32 Flashcards
GI and Surgery
Epidemiology UC
- Incidence: 21 per 100,000
- Prevalence: 240 per 100,000
- Occurs more in Caucasians and Ashkenazic Jews
- F:M ratio 1:1
- Peak incidence in 15-25 and 55-65 years
- Can present in very young children or elderly
S+S 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.
Malignant potential.
Negatives: No skin lesions. No mural thickening, no strictures, no fistulas. No malabsorption . 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 and 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
- Haemorrhage
- Toxic megacolon
- Colorectal carcinoma
- Fatty liver
- Primary sclerosing cholangitis
Epidemiology of Crohn’s
- Genetic link - NOD2
- Smoking is a big risk factor
- Most common in ileocaecal region
- Incidence: 4 per 100,000
- Prevalence: 150 per 100,000
- Caucasians and Ashkenazic Jews
- F:M ratio 1.5:1
- Peak incidence in 15-25 and 50-80 years
- More common in smokers
- Can occur in children (usually with FHx)”
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’s
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
19
Complications of Crohn’s
- Malabsorption (short loop/bowel syndrome due to repeated resection)
- Stricturing
- Anal lesions (60%): fissures, fistula
- Perforation
- Cholelithiasis
- Fatty liver
- Increased risk of malignancy of SI but less frequent than ulcerative colitis
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 flexible 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 anaemia
- 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?
- 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.
Process:
- 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 microcytic hypochromic anaemia
LISTS:
Lead poisoning
Iron-deficiency - blood loss, increased demand (growth and pregnancy), decreased absorption (post-gastrectomy, Crohn’s), poor intake.
Sideroblastic
Thalassemia
Sickle cell
Causes of normocytic normochromic anaemia
HAHAC:
Haemolytic Acute blood loss Hypersplenism Aplastic – bone marrow infiltration CKD
Causes of macrocytic anaemia
PPMATRC:
Pregnancy
Pernicious – intrinsic factor def leading to B12 deficiency
Megaloblastic – B12 / B9 deficiency:
B12 - gastrectomy, ileal disease, resection.
B9 - alcohol, coeliac, Crohn’s, partial gastrectomy, cancer, drugs.
Alcoholism
hypoThyroidism
Reticulocytosis
Cirrhosis – liver disease
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
47.
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 para-umbilical.
Incisional.
Ventral and epigastric.
Types of hernias: reducible/irreducible/strangulation.
Reducible:
- 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 (anatomy, epidemiology)
Anatomy:
- Passes through the femoral canal.
- Medial to the femoral sheath.
- Femoral sheath contains the femoral artery and vein.
Epidemiology:
- Females > Males.
- More common in the middle aged and elderly.
- Swelling BELOW and LATERAL to pubic tubercle.
- Enlarges on standing and coughing.
- DIsappears on lying down.
Strangulation 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, presents as respiratory distress shortly after birth and require urgent surgery.
Other examples: large oesophageal hiatus which present with regurgitation, vomiting, dysphagia and progressive weight loss in the child.
List the types of acquired hiatus hernias.
Sliding (80%)
- Stomach (GO junction and cardia sometimes) slides through diaphragmatic hiatus.
- It is covered anteriorly with peritoneal sac, posteriorly with extraperitoneum.
- It disturbs cardio-oesophageal mechanism.
Rolling (20%)
- Cardia remains in position.
- Gastric fundus moves up and lies alongside the GOJ, which creates a bubble of stomach in the thorax.
- This is a true hernia within a peritoneal sac.
- No regurgitation symptoms.
- Represents progressive weakening of hiatus muscles.
- 4x more common in females.
- Occurs in obese, middle aged and elderly.
Presentation of acquired hiatus hernia.
Cough. Dyspnoea. Palpitations. Hiccoughs. Retrosternal burning. Pain worse on lying and swooping.
Occult bleeding from oesophagitis.
Treatment of hiatus hernias.
Treat symptomatically.
If unsuccessful, laparoscopic repair indicated.
Epidemiology of colon cancer.
Epidemiology:
- 50 per 100,000.
- 3rd most common malignancy.
- Risk increases with age.
- Males > Females.
- FHx (HNPCC, FAP)
Risk factors of colon cancer.
Risk Factors:
- UC or Crohn’s
- Pelvic radiotherapy
- Smoking
- Alcohol
- Obesity
- Sedentary lifestyle
- Red meat
- DMII
- Aspirin/NSAIDs
- Cholecystectomy
- Low fibre diet
Gram-negative, oxidase positive, non-lactose fermenting bacilli.
Pseudomonas aeruginosa.
This bacterium can cause a range of infection such as pneumonia, urinary tract infections and skin infections amongst others.
Gram-negative, maltose-utilising diplococci
Neisseria meningitidis
Which is mostly known for causing meningitis.
Gram-negative, oxidase positive, growth at 42 C, comma-shaped rods
Vibrio cholerae
Which can cause severe rice-water diarrhea in places where water has been contaminated with the organism.
Dehydration and electrolyte imbalance is a common cause of death, and therefore proper hydration is vital to prevent death.
Gram-negative, oxidase positive, catalase positive comma-shaped rods
Helicobacter pylori
Which causes chronic gastritis and peptic ulcer disease.
Gram-positive, urease positive, catalase positive cocci
Staphylococcus epidermidis
Which is part of the normal skin flora but can also be responsible for infection of catheters and other devices such as mechanical heart valves.
Gram-positive, catalase positive cocci
Staphylococcus bacteria
Which can further be differentiated based on the coagulase positivity and novobiocin sensitivity.
Gram-positive aerobic bacilli
Listeria, Bacillus and Corynebacterium bacteria.
Gram-negative, oxidase-positive comma-shaped rods
Campylobacter jejuni which grows at 42 degrees celcius,
Vibrio cholerae which grows in alkalin media
Helicobacter pylori which produces urease.
Gram-negative, maltose-utilising diplococci
Neisseria meningitidis bacteria.
Tumour marker of colonic cancer
Carcinoembryonic antigen (CEA)
Note: Screening for colonic cancer using CEA is not justified!
It is falsely elevated in a number of non-malignant disease states such as cirrhosis and colitis.
Metoclopramide (antiemetic) is contraindicated in which disease?
Parkinson’s disease (PD)
Metoclopramide is a dopamine antagonist which can make the symptoms of PD worse. There is a degeneration of the basal ganglia in PD and a lack of dopamine. Further inhibiting the action of dopamine increases the symptoms of PD.
Carcinoid tumour markers?
Urinary 5-HIAA
Plasma chromogranin A
Causative organism that causes fat malabsorption, therefore greasy stool can occur.
It is resistant to chlorination, hence risk of transfer in swimming pools.
Giardia lamblia
Which bacteria is seen with antibiotic use?
Clostridium difficile
Borders of the femoral canal?
Laterally - Femoral vein
Medially - Lacunar ligament
Anteriorly - Inguinal ligament
Posteriorly - Pectineal ligament
Types of shock
Septic Haemorrhagic Neurogenic Cardiogenic Anaphylactic
Hesselbach’s triangle boundaries?
Note:
Direct hernias pass through Hesselbachs triangle.
Superolaterally - Epigastric vessels
Medially - Lateral edge of rectus muscle
Inferiorly - Inguinal ligament
Most common complication of endoscopic retrograde cholangiopancreatography (ERCP)?
Acute pancreatitis is the most common complication of ERCP
Linitis plastica
Linitis plastica produces a diffuse infiltrating lesion, the stomach is fibrotic and rigid and will not typically distend.
This may be described as a ‘leather bottle stomach’.
Diagnosis is made with a combination of pathology examination with endoscopy, radiological or surgical assessment.
Pathologically signet-ring cell proliferation occurs.
Indirect inguinal
Indirect inguinal hernia is lateral to epigastric vessels
Indirect inguinal hernias occur due to failure of the processus vaginalis to regress.
The protrusion occurs through the deep inguinal ring and enters the inguinal canal.
It may progress and enter the scrotum in males or labia in females.
Sulphasalazine important side effect.
Sulphasalazine can cause oligospermia and infertility in men
Aminosalicylate drugs
5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit prostaglandin synthesis
Sulphasalazine
a combination of sulphapyridine (a sulphonamide) and 5-ASA
many side-effects are due to the sulphapyridine moiety: rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis
other side-effects are common to 5-ASA drugs (see mesalazine)
Mesalazine
a delayed release form of 5-ASA
sulphapyridine side-effects seen in patients taking sulphasalazine are avoided
mesalazine is still however associated with side-effects such as GI upset, headache, agranulocytosis, pancreatitis*, interstitial nephritis
Olsalazine
two molecules of 5-ASA linked by a diazo bond, which is broken by colonic bacteria
*pancreatitis is 7 times more common in patients taking mesalazine than sulfasalazine
Metoclopramide
Metoclopramide is a D2 receptor antagonist mainly used in the management of nausea. Other uses include:
gastro-oesophageal reflux disease
prokinetic action is useful in gastroparesis secondary to diabetic neuropathy
often combined with analgesics for the treatment of migraine (migraine attacks result in gastroparesis, slowing the absorption of analgesics)
Adverse effects extrapyramidal effects: oculogyric crisis. This is particularly a problem in children and young adults hyperprolactinaemia tardive dyskinesia parkinsonism
List 2 opioid agonists used as antidiarrhoeal agents.
Loperamide
Diphenoxylate
They act on u-opioid channels in GIT.
Clinical features 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
- Mass in RIF
Colicky pain
Weight loss
Obstruction or perforation
Hepatomegaly/ascites if mets
Peritonitis
Signs of peritonitis
Rock hard abdomen
Rebound tenderness
Absent bowel sounds
Most common places for bowel cancer?
Rectosigmoid 45%
Ascending colon 30%
Descending colon 15%
Transverse colon 10%
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.
- 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 GI 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%
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