inguinal canal via tension-free mesh
  • Laparascopic (for recurrent, bilateral, female or risk of chronic pain)
    • Total Extraperitoneal (TEP)
    • Transabdominal Preperitoneal (TEPP)
97
Q

Name some complications of an inguinal hernia

A
  • Incarceration (irreducible)
  • Strangulation
  • Obstruction
  • Recurrence
  • Chronic pain (> 3 months)
  • Vas deferens/testicular vessel damage (iscaemic orchitis)
98
Q

What does the inguinal canal contain?

A
  • Ilioinguinal nerve
  • Spermatic cord
    • 3 arteries - testicular, cremisteric, vas
    • 3 fascial coverings - external spermatic, cremasteric, and internal spermatic
    • Vas deferens
    • Pampinform venous plexus
    • Lymphatics
99
Q

What are the risk factors for developing a femoral hernia?

A
  • Female
  • Older age
  • Pregnancy
  • Increased abdominal pressure
100
Q

What are the clinical features of femoral hernia?

A
  • Lump in groin
    • Inferolateral to pubic tubercle
    • Medial to femoral pulse
  • 30% as emergency - obstruction or strangulation
  • Unlikely to be reducible (tight ring)
101
Q

How is a femoral hernia managed?

A

All need surgical repair due to risk of strangulation

  • Reduction of hernia
  • Narrowing of femoral ring

Low approach = incision below inguinal ligament (elective)

  • Doesn’t interfere with inguinal structures
  • Limited space for bowel resection

High approach = incision above inguinal ligament with dissection through posterior inguinal canal (emergency)

102
Q

What is appendicitis?

A

Inflammation of the appendix (usually retrocaecal) caused by direct luminal obstruction secondary to a faecolith, lymphoid hyperplasia, impacted stool or cancer

  • Mucosal (mildest form)
  • Phlegmanous (slow onset and progression)
  • Necrotic (bacterial infection with ischaemic necrosis)
103
Q

Name some clinical features of appendicitis

A
  • Abdominal pain
    • Peri-umbilical initially then RIF when inflammation irritates parietal peritoneum
    • Worse with coughing and moving
  • Vomiting (after pain)
  • Diarrhoea
  • Anorexia
  • Tachycardia / pnoea
  • Rebound tenderness at McBurney’s point
  • Rovsings sign = RIF pain when palpating LiF
  • Psoas sign = RIF pain with extension of right hip
104
Q

Where is McBurneys point?

A

2/3rds of distance from umbilicus to ASIS

105
Q

How is appendicitis investigated?

A
  • Urinanalysis - exclude UTI, renal cause and pregnancy
  • Bloods - FBC, CRP, U+E, LFTs
  • Trans-abdominal US
  • CT (if > 65 and complication/malignancy suspected)
106
Q

How is appendicitis managed?

A
  • IV fluids and fluid balance chart
  • Analgesia
  • Open / laparascopic appendicectomy
  • IV antibiotics for perforation or abscess
    • Ceruforxime 750mg tds + metronidazole 500mg tds
107
Q

Name some complications of appendicitis

A
  • Perforation
  • Abscess (RIF/pelvic)
  • Wound infection
  • Appendix mass (omentum and small bowel adhere to appendix)
108
Q

Name a scoring system for appendicitis

A

Alvarado score

109
Q

Name some common surgical scars

A
110
Q

How can a femoral and inguinal hernia be differentiated?

A
  • Feel femoral pulse
  • Place hand one finger breadth medially
  • Ask patient to cough
  • Femoral hernias will remain reduced
  • Inguinal hernias will bulge out
111
Q

How do gallstones cause pancreatitis?

A

Gallstones obstruct common bile duct and stop the passage of pancreatic enzymes from the pancreas to the duodenum. This causes an accumulation of enzymes in the pancreas which causes irritation and inflammation

112
Q

What is ulcerative colitis?

A

Diffuse continual mucosal inflammation of the large bowel

  • Begins in the rectum and spreads proximally
  • Can affect distal ileum (backwash ileitis)
113
Q

Name some intestinal features of UC

A
  • Bloody diarrhoea
    • Dehydration
    • Electrolyte imbalance
  • Proctitis (inflammation of rectal lining)
    • PR bleeding
    • Urgency/frequency
    • Mucus discharge
    • Tenesmus
  • Left-sided colitis / pancolitis
114
Q

How is UC investigated?

A
  • Bloods (FBC, U&Es, CRP, LFT, clotting)
  • Stool - faecal calprotectin, M, C & S
  • AXR = thumbprinting (oedematous, colonic mucosa) or toxic megacolon
  • Flexible sigmoidoscopy (avoid in acute flare up) = erythema, granular, ulcerated mucosa with mucus and blood
  • Barium enema - lead pipe colon (loss of haustral markings)
115
Q

How is UC acutely managed / induction of remission in mild to moderate flare up?

A

Mild to moderate:

  • Fluid resuscitation
  • Topical / suppository aminosalicylate (5-ASA/mesalazine, sulfasalazine)
  • Add oral aminosalicylate
  • Add topical corticosteroid or oral prednisolone (4 weeks after)
  • Add oral tacrolimus (2-4 weeks after)
116
Q

How is UC acutely managed / induction of remission in severe flare up?

A
  • IV fluids
  • IV hydrocortisone 100mg qds
  • IV cyclosporin if not responding to steroids
  • Surgery if:
    • No improvement within 72 hours
    • Worsening symptoms
117
Q

How is remission maintained in UC?

A
  • Topical and/or oral aminosalicylate (5-ASA)
  • Add oral azathioprine or mercaptopurine
  • Add biologics (infliximab)
  • Surgery if fails to respond to treatment
    • Proctoscopy (removal of rectum and colon)
    • Panproctocolectomy (removal of anus, rectum and colon)
    • Total abdominal colectomy (removal of whole colon)
  • Refer to IBD nurse and support group
118
Q

Name some complications of UC

A
  • Toxic megacolon = dilatation of colon
    • Urgent decompression is required
  • Colorectal carcinoma
  • Osteoporosis (chronic steroids)
  • Pouchitis (ileal pouch)
119
Q

Name a system that scores the severity of a UC exacerbation

A

Truelove and Witt criteria

120
Q

Name some extra-intestinal features of UC

A
  • Systemic - malaise, anorexia, fever, anaemia
  • MSK - enteropathic arthritis, nail clubbing
  • Skin - erythema nodosum
  • Eyes - episcleritis, anterior uveitis, iritis
  • HPB - Primary sclerosing cholangitis
121
Q

What is Crohn’s disease?

A

A chronic inflammatory, non-caseating granulomatous disease affecting any part of the GI tract

  • Commonly affects 15-30 and 60-80 years old
  • Less common than UC
122
Q

Name some risk factors for developing crohn’s

A
  • Family history
  • Smoking
  • Caucasian
  • Appendicectomy
123
Q

Name some GI features of Crohn’s

A

Acute, episodic attacks:

  • Abdominal pain (RIF)
  • Diarrhoea
  • Oral apthous ulcers
  • Perianal disease
  • Fistula formation
  • Distension
124
Q

Name some extra-intestinal features of Crohn’s

A
  • Systemic - weight loss, fever, fever, malaise
  • MSK - eneteropathic arthritis, nail clubbing, metabolic bone disease, ankylosing spondylitis
  • Skin - erythema nodosum, pyoderma gangrenosum
125
Q

How is Crohn’s investigated?

A
  • Bloods (FBC, CRP, U&Es, LFTs, clotting)
  • Stool - faecal calprotectin, M, C & S
  • AXR in acute presentation (obstruction)
  • Colonoscopy + biopsy (avoid in acute flare up)
    • Cobblestoning, non-caseating granulomas
  • CT if complications suspected
  • Barium swallow - string sing of Kantor
  • Pelvic MRI if perianal disease
126
Q

How is remission induced in Crohn’s?

A
  • Fluid resuscitation
  • Nutritional support
  • Oral prednisolone or IV hydrocortisone
  • Add azathioprine or mercatopurine if:2 or more inflammatory exacerbations in 12 months
    • Assess TPMT levels before
    • If TPMT deficient, add methotrexate
  • Consider changing to infliximab
127
Q

How is remission maintained in Crohn’s?

A
  • Smoking cessation
  • Oral azathioprine or mercaptopurine
  • OR methotrexate if contraindicated
  • Consider anti TNF-a (infliximab)
  • Surgery (ileocaecal resection/terminal ileum removal) if:
    • Medical failure
    • Severe complications
    • Growth impairment (children)
128
Q

Name some complications of Crohn’s

A
  • Stricture
  • Fistula
  • Perianal abscess/fistula
  • GI malignancy
  • Malabsorption - growth retardation
  • Osteoporosis (steroids)
  • Gallstones
  • Renal stones
  • Short gut syndrome (after surgery)
129
Q

Name some differences in the pathology (distribution, site, inflammation, micropscopic and macroscopic) of UC and Crohn’s

A
130
Q

Name some differences in the clinical features (diarrhoea, rectal bleeding, pain, mass) of UC and Crohn’s

A
131
Q

Name some differences in the complications (strictures, fistulae, perianal, toxic megacolon, malignancy, obstruction) of UC and Crohn’s

A
132
Q

Describe the pathophysiology of diveritcular disease

A
  • High pressure contractions cause chronic pressure on bowel wall
  • Causes naturally weakened areas of bowel to protrude
  • Hypertrophy/thickening of surrounding colonic mucosa
  • Bowel contents and bacteria accumulate in pockets to cause inflammation
  • Tends to occur along the lines where the penetrating colonic arteries transverse the colonic wall between the taenia coli
133
Q

Name some risk factors for developing diverticular disease

A
  • Low fibre
  • Obesity
  • Smoking
  • Family history
  • NSAIDs
134
Q

What are the clinical features of diverticular disease?

A
  • Intermittent LIF pain
    • If perforated - peritonism/guarding
  • Nausea
  • Fever
  • Loose stools
  • PR bleeding
135
Q

How is diverticular disease investigated?

A
  • Bloods - FBS, U&Es, clotting, LFTs, group and save
  • ABG (lactate) - assess if septic
  • Urine dip - exclude urological causes
  • AXR - exclude obstruction
  • Erect CXR if perforation suspected
  • CT if complications suspected
  • Barium enema (elective)
  • Colonoscopy if malignancy suspected
136
Q

What is the management of diverticular disease?

A
  • High fibre and fluid intake
  • Analgesia
  • Stool softeners
  • IV antibiotics if infected (amoxicillin, metronidazole, gentamicin)
  • Surgery (if perforated, septic or failure to improve)
    • Bowel resection +/- anastamosis/colostomy
137
Q

Name some complications of diverticular disease

A
  • Pericolic abscess
  • Peritonitis
  • Fistula (colovesical/colovaginal)
  • Stricture
138
Q

What is a volvulus?

A

Twisting of a loop of bowel around its mesenteric attachment, resulting in a closed loop bowel obstruction with risk of ischaemia, necrosis and perforation

  • Common at sigmoid colon due to its long mesentery
139
Q

Name some risk factors for developing a volvulus

A
  • Neuropsychiatric disorders
  • Male
  • Nursing home
  • Chronic constipation
  • Previous abdominal surgery
  • Diabetes
140
Q

Name some clinical features of volvulus

A
  • Colicky pain
  • Distension
  • Absolute constipation (early)
  • Vomiting (late)
  • Increased bowel sounds
  • Tympanic percussion
141
Q

How is a volvulus investigated?

A
  • Bloods (ca2+, electrolytes, TFTs to exclude pseudoobstruction)
  • AXR
    • Coffee bean sign from LIF
    • Small bowel dilatation
  • CT (if unclear or ischaemic)
    • Whirl sign
  • Erect CXR
142
Q

How is a volvulus managed?

A
  • Decompression with a sigmoidoscope and flatus tube
  • Surgery (if failed decompression, necrosis or perforation)
    • Sigmoidectomy with primary anastamosis
143
Q

Name some complications of volvulus

A
  • Bowel ischaemia
  • Perforation
  • Recurrence (90%)
  • Stoma complications
144
Q

Name some causes of bowel obstruction

A
  • Intraluminal
    • Gallstone ileus
    • Foreign body
    • Impaction
  • Mural
    • Carcinoma
    • Strictures
    • Diverticula
    • Intussusception (CF)
  • Extramural
    • Hernia
    • Adhesions
    • Volvulus
    • Peritoneal metastases
145
Q

Name some clinical features of bowel obstruction

A
  • Colicky abdominal pain
    • Secondary to peristalsis
  • Vomiting (gastric - bile - faeculent)
  • Distension
  • Absolute constipation (cannot pass flatus and faeces)
146
Q

How is bowel obstruction investigated?

A
  • Bloods - FBC, CRP, U&E (dec K+, inc urea) group and save
  • ABG - ischaemia or metabolic derangement
  • AXR
    • Small bowel (> 3cm) and central with valvulae conniventes (whole circumference)
    • Large bowel (> 6cm) and peripheral with haustra
  • Erect CXR
  • CT - site and cause, metastases
147
Q

How is bowel obstruction managed?

A
  • NBM
  • NG tube
  • IV fluids
  • Analgesia (+ anti emetic)
  • Surgery if
    • Ischaemic
    • Small bowel obstruction in ‘virgin’ abdomen
    • Cause requires surgery (tumour, strangulated hernia)
    • > 48 hours of conservative therapy with no improvement
148
Q

Name some complications of bowel obstruction

A
  • Ischaemia
  • Perforation
  • Dehydration - renal impairment
  • Malnutrition
149
Q

Name some emergency and non-emergency causes of haematemesis

A

Emergency:

  • Oesophageal varices = porto-systemic anastamoses prone to rupture (dark red venous blood)
  • Gastric ulcer via erosion to blood vessels (gastroduodenal) fresh blood red

Non-emergency:

  • Mallory-Weiss tear = tears in the epithelial lining caused by forceful vomiting (fresh bright blood)
  • Oesophagitis / gastritis
  • Vascular malformations (Dieu la Foy)
  • Gastric carcinomas
150
Q

How is haematemesis investigated?

A
  • Bloods - FBC, U&E (digested HB - urea), LFTs, cross-match, clotting
  • ABG - pH, pO2, pCO2, lactate
  • Urgent OGD (within 12 hours)
  • Erect CXR if perforated ulcer suspected
151
Q

How is haematemesis treated?

A
  • 2 large bore cannulas - crystalloid up to 1L
    • O neg if critical (wait for cross match if not)
    • Fresh frozen plasma if abnormal clotting
  • Catheterise and fluid balance
  • IV PPI

Varices - endoscopic banding, IV vasopressin +/- Sengstaken-Blakemore tube

Ulcer - Endoscopic coagulation/excision or partial gastrectomy

Carcinomas - surgical resection

152
Q

Name a scoring system for predicting mortality in acute upper GI bleed

A

Rockall

153
Q

Name some causes of malaena

A

Upper GI bleed

  • Peptic ulcer
  • Variceal bleed
  • Oesophagitis
  • Upper GI malignancy
  • Mallory-Weiss tear
154
Q

How is malaena investigated?

A
  • Bloods - FBC, U&Es, LFTs, clotting, group and save
  • ABG
  • OGD
155
Q

How is malaena treated?

A

Ulcer:

  • Adrenaline
  • PPI
  • Cauterisation

Varices:

  • Endoscopic banding
  • Antiobiotics
  • Somatostatin analogue (terlipressin)
  • Sengstaken-Blakemore tube if severe
156
Q

What is an anal fissure?

A

Tear in the mucosal lining of the anal canal

  • Acute < 6 weeks
  • Chronic > 6 weeks
157
Q

Name some risk factors for developing an anal fissure

A
  • Constipation
  • Dehydration
  • IBD
  • Chronic diarrhoea
158
Q

How are anal fissures managed?

A
  • Increase fibre and fluid in diet
  • Analgesia
  • Laxatives (lactulose)
  • Anal sphincter muscle relaxants (GTN cream)
  • Lateral sphincterotomy if chronic and unresolved
159
Q

What is an anal fistula?

A

Abnormal connection between the anal canal and the perianal skin, usually as a result of an anal abscess

160
Q

Name some risk factors for developing an anal fistula

A
  • Anal abscess
  • IBD
  • Trauma
  • Systemic diseases - TB, diabetes, HIV
  • Radiation therapy
161
Q

What are the clinical features of an anal fissure?

A
  • Acute ‘knife-like’ pain post-defaecation
  • Bleeding (blood on paper)
  • Itching
  • Deep throbbing pain
  • May refuse DRE due to pain
162
Q

How are anal fistulas classified?

A
  • Inter-sphincteric (most common - does not cross external sphincter
  • Trans-sphincteric - through external sphincter ito ischiorectal fossa
  • Supra-sphincteric (least common) - through iliococcygeus muscle
  • Extra-sphincteric
163
Q

What are the clinical features of anal fistulas?

A
  • Chronic anal infection - discharge, mucus, blood
  • Acute perianal abscess - rapid onset perianal pain, erythema, tachycardia, fever
  • Recurrent perianal sepsis - discharge of blood-stained, purulent fluid
  • Change in bowel habit
  • External opening on perineum
  • Fibrous tract on DRE
164
Q

How can the projectory of an anal fistula be predicted?

A

Goodsall rule:

  • External opening posterior to transverse anal line = curved course to posterior midline
  • External opening anterior to transverse anal line = straight radial course to pectinate line
165
Q

How are anal fistulas investigated?

A
  • DRE - palpable fibrous track
  • Endoanal ultrasound (+ hydrogen peroxide)
  • MRI
  • Rigid sigmoidoscopy
166
Q

How are anal fistulas managed?

A
  • Antibiotics if septic
  • IBD control
  • Fistulotomy (if low course) = lay open track via probe, remove chronic granulation tissue and allow to heal by secondary intention
  • Fistulectomy = remove track and close opening
    • Increased risk of infection
  • Cutting seton (if high course) = divide sphincter tissue between fistula and skin
167
Q

What is an anorectal abscess?

A

Collection of pus in the anal/rectal region, caused by plugging of anal ducts - stasis - normal floral overgrowth (E coli, enterococcus, bacteriodes)

Categorised by area: perianal, ischiorectal, intersphncteric or supralevator

168
Q

What are the clinical features of an anorectal abscess?

A
  • Gradual onset, constant perianal pain
    • Exacerbated by sitting down
  • Swelling
  • Itching
  • Discharge
  • Systemic features - fever, rigors, malaise, sepsis
  • Red and tender abscess with discharge of purulent fluid
169
Q

How is an anorectal abscess investigated?

A
  • DRE - fluctuant, tender mass
  • MRI if complicated or chronic
170
Q

How is an anorectal abscess managed?

A
  • Antibiotics for acute infective states
  • Surgical incision and drainage (general aneasthetic)
    • Allow healing by secondary intention
171
Q

What is a pilonidal sinus?

A

Formation of a sinus in the cleft of the buttocks

  • Usually contains hair
  • Males aged 15-30
172
Q

Describe the pathophysiology of a pilonidal sinus

A
  • Hair follicle in intergluteal cleft becomes inflamed/infected
  • Obstructs opening of follicle which extends into a pit
  • Foreign body reaction creates a cavity
  • Chronic inflammation
173
Q

What are the risk factors for developing a pilonidal sinus?

A
  • Course dark body hair
  • Increased sweating
  • Prolonged sitting (drivers)
  • Obesity
  • Poor hygiene
  • Buttock friction
174
Q

What are the clinical features of a pilonidal sinus?

A
  • Intermittent, red, painful mass in sacrococcygeal region
  • Discharge
  • Acute abscess - sepsis
175
Q

How is a pilonidal sinus investigated?

A
  • Test for occult diabetes
  • Rigid sigmoidoscopy - differentiate between fistula
    • Pilonidal sinus does not open into anal canal
  • MRI
176
Q

How is a pilonidal sinus managed?

A
  • Shave local hairs
  • Pluck sinus of hair
  • Washout of accessible sinus
  • Abscess drainage
  • Antibiotics for septic episodes
  • Surgery
    • Primary excision with laying open of wound and allowing healing by secondary intention
    • Tension-free apposition of skin edges
177
Q

What are haemorrhoids?

A

Abnormal swelling of the anal vascular cushions

  • Comprise anorectal mucosa, submucosal tissue and submucosal blood vessels
  • Occurs at 3, 7 and 11 o clock positions (lithotomy)
  • Upper anal canal = internal
  • Lower anal canal = external
178
Q

How are haemorrhoids classified?

A
  • 1st degree = remain in rectum
  • 2nd degree = prolapse through anus on defaecation but spontaneously reduce
  • 3rd degree = prolapse through anus on defaecation but require digital reduction
  • 4th degree = permenantly prolapsed
179
Q

What are the risk factors for developing haemorrhoids?

A
  • Excessive straining
  • Age
  • Raised intra-abdominal pressure
    • Cough
    • Pregnancy
    • Obesity
    • Ascities
  • Cardiac failure
  • Portal hypertension
180
Q

What are the clinical features of haemorrhoids?

A
  • Post-defaecation bleeding (bright red on paper)
  • Pruritis (chronic mucus discharge)
  • Prolapse
  • Impaired continence
  • If thrombosed:
    • Purple/blue
    • Oedematous
    • Tense
    • Tender
181
Q

How are haemorrhoids investigated?

A
  • Proctoscopy
  • FBC (if prolonged bleeding/signs of anaemia)
  • Flexible sigmoidoscopy if malignancy suspected
  • Look for cause
    • LFTs
    • ECG
182
Q

How are haemorrhoids managed?

A
  • Increase fibre and fluids in diet
  • Laxatives
  • Topical analgesia (lignocaine gel)
  • Rubber band ligation (1st/2nd degree)
  • Harmorrhoidal Arterial Ligation (HAL)
  • Stapled anopexy
  • Haemorrhoidectomy (large, external haemorrhoids)
183
Q

Name some complications of haemorrhoids

A
  • Ulceration (due to thrombosis)
  • Ischaemia, thrombosis and gangrene (4th degree)
  • Skin tags
  • Perianal sepsis

Haemorrhoidectomy surgery:

  • Bleeding
  • Infection
  • Constipation
  • Stricutre
  • Fissure
  • Incontinence
184
Q

What is a rectal prolapse?

A

Mucosal or full-thickness layer of rectal tissue protrudes out of anus

  • Partial thickness = rectal mucosa protrudes out
  • Full thickness = rectal wall protrudes out
185
Q

Name some risk factors for developing rectal prolapse

A

Defect in fascia of pelvice region

  • Chronic constipation
  • Chronic cough
  • Vaginal delivery
  • Weakening of anal sphincter
  • Neurological damage
186
Q

Name some clinical features of rectal prolapse

A
  • Mucus discharge
  • Incontinence
  • Bright red blood on paper
  • Ulceration
  • Sensation of rectal fullness/mass
  • Incomplete defaecation
187
Q

How is rectal prolapse investigated?

A
  • Ask to cough/strain
  • DRE - weakened sphincter
  • Defaecating proctogram (internal prolapse)
  • Rigid sigmoidoscopy - mucosal inflammation
188
Q

How is rectal prolapse managed?

A
  • Increase fibre and fluid diet
  • Decrease straining
  • Stool softeners / bulking agent
  • Mucosal prolapse:
    • Recurrent banding
    • Mucosal excision
    • Stapled anoplexy
  • Surgery for full thickness prolapse
189
Q

How is primary biliary cirrhosis diagnosed?

A

M rule:

  • Middle aged females
  • IgM
  • Anti-Mitochondrial antibodies
190
Q

What is Wilsons disease? Name some clinical features

A

Autosomal recessive disease where copper is deposited in tissue

  • Jaundice
  • Hepatocellular LFTs
  • Neuropsychiatric disease
    • Depression
    • Dementia
    • Behavioural change
    • Tremor
  • Kayser-Fleischer rings
  • Blue nails
191
Q

What is haemochromatosis? Name some clinical features

A

An autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation

  • Arthralgia (MCP and PIP)
  • Liver disease
  • Impotence
  • Skin pigmentation (grey skin)
192
Q

How is haemachromatosis diagnosed and treated?

A

Diagnosed:

  • Serum transferrin saturation and serum ferritin
  • Genetic testing
  • Liver biopsy (Perl’s stain)

Treated:

  • Regular venesection
  • Iron chelator if venesection not tolerated
193
Q

Name the different hepatitis serology

A
  • HBsAg - infected with Hep B (and infectious)
  • Anti-HBs - immunity/recovering
  • Anti-HBc - previous or current infection
  • IgM anti-HBc = acute infection
194
Q

What can cause C diff infection?

A

Gram positive rod caused by suppression by broad-spectrum antibiotics

  • Clindamycin
  • Cephalosporins (ceftriaxone)
195
Q

How is C diff infection treated?

A
  • Oral metronidazole for 10-14 days
  • If not responding - vancomycin

IPE (13 decks)

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