Abdominal pain- IBS Flashcards

1
Q

IBS: who gets it

A

Presents in young adults 20-30s
Females more then males
Runs in families

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2
Q

IBS- mechanism and risk factors

A

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

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3
Q

Symptoms of IBS

A

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

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4
Q

Diagnosis of IBS

A

Normally a diagnosis of exclusion, you will find nothing on examination but distension of the abdomen and generalised tenderness

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5
Q

Red flags for IBS symptoms

A

Unexplained weight loss, new onset of symptoms over 50, bleeding per rectum, fevers, night sweats, localised tenderness/rigidity

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6
Q

Investigating IBS

A

Bedside examinations- digital rectal examination, body mass index
Other tests- FBC, inflammatory markers i.e. CRP/ESR, stool sample id suspect infection, coeliac screening

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7
Q

Management of IBS

A

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

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8
Q

Management of Crohns- inducing remission

A

First line: steroids i.e. oral prednisiolone or IV hydrocortisione
Second line: Azathioprine, Mercaptopurine, Methotrexate, Infliximab, Adalimumab

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9
Q

Management of Crohns- maintaining remission

A

First line: Azatthioprine, Mercaptopurine
Second line: Methotrexate, Infliximab, Adalimumab

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10
Q

Crohns surgery

A

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.

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11
Q

Management of UC- inducing remission

A

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

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12
Q

Management of UC: maintaining remission

A

Aminosalicylate (e.g. mesalazine oral or rectal)
Azathioprine
Mercaptopurine

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13
Q

Management of UC- surgery

A

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.

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14
Q

Biliary colic

A

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.

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15
Q

Cholecystitis

A

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

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16
Q

Macroscopic and Microscopic changes with Ulcerative colitis

A

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

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17
Q

UC summary

A

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.

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18
Q

General examination findings for uc

A

Features of anaemia (e.g. pallor, fatigue)
Joint pain
Clubbing
Erythema nodosum
Pyoderma gangrenosum
Uveitis
Episcleritis

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19
Q

UC: classification

A

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

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20
Q

Diabetic ketoacidosis

A
  • Associated with type 1 diabetes mellitus
  • Ketone bodies are generated in excess of clearance. Ketone bodies are produced when there is scarcity of glucose
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21
Q

Appearance of diabetic ketoacidosis

A

Acute deterioration – abdominal pain, nausea, vomiting

Examination – Hypotension, Tachycardia, fever, reduced GCS

Causes: Missed insulin dose(s), Sepsis, Myocardial Ischaemia, Alcohol

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22
Q

Investigations into diabetic ketoacidosis

A

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

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23
Q

Treatment of diabetic ketoacidosis

A

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!!!!

24
Q

Hypoglycaemia symptoms

A

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

25
Q

Hyperosmolar Hyperglycaemic state (HHS)

A

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

26
Q

Primary, secondary and tertiary disease of the Thyroid

A

Primary – disease of thyroid gland
Secondary – disease of pituitary
Tertiary – disease of hypothalamus (rare e.g.craniopharyngioma)

27
Q

Synthesis of thyroid hormones

A
  • 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
28
Q

Metabolic functions of T3

A

Thermogenesis
Basal metabolic rate
Lipid metabolism
Salt and water balance
Reflex times & muscle strength
Heart rate and contraction time

29
Q

Hyperthyroidism

A

Core symptoms: Weight loss, heat intolerance, palpitations, goitre

Other symptoms: anxiety, temor, fatigue, weakness, menstrual change, breathlessness, eye signs, sweating, hyperkinesia, diarrhoea

30
Q

Hyperthyroidism- Examination

A

Tachycardia
Palmar erythema
Tremor
Proximal myopathy
Hyper-reflexia
Eye signs
Goitre

31
Q

Hyperthyroidism- eyes

A

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

32
Q

Hyperthyroidism: hands

A

Dermopathy – glycosaminoglycan deposition (skin of hands, or pretibial myxoedema!)

Thyroid acropachy – clubbing, skin tightness, soft tissue oedema and periosteal reaction

33
Q

Aetiology of Hyperthyroidism

A

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

34
Q

How the Thyroid hormones interacr

A

Raised TRH- causes increased TSH
Raised TSH- causes increased T3 and T4
T3 and T4- causes decreased TSH

35
Q

Investigations into Hyperthyroidism

A

Thyroid Function Tests: ↓TSH, ↑FT3/FT4

Autoantibodies: TPO, Thyroglobulin, TSH-Receptor antibody

Thyroid Uptake scan

36
Q

Treatment for hyperthyroidism

A

Carbimazole, Propylthiouracil (PTU)

Propranolol

Radio-Iodine

Thyroid Surgery

37
Q

Hypothyroidism symptoms

A

Symptoms: weight gain, constipation, goitre
Other symptoms: cold intolerance, depression, fatigue, weakness, dry skin, puffy face, menorrhagia, Paraesthesia,Hoarse voice, yellow skin, bradycardia, bradykinesia

38
Q

Causes of Hypothyroidism

A

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

39
Q

Hypothyroidism- investigations

A

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

40
Q

X-ray: Abdominal structures and density

A

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

41
Q

What to look for in an abdominal x-ray

A

Personal details
Film details
Adequacy
Gas pattern
Organs
Bones- blood vessels
Calcification
Review area
Objects

42
Q

Abdominal x-ray specialist procedures

A

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

43
Q

Ultrasound (transabdominal)

A

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

44
Q

Abdomen: Computed Tomography

A

Fast
Non-invasive
Accurate
Usually requires IV contrast
Good views of the organs of upper abdomen
However: Significant radiation

45
Q

What do you use CT to diagnose in the abdomen

A
  • 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
46
Q

Systematic approach to AXR

A

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

47
Q

Small bowel obstruction

A
  • 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
48
Q

Causes and presentation of small bowel obstruction

A
  • 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
49
Q

Large bowel obstruction

A
  • Colonic distension proximal to the obstruction
  • Dilatation of >6cm for colon, >9cm for caecum
  • Haustra are visible
  • Less common than SBO (20% of cases
50
Q

Causes and complications of large bowel obstruction

A

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

51
Q

Volvulus

A
  • 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
52
Q

AXR- IBD

A
  • Can be entirely normal
  • Signs of acute inflammation causing bowel wall thickening
  • Thickening of haustral folds causes a ‘thumbprinting’ appearance
53
Q

Toxic megacolon

A
  • Secondary to Clostridium Difficile Colitis
  • Look for bowel wall thickening and mucosal islands
54
Q

Gas in the biliary tree

A

The patient has a biliary stent in situ, the gas in the biliary tree proves the stent is patent

55
Q

Endoscopic ultrasound

A

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