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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
How is jaundice investigated?
* 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)
26
What pattern of LFTs would you see in each type of jaundice
27
How is jaundice managed?
* 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
28
Name some complications of jaundice
* Hepatorenal syndrome * Deranged coagulation * Cholangitis * Hepatic encephalopathy * Immunosuppresion
29
What is hepatorenal syndrome?
The development of kidney failure in patients with advanced liver disease. Thought to be caused by systemic vasoconstriction
30
What are the different types of hiatus hernia?
31
Name some risk factors for developing hiatus hernia
* Age * Loss of diaphragmatic tone * Increasing intra-abdominal pressures * Increased size of oesophageal hiatus * Pregnancy * Obesity * Ascites * Female * Previous surgery
32
What are clinical features of hiatus hernia?
* GORD - burning epigastric pain * Worse lying flat * Vomiting * Weight loss * Early satiety * Bleeding * Hiccups * Dysphagia
33
How is hiatus hernia investigated?
* OGD (endoscopy) * Barium swallow * CT abdo and thorax (exclude malignancy)
34
How is hiatus hernia managed?
* 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
35
Name some complications of hiatus hernia
* 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
36
What is a peptic ulcer? Where is it most common?
Break in the lining of the GI tract Most common in lesser curve of stomach and proximal duodenum
37
Name some causes of peptic ulcers
* H-pylori (gram negative bacillus) * Female * NSAIDs (inhibit prostaglandin synthesis) * High alcohol intake * Steroid use * Chemotherapy
38
What are the clinical features of peptic ulcers?
* Epigastric pain * Worse with eating if stomach * Worse with empty stomach if duodenal * Nausea * Anorexia * Weight loss
39
How are peptic ulcers investigated?
* 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)
40
How are peptic ulcers managed?
* 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
41
How is H pylori treated?
7 day, twice daily course of: * PPI (omeprazole 20-40mg) * Amoxicillin * Clarithromycin or metronidazole If allergic to penicillin = PPI, clarithromycin and metronidazole
42
Name some complications of peptic ulcers
* Acute upper GI bleeding * Pyloric stenosis * Iron deficiency anaemia * Perforation * Gastric outlet obstruction
43
What is Zollinger-Ellison syndrome?
Hypergastrinaemia causing extensive ulceration. Caused by gastrinoma (intrapancreatic)
44
Name some risk factors for developing a gastic adenocarcinoma
* \> 50 * Male * H pylori * Smoking * East asian * Chronic gastritis * Blood group A * Excess alcohol * High salt diet * Family history
45
What are the clinical features of gastic adenocarcinoma?
* Dyspepsia * Dysphagia * Nausea and vomiting * Melaena * Haematemesis * Systemic = weight loss, anaemia, lethargy * Epigastric mass * Virchow's node
46
How is gastic adenocarcinoma investigated?
* Bloods * CEA (carcinoembryonic antigen) in 50% * FBC * LFTs * OGD / endoscopy * Biopsies * CT chest-abdo-pelvis (metastases) * Staging laparascopy (peritoneal metastases)
47
How is gastic adenocarcinoma treated?
* 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
48
What are the complications of gastic adenocarcinoma?
* Gastric outlet obstruction * Iron deficiency anaemia * Perforation * Malnutrition
49
What are the risk factors for developing GORD?
* Age * Obesity * Alcohol * SMoking * Caffeine * Fatty foods * Previous surgery
50
What is GORD? What causes it?
Acid from the stomach leaks up into the oesophagus * Reduced LOS tone * Increased intragastric pressure
51
What are the clinical features of GORD?
* Dyspepsia / chest pain * Burning * Retrosternal * Worse with lying down, straining, after meals and bending over * Excessive belching * Odynophagia * Chronic cough
52
What are the red flags of GORD symptoms?
* Dysphagia * Weight loss * Early satiety * Loss of appetite
53
How is GORD investigated?
* 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
54
How is GORD managed?
* 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
55
What are the complications of GORD?
* Aspiration pneumonia * Barrett's oesophagus * Oesophagitis * Stricutres * Malignancy
56
What are the complications of fundoplication surgery?
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
57
What is Barrett's Oesophagus?
Metaplasia of the lower oesophageal epithelial lining from stratified squamous to simple columnar due to chronic acid reflux
58
How is Barrett's oesophagus investigated?
Biopsy of oesophageal epithelium via endoscopy
59
How is Barrett's oesophagus managed?
* 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
60
What are the types of oesophageal cancer and risk factors for both?
* Squamous cell (middle and upper thirds) * Smoking * Alcohol * Low vit A * Chronic achalasia * Adenocarcinoma (lower third) * Barrett's * GORD * High fat diet
61
What are the clinical features of oesophageal cancer?
* 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)
62
What is the NICE guidance on criteria for urgent endoscopy?
* New onset dysphagia * \> 55 years with * Weight loss * Upper abdominal pain * Dyspepsia
63
Name some oesophageal motility disorders
Achalasia = failure of smooth muscle/LOS relaxation Diffuse oesophageal spasm = multi-focal, high amplitude contractions of the oesophagus
64
How are oesophageal motility disorders investigated?
* Manometry * Hypertonicity * Failure of relaxation * Repetitive, simultaneous, ineffective contractions (DOS) * Barium swallow * Cork screw (DOS) * Bird's beak (achalasia) * OGD to exclude malignancy
65
How is achalasia managed?
* Conservative - lots of pillows, eat slowly, lots of fluids * Botox injection into LOS * Endoscopic balloon dilatation * Laparascopic Heller's myotomy
66
How is diffuse oesophageal spasm managed?
* Smooth muscle relaxants * Nitrates * CCB * Benzodiazepines * Pneumatic dilatation (rupture muscle fibres via balloon) * Myotomy
67
Name some causes of acute pancreatitis
GET SMASHED * Gallstones * Ethanol * Trauma * Steroids * Mumps * Autoimmune * Scorpion sting * Hypercalcaemia * ERCP * Drugs - azathioprine, NSAIDs, thiazide
68
How is acute pancreatitis classified?
* Oedematous (70%) = transient fluid collections * Severe/necrotising = necrosis with psuedocysts * Haemorrhagic (5%)
69
Name some clinical features of acute pancreatitis
* 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)
70
How is acute pancreatitis investigated?
* Bloods * Amylase (\>1000 U) / lipase * LFTs (cholestatic) * FBC * U+E * Glucose * AXR * CT - pancreatic oedema, swelling * US - identify gallstones
71
What AXR signs are present in acute pancreatitis?
* Absent psoas shoadow * Sentinel loop sign * Colon cut off sign (splenic flexure) * Gallstones
72
Name a criteria for severe pancreatitis
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
73
How is acute pancreatitis managed?
* 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
74
Name some causes of chronic pancreatitis
* Chronic alcoholism * Idiopathic * Cystic fibrosis * Recurrent acute pancreatitis * Infection (HIV, mumps) * Obstruction (stricture/tumour) * Autoimmune (SLE, PBC)
75
Name some clinical features of chronic pancreatitis
* 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
76
How is chronic pancreatitis managed?
* 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
77
Name some complications of chronic pancreatitis
* Pseudocyst * Steatorrhoea * Malabsorption * Diabetes * Effusions * Ascites * Malignancy * Acute-on-chronic pancreatitis
78
Name some risk factors for pancreatic cancer
* Smoking * Chronic pancreatits * Diabetes * High fat diet * Alcoholism * Genetics (MEN-1 syndrome)
79
What is Courvoisiers law?
When jaundice and an enlarged/palpable gall bladder are present, the cause is rarely gallstones and malignancy should be considered
80
What is a pancreatic cysts? What types are there?
Collection of fluid within the pancreas * Serous cyst = low malignancy risk * Mucinous cyst = high malignancy risk
81
What are gallstones?
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
What are the different types of gallstone?
* 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
Name some risk factors for developing gallstones
5 Fs: * Fat * Female * Fertile * Forty * Family history * Pregnancy * OCP (oestrogen increases cholesterol into bile) * Haemolytic anaemia
84
Name some clinical features of gallstones
* 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
How are gallstones investigated?
* Bloods * FBC * CRP * U+E * LFTs (inc ALP) * Amylase * Culture * Urinanalysis (+ pregnancy test) * Transabdominal ultrasound * MRCP * Abdominal x-ray
86
How are gallstones managed?
* 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
Name some complications of gallstones
* 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
Name some risk factors for cholangiocarcinomas
* Primary sclerosing cholangitis * UC * Toxins (rubber, aircraft industry) * Infective (HIV, hepatitis) * Congenital * Alcohol * DIabetes
89
Name some clinical features of cholangiocarcinomas
* Post-hepatic jaundice * Pruritis * RUQ pain * Early satiety * Weight loss * Anorexia * Malaise
90
How are cholangiocarcinomas investigated?
* Obstructive jaundice markers - (inc bilirubin, ALP, GGT) * Tumour markers (CEA, CA19-9) * Ultrasound * MRCP * ERCP - biopsy, brush cytology * CT scan - assess local spread
91
How are cholangiocarcinomas managed?
* 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
Describe the different types of inguinal hernia
* 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
How can inguinal hernias be differentiated clinically and surgically?
* 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
What are the risk factors for developing an inguinal hernia?
* Male * Older age * Obesity * Raised intra-abdominal pressure
95
Name some clinical features of an inguinal hernia
* Lump in groin * Mild discomfort * Worse with standing/activity * If irreducible - painful, tender, erythematous * If causing obstruction - distension, vomiting, constipation
96
How is an inguinal hernia managed?
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
Name some complications of an inguinal hernia
* Incarceration (irreducible) * Strangulation * Obstruction * Recurrence * Chronic pain (\> 3 months) * Vas deferens/testicular vessel damage (iscaemic orchitis)
98
What does the inguinal canal contain?
* 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
What are the risk factors for developing a femoral hernia?
* Female * Older age * Pregnancy * Increased abdominal pressure
100
What are the clinical features of femoral hernia?
* Lump in groin * Inferolateral to pubic tubercle * Medial to femoral pulse * 30% as emergency - obstruction or strangulation * Unlikely to be reducible (tight ring)
101
How is a femoral hernia managed?
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
What is appendicitis?
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
Name some clinical features of appendicitis
* 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
Where is McBurneys point?
2/3rds of distance from umbilicus to ASIS
105
How is appendicitis investigated?
* Urinanalysis - exclude UTI, renal cause and pregnancy * Bloods - FBC, CRP, U+E, LFTs * Trans-abdominal US * CT (if \> 65 and complication/malignancy suspected)
106
How is appendicitis managed?
* IV fluids and fluid balance chart * Analgesia * Open / laparascopic appendicectomy * IV antibiotics for perforation or abscess * Ceruforxime 750mg tds + metronidazole 500mg tds
107
Name some complications of appendicitis
* Perforation * Abscess (RIF/pelvic) * Wound infection * Appendix mass (omentum and small bowel adhere to appendix)
108
Name a scoring system for appendicitis
Alvarado score
109
Name some common surgical scars
110
How can a femoral and inguinal hernia be differentiated?
* Feel femoral pulse * Place hand one finger breadth medially * Ask patient to cough * Femoral hernias will remain reduced * Inguinal hernias will bulge out
111
How do gallstones cause pancreatitis?
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
What is ulcerative colitis?
Diffuse continual mucosal inflammation of the large bowel * Begins in the rectum and spreads proximally * Can affect distal ileum (backwash ileitis)
113
Name some intestinal features of UC
* Bloody diarrhoea * Dehydration * Electrolyte imbalance * Proctitis (inflammation of rectal lining) * PR bleeding * Urgency/frequency * Mucus discharge * Tenesmus * Left-sided colitis / pancolitis
114
How is UC investigated?
* 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
How is UC acutely managed / induction of remission in mild to moderate flare up?
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
How is UC acutely managed / induction of remission in severe flare up?
* IV fluids * IV hydrocortisone 100mg qds * IV cyclosporin if not responding to steroids * Surgery if: * No improvement within 72 hours * Worsening symptoms
117
How is remission maintained in UC?
* 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
Name some complications of UC
* Toxic megacolon = dilatation of colon * Urgent decompression is required * Colorectal carcinoma * Osteoporosis (chronic steroids) * Pouchitis (ileal pouch)
119
Name a system that scores the severity of a UC exacerbation
Truelove and Witt criteria
120
Name some extra-intestinal features of UC
* Systemic - malaise, anorexia, fever, anaemia * MSK - enteropathic arthritis, nail clubbing * Skin - erythema nodosum * Eyes - episcleritis, anterior uveitis, iritis * HPB - Primary sclerosing cholangitis
121
What is Crohn's disease?
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
Name some risk factors for developing crohn's
* Family history * Smoking * Caucasian * Appendicectomy
123
Name some GI features of Crohn's
Acute, episodic attacks: * Abdominal pain (RIF) * Diarrhoea * Oral apthous ulcers * Perianal disease * Fistula formation * Distension
124
Name some extra-intestinal features of Crohn's
* Systemic - weight loss, fever, fever, malaise * MSK - eneteropathic arthritis, nail clubbing, metabolic bone disease, ankylosing spondylitis * Skin - erythema nodosum, pyoderma gangrenosum
125
How is Crohn's investigated?
* 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
How is remission induced in Crohn's?
* 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
How is remission maintained in Crohn's?
* 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
Name some complications of Crohn's
* Stricture * Fistula * Perianal abscess/fistula * GI malignancy * Malabsorption - growth retardation * Osteoporosis (steroids) * Gallstones * Renal stones * Short gut syndrome (after surgery)
129
Name some differences in the pathology (distribution, site, inflammation, micropscopic and macroscopic) of UC and Crohn's
130
Name some differences in the clinical features (diarrhoea, rectal bleeding, pain, mass) of UC and Crohn's
131
Name some differences in the complications (strictures, fistulae, perianal, toxic megacolon, malignancy, obstruction) of UC and Crohn's
132
Describe the pathophysiology of diveritcular disease
* 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
Name some risk factors for developing diverticular disease
* Low fibre * Obesity * Smoking * Family history * NSAIDs
134
What are the clinical features of diverticular disease?
* Intermittent LIF pain * If perforated - peritonism/guarding * Nausea * Fever * Loose stools * PR bleeding
135
How is diverticular disease investigated?
* 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
What is the management of diverticular disease?
* 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
Name some complications of diverticular disease
* Pericolic abscess * Peritonitis * Fistula (colovesical/colovaginal) * Stricture
138
What is a volvulus?
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
Name some risk factors for developing a volvulus
* Neuropsychiatric disorders * Male * Nursing home * Chronic constipation * Previous abdominal surgery * Diabetes
140
Name some clinical features of volvulus
* Colicky pain * Distension * Absolute constipation (early) * Vomiting (late) * Increased bowel sounds * Tympanic percussion
141
How is a volvulus investigated?
* 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
How is a volvulus managed?
* Decompression with a sigmoidoscope and flatus tube * Surgery (if failed decompression, necrosis or perforation) * Sigmoidectomy with primary anastamosis
143
Name some complications of volvulus
* Bowel ischaemia * Perforation * Recurrence (90%) * Stoma complications
144
Name some causes of bowel obstruction
* Intraluminal * Gallstone ileus * Foreign body * Impaction * Mural * Carcinoma * Strictures * Diverticula * Intussusception (CF) * Extramural * Hernia * Adhesions * Volvulus * Peritoneal metastases
145
Name some clinical features of bowel obstruction
* Colicky abdominal pain * Secondary to peristalsis * Vomiting (gastric - bile - faeculent) * Distension * Absolute constipation (cannot pass flatus and faeces)
146
How is bowel obstruction investigated?
* 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
How is bowel obstruction managed?
* 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
Name some complications of bowel obstruction
* Ischaemia * Perforation * Dehydration - renal impairment * Malnutrition
149
Name some emergency and non-emergency causes of haematemesis
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
How is haematemesis investigated?
* 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
How is haematemesis treated?
* 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
Name a scoring system for predicting mortality in acute upper GI bleed
Rockall
153
Name some causes of malaena
Upper GI bleed * Peptic ulcer * Variceal bleed * Oesophagitis * Upper GI malignancy * Mallory-Weiss tear
154
How is malaena investigated?
* Bloods - FBC, U&Es, LFTs, clotting, group and save * ABG * OGD
155
How is malaena treated?
Ulcer: * Adrenaline * PPI * Cauterisation Varices: * Endoscopic banding * Antiobiotics * Somatostatin analogue (terlipressin) * Sengstaken-Blakemore tube if severe
156
What is an anal fissure?
Tear in the mucosal lining of the anal canal * Acute \< 6 weeks * Chronic \> 6 weeks
157
Name some risk factors for developing an anal fissure
* Constipation * Dehydration * IBD * Chronic diarrhoea
158
How are anal fissures managed?
* Increase fibre and fluid in diet * Analgesia * Laxatives (lactulose) * Anal sphincter muscle relaxants (GTN cream) * Lateral sphincterotomy if chronic and unresolved
159
What is an anal fistula?
Abnormal connection between the anal canal and the perianal skin, usually as a result of an anal abscess
160
Name some risk factors for developing an anal fistula
* Anal abscess * IBD * Trauma * Systemic diseases - TB, diabetes, HIV * Radiation therapy
161
What are the clinical features of an anal fissure?
* Acute 'knife-like' pain post-defaecation * Bleeding (blood on paper) * Itching * Deep throbbing pain * May refuse DRE due to pain
162
How are anal fistulas classified?
* 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
What are the clinical features of anal fistulas?
* 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
How can the projectory of an anal fistula be predicted?
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
How are anal fistulas investigated?
* DRE - palpable fibrous track * Endoanal ultrasound (+ hydrogen peroxide) * MRI * Rigid sigmoidoscopy
166
How are anal fistulas managed?
* 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
What is an anorectal abscess?
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
What are the clinical features of an anorectal abscess?
* 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
How is an anorectal abscess investigated?
* DRE - fluctuant, tender mass * MRI if complicated or chronic
170
How is an anorectal abscess managed?
* Antibiotics for acute infective states * Surgical incision and drainage (general aneasthetic) * Allow healing by secondary intention
171
What is a pilonidal sinus?
Formation of a sinus in the cleft of the buttocks * Usually contains hair * Males aged 15-30
172
Describe the pathophysiology of a pilonidal sinus
* 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
What are the risk factors for developing a pilonidal sinus?
* Course dark body hair * Increased sweating * Prolonged sitting (drivers) * Obesity * Poor hygiene * Buttock friction
174
What are the clinical features of a pilonidal sinus?
* Intermittent, red, painful mass in sacrococcygeal region * Discharge * Acute abscess - sepsis
175
How is a pilonidal sinus investigated?
* Test for occult diabetes * Rigid sigmoidoscopy - differentiate between fistula * Pilonidal sinus does not open into anal canal * MRI
176
How is a pilonidal sinus managed?
* 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
What are haemorrhoids?
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
How are haemorrhoids classified?
* 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
What are the risk factors for developing haemorrhoids?
* Excessive straining * Age * Raised intra-abdominal pressure * Cough * Pregnancy * Obesity * Ascities * Cardiac failure * Portal hypertension
180
What are the clinical features of haemorrhoids?
* Post-defaecation bleeding (bright red on paper) * Pruritis (chronic mucus discharge) * Prolapse * Impaired continence * If thrombosed: * Purple/blue * Oedematous * Tense * Tender
181
How are haemorrhoids investigated?
* Proctoscopy * FBC (if prolonged bleeding/signs of anaemia) * Flexible sigmoidoscopy if malignancy suspected * Look for cause * LFTs * ECG
182
How are haemorrhoids managed?
* 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
Name some complications of haemorrhoids
* Ulceration (due to thrombosis) * Ischaemia, thrombosis and gangrene (4th degree) * Skin tags * Perianal sepsis Haemorrhoidectomy surgery: * Bleeding * Infection * Constipation * Stricutre * Fissure * Incontinence
184
What is a rectal prolapse?
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
Name some risk factors for developing rectal prolapse
Defect in fascia of pelvice region * Chronic constipation * Chronic cough * Vaginal delivery * Weakening of anal sphincter * Neurological damage
186
Name some clinical features of rectal prolapse
* Mucus discharge * Incontinence * Bright red blood on paper * Ulceration * Sensation of rectal fullness/mass * Incomplete defaecation
187
How is rectal prolapse investigated?
* Ask to cough/strain * DRE - weakened sphincter * Defaecating proctogram (internal prolapse) * Rigid sigmoidoscopy - mucosal inflammation
188
How is rectal prolapse managed?
* 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
How is primary biliary cirrhosis diagnosed?
M rule: * Middle aged females * IgM * Anti-Mitochondrial antibodies
190
What is Wilsons disease? Name some clinical features
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
What is haemochromatosis? Name some clinical features
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
How is haemachromatosis diagnosed and treated?
Diagnosed: * Serum transferrin saturation and serum ferritin * Genetic testing * Liver biopsy (Perl's stain) Treated: * Regular venesection * Iron chelator if venesection not tolerated
193
Name the different hepatitis serology
* HBsAg - infected with Hep B (and infectious) * Anti-HBs - immunity/recovering * Anti-HBc - previous or current infection * IgM anti-HBc = acute infection
194
What can cause C diff infection?
Gram positive rod caused by suppression by broad-spectrum antibiotics * Clindamycin * Cephalosporins (ceftriaxone)
195
How is C diff infection treated?
* Oral metronidazole for 10-14 days * If not responding - vancomycin

IPE (13 decks)

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