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Medicine > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is the pathophysiology of gastro-oesophageal reflux disease

A

The dysfunctional LES loosens independently of swallowing and has a decreased ability to constrict, which allows stomach contents to uncontrollably flow back into the oesophagus

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2
Q

Diagnosis of Gastro-oesophageal relfux disease

A
  1. A short trial of a Proton Pump Inhibitor and lifestyle therapy should be started in patients with typical symptoms – symptoms relief is diagnostic, but liver failure doesn’t exclude GORD
  2. Endoscopy indicated in patients with atypical relapsing or persistent symptoms
  • Reveals hyperplasia of squamous epithelium, thickening of basal cell layer and elongated sub-epithelial papillae. Along with swollen cells, inflammatory cells, erosion and ulceration.
  1. Oesophageal pH monitoring – done through 24 hours via nasogastric tube
  2. Oesophageal manometry
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3
Q

Treatment of Gastro-oesophageal reflux disease

A
  1. Lifestyle –> avoid alcohol, spicy food, carbonated drinks, smoking, reduce body weight, smaller portions, avoid high fat content
  2. Antacids e.g. Myalnta, quick eze (Aluminium hydroxide)
  3. H2 antagonists e.g. ranitidine 150mg orally OD or BD
  4. Proton Pump Inhibitors e.g. esomeprazole 20mg orally

If mild and infrequent use antacids, if more severe PPI (can double dose and try for 12 weeks to improve symptoms) . if not relieved consider endoscopy

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4
Q

What are the bacterial, viral and protozoal causes of acute diarrhoea

A

Bacterial

  • C. difficile (Antibiotic association, treat with vancomycin)
  • E. coli (Enterotoxigenic - travellers, enterohaemorrhagic)
  • Campylobacter (blood)
  • Salmonella
  • Shigella (blood)
  • Listeria monocytogenes (pregnancy)
  • Yersinia

Viral

  • Norovirus
  • Rotavirus

Protozoal

  • Guardia
  • Cryptosporidia
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5
Q

Symptoms associated with diarrhoea that indicate severe/ bacterial infection

A
  • high fever
  • tachycardia
  • leucocytosis
  • abdominal tenderness or severe pain
  • high volume diarrhoea with hypovolaemia
  • blood in stool

*Viral more likely if sick contacts

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6
Q

Investigations for diarrhoea

A
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7
Q

Treatment for acute infectious diarrhoea

A

*Most acute diarrhoea is viral and does not require antibiotic therapy. Most cases are self-limiting and resolve without specific treatment. Antibiotics are not required or appropriate for many cases of bacterial diarrhoea. When used, their role is to reduce the duration and severity of infection. In infants, bacterial gastroenteritis is treated more aggressively with antibiotics due to the greater risk of developing sepsis.

  1. Rehydration – oral rehydration unless showing signs of severe dehydration then IV
  2. Electrolyte supplementation
  3. Antidiarrheal agents
  • Mu-opioid receptor agonist – loperamide, diphenoxylate, codeine sulfate
    1. Empirical Antibiotics
  • Indicated if symptoms of severe disease or immunocompromised
  • Antibiotics is not recommended in children with bloody diarrhoea without fever due to potential for haemolytic uraemic syndrome if caused by enterohaemorrhagic E.coli
  • Before starting therapy, obstain microbiological tests
  • Ciprofloxacin 500mg orally, 12 hourly for 3 days (12.5mh/kg up to 500 for children)
  • Norfloxacin 400mg orally, 12 hours for 3 days
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8
Q

Causes of undernutrition

A
  1. low intake of food
  2. mental health - anorexia nervosa
  3. social problems
  4. digestive disorders - coeliac, crohns
  5. alcoholism
  6. lack of breastfeeding
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9
Q

Symptoms of Malnutrition

A

CNS –> hypothermia, disturbed memory and concentration

Endocrine –> adrenaline increase, euthyroid sick syndrome, lack of sex drive

Electrolytes –> hypokalaemia

Heart –> bradycardia, hypotension

Bones –> osteoporosis

Skin –> slin strophy, skin dryness, poor wound healing, alopecia

Blood –> pancytopenia

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10
Q

What is refeeding syndrome

A

Very rapid increase in food intake can cause massive insulin release –> increased displacement of magnesium, potassium and phosphate

  • Clinical features: oedema, tachycardia, seizures, ataxia
  • Treatment – electrolyte substitutions
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11
Q

Disease/conditions associated with obesity

A
  • High triglycerides and low HDL
  • T2DM
  • HTN
  • Metabolic syndrome – high BSL, HTN, high triglycerides and low HDL
  • Heart disease
  • Stroke
  • Cancer
  • Breathing disorders – OSA
  • Gallbladder disease
  • Gynaecological problems – infertile, irregular periods
  • Erectile dysfunction
  • Non-alcoholic fatty liver disease
  • Osteoarthritis
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12
Q

What is cholelithiasis and choledocholithiasis?

A

Cholelithiasis is the presence of solid concentrations in the gallbladder gallstones form in the gallbladder but may exit into the bile duct (Choledocholithiasis). Symptoms ensue if a stone obstructs the cystic, bile or pancreatic duct. Most gallstones in developed countries consist of cholesterol.

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13
Q

Types of gallstones

A

Cholesterol GS

Female, Fat, Fertile, 40, fair

  1. Obesity
  2. Rapid weight loss after bariatric surgery
  3. Medications – estrogen and ceftriaxone
  4. Female
  5. Family history

Black GS

Disorders that lead to elevated unconjugated bilirubin in bile

  1. Chronic haemolytic anaemia
  2. Cirrhosis
  3. Cystic fibrosis
  4. Ileal disease

Brown GS

Contain bacterial degradation

  1. Infection
  2. Stasis due to biliary stricture – inflammatory/ neoplastic
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14
Q

Clinical features of cholelithiasis and choledocholithiasis

A

Cholelithiasis

  • 80% of people remain asymptomatic
  • biliary colic pain, postprandial pain
  • may radiate to epigastrium, right shoulder and back
  • nausea, vomiting, feelings of satiety
  • bloating, dyspepsia

Choledocholithiasis

  • Colicky RUQ/ epigastric pain
  • Nausea, vomiting
  • Extrahepatic cholestasis
  • Obstructive jaundice, pale stool, dark urine
  • Pruritus with obstruction of gallbladder drainage
  • If complicated may present with pancreatitis and acute cholangitis

Pain usually lasts up to 4 hours

Once symptomatic, 70% reoccurrence in 2 years

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15
Q

Complications of choledocholithiasis

A
  • Cholecystitis
  • Empyema
  • Perforation
  • Fistula
  • Cholangitis
  • Obstructive cholestasis
  • Pancreatitis
  • Gallstone ileus
  • Increased risk of carcinoma
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16
Q

Investigations in cholelithiasis and choledocholithiasis

A
  1. FBC – normal in uncomplicated biliary colic
  2. LFTs – In choledocholithiasis à Elevated alkaline phosphate (ALP), ­GGT, elevated conjugated bilirubin
  3. U/S – stones in gallbladder = cholelithiasis
  4. Endoscopic U/S of bile duct – to exclude choledocholithiasis
  5. Gastroscopy – exclude other aetiologies of abdominal pain
  6. Serum lipase and amylase – elevated in acute pancreatitis
  7. ERCP
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17
Q

Management of cholelithiasis

A

Conservative

  • Fasting or dietary modification (decrease fat intake)
  • Analgesia – NSAIDs
  • Spasmolytic (e.g. dicyclomine)

Interventional

  • Endoscopic retrograde cholangiopancreatography (ERCP) with papillotomy
  • Procedure that displays bile and pancreatic ducts by introducing a gastroduodenal endoscope and injecting constrast through the ampulla of Vater
  • Papillotomy widens the ampulla of Vater to facilitate better passage of bile and pancreatic secretions
  • Indications à symptomatic cholelithiasis, choledocholithiasis, acute cholangitis, gallstone pancreatitis
  • Complications
  • Post ERCP pancreatitis
  • Haemorrhaging
  • Cholangitis
  • Perforation
  • Medical litholysis
  • Administration of oral bile changes the lithogenicity of the bile
  • Possibly indicated in cholesterol stones without calcification
  • Success rate 50% and treatment duration 6 months minimum
  • Extracorporeal shock wave lithotriosy (ESWL)
  • Possible in up to 3 non-calcified gallstones. With a maximal diameter of 3 cm
  • Retained contraction capacity must be present
  • Additional medical litholysis is necessary
  • Success rate – 90%
  • Contraindications – pregnancy, infection, coagulopathy
  • Surgical – Elective Laparoscopic Cholecystectomy (after ERCP)
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18
Q

Major classification/ causes of cholecystitis

A
  1. Acute calculous cholecystitis
  2. Acute acalculous cholecystitis
  • Acute necroinflammatory disorder of the gallbladder, usually seen in critically ill patients. It usually presents with secondary infection. Due to starvation, sepsis, total parenteral nutrition, narcotic analgesia, burns.
    1. Emphysematous cholecystisis
  • Rare form of acute cholecystitis with gas-formiing bacteria that occurs more often in elderly diabetic males
    1. Chronic cholecystitis
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19
Q

Clinical symptoms of cholecystitis

A
  • RUQ pain
  • More severe and prolonged (>6 hours) than in cholelithiasis
  • Worse after meals
  • Radiation to the right scapula
  • Guarding
  • Positive Murphy’s sign – sudden inspiratory arrest during RUQ palpation
  • Fever, malaise
  • Nausea and vomiting
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20
Q

Investigations of cholecystitis and ascending cholangitis

A
  1. FBC – elevated WBC (if infection)
  2. CRP – elevated
  3. LFTs – elevated ALP, GGT, bilirubin (possible ­AST, ALT)
  4. serum urea and creatining - raised in severe
  5. U/S
  • Enlargement of gallbladder wall thickening
  • Gallstone
  • Double wall sign - Inner and outer walls remain hyperechoic, whereas the wall in between remains hypoechoic because of fluid retention.
  1. Tc-HIDA nuclear medicine scan – radioactive tracer excreted into bile
  • Perform if U/S not diagnostic
  • Failure of gallbladder filling with normal hepatic uptake and biliary excretion
  1. CT if U/S unreliable (obesity), MRI in pregnant women
  2. Cholangiogram: ERCP, Percutaneous trans-hepatic cholangiography
  3. Blood cultures
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21
Q

complications of cholecystitis

A
  • Perforation and sepsis
  • Obstruction of CBD
  • Obstruction of pancreatic duct – ampulla of Vater
  • Gangrene fistula
  • Emphysematous cholecystitis – secondary to gas forming organisms in GB wall
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22
Q

Treatment of cholecystitis and acute cholangitis

A

Conservative

  • IV antibiotic therapy – Pipracillin-tazobactam (Tazocin)
  • Analgesia (meperidine)
  • Fluid and electrolyte correction
  • Antiemetic’s

Surgery

  • Gold standard - laparoscopic cholecystectomy
  • Open surgery if gangrene or empyema

In acute cholangitis need to remove the blockage and treat with antibiotics.

  1. Broad spectrum antibiotics (Tazocin or gentamicin)
  2. Fluid, electrolytes, analgesia
  3. ERCP and cholecystectomy
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23
Q

What is ascending cholangitis

A

Infection of the biliary system due to blockage of common bile duct, by gallstone, tumour or stricture

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24
Q

Typical clinical features of acute cholangitis (Charcots cholangitis triad)

A

Charcots cholangitis triad

  1. RUQ pain
  2. fever
  3. juandice

Reynolds pentad

also includes… charcots cholangitis triad + hypotension + altered mental status in severe cholangitis

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25
Q
A
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26
Q

Familial causes of colorectal cancer and risk factors

A

The majority of colorectal cancers are sporadic rather than familial. However, there is a 2-3 fold increased risk of colorectal cancer in people with a family history in a single first-degree relative. Familial syndromes include:

  • Familial adenomatous polyposis syndrome (FAP) 

  • 100% risk by age 40
  • Hereditary non-polyposis colorectal carcinoma (HNPCC)
  • 80% progress to CRC

Risk factors 


  • Increasing age 

  • Smoking
  • Alcohol
  • Processed meat: high fat, low fiber diet
  • Obesity
  • Inflammatory bowel disease 

  • Endocarditis and bacteraemia due to Streptococcus gallolyticus
  • APC mutation 

  • MYH-associated polyposis 

  • Hamartomatous polyposis syndrome
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27
Q

The 4 major classifications of colorectal cancer

A
  1. Colorectal carcinoma
  • Most are adenocarcinoma (colorectal mucosa) – 95%
  • Arise from adenomatous polyps
  • Mutation in oncogenes (KRAS) and tumour suppressor genes (APC, TP53)
  1. Neuroendocrine tumours (carcinoid)
  • Neuroendocrine cell lineage
  • Most low grade
  • Appendix most common site
  1. Gastrointestinal stromal tumours (GIST)
  • Spindle cell neoplasm
  • 80% CD117 (C-kit) and 10% PDGFRA (platelet derived growth factor receptor alpha)
  • high and low malignant potential
  1. Lymphomas
  2. B-cell lymphomas: Marginal zone lymphoma (MALT), diffuse large b cell lymphoma, Burkitt lymphoma
  3. T-cell lymphoma: associated with malabsorption syndrome i.e. coeliac disease
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28
Q

Clinical features of CRC

A
  • Blood in stool, irone deficiency anaemia
  • Change in bowel habits
  • Colicky abdominal pain due to obstruction
  • Tenesmus - a distressing and persistent urge to empty rectum
  • signs of metastasis
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29
Q

Investigations for CRC

A
  1. Digital Rectal Exam
  2. Complete colonoscopy (gold standard)
  3. FBC - anaemia
  4. Staging CT
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30
Q

Curative for Colon Tumour

  1. Surgical Resection - colectomy, regional lymph node dissection, resection of resectable metastases in liver and/ or lungs
  2. Systemic therapy
  • Chemotherapy - Golinic acid + 5-fluorouracil + oxiplatin
  • Biologics - anti-VGEF antibodies e.g. cetuximab

Curative for rectal tumour

  1. Surgical - transanal exciion, low anterior resection, abdominoperineal resection
  2. systemic - adjuvant radiochemotherapy
A
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31
Q

Screening protocol for CRC

A

Screening for colorectal cancer and adenomatous polys is performed in asymptomatic men and women > 50 yo

Low-risk (3 options)

  1. Colonoscopy every 10 years if not polyps/ carcinomas detected
  2. Annual Faecal Occult Blood test
  3. Sigmoidoscopy every 5 years and FOBT every 3 years

High risk

  1. Complete colonoscopy 10 years earlier than the index patients age at diagnosis or no later than 40yo
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32
Q

Definitions of dyslipidaemia, hyperlipidaemia, hypercholesterolaemia, hypertriglyceridaemia, hypolipoproteinemia

A
  1. Dyslipidaemia – Abnormal lipoprotein levels (LDL > 130 mg/dL, HDL < 40mg/dL) .in association with an increased risk of cardiovascular disease
  2. Hyperlipidaemia – elevated blood lipid levels (total cholesterol, LDL, triglycerides)
  3. Hypercholesterolemia – elevated total cholesterol (>200mg/dL)
  4. Hypertriglyceridemia – elevated triglyceride levels (associated with increased risk of acute pancreatitis)
  5. Hypolipoproteinaemia – elevated levels of a certain lipoprotein
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33
Q

causes of dyslipidaemia

A

Acquired

  • Obesity
  • Diabetes mellitus
  • Physical inactivity
  • Alcoholism
  • Hypothyroidism
  • Nephrotic syndrome
  • Cholestatic liver disease
  • Cushing’s disease
  • Drugs: OCP, metoprolol, high dose diuretic

Congenital

  • Hyperchylomicronemia
  • Familial hypercholesterolemia (mutation of LDL receptor leading to increased LDL)
  • Familial hypertriglyceridemia
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34
Q

Signs of hyperlipidaemia

A
  1. Xanthomata
  2. xanthalesmata
  3. arcus senalis
  4. fatty liver
  5. atherosclerosis with secondary disease –> CAD< PAD, stroke, MI, Carotid artery stenosis
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35
Q

Cholesterol reducing treatment

A
  1. General measures – lifestyle modification, dietary changes (reduce saturated fat and cholesterol intake), weight management, physical activity
  2. Medical therapy
  • Statins (Atorvastatin)
  • Inhibits HMG-CoA reductase, prevents synthesis of cholesterol in liver
  • Ezetimibe
  • Used with statins, when statins don’t work alone, decreased cholesterol absorption in small intestine
  • PCSK9 inhibitors (Evolocumab)
  • Monoclonal Ab inhibit PCSK9 from degrading LDL receptors
    1. Treatment xanthomas and xanthelasmas – surgical
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36
Q

Pathogens causing primary and secondary peritonitis

A

Primary

  • Rare type seen in patients who have ascites and end-stage liver disease
  • Continuous Ambulatory Peritoneal dialysis
  • Gram -ve: E.coli, Klebsiella pneumoniae
  • Gram +ve: Streptococcus pneumoniae, Staph aureus

Secondary

  • Usually polymicrobial, enteric bacteria
  • Aerobic: E.coli, Klebsiella, Enterobacter, Streptococci, Enterococci
  • Anaerobic: Bacterioides, Clostridia, Eubacteria
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37
Q

Signs and Symptoms of peritonitis

A

General Symptoms

  • Diffuse abdominal pain with abdominal guarding and/or rebound tenderness
  • Nausea, vomiting
  • Fever and chills
  • Possibly shoulder pain
  • Ascites in spontaneous bacterial peritonitis

Physical examination

  • Distressed patient, knees drawn up when supine, avoids movement
  • Abdominal pain and rigidity, rebound tenderness
  • Sparse peristaltic sounds
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38
Q

Investigations for suspected peritonitis

A

Lab

  1. FBC
  2. CRP
  3. Peritoneal fluid analysis - Neurtophil count, glucose, LDH, pH, gram stain and culture
  4. Serum creatinine and LFTs - underlying liver dysfunciton
  5. Blood culture

Imaging

  1. U/S (Underlying disease - pancreatitis, appendicitis, cholangitis), peritoneal fluid
  2. Abdominal X-ray - air fluid levels, free air secondary to organ perforation
  3. CT abdomen and pelvis
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39
Q

Treatment of peritonitis

A

Primary Peritonitis

  • Broad spectrum antibiotics - cefotaxime, ceftriaxone

Secondary peritonitis

  • Fluid replacement
  • Drainage of asbcess
  • Broad spectrum antibiotics - Tazocin OR Ciprofloxacin + metronidazole
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40
Q

Causes of Malabsorption

A

Maldigestion

  1. Chronic pancreatitis à exocrine pancreatic insufficiency à lack of enzymes à reduced hydrolysis of carbohydrates, proteins and lipids
  2. GI surgery (resections) à lack of gastric acid à impaired breakdown of nutrients
  3. Bile acid deficiency (cholestasis, bile acid malabsorption) à incomplete emulsification of fats
  4. Medications (orlistat) à inhibits gastric and pancreatic lipase

Malabsorption

  1. Inflammation
    * Crohn’s disease, Ulcerative colitis
  2. Infection
    * Tropical sprue, giardiasis, traveller’s diarrhoea, Whipple’s disease
  3. Coeliac disease
  4. Lactose Intolerance (lactase deficiency)
  • Dietary elimination and challenge are generally diagnostic
  • If elimination of lactose is necessary for Tx – alternative calcium source recommended
  1. HIV enteropathy
  2. Cystic fibrosis
  3. Irritable bowel syndrome
  4. Diagnosis of exclusion
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41
Q

What are the fat volume vitamins and the symptoms of their deficiencies

A

Vitamin A

  • Night blindness, retinopathy, xerophthalia

Vitamin D

  • Osteomalacia and rickets

vitamin E

  • Demyelination of posterior column (neuromuscular deficiency)

Vitamin K

  • Increased bleeding tendency
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42
Q

Water-soluble vitamin Deficiencies (B1 - thiamine, B3 - niacin, B12 - cobalamin)

A
  • B1 - beriberi –> symmetrical peripheral neuropathy, muscle wasting, confusion, cardiomyopathy
  • B3 - pallegra –> Dermatitis, Dementia, Diarrhoea, Da big tongue (glossitis)
  • B12 - Megaloblastic anaemia
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43
Q

Investigations for malabsorption

A
  1. FBC
  • Macrocytic or microcytic anaemia
  • Decreased electrolytes, decreased total protein, vitamin deficiencies
  1. Stool test
  • Analysis of faecal fat over 72 hours
  • Detection of pathogens
  1. X-xylose absorption test – assesses the absorptive function of the upper small intestine
  2. Blood tests
  • Vitamin B-12
  • Vitamin D
  • Folate
  • Iron
  • Calcium
  • Phosphorus
  • Carotene
  • Albumin
  • Protein
  1. Lactose Hydrogen Breath test
  2. Imaging – Structural problems e.g. Crohn’s disease
  3. Tissue transglutimase and Biopsy e.g. coeliac
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44
Q

What is coeliac disease and its clinical features

A

malabsorption due to chronic immune-mediated reaction to dietary gluten

GI symptoms

  • chronic diarrhoea, steatorrhoea
  • Flatulence, abdominal bloating
  • lack of appetite

Extra-intestinal

  • Dermititis herpatiformis
  • fatigue, weight loss, vitamin deficiency, osteoporosis
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45
Q

Investigations for coeliac disease

A
  1. Tissue transglutimase - first line test
  2. Anti-emdomysial antibody (EMA) - harder to perform
  3. FBC - low Hb and microcytic RBCs
  4. Biopsy - confirmatory test showing atrophic villi
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46
Q

Causes of dehydration

A
  • Insufficient water intake (particularly in elderly and critically ill)
  • Increased free water loss
  • Renal loss
  • Diuretics
  • Hyperglycaemia
  • Polyuric phase of renal failure
  • Diabetes insipidus
  • Extra-renal loss
  • Diarrhoea
  • Vomiting
  • Burns
  • Increased sweating
  • Fever
  • Inflammation
  • Ascites
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47
Q

Signs and symptoms of dehydration

A

Symptoms

  • thirst
  • headaches, dizziness, disorientation
  • weakness, fatigue

Signs

  • Sunken eyes
  • decreased skin turgor
  • dry skin and dru mucous membranes
  • in infants - sunken fontanelle
  • in children - no tears
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48
Q

Investigations for dehydration

A
  1. Serum sodium - hypernatraemia
  2. Increased haematocrit (hypovolaemia)
  3. Decreased bicarbonate levels (lactic acidosis)
  4. BUN to serum creatinine ration > 20:1 (renal hypoperfusion in hypovolaemia)
  5. Urine osmolality <800 - renal, > 800 - extra-renal
  6. BGL - (hypo could mean decreased fluid intake, hyper could mean osmotic diuresis)
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49
Q

Treatment of dehydration

A

Patients who are hypovolemic as result of severe dehydration require immediate fluid resuscitation with crystalloids

  1. Fluid resuscitation
  • Adults: rapid infusion of isotonic crystalloids
  • Children: rapid infusion of isotonic saline
  1. Correction of electrolyte abnormalities
    * Hypernatraemia or hyponatramia once volume resuscitated
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50
Q

Types of abdominal hernias

A
  • Ventral Hernias
    • Epigastric hernia
    • Umbilical hernia
    • Incisional hernia
    • Spigellan hernia
    • Parastomal hernia
  • Groin hernias
    • Inguinal hernia
    • Femoral hernia
  • Pelvic hernias (rare)
    • obturator, sciatic, perineal hernias
  • Flank hernia
    • Incisional, lumbar hernia
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51
Q

Difference in clinical features between reducible and irreducible hernias

A

*Most are asymptomatic

Reducible hernia

Can be pushed back with minimal pressure

  • Completely reducible non-tender mass on the abdominal wall (epigastric region, umbilicus, groin, etc.)
  • Increases on straining (coughing, lifting heavy object)
  • Decreases on lying down
  • Edges of the fascial defect are palpable
  • Bowel sounds may be heard

Irreducible/ incarcerated hernias

Cannot be pushed back with pressure

  • Absent cough impulse
  • May lead to obstructed hernia (features of acute bowel obstruction)
  • If left untreated, can lead to a strangulated hernia (blood supply cut off) with ischaemia of the hernia contents
  • Acute pain at site of hernia
  • Edematous, erythematous, warm overlying skin
  • Possibly features of bowel obstruction
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52
Q

inguinal canal anatomy and the difference between direct and indirect inguinal hernias

A
  • Floor* – inguinal ligament
  • Roof* – transversalis and internal oblique
  • Front* – external oblique aponeurosis + internal oblique for the lateral
  • Back* – laterally, transversalis fascia; medially; conjoined tendon

Deep ring – created by transversalis fascia

Superficial ring – formed by external oblique

Direct

  • Enters through the fascia transversalis on the posterior wall of the inguinal canal in the area known as Hasselbach’s triangle (Lateral = inferior epigastric artery, medial = rectus abdominus, inferior = inguinal ligament)
  • Hernia does not pass through deep ring -> not covered by internal spermatic fascia

Indirect

  • Indirect hernias pass through the deep inguinal ring following the path of the spermatic cord, may protrude into the superficial ring; congenital
  • Lateral to the inferior epigastric artery
  • Commonly seen in children
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53
Q

Appendicitis pathophysiology of obstructed lumen

A

Obstruction of appendiceal lumen by:

  1. Lymphoid tissue
  2. Hardened faecal matter
  3. Less common: foreign bodies, worm infestation, intestinal infections, tumours (carcinoid), haemolytic disease

Stasis of mucus and fluid à bacterial growth and local inflammation à rising intraluminal pressure à vascular compromise à ischaemia à necrosis à perforation and peritonitis

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54
Q

Clinical features of appendicitis

A

Non-specific

  • Progressive fever
  • Anorexia (hamburger sign)
  • Nausea, vomiting,
  • Constipation (maybe)

Abdominal pain

  • Initially dull, migratory periumbilical pain (due to visceral peritoneum irritation)
  • After 4-24 hours, sharp RLQ pain (due to parietal peritoneum irritation by a distended and inflamed appendix) with rebound tenderness

Signs of appendicitis

  1. Blumberg’s sign; rebound tenderness caused upon suddenly ceasing deep palpation of the RLQ
  2. McBurney point tenderness: an area one-third of the distance from the anterior superior iliac spine to the umbilicus (in the RLQ)
  3. Rovsing’s sign; deep palpation of the LLQ causes RLQ referred pain
  4. Psoas sign: RLQ pain with extension of the right leg against resistance
  5. Obturator sign: RLQ pain with flexion and internal rotation of the right leg
55
Q

Investigations in suspected appendicitsis

A
  1. CRP
  2. FBC
  3. B-hCG
  4. Urinalysis - rule out UTI
  5. UEC - sepsis, kidneys
  6. LFTs
  7. Lipase - pancreatitis
  8. Imaging - U/S, CT
56
Q

Treatment of appendicitis

A
  1. Bowel rest (nil by mouth), IV fluid therapy, observation
  2. Analgesia
  3. Antibiotics with anaerobic and gram negative cover (cefazolin and metronidazole)
  4. DVT prophylaxis
  5. Appendectomy
  • Body can still function properly without an appendix
  • When appendix become inflamed and swollen and can lead to perforation, want to remove before it ruptures
  • May lead to serious infection peritonitis or abscess
  • Risks: bleeding, infection, injury to nearby organs, blocked bowels
  • Laparoscopic incision
57
Q

Causes of constipation

A
  • Primary
    • Low dietary fibre
    • Lack of exercise
    • Dehydration
  • Secondary
    • Mechanical - bowel obstruction - colorectal carcinoma, stenosis
    • Medications - opioids, iron supplements, antacids
    • Endocrine - hypothyroidism, DM, electrolyte imbalance
    • Neurological - MS, diabetic neuropathy
    • Post-surgical ileus
    • GI conditions e.g. IBD
58
Q

Treatment for constipation

A
  1. Discontinue non-essential medications causing the constipation
  2. Use PO or IV rehydration with normal saline to correct dehydration and electrolytes
  3. Insert a catheter in cases of urinary retention secondary to distal faecal impaction
  4. Oral laxatives
  • Stool softener (Coloxyl) [Docusate sodium]
  • Osmotic laxatives (Movicol)
  1. Rectal laxatives
  • Osmotic laxatives (glycerine suppository)
  • Stimulant laxative (bisacodyl suppository or Senna)
  1. Enemas
  • Rectal stool softener (microlax)
  • Sodium phosphate hypertonic enema
  1. Opioid antagonist – methylnaltraxone
  2. 5-HT4 receptor antagonist – prucalopride
  3. Digital manual faecal disimpaction
59
Q

Causes of PR bleed

A

Frank Haematochezia

  • Anal fissue
  • haemorrhoids
  • Rectal cancers
  • Rectal varices
  • traums

Frank mixed

  • Diverticulitis
  • Colorectal cancer
  • IBD
  • Polyps
  • angiodysplasia
  • Mesenteric ischaemia

Melaena

  • Upper GI bleed - duodenal ulcer, oesophageal perforation
  • Upper GI malignancy
  • oesophageal varices
  • gastritis
60
Q

Clinical features and Pathology differences between Crohn’s disease and Ulcerative Colitis

A

Crohn’s

Pathology

  • Tranmural inflammation
  • Dicontinuous inflammation (skip lesions)
  • Can affect entire GI tract, but typically terminal ileum
  • commonly leads to fistulas, abscesses and stenosis
  • Linear ulceration

Clinical

  • Constant pain, mainly RLQ
  • malnourished
  • Increased frequency of bowel movements or contripated
  • typically non-bloody watery diarrhoea

Ulcerative colitis

Pathology

  • Continuous inflammation
  • Starts from rectum and goes upwards
  • only mucosal and submucosal inflammation
  • No granulomas
  • Fistulas are very rare

Clinical features

  • Bloody diarrhoea with mucus
  • greatly increased frequency of bowel movements
  • normally dont have weight loss
  • pain mostly before defecation or during defecation, mainly LLQ
61
Q

Investigations for Crohn’s Disease

A

Lab tests

Blood

  1. Increased inflammatory markers – CRP, ESR, thrombocytes, leukocytes
  2. FBC – anaemia, leukocytosis
  3. ASCA – elevated

Faeces

  1. Stool analysis to rule out gastroenteritis caused by bacteria
  2. Detection of fecal calprotectin and/ or lactoferrin

Imaging

  1. Plain abdominal X-rays: bowel distention, pneumoperitoneum
  2. Plain radiography with barium swallow (enteroclysis) to detect fistulas or stenosis
  3. U/S – GI wall thickness caused by inflammation and oedema

Endoscopy – confirms diagnosis

  • Ileocolonoscopy or Oesophagogastroduodenoscopy findings
  • Segmental/ discontinuous patterns (Skip lesions)
  • Linear ulcers
  • Fissures, fistulas
  • Transmural and erythematous inflammation
62
Q

Treatment for Crohn’s Disease

A

Pharmacotherapy

Symptoms

  1. Anti-diarrhoeal agents (Loperamide)
  2. Topical corticosteroids (Triamcinolone)
  • For pain relief in oral lesions
    1. Topical 5-Aminosalicyclic acid derivatives (5-ASA)
  • In the case of inflammation of the distal colon

Acute exacerbations

Mild

  1. Topical corticosteroids: Oral budesonide
  2. 5-ASA: Sulfasalazine, metronidazole
  3. Antibiotics: Metronidazole, ciprofloxacin
  • Indicated for fistulas, perianal abscess
  • Reduces intestinal bacteria, immune response and risk of infection

Moderate to severe

  1. Systemic corticosteroids (Prednisolone)

Steroid-refractory

  1. Immunosuppressant’s
  2. TNF-alpha antibodies (infliximab, adalimumab)
  3. If necessary in combination with azathioprine
  4. Alsternative – methotrexate

Maintenance therapy

  1. First line: 5-ASA

Alternatives: Azathioprine, methotrexate of TNF-alpha antibodies

Surgery

  • Resect affected and non-functional intestinal loops
  • Indicated in failed medical therapy or severe complications e.g. abscess, perforation, toxic megacolon, obstruction, stricture
63
Q

Investigations for ulcerative colitis

A

Lab tests

Blood

  1. FBC – anaemia, leukocytosis
  2. CRP
  3. Perinuclear ANCA

Stool analysis

  • Test for bacteria to rule out other causes
  • Calprotectin and lactoferrin are indicators of mucosal inflmattation

Imaging

  1. Colonoscopy
  • Inflamed, reddened mucosa
  • Bleeding on contact with endoscope
  • Fibrin-covered ulcers
  • Adjunct imaging can include x-ray, CT, MRI, U/S
64
Q

Treatment of ulcerative colitis

A

Pharmacotherapy

Symptoms

  1. Anti-diarrhoeal agents (Loperamide)

Acute exacerbations

Mild

  1. 5-ASA: Sulfasalazine, mesalamine

Moderate to severe

  1. Systemic corticosteroids (Prednisolone)

Steroid-refractory

  1. Immunosuppressant’s
  2. TNF-alpha antibodies (infliximab, adalimumab)
  3. If necessary in combination with azathioprine
  4. Alsternative – methotrexate

Maintenance therapy

  1. First line: 5-ASA

Alternatives: Azathioprine, methotrexate of TNF-alpha antibodies

Surgery

  • Resect affected and non-functional intestinal loops
  • Indicated in failed medical therapy or severe complications e.g. abscess, perforation, toxic megacolon, obstruction, stricture
65
Q

Pathophysiology and particular pathogen associated with antibiotic induced diarrhoea

A

Disturbance of the normal colonic microflora

  • Alterations in bacterial degradation -> osmotic diarrhea
  • Direct effect of antibiotic e.g. erythromycin stimulate intestinal motility
  • Infection by organisms

Clostridium difficile is a gram-positive rod bacillus that is commonly involved in AAD. C. difficile infection rate particularly high among hospitalized patients. The resulting damage to the intestinal flora promotes infection. The most severe C.difficile infection is pseudomembranous colitis, which may lead to ileus, sepsis, and toxic megacolon,

66
Q

Causes of acute pancreatitis (I GET SMASHED)

A
  • Idiopathic
  • Gall stone
  • Ethanol
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion bite
  • Hypertriglyceridaemia, hypercalcaemia
  • ERCP
  • Drugs - azathroprine, sulfonamides
67
Q

Clinical features of acute pancreatitis

A
  • Constant severe epigastric pain
  • Classically radiating towards the back
  • Worse after meals and when supine
  • Improves on leaning forwards
  • Nausea and vomiting
  • General physical examination
  • Shock, tachycardia, hypotension, oliguria/anuria
  • Abdominal examination
  • Abdominal tenderness, distention, guarding
  • Ileus with reduced bowel sounds and tympany on percussion
  • Ascites
  • Skin changes (rare)
  • Cullen’s sign – periumbilical ecchymosis and discoloration
  • Grey-turner’s sign – flank ecchymosis and discoloration
  • Fox’s sign – ecchymosis over inguinal ligament
68
Q

3 criteria to diagnose acute pancreatitis:

A

Diagnosis of acute pancreatitis requires 2 of the following 3 features:

  1. Abdominal pain consistent with acute pancreatitis (acute onset, persistent, severe epigastric pain often radiating to the back)
  2. Serum lipase/ amylase at least 3 times greater than upper limit of normal
  3. Characteristic findings on U/S, CT or MRI
69
Q

Other investigations to order for suspected pancreatitis

A

Lab tests

  1. ­ serum pancreatic enzymes (normal enzymes don’t rule out pancreatitis)
  • lipase if >= 3 times upper reference range
  • amylase
  • note that the enzyme levels are not directly proportional to severity or prognosis
  1. Haematocrit
  • Should be conducted at presentation and 12 and 24 hours after admission
  • ­ Hct indicates third space fluid loss and inadequate fluid resuscitation
  • ¯ Hct indicates the rarer acute haemorrhagic pancreatitis
  1. WBC count – leukocytosis indicates severe pancreatitis
  2. Blood urea nitrogen
  • Rising blood urea nitrogen levels > 48 hours of resuscitation indicates persistent third spacing of fluid and is a predictor of severe pancreatitis.
    1. ­CRP and prolactin levels
  • Procalcitonin levels help determine if a rise in CRP is due to necrosis caused by bacterial pancreatitis, as procalcitonin typically indicates bacterial infection, whereas CRP may be elevated in either sterile or bacterial pancreatitis.
    1. LFTs
  • ­ ALT (> 150 U/L) indicates pancreatitis caused by biliary disorders (in 85% of cases) and a more fulminant disease course.
  • ­ALP, ­bilirubin à gallstone
  1. Serum calcium levels
    * Hypercalcemia may cause pancreatitis, then in turn cause hypocalcaemia
  2. Serum triglyceride levels
  3. Electrolytes (K, Ca)
  4. Renal function tests

I_maging_

  1. U/S – most useful initial test
  2. CT scan – not routine, only when diagnosis is in doubt
  3. MRCP - Magnetic resonance cholangiopancreatography (noninvasive but less sensitive than ERCP)
  4. ERCP – Endoscopic retrograde cholangiopancreatography – may worsen pancreatitis but can extract stone
  5. X-ray
70
Q

Treatment of acute pancreatitis

A

General

  1. Fluid resuscitation
  2. Analgesia – IV opioids
  3. Bowel rest

Drug therapy

  1. Analgesics – fentanyl or hydromorphone
  2. Antibiotics – only used if evidence of infected necrosis (Tazocin)

Surgery

  1. Biliary pancreatitis
  • Urgent ERCP and sphincterotomy in patients with evidence of choledocholithiasis or cholangitis
  • Cholecystectomy followed – in all patients with biliary pancreatitis
71
Q

Clinical features of chronic pancreatitis

A

Epigastric abdominal pain

  • Pain radiates to the back, is relieved on bending forwards and exacerbated after eating
  • Pain is initially episodic and becomes persistent as the disease progresses
  • Often associated with nausea and vomiting

Features of pancreatic insufficiency

  • Late manifestation (after 90%) of the pancreatic parenchyma is destroyed
  • Steatorrhoea (exocrine hormone deficiency)
  • Cramping abdominal pain, bloating, diarrhea, weight loss
  • May cause fat-soluble vitamin deficiency
  • Malabsorption and weight loss
  • Pancreatic diabetes
72
Q

treatment of chronic pancreatitis

A

General measures

  1. Abstinence from alcohol and nicotine
  2. Small regular meals low in fat
  3. Pancreatic enzyme replacement with meals
  4. Parenteral administration of fat-soluble vitamins (A,D,E,K)
  5. Endocrine insufficiency - insulin administration

Pain management

  1. Analgesics: NSAIDs, opioid for severe pain (fentanyl, morphine), low dose tricyclic antidepressants (amitriptyline)
  2. Intractible pain
  3. Celiac ganglion block (offers temporary relief)
  4. Endoscopic papillotomy _ductal dilation and stent placement + remove stone
  5. Extracorporeal show wave lithotripsy

Surgery

If pancreatic cancer is suspected or in those with intractable pain

  1. Pancreaticojejunostomy
  2. Resection of affected pancreas (distal pancreatomy, Whipple’s procedure)
  3. Thoracoscopic bilateral splanchiectomy (destroys sensory nerves)
73
Q

What is metabolic syndrome

A

Metabolic syndrome describes a constellation of medical conditions which increase the risk for several health problems:

  • primarily CVD disease
  • T2DM
  • Fatty liver (Non-alcoholic steatohepatitis à increased risk of liver cirrhosis and hepatocellular carcinoma)

Presence of >= 3 of the following conditions:

  1. Insulin resistance (fasting glucose > 5.6mmol/L)
  2. Hypertension (>= 130/85 mmHg)
  3. Dyslipidaemia
  • Elevated triglycerides: (>= 1.8 mmol/L)
  • Low HDL (<1.0mmol/L in men and < 1.3 mmol/L in women)
  1. Abdominal obesity (waist cirfumference >=102cm in men, >= 88cm in women)
74
Q

Causes of Peptic Ulcer Disease (Gastric or Duodenal Ulcer)

A
  • Helicobacter Pylori
  • Long term use of NSAIDs
  • Zollinger-Ellison Syndrome
75
Q

Clinical features of peptic ulcer disease

A
  • Abdominal pain
  • Epigastric tenderness
  • Upper GI bleeding
  • Pain after eating
  • Nocturnal pain/ worse lying down
76
Q

Investigations for H.Pylori infection

A
  • Serology IgG (Blood test)
  • Urea Breath Test - fasting
  • Faeces Antigen
  • Urease Test (endoscopy and biopsy)
  • Culture main lab (endoscopy and biopsy)
  • Histology (endoscopy and biopsy)

List increases in complexity and cost

77
Q

Treatment for H. Pylori Infection

A
  • PPI (esomeprazole 20mg)
  • Amoxicillin
  • Metronidazole/ Clindamycin

(If ulcer caused by NSAIDs - stop NSAIDs and use PPI)

78
Q

What cancers are associated with H. Pylori infection

A
  • Gastric adenocarcinoma
  • MALT lymphoma
79
Q

Causes of ischaemic colitis

A

Ischaemic colitis – Hypo perfusion of the large bowel, which is mostly transient and self-limiting, but can also lead to severe acute ischaemia with bowel infarction

Acute mesenteric ischaemia – acute inadequate blood flow to the small intestine that can result in bowel infarction

Chronic mesenteric ischemia – constant or episodic hyoperfusion of the small intestine, usually due to atherosclerosis

Acute ischaemia

  1. Acute arterial embolism (AF, MI, Valvular heart disease, endocarditis)
  2. Arterial thrombosis (atherosclerosis, arteritis, aortic aneurysm, dissection)
  3. Non-occlusive mesenteric ischaemia (low cardiac output, hypotension, vasopressive drugs , cocaine)
  4. Venous thrombosis (infection, malignancies, Oestrogen therapy, hypercoagulability disorders)

Chronic Ischaemia

  1. iAtherosclerosis
    * Risk factors: HTN, smoking, DM, high cholesterol
80
Q

Which arteries supply the adominal GI tract

A

The splenic flexure and the rectosigmoid junction are at high risk for colonic ischemia because they are “watershed areas”.

81
Q

Clinical features of ischaemic colitis

A
  • Hyperactive phase (80% of patients don’t progress past this phase)
  • Sudden onset of crampy abdominal pain (usually LLQ)
  • Bloody, loose stools
  • Paralytic phase
  • Pain more diffuse
  • Bowel sounds absent
  • Bloating
  • Bloody stools cease
  • Stock phase
  • Acute abdomen with abdominal guarding and rebound tenderness
  • Signs of septic shock

*Classic case – bloody diarrhea and severe abdominal pain after abdominal aortic aneurysm repair

82
Q

Investigations for ischaemic colitis

A

Lab tests

Severe ischaemic colitis

  1. ­lactate (increases in hypoperfusion and decreased aerobic metabolism) ­LDH, ­creatinine kinase
  2. leukocytosis
  3. metabolic acidosis

Imaging

  1. Colonoscopy
  2. CT scan
83
Q

Treatment for ischaemic colitis

A

Mild-moderate

  • Supportive care (IV fluids, bowel rest)
  • Antiplatelet drugs
  • Reduce risk of atherosclerosis

Severe

Surgical intervention – laparotomy or bowel resection

84
Q

What is haemodynamic instability and its signs and symptoms

A

hemodynamic instability will be defined as global or regional perfusion that is not adequate to support normal organ function

Signs and symptoms

  1. Hypotension
  2. Abnormal HR
  3. SOB
  4. Cold extremities, peripheral cyanosis
  5. Decreased urine output
  6. Alternative consciousness
  7. Chest pain
85
Q

Causes of Bowel obstruction

A

Mechanical Bowel Obstruction

Small bowel obstruction

  • Adhesions (post-operative, prior abdominal surgery)
  • Incarcerated hernia
  • Malignant tumours or metastases
  • Strictures (Crohn’s Disease, congenital, radiation, enteritis)
  • Foreign body
  • Superior mesenteric artery syndrome (SMA passes in close proximity anterior to the third segment of the duodenum à duodenum compressed between SMA and aorta)
  • In children – pyloric stenosis, congenital intestinal atresia, intussusception

Large bowel obstruction

  • Malignant tumours
  • Strictures (diverticulitis, IBD, congenital)
  • Volvulus
  • Adhesions (post-operative, prior abdominal surgery)
  • Infective mass (TB, appendiceal mucocele)
  • Fecal impaction

Paralytic ileus

  • Intra-abdominal surgery or trauma (e.g. laparotomy, retroperitoneal haemorrhage)
  • Endocrine (DM, hypothyroidism, porphyria, uraemia)
  • Electrolyte disturbances (hypokalaemia)
  • Neurosurgical procedures e.g. spinal surgery
  • Vascular (mesenteric infarct)
  • Inflammation of intra-abdominal organs (appendicitis, cholecystitis) and peritonitis
  • Medication (anticholinergics, opioids, antidepressants
86
Q

Clinical features of bowel obstruction

A
  • Nausea and vomiting
  • Dehydration, possible fever
  • Constipation with abdominal distention
  • Abdominal pain and discomfort – vague or periumbilical cramping, colicky pain
  • Persistent, focal pain usually implies bowel necrosis
  • Sudden acute pain, followed by temporary pain relief indicates bowel perforation

Auscultation

  1. Mechanical bowel obstruction - increased high pitched, tinkling bowel sounds
  2. Paralytic ileus - absent bowel sounds
87
Q

Investigations for bowel obstruction

A

Imaging

  1. Abdominal X-ray
  • SBO/ LBO: dilated loops of small or large bowel, air-fluid levels proximal to the obstruction, distal bowel collapse, minimal gas in colon
  • LBO: air-fluid levels in the colon, bowel distention before obstruction
  • Paralytic ileus: uniform distribution of gas in the small bowel, colon and rectum
  • Bowel perforation: free air in abdomen
  1. CT abdomen with IV and oral contract
  2. Abdominal U/S
  3. Barium or gastrografin enema

Lab tests

  1. FBC – leukocytosis (indicates ischaemia or necrosis)
  2. Blood gas analysis (metabolic alkalosis due to severe vomiting, metabolic acidosis if ischaemia or sepsis)
  3. Inflammatory markers - ­ in paralytic ileus
  4. Coagulation profile – pathological in sepsis
88
Q

Treatment of bowel obstruction (Mechanical and paralytic)

A

Mechanical Obstruction

Conservative (partial obstruction, no signs of ischaemia, or necrosis or clinical deterioration

  • Fluid resuscitation, electrolyte correction
  • Nasogastric tube
  • Bowel rest
  • Antibiotics (suspected bowel perforation, prophylaxis for surgery)

Surgical

  • Surgical bowel decompression (removal of adhesions, bowel resection, stenting for tumours, herniotomy)

Paralytic ileus

  • Conservative treatment
  • Specific to underlying condition e.g. reducing postoperative opioid use
  • Possible surgical management
89
Q

What are three benign liver tumours

A
  1. Hepatocellular adenoma (rare)
  • Young women on oral contraception or anabolic steroid use
  • Complications – rupture or progression to HCC
  1. Hepatic Haemangioma
    * Composed of endothelium-lined blood-filled sinuses. More common in women between 30-50 years.
  2. Bile duct adenoma
90
Q

Most common malignant tumours of the liver

A
  1. Metastatic
  2. Hepatocellular carcinoma
  3. cholangiocarcinoma
  4. hepatoblastoma
91
Q

Aetiology and investigation for diagnosis of hepatocellular carcinoma

A

Epidemiology

  • Highest incidence in asia
  • Higher incidence in countries with high HBV and HCV

Aetiology

  • HBV, HCV
  • Food contamination by alfatoxins
  • Hemochromatosis

Investigations

  • Core needly biopsy
92
Q

Three stages of alcoholic liver disease

A
  • fatty liver (steatosis)
  • alcoholic hepatitis (inflammation and necrosis)
  • alcoholic liver cirrhosis
93
Q

symptoms of alcoholic liver disease

A
  • Abdominal pain
  • Hepatomegaly
  • Ascites
  • Weight gain/ loss
  • Malnutrition and wasting
  • Anorexia
  • Fatigue
  • Splenomegaly
  • Jaundice
  • Palmar erythema
  • Asterixis
  • Hematemesis and melena
94
Q

Investigations of alcoholic liver disease

A
  1. LFTs – elevated AST and ALT, normal or elevated ALP
  2. GGT increased in ETOH
  3. Serum ferritin - increased
  4. Elevated bilirubin
  5. FBC – macrocytic anemia, leukocytosis, thrombocytopenia
  6. Urea – decreased due to muscle wasting
  7. Electrolyte disturbances
  8. U/S – mild hepatomegaly
95
Q

Treatment of alcoholic liver disease

A
  • Alcohol abstinence
  • Weight reduction
  • Nutritional supplement
  • Immunizations
  • 2nd line liver transplant
96
Q

Causes of acute hepatitis and acute liver failure

A

Heptatitis for < 6 months

  • Viral
    • Hep A, E, (majority) and B, C, D 

    • In immunosuppressed/ transplant – CMV, EBV, HSV 

  • Other infections – toxoplasma, Q fever, Leptospirosis, Brucellosis 

  • Alcohol 

  • Drugs – paracetamol 

  • Toxins – mushrooms, carbon tetrachloride 

  • Ischaemia (double blood supply so hard) 

  • Pregnancy 

  • Autoimmune conditions 

  • Metabolic – Wilson’s disease 

97
Q

causes of chronic hepatitis and cirrhosis

A
  • Viral–Hep B,C, D
  • Alcohol
  • Drugs – methotrexate, amiodarone, isoniazid
  • Autoimmune hepatitis (AIH) 

  • Biliary
    • Primary biliary cirrhosis (PBC) 

    • Primary sclerosing cholangitis (PSC) 

    • biliary obstruction (gallstone, stricture)
  • Metabolic
    • Alpha-1-antitrypsin deficiency 

    • Hereditary haemochromatosis 

    • Wilson’s disease 

    • NAFLD (Non-alcoholic fatty liver disease) 

98
Q

Serology levels for acute and chronic Hep B infections

A
  • HBsAg and resulting HBsAb
  • HBcAg (not present in blood), resulting ABcAb in blood
  • HBeAg and resulting HBeAb
99
Q

Flow diagram of Hep B serology - what would you expect to find in blood results for someone vaccinated for Hep B

A
100
Q

What are the 4 stages of hepatitis B

A
101
Q

Treatment of Hep B

A

Aim of treatment is to suppress HBV to improve diagnosis.

  • HBeAg seroconversion to HBeAb antibody
  • Reduce HBV DNA below detectable elvels
  • Settling of liver inflammation (raised ALT)
  1. Nucleosides and Nucleotides analogue – e.g. (Lamivudine, Tenofovir, Entacavir)
    OR
  2. Interferon – blocks viral mRNA synthesis, many side effects

Also stop ETOH consumption and caution with sexual contacts.

102
Q

How is hep A, B and C transmitted

A

Hep A - faecal-oral

Hep B and C

  • Parenteral (blood exposure) – IDVU, tattoos, transfusion
  • Vertically – 3-5% risk from HCV RNA +ve mothers
  • Sexual – very low risk, higher with anal intercourse
  • Developing countries – medical practices
103
Q

Complications of HCV

A
104
Q

Investigations for Hep C

A
  1. HCV antibody
    * Indicate infection at some point, takes 7-8 weeks to seroconvert
  2. PCR (HCV RNA)
  • Defines active infection, becomes positive within 1-2 weeks
  • Used to monitor treatment success (Sustained viralogical response = PCR –ve 3/12 after Tx)
  • Persistence past 6/12 indicates chronic infection
  1. ALT
105
Q

Treatment for Hep C

A
  • 12 weeks of oral medication with a 90% SVR success rate

Sofosbuvir (polymerase inhibitor) + Ledipasivir (asembly inhibitor) combination

106
Q

What is hep D

A

Defective RNA virus. Can only be effective if there is also HBsAg present.

Diagnose using serology - IgM and IgG

Nil Vaccine

107
Q

Which viral hepatitis’ have vaccines, and which hepatitis’ are chronic

A

Vaccine for A and B

Chronic are B,C D

108
Q

Investigations in liver failure and what you’d expect to see from them

A
  1. LFTs (LFTs do not correspond to the degree of hepatocellular damage)
  • AST and ALT increase with hepatocellular damage
  • Albumin
  • GGT increased in ETOH
  1. Serum bilirubin
    * Raised à jaundice
  2. Serum albumin
    * Reduced and associated with ascites
  3. Coagulation profile
    * Prothrombin time – prolonged as liver produces coagulation factors I, II, V, VII, VIII, IX, X, XI, XIII, protein C&S
  4. Platelet count - reduced due to portal HTN with hypersplenism
  5. FBC
  • Portal hypertension – splenic enlargement – thrombocytopenia
  • Liver disease affects EPO leves
  • MCV à alcoholic anaemia
  • WCC decreased due to hypersplenism
  1. Viral serology
    * Hep B and C
  2. Urea
    * Hepatic encephalopathy
  3. VBGs + ABGs
    * Metabolic acidosis
  4. Creatinine
    * Hepato-renal syndrome
  5. Glucose
    * Elevated at liver stores glucose
  6. Abdominal MRI – Increased caudate lobe, smaller islands of regenerating nodules à alcoholic cirrhosis

Liver biopsy - diagnostic for Liver cirrhosis

109
Q

Complications throughout the body of liver failure

A
  • Encephalopathy
  • Coagulopathy
  • Hepatorenal syndrome and renal failure
  • Metabolic derrangements (hyponatraemia, hypoglycaemia, hypokalaemia, metabolic alkalosis)
  • SIRS
  • ascites
  • gastro-oesophageal varices
  • spontaneous bacterial peritonitis
  • hypogonadism and feminisation
110
Q

What are the triggers for hepatic encephalopathy

A
  • Deterioration of liver function
  • Infections – spontaneous bacterial peritonitis
  • Gastrointestinal bleeding
  • Constipation
  • Portal vein thrombosis
  • Hypovolaemia/ electrolyte disturbances
  • Renal failure
  • Excessive protein consumption
111
Q

what is hepatic encephalopthy and how does it present clinically

A

Hepatic encephalopathy encompasses a severe spectrum of neuropsychiatric abnormalities in patients with severe liver dysfunction.

Caused by elevated blood ammonia levels

Disturbances of consciousness, ranging from mild confusion to coma

Multiple neurological and psychiatric disturbances:

  • Asterixis
  • Fetor hepaticus
  • Fatigue, lethargy, apathy
  • Memory loss
  • Impaired sleeping patterns
  • Irritability
  • Disorientated, socially aberrant behaviour
  • Slurred speech
  • Muscle rigidity
112
Q

What is hepatorenal syndrome

A

Deterioration of kidney function in patients with advanced liver disease. The condition is cause by renal vasoconstriction resulting in hypoperfusion of the kidneys.

Diagnostic criteria

  1. Cirrhosis with ascites
  2. Serum creatinine > 1.5mg/dL
  3. No improvement of serum creatinine after at least 2 days with diuretic withdrawal and volume expansion with albumin
  4. Absence of shock
  5. No current or recent treatment with nephrotoxic drug
  6. Absence of parenchymal kidney disease Protein excretion < 500mg/d, microhaematuria (>50 RBC per high power field)

Treatment

  1. General – improve liver function if possible (stop alcohol consumption)
  2. Pharmacotherapy: combination of midodrine, octreotide, and albumin
  3. Surgical – placement of transjugular intrahepatic portosystemic shunt or liver transplant
113
Q

What are the 4 Main functions of the liver and what symptoms and signs would one get if these functions of the liver failed.

A
  1. Mechanical filter – acts as a sieve to remove particular matter
  2. Portal hypertension due to increasing obstruction of blood flow through liver
  3. abdominal swelling (ascites, splenomegaly, irregular hepatomegaly, portosystemic shunts (bypass liver to systemic), varices (caput medusa), hepatorenal syndrome
  4. haematemesis, malena and oesophageal varices bleeding
  5. Detoxification – removes toxins and metabolites from blood and either breaks them down or excretes them in the bile
  6. Nitrogen - encephalopathy – mental confusion, asterixis, fetor hepaticus
  7. Bile (hyperbilrubinaemia) – jaundice, itch
  8. Oestrogen – gynecomastia, hypogonadism, spider naevi
  9. Digestion – metabolises nutrients, produces bile which aids in digestion of fats in gut
  10. Decreased bile excretion - diarrhoea, steatorrhoea, malabsorption of fat soluble vitamins
  11. Decreased metabolism – LOA, LOW
  12. Protein manufacture
  13. Decreased albumin production – ascites, peripheral oedema
  14. Decreased clotting factor production – coagulopathy and bruising
114
Q

what is liver cirrhosis

A

Cirrhosis is a diffuse pathological process, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules, separated by a fibrous septum. It can arise from a variety of causes and is the final stage of any chronic liver disease. It leads to portal hypertension, liver insufficiency, and hepatic failure, in general, it is considered to be irreversible in its advanced stages.

115
Q

What is diverticulosis andits symptoms

A

Chronic constipation and increasing weakness of CT due to age –> protrusion of herniated intestinal mucosa and submucosa through gaps in the muscular layer of the intestinal wall

Symptoms

  • Mostly asymptomatic
  • Most common cause of lower GI bleeding in adults
  • Can present with abdominal pain in patients with chronic constipation
116
Q

What is diverticulitis and how does it present

A

Stool gets lodged in diverticula à obstruction of intestinal lumen à increased intraluminal pressure and erosion of diverticula wall à inflammation

Symptoms:

  • Low grade fever
  • Sigmoid colon most commonly affected - LLQ pain
  • Possible tender, palpable mass
  • Change in bowel habits (50% constipation, 25-35% diarrhea)
  • Nausea and vomiting; caused by bowel obstruction or ileus
  • ­ urinary urgency and frequency (15%)
  • acute abdomen –> perforation +/- peritonitis
117
Q

Investigations for diverticulitis

A

Lab tests

Blood tests

  • Leukocytosis
  • decreased Hb (bleeding)
  • CRP ­

Stool test – rule out pathogens in diarrhea

Imaging

  • 1st line à Abdominal CT with oral and IV contrast
  • Abdominal U/S

Colonoscopy

  • Not indicated during an acute episode à increased risk of perforation and exacerbating diverticulitis
  • Performed once inflammation has subsided (6 weeks) to assess extent of diverticulitis and rule out malignancy
118
Q

Treatment of diverticulitis

A

Conservative management

  • IV fluids and bowel rest
  • broad spectrum antibiotics e.g. tazocin
  • Analgesia - moephine, paracetamol

Surgical management

If complicated with say an abscess

  • CT-guided percutenous abscess drain

If complicated by peritonitis, sepsis, intestinal obstruction

  • resection of affected segment

If reccurent disease unresponsive to antibiotics, patient can have elective

  • resection of affected segment
119
Q

What are colonic polys and their substypes

A

Colonic polyps are abnormal colonic mucosal overgrowths. Subtypes based on histology:

Low malignant potential

  • Hamartomatous polyps (Increased risk of malignancies)
    • Juvenile polyposis syndrome
    • Peutz-Jeghers syndrome
    • Cowden syndrome
  • Inflammatory polyps (Seen in Ulcerative colitis)
  • Mucosal polyps
  • Submucosal polyps

Moderate malignant potential

  • Serrated polyps
    • Hyperplastic polyps (minimal risk of mal)
    • Sessile serrated polyps (risk of mal 5%)
    • Traditional serrated adenome (risk 5%)

High malignangt potential

  • tubular adenoma (<5% mal risk)
  • Tubulovillous (20% mal)
  • Villous adenoma (50% risk)
120
Q

What is familail adenamatous polyposis (FAP)

A
  • Mutation of tumour suppressor gene APC (Autosomal Dominant)
  • <1% of colorectal cancers, but lifetime risk of colorectal cancer is 100% at age 45
  • Diagnosis: > 100 polyps in the entire Gi tract, particularly colon
  • Screening beginning at 10yo
  • Tx – prophylactic proctocolectomy + ileoanal anastomosis at time of diagnosis
121
Q

What is pyloric stenosis

A

Hypertrophic pyloric stenosis – the most common cause of gastric outlet obstruction in infants – is characterised by hypertrophy and hyperplasia of the pyloric sphincter in the first months of life.

Symptoms

  • frequent regurtitation
  • olive-shape palpable in epigastrum
  • peristaltic wave in epigastrum
  • hungry vomiters

Investigating

  • U/S

Tx

  • IV rehydration, correct electrolytes
  • Frequent small meals, elevate head
  • Surgery - pyloromyotomy
122
Q

What is Barret’s oesophagus

A

Metaplasia – change from the specified squamous epithelium of the tubular oesophagus to specialized intestinal type glandular mucosa with mucin secreting goblet cells

symptoms

  • Heartburn, cough, reflux symptoms

complications

  • adenocarcinoma
  • squamous cell carcinoma

Treatment

  • PPI and surveillance
123
Q

What is achalasia

A

Achalasia is a failure of the lower oesophageal sphincter to relax that is caused by the degeneration of inhibitory neurons within the oesophageal wall.

Clinical features:

  • Dysphagia to solids and liquids
  • Regurgitation
  • Retrosternal pain and cramps
  • Weight loss

Investigations

  1. Endoscopy – to rule out pseudoachalasia (usually normal)
  2. Barium oesophagram
  3. Oesophageal manometry (confirmatory test)
  • Lack of peristalsis in the lower two thirds of oesophagus
  • Incomplete or absent relaxation of LES
  • No evidence of mechanical obstruction
  1. CXR
  • Widened mediastinum
  • Air-fluid level on lateral view
  • Possible absence of gastric air bubble

Treatment

Surgery

  • Pneumatic dilation – endoscope-guided graded dilation of the LEW that tears the surrounding muscle fibres with the help of a balloon
  • LES myotomy (heller myotomy)
124
Q

Causes of Pancreatic Cancer

A

Pancreatic adenocarcinoma (pancreatic duct carcinoma)

  • Precursor lesions include:
  • MCN and IPMN
  • Pancreatic intraepithelial neoplasm dysplasia of pancreatic duct
  • Aetiology
  • Old age
  • Smoking
  • Diabetes
  • Precursor lesion
  • FHx
  • Chronic pancreatitis
  • Molecular carcinogens
  • K-ras, G-nas, P53, SMAD4, HER2
  • Poor prognosis, direct infiltration

Acinar cell carcinoma

125
Q

Clinical features of pancreatic cancer

A
  • Belt-shaped epigastric pain which radiate to the back
  • Jaundice
  • Courvoiseier sign: enlarged gallbladder and painless jaundice
  • Pale stools, dark urine, and pruritis
  • Weight loss, nausea, weakness, poor apetite
  • Diarrhea (possible steatorrhea secondary to exocrine pancreatic insufficiency)
  • Superficial thrombophlebitis
  • Thrombosis
  • Impaired glucose tolerance (rare)
126
Q

investigations for pancreatic cancer

A

Lab tests

  • Tumour markers – CEA, CA 19-9
  • Lipase ­

Imaging

  • First test: usually contrast-enhanced abdominal CT or U/S
  • Endoscopic retrograde cholangiopancreatography
127
Q

4 types of gastric cancers

A
  1. Gastrointestinal stromal tumours (associated with KIT mutation)
  2. MALT (mucosal asssociated lymphoid tissue) [related to H. pylori]
  3. Neuroendocrine (carcinoid)
  4. Hereditary Diffuse Gastric Carcinoma
128
Q

Two types of hiatal hernia and their differences

A

Sliding Hernia

  • Most common type 

  • Part of the stomach is pulled up above the diaphragm forming a cell shaped dilated 
segment 

  • This is due to congenitally short oesophagus 

  • Or due to a secondary defect like scaring of the oesophagus following chronic injury 


Rolling Hernia (Paraoesophageal hernia) 


  • Portion of the cardiac end of the stomach pushes through the diaphragm rolling up alongside the oesophagus 

  • This is usually small and the lower end of the oesophagus is normally placed 

  • Less than 10% of hernias are this type 

129
Q

symptoms of hiatal hernia

A
  • Epigastric/ substernal pain
  • Early satiety
  • Retching
  • Symptoms of GORD can occur

Saint’s triad: cholelithiasis, diverticulosis, hiatal hernia

130
Q

Investigations and treatment for hiatal hernia

A

Investigations

  • barium swallow
  • endoscopy
  • CXR

treatment

  • surgery
  • PPI
  • lifestyle mod
131
Q

What is oesophageal atresia and its symptoms

A

Congenital defect in which the upper oesophagus is not connected to the lower oesophagus, ending blindly instead. It is caused by the abnormal development of the tracheoesophageal septum.

Oesophageal atresia with a fistula connected distally to the trachea is the most common kind of oesophageal malformation. It prevents immediately after birth with cyanotic attacks, foaming at the mouth and coughing and prevents any attempts to pass a feeding tube into the stomach.

Prenatal

  • Polyhydramnios - increased risk of premature birth

Postnatal

  • Oesophageal atresia à pooling of secretions à excessive mouth secretions/ foaming at mouth
  • Transoesophageal fistula
    ​–> If the fistula is connected to the proximal oesophageal segment: aspiration and subsequent aspiration pneumonia
    • Coughing spells
    • Rales
    • Cyanotic attacks

—> if the fistula is connected to the distal oesophageal segment - gastric distention

132
Q

What is Hirschprung’s disease

A

Congenital ananglionic megacolon, is an inherited disorder primarily affecting newborns. The conditions is characterised by an aganglionic colon segment, usually the rectosigmoid region, which fails to relax leading to functional intestinal obstruction.

Early presentation

  • Delayed passage of meconium
  • Distal intestinal obstruction: abdominal distention and bilious vomiting
  • Tight anal sphincter with explosive release of stools and air upon removal of the finger
  • Failure to thrive/ poor feeding
  • Palpation of faeces via the abdominal wall

Late presentation

  • Chronic constipation with possible inability to pass gas
133
Q

What is Kwashiorkor and Marasmus

A

Oedematous malnutrition affecting children, characterised by bilateral pitting oedema in the absence of another medical cause of oedema, generally occurring while receiving a monotonous cereal-based diet.

Marasamic kwashiorkor is the presence of severe wasting in addition to oedema.

Medicine (11 decks)

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