NMDE Flashcards
Epidemiology UC
2-10 per 100,000 Increased in females Increased in Caucasians Bimodal peaks 15-25 and 55-65 FHx component
Decreased in smokers
Symptoms & signs of UC
relapsing and remitting in nature Diarrhoea PR bleeding Frequency of stools, associated with urgency Fatigue and malaise Fever Mucus discharge
Tachycardia
Fever
Abdominal tenderness
Disease features of UC
Only affects the colon, always affects the rectum Inflammation limited to the mucosa Mucosal atrophy, walls appear thin Ulcers are superficial with a broad base No skin lesions No mural thickening, no strictures, no fistulas No malabsorption Malignant potential No recurrence post-op
Pathophysiology of UC
Defects in host interaction with intestinal bacteria
Intestinal epithelial dysfunction
Inappropriate mucosal immune responses
TH17 and TH2 are increasingly active
Defects in epithelial tight junctions increased passage of bacteria to cause a reaction
Increased cytokine activity
No specific gene.
Investigations for UC
FBC - anaemia or thrombocytosis
LFTs - raised ALP, hypoalbuminaemia, hypokalaemia, hypomagnesaemia
Raised ESR and CRP
Test iron, B12, folate
Foetal calprotectin, usually used for monitoring.
Stool samples for infection,
ANCA positive
Colonoscopy/sigmoidoscopy + biopsy - abnormal erythematous mucosa with ulceration - biopsy for confirmation
Abdominal X-ray to check for perforation.
Double contrast barium enema - lead piping
Foetal calprotectin, usually used for monitoring
Can use CT enterography
Measuring severity of UC
Using Truelove & Witt’s severity index
MILD - diarrhoea <4 times /day, no anaemia, no fever, no tachycardia, no weight loss
MODERATE - diarrhoea 4/5 times per day, Small amount of blood in stool, no fever, no tachycardia, raised CRP (mild)
SEVERE - diarrhoea 6+ times a day, blood in stool, fever, tachycardia, anaemia, raised CRP
Extracolonic manifestations of UC
Uveitis Pleuritis Erythema nodosum Ankylosing spondylitis Pyoderma gangrenosum
Primary sclerosing cholangitis
MS
Management of UC - inducing remission
- Amniosalicylates - mesalazine
- Corticosteroids - oral prednisolone
- Immunomodulators - azathioprine, methotrexate, ciclosporin
- Mabs - Infliximab in severe cases
- Surgery
Complications of UC
Bleeding
Toxic megacolon
Increased risk of colon cancer
Perforation
Epidemiology of Crohn’s
1-6 per 100,000 Increased in females Increased in Caucasians Bimodal age peak 15-25 and 55-65 Genetic link - NOD2
Smoking is a big risk factor
Most common in ileocaecal
Symptoms of Crohn’s
Diarrhoea PR bleeding Abdominal pain Weight loss Fatigue Mouth ulcers
Features of Crohn’s
Any part of GI tract Transmural, can form strictures Skip lesions Oedema and loss of mucosal texture Triggered by emotional stresses or smoking Cobblestone appearance Ulcers deep and knife like Fistulas common Fat/vitamin malabsorption Malignant potential if in colon Recurrence post-op is common
40% ileocecal, 30% small intestine, 25% colon
Pathophysiology of Crohn’
Defects in host interaction with intestinal bacteria
Intestinal epithelial dysfunction
Inappropriate mucosal immune responses
TH17 and TH2 are increasingly active
Defects in epithelial tight junctions increased passage of bacteria to cause a reaction
Increased cytokine activity
NOD 2 gene
Investigations in Crohn’s
FBC - anaemia
Raised CRP
Nutrient deficiency, B12, folate
LFTs hypoalbuminaemia
Stool culture for C.diff
ASCA (not ANCA as in UC)
Endoscopy - ileocolonoscopy + biopsies, occasionally OGD
Abdominal X-ray for perforation
Small bowel follow through - cobblestone appearance
Can have CT enterography
Management of Crohn’s - inducing remission
- Steroid - prednisolone
- Aminosallicylate - mesalazine
- Azathioprine / mercaptopurine
- Methotrexate
- Infiximab or adalimumab
Surgery is last line
Management of Crohn’s - maintenance
Azathioprine or mercaptopurine
Extraintestinal features of Crohn’s
Uveitis Migrating polyarthritis Ankylosing spondylitis Clubbing Pyoderma gangrenosum (greater incidence than in UC) Erythema nodosum Aphthous ulcers
Classification of Crohn’s disease
Crohn’s disease activity index
<150 remission, 150-300 active, 300+ severe
Depends on number of stools, pain, well being, extra intestinal manifestations, pyrexia, etc.
Harvey Bradshaw Index
<4 = remission, 5-8 moderate, 8+ severe
Complications of Crohn’s
Small bowel obstruction Perianatal fistula/fissure bowel fistula Bowel perforation GI blood loss Cancer
Causes of upper GI bleeding
Gastritis - dyspepsia
Oesophagitis - dyspepsia , worse on lying
Gastric/duodenal ulcer - nausea, vomiting, weight loss, dyspepsia
Oesophageal/gastric varices - Hx of liver disease, alcohol excess
Cancer - malaise, weight loss, vomiting, early satiety
Mallory-Weiss tear = young, history of vomiting, small amounts
Gastric/duodenal erosions = NSAID or alcohol history, epigastric pain
Drugs = aspirin, NSAIDs, steroidsm thrombolytics, anticoagulants
Rare = bleeding disorders, aorto-enteric fistula, Meckel’s diverticulum
Symptoms and Signs of upper GI bleeding
Fresh haematemesis or coffee grounds
Melaena
Medication and alcohol history
Tachycardic and hypotensive
Cap refill may be reduced
Postural BP drop
Anaemia - pallor
Stigmata of liver disease - hepatic flap, caput medusa, ascites, hepatomegaly, spider naevi
Investigations for GI bleeding
FBC - haemoglobin and MCV (if low MCV, may be chronic)
U&E - raised urea to creatinine ratio
LFTs - clotting and signs of chronic liver disease
Upper GI endoscopy - NBM for 4 hours.
Classification of GI bleeds
Rockall risk scoring
- relies on BP, HR, endoscopy
Low risk - 0-1, moderate 2-3, severe 4+
Blatchford score
No endoscopy required
Predicts who needs intervention - 6+ needs intervention
Management of upper GI bleed
Non-variceal
- Resuscitate
- Endoscopy within 4/24 hours, urgent/non-urgent, no routine PPI pre-endoscopy
Variceal
- Resuscitate
- Terlipressin
- Variceal band, ligation/adrenaline injections/ TIPS/ glue
- Balloon tamponade - Sengstaken-Blakemore tube
- antibiotics
Side effects of blood transfusions
Hypothermia as products stored at fridge temperature
Hypocalcaemia - blood contains citrate which chelates calcium
Hyperkalaemia
Causes of lower GI bleeding visible
Haemorrhoids Fissures Carcinoma Polyps Proctitis Diverticular disease IBD Angiodysplasia Infection - E.coli, shigella, salmonella, campylobacter
Investigations for lower GI bleeding visible
FBC U&Es Clotting LFTs Colonoscopy or flexi sig Rectal exam Stool cultures
Causes of occult GI bleeding
Coeliac disease Gastric cancer Peptic ulcer disease Colorectal cancer IBD
Management of occult GI bleeding
Treat underlying cause
Replace iron stores if deficient
Check blood count after 1 month to see if it improves
Signs, symptoms and deficiency states for fat soluble vitamins
A
- Night blindness
D
- Osteomalacia
- Proximal limb weakness
E
- Anaemia
K
- Clotting deficiency
- Bruising
Signs, symptoms and deficiency state for vitamins B6, B12, C and folate
B6
- Dermtitis, anaemia
B12
- Pernicious anaemis
- Tired/fatigue/pale/peripheral neuropathy
Folate
- megaloblastic anaemia
- tired.fatigue.pale
C
- Scurvy
- bruising, gingivitis
Reasons for malnutrition in hospitals
Secondary to pathological disease - raised metabolic demand
Neglect - by patient or staff
NBM
Who should receive nutritional support in hospitals
Consider in all
- BMI < 18.5
- Unintentional weight loss >10% in 3-6 months
- BMI < 20 and unintentional weight loss >5% in 3-6 months
- Eaten little or nothing for 5 days and not likely to in next 5 days
- Poor absorptive capacity
Methods of enteral feeding
Oral - supplementation e.g, fortisips
Tube feeding - NG tube if inadequate or unsafe oral intake
Enterostomy feeding - if for over 4-6 weeks
PEG tube - can get perforation, infection or peritonitis
Parenteral feeding
- Only if other routes not suitable e.g. perforated GI tract
If short term can use peripheral cannula <14 days
If not the PICC line
Complicated by thrombophlebitis
Refeeding syndrome
Complication from too rapid reintroduction of feeding following starvation.
Low insulin levels secondary to starving.
When feeding restarted, increased insulin.
Insulin causes cellular uptake of phosphate
Low phosphate causes respiratory/cardiac failure, muscle weakness, seizures, coma
usually occurs in day 4 of refeeding
Which patients are at high risk of refeeding syndrome
BMI < 16
History of alcohol abuse
Little or no intake for 10 days
Low levels of phosphate, potassium or magnesium prior to feed
Unintentional weight loss of >15% in last 3-6 months
Clinical features of malabsorption
Diarrhoea Steatorrhoea Weight loss Fatigue Flatulence and abdominal distension Oedema from hypoalbuminaemia Bleeding disorders (vit K) Metabolic defects in bones Neurological manifestation (low Ca, Mg - tetany)
Orthostatic hypotension Decreased subcut fat Signs of muscle loss or wasting Hyperactive bowel sounds Ascites Pallor Peripheral oedema Glossitis
Causes of hypochromic microcytic anaemia
Iron deficiency anaemia - blood loss, increased demand (growth and pregnancy), decreased absorption (post-gastrectomy, Crohn’s), poor intake
Thalassaemia
Anaemia of chronic disease
Sideroblastic anaemia
Causes of normocytic normochromic anaemia
Acute blood loss CKD Anaemia of chronic disase Autoimmune rheumatic disease Endocrine disease Marrow infiltration Haemolytic anaemia
Causes of macrocytic anaemia (megaloblastic)
Vitamin B12 or folate deficiency
B12 - gastrectomy, ileal disease, resection
Folate - alcohol, coealiac, Crohn’s, partial gastrectomy, cancer, drugs
Clinical features of anaemia
Fatigue headache angina, breathlessness pallor palpitations tachycardia
Epidemiology of coeliac disease
Increased in females (2 to 1)
Age peaks in early childhood and again 40-50
1-2% prevalence
FHx - HLA DQ2
RF - other autoimmune disease
Signs and symptoms of coeliac disease
Tiredness, malaise GI symptoms may be absent or mild Diarrhoea or steatorrhoea Abdominal pain diffuse Weight loss
Mouth ulcers
Angular stomitis
Anaemia/pallor
Dermatitis herpetiformis
Subgroups of coeliac disease
Classic - 50%
Typical symptoms
Atypical
Lacks GI symptoms but presents with deficiency state or extra intestinal features
Silent - 20%
No signs of symptoms
Non-responsive
Refractory - 1%
Pathophysiology of coeliac disease
Proteins in wheat, barley, rye are broken down by tissue transglutaminase into GLIADIN
Gliadin then presents to T cells via HLA class 2 DQ2 and DQ8
T cells produce inflammatory cytokines
Over expression of IL 15
Investigations for coeliac disease
IgA anti-tissue transglutaminase antibodies - highly specific and sensitive. They become undetectable after 6 months of a gluten free diet
FBC - microcytic anaemia from iron deficiency
Howell-Jollie bodies (leukocytes)
LFTs - raised transaminases
Small bowel biopsy is gold standard - need to still be consuming gluten
Treatment of coeliac disease
GLUTEN FREE DIET!
NHS can subsidise gluten free products
Recommended to have 5 yearly pneumococcal vaccinations
Hernias - most to least common
Inguinal (indirect or direct) Femoral Umbilical and parumbilical Incisional Ventral and epigastric
Types of hernias:
reducible/irreducible/strangulation
Reducible - contents replaced completely back into peritoneal cavity
Lump disappears lying down, not painful
Cough impulse
Irreducible Adhesions to sac wall mass larger than neck not reducible Cough impulse
Strangulation
Contents restricted by neck so circulation is cut off - gangrene inevitable
Severe pain, central, colicky
vomiting, distension, constipation (from obstruction)
Tender,tense
No cough impulse
Noisy bowel sounds
Hernias most likely to strangulate
- Femoral
- Indirect inguinal
- Umbilical
Indirect inguinal hernia
Pass through internal ring Lateral to inferior epigastric vessels May be congenital Can be controlled by pressure over internal ring Commonly strangulates due to narrow neck Often extends to scrotum Does not readily reduce on lying
Hernia does not reach full size until the patient has been up for some time, does not reduce on lying
Direct inguinal hernia
Pass through posterior wall of inguinal canal
MEDIAL to inferior epigastric vessels
Always acquired
Not controlled by pressure over internal ring
Rarely strangulate due to wide neck
Reduces spontaneous on lying
Borders of the inguinal canal
Anterior - skin, external oblique aponeurosis
Posterior - conjoint tendon forms posterior well medially, transversalis fascia laterally
Above - internal oblique and transversus abdominis
Below - inguinal ligament
Describe a femoral hernia
passes through the femoral canal
Medial to the femoral sheath
Femoral sheath contains the femoral artery and vein
Occurs more commonly in women Usually seen in elderly and middle aged Non-strangulated swelling, BELOW and LATERAL to pubic tubercle Enlarges on standing and coughing Disappears on lying down
STRAGULATION COMMON due to narrow neck`
Exomphalos
Rare condition
Failure of all or part of midgut to return to abdominal cavity in foetal life
Presentation of congenital diaphragmatic hernias
Different types
In more serious cases - present as respiratory distress shortly after birth and require urgent surgery
Others e.g. large oesophageal hiatus = present as regurgitation, vomiting, dysphagia and progressive weight loss in the child
Types of acquired hiatus hernia
Sliding (90%)
stomach slides through hiatus and is covered anteriorly with peritoneal sac, posterior = extraperitoneal.
It disturbs cardio-oesophageal mechanism and produces the effect of a space occupying lesion
Rolling (10%)
Cardia remains in position, stomach rolls up anteriorly through volvulus - partial volvulus. No symptoms of regurgitation.
Represents progressive weakening of hiatus muscles.
Occur in obese, middle aged and elderly. 4x more common in women
Presentation of acquired hiatus hernia
cough dyspnoea palpitations hiccough burning retrosternal pain worse on lying and swooping occult bleeding from oesophagitis
Treatment of hiatus hernia
Treat symptomatically
If not controlled then laparoscopic repair
Epidemiology of colon cancer
50 per 100,000 3rd most common malignancy Increases with age More common in men FHx is associated especially regarding HNPCC, FAP
RFs UC or Crohn's Pelvic radiotherapy Smoking Alcohol Obesity Sedentary lifestyle High red meat in diet Type 2 diabetes aspirin/NSAIDs Cholecystectomy Low fibre diet
Signs and symptoms of colon cancer
Dependent on site of cancer
Left - fresh rectal bleeding, early obstruction, tenesmus, mucus (if rectal), early change in bowel habit, mass in LIF
Right - anaemia from occult bleeding, altered bowel habit (alternating diarrhoea and constipation), mass in RIF
Colicky pain Weight loss Can present with obstruction or perforation SOB/fatigue (from anaemia) Hepatomegaly/ascites if mets Signs of peritonitis
Signs of peritonitis
Rock hard abdomen
rebound tenderness
absent bowel sounds
most common places for bowel cancer
45% rectosigmoid
30% ascending colon
15% descending colon
10% transverse colon
Pathophysiology of colon cancer
Malignant transformation of benign adenomatous polyp
Accumulation of multiple genetic mutations
APC gene
K-ras gene - failure leads to cell proliferation
DCC gene - has a role in invasion and metastasis
p533 gene - role in impaired apoptosis and cell proliferation
HNPCC
Hereditary non-polyposis colon carcinoma
Also known as Lynch syndrome
Occurs at a young age with family history
- autosomal dominant
Mean age 45, lifetime risk 80%
It is the most hereditary syndrome
Majority occur proximally
Increased risk of other cancers: endometrium, ovary, urinary tract, stomach, small intestine, pancreas, CNS
Regular colonoscopy every 1-2 years from 25
Criteria for diagnosis - 3+ relatives with colon cancer (1 must be 1st degree, must be across 2 generations) & 1 family member affected under 50, FAP excluded
FAP
Familial adenomatous polyposis
Hereditary disorder causing numerous polyps and resulting in colon carcinoma before 40
Autosomal dominant
Patients usually asymptomatic
Diagnosis by colonoscopy (100+ polylps) and genetic testing (APC gene)
Treated with colectomy
Polyps present in 50% by 15 and 95% by 35
Extra intestinal manifestations:
- osteoma of skull/mandible
- sebaceous cysts
- increase in cancer: small intestine, pancreas, thyroid, brain, liver and gastric cancer
Treatment of colon cancer
surgery - without metastatic disease. Tumour + resection margins+ pericolic lymph nodes removed
May reanastamose or stoma
Adjuvant therapy =
if lymph spread it can’t be controlled with surgery alone
Chemotherapy with 5-FU or carbecitabine or irinotecan
Investigations for colon cancer
FBC - anaemia
LFTs - for mets
Colonoscopy for diagnosis + biopsy (GOLD STANDARD)
CT colongraphy
CT or MRI and liver US for staging
PET for recurrent but not initial cancer
CEA is raised in colon cancer but is not useful for screening. Good prognostic factor, better outcome if CEA negative,
Screening for colon cancer
Faecal occult blood
Every 2 years after 60
When to refer for suspected bowel cancer?
> 40 + rectal bleeding + loose stools for over 6 weeks
> 60 with rectal bleeding OR loose stools >6 weeks regardless of other symptoms
If right lower abdominal mass consistent with large bowel
Palpable rectal mass (NOT pelvic - urology or gynae referral)
Men with unexplained iron deficiency anaemia <11
Non-menstruating women with unexplained iron deficiency anaemia <10
Staging for bowel cancer
Dukes A - tumour confined to bowel (10%) B - extension through bowel wall (35%) C - tumour involving lymph nodes (30%) D - distant mets (25%)
Or can use TNM
T - 1 submuscosa, 2 muscularis propria, 3 pericolorectal tissues, 4A surface of visceral peritoneum, 4B directly invades
Symptoms of peritonitis
Abdominal pain ** Localised pain if contained, generalised after rupture Anorexia Nausea Vomiting Fever and chills Diarrhoea
Signs of peritonitis
High fever in early stages
Rebound tenderness
Absent bowel sounds
Rock hard abdomen
Guarding and rigid abdomen
Hypotensive
Signs of septic shock
DRE increases abdominal pain
Aetiology of primary peritonitis
Spontaneous bacterial peritonitis is acute bacterial of infection of ascitgic fluid resulting from translocation ofbacteria across gut wall
Complications of ascites
90% is mono-microbial
40% E.coli, 7% Klebsiella pneumonia, 15% strep 30%
Predominantly gram negative
Aetiology of secondary peritonitis
Pathogens depend on location in GI tract
Mainly gram positive in upper HI tract
Colon perforation generally multi-microbial and predominantly gram negative
All caused by perforation
Causes of peritonitis
Malignancy Penetrating trauma Ulcer perforation Stone perforation Iscahemic bowel Bowel obstruction Crohn's Appendicitis Post-operative Peritoneal dialysis Pancreatitis
Investigations for peritonitis
FBC - raised WBC, CRP
LFTs, amylase and lipase for pancreatitis
Blood cultures - sepsis
Peritoneal fluid for culture
Urinalysis to rule out urinary tract pathology
Abdominal x=ray
CT/MRI
Treatment for peritonitis
Correction of underlying pathology
Systemic antibiotics
Supportive therapy to prevent organ system failure
Antibiotics are dependent on the cause - usually 3rd generation cephalosporin
Haemodynamic, pulmonary and renal support = fluid resuscitation, monitor renal function, blood gases, urine output, BP, HR
Nutrition support - high requirement in sepsis
Surgery to correct pathology
Describe pain coming from fore, mid and hindgut
Foregut = stomach, duodenum, liver, pancreas. Pain described as upper abdominal pain.
Midgut = small bowel, proximal colon and appendix. Pain felt in umbilicus
Hindgut = distal colon and genito-urinary tract. Lower abdominal pain
Causes of diffuse abdominal pain
Pancreatitis Diabetic ketoacidosis Early appendicitis Gastroenteritis Intestinal obstruction Mesenteric ischaemia Peritonitis Sickle cell anaemia crisis Spontaneous bacteria peritonitis Typhoid fever
Red flags for abdominal pain
Severe pain Tachycardia Hypotension Confusion Signs of peritonitis Abdominal distension
Causes of RUQ pain
Appedicitis with gravid uterus Cholecystitis Biliary colic Congestive hepatomegaly Hepatitis Perforated duodenal ulcer
Causes of RLQ pain
Appendicitis
Caecal diverticulitis
Merkel diverticulitis
Mesenteric adenitis
Causes of lower abdominal pain - R or L
Abdominal or psoas abscess Abdominal wall haematoma Cystitis Endometriosis Strangulated hernia IBD PID Renal stone Ruptured AAA Ectopic pregnancy Ovarian cyst torsion
Define diarrhoea
Passage of >200g of stool per day
Can be acute or chronic
Categories of diarrhoea
OSMOTIC
- when unabsorbable water solutes remain in the bowel and retain water
- Stops with fasting
- Examples: sorbitol, malabsorption causing high concentration in lumen, absorptive defect e.g. lactase deficiency
SECRETORY
- Bowel secretes more electrolytes and water
- Persists with fasting
- Causes: infection, malabsorption. drugs (colchicine, quinine), endocrine tumours
- Enterotoxins cause block of Na/H+ exchange or absorption of Cl-
INFLAMMATORY
- reduced surface area or contact time
- Causes: bowel resection, IBD, Coeliac, shigella
Causes of acute diarrhoea
Likely to be infective
bacteria: salmonella, campylobacter, shigella, E.coli, C. Diff. bacillus cereus
viral: norovirus, rotavirus, CMV, hep A
parasite: giardia,
Drugs: antibiotics, cytotoxic drugs, PPIs, NSAIDs
Ask about recent travel abroad
Causes of chronic diarrhoea
IBS IBD Bowel resection Coeliac disease Pancreatic insufficiency Lactose intolerance Colon cancer Lymphoma Hyperthyroidism Diabetes
Red flags for diarrhoea
Blood Pus Fever Signs of dehydration Chronic Weight loss
Management of acute diarrhoea
- Enquire about red flag symptoms
- Assess for dehydration
- Offer Oral rehydration therapy - 100ml per episode. if sever then IV 5% dextrose
- Stool cultures
- Faecal examinati0on for parasites and ova
- Faecal alpha 1 antitrypsin levels - high in entroinvasive infections
usually self-limiting
Only requires supportive treatment
Causes of constipation
- lack of fibre or fluid intake
- immobility
- old age
- bowel obstruction: volvulus, adhesions, hernia, faecal impaction, strictures
- IBS
- Drugs: opiates, anti-cholinergic, calcium antagonists, iron supplements, anatacids, antipsychotics, antispasmodics, general anaesthetics
- Colon cancer
- Obstruction: strictures, Crohn’s, pelvic mass
- Metabolic/endocrine: hypothyroid, hypercalcaemia, hypokalaemia
- Neuromuscular: spinal or pelvic nerve injury, diabetic neuropathy
- Parkinsonism
- Diabetes
- Pregnancy
- Depression
Red flags for constipation
Distended abdomen Vomiting Blood in stool Weight loss Severe constipation with recent onset or worsening Over 50
Investigations for constipation
Blood tests
FBC, U&E, TFTs, calcium
Blood glucose
Abdominal X-ray for masses or obstruction
PR exam
barium enema or colonoscopy/sigmoidoscopy
Rome III criteria for functional constipation
Functional constipation. must include 2 or more of:
- straining
- lumpy/hard stools
- sensation of incomplete evacuation
- Sense of anorectal obstruction
- Manual manoeuvres
- Less than 3 per week
Each symptom must be present >25%
Bristol Stool Chart
- Separate hard lumps
- Lumpy sausage shape
- Like sausage with cracks
- Sausage, smooth and soft
- Soft blobs with clear cut edges
- Fluffy with ragged edges (mushy)
- Watery, no solid pieces
Management of constipation
INITIAL if no alarm
- Patient education
- High fibre diet
- Increase fluids
- Increase exercise
- Bulk laxatives
- Bulk laxatives e.g. ispaghula husk
- Osmotic or stimulant laxatives
- Refer
Symptoms of IBS
6 month history of either: abdominal pain or discomfort, bloating or change in bowel habit
- Pain improves in defaecation
- Altered passage of stool: straining, urgency, incomplete evacuation
- Abdominal bloating
- Distention
- Symptoms aggravated by eating
- Rectal mucus
- lethargy
- Nausea
- Backache
- Urinary frequency and urgency
- Headaches and migraine
Epidemiology of IBS
10-20% of population
Increased in women (2:1)
Peak between 20-40
RF
Emotional stress
Food poisoning or gastroenteritis
Mental health condition
Criteria for IBS
Rome III Criteria
Recurrent abdominal pain for over 3 months, at least 3 days per month, PLUS 2 or more of:
- Pain improves with defaecation
- Change in stool frequency
- change in stool form
Pathophysiology of IBS
Psychological factors, altered GI motility, altered visceral sensation
7-30% develop IBS following gastroenteritis
Investigations for IBS
FBC, ESR, CRP Coeliac screen CA-125 if ?ovarian cancer Faecal calprotectin if ?IBD Colonoscopy or sigmoidoscopy Refer if any RED FLAGS
Classification for IBS
IBS-C - constipation - loose stool <25%, Hard stools >25%
IBS-M - mixed - both hard and soft stools >25% of the time
IBS-D - diarrheoa - loose stool >25%, hard <25%
Treatment of IBS
Constipation
- high fibre diet, bulk forming laxatives (ispaghula husk) or osmotic (but avoid lactulose)
Diarrhoea
- reduce fibre + loperamide, codeine, colestyramine
Pain and bloating - use spasmolytic drugs e.g. amitryptiline
Treat the symptoms of the patient
CBT, hypnotherapy, psychotherapy
Symptoms of achalasia
Dysphagia Affecting solids more than liquids Regurgitation in 80% Chest pain in 50% - occurs after eating, retrosternal Heartburn is common Weight loss suggests malignancy Nocturnal cough No signs!
Pathophysiology of achalasia
Smooth muscle layer of oesophagus has impaired peristalsis and failure of the sphincter to relac causes functional stenosis or stricture
Most have no underlying cause
Investigations for achalasia
CXR - vastly dilated oesophagus
Barium swallow - usually precedes endoscopy when investigating dysphagia as can perforate malignancy with endoscope.
Birds beak - narrow segment in distal oesophagus.
Endoscopy
Manometry - is GOLD STANDARD - can detect 90% of cases. High resting pressure in cardiac sphincter, incomplete relaxation on swallowing and absent peristalsis
If no radiological evidence - it may be pseudoachalasia
Management of achalasia
Calcium channel blockers and nitrates - reduce pressure in lower sphincter. Only works in 10%
Heller myotomy - divide muscles longitudinally (90% success)
Pneumatic dilation - balloon inflated to rupture muscle, leaving mucosa intact
Enodscopic injection of botulinum but recurs in the majority.
Endoscopic stent insertion
Causes of dysphagia
benign stricture: schataki ring, GORD Malignant stricture: SCC, adenocarcinoma Stroke Achalaisa Parkinson's Motor neurone disease Myasthenia gravis
Epidemiology of oesophageal cancer
13th most common in the UK, 8th most common worldwide
Increased in age - most are over 60
Increased in men
High in East African and Asia
Increasing prevalence of adenocarcinoma, decreasing SCC
RF Adenocarcinoma - Caucasian - Barrett's oesophagus - Obesity
SCC
- Achalasia
- Corrosive strictures
- Coeliac
- African
Both
- Smoking
- Alcohol
- Radiation to area
- Genetics
- Diet (high sat fat)
Symptoms of oesophageal cancer
Dysphagia (initially liquids then solids) Vomiting Anorexia Weight loss Blood loss/ melaena Odynophagia (painful swallowing) Hoarseness Retrosternal or epigastric pain Persistent cough Lymphadenopathy
Types of oesophageal cancer
Adenocarcinoma - more common in lower oesophagus. Mainly progression from Barrett’s oesophagus
Squamous cell carcinoma - can be anywhere along the oesophagus
Investigations for oesophageal cancer
FBC - anaemia
U&Es, LFTs for baseline
CRP - can be raised
Glucose
Urgent endoscopy and biopsy
CXR for mets and spread
Double contrast barium swallow
Staging - FDG PET/CT or MRI
Endoscopic Ultrasound
Prognosis of oesophageal cancer
50% have mets at diagnosis
presents late as 75% of lumen needs to affected around the circumference before difficulties present
20-25% 5 year survival rate
AC and SCC have the same prognosis
Management of oesophageal cancer
Primary = surgery +/- chemo +/- radiotherapy
Surgery
- antibiotic and antithrombotic prophylaxis given
- If early, endoscopic muscosal resection
- If late: oesophagectomy endoscopically if possible
- Abdominal lymphadenectomy is beneficial
- Chemo and radiotherapy shrink tumour prior to resection
Palliative
- Can use chemo/radiotherapy to decrease bulk
- Fit stent to allow swallowing
- PEG for feeding
- ANALGESIA
Epidemiology of GORD
25% of adults, 5% have daily symptoms
More common in men
RFs
- Obesity
- Pregnancy
- Systemic sclerosis
- Drugs: nitrates, TCAs, anticholinergics, calcium channel blockers
- Hiatus hernia
- Increased intra abdominal pressure
- Smoking
- Alcohol
- Large meals
Symptoms of GORD
Heartburn worsened on lying or bending down Retrosternal discomfort Regurgitation Pain on swallowing Nocturnal cough Excessive salivation Chronic hoarseness Acid brash Pain relieved by antacids
No signs
Endoscopic findings in GORD
60-70% have normal endoscopy (non-erosive reflux disease)
20-30% erosive oesophagitis
6-10% Barrett’s oesophagus
Can show basal hyperplasia, inflammation, Goblet cell metaplasia, thinning of squamous layer or dysplasia
Pathophysiology of GORD
Spectrum of disorders from endoscopy negative GORD to oesophageal damage
3 main causes:
- Poor oesophageal motility
- Dysfunction of lower oesophageal sphincter (permanent or intermittent relaxation or increase in abdominal pressure)
- Delayed gastric emptying
Investigations for GORD
FBC to exclude anaemia
H.pylori stool test (stool antigen test)
Endoscopy +/- biopsy (must be drug free for 2 weeks)
Barium swallow
Management of GORD
Assess for possibility of GI bleed
Simple lifestyle advice: healthy eating, weight reduction, smoking cessation.
Avoid precipitants: smoking, alcohol, coffee, chocolate, fatty foods, acidic foods e.g. tomatoes, oranges
Raised head of bed
Avoid eating late at night
If H.pylori positive, treat
Full dose PPI for 4 weeks.
Can offer H2 receptor agonist therapy as alternative.
Antacids as required
If very severe and uncontrollable, can fit magnetic band around LOS to aid closure.
Urgent referral criteria for GORD
Dysphagia Dyspepsia + weight loss/anaemia Dyspepsia new onset in over 55s Dyspepsia plus one of: - FHx of upper GI cancer - Barrett's - Pernicious anaemia - upper abdominal mass - known dysplasia
Complications of GORD
Oesophagitis Ulceration Anaemia Stricture Barrett's oesophagus
What is Barrett’s oesophagus
Premalignant condition
Normal squamous lining is replaced by columnar cells
Adaptive response to GORD
Classification of GORD
Savary-Miller Grading system
- single or multiple erosions on single fold
- multiple on multiple folds
- multiple circumferential erosions
- ulcers, stenosis or oesophageal shortening
- Barrett’s
Can use Los Angeles Grades A-D
Epidemiology of peptic ulcer disease
Of the 1% with reflux receiving endoscopy, 13% will have peptic ulcer disease
1 per 1000 (0.1%)
Decreasing in Western populations
Increased in males
RFs
- Smoking
- Alcohol
- NSAID or steroid use
Symptoms of peptic ulcer disease
Post-prandial epigastric pain Relieved by food Nausea Oral flatulence Bloating Intolerance of fatty foods Heartburn Pain can radiate to the back if ulcer is posterior Fatigue or dyspnoea if anaemia melena
Signs
Epigastric tenderness
Aetiology of peptic ulcers
H. pylori Bile acids NSAIDs Steroids pepsin Stress Smoking Changes in mucus consistency Alcohol
Pathophysiology of H.pylori
Gram negative spiral Lives deep beneath mucus layer Closely adheres to epithelial surface Uses an adhesin (BabA) Any acidity is buffered by urease
Pathphyiology of peptic ulcers
- Depletion of somatostatin
- increase gastrin release from G cells
- Increased acid secretion
- Increased acid load in duodenum will cause metaplasia
Investigations for peptic ulcer disease
FBC - iron deficiency anaemia
H. pylori test - 13C breath test or stool antigen test
Endoscopy if there are any warning signs
Treatment of peptic ulcers
Lifestyle advice: stop smoking and alcohol
If H.pylori positive treat
If taking NSAIDs = STOP
If neither is positive (rare), endoscopy for ? Zollinger-Ellison syndrome
Endoscopic ablation if actively bleeding
Complications of peptic ulcers
Perforation (more common in duodenal)
Gastric outlet obstruction
Bleeding
Anaemia
Treatment of H.pylori
TRIPLE therapy for 7 days
Clarithromycin
PPI
Amoxicillin or metronidazole
Functional dyspepsia
Chronic discomfort in the upper abdomen without any organic disease (as seen in GORD)
Drug treatment not useful.
Prokinetic drugs e.g. metoclopramide may be helpful
Define cholelithiasis and choledolithiasis
Formation of gall stones within the gall bladder
Choledocholithiasis - stones in the common bile duct
Epidemiology of gallstones
10-15% of Western population but only 10-25% of these become symptomatic
Increases with age
Increased in women
increased in middle age
Fair, fat, fertile, female and 40
RF FHx Obesity Pregnancy Sudden weight loss Haemolysis (sickle cell) Loss of bile salts (ileal resection) Drugs (oestrogens, fibrates, somatostatin) Diabetes Oral contraception Crohn's
Symptoms of gallstones
70% are asymptomatic
Pain in RUQ or epigastrium, can radiate to the back
Pain begins post-prandially
Pain is intense and dull
Subsides spontaneously, after analgesia, vomiting, antacids, defaecation, flatus or positional changes
Sporadic and unpredictable episodes
Persists from 5 minutes to 24 hours
Nausea or vomiting can accompany pain
Intolerances to fats
Abdominal distension
Can have diaphoresis (excessive sweating)
Signs of gallstones
No findings if asymptomatic
Tachycardia (due to pain)
No peritoneal signs
If complications: can have jaundice, positive Murphy’s sign or pancreatitis
Types of gallstones
Cholesterol stones (80%)
Large, solitary and radiolucent
Increased with increased cholesterol
Pigment stones (20%)
Small, black and friable, irregular radiolucent
RFs - haemolysis and cirrhosis
Occurs with high levels of unconjugated bilirubin
Calcium bilirubinate can crystalise to form stones
Mixed stones - calcium salts, pigment and cholesterol, 10% are radio-opaque
Brown pigment stones <5%, due to stasis and generally present with E.coli or Klebsiella infection
4 stages of gallstone formation
- Lithogenic state in which conditions favour gall stones: high cholesterol, low bile sales
- Asymptomatic gallstones
- Symptomatic gallstones with episodes of biliary colic
- Complicated cholethiasis
Investigations for gallstones
Blood tests: FBC, LFTs, amylase and lipase
If uncomplicated or simple biliary colic, will be normal
Abdominal x-ray to rule out obstruction
US - best way to see stones. They are usually echogenic, mobile and cast an acoustic shadow.
ERCP - can be used to see and remove stones in CBD
MRCP - using MRI, reserved for suspected choledolithiasis.
Management for gallstones
Manage with pain with morphine
Laparoscopic cholecystectomy
If unfit for surgery can surgical drain the gallbladder (cholecystotomy)
If stones in bile duct then - cholecystectomy and CBD exploration and stone extraction
Consider mechanical or shock wave lithotripsy
If asymptomatic watch and wait.
Reasons for cholecystectomy in asymptomatic patients
stone > 2cm high risk of GB carcinoma Non-functioning GB Sensory neuropathy of abdomen Sickle cell anaemia Cirrhosis or portal hypertension Children Transplant candidates Diabetics
Complications of gallstones
Cholangitis if in biliary tree GB empyema Gallstone ileus Fibrosis of gallbladder Loss of gallbladder function GB carcinoma
Epidemiology of cholecystitis
10% have gallstones 1/3 get cholecystitis Increases with age increased in females Although acalculus is more common in men
RFs Gallstones Trauma Obesity Rapid weight loss Pregnancy Crohn's Hyperlipidaemia
RF for acalculus Major surgery Long term parenteral nutrition Sepsis Prolonged fasting
Symptoms of cholecystitis
Upper abdominal pain
may radiate to right shoulder or scapula
Pain begins in epigastrium and localises to RUQ
Starts colicky but becomes constant in all cases
nausea and vomiting
Fever
Signs of cholecystitis
Raised WCC Positive Murphy's sign Local peritonism Fever Tenderness in epigastrium/RUQ Tachycardia Jaundice Guarding/rebound tenderness palpable GB
Pathophysiology of cholecystitis
90% are calculous
Stone obstructs cystic duct causing distension of GB
Blood flow and lymph drainage of the gallbladder are compromise and can cause ischaemia and necrosis
Acalculous 10%
Cause unclear.
If fasting GB has no CKK stimulus and so bile remains stagnant
Causes of cholecystitis
GALLSTONES
Acalculus MI Sickle cell Salmonella Diabetes AIDS CMV pregnancy
Investigations for cholecystitis
Blood tests -
Raised WCC
Raised ALT and AST
Check amylase and lipase for pancreatitis
Urinalysis to rule out pyelonephritis and renal stones
Pregnancy test
CXR to rule out lower lobe pneumonia or see radiopaque stones
US - thickened gall bladder wall >3mm, pericholecystic fluid or air on GB or GB wall
CT with IV contrast
Treatment for cholecystitis
Rest IV hydration Bowel rest - no intake Correct electrolyte imbalance Analgesia IV antibiotics (tazocin/metronidazole) Laparoscopic cholecystectomy ERCP
Triad of ascending cholangitis
Charcot’s triad
RUQ pain
Jaundice
Fever
Reynold’s pentad adds confusion and hypotension
Cholangitis
Infection of biliary tract
Majority of cases are due to gall stones
10-30% are due to benign strictures, post-op damage, tumours, bacteria (anaerobes) and parasites
Carries significant risk of death due to shock or multi organ failure
Blood test results in cholangitis
Raised CRP or WCC Increased LFTs (ALP, AST, ALT, GGT)
Epidemiology of gastric cancer
8th most common cancer
Increases in Asia and South America
Increases with age
More common in men
50% in pylorus, 25% in lesser curve, 10% cardia, 2-8% lymphomas
RFs H.pylori infection Smoking Diet: rich in pickles, salt, smoked meats and fish FHx Poor socioeconomic status Previous gastric surgery Obesity
Pathophysiology of gastric cancer
Correa’s cascade
- Chronic non-atrophic gastritis
- Atrophic gastritis
- Intestinal metaplasia
- Dysplasia
- Cancer
Can spread to ovaries
2 main types:
- Intestinal (type 1) with well formed glandular structures. Ulcerating lesions with heaped rolled edges. Strong environmental association
- Diffuse (type 2) poorly cohesive cells. Poorer prognosis. Loss of expression of E=cadherin molecule
Investigations for gastric cancer
FBC for anaemia
LFTs
Rapid access flexible endoscopy: Gastroscopy and biopsy
Endoscopic US for local staging and depth
Chest/Abdo/Pelvis CT
18F PET/CT
Management of gastric cancer
Surgery is treatment of choice
If distal then subtotal gastrectomy, if proximal then total
If curable remove D2 lymph nodes
Perioperative chemotherapy is standard with 5-FU, but can be palliative
Blood transfusion if anaemia
Corticosteroids for management of anorexia
Prognosis of gastric cancer
Overall survival rate 15%
11% live 10 years
Younger patients have a better prognosis
Poorer prognosis if paraneoplastic syndrome
Epidemiology of pancreatitis
150 per million
3% of all abdominal pain in hospital
High in USA & Scandinavia
Equal gender distribution
RF
- Alcohol abuse
- Some family history (alpha 1 antitrypsin deficiency)
- Hyperlipidaemia
- Gallstones
- CF
- Smoking
- Oestrogens
- Hypothermia
- Congenital abnormalities
- Vasculitis
Symptoms of acute pancreatitis
Severe upper abdominal pain Decreases steadily over 72 hours Pain focused in LUQ or epigastrium Penetrates tot he back Sudden onset vomiting
Signs of acute pancreatitis
Mild pyrexia (common), rare but can have hypothermia Hyperlipidaemia Tachycardia Jaundice Abdominal tenderness and rigidity Bowel sounds in early phase Paralytic ileus causes absent bowel sounds Hypoxaemia
In severe: Gross hypotension Pyrexia Tachypnoea Ascites Pleural effusion Body wall staining around umbilicus (Cullens sign) or Grey Turner's (flanks)
Cullen’s sign
Body wall staining around the umbilicus
Grey Turner’s sign
Body wall staining on the flanks
Aetiology of acute pancreatitis
90% are caused by gallstones, alcohol, post-ERCP or idiopathic
Idiopathic Gallstones Ethanol Trauma Steroids Mumps/malignancy Autoimmune Scorpion bite Hyperlipidaemia ERCP Drugs
Viral causes - Coxsackie B, hepatitis, mumps
Drugs - thiazides, valproate, azathioprine
IBD
Alpha 1 antitrypsin deficiency
Sclerosing cholangitis
Vasculitis
Hyperparathyroidism
Pathophysiology of acute pancreatitis
Occurs as a consequence of premature activation of zymognes releasing proteases that digests surrounding tissues.
Severe is dependent on balance between proteases and anti-proteolytic factors (Alpha anti-trypsin_
Occurs because of one of:
- Defective intracellular transport and secretion of pancreatic zymogens
- Pancreatic duct obstruction
- Hyperstimulation of pancreas (alcohol/fat)
- Reflex of infected contents into CBD
Investigations for acute pancreatitis
FBCs, U&Es, LFTs, CRP, glucose
- Amylase 3x normal
- Lipase is more sensitive and specific
- Hypocalcaemia is common
Abdominal x-ray - rule out perforation and obstruction
CXR - at show pleural effusions or ARDS
CT + contrast is bloods unclear
After 4 days can assess for complications - pancreatic swelling, fluid collection, change in density of gland
US - poorly visualised in 25-50% of cases
See swollen pancreas, dilated CBD, free peritoneal fluid
MRI for acute abdominal wall oedema
Laparoscopy if inconclusive results
Treatment of acute pancreatitis
MILD
- Manage on general ward
- Pain relief with pethidine +/- benzos
- NBM
- IV fluids
- Nasogastric tube if severe vomiting
- Antibiotics for specific infections
- resume oral fluids once symptoms resolve and normal blood tests
MODERATE
- Treat in HDU or ITU
- If pancreaitic necrosis - IV antibiotics and peritoneal fluid culture
- Enteral nutrition via NG below Ligament of Treitz
- Surgery only if infection and necrosis = open surgical debridement
- Early ERCP for co-existing cholangitis
Complications of acute pancreatitis
Pancreatic necrosis (if infected then 3x mortality) - confirmed by CT.
Infected necrosis - fatal without intervention (Infection in 30-70% of necrosis) - IV antibiotics and agrressive surgical debridemnt
Fluid collections
Pancreatic abscess - occurs several months after the attack, requires surgery
Acute pseudo-cyst - occurs 4 weeks after the attack. Can rupture/haemorrhage, requires surgery
Pancreatic ascites from collapsed pseudocyst
Acute cholecystitis
Systemic complications - pulmonary oedema, pleural effusions, consolidation, hypovolaemia, shock, renal dysfunction, hypocalcaemia, hypomagnesaemia, hyperglycaemia, GI haemorrhage, Weber-Christian disease
Prognosis of acute pancreatitis
80% have mild and recover without complications
5% mortality in mild
30% mortality in severe
Classification of acute pancreatitis
Glasgow Prognostic Score
Ranson’s criteria (very similar)
3+ = severe pancreatitis
Can also use APACHE II = 8 or more is severe
Causes of raised amylase
Pancreatitis Renal failure Ectopic pregnancy Diabetic ketoacidosis Perforated duodenal ulcers Mesenteric ischaemia
Symptoms of chronic pancreatitis
Episodes of exacerbation with intervening remission or continuous pain Abdominal pain Epigastric and radiating to the back Nausea and vomiting Decreased appetite Weight loss Steatorrhoea
Signs of chronic pancreatitis
Exocrine dysfunction
- Malabsorption
- Diarrhoea/steatorrhoea
- Protein deficiency
Endocrine dysfunction - diabetes mellitus
Abdominal tenderness
Risk factors for chronic pancreaitis
Alcohol abuse Smoking Genetics (PRSS1, CFTR, SPINK1) Male Black
Pathophysiology of chronic pancreatitis
Obstruction OR reduction of bicarbonate excretion
These lead to the activation of pancreatic enzymes - causing pancreatic necrosis
Alcohol causes proteins to precipitate in pancreatic ducts leading to pancreatic dilation and fibrosis.
It leads to ductal plugging and obstruction
- Alcohol most common cause
- Increased protein secretion, decreases fluid, decreased bicarbonate production
2 pathological subtypes:
- LARGE DUCT: dilation and dysfunction of large ducts visible on imaging.
- Occurs more in men, steatorrhoea common, requires surgery to alleviate symptoms
- SMALL DUCT: occurs more in women, no diffuse pancreatic calcification. Imaging normal - hard to diagnose.
- Patients respond to pancreatic enzyme replacement
Hereditary pancreatitis
Rare
Similar to chronic
Genetic mutation in PRSS1
This increases autoactivation of chymotrypsin C
Presents at a young age with epigastric pain
Exocrine and endocrine dysfunction
High incidence of pancreatic carcinoma
Tropical chronic pancreatitis
Developing countries
Associated with type 1 diabetes
Associated with CFTR and SPINK1 genes
Similar to alcoholic pancreatitis presentation
Autoimmune chronic pancreatitis
High prevalence in Japan Elevated IgG and serum gammaglobulins Autoantibodies may be increased Steroid responsive. Reversible
Investigations for chronic pancreatitis
Blood tests
- FBC
- U&Es
- LFTs
- Calcium (hypocalcaemia)
- Amylase (raised)
- Glucose and HbA1c
Secretin stimulation test - positive if pancreatic exocrine function damaged
Serum trypsinogen, urinary D-xylose
Faecal elastase
All seen in malabsorption
US - first line then CT -> ERCP
- See pancreatic calcification
MRCP
Pancreatic biopsy - chronic inflammation, irregularly placed fibrosis, Rarely performed as high risk
Tests of pancreatic function:
- GOLD standard is collection of pure pancreatic juice after secretin injection (rarely used due to invasive nature)
- Pancreolauryl test or PABA test
- Faecal pancreatic elastase
Treatment of chronic pancreatitis
Supportive measures
Lifestyle advice - smoking cessation, alcohol abstinence
Pain relief - opiates
ERCP may reduce pain
Malabsorption is treated by pancreatic enzyme replacement - Lipase treatment of choice
Octreotide (somatostain analogue) inhibits pancreatic enzyme secretion and CCK levels
Surgery - pseudocyst decompression, ERCP + lithotripsy
- If large duct dilation: pancreaticojejunostoy
- Pancreatoduodenectomy
Complications of chronic pancreatitis
Cobalamin Deficiency (B12) Diabetes Pericardial, peritoneal and pleural effusions Pseudocysts Pancreatic carcinoma
Increased risk of morbidity and mortality. 1/3 die in 10 years
Epidemiology of hepatitis A
Very common in developing countries, particularly in early life
Most common viral hepatitis
High risk: India, Africa, South and Central America, Middle Esat
RFs - Personal contact - Occupation - residential home staff, sewage worker - Travel to high risk areas -
Hep A virus
Small unenveloped RNA virus Enterovirus in picornaviridae family Incubation period 2-6 weeks Spread through faecal oral route Can be vaccinated with
Symptoms of Hep A infection
More severe in older patients, children can be asymptomatic
- Mild-flu like symptoms
- Anorexia, nausea, fatigue, malaise, joint pain, mild headache
- Following this: jaundice
- Icteric phase: dark urine, pale stools, jaundice, abdominal pain, pruritus, arthralgia, skin rash
Pathophysiology of hepatitis A
- Receptor binding
- RNA uncoating
- Tranlocation and proteolytic processing. Host ribosomes bind to form polysomes
- RNA replication. Genome copied by viral RNA polymerase
- Virion assembly
- maturation and release. Shed via biliary tree into faeces
Shedding greatest between 14-21 days after infection
Investigations for Hep A infection
Specific antibody tests - IgM antibody to Hep A (positive for 3-6 months)
IgG occurs after and persists for many years
LFTs - ALT>AST. Raised ALP
Levels return to normal over several weeks
Raised bilirubin
Modest decrease in albumin
Mild lymphocytosis common
Treatment for Hep A infection
Mainly supportive - fluids, antiemetics, rest
Avoid alcohol until liver enzymes return to normal
For immediate protection can give immune serum globulin
Prognosis of hep A infection
Excellent
Self limiting
No long term sequale
No carrier state. No chronic liver disease
Complications - cholestatichepatitis, autoimmune hepatitis, relapsing hep A infection 4-15 weeks after first illness.
Epidemiology of Hep B infection
High prevalence in sub-Saharan Africa, most of Asian and Pacific Islands
1 in 350 in UK
Starting to decline due to vaccinations
RFs
- Homosexual males
- Sex workers
- IV drug users
- HIV + patients
- Sexual assault victims
- Healthcare workers/needle stick injuries
Hep B virus
Double stranded DNA
Hepadnoviridae family
Incubation period 40-160 days (average 60-90)
Can be e antigen positive or negative (positive = increase rate of replication)
Transmission: vaginal or anal intercourse, blood to blood contact, vertical transmission
Hep B antibodys
HBsAg - hep B surface antigen
Indicator of active infection
If present after 6 months then chronic infection
HBcAg - Hep B core antigen
Detected by its antibody IgM then IgG
HBeAg - Hep B e antigen
Indicator of viral replication
Chronic infection = HbsAg and anti-HBcAg (IgG)
Investigations for Hep B infection
Blood tests
- HBsAg (only detected in first 3-5 weeks after infection - unless chronic infection)
- HBsAg antibodies - in vaccinated people
- HBeAg - if positive, active infection
- HBcAg antibodies - past infection
- Dane particles are Hep B virions, can have anti-Dane antibodies
- Quantitative Hep B DNA
- FBC, bilirubin, LFTs, clotting, ferritin, lipid profile, caeruloplasmin
- Test for Hep C and HIV
- Alpha fetoprotein and liver US for hepatocellular carcinoma screen
Management of Hep B infection
Avoid unprotected intercourse
Notify HPA
Supportive treatment - fluids, antiemetics, rest
Avoid alcohol. Stop unnecessary medications
Give antiviral agents if - Fulminant hepatitis - HBeAg positive - Pregnancy with high HBV DNA Give: peginterferon alpha-21 or tenofovir
- Monitor ALT every 24 weeks, more often if cirrhosis
- Test for HCC (US and alpha fetoprotein)
Can give hepatitis B immunoglobulin to baby to reduce risk of vertical transmission or just after infection to decrease risk
Prognosis of Hep B infection
Cirrhosis 20%
Faster progression in Hep C or HIV positive as well
Signs and symptoms of Hep B infection
Flu like illness - nausea, anorexia, mlaise, ache in RUQ Jaundice Disinclination to drink alcohol Dark urine Pale stool
Fever
In decompensated - ascites, encephalopathy, Gi haemorrhage
Signs and symptoms of Hep C infection
Acute - asymptomatic, often diagnosed on routine blood testing
20-30% get jaundice
Chronic - malaise, weakness, anorexia, abdominal pain
Symptoms are worse with increased alcohol intake
Epidemiology of Hep C infection
Large number undiagnosed
214,000 in UK
RF
- Drug misuse
- Blood transfusion pre-1991
- Sexual intercourse
- Infected pregnant mother
- Healthcare worker
- Needlestick injury
- Tattoo, body piercing
- Sharing razors/toothbrushes
Hep C virus
Enveloped RNA virus
Flavivirdae family
Incubation period 6-9 weeks
Hep C RNA can be found after 2-4 weeks, antibodies at 6-12 weeks
Transmission - Parenteral, blood born, sexual contact, vertical transmission
6 genotypes
- 1 = most common
- 2, 3, 4, 5, 6
Investigations for Hep C infection
- Anti HCV serology
- HCV RNA quantitative PCR
- HCV antibody positive for life regardless of treatment
- US: focal lesions, splenomegaly, cirrhosis
- Liver biopsy to assess severity
- Measures of severity: macroglobulin, haptoglobulin, apolipoprotein A1, GGT, total bilirubin, transient elastography
- Test for Hep B and HIV
Treatment of Hep C infection
Advice - counselling, barrier contraception, alcohol abstinence, implications of being positive
Drugs effectiveness is related to genotype
Better response in type 2 and 3
- Weekly subcut peginterferon alpha2a
Prognosis of Hep C infection
50-85% become chronic carriers
15% will clear virus completely
Cirrhosis in 20-30% of chronic
1-4% get HCC, 2-5% get liver failure
Co-infection with Hep B or HIV = worse prognosis
Type 1 more likely to clear spontaneously
Hep D virus
Single stranded RNA virus Enveloped spherical deltavirus Requires presence of Hep B to replicate Patients must be HBsAg positive Delta virus Blood bourne Clinically indistinguishable from Hep B infection
Replicated only in liver cells
Increases risk of fulminant hepatic failure, chronic liver disease, cirrhosis and HCC with B+D
Chronic in 30-50%
Incubation 3-20 weeks
Hep E virus
Hepeviridae
Non-enveloped single stranded RNA
Spread via faecal oral route
Self-limiting with no chronic infections
Incubation 2-9 weeks
Fulminant disease in 10%
Mild flu like symptoms
Hep B blood test results - vaccinated
HBsAg antibody - positive
HBsAg - negative
HBcAg antibody - negative
Hep B blood test results - Acute infection
HBsAg - positive
HBcAg antibody - positive
HBcAg IgM - positive
HBsAg antibody - negative
Hep B blood test results - chronic infection
HBsAg - positive
HBcAg IgG - positive
HBsAg antibody - negative
Hep B blood test results - natural infection (cleared)
HBsAg antibody - positive
HBcAg antibody - positive
HBsAg - negative
Define acute liver failure
Occurs when liver loses the ability to regenerate or repair so that decompensation occurs.
Characterised by -
- Hepatic encephalopathy
- Abnormal bleeding
- Ascites
- Jaundice
Fulminant hepatic failure - when failure takes place within 8 weeks of the onset of underlying illness
Late onset/subacute fulminant - when it occurs during 8-26 weeks
Chronic decompensated hepatic failure - after 6 months
Risk factors for acute liver failure
Chronic alcohol abuse Poor nutritional status Female Chronic Hep B/C infection Chronic pain and narcotic use Pregnancy Paracetamol Antidepressant therapy Medications Illicit drug use
FHx - Wilson’s disease, haemochromatosis
Aetiology of acute liver failure
Toxins - alcohol, Paracetamol, Reye’s syndrome, drugs (co-amoxiclav, ciprofloxacin, doxycycline, erythromycin), ectasy, cocaine
Infections - viral hepatitis, EBV, CMV, viral haemorrhagic fevers
Cancer - HCC or mets
Pregnany related - acute fatty liver of pregnancy
Autoimmune liver disease
Metabolic - Wilson’s disease, alpha 1 antitrypsin deficiency
Vascular - ischaemia or veno-occulsive disease. Budd-Chiari syndrome
Presentation of acute liver failure
Nausea and vomiting Malaise Abdominal pain RUQ tenderness Drowsiness and possibly confusion Jaundice Abdominal distension - ascites, hepatomegaly Papilledema,, hypertension, bradycardia (from cerebral oedema) Asterixis Palmar erythema Hepatic encephalopathy
Investigations for acute liver failure
FBC - thrombocytopaenia, leucocytosis, anaemia
LFTs - Very raised transaminases, raised ALP
Raised INR, Raised bilirubin, raised ammonia, low glucose
May have: raised lactate, raised creatinine
Blood cultures - very susceptible to infection
Viral serology
Free copper (Wilson’s), Paracetamol levels for OD
ABG - metabolic acidosis
Dopper US, CT or MRI
Avoid contrast
Management of acute liver failure
Intensive care management
Mannitol to decrease ICP
Lactulose + neomycin to reduce ammonia
AKI may require haemodialysis or haemofiltration
FFP, platelets and anti-fibrinolytic drugs for abnormal bleeding
Replace glucose as required
Complications and prognosis of acute liver failure
Infection - Spontaneous peritonitis common
Cerebral oedema
Haemorrhage
Bleeding, sepsis, cerebral oedema, AKI, respiratory failure
High morbidity and mortality
Cause depends on outcome
Higher survival if Paracetamol, hep A, pregnancy
Define Jaundice
Yellow discolouration caused by accumulation of bilirubin in tissue
Not apparent until serum bilirubin is over 35
It can be pre-hepatic, hepatocellular, post-hepatic
Breakdown of haemoglobin
Haemoglobin broken down in spleen to biliverdin.
Biliverdin in plasma converted to unconjugated bilirubin and bound with bilirubin
Unconjugated becomes conjugated in liver by glucaronic acid
Secreted into bowels where converted to urobilinogen by bacteria, secreted in stool as stercobilin
Presentation of jaundice
Any prodromal flu like illness may suggest viral hepatitis Pain suggest gallstones painless suggests cancer Change in colour of urine and stools Pruritus Weight loss Alcohol or drug use medication history! amitriptyline, erythromycin, COCP, rifampicin, salicylates
Examination of a patient with jaundice/signs of liver disease
Jaundice - skin and sclera Spider naevi Palmar erythema Gynaecomastia Testicular atrophy Flapping tremor Ascites Splenomegly Finger clubbing Peripheral oedema
Aetiology of pre-hepatic jaundice
Gilbert’s syndrome - unconjugated hyperbilirubinaemia
Haemolytic anaemia - spherocytosis, pernicious anaemia
Thalassaemia
Trauma
Crigler-Najjar syndrome
Aetiology of hepatic jaundice
Viral hepatitis HCC Alcoholic hepatitis Autoimmune hepatitis Drug induce hepatitis (Paracetamol) Decompensated cirrhosis
Aetiology of post-hepatic jaundice
Gall stones Bile duct strictures Common duct stone Head of pancreas cancer Tumour at ampulla of Vater Pancreatitis GB cancer Primary biliary cirrhosis Primary sclerosing cholangitis
Blood test results in Pre-hepatic jaundice
Raised unconjugated bilirubin
Normal AST, ALP, GGT
Raised reticulocytes
Normal INR, PT
Blood test results in hepatic jaundice
Raised bilirubin ** Raised AST ALT>AST Raised ALP Raised GGT Raised INR and PT Raised urobilinogen with raised or normal bilirubin
Blood test results in Post-hepatic jaundice
Very high bilirubin Raised AST ** Raised ALP ** Raised GGT Rasied INR and PT ALT>AST Raised urine bilirubin
Investigations for jaundice
FBC - reticulocytes and blood smear LFTs Hepatitis viral serology Serum ANA and anti-smooth muscle antibody for primary biliary cirrhosis Ferritin for ?haemochromatosis Alpha 1 antitrypsin levels Abdominal US MRI/MRCP Liver biopsy
What is anti-mitochondrial antibody seen in?
Primary biliary cirrhosis
What is anti-nuclear and anti-smooth muscle and microsomal antibody seen in?
Autoimmune hepatitis
What is alpha fetoprotein an indicator of?
Hepatocellular carcinoma
