GIT management and diagnosis Flashcards
GI causes of finger clubbing
My Inflamed Liver:
Malabsorption
Inflammatory bowel disease
Liver cirrhosis
Abdominal exam clinical signs to look out for initially
Confusion: end stage liver disease/hepatic encephalopathy
Jaundice: high bilirubin from acute hepatitis, liver cirrhosis, cholangitis, pancreatic cancer
Pallor: underlying anaemia
Abdominal distension: ascites or bowel obstruction or organomegaly
Hyperpigmentation: haemochromatosis
Oedema: liver cirrhosis
Cachexia: malignancy and advanced liver failure
Hernias: coughing may make these more pronounced
Also look for:
stoma, surgical drains, feeding tubes, mobility aids, vital signs, fluid balances and prescriptions
Hand clinical signs for abdominal problems
Palmar erythema: red heel or palm: chronic liver disease (normal in pregnancy)
Dupuytren’s contracture
Koilonychia: spoon shaped nails associated with iron deficiency anaemia (eg in Crohn’s disease)
Leukonychia: Whitening nail bed - hypoalbuminaemia eg end stage liver disease, protein losing enteropathy
Finger clubbing: IBD, coeliac disease, liver cirrhosis, lymphoma of GIT
Asterixis (flapping tremor): hepatic encephalopathy or renal failure
Arms and axillae clinical signs for abdominal disease
Bruising: clotting problems secondary to liver disease
Needle marks: increased risk of viral hepatitis
Acanthosis nigricans: insulin resistance or GI malignancy (stomach cancer most common)
Hair loss: iron deficiency anaemia and malnutrition
Facial clinical signs for abdominal disease
Conjunctival pallor: anaemia
Jaundice: acute hepatitis, liver cirrhosis, cholangitis, pancreatic cancer
Corneal arcus and Xanthelasma: hypercholesterolaemia
Kayser-fleischer rings: Dark rings around iris - Wilsons disease (liver cirrhosis)
Perilimbal injection: inflammation adjacent to iris associated with IBD
Glossitis: smooth enlarged tongue - iron, B12 and folate deficiency
Oral candidiasis: immunosuppression
Aphthous ulceration: round ulcers inside mouth - stress, trauma, iron, B12 and folate deficiency
Hyperpigmented macules: Peutz-Jeghers syndrome
Enlargement of the left supraclavicular lymph node (Virchow’s node) - metastatic abdominal malignancy
Chest and abdomen clinical signs of abdominal disease
Spider naevi: liver cirrhosis, pregnancy, combined oral contraceptive (more than 5 = pathology)
Gynaecomastia: liver cirrhosis, digoxin and spironolactone medications
Caput medusae: engorged paraumbilical veins associated with portal HTN (liver cirrhosis)
Striae: ascites, malignancy, Cushings, obesity, pregnancy
Cullen’s sign: bruising around umbilicus - late sign of haemorrhagic pancreatitis
Grey-Turner’s sign: bruising in flanks - late sign of haemorrhagic pancreatitis
Stoma assessment
Location: type of stoma (e.g. colostomies are typically located in the left iliac fossa, ileostomies and urostomies are typically located in the right iliac fossa).
Contents: can be stool (e.g. colostomy or ileostomy) or urine (e.g. urostomy).
Consistency of stool: note if it is liquid (ileostomy) or solid (colostomy).
Spout: colostomies are flush to the skin with no spout whereas ileostomies and urostomies have a spout.
Murphy’s sign
- Position your fingers at the right costal margin in the mid-clavicular line at the liver’s edge.
- Ask the patient to take a deep breath.
If the patient suddenly stops mid-breath due to pain, this suggests the presence of cholecystitis (known as “Murphy’s sign positive”).
Causes of splenomegaly
Portal hypertension secondary to liver cirrhosis Haemolytic anaemia Congestive heart failure Splenic metastases Glandular fever
Anatomy of the colon and relevant clinical points
The widest area of the colon is the cecum, the narrowest is the sigmoid colon; meaning any blockages have highest likelihood of perforation in the sigmoid and chance of diverticulitis is highest in the sigmoid colon
Divisions of the abdomen and contents
right hypochondriac: liver, gallbladder, right kidney, small intestine
epigastric region: stomach, liver, pancreas, duodenum, spleen, adrenal glands
left hypochondriac: spleen, colon, left kidney and pancreas
right lumbar: gallbladder, liver and right colon
umbilical: umbilicus, parts of small intestine, duodenum
left lumbar: descending colon and left kidney
right iliac fossa: appendix and cecum
pelvic/hypogastric: bladder, sigmoid colon, uterus, reproductive organs
left iliac fossa: descending colon, sigmoid colon
water and electrolyte turnover in GIT
On average/24h (in rounded numbers)
+ 2000 CC Water intake (drinking and eating)
+ 8000 CC Secreted water in upper GI
(Saliva, gastric, duodenal, intestinal secretions, and bile)
_______________
+ 10,000 CC Water, exposed to the small intestinal mucosa
- 9000 CC Water, absorbed by the small intestinal mucosa - 90%
_______________
+ 1000 CC Water, exposed to the colon mucosa
- 900 CC Water, absorbed by the colon mucosa - 90%
_______________
+ 100 CC Water, lost in stool (≡ 1% of the 10,000 CC)
If this 1% becomes 2%, it means diarrhoea!
If this 1% becomes 0.5%, it means constipation!
In conditions like obstruction, diarrhoea and perforation, water and electrolyte imbalance is a major and early issue.
Considering 70-80% of body weight in neonates is composed of water, these disorders are more dangerous in children.
Define acute abdomen
An abdominal condition of abrupt onset associated with severe abdominal pain resulting from (ethiology):
Inflammation
Obstruction
Infarction
Perforation
Rupture of intra-abdominal organs.
Acute abdomen requires urgent evaluation and diagnosis, because it may indicate a condition that requires urgent surgical intervention.
Presenting complaint of acute abdomen
SOCRATES characteristics of pain
Site - Where is the pain, is it localized, in a region, or generalized?
Diffuse
Epigastrium, Peri-Umbilical, Hypogastrium
Four Quadrants
Onset - Gradual, rapid, or sudden? Intermittent or constant? Happened before?
Character - Sharp, stabbing, dull, aching, tight, sore, colicky, burning?
Radiation - Does it spread to other areas e.g. back or shoulder?
Associated symptoms - Nausea, Vomiting, Dysuria, Jaundice?
Timing - Does it occur at any particular time?
Exacerbating or Relieving factors.
Surgical history - Does the pain relate to surgical interventions? / Severity
Characteristics
Sharp in nature
Well-localised
Made worse by movement or cough
Relieved by lying still
Mild forms – dull in nature and vague description from patient
Severe forms – nausea and vomiting, poorly-localised
Foregut – epigastrium
Midgut – peri-umbilical
Hindgut – suprapubic
Interpreting abdominal imaging
Check the name, date and type of imaging
Ask about clinical findings
Describe the image (type, position, view, plain/contrast) and landmarks
Describe abnormalities
Translate these abnormalities to pathologies
Differential pathologies
Management plan and further investigations if needed
Acute abdominal series XR
Indicated for:
Determining the amount of bowel gas and possibly bowel distension
Assess air fluid levels
Query pneumoperitoneum
Projections used:
AP supine: most information is gathered via this view
PA erect AXR: This clarifies air-fluid levels
PA erect chest XR: This is for greater sensitivity for pneumoperitoneum and to exclude any chest pathologies which may be presenting with abdominal pain
Modified view (for those who cannot stand):
AP supine
Left lateral decubitus view: most sensitive for intraperitoneal free gas evaluation
AP supine chest view
In order to adequately evaluate for free intraperitoneal gas, the patient should be positioned in the erect and decubitus views for enough time to allow small amounts of free gas to drift up to the diaphragm or lateral liver edge, respectively. This often takes ~5-10 minutes
KUB XR
Indicated for visualising any calcifications within the urinary tract (kidneys, ureter, urinary bladder and urethra)
Is an AP projection
Taken with patient lying straight, supine, taken on full inspiration to squash all organs down to fit in one image
Intestinal obstruction types
Mechanical: physical blockage of the intestinal lumen (either through extra, intra or inter-mural means) such as adhesion bands, neoplasms and hernias
Paralytic Ileius (pseudo-obstruction): a functional condition causing loss of peristalsis, such as bacterial or viral infections, electrolyte imbalances etc.
Mechanical bowel obstruction complications
Loss of intra-luminal fluid and vomiting leads to hypovolaemia, water and electrolyte imbalances
Bowel distension and intraluminal and intramural pressures increase which can lead to intestinal ischaemia and necrosis due to perfusion impairment (STRANGULATED BOWEL OBSTRUCTION) is a vascular emergency
Luminal flora of the bowel changes and BACTERIAL OVERGROWTH occurs
Perforation
Respiratory distress (elevated diaphragm)
Aspiration pneumonitis
Acute renal failure
Bowel obstruction investigations/diagnosis
History of bowel changes (prior abdominal operations may suggest adhesions, abdominal disorders)
Abdominal examination; assess for hernias or previous scar tissues
Bloods: FBC, U+Es, Amylase, LFTs, CRP, clotting screen
ABG (strangulation)
Urinary output
In partial or early (first 1-2 days) small bowel obstruction they may appear identical to an ileus, therefore follow up imaging is usually used to see how it involves and then determine the cause
Acute abdominal series Ix:
AXR supine
AXR upright
CXR upright
CT scan more sensitive for SBO detection
Small bowel obstruction and causes
Caused by lesion obstructing lumen of the bowel
Results in dilatation of bowel proximal to obstruction and compression after obstructing lesion
caused by: Adhesions Tumors Hernia Irritable bowel disease Intussusception (tunneling within bowel) Intraluminal lesions other than tumors (foreign body, gallstones, bezoars)
bowel obstruction diagnostic criteria
Dilated small bowel loops >3 cm (SBO) >5/6cm LBO
Air-fluid levels
Paucity of air in colon (lack of air past the obstruction if complete obstruction)
SBO:
Can look very similar to ileus when early within first few days, need follow up monitoring to see how it develops
Will show dilated loops of small bowel >3cm
Transition point
Collapsed bowel distal to transition point
Maybe a small bowel faeces sign: stool seen within the small bowel
Closed loop bowel obstruction
Obstruction of a loop of bowel in 2 separate places
Will not see any significant dilatation proximal to the closed loop
Often caused by adhesions from prior surgery
Can result in strangulation (surgical emergency)
There will be blocked blood flow to bowel resulting in necrosis
Imaging will show wall thickening and decreased enhancement of bowel wall
Closed loop obstructions need immediate surgical management due to high risk of perforation from strangulation
Strangulated bowel and red flags
Refers to ischaemia/infarction of an obstructed loop of bowel
Most commonly seen in context of a closed loop obstruction
Will show reduced mural enhancement on CT scan
Red flags: indicate early surgical interventions:
Patient is usually more ill than expected
Severe abdominal pain disproportionate to clinical findings suggests ischaemia (sharp, constant, localised pain with peritonism)
Localised abdominal tenderness and rigidity
Tachycardia
Fever
Marked raised leukocytes
Acidosis
Comparison of SBO and paralytic Ileus
Both conditions cannot promote bowel contents (impaired motility)
Both show distended loops of small intestine detected by XR or CT
OBSTRUCTION physically blocks the contents: the lumen is closed
ILEUS: the paralysis of the intestinal wall muscles makes contents stagnant: the lumen in open, this is a FUNCTIONAL obstruction
Ileus has no hyper-secretion and therefore no colic usually
Bowel sounds are absent/diminished in ileus but are hyperactive in SBO
Ileus is temporary motility disorder, reversed by correction of the cause
Localised functional paralytic Ileus and causes
Dilatation of a loop(s) of small bowel called sentinel loops are seen on AXR
Results from abdominal pathology causing focal inflammation of the small bowel
Causes: Cholecystitis Pancreatitis Appendicitis Diverticulitis Ureteral stones
Generalised functional Ileus and causes
Most often post operative
Involves the entire bowel, large and small
Cause of generalised function ileus: operations, infection and inflammation, electrolyte imbalances, drugs
Abdominal surgery
Infection: sepsis, intra-abdominal abscess, peritonitis, pneumonia, electrolyte abnormalities (hypokalaemia, hypomagnesemia, hypermagnesemia, hyponatremia)
Medication: anticholinergics, opiates, phenothiazines, CCB, tricyclic antidepressants
Hypothyroidism
Retroperitoneal haemorrhage
Spinal cord injury
Myocardial infarction
Mesenteric ischaemia
Paralytic Ileus presentation
Inability to tolerate liquids or solids by mouth
Nausea
Lack of flatus or bowel movements
Vomiting and abdominal distension MAY occur
Large bowel obstruction and causes
Far less common than small bowel (20% bowel obstructions)
Causes:
Malignancies
Diverticular disease
Colonic volvulus
Bowel obstruction presentation
Nausea and vomiting Abdominal colics Abdominal distension Lack of wind/gas passage ie constipation or obstipation Loss of lots of fluid: hypovolemic
Upper obstruction (small intestine):
Vomiting occurs earlier on
Distance between colics are SHORTER
Abdominal distension and constipation are LATE presenting
Lower obstruction (large intestine): Abdominal distension and constipation occur earlier on Distance between colics is longer Vomiting occurs later on *in complete obstruction, symptoms are complete, but in partial obstruction symptoms are more mild usually and they may also develop diarrhoea (hyper-secretion)*
SBO and LBO AXR comparisons
SBO: Central gas shadows No gas in large bowel Mucosal folds (valvulae conniventes) completely cross lumen May show fecal impact sign
LBO:
Peripheral gas shadows
Dilation >6 cm
Gas proximal to blockage but not in rectum (unless PR exam done beforehand)
Mucosal folds (haustra) do NOT cross all lumen width
Bowel obstruction management
ALL bowel obstructions need fluid resuscitation and correction of electrolyte imbalances
Conservative: usually successful secondary to adhesions, Ileus and partial obstructions
- Monitor patient regularly, regular examinations and imaging to monitor progress, NBM, if signs of strangulation, ischaemia, peritonitis or toxaemia then ready for emergency surgery
Surgical intervention: strangulation, frank perforations, peritonitis, LBO all need immediate surgical intervention
Fluid resus steps
Two large IV lines administer saline or hartmann
Bloods: FBC (Hb, WCC), U+Es (Na, K), CRP, amylase, lipase, group and save
NBM, NG tube insertion
Catheterise
Fluid balance chart
ABG needed if in shock, suspected ischaemic bowel or pancreatitis
Acute appendicitis
Appendix is attached to cecum found in left inguinal fossa (RIF)
Most common acute abdomen complaint
Highest incidence between 10-20 years but can occur at any age
Very wide range of presentations
Acute appendicitis causes and pathophysiology
Causes:
Fecalith (poop rock)
Undigested seeds
Pinworm infection
Pathophysiology:
Obstruction blocks the blind ending lumen
The appendix continues secreting fluid and becomes oedematous
Causing inflammation of the appendix and leading to compression of afferent visceral nerves nearby causing pain
Can lead to gangrene if the obstruction of blood vessels supplying the organ persists
Acute appendicitis presentation
Epigastric or periumbilical pain that moves to the right inguinal fossa (RIF)
Gradual pain onset, constant and moderate-severe
Peritonism: Shows guarding and rebound tenderness or percussion tenderness in RIF
Tachycardia
Fever
Anorexia
Nausea may be present but vomiting is rare
Constipation in adults, diarrhoea in children
Rovsing’s sign (pain greater in RIF than LIF when LIF pressed)
Psoas sign (pain on flexion and internal rotation of right hip if appendix close relation to obturator internus)
Acute appendicitis complications
Perforation: if faecolith present and diagnosis delayed can cause generalised peritonitis Gangrenous appendix Appendix abscess (usually treat with drainage or antibiotics) Appendix mass (inflamed and covered with omentum) diagnosed with US/CT, early surgery or conservative NBM and antibiotics treatment used +/- delayed appendectomy
Acute appendicitis investigations
Bloods: neutrophil leucocytosis, elevated CRP
CT scan has high diagnostic accuracy!!
Mcburney’s point +ve
acute appendicitis management
Mild: rest GI and antibiotics for inflammation
Appendectomy +/- antibiotics
Laparoscopic appendicectomy (esp. Good for women and obese with suspected gangrenous perforation)
Meckels diverticulum
Outpouching of the lower part of the small intestine
It is a remnant of the vitello-intestinal duct (leftover umbilical cord should obliterate during fifth week foetal development)
Most common congenital defect of the GIT (2-3% population)
Usually asymptomatic
The majority of symptomatic pts begin presenting before age 2
Meckel’s diverticulitis occurs in 20% patients who become symptomatic, it is clinically indistinguishable from appendicitis
Meckels diverticulum disease of 2s
2% people have this
2:1 M:F ratio
2 inches in length usually
2 more common ectopic tissues: pancreas and stomach
2 complications other than diverticulitis: obstruction, bleeding
2 mechanisms of obstruction: secondary intussusception (inverted diverticulum acts as lead point), volvulus (loops around band between diverticulum and umbilicus)
Meckels disease presentation, diagnosis and management
Presentation:
GI bleeding
Obstructive symptoms
Diagnosis:
technetium -99m pertechnetate scan (Meckel’s scan)
Management:
Asymptomatic - no treatment needed
Symptomatic - monitoring
Meckel’s diverticulitis - laparoscopic surgery
Peritonitis
Inflammation of the peritoneum
Generally secondary generalised bacterial infection
Common complication of many abdominal pathologies
Classification:
Chemical, viral, bacterial (primary or secondary)
Local peritonitis - localised tenderness
Generalised peritonitis - generalised tenderness
Causes of peritonitis
Post-surgical eg anastomotic leak, enteric injury (30%)
Acute perforated appendicitis (most common esp <45 yrs (20%)
Acute diverticulitis (most common in elderly)
Peptic ulcer perforation - 10% (or other upper GI perforation)
Perforated acute cholecystitis
Perforated tumours (colonic or gastric)
Perforated ischaemic bowel (eg acute mesenteric ischaemia)
Acute pancreatitis
Peritoneal dialysis-related
Peritonitis pathophysiology
Widespread absorption of toxins from large, inflamed surface (peritoneum)
Paralytic ileus with loss of fluid, electrolytes and protein
Gross abdominal distension with elevation of diaphragm, increases susceptibility to lung collapse and pneumonia
Primary (rare): monomicrobial, typically streptococcal. Probable port of entry via the bloodstream
Secondary (common): polymicrobial, gram - and +ve and anaerobes. Portal of entry from intra-abdominal organs (secondary to perforation, ischaemia or infection of other organs etc)
Usually shows mixed faecal flora (E.coli, strep facalis, pseudomonas)
Peritonitis presentations
Anorexia
Fever
Severe generalised abdominal pain, radiating to shoulder and back
Abdo pain worse with movement, coughing, sneezing
Alleviated when lying still
Tachycardia
Generalised abdominal tenderness, rebound tenderness, guarding and rigidity
Max tenderness may indicate underlying cause if in one particular area
May be abdominal mass present
Advanced stages: Distended abdomen and tympanic on percussion Increasingly toxin and ill Feculent vomit Sunken eyes (severe dehydration) Rapid, febril pulse (shock) Moist, cold, cyanosed skin (shock) drowsy/confused (shock)
Peritonitis investigations
ABCDE assessment and act accordingly
Analgesia
Find cause: Bloods show infection markers, Abdo CT scan confirms or excludes acute pancreatitis or locates probably source of pathology
Laparoscopy
Prep patient for possible surgery: most causes of peritonitis need surgery, however, acute pancreatitis is contraindicated for surgery!
Management of peritonitis
Early: IV antibiotics (wide coverage) eg metronidazole 500mg IV tds + Cefuroxime 750mg IV tds
Oxygen therapy, serum therapy (IVI), correction of electrolyte abnormalities
Definite specific management should then be based on diagnosis of cause: surgery, medications ect.]
if there is swelling, swinging fever, high WCC then suspect ABSCESS FORMATION and US/CT guided drainage is needed or by laparotomy
Bacteroides fragilis - antibiotics in peritonitis needs to cover this bacteria (common gut flora causing abdo infections)
Local peritonitis causes
Diverticulitis
Cholecystitis
Salpingitis
Appendicitis
local peritonitis presentation and investigation
Presentation:
Localised tenderness/rebound tenderness
Presentation of cause
Investigations: Bloods CT US CXR AXR *if there is swelling, swinging fever, high WCC then suspect ABSCESS FORMATION and US/CT guided drainage is needed or by laparotomy*
Gastroenteritis
(adults)
An infection of the GIT, nonspecific term to describe a condition with a combination of nausea, vomiting, diarrhoea and abdominal pain
About 20% of the UK develops every year
Viral infections cause 30-40% of gastroenteritis in adults (higher in children)
Management is not usually dependent on cause as it is never isolated and the responsible agent never diagnosed
(children):
Infective gastroenteritis in young children by the sudden onset of diarrhoea with/without vomiting
Mostly due to viral infection but can be from bacterial or protozoal infections.
Usually resolves within days but can cause severe dehydration and become life threatening
Gastroenteritis causes
children:
Retrovirus most common (56%), campylobacter spp., salmonella spp., norovirus, E.coli
Cause never isolated and responsible agent never diagnosed
adults:
A variety of viral (norovirus, rotavirus, adenovirus), bacterial (E. coli, salmonella, staph.aureus toxins) and parasitic pathogens
Gastroenteritis risk factors
Poor hygiene, lack of sanitation
Compromised immunity
Achlorhydria: lack of HCL in digestive juices (especially for salmonella and campylobacter) can result from acid-suppressing drugs
Poorly cooked food, cooked food left too long, insufficient reheating etc
Gastroenteritis presentations
History of eating mispreppared food (incubation usually around 24-36 hours for virus’, few hours to 4 days for bacillary dysentery and 7-10 days for parasites) or may have recently been to exotic location
Vomiting and nausea
Abdominal pain
Diarrhoea (bloody diarrhoea may indicate bacterial infection especially E. coli)
Pyrexia (in adults can indicate invasive organism)
Complications of gastroenteritis
Dehydration and electrolyte disturbance
Haemolytic uraemic syndrome (HUS): AKI, haemolytic anaemia and thrombocytopenia
Reactive complications such as urticaria, reactive arthritis, erythema nodosum etc.
IBS
Gastroenteritis investigations
Vitals: temp, BP, pulse, HR, respiratory rate
Abdominal examination to exclude other diagnoses (appendicitis)
Assess for dehydration
Stool microscopy, culture and sensitivity if there is blood/mucus in stool or the patient is immunocompromised or the patient has been abroad to anywhere other than western europe, north america, australia or NZ recently, if diarrhoea has not improved by day 7 or uncertain diagnosis.
Unwell patients may need FBC, renal function and electrolytes
Gastroenteritis prevention and management
Prevention:
Good hand hygiene
Good food hygiene and preparations (cooking)
Management:
All dysentery and food poisoning are notifiable diseases
Hospital admission if unable to retain oral fluids, features of shock or severe dehydration
Assess the extent of dehydration and manage accordingly, patient education of infection prevention, advising small light meals, avoiding spice or heavy food while ill.
Oral rehydration salt (ORS) can be used in frail elderly patients
Advise exclusion from work or other settings until at least 48 hours after being free from diarrhoea and vomiting
Can advise antimotility drugs if these will enable quicker resolution to essential activities in those with mild to moderate diarrhoea (loperamide 1st line). AVOID if blood or mucus in stool or high fever present
CHILDREN
Encourage fluid intake and normal breastfeeding etc. but avoid solid foods if during rehydration therapy
Offer oral rehydration salts to those at increased risk of dehydration
Racecadotril can be used with oral rehydration in infants over 3 months
Monitor vitals very well.
Gastroenteritis red flags
Appears unwell or deteriorating Altered responsiveness Sunken eyes Tachycardia Tachypnoea Reduced skin turgor
Signs of shock
Decreased level of consciousness Pale or mottled skin Cold extremities Decreased level of consciousness Tachycardia Tachypnoea Weak peripheral pulses Prolonged capillary refill Hypotension
Dehydration assessment
Mild: lassitude (weak, lacks energy), anorexia, nausea, light-headed, postural hypotension
Moderate: apathy (lack of interest or concern), tiredness, dizzy, muscle cramps, dry tongue, sunken eyes, reduced skin elasticity, postural hypotension, tachycardia, oliguria
Severe: profound apathy, weakness, confusion, shock, tachycardia, marked peripheral vasoconstriction, hypovolemia, oliguria or anuria
Cholelithias
70% patients with gallstones are asymptomatic and have no issues
Can cause acute or chronic cholecystitis, biliary colic, pancreatitis or obstructive jaundice
Biliary colic is most common, caused by gallstone impacting in the cystic duct or the ampulla of Vater, blocking the tubes.
Second most common is acute cholecystitis, caused by gallbladder distension and subsequent necrosis and ischemia of mucosal wall
Cholelithias pathophysiology
Bile is formed of cholesterol, phospholipids and bile pigments, stored in the gallbladder before passing into the duodenum
the cystic duct travels from the GB, joins the common hepatic duct to form the common bile duct, joined by the pancreatic duct close to the duodenum to form the hepatopancreatic ampulla of Vater which deposits bile into the duodenum.
Gallstones form as a result of supersaturation of bile
Types of gallstone
Cholesterol stones: composed purely of cholesterol from excess cholesterol production. Highly linked to poor diet and obesity.
Pigment stones: composed purely of bile pigments from excess bile pigments production. Commonly seen in those with haemolytic anaemia
Mixed stones: mixture of both
Risk factors for cholelithias
5 Fs: Fat, forty, fertile, female, family history
Increasing age
Positive family history
Female
Loss of bile salts (after obesity surgery)
Diabetics (metabolic syndrome)
Oral contraception, particularly in young women
Management of cholelithias
Case by case basis: very small risk of complications so mostly a ‘watch and wait’ policy
Younger patients are more likely to develop complications more frequently due to having gallstones for longer - monitor more frequently
Modify risk factors if possible
Biliary colic
Occurs when the gallbladder neck becomes impacted by a gallstone.
No inflammatory response, but the contraction of the gallbladder against the occluded neck will cause pain
Over 50% symptomatic pts with gallstones will present with biliary colic
Biliary colic presentations
Sudden, dull pain
Colicky
Focussed often in the RUQ, although may radiate to epigastrium and/or the back
Pain may be precipitated by consumption of fatty foods (stimulates CCK release from duodenum, causing contraction of GB)
Nausea/vomiting
Often relieved quickly with pain relief
Cholecystitis
Inflamed gallbladder
Most often caused by gallstones
More common in women
25% pts with cholelithias will present with acute cholecystitis
Cholecystitis pathology
Most individuals with gallstones are asymptomatic, the gallstones mostly stay within the gallbladder and cause no harm
Cholecystitis is usually caused when a gallstone seemingly becomes stuck in the cystic duct
Bile then builds up in the gallbladder, which becomes distended and the walls of the gallbladder consequently become inflamed or may even become infected
Infection is more prone to complications
Repeated attacks of acute cholecystitis leads to chronic cholecystitis; the walls of the gallbladder become thickened and scarred and the gallbladder becomes shrivelled
Risk factors for cholecystitis
5 Fs: fat, fertile, female, forty, family history
Gallstones or biliary sludge Hospitalisation for trauma or acute biliary illness Female Increasing age Obesity Rapid weight loss Pregnancy Crohn's disease Hyperlipidaemia
Cholecystitis presentation
Upper abdomen pain, usually worse on the right side under the ribs (RUQ) continuous epigastric pain
May radiate to the back or to the right shoulder and tends to last several hours
Nausea and vomiting
Fever, lethargy
+ve Murphy’s sign
May have previous history of cholecystitis
Murphy’s sign positive: increased pain when placing hand under the ribs on the right hand sign and asking patient to take deep breath, putting pressure on the gallbladder
Cholecystitis investigations
Vitals: BP, temperature, pulses, urine output
Abdominal examination including Murphy’s sign
Ultrasound: thickened GB walls (>3mm), gallstones
Bloods: WWC raised, mildly abnormal liver enzymes
CT of abdomen if indicated
Magnetic resonance cholangiopancreatography (MRCP): shows potential defects in biliary tree with almost 100% sensitivity
trans-abdominal US is most sensitive!! = FIRST LINE
Management of acute cholecystitis
Acute cholecystitis:
Opioid (morphine or pethidine) given parenterally and/or diclofenac by suppository - overcomes absorption difficulties due to vomiting.
Pain lasting >24 hours with fever needs hospital admission
IV antibiotics (coamoxiclav + metronidazole)
Open cholecystectomy surgery to remove stones in emergency - very rarely perform cholecystectomy for acute cases
Sepsis 6 if septic
Management of chronic cholecystitis
Laparoscopic cholecystectomy preferred Percutaneous cholecystostomy (surgical drainage) is useful for those not fit for cholecystectomy *Post op complications are rare but include bile duct injury, fat intolerance and post-cholecystectomy syndrome (abdominal pain, jaundice or dyspeptic symptoms*
Prognosis is good however there is a high chance they may experience more bouts of cholecystitis which is why usual treatment is to remove the gallbladder entirely
Cholangitis and causes
Infection of the biliary tract
Associated with high morbidity and mortality if untreated
Cause:
Biliary outflow obstruction
Gallstones
ERCP (iatrogenic)
Cholangiocarcinoma
Most common organisms are E. coli, Klebsiella and enterococcus
Pancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy and parasitic infections (rare)
Cholangitis pathophysiology ad risk factors
Pathophysiology:
During obstruction the stasis of fluid combined with elevated intraluminal pressure allows bacterial colonisation of the biliary tree to become pathological
Risk factors:
Oral contraceptive
Fibrates
Lipid-rich diet
Cholangitis presentation
Charcot’s triad: jaundice, fever, RUQ pain
RUQ pain Fever Jaundice (when bilirubin >50 umol/L) Pruritus (as result of bile accumulation) Pale stool Dark urine Pyrexic Rigors Confusion Hypotension, tachycardia May have history of cholelithias, recent biliary tract procedure (ERCP/cholecystectomy) or previous history of cholangitis
Cholangitis investigations
Bloods: FBC (Hb and WCC) shows leukocytosis, LFTs (raised ALP and GGT)
Blood cultures
Biliary tract USS shows bile duct dilation >6mm and may indicate underlying cause
GOLD STANDARD: ERCP is diagnostic and therapeutic
Cholangitis management
Vitals: check for sepsis, manage as needed
Gain IV access for fluid resus
Routine bloods and blood cultures taken early
Broad spectrum antibiotics therapy (co amoxiclav + metronidazole)
Definitive management given via endoscopic biliary decompression (ERCP +/- sphincterotomy and stenting)
PTC percutaneous transhepatic cholangiography 2nd line
In long term may need cholecystectomy if gallstones are underlying cause
Acute pancreatitis
Sudden inflammation of the pancreas
Typically caused by hypersecretion of backflow (obstruction) of exocrine digestive enzymes, resulting in autodigestion of the pancreas
Can be mild or life threatening
With effective treatment has good prognosis
Acute pancreatitis pathology
Occurs when digestive enzymes are activated before release into the duodenum and so attack the pancreas
If the enzymes enter the bloodstream other organs can become affected which can lead to life threatening shock symptoms
Pancreatic damage can be classified into two major categories: interstitial oedematous (most common, better prognosis) and necrotising (5-10% cases, more severe)
The damage is potentially reversible whereas chronic pancreatitis results in irreversible damage from ongoing inflammation
Causes of acute pancreatitis
I GET SMASHED
Iatrogenic Gallstones Ethanol Trauma Steroids Mumps/malignancy Autoimmune disease Scorpion sting Hypercholesterolaemia/hypertriglyceridaemia ERCP Drugs: thiazides, septrin, tetracyclines, azathioprine
Risk factors of acute pancreatitis
Male Increasing age Obesity Smoking Family history
Acute pancreatitis presentations
Severe, sudden epigastric pain
Sharp, stabbing pain, may radiate to sides or back if cholecystitis present too
Vomiting
Pain rapidly crescendos, duration likely 1 day
May have history of biliary colic, recent surgery or illness
Exacerbated by movement, alleviated partially by leaning forward or adopting foetal position
Tetany may occur from hypocalcemia (secondary to fat necrosis)
Acute pancreatitis investigations
Abdominal examination: epigastric tenderness, abdominal distension
Cullen’s sign: periumbilical bruising (LATE sign of retroperitoneal haemorrhage)
Grey-Turner’s sign: flank bruising (LATE sign of retroperitoneal haemorrhage)
Bloods: FBC, CRP, U+Es, LFTs, Lipase, serum amylase, VBG, ABG, Beta-hCG (rule out pregnancy and permit safe investigation of XR and CT)
ECG to ensure no MI
Urinalysis
CXR to look for free gas under diaphragm (pneumoperitoneum)
USS - abdominal ultrasound
CT of abdomen and pelvis
glasgow-Imrie scale
Diagnosis of acute pancreatitis
two of three criteria
Abdominal pain + history suggestive of acute pancreatitis
Serum amylase/lipase of over 3 times upper limit of normal
Imaging characteristic of acute pancreatitis
Classification of acute pancreatitis
Mild: most common, no organ dysfunction/complications, resolves within 1 week
Moderate: initially some evidence of organ failure which improves within 48 hours
Severe: persistent organ dysfunction >48 hours with local or systemic complications
Management of acute pancreatitis
PANCREAS:
Perfusion: fluid resus and oxygenation
Analgesia
Nutrition: enteral feeding <48 hours
Clinical: APACHE II or APACHE I scores to assess need to transfer to HDU
Radiology: USS for gallstones, choledocholithias and local complications. CECT after 48-72 hours pain onset to determine degree and extent of necrosis. Percutaneous catheter drainage USS guided helpful to manage necrosis
ERCP: within 72 hours if cholangitis or severe acute pancreatitis with persistent obstruction
Antibiotics: empirical ABs if infection suspected
Surgery: multiorgan failure with necrosis not responding to conservative management
Predict severity using the glasgow-Imrie scale, predict mortality using APACHE II scoring
Once diagnosis is confirmed, largely supportive management: fluid resuscitation, analgesia (IV paracetamol and opioids)
Nil-by-mouth until initial pain improves - gradual feeding re-introduced via oral feeding or nasojejunal feeding
Antiemetics: IV ondansetron
Calcium derangement corrected
Control glucose
Antibiotics for prophylaxis PRN
Infected necrotic tissue needs to be removed via: percutaneous drainage or surgical necrosectomy
Gallstone pancreatitis:
Obstructed bile duct needs ERCP to relieve obstruction with/without sphincterotomy to dilate the sphincter of Oddi to allow removal of ductal stones, biliary sludge etc.
Cholecystectomy for all patients with gallstone pancreatitis during same admission of acute episode
Alcoholic pancreatitis:
Benzodiazepines for withdrawal agitation and seizures
Thiamine, folate and B12 replacement
Glasgow-Imrie scale: PANCREAS
PaO2 <7.9 Age >55 Neutrophils/WCC >15 Calcium <2 Renal function/ urea >16mmol Enzymes (LDH >60) Albumin <32 g/l Sugar >10mmol
*if CRP >150mg/l likely to be severe
Chronic pancreatitis and cause
Chronic inflammation resulting in progressive and irreversible damage to the pancreas parenchyma
Male to female ratio 4:1
Cause: Chronic alcohol abuse (60%) Idiopathic (30%) Hyperlipidaemia Infection (viral and bacterial) Hereditary (CF) Autoimmune
Presentation of chronic pancreatitis
Chronic pain, complicated by recurring attacks of acute pancreatitis (acute-on-chronic pain)
Typically in epigastrium and back
Nausea and vomiting
Endocrine insufficiency (secondary to islet of langerhans damage)
Exocrine insufficiency (secondary to acinar cell damage causing malabsorption - weight loss, diarrhoea, steatorrhoea)
Abdo examination: soft abdomen but tender epigastrium, may have signs of cachexia and malabsorption
Chronic pancreatitis investigations
Urine dip
Bloods: FBC, CRP, serum amylase/lipase (often not raised in established disease), BLOOD GLUCOSE, LFTs (obstructive jaundice)
Faecal elastase level will be low
Chronic pancreatitis management
Treat underlying cause (alcohol cessation, statin therapy for hyperlipidaemia)
Analgesia (opioid or neuropathic analgesics)
Enzyme replacement for malabsorption
Vitamins A, D, E and K (fat soluble)
Regularly check for endocrine insufficiency, (HbA1c annually) treat as needed, also screen bone density regularly
Cholesterol and pigment gallstones
Cholesterol gallstones often appear yellow and are the most common type of gallstone. Scientists believe that cholesterol stones are caused by bile that contains:
too much cholesterol
too much bilirubin
not enough bile salts
The cause of pigment stones is not known. They seem to occur in people who have:
cirrhosis of the liver
biliary tract infections
hereditary blood disorders in which the liver makes too much bilirubin
Choledocelithias
(also called bile duct stones or gallstones in the bile duct) is the presence of a gallstone in the common bile duct.
Choledocelithias presentation
abdominal pain in the RUQ or epigastric region
fever
jaundice (yellowing of the skin and eyes)
loss of appetite
nausea and vomiting
clay-colored stools
Pain severity can vary throughout, can be sporadic or can linger
Complications of choledocelithias
Cholangitis
Biliary cirrhosis
pancreatitis
Choledocelithias investigations
transabdominal ultrasound (TUS)
abdominal CT scan
endoscopic ultrasound (EUS)
endoscopic retrograde cholangiography (ERCP)
magnetic resonance cholangiopancreatography (MRCP)
percutaneous transhepatic cholangiogram (PTCA)
complete blood count
bilirubin
pancreatic enzymes
liver function tests
Choledocelitheias management
stone extraction via biliary endoscopic sphincterotomy (BES) using balloon/basket device
fragmenting stones (lithotripsy)
surgery to remove the gallbladder and stones (cholecystectomy)
surgery that makes a cut into the common bile duct to remove stones or help them pass (sphincterotomy)
biliary stenting
Intussusception
Common in infants 3-12 months
Boys:girls 3:1 ratio
Usually occurs in the ileocecal region (usually ileum telescoping into cecum)
Primary: 95% in infants and children, most often due to lymphoid hyperplasia from peyer’s patches
Secondary: adults mostly, much less common, lead point/apex is a polyp, tumour or inverted Meckel’s diverticulum etc.
Low mortality within 24 hours, but very high in irreducible or gangrenous cases
Pathophysiology:
Telescoping of portion of the intestine
Mesentery is dragged alongside proximal bowel wall into the distal lumen, obstructing venous return
Causes Oedema, mucosal bleeding and increased pressure
If arterial flow is compromised then causes ischaemia, necrosis and perforation can result
Intussusception presentation
classic triad: sudden severe paroxysmal colicky pain, bilious vomiting, red currant jelly stools
Colicky abdominal pain and guarding Leg flexing Fever (if septic) Lethargy Vomiting Blood in stool: red currant jelly stool Poor feeding Dance’s sign: empty RIF + sausage shaped mass in mid/RUQ Abdominal distension Signs of shock in late presentation
Intussusception investigations
USS if stable may show bullseye sign, doughnut sign or crescent in doughnut Diagnostic enema (CI if peritonitis, shock, perforation or pt unstable) shows meniscus sign/coiled spring sign
Intussusception management
Acute: clinically stable, no CI to contrast enema reduction:
NBM, nasogastric tube, Fluid resus and contrast enema reduction
Broad spectrum antibiotics IF sign of infection/ischaemia
Clinically unstable or CI contrast enema
Fluid resus and surgical reduction
Broad spectrum antibiotics IF sign of infection/ischaemia
Achalasia
Rare disorder of the oesophagus making it difficult to swallow food or drink
Motility disorder of the lower oesophageal or cardiac sphincter
This layer of muscle has impaired peristalsis and failure of relaxation causing functional stenosis or stricture
Exact cause is unknown but can occur secondary to other conditions such as oesophageal cancer
Tends to present in adult life, children is very rare
achalasia pathophysiology
Muscle tone and activity are controlled by a balance of excitatory transmitters such as ACh and substance P and inhibitory transmitters such as NO and Vasoactive intestinal peptide (VIP)
The interstitial cells of Cajal (cells within the intestinal wall which provide the pacemaker function of the musculature) are thought to be involved in the condition
Autoimmune reactions to viral infections and genetic factors have also been implicated to trigger the condition
Achalasia presentation
Dysphagia
Food bolus impaction
Regurgitation (may also induce regurgitation to reduce pain)
Retrosternal chest pain in some pts, after eating
Heartburn also common and can be aggravated by treatment
Weight loss
Nocturnal cough (later sign of disease)
Inhalation of refluxed contents - inhalation pneumonia incidences! (later sign)
Achalasia investigations
Examinations are unlikely to reveal anything!! Sometimes high incidences of inhalation pneumonia may indicate
CXR may show signs of inhalation or may show dilated oesophagus behind the heart (rare to see in practice)
Barium swallow (contrast material) to rule out malignancy
Endoscopy
Manometry GOLD STANDARD: detects up to 9-% cases, high resting pressure in cardiac sphincter, incomplete relaxation on swallowing and absent peristalsis. If this shows normal results but there are symptoms of achalasia then pseudoachalasia might be present
Lower oesophageal pH monitoring to exclude GORD
Achalasia management
CCB and nitrates may reduce pressure in lower oesophageal sphincter but only effective in 10% pts.
Heller myotomy is considered best treatment if pts are fit, performed by laparoscope (success rate 85-95%, low complication rate)
For older pts can use pneumatic dilatation: insert balloon and inflate to rupture muscle while leaving mucosa intact (multiple dilations over months or years has better success rates)
Endoscopic injection of botulinum toxin
Peroral endoscopic myotomy and endoscopic stent
Achalasia complications
Nocturnal inhalation
Aspiration pneumonia
GORD (from treatments)
Oesophageal cancers
Dyspepsia
Indegestion Complex of upper GI symptoms present for typically more than four weeks Includes abdominal pain or discomfort Heartburn Acid reflux Nausea Vomiting
Dyspepsia presentation and red flags
Epigastric discomfort Fullness and bloating Excessive flatus Nausea Fatty food intolerance
Red flags:
Weight loss
Recurrent vomiting
Dysphagia
Evidence of GI bleeding (blood in stool etc)
Urgent 2WW referral for chronic GI bleeding or for >55 years with weight loss
Dyspepsia investigations
Abdominal exam: always check for masses
Bloods: FBC for iron deficiencies
Test for helicobacter pylori
Endoscopy (considered in >55 years who are treatment resistant, raised platelet count, nausea or vomiting, previous Barrett’s oesophagus)
Dyspepsia management
Uninvestigated without alarm features:
Review medications: NSAIDs, steroids, Ca antagonists, nitrates, theophyllines, bisphosphonates
Lifestyle advice: smoking cessation, regular meals, cease excessive alcohol consumption, avoid triggering foods, reduce stress, anxiety and depression if needed
Antacids for occasional symptom relief
Test for H.pylori and treat if positive
Empirical acid suppression (with proton pump inhibitors) for 1 month with full dose, continue long term either PPI, H2RA on lowest effective dose (eg ranitidine)
Investigate to find underlying cause and treat best as possible
Review at end of treatment course to confirm outcome
H pylori eradication 1st line
Lansoprazole 30 mg, omeprazole 20–40 mg, esomeprazole 20 mg, pantoprazole 40 mg, or rabeprazole 20 mg.
7-day triple therapy regimen of:
PPI twice-daily and amoxicillin 1 g twice-daily and
Either clarithromycin 500 mg twice-daily or metronidazole 400 mg twice-daily.
PENICILLIN ALLERGY: 7-day triple therapy regimen of:
A PPI twice-daily and clarithromycin 500 mg twice-daily and metronidazole 400 mg twice-daily.
If the person is allergic to penicillin and has had previous exposure to clarithromycin, offer a 7–10 day triple therapy regimen of:
A PPI twice-daily and metronidazole 400 mg twice-daily and levofloxacin 250 mg twice-daily.
If re-testing is indicated, wait at least 4 weeks (ideally 8) after initial eradication therapy
Oesophagitis and presentation
Inflammation of the oesophagus lining, mostly due to reflux of stomach contents leading to chronic irritation
Presentation: Heartburn Upper chest and abdomen pain Nausea Bloating Dyspepsia (indigestion) Tend to be related to meal intake Persistent cough particularly at night Mouth and gum problems, bad breath
Endoscopic grading of oesophagitis
Stage 1: Single of multiple erosions on single fold. May be exudative or erythematous
Stage 2: Multiple erosions on multiple folds. May be confluent
Stage 3: Multiple circumferential erosions
Stage 4: Ulcer, stenosis or oesophageal shortening
Stage 5: Barrett’s epithelium. Columnar metaplasia in form of circular or non-circular extensions (Islands or tongues)
OR
A - one or more mucosal breaks <5mm none extending to tops of mucosal folds
B - one or more mucosal breaks >5mm none extending between tops of two mucosal folds
C - mucosal breaks extending between tops of two or more mucosal folds, involving <75% mucosal circumference
D - mucosal breaks involving >75% mucosal circumference
GORD
Acid from stomach leaks up into oesophagus, usually as result of cardia sphincter weakening
2-3 x more common in men
25% adults experience heartburn
5% have daily symptoms
Spectrum of disorders ranging from the most common endoscopy negative GORD to oesophageal mucosal damage, which can progress to ulceration, stricture (although only 8% will have mod-severe oesophagitis)
GORD pathophysiology
Gastro-oesophageal reflux is a natural protective mechanism of the lower oesophagus
If reflux is prolonged or excessive it can cause breakdown of protection with inflammation of the oesophagus (oesophagitis)
Abnormalities of the lower oesophageal sphincter may facilitate excessive reflux of the gastric and sometimes bile contents into the oesophagus
Reflux of duodenal contents (bile) is more severe
GORD risk factors:
Increased intra-abdominal pressure Weak cardiac sphincter Smoking Alcohol Fat Coffee Pregnancy Obesity Tight clothes Large meals Surgery in achalasia of the cardia Systemic sclerosis Hiatus hernia Drugs: tricyclic antidepressants, NSAIDs, anticholinergics, nitrates, CCBs
*most of these factors increase intra-abdominal pressure
GORD presentations
Heartburn, related to eating, lying down, stooping, straining
Relieved by antacids
Retrosternal discomfort
Acid brash (regurgitation of acid or bile)
Water brash (excessive salivation)
Odynophagia (pain on swallowing) can indicate stricture or severe oesophagitis
Atypical symptoms: found in up to 50% cases
Chest pain
Epigastric pain
Bloating
GORD investigations
ENDOSCOPY - gold standard
Bloods: FBC to exclude anaemia
Barium swallow
Oesophageal pH monitoring (24 naso-oesophageal study or wireless pH capsule)
Dyspepsia red flags
Dysphagia
Dyspepsia with weight loss, proven anaemia or vomiting
Dyspepsia >55 years with <1 onset or continuous symptoms since onset
Dyspepsia with at least 3 risk factors
GORD management
Lifestyle: reduce weight, smoking cessation, decreased alcohol consumption, raise head of bed at night, small regular meals, avoid hot drinks and eating <3 hours before going to bed, avoid triggering drugs (nitrates, NSAIDs, anticholinergics, antidepressants)
PPI full dose for one month (two months if severe oesophagitis), can add H2RA (ranitidine) at bedtime, or switch entirely to H2RA if needed with confirmed oesophagitis
H. pylori eradication if indicated
Long term acid suppression for recurring symptoms after initial management (healing dose for one-two months then taper to lowest dose providing symptom relief)
Referral for endoscopy
Surgery: laparoscopic insertion of magnetic bead band
Review patients annually if on long term treatments or as needed
Peptic ulcer disease and causes
Break in inner lining of stomach, duodenum or lower oesophagus
Gastric ulcers in stomach, duodenal ulcers, oesophageal ulcers
Helicobacter pylori infection associated with 95% duodenal ulcers and 80% gastric ulcers
Pathophysiology:
Stomach mucosa is prone to ulceration from: breakdown of protective layer of the stomach and duodenum and an increase in stomach acid (stress, excessive caffeine, smoking, spicy foods etc)
Cause: H pylori NSAIDs Pepsin Smoking Alcohol Bile acids Steroids Stress Changes in gastric mucin consistency (genetically determined)
Peptic ulcer disease presentation
very nonspecific presentation sometimes
Epigastric pain usually 1-3 hours postprandial, may sometimes wake patient in night
Relieved by food (DUODENAL ulcer)
Worsened by food (GASTRIC ULCER)
Nausea and vomiting
Oral flatulence
Bloating, distension and intolerance of fatty foods
Heartburn (sometimes)
Posterior ulcer may cause pain radiating to back
Symptoms relieved by antacids
Epigastric tenderness
Succussion splash (if gastric emptying is slow)
Melaena
Haematemesis
Dyspepsia
Iron deficiency anaemias
SILENT Peptic ulcer disease risk factors
can present with unheralded perforation or bleeding
Increasing age Male sex Smoking H pylori infection Absence of atrophic gastritis
PUD investigations
Bloods: FBC for iron deficiencies
H pylori testing
Endoscopy
PUD management
Lifestyle: avoid triggering medications, smoking cessation
H pylori +ve = eradication treatment, follow up for proof of eradication
PPIs or H2RA for H pylori -ve
Exclude rare conditions (if not caused by common eg infection or NSAIDs) such as Zollinger-Ellison syndrome - take samples from ulcer and mucosa
Treat bleeding ulcers PRN (correct fluid loss, transfusions, surgical interventions)
Annual reviews for regular intermittent treatments
GI associated symptoms for history taking
Abdominal pain Nausea and vomiting Change in bowel motions, constipation, diarrhea, incontinence Blood in stool Anorectal pain, masses or sensation of incomplete emptying (tenesmus) Weight change Jaundice Dysphagia Dyspepsia
GI history taking past medical history conditions
Common GI disorders: GORD Peptic ulcer disease IBD; Crohn’s, ulcerative colitis Coeliac disease Diverticular disease Anorectal disease; fissures, fistulas, ulcers, haemorrhoids Hernia; inguinal, femoral, umbilical ventral IBS
Hepatobiliary disease: Liver cirrhosis Alcoholic liver disease Non-alcoholic fatty liver disease Hepatitis B or C Chronic pancreatitis
also ask about procedural history!
Antiemetics examples and function
Antidopaminergics:
- Metoclopramide
- Domperidone
- Droperidol
- Antagonise dopamine D2/3 receptors
Serotonin receptor blockers (5-HT):
- Ondanstetron
- Selectively inhibit serotonin receptors
Phenothiazines:
- Prochlorperazine
- Blocks D2 receptors and alpha adrenoreceptors
Gastric secretion modulators examples and functions
H2 receptor antagonists:
- Ranitidine
- Inhibits histamine H2 receptors, decreasing acid H+
Proton pump inhibitor (PPIs):
- Omeprazole
- Esomeprazole
- Pantoprazole
- inhibit H+/K+ ATPase (acid secretion)
Laxatives examples and functions
Bulking agents:
- Psyllium
- carbohydrates that retain water
Osmotic laxatives:
- MgSO4 (epsom salt)
- Lactulose
- Macrogol 3350
- Osmotically draws water into the GIT
Secretory laxatives:
- Senna
- Sodium picosulphate
- Stimulate GI elec. and water secretion
Stool softeners:
- Docusate sodium
- Softens faeces, doesn’t affect motility
IBD medications
Systemic corticosteroids:
- Prednisolone
- Hydrocortisone
- Systemic anti-inflammatory action
Aminosalicylates:
- Mesalazine
- Sulfasalazine
- Adenosine release, decreases inflammation
Thiopurines:
- Azathioprine
- Mercaptopurine
- Inhibits purine synthesis decreasing DNA synthesis
Methotrexate:
*Inhibition of IL-1 and other cytokines
TNF-Inhibitors:
- Infliximab
- Adalimumab
- Inhibit tumour necrosis factor alpha, decreasing inflammation
Abdominal regions and related pains and conditions
RUQ pain: Hepatobiliary Hepatic flexure Right renal Right lower lobe pathology Gallbladder pathology
RLQ pain: Colonic Appendicitis Gynaecologic Right renal pathology
Generalised pain: Bowel obstruction Perforation Bacterial peritonitis IBD
Epigastrium: Hepatobiliary Gastric Pancreatic Vascular or cardiac pathology
LUQ pain: Gastric Pancreatic Splenic flexure Spleen Left renal Left lower lobe Vascular pathology
Umbilical:
Gastric
Small bowel
Vascular pathology
LLQ pain:
Colonic
Gynaecologic
Renal pathology
Suprapubic:
Colonic
Gynaecologic
Right renal pathology
Moving from umbilical to RLQ:
Characteristic of appendicitis
Abdominal character and radiating pain and indications
Character:
Dull, diffuse pain - visceral pain eg from intra-abdominal organs
Sharp, localised pain - parietal pain eg from peritoneum
Burning pain in epigastrium - suggestive of oesophagitis, gastritis or peptic ulcer disease
Radiation:
To flank: renal or biliary cause
To back: pancreatitis, ruptured AAA, aortic dissection, duodenal ulcer
To shoulder: diaphragm irritation eg intra-abdominal gas or blood
GI associated symptoms and indications
Nausea and vomiting
Feculent vomiting: bowel obstruction
Bloating: gastroparesis
Diarrhoea: gastroenteritis
Constipation: faecal impaction or bowel obstruction
Lack of flatus: bowel obstruction
Blood in stool: diverticulitis or ischaemic colitis
Frank PR blood: lower GI bleed or massive upper GI bleed
Haematemesis or melaena: peptic ulcer
Fevers: infection (appendicitis, peritonitis, cholecystitis, diverticulitis, cholangitis etc)
RUQ/LUQ pain with cough and fever: pneumonia
Heartburn: gastritis, peptic ulcer
Dysuria: cystitis, pyelonephritis
Haematuria: nephrolithiasis
Vaginal discharge: pelvic inflammatory disease
Anorexia: appendicitis
Weight loss: malignancy
GI exacerbating and relieving factors and indications
Exacerbating factors:
Coughing or movement: peritonitis, perforation, pancreatitis
After eating: gastric ulcer, gastritis, cholelithiasis, mesenteric ischaemia
Eating fatty foods: cholelithias
Alleviating factors:
Eating: duodenal ulcer
Vomiting: small bowel obstruction
Regurgitation: achalasia
Vomiting and nausea timing indications
Worst in morning: pregnancy, alcohol intake, uraemia, raised intracranial pressure
Vomiting 1-2 hours after eating: gastric outlet obstruction
Vomiting during meals: anorexia/bulimia
Is it affecting daily lifestyle
Are they able to keep any solid or fluids down at all
Were they in contact with any sick coworkers or family or friends etc.
Causes of hematochezia
Lower GI bleed
Inflammation: IBD, diverticular disease, infectious colitis, ischaemic colitis
Mass: carcinoma, polyp
Anorectal disorder: haemorrhoids, fissure, fistula, ulcer, anal SCC
Arteriovenous malformation
Trauma
Massive upper GI bleed:
Variceal bleed
Peptic ulceration
GI Bleeding history taking and indications
Blood on toilet paper only: anorectal disorder
Blood in stool: colorectal disease
Blood in toilet bowl: high volume bleed
Heavy bleeding: diverticular bleed or AV malformation
Minor bleeding: haemorrhoids, polyp, cancer
RED FLAG
Weight loss: cancer
presyncope/syncope: hypovolaemia
Melaena and causes
Jet black, tarry, sticky, foul-smelling stool
Highly suggestive of upper GI bleeding
Medications containing iron and bismuth can also cause stools to look similar in appearance
CAUSES:
Oesophageal: varices, AVM, tumour, oesophagitis, Mallory-Wiess tear
Gastric: gastritis, gastric ulcer, gastric carcinoma, hiatus hernia
Duodenal: duodenal ulcer, duodenitis
GI causes of weight loss
peptic ulcer disease, obstruction, IBD, chronic pancreatitis, coeliac disease, gastric bypass surgery
toxic megacolon
When IBD cause the colon to expand, dilate and distend >6cm (toxic colitis with dilated colon = toxic megacolon)
The colon is becomes obstipated (no gas or faeces)
Is life threatening and may lead to perforations
Toxic megacolon risk factors
Ulcerative colitis Crohn’s colitis Pseudomembranous colitis Infectious colitis HIV/AIDS immunosuppression Discontinuation of IBD medications Antimotility agents
Toxic megacolon presentation
Fever/chills Tachycardia Mental status alterations Diarrhoea Abdominal pain and tenderness Hypotension Abdominal distension
Toxic megacolon investigations
History of risk factors (IBD, medications)
Clinical diagnosis from presentation and history
Bloods: FBC, electrolytes, albumin levels, lactic acid, CRP, blood cultures
Stool samples
CT of abdomen/pelvis
Acute AXR series
Toxic megacolon management
1st line resus and monitoring
Broad spectrum antibiotics
Supportive care
Nasogastric decompression
With suspected severe C difficile colitis: antibiotics
With inflammatory colitis: IV corticosteroids
No improvement within 72 hours: surgery
Diverticular disease and complications
Out-pouching of the wall of the gut
May be result of smooth muscle over activity
Mostly asymptomatic but can cause a wide array of symptoms and complications
Diverticulitis is inflammation of a diverticulum and can be caused by infection
Classification:
Congenital ‘true’ diverticula: all 3 coats of bowel are present in the wall (eg Meckel’s diverticulum)
Acquired ‘false’ pulsion diverticula: no muscularis layer, herniation of mucosa and muscularis mucosa through the colonic wall where main blood vessels penetrate the colonic wall (eg sigmoid diverticula, Zenker diverticulum)
complications Diverticulitis Segmental colitis Lower GI bleeding Infection Abscess Perforation Peritonitis Fistula formation Obstruction
Diverticular disease risk factors
Low fibre diet Western diet >50 years BMI >30 NSAID use
Diverticular disease presentation
majority asymptomatic found incidentally on colonoscopy History: presence of risk factors LLQ abdominal pain (colicky persisting pain) After eating, relieved by defecation Leukocytosis Fever Guarding in LLQ, tenderness Bloating Constipation, obstipation Diarrhea Anorexia Nausea Flatulence *pain and tenderness on right side as well as if pt is on steroids indicates sigmoid diverticular disease*
Diverticular disease management
Asymptomatic: no treatment needed
Symptomatic diverticular disease:
1st line: diet modification increase fibre with Oral antibiotics
Symptomatic diverticulitis (uncomplicated):
1st line analgesia and oral antibiotics with Low residue diet
2nd line IV antibiotics to cover gram -ve and anaerobes, analgesia and low residue diet
Symptomatic diverticulitis (complicated): 1st line with rectal bleeding: endoscopic haemostasis, supportive therapy, low residue diet and analgesia 2nd line surgery plus all above aside from endoscopic haemostasis
Unresponsive to IV antibiotics or with >3cm abscess, perforation, fistulae, obstruction: 1st line radiological drainage/surgery, IV antibiotics, analgesia and low residue diet
Recurrent diverticulitis:
Elective surgery
Ischaemic bowel disease
Group of disorders caused by acute or chronic processes, arising from occlusive or nonocclusive aetiologies resulting in decreased blood flow to the GIT
May range from transient to reversible to fulminant (sudden and severe)
Classification:
Acute mesenteric ischaemia (further split into embolic, thrombotic or venous)
Colonic ischaemia (most common with best prognosis)
Chronic mesenteric ischaemia
Ischaemic bowel disease risk factors
Old age Smoking Hypercoagulable states AF MI Structural heart defects Vasculitis history
Ischaemic bowel disease presentations
Abdominal pain and tenderness (general or specific depending on area of ischaemia) Hematochezia/melaena Diarrhoea Weight loss Abdominal bruit (stenosis of vessel)
Ischaemic bowel disease investigations
Bloods: FBC (leukocytosis, anaemia, haemoconcentration), serum lactate, coagulation, ABG
Acute abdominal series
ECG
CT scan
Sigmoidoscopy or colonoscopy
Mesenteric angiography, duplex US or MRI angiography if indicated
