Abdominal pain- IBS Flashcards
IBS: who gets it
Presents in young adults 20-30s
Females more then males
Runs in families
IBS- mechanism and risk factors
Mechanism- Hypersensitive viscera, abnormalities to the GI immune function, colonic microbiota, autonomic activity and GI motility
Risk factors- Genetic, previous inflammation/infection of the gut, dietary factors, medication, psychological factors
Symptoms of IBS
Abdominal pain/bloating or changes in bowel habit- tend to have the symptoms for over 6 months
Associated symptoms: altered stool passage, abdominal bloating, distension, hardness, symptoms worsened by eating, passage of rectal mucus
Diagnosis of IBS
Normally a diagnosis of exclusion, you will find nothing on examination but distension of the abdomen and generalised tenderness
Red flags for IBS symptoms
Unexplained weight loss, new onset of symptoms over 50, bleeding per rectum, fevers, night sweats, localised tenderness/rigidity
Investigating IBS
Bedside examinations- digital rectal examination, body mass index
Other tests- FBC, inflammatory markers i.e. CRP/ESR, stool sample id suspect infection, coeliac screening
Management of IBS
May be useful to keep a food diary to identify triggers. Avoid short-chain fermentable carbohydrates (see FODMAP diet), eat regular balanced meals, limit alcohol, coffee, foods high in insoluble fibre, and sugar-free products.
Medications- if constipation is the main symptoms then take soluble fibre supplements i.e. ispaghula husk or anti-spasmodic agents like mebevarine or buscopan. Tricyclic antidepressants and SSRI can also be considered
Management of Crohns- inducing remission
First line: steroids i.e. oral prednisiolone or IV hydrocortisione
Second line: Azathioprine, Mercaptopurine, Methotrexate, Infliximab, Adalimumab
Management of Crohns- maintaining remission
First line: Azatthioprine, Mercaptopurine
Second line: Methotrexate, Infliximab, Adalimumab
Crohns surgery
When the disease only affects the distal ileum it is possible to surgically resect this area and prevent further flares of the disease. Crohns typically involves the entire GI tract
Surgery can also be used to treat strictures and fistulas secondary to Crohns disease.
Management of UC- inducing remission
Mild to moderate disease
First line: aminosalicylate (e.g. mesalazine oral or rectal)
Second line: corticosteroids (e.g. prednisolone)
Severe disease
First line: IV corticosteroids (e.g. hydrocortisone)
Second line: IV ciclosporin
Management of UC: maintaining remission
Aminosalicylate (e.g. mesalazine oral or rectal)
Azathioprine
Mercaptopurine
Management of UC- surgery
Ulcerative colitis typically only affects the colon and rectum. Therefore, removing the colon and rectum (panproctocolectomy) will remove the disease. The patient is then left with either a permanent ileostomy or something called an ileo-anal anastomosis (J-pouch). This is where the ileum is folded back in itself and fashioned into a larger pouch that functions a bit like a rectum. This “J-pouch” which is then attached to the anus and collects stools prior to the person passing the motion.
Biliary colic
Is caused by an impacted stone at the neck of the gallbladder and typically presents with crampy abdominal pain in the absence of infective features (e.g. fever/raised inflammatory markers). Biliary colic is typically triggered by the consumption of fatty foods.
Cholecystitis
Typically presents with constant RUQ pain, fever and raised inflammatory markers. However, jaundice is absent in most cases as there is no associated biliary obstruction (except if the gallbladder is compressing the common bile duct, as in Mirizzi syndrome). Inflammation of the gallbladder, usually due to a gallstone blocking the cystic duct
Macroscopic and Microscopic changes with Ulcerative colitis
Macroscopic findings:
Continuous, uniformly inflamed mucosa
Erythematous, friable mucosa
Abnormal vascular pattern
Ulceration
Inflammatory polyps (‘pseudopolyps’)
Microscopic findings (biopsy):
Crypt abscesses
Decreased goblet cell abundance
UC summary
UC is the most common type of inflammatory bowel disease and has a relapsing-remitting course.
Common symptoms of UC include episodic diarrhoea with urgency, rectal bleeding and abdominal pain.
Extra-intestinal manifestations include; erythema nodosum, uveitis and joint pain.
Topical and oral aminosalicylates are the mainstay therapies used in UC.
Surgical intervention should not be delayed for urgent indications and usually involves partial or complete resection of the colon.
UC increases the lifetime risk of colorectal cancer and thromboembolic events.
General examination findings for uc
Features of anaemia (e.g. pallor, fatigue)
Joint pain
Clubbing
Erythema nodosum
Pyoderma gangrenosum
Uveitis
Episcleritis
UC: classification
Proctitis: rectum
Proctosigmoiditis: rectum and sigmoid colon
Left-sided colitis: rectum, sigmoid colon and descending colon
Extensive colitis: rectum, sigmoid colon, descending colon and transverse colon
Pancolitis: rectum and entire colon
Diabetic ketoacidosis
- Associated with type 1 diabetes mellitus
- Ketone bodies are generated in excess of clearance. Ketone bodies are produced when there is scarcity of glucose
Appearance of diabetic ketoacidosis
Acute deterioration – abdominal pain, nausea, vomiting
Examination – Hypotension, Tachycardia, fever, reduced GCS
Causes: Missed insulin dose(s), Sepsis, Myocardial Ischaemia, Alcohol
Investigations into diabetic ketoacidosis
Blood glucose (>11 mmol/L)
Blood Ketones (>3 mol/L) or Urine Ketones (2+)
Arterial or Venous blood gas – Metabolic Acidosis (pH < 7.3, HCO3 <15 mmol/L)
Other tests – raised inflammatory markers, Urea and Electrolytes, ECG, septic screen
Treatment of diabetic ketoacidosis
Aim of treatment is to correct underlying abnormal physiology
Intravenous insulin
Intravenous Rehydration= 500ml of IVT STAT if BP is low i.e. <90mmHg
Correction of electrolyte abnormalities – Potassium, Sodium
Treat underlying cause!!!!
Hypoglycaemia symptoms
Autonomic response (BG < 3.3 mmol/L) – Hunger, tremor, sweats, anxiety, palpitations, nausea
Severe hypoglycaemia (BG < 2.8 mmol/L) – Neuroglycopaenia: weakness, confusion, lethargy, change in behaviour. can lead to convulsions, coma and death
Hyperosmolar Hyperglycaemic state (HHS)
Occurs in Type 2 Diabetics
Hyperglycaemia (>30 mmol/L)
Hyperosmolar (>320 mosmol/L)
Treatment: Intravenous fluid +/- intravenous insulin
Cautious correction to prevent fluid shifts e.g. cerebral oedema
Primary, secondary and tertiary disease of the Thyroid
Primary – disease of thyroid gland
Secondary – disease of pituitary
Tertiary – disease of hypothalamus (rare e.g.craniopharyngioma)
Synthesis of thyroid hormones
- Tyrosine attaches to Thyroglobulin
- It is then Iodinated to MIT and DIT
- MIT and DIT are coupled together
- Through Proteolysis and secretion Thyroxine (T4) is released
Metabolic functions of T3
Thermogenesis
Basal metabolic rate
Lipid metabolism
Salt and water balance
Reflex times & muscle strength
Heart rate and contraction time
Hyperthyroidism
Core symptoms: Weight loss, heat intolerance, palpitations, goitre
Other symptoms: anxiety, temor, fatigue, weakness, menstrual change, breathlessness, eye signs, sweating, hyperkinesia, diarrhoea
Hyperthyroidism- Examination
Tachycardia
Palmar erythema
Tremor
Proximal myopathy
Hyper-reflexia
Eye signs
Goitre
Hyperthyroidism- eyes
Exclusively associated with Grave’s Disease (Autoimmune)
Early signs: Lid lag, lid retraction, stare (note can occur with any cause of hyperthyroidism – adrenergic stimulation)
Conjunctival erythema and swelling
Proptosis, Exopthalmos
Opthalmoplegia
Optic nerve compression
Hyperthyroidism: hands
Dermopathy – glycosaminoglycan deposition (skin of hands, or pretibial myxoedema!)
Thyroid acropachy – clubbing, skin tightness, soft tissue oedema and periosteal reaction
Aetiology of Hyperthyroidism
Primary Disease
Autoimmune (Grave’s disease)
Toxic adenoma- raised T3, normal FT4, often large palpable nodules in one lobe
Toxic multinodular goitre- elderly patients generally, raised FT3, relatively normal FT4
Thyroiditis (viral/postpartum/drug-induced e.g. Amiodarone)
Secondary Disease
TSH-oma
Thyroid Hormone Resistance
How the Thyroid hormones interacr
Raised TRH- causes increased TSH
Raised TSH- causes increased T3 and T4
T3 and T4- causes decreased TSH
Investigations into Hyperthyroidism
Thyroid Function Tests: ↓TSH, ↑FT3/FT4
Autoantibodies: TPO, Thyroglobulin, TSH-Receptor antibody
Thyroid Uptake scan
Treatment for hyperthyroidism
Carbimazole, Propylthiouracil (PTU)
Propranolol
Radio-Iodine
Thyroid Surgery
Hypothyroidism symptoms
Symptoms: weight gain, constipation, goitre
Other symptoms: cold intolerance, depression, fatigue, weakness, dry skin, puffy face, menorrhagia, Paraesthesia,Hoarse voice, yellow skin, bradycardia, bradykinesia
Causes of Hypothyroidism
Primary Hypothyroidism
- Hashimoto’s Thyroiditis (Autoimmune)
- Thyroiditis (Viral, Postpartum)
- Post-treatment for Hyperthyroidism
Drug-induced
- Iodine deficiency or excess
- Dyshormonogenesis (inborn errors of hormone synthesis)
Secondary Hypothyroidism
- Pituitary Disease
Hypothyroidism- investigations
Tests
- Thyroid Function Tests: ↑TSH, ↓FT3/FT4
- Autoantibodies: TPO, Thyroglobulin, TSH-Receptor blocker
Treatment
- Replacement T4 (Levothyroxine once daily)
- Regular monitoring of Thyroid function every 6 – 12 months
X-ray: Abdominal structures and density
High density(white)-bone,stones,metal,NG tubes.
Medium density(grey)-soft tissue -liver,spleen,kidneys,psoas muscles.
Low density(black)-air and fat-bowel gas,subcutaneous fat
What to look for in an abdominal x-ray
Personal details
Film details
Adequacy
Gas pattern
Organs
Bones- blood vessels
Calcification
Review area
Objects
Abdominal x-ray specialist procedures
Small bowel study: patient drink barium and an x-ray is taken, valvulae conniventes will be seen in small bowel obstruction
Barium meal: visualisation of the stomach
Barium enema: visualisation of the colon, there is an ‘apple core’ stricture in colonic cancer
Ultrasound (transabdominal)
Non-invasive
Cheap
Widely available
Safe (no radiation)
Good at looking at soft tissues
Images available in real-time (can be combined with biopsies)
First-line investigation in patients with hepatobiliary or pancreatic disease
Measure size of AAA avoiding the need for CT
However: Operator dependant, Images can be difficult to obtain eg obesity
Abdomen: Computed Tomography
Fast
Non-invasive
Accurate
Usually requires IV contrast
Good views of the organs of upper abdomen
However: Significant radiation
What do you use CT to diagnose in the abdomen
- infections such asappendicitis,pyelonephritisand abscesses.
- inflammatory bowel disease,pancreatitis (including complications)and liver cirrhosis.
- cancers of the liver, kidneys, pancreas, ovaries and bladder.
kidney and bladder stones. - abdominal aortic aneurysms (AAA), injuries to abdominal organs such as the spleen, liver, kidneys or other internal organs in cases of trauma
Systematic approach to AXR
1) Projection: normally AP with patient supine
2) Patient details
3) Technical adequacy- the entre abdomen should be included
4) Obvious abnormalities- i.e. small bowel dilation
5) Systematic review: large and small bowel, diameter of the bowel, bowel wall thickness. The large bowel should be no wider then 6cm and the sall bowel no more than 3cm
6) Other- foreign bodies, bones etc
Small bowel obstruction
- Dilated loops of small bowel proximal to obstruction
- Often multiple and centrally located
- Dilatation over 3cm in at least 3 places
- Valvulae Conniventes are visible
- More common than large bowel obstruction
- AXR 50% sensitive for SBO
Causes and presentation of small bowel obstruction
- Presentation: abdominal pain, abdominal distension, vomiting, abslute constipation, lack of bowel sounds/tinckling bowel sounds
- Causes: congenital causes, extrinsic bowel lesions, intrinsic bowel wall lesions, luminal occlusions
Large bowel obstruction
- Colonic distension proximal to the obstruction
- Dilatation of >6cm for colon, >9cm for caecum
- Haustra are visible
- Less common than SBO (20% of cases
Causes and complications of large bowel obstruction
Causes:
50-60% malignancy
colonic diverticulitis
volvulus (Caecal vs Sigmoid)
ischaemic stricture,
faecal impaction/faecoloma
hernias(uncommon)
Complications: Perforation, the more distended the greater the risk. At site of obstruction or proximal to obstruction due to ischaemia
Volvulus
- Can be caecal or sigmoid
- Only 11% are caecal- torsion of the caecum around its own mesentery
- Cause of large bowel obstruction
- Due to chronic constipation and/or laxative abuse, fibre rich diet and chagas disease
- Presents with the coffee bean sign on x-ray
AXR- IBD
- Can be entirely normal
- Signs of acute inflammation causing bowel wall thickening
- Thickening of haustral folds causes a ‘thumbprinting’ appearance
Toxic megacolon
- Secondary to Clostridium Difficile Colitis
- Look for bowel wall thickening and mucosal islands
Gas in the biliary tree
The patient has a biliary stent in situ, the gas in the biliary tree proves the stent is patent
Endoscopic ultrasound
Ultrasound transducer on the end of an endoscope
Gives good images of gallbladder, bile duct and pancreas
Useful for identifying bile duct stones and gallbladder microlithiasis
Detecting and staging pancreatobiliary tumours
Assessing pancreatic cystic lesions
Can take fine needle aspirate
