Meeran Flashcards
A gram negative intracellular diplococcus that causes meningitis
Neisseria or Neisseria Meningitides
A gram positive diplococcus that causes pneumonia
Pneumococcus or streptococcus pneumoniae
A gram positive organism that grows in bunches and causes abscesses
Staphylococcus Aureus
The organism that causes tetanus
Clostridium tetanae
A gram negative rod that commonly causes urinary tract infections
E-coli
Cystic dilatation of duct during lactation caused by obstruction
duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating adenoma
galactocoele
Infection of the breast that occurs during lactation
duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating adenoma
mastitis
Occurs in males with liver disease
duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating adenoma
gynaecomastia
Occurs in the presence of a high prolactin
duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating adenoma
galactorrhoea
The commonest benign tumour of the female breast
duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating adenoma
fibroadenoma
Causes an increased loss of HCO3-
Diabetic ketoacidosis Intestinal fistula Metabolic acidosis Metabolic alkalosis Poor lung perfusion Pyloric stenosis Renal failure Respiratory acidosis Respiratory alkalosis
Intestinal fistula
2. Causes increased H+ production Diabetic ketoacidosis Intestinal fistula Metabolic acidosis Metabolic alkalosis Poor lung perfusion Pyloric stenosis Renal failure Respiratory acidosis Respiratory alkalosis
Diabetic ketoacidosis
3. Causes increased H+ loss Diabetic ketoacidosis Intestinal fistula Metabolic acidosis Metabolic alkalosis Poor lung perfusion Pyloric stenosis Renal failure Respiratory acidosis Respiratory alkalosis
Pyloric stenosis
4. Can be compensated by increased renal excretion of H+ Diabetic ketoacidosis Intestinal fistula Metabolic acidosis Metabolic alkalosis Poor lung perfusion Pyloric stenosis Renal failure Respiratory acidosis Respiratory alkalosis
Metabolic acidosis
Be aware that compensation for a metabolic acidosis is with hyperventilation. Renal excretion (question 4) of acid is not really compensation, but just correcting the problem.
5. Can be compensated by hypoventilation Diabetic ketoacidosis Intestinal fistula Metabolic acidosis Metabolic alkalosis Poor lung perfusion Pyloric stenosis Renal failure Respiratory acidosis Respiratory alkalosis
Metabolic alkalosis
Also although hypoventilation would compensate for a metabolic alkalosis, that effect is minimised in humans by hypoxia.
- Gain in bicarbonate ions or loss of H+ ions resulting in raised pH.
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis with Respiratory Compensation
Metabolic Alkalosis with Respiratory Compensation
Respiratory Acidosis with Metabolic Compensation
Respiratory Alkalosis with Metabolic Compensation
a. Metabolic Alkalosis
- 24 year old female presents at A&E with a broken ankle. The interpretation of her blood gas results (pH 7.62, PCO2 3.59, PO2 14.1, HCO3 23, Base Excess 0) demonstrates a ____.
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis with Respiratory Compensation
Metabolic Alkalosis with Respiratory Compensation
Respiratory Acidosis with Metabolic Compensation
Respiratory Alkalosis with Metabolic Compensation
a. Respiratory Alkalosis
- 22 year old model is admitted to A&E with weakness and tingling sensations in both hands and feet, and “poor balance”. Patient denies pill ingestion but admits she has been on a strict diet regimen to meet her agency’s expectations. Her ABG results (pH 7.55, PCO2 6.67, PO2 12.0, HCO3 45) demonstrate ____.
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis with Respiratory Compensation
Metabolic Alkalosis with Respiratory Compensation
Respiratory Acidosis with Metabolic Compensation
Respiratory Alkalosis with Metabolic Compensation
a. Metabolic Alkalosis
- A 40 year old lady with severe chronic back pain (treated aggressively with OTC NSAIDs) for several years was found to have BP 155/95 at her routine GP visit. Her urine dipstick demonstrated ++ protein and increased white blood cells. Her ABG results (pH 7.30, PCO2 4.27, HCO3 15) demonstrate _____.
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis with Respiratory Compensation
Metabolic Alkalosis with Respiratory Compensation
Respiratory Acidosis with Metabolic Compensation
Respiratory Alkalosis with Metabolic Compensation
a. Metabolic Acidosis with Respiratory Compensation
- A 45 year old man with a history of solvent (inhalant) abuse presents to A&E complaining of dyspnoea (SPO2 99% on room air). He is tachypnoeic on examination and demonstrates Kussmaul breathing. His ABG (pH 6.95, PCO2 1.20, PO2 17.0, HCO3- 2) demonstrates ___.
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis with Respiratory Compensation
Metabolic Alkalosis with Respiratory Compensation
Respiratory Acidosis with Metabolic Compensation
Respiratory Alkalosis with Metabolic Compensation
a. Metabolic acidosis with respiratory compensation
An elderly patient on the ward has RR 16, HR 65, temp 37.5 degrees C. His blood gases are pH 7.35 (7.35-7.45), pCO2 9.0 (4.7-6 kPa), pO2 8.1(10.0-13.3 kPa), HCO3 45 (22-30). Rank the underlying diseases below in order of likelihood, going from most to least likely:
Pulmonary embolism Tension pneumothorax COPD Hyperventilation Pneumonia
Answer:
- COPD
- Pneumonia
- Pulmonary embolism
- Tension pneumothorax
- Hyperventilation
Explanation: this is a picture of respiratory acidosis with metabolic compensation. Hyperventilation would cause alkalosis so is least likely. A tension pneumothorax would not have time to establish compensation so is next least likely. The carbon dioxide is high and the oxygen is low so this is type 2 respiratory failure with no v/q mismatch. while a number of small PEs might result in compensation over time they would give a type 1 picture with low oxygen and normal carbon dioxide. Both pneumonia and COPD might give this blood gas picture but this patient’s vital measurements show no sign of infection so COPD is most likely.
- A 42 year old man with heartburn presents with the following blood gases: pH 7.51, pCO2 5.2kPa, bicarbonate = 30 mmol/l.
Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Compensated Respiratory Alkalosis Compensated Respiratory Acidosis Compensated Metabolic Alkalosis Compensated Metabolic Acidosis Type I Respiratory Failure Type II Respiratory Failure
a. Metabolic Alkalosis
- 65 year old long- term smoker is admitted with drowsiness and confusion. ABG reveals pH 7.36, pO2 7kPa, pCO2 8kPa, bicarbonate 24 mmol/l.
Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Compensated Respiratory Alkalosis Compensated Respiratory Acidosis Compensated Metabolic Alkalosis Compensated Metabolic Acidosis Type I Respiratory Failure Type II Respiratory Failure
a. Type II Respiratory Failure
- Treat with IV sodium bicarbonate
Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Compensated Respiratory Alkalosis Compensated Respiratory Acidosis Compensated Metabolic Alkalosis Compensated Metabolic Acidosis Type I Respiratory Failure Type II Respiratory Failure
a. Metabolic Acidosis
- 24 year old female presents with an aspirin overdose. She appears to be breathing heavily. pH 7.38, pO2 12kPa, pCO2 2.5kPa, bicarbonate 16 mmol/l.
Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Compensated Respiratory Alkalosis Compensated Respiratory Acidosis Compensated Metabolic Alkalosis Compensated Metabolic Acidosis Type I Respiratory Failure Type II Respiratory Failure
a. Compensated Metabolic Acidosis
- 55 year old male with difficulty breathing is diagnosed with Guillain- Barre syndrome. pH 7.25, pO2 12kPa, pCO2 9kPa, bicarbonate 25 mmol/l.
Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Compensated Respiratory Alkalosis Compensated Respiratory Acidosis Compensated Metabolic Alkalosis Compensated Metabolic Acidosis Type I Respiratory Failure Type II Respiratory Failure
a. Respiratory Acidosis
- 22 year old man presents with a painless, red ulcer on his penis. Microscopy reveals spiral shaped organisms.
Benzylpenicillin Ceftriaxone Chloramphenicol Clarithromycin Colistin Gentamicin Intravenous Meropenem Moxifloxacin Orally Rifampicin Trimethoprim Vancomycin Rectally
a. Benzylpenicillin
- On a routine swab for a pre-op patient, the lab is able to culture Staphylococcus aureus. The lab also reports that this particular strain is not sensitive to Penicillins.
Benzylpenicillin Ceftriaxone Chloramphenicol Clarithromycin Colistin Gentamicin Intravenous Meropenem Moxifloxacin Orally Rifampicin Trimethoprim Vancomycin Rectally
a. Vancomycin
- The route of administration when administering Vancomycin to treat serious C.difficile infection.
Benzylpenicillin Ceftriaxone Chloramphenicol Clarithromycin Colistin Gentamicin Intravenous Meropenem Moxifloxacin Orally Rifampicin Trimethoprim Vancomycin Rectally
a. Orally
- This antibiotic which is usually administered as eye drops, can cause grey baby syndrome in neonates, because of an inability to metabolise the drug.
Benzylpenicillin Ceftriaxone Chloramphenicol Clarithromycin Colistin Gentamicin Intravenous Meropenem Moxifloxacin Orally Rifampicin Trimethoprim Vancomycin Rectally
a. Chloramphenicol
- A 21 year old university student presents with meningococcal infection, and he is successfully treated. What prophylaxis might be given to his housemates and closest contacts?
Benzylpenicillin Ceftriaxone Chloramphenicol Clarithromycin Colistin Gentamicin Intravenous Meropenem Moxifloxacin Orally Rifampicin Trimethoprim Vancomycin Rectally
a. Rifampicin
- 36-year old male presents with hypertension. Lab results: Na+ = 155mmol/L, K+ = 2.9mmol/L, pH = 7.46, low plasma renin activity.
Pituitary dependent Cushing’s disease Adrenal tumour causing Cushing’s syndrome Ectopic ACTH causing Cushing’s syndrome Normal obese person Cushing’s syndrome of indeterminate cause Pituitary adenoma Phaeochromocytoma Primary adrenal insufficiency Secondary adrenal insufficiency Primary hyperaldosteronism Secondary hyperaldosteronism Adrenal medulla Zona glomerulosa Zona fasciculata Zona reticularis
a. Primary hyperaldosteronism
- 50-year old female with the following lab results: Na+ = 130mmol/L, K+ = 5.9mmol/L, glucose = 3.4mmol/L, urea = 7.2 mmol/L, Ca2+ = 2.8 mmol/L. A short SynACTHen test shows cortisol = 600nmol/L half an hour after administration.
Pituitary dependent Cushing’s disease Adrenal tumour causing Cushing’s syndrome Ectopic ACTH causing Cushing’s syndrome Normal obese person Cushing’s syndrome of indeterminate cause Pituitary adenoma Phaeochromocytoma Primary adrenal insufficiency Secondary adrenal insufficiency Primary hyperaldosteronism Secondary hyperaldosteronism Adrenal medulla Zona glomerulosa Zona fasciculata Zona reticularis
a. Secondary adrenal insufficiency
- A 45-year old female patient presents with cushingoid features. A dexamethasone suppression test shows undetectable ACTH, cortisol = 750nmol/L.
Pituitary dependent Cushing’s disease Adrenal tumour causing Cushing’s syndrome Ectopic ACTH causing Cushing’s syndrome Normal obese person Cushing’s syndrome of indeterminate cause Pituitary adenoma Phaeochromocytoma Primary adrenal insufficiency Secondary adrenal insufficiency Primary hyperaldosteronism Secondary hyperaldosteronism Adrenal medulla Zona glomerulosa Zona fasciculata Zona reticularis
a. Adrenal tumour causing Cushing’s syndrome
- A 65-year old male patient presents with cushingoid features. A high dose dexamethasone suppression test shows ACTH 25 pmol/L (high), cortisol = 750nmol/L.
Pituitary dependent Cushing’s disease Adrenal tumour causing Cushing’s syndrome Ectopic ACTH causing Cushing’s syndrome Normal obese person Cushing’s syndrome of indeterminate cause Pituitary adenoma Phaeochromocytoma Primary adrenal insufficiency Secondary adrenal insufficiency Primary hyperaldosteronism Secondary hyperaldosteronism Adrenal medulla Zona glomerulosa Zona fasciculata Zona reticularis
a. Ectopic ACTH causing Cushing’s syndrome
- A 28-year old man presents with hypertensive episodes. Lab results: Na+ 140mmol/L, K+ = 4.1mmol/L, random cortisol = 200nmol/L. CT shows an adrenal mass, which region is most likely to be affected?
Pituitary dependent Cushing’s disease Adrenal tumour causing Cushing’s syndrome Ectopic ACTH causing Cushing’s syndrome Normal obese person Cushing’s syndrome of indeterminate cause Pituitary adenoma Phaeochromocytoma Primary adrenal insufficiency Secondary adrenal insufficiency Primary hyperaldosteronism Secondary hyperaldosteronism Adrenal medulla Zona glomerulosa Zona fasciculata Zona reticularis
a. Adrenal medulla
- What is the first line of treatment in phaeochromocytomas?
Phaeochromocytoma Conn’s syndrome Cushing’s syndrome Alpha blockade Beta blockade Surgery Pituitary MRI High dose dexamethasone test Adrenal CT Scan Spironolactone Zona glomerulosa Zona fasciculata Low dose dexamethasone test 24 hour ambulatory blood pressure Aldosterone- renin ratio Glucose tolerance test
a. Alpha blockade
- A 25 year old female patient presents with high levels of aldosterone and low levels of renin. On examination the patient is found to be hypertensive.
Phaeochromocytoma Conn’s syndrome Cushing’s syndrome Alpha blockade Beta blockade Surgery Pituitary MRI High dose dexamethasone test Adrenal CT Scan Spironolactone Zona glomerulosa Zona fasciculata Low dose dexamethasone test 24 hour ambulatory blood pressure Aldosterone- renin ratio Glucose tolerance test
a. Conn’s syndrome
- A 75 year old lady reports to her GP of very frequent panic attacks. She complains of excessive sweating and following investigations, hypertension is detected and raised levels of catecholamines are found in the urine.
Phaeochromocytoma Conn’s syndrome Cushing’s syndrome Alpha blockade Beta blockade Surgery Pituitary MRI High dose dexamethasone test Adrenal CT Scan Spironolactone Zona glomerulosa Zona fasciculata Low dose dexamethasone test 24 hour ambulatory blood pressure Aldosterone- renin ratio Glucose tolerance test
a. Phaeochromocytoma
- A 53 year old male patient presents with constantly high blood pressure. He is an investment banker and initially the elevation is thought to be related to stress. The patient’s Na, K and urea are all normal. His glucose is however taken randomly and is found to be elevated at 7.9mmol/L. What is the first investigation that needs to be carried out in this patient ?
Phaeochromocytoma Conn’s syndrome Cushing’s syndrome Alpha blockade Beta blockade Surgery Pituitary MRI High dose dexamethasone test Adrenal CT Scan Spironolactone Zona glomerulosa Zona fasciculata Low dose dexamethasone test 24 hour ambulatory blood pressure Aldosterone- renin ratio Glucose tolerance test
a. 24 hour ambulatory blood pressure
- Which part of the adrenal cortex produces glucocorticoids in response to the Adrenocorticotrophic hormone ? (ACTH)
Phaeochromocytoma Conn’s syndrome Cushing’s syndrome Alpha blockade Beta blockade Surgery Pituitary MRI High dose dexamethasone test Adrenal CT Scan Spironolactone Zona glomerulosa Zona fasciculata Low dose dexamethasone test 24 hour ambulatory blood pressure Aldosterone- renin ratio Glucose tolerance test
a. Zona fasciculata
- Distressed parents rush their 7-year-old boy to A&E. He’s experiencing difficulty breathing and facial swelling, which started suddenly during a family picnic. His father mentions there was a dead wasp close to where his son collapsed.
Medication side effect Acute urticaria Asthma C1 inhibitor deficiency Chronic Granulomatous Disease Chronic urticaria Contact dermatitis Dermatitis herpetiformis Food intolerance Hayfever Hyper IgM Type I hypersensitivity Type II hypersensitivity Type III hypersensitivity Type IV hypersensitivity
a. Type I hypersensitivity
- A student presents with ‘a lot of sneezing’ and a runny nose. He’s anxious as he cannot concentrate on his upcoming summer exams, and mentions this happened to him the last 2 years.
Medication side effect Acute urticaria Asthma C1 inhibitor deficiency Chronic Granulomatous Disease Chronic urticaria Contact dermatitis Dermatitis herpetiformis Food intolerance Hayfever Hyper IgM Type I hypersensitivity Type II hypersensitivity Type III hypersensitivity Type IV hypersensitivity
Hayfever
- A 16-year-old boy has had several bouts of facial swelling and unexplained severe abdominal pain.
Medication side effect Acute urticaria Asthma C1 inhibitor deficiency Chronic Granulomatous Disease Chronic urticaria Contact dermatitis Dermatitis herpetiformis Food intolerance Hayfever Hyper IgM Type I hypersensitivity Type II hypersensitivity Type III hypersensitivity Type IV hypersensitivity
a. C1 inhibitor deficiency
- A 10-year-old girl experiences significant weight loss, abdominal pain and diarrhoea. Her parents are particularly worried about a blistering rash on her elbows and knees that she only experienced after they moved from Ireland.
Medication side effect Acute urticaria Asthma C1 inhibitor deficiency Chronic Granulomatous Disease Chronic urticaria Contact dermatitis Dermatitis herpetiformis Food intolerance Hayfever Hyper IgM Type I hypersensitivity Type II hypersensitivity Type III hypersensitivity Type IV hypersensitivity
a. Dermatitis herpetiformis
- A 48-year-old man develops and itchy rash on his hands that makes his skin dry and cracked. It’s particularly worse if he’s been gardening.
Medication side effect Acute urticaria Asthma C1 inhibitor deficiency Chronic Granulomatous Disease Chronic urticaria Contact dermatitis Dermatitis herpetiformis Food intolerance Hayfever Hyper IgM Type I hypersensitivity Type II hypersensitivity Type III hypersensitivity Type IV hypersensitivity
a. Contact dermatitis
- A 30-year-old overweight Asian gentleman presents to his GP several hours after noticing that his skin is becoming increasingly itchy and the appearance of hives after admitting to have consumed a ‘cheeky packet of peanuts’ at work. What is the most likely causative factor in mediating his symptoms?
Adrenaline b-Defensin Complement C3 Contrast medium Corticosteroids Diluent Filaggrin Histamine IgA IgE IgG Mast cell (serum) tryptase Noradrenaline Peanuts Penicillin
a. IgE
- You are a medical student attending an atopy clinic and are observing a doctor administer a skin prick test. The doctor asks you to explain what she is injecting into the patient’s skin as a ‘positive control’. What component makes up the positive control?
Adrenaline b-Defensin Complement C3 Contrast medium Corticosteroids Diluent Filaggrin Histamine IgA IgE IgG Mast cell (serum) tryptase Noradrenaline Peanuts Penicillin
a. Histamine
- You are an anaesthetic doctor in surgery and notice that your patient has suddenly developed unexpected widespread rashes and is becoming increasingly hypotensive. You suspect the patient may be having an anaphylactic reaction. What is the best test to determine if the patient is undergoing a systemic allergic reaction in this situation?
Adrenaline b-Defensin Complement C3 Contrast medium Corticosteroids Diluent Filaggrin Histamine IgA IgE IgG Mast cell (serum) tryptase Noradrenaline Peanuts Penicillin
a. Mast cell (serum) tryptase
- A miserable-looking child of European descent presents to your clinic with a long, troublesome history of atopic dermatitis. Which component is a potential genetic cause of the child’s atopy that should be considered?
Adrenaline b-Defensin Complement C3 Contrast medium Corticosteroids Diluent Filaggrin Histamine IgA IgE IgG Mast cell (serum) tryptase Noradrenaline Peanuts Penicillin
a. Filaggrin
- A patient with nephrolithiasis is seen by your on-take team at the beginning of a long night shift. You see the patient and refer the patient for appropriate investigations and decide to take a short coffee break. Returning from your break a few hours later, to your dismay, you learn that the patient has developed severe abdominal pain and diarrhoea. The patient also appears to be a little confused. The registrar suggests to you that this may be a non-IgE mediated reaction. What could have happened, and what is the likely cause of the patient’s symptoms?
Adrenaline b-Defensin Complement C3 Contrast medium Corticosteroids Diluent Filaggrin Histamine IgA IgE IgG Mast cell (serum) tryptase Noradrenaline Peanuts Penicillin
a. Contrast medium
- First line treatment for mild to moderate C. Difficile
Amoxicillin Ceftriaxone Chloramphenicol Ethambutol Erythromycin Flucloxacillin Gentamicin Isoniazid Metronidazole Pyrazinamide Rifampicin Vancomycin
a. Metronidazole
- Treatment of infections resistant to penicillin e.g. MRSA
Amoxicillin Ceftriaxone Chloramphenicol Ethambutol Erythromycin Flucloxacillin Gentamicin Isoniazid Metranidazole Pyrazinamide Rifampicin Vancomycin
a. Vancomycin
- May cause deafness an unwanted side effect
Amoxicillin Ceftriaxone Chloramphenicol Ethambutol Erythromycin Flucloxacillin Gentamicin Isoniazid Metranidazole Pyrazinamide Rifampicin Vancomycin
a. Gentamicin
- 20 year old male, with true resistance to penicillin, presents with a severe headache, neck stiffness, fever and photophobia
Amoxicillin Ceftriaxone Chloramphenicol Ethambutol Erythromycin Flucloxacillin Gentamicin Isoniazid Metranidazole Pyrazinamide Rifampicin Vancomycin
a. Chloramphenicol
- Treatment of TB but may cause optic neuritis.
Amoxicillin Ceftriaxone Chloramphenicol Ethambutol Erythromycin Flucloxacillin Gentamicin Isoniazid Metranidazole Pyrazinamide Rifampicin Vancomycin
Ethambutol
- Which group of antibiotics is not recommended for use in children or pregnant women?
Glycopeptides Cephalexin Cefotaxime Tetracyclines Macrolides Cefuroxime Beta-lactams Aminoglycosides 3 days 7 days Tazocin Doxyclycline Amoxicillin Flucloxacillin Ceftriaxone Trimethoprim
a. Tetracyclines
- Give an example of a second-generation cephalosporin.
Glycopeptides Cephalexin Cefotaxime Tetracyclines Macrolides Cefuroxime Beta-lactams Aminoglycosides 3 days 7 days Tazocin Doxyclycline Amoxicillin Flucloxacillin Ceftriaxone Trimethoprim
Cefuroxime
- Which group of antibiotics is bacteriostatic and acts on 50S ribosomes to interfere with mRNA translation?
Glycopeptides Cephalexin Cefotaxime Tetracyclines Macrolides Cefuroxime Beta-lactams Aminoglycosides 3 days 7 days Tazocin Doxyclycline Amoxicillin Flucloxacillin Ceftriaxone Trimethoprim
Macrolides
- A 23-year-old intubated male in ITU developes a chest infection 14 days after admission, which antibiotic would you prescribe?
Glycopeptides Cephalexin Cefotaxime Tetracyclines Macrolides Cefuroxime Beta-lactams Aminoglycosides 3 days 7 days Tazocin Doxyclycline Amoxicillin Flucloxacillin Ceftriaxone Trimethoprim
Tazocin
A 28-year-old woman is diagnosed with community-acquired cystitis, what is the recommended duration of antibiotic treatment for this diagnosis?
Glycopeptides Cephalexin Cefotaxime Tetracyclines Macrolides Cefuroxime Beta-lactams Aminoglycosides 3 days 7 days Tazocin Doxyclycline Amoxicillin Flucloxacillin Ceftriaxone Trimethoprim
a. 3 days
- A 3-week old baby presents with a fever, irritability and painful, vesicular lesions on the tongue, buccal mucosa, lips and face.
IV Acyclovir Oseltamivir Interferon-beta Symptomatic treatment and reassurance IV Gancyclovir Oral Acyclovir Ribavarin Palivizumab Antiretroviral Therapy Interferon-alpha and Ribavarin
a. Oral Acyclovir
- On examination of a newborn child you notice that although they are small their head is unusually out of proportion and seems much smaller than the rest of their body, additionally their skin appears slightly yellow, with a petechial rash.
IV Acyclovir Oseltamivir Interferon-beta Symptomatic treatment and reassurance IV Gancyclovir Oral Acyclovir Ribavarin Palivizumab Antiretroviral Therapy Interferon-alpha and Ribavarin
a. IV Gancyclovir
- A 2-year old child presents with persistent lymphadenopathy, recurrent fevers and parotid swelling. His adopted parents are unaware of any FH or PMH.
IV Acyclovir Oseltamivir Interferon-beta Symptomatic treatment and reassurance IV Gancyclovir Oral Acyclovir Ribavarin Palivizumab Antiretroviral Therapy Interferon-alpha and Ribavarin
a. Antiretroviral Therapy
- A primary school teacher brings in her 4-year old child with a fever and an itchy, vesicular rash on his trunk and face.
IV Acyclovir Oseltamivir Interferon-beta Symptomatic treatment and reassurance IV Gancyclovir Oral Acyclovir Ribavarin Palivizumab Antiretroviral Therapy Interferon-alpha and Ribavarin
a. Symptomatic treatment and reassurance
- An 8-month old child suddenly develops a high fever, headache and a chesty cough. Her mum is concerned as she seems to have lost her appetite over the past 24 hours and is not improving
IV Acyclovir Oseltamivir Interferon-beta Symptomatic treatment and reassurance IV Gancyclovir Oral Acyclovir Ribavarin Palivizumab Antiretroviral Therapy Interferon-alpha and Ribavarin
Oseltamivir
A 70 year man old presented with acute onset of vertigo. On neurological examination he has left-sided loss of pain and temperature sensation with partial right-sided ptosis and miosis as well as right sided diplopia. He has a mild left-sided weakness and an ataxic gait. He reports numbness on the right side of his face.
Acute Extradural Haemorrhage Acute Subdural Haemorrhage Chronic Extradural Haemorrhage Chronic Subdural Haemorrhage Lacunar Infarction Left Anterior Cerebral Occlusion Left Middle Cerebral Occlusion Left Posterior Cerebral Occlusion Left Posterior Inferior Cerebellar Artery (PICA) Occlusion Right Anterior Cerebral Occlusion Right Middle Cerebral Occlusion Right Posterior Cerebral Occlusion Right Posterior Inferior Cerebellar Artery (PICA) Occlusion Watershed Infarction Weber’s syndrome Vascular/Multi-infarct Dementia
Right Posterior Inferior Cerebellar Artery (PICA) Occlusion
PICA occlusion is also known as lateral medullary syndrome.
A 70 year old man with a history of congestive heart failure presents with bilateral visual loss. On examination there is weakness in the proximal limbs that spared both the hands and feet.
Acute Extradural Haemorrhage Acute Subdural Haemorrhage Chronic Extradural Haemorrhage Chronic Subdural Haemorrhage Lacunar Infarction Left Anterior Cerebral Occlusion Left Middle Cerebral Occlusion Left Posterior Cerebral Occlusion Left Posterior Inferior Cerebellar Artery (PICA) Occlusion Right Anterior Cerebral Occlusion Right Middle Cerebral Occlusion Right Posterior Cerebral Occlusion Right Posterior Inferior Cerebellar Artery (PICA) Occlusion Watershed Infarction Weber’s syndrome Vascular/Multi-infarct Dementia
Watershed infarction
Watershed infarcts are cortical infarcts caused by prolonged periods of low perfusion, common in patients with a history of cardiovascular disease.
A 70 year lady old collapsed at home and is taken to hospital. She regains consciousness but has a right sided hemiplegia, hemianesthesia and hemianopia with eye deviation towards the left. She also has an expressive aphasia.
Acute Extradural Haemorrhage Acute Subdural Haemorrhage Chronic Extradural Haemorrhage Chronic Subdural Haemorrhage Lacunar Infarction Left Anterior Cerebral Occlusion Left Middle Cerebral Occlusion Left Posterior Cerebral Occlusion Left Posterior Inferior Cerebellar Artery (PICA) Occlusion Right Anterior Cerebral Occlusion Right Middle Cerebral Occlusion Right Posterior Cerebral Occlusion Right Posterior Inferior Cerebellar Artery (PICA) Occlusion Watershed Infarction Weber’s syndrome Vascular/Multi-infarct Dementia
Left Middle Cerebral Occlusion
A 70 year old man is presents with headache, being unable to read the right pages of his book and walking into a lamppost. Neurological examination revealed left sided sensory loss in the head and limbs.
Acute Extradural Haemorrhage Acute Subdural Haemorrhage Chronic Extradural Haemorrhage Chronic Subdural Haemorrhage Lacunar Infarction Left Anterior Cerebral Occlusion Left Middle Cerebral Occlusion Left Posterior Cerebral Occlusion Left Posterior Inferior Cerebellar Artery (PICA) Occlusion Right Anterior Cerebral Occlusion Right Middle Cerebral Occlusion Right Posterior Cerebral Occlusion Right Posterior Inferior Cerebellar Artery (PICA) Occlusion Watershed Infarction Weber’s syndrome Vascular/Multi-infarct Dementia
Right Posterior Cerebral Occlusion
A 70 year old lady presented with a headache, mild weakness and drowsiness. She says she can’t remember when it started. On CT the lesion is hypo-dense to the brain parenchyma.
Acute Extradural Haemorrhage Acute Subdural Haemorrhage Chronic Extradural Haemorrhage Chronic Subdural Haemorrhage Lacunar Infarction Left Anterior Cerebral Occlusion Left Middle Cerebral Occlusion Left Posterior Cerebral Occlusion Left Posterior Inferior Cerebellar Artery (PICA) Occlusion Right Anterior Cerebral Occlusion Right Middle Cerebral Occlusion Right Posterior Cerebral Occlusion Right Posterior Inferior Cerebellar Artery (PICA) Occlusion Watershed Infarction Weber’s syndrome Vascular/Multi-infarct Dementia
Chronic subdural haemorrhage
Chronic sub-durals are iso-dense or hypo-dense on CT, compared to acute sub-durals which are hyper-dense.
Number of B cells /μL required to diagnose CLL
70 30 50 500 5000 80 100 1000 20 40
5000
% of CLL patients older than 65 years at time of diagnosis
70 30 50 500 5000 80 100 1000 20 40
70
% of cases that present with no anaemia or thrombocytopenia, with three or more areas of lymphoid involvement (Rai Stages I and II, Binet Clinical Stage B)
70 30 50 500 5000 80 100 1000 20 40
50
% of CLL patients in which one or more cytogenetic abnormalities have been found
70 30 50 500 5000 80 100 1000 20 40
80
A 50 year old man presents with weight loss, fatigue and night sweats. He is diagnosed with chronic myeloid leukaemia and treatment is commenced. Several months later it becomes clear that he is resistant to the main class pharmaceutical agents that were used.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
Allogenic blood transfusion Allogenic stem cell transplantation Autologous blood transfusion Autologous stem cell transplantation Azathioprine Daunorubicin infusion Donor granulocyte infusion Donor lymphocyte infusion Dosatinib Fresh frozen plasma Golimumab Hydroxychloroquine IFN-α infusion Imatinib Methotrexate None of the above
Allogenic stem cell transplantation
A 57 year old woman is known to have chronic myeloid leukaemia. She presents acutely unwell, with 25% myeloblasts on her blood film, and is appropriately treated. 24 months later she relapses.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
Allogenic blood transfusion Allogenic stem cell transplantation Autologous blood transfusion Autologous stem cell transplantation Azathioprine Daunorubicin infusion Donor granulocyte infusion Donor lymphocyte infusion Dosatinib Fresh frozen plasma Golimumab Hydroxychloroquine IFN-α infusion Imatinib Methotrexate None of the above
Donor lymphocyte infusion
A 60 year old woman presents with weight loss and lethargy. On examination, she is cachectic with splenomegaly. Her white cell count is 150 x 109/l. Her blood film showed 25% myeloblasts. Cytogenetic analysis showed presence of the Philadelphia chromosome.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
Allogenic blood transfusion Allogenic stem cell transplantation Autologous blood transfusion Autologous stem cell transplantation Azathioprine Daunorubicin infusion Donor granulocyte infusion Donor lymphocyte infusion Dosatinib Fresh frozen plasma Golimumab Hydroxychloroquine IFN-α infusion Imatinib Methotrexate None of the above
Allogenic stem cell transplantation
A 55 year old man presents with weight loss and lethargy. On examination, he is cachectic with splenomegaly. His white cell count was 135 x 109/l. Cytogenetic analysis showed presence of the Philadelphia chromosome.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
Allogenic blood transfusion Allogenic stem cell transplantation Autologous blood transfusion Autologous stem cell transplantation Azathioprine Daunorubicin infusion Donor granulocyte infusion Donor lymphocyte infusion Dosatinib Fresh frozen plasma Golimumab Hydroxychloroquine IFN-α infusion Imatinib Methotrexate None of the above
Imatinib
A 57 year old man with a history of chronic myeloid leukaemia presents with night sweats, fatigue and weight loss. He was started on first line therapy 6 months ago but his doctor is concerned that he has relapsed. He wants to try a new treatment option.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
Allogenic blood transfusion Allogenic stem cell transplantation Autologous blood transfusion Autologous stem cell transplantation Azathioprine Daunorubicin infusion Donor granulocyte infusion Donor lymphocyte infusion Dosatinib Fresh frozen plasma Golimumab Hydroxychloroquine IFN-α infusion Imatinib Methotrexate None of the above
Dosatinib
A 50 year old man presented with fatigue, lethargy and weight loss. On examination, he was pale and had gross splenomegaly. His blood film showed an increase in white blood cells (both myelocytes and mature granulocytes). Cytogenetic analysis showed a t(9;22) chromosomal translocation.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
IFN-α Hydroxycarbamide Allogeneic stem cell transplantation Imatinib Chlorambucil Cyclosphosphamide Monitor clinically and give annual influenza vaccine Radiotherapy and 6-8 cycles of chemotherapy Dosatinib Chemotherapy + all-trans-retinoic acid Chemotherapy (R-CHOP regimen) Chemotherapy (ABVD regimen) Chemotherapy (R-CVP regimen) Donor lymphocyte infusion
Imatinib
A 74 year old patient has been diagnosed with chronic myeloid leukaemia and 6 months after starting therapy with the first line drug has shown no improvement in FBC or cytogenetics. His physician switches him to another drug.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
IFN-α Hydroxycarbamide Allogeneic stem cell transplantation Imatinib Chlorambucil Cyclosphosphamide Monitor clinically and give annual influenza vaccine Radiotherapy and 6-8 cycles of chemotherapy Dosatinib Chemotherapy + all-trans-retinoic acid Chemotherapy (R-CHOP regimen) Chemotherapy (ABVD regimen) Chemotherapy (R-CVP regimen) Donor lymphocyte infusion
Dosatinib
A 48 year old patient with chronic myeloid leukaemia becomes acutely unwell. A peripheral blood film shows 30% myeloblasts.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
IFN-α Hydroxycarbamide Allogeneic stem cell transplantation Imatinib Chlorambucil Cyclosphosphamide Monitor clinically and give annual influenza vaccine Radiotherapy and 6-8 cycles of chemotherapy Dosatinib Chemotherapy + all-trans-retinoic acid Chemotherapy (R-CHOP regimen) Chemotherapy (ABVD regimen) Chemotherapy (R-CVP regimen) Donor lymphocyte infusion
Allogeneic stem cell transplantation
A 59 year old patient with chronic myeloid leukaemia has been found to be positive for the Philadelphia chromosome several years following his stem cell transplantation.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
IFN-α Hydroxycarbamide Allogeneic stem cell transplantation Imatinib Chlorambucil Cyclosphosphamide Monitor clinically and give annual influenza vaccine Radiotherapy and 6-8 cycles of chemotherapy Dosatinib Chemotherapy + all-trans-retinoic acid Chemotherapy (R-CHOP regimen) Chemotherapy (ABVD regimen) Chemotherapy (R-CVP regimen) Donor lymphocyte infusion
Donor lymphocyte infusion
A 61 year old patient with chronic myeloid leukaemia has not responded to different tyrosine kinase inhibitors available.
For each scenario, choose the most appropriate treatment option from the list. Each option may be used once, more than once or not at all.
IFN-α Hydroxycarbamide Allogeneic stem cell transplantation Imatinib Chlorambucil Cyclosphosphamide Monitor clinically and give annual influenza vaccine Radiotherapy and 6-8 cycles of chemotherapy Dosatinib Chemotherapy + all-trans-retinoic acid Chemotherapy (R-CHOP regimen) Chemotherapy (ABVD regimen) Chemotherapy (R-CVP regimen) Donor lymphocyte infusion
Allogeneic stem cell transplantation
- A 17 year old was diagnosed with Infectious Mononucleosis (EBV). Confirmatory blood tests also revealed anaemia. Direct Coombs test was positive (but not “strongly positive”). On more detailed analysis, IgM antibodies were eluted from red cells with C3d remaining.
A Burns B Cold Autoimmune HA C Direct membrane damage (drugs) D G6PD deficiency E Haemolytic transfusion reaction F Hereditary spherocytosis G Hypersplenism H Immune (drug induced) I Malaria J March haemoglobinuria K Mechanical haemolysis L Microangiopathic HA M Paroxysmal nocturnal haemoglobinuria N Sickle Cell disease O Thalassaemia P Warm Autoimmune HA
B Cold Autoimmune HA
- A 4 year old African boy attends your clinic with recurrent pain in the hands. While in the cold waiting room he suddenly grasps his chest in pain and starts breathing rapidly. Investigations reveal hypoxia and new chest X-ray changes that look like consolidation.
A Burns B Cold Autoimmune HA C Direct membrane damage (drugs) D G6PD deficiency E Haemolytic transfusion reaction F Hereditary spherocytosis G Hypersplenism H Immune (drug induced) I Malaria J March haemoglobinuria K Mechanical haemolysis L Microangiopathic HA M Paroxysmal nocturnal haemoglobinuria N Sickle Cell disease O Thalassaemia P Warm Autoimmune HA
N Sickle Cell disease
- An 18 year old attending a routine check up at her new GP practice is noted to have mild splenomegaly and a leg ulcer. Upon questioning she mentions that she had jaundice as a child, and that one of her parents (and grandparents) suffer from anaemia. Blood results reveal slight anaemia with hyperchromic cells lacking central pallor. Coombs test is negative.
A Burns B Cold Autoimmune HA C Direct membrane damage (drugs) D G6PD deficiency E Haemolytic transfusion reaction F Hereditary spherocytosis G Hypersplenism H Immune (drug induced) I Malaria J March haemoglobinuria K Mechanical haemolysis L Microangiopathic HA M Paroxysmal nocturnal haemoglobinuria N Sickle Cell disease O Thalassaemia P Warm Autoimmune HA
F Hereditary spherocytosis
- A 58 year old man from South East Asia attends for a clinic feeling anaemic on return from holiday in Africa. On direct questioning he admits that he did start taking the Primaquine and Quinine you prescribed until a couple of days ago. Blood film revealed Heinz bodies and bite cells.
A Burns B Cold Autoimmune HA C Direct membrane damage (drugs) D G6PD deficiency E Haemolytic transfusion reaction F Hereditary spherocytosis G Hypersplenism H Immune (drug induced) I Malaria J March haemoglobinuria K Mechanical haemolysis L Microangiopathic HA M Paroxysmal nocturnal haemoglobinuria N Sickle Cell disease O Thalassaemia P Warm Autoimmune HA
D G6PD deficiency
- A 31 year old student nurse returns from her elective in Indonesia feeling generally unwell, with rigors and fever. Clinical examination reveals slight splenomegaly and haematuria.
A Burns B Cold Autoimmune HA C Direct membrane damage (drugs) D G6PD deficiency E Haemolytic transfusion reaction F Hereditary spherocytosis G Hypersplenism H Immune (drug induced) I Malaria J March haemoglobinuria K Mechanical haemolysis L Microangiopathic HA M Paroxysmal nocturnal haemoglobinuria N Sickle Cell disease O Thalassaemia P Warm Autoimmune HA
I Malaria
- A 22 year old woman presents with dark urine and tachycardia. She believes the dark urine is related to some “problems with the water works” she is currently being treated for. Direct antiglobulin test is positive.
A Cold Type AIHA B Drug induced/Iatrogenic C Glucose-6-phosphate deficiency D Hereditary elliptocytosis E Hereditary spherocytosis F Isoimmune paroxysmal cold haemoglobin urea G Malaria H Microangiopathic haemolytic anaemia (MAHA) I Paroxysmal nocturnal haemoglobinurea J Pyruvate kinase deficiency K Sickle cell disease L Thalassaemia M Warm Type AIHA
B Drug induced/Iatrogenic
- A 72 year old woman presents with haemolytic anaemia. FBC shows Hb 10.7 g/dL, WBC 108x10^3/uL, Platelets 90x10^3/uL. On examination the patient also has splenomegaly.
A Cold Type AIHA B Drug induced/Iatrogenic C Glucose-6-phosphate deficiency D Hereditary elliptocytosis E Hereditary spherocytosis F Isoimmune paroxysmal cold haemoglobin urea G Malaria H Microangiopathic haemolytic anaemia (MAHA) I Paroxysmal nocturnal haemoglobinurea J Pyruvate kinase deficiency K Sickle cell disease L Thalassaemia M Warm Type AIHA
M Warm Type AIHA
- A 32 year old woman is brought in by her concerned husband. She has a 5 month history or amenorrhea and is grossly distended. Her BP is 154/98. A urine sample is taken and results confirm your suspicion.
A Cold Type AIHA B Drug induced/Iatrogenic C Glucose-6-phosphate deficiency D Hereditary elliptocytosis E Hereditary spherocytosis F Isoimmune paroxysmal cold haemoglobin urea G Malaria H Microangiopathic haemolytic anaemia (MAHA) I Paroxysmal nocturnal haemoglobinurea J Pyruvate kinase deficiency K Sickle cell disease L Thalassaemia M Warm Type AIHA
H Microangiopathic haemolytic anaemia (MAHA)
- A young boy presents with splenomegaly and jaundice. His blood film shows Howell-Jolly bodies and poikilocytosis. An osmotic fragility test confirms the diagnosis.
A Cold Type AIHA B Drug induced/Iatrogenic C Glucose-6-phosphate deficiency D Hereditary elliptocytosis E Hereditary spherocytosis F Isoimmune paroxysmal cold haemoglobin urea G Malaria H Microangiopathic haemolytic anaemia (MAHA) I Paroxysmal nocturnal haemoglobinurea J Pyruvate kinase deficiency K Sickle cell disease L Thalassaemia M Warm Type AIHA
E Hereditary spherocytosis
- A teenage boy originally from Lebanon presents with acute haemolytic anaemia after switching to a vegan diet. Blood film shows bite cells and blister cells.
A Cold Type AIHA B Drug induced/Iatrogenic C Glucose-6-phosphate deficiency D Hereditary elliptocytosis E Hereditary spherocytosis F Isoimmune paroxysmal cold haemoglobin urea G Malaria H Microangiopathic haemolytic anaemia (MAHA) I Paroxysmal nocturnal haemoglobinurea J Pyruvate kinase deficiency K Sickle cell disease L Thalassaemia M Warm Type AIHA
C Glucose-6-phosphate deficiency
Innate immune deficiency
Recurrent infections with high neutrophil count on FBC but no abscess formation • Lymphocyte adhesion deficiency • Chronic granulomatous disease • Kostmann syndrome • IFN gamma receptor deficiency
Lymphocyte adhesion deficiency
Innate immune deficiency
Recurrent infections with hepatosplenomegaly and abnormal dihydrorhodamine test • Lymphocyte adhesion deficiency • Chronic granulomatous disease • Kostmann syndrome • IFN gamma receptor deficiency
Chronic granulomatous disease
Innate immune deficiency
Recurrent infections with no neutrophils on FBC • Lymphocyte adhesion deficiency • Chronic granulomatous disease • Kostmann syndrome • IFN gamma receptor deficiency
Kostmann syndrome
Innate immune deficiency
Infection with atypical mycobacterium. Normal FBC • Lymphocyte adhesion deficiency • Chronic granulomatous disease • Kostmann syndrome • IFN gamma receptor deficiency
IFN gamma receptor deficiency
T-cell deficiency
Severe recurrent infections from 3 months,CD4 and CD8 T cells absent, B cell present, IgM present, IgA and IgG absent • X-linked SCID • IFN gamma receptor deficiency • DiGeorge’s syndrome • Bare lymphocyte syndrome type II
• X-linked SCID
T-cell deficiency
Young adult with chronic infection with Mycobacterium marinum • X-linked SCID • IFN gamma receptor deficiency • DiGeorge’s syndrome • Bare lymphocyte syndrome type II
• IFN gamma receptor deficiency
T-cell deficiency
Recurrent infections in childhood, abnormal facial features, congenital heart disease, normal B cells, low T cells, low IgA and IgG • X-linked SCID • IFN gamma receptor deficiency • DiGeorge’s syndrome • Bare lymphocyte syndrome type II
• DiGeorge’s syndrome
T-cell deficiency
6 month baby with two recent serious bacterial infections. T cells present – but only CD8+ population. B cells present. IgM present but IgG absent • X-linked SCID • IFN gamma receptor deficiency • DiGeorge’s syndrome • Bare lymphocyte syndrome type II
• Bare lymphocyte syndrome type II
B-cell deficiency
Adult with bronchiectasis, recurrent sinusitis and development of atypical SLE
- Common variable immunodeficiency
- X linked hyper IgM syndrome due to CD40ligand mutation
- Bruton’s X linked hypogammaglobulinaemia
- IgA deficiency
• Common variable immunodeficiency
B-cell deficiency
Recurrent bacterial infections in a child, episode of pneumocystis pneumonia, high IgM, absent IgA and IgG
• Common variable immunodeficiency
• X linked hyper IgM syndrome due to CD40ligand mutation
• Bruton’s X linked hypogammaglobulinaemia
• IgA deficiency
• X linked hyper IgM syndrome due to CD40ligand mutation
B-cell deficiency
1 year old boy. Recurrent bacterial infections. CD4 and CD8 T cells present. B cells absent, IgG, IgA, IgM absent
• Common variable immunodeficiency
• X linked hyper IgM syndrome due to CD40ligand mutation
• Bruton’s X linked hypogammaglobulinaemia
• IgA deficiency
• Bruton’s X linked hypogammaglobulinaemia
B-cell deficiency
Recurrent respiratory tract infections, absent IgA, normal IgM and IgG
• Common variable immunodeficiency
• X linked hyper IgM syndrome due to CD40ligand mutation
• Bruton’s X linked hypogammaglobulinaemia
• IgA deficiency
• IgA deficiency
Complement deficiency
Membranoproliferative nephritis and bacterial infections
• C3 deficiency with presence of a nephritic factor
• C9 deficiency
• C1q deficiency
• MBL deficiency
• C3 deficiency with presence of a nephritic factor
Complement deficiency
Meningococcus meningitis with family history of sibling dying of same condition aged 6
• C3 deficiency with presence of a nephritic factor
• C9 deficiency
• C1q deficiency
• MBL deficiency
• C9 deficiency
Complement deficiency
Severe childhood onset SLE with normal levels of C3 and C4
• C3 deficiency with presence of a nephritic factor
• C9 deficiency
• C1q deficiency
• MBL deficiency
• C1q deficiency
Complement deficiency
Recurrent infections when receiving chemotherapy but previously well
• C3 deficiency with presence of a nephritic factor
• C9 deficiency
• C1q deficiency
• MBL deficiency
• MBL deficiency
Expresses Foxp3 and CD25 and secretes IL-10. Deficient in the monogenic autoimmune disease known as IPEX (immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome)
- Th17 cell
- Macrophage
- Epithelial cell
- T reg cell
- Dendritic cell
- CD4+ T cell
- Neutrophil
- Th1 cell
- Plasma cell
- Megakaryocyte
- Lymphocyte
• 4. T reg cell
In the immature form these cells are adapted for recognition and uptake of pathogens. Maturation is associated with expression of CCR7, migration to lymph nodes and enhanced capacity for antigen presentation.
- Th17 cell
- Macrophage
- Epithelial cell
- T reg cell
- Dendritic cell
- CD4+ T cell
- Neutrophil
- Th1 cell
- Plasma cell
- Megakaryocyte
- Lymphocyte
• 5. Dendritic cell
These cells can be rapidly mobilised from bone marrow. They express pathogen recognition receptors and Fc receptors and are able to engage in oxidative and non-oxidative killing. They do not express HLA class II molecules and so do not activate CD4 T cells. They are the predominant cell type in synovial fluid taken from patients with gout,
- Th17 cell
- Macrophage
- Epithelial cell
- T reg cell
- Dendritic cell
- CD4+ T cell
- Neutrophil
- Th1 cell
- Plasma cell
- Megakaryocyte
- Lymphocyte
Neutrophil
These cells may be formed following a germinal centre reaction involving isotype switching and affinity maturation of receptors. They are long-lived and reside in bone marrow.
- Th17 cell
- Macrophage
- Epithelial cell
- T reg cell
- Dendritic cell
- CD4+ T cell
- Neutrophil
- Th1 cell
- Plasma cell
- Megakaryocyte
- Lymphocyte
• 9. Plasma cell
These cells express CD3 and secrete IL-17 and IL-22. They are thought to be important in some auto-immune conditions including rheumatoid arthritis.
- Th17 cell
- Macrophage
- Epithelial cell
- T reg cell
- Dendritic cell
- CD4+ T cell
- Neutrophil
- Th1 cell
- Plasma cell
- Megakaryocyte
- Lymphocyte
• 1. Th17 cell
These cells may be resident in peripheral tissues (eg Kupffer cells in liver, microglia in neural tissue) express pathogen recognition receptors and Fc receptors and are able to engage in oxidative and non-oxidative killing. They are an important source of cytokines such as IL-1 and TNF-alpha and are thought to play an important role in some auto-inflammatory and auto-immune diseases.
- Th17 cell
- Macrophage
- Epithelial cell
- T reg cell
- Dendritic cell
- CD4+ T cell
- Neutrophil
- Th1 cell
- Plasma cell
- Megakaryocyte
- Lymphocyte
• 2. Macrophage
The normal function of these cells is to express cytokines in response to recognition of specific peptides presented by HLA class II molecules. Depletion of these cells during HIV infection is an important factor in development of AIDS.
- Th17 cell
- Macrophage
- Epithelial cell
- T reg cell
- Dendritic cell
- CD4+ T cell
- Neutrophil
- Th1 cell
- Plasma cell
- Megakaryocyte
- Lymphocyte
• 6. CD4+ T cell
Play a role in protective immunity against HIV infection by killing virus infected cells via perforin and FAS.
- Gp120
- Anti-metabolites
- CCR5
- Reverse transcriptase
- Basophils
- Gastric parietal cells
- Protease inhibitors
- CCR7
- Macrophages
- CD8 T cells
- 11.IL-8
• 10. CD8 T cells
Acts as a co-receptor for HIV entry to cells
- Gp120
- Anti-metabolites
- CCR5
- Reverse transcriptase
- Basophils
- Gastric parietal cells
- Protease inhibitors
- CCR7
- Macrophages
- CD8 T cells
- 11.IL-8
• 3. CCR5
Serves to generate complementary DNA from RNA, which can then be integrated into host cell genes
- Gp120
- Anti-metabolites
- CCR5
- Reverse transcriptase
- Basophils
- Gastric parietal cells
- Protease inhibitors
- CCR7
- Macrophages
- CD8 T cells
- 11.IL-8
• 4. Reverse transcriptase
Directs homing of dendritic cells to lymph nodes
- Gp120
- Anti-metabolites
- CCR5
- Reverse transcriptase
- Basophils
- Gastric parietal cells
- Protease inhibitors
- CCR7
- Macrophages
- CD8 T cells
- 11.IL-8
• 8. CCR7
Are often infected by HIV if they express CD4
- Gp120
- Anti-metabolites
- CCR5
- Reverse transcriptase
- Basophils
- Gastric parietal cells
- Protease inhibitors
- CCR7
- Macrophages
- CD8 T cells
- 11.IL-8
• 9. Macrophages
Antibodies against this target are partially protective against HIV infection
- Gp120
- Anti-metabolites
- CCR5
- Reverse transcriptase
- Basophils
- Gastric parietal cells
- Protease inhibitors
- CCR7
- Macrophages
- CD8 T cells
- 11.IL-8
• 1. Gp120
Are effective in management of HIV infection if used in combination with other drugs
- Gp120
- Anti-metabolites
- CCR5
- Reverse transcriptase
- Basophils
- Gastric parietal cells
- Protease inhibitors
- CCR7
- Macrophages
- CD8 T cells
- 11.IL-8
• 7. Protease inhibitors
Mutation in MEFV leads to failure to regulate neutrophil function
Rheumatoid arthritis Familial Mediterranean Fever IPEX (immune dysregulation polyendocrinopathy, enteropathy, X linked syndrome) Crohn’s disease Ankylosing Spondylitis
Familial Mediterranean Fever
Polygenic auto-inflammatory disease in which NOD-2 (CARD 15) mutations are common
Rheumatoid arthritis Familial Mediterranean Fever IPEX (immune dysregulation polyendocrinopathy, enteropathy, X linked syndrome) Crohn’s disease Ankylosing Spondylitis
Crohn’s disease
Mixed pattern disease with very high heritability (>90%) and a strong association with HLA-B27
Rheumatoid arthritis Familial Mediterranean Fever IPEX (immune dysregulation polyendocrinopathy, enteropathy, X linked syndrome) Crohn’s disease Ankylosing Spondylitis
Ankylosing Spondylitis
Polygenic auto-immune disease associated with polymorphisms in PAD enzymes (which citrullinate proteins). Environmental factors including smoking and gum infection are associated with disease.
Rheumatoid arthritis Familial Mediterranean Fever IPEX (immune dysregulation polyendocrinopathy, enteropathy, X linked syndrome) Crohn’s disease Ankylosing Spondylitis
Rheumatoid arthritis
Monogenic auto-immune disease due to a mutation in Foxp3
Rheumatoid arthritis Familial Mediterranean Fever IPEX (immune dysregulation polyendocrinopathy, enteropathy, X linked syndrome) Crohn’s disease Ankylosing Spondylitis
IPEX (immune dysregulation polyendocrinopathy, enteropathy, X linked syndrome)
Congenital heart block in infants of mothers with SLE
Anti-DNA antibody Anti-RNP antibody Anti-GAD antibody Anti-centromere antibody Anti-Ro antibody
Anti-Ro antibody
Lupus nephritis
Anti-DNA antibody Anti-RNP antibody Anti-GAD antibody Anti-centromere antibody Anti-Ro antibody
Anti-DNA antibody
Mixed connective tissue disease
Anti-DNA antibody Anti-RNP antibody Anti-GAD antibody Anti-centromere antibody Anti-Ro antibody
Anti-RNP antibody
Limited cutaneous systemic sclerosis
Anti-DNA antibody Anti-RNP antibody Anti-GAD antibody Anti-centromere antibody Anti-Ro antibody
Anti-centromere antibody
Sjogren’s syndrome
Anti-DNA antibody Anti-RNP antibody Anti-GAD antibody Anti-centromere antibody Anti-Ro antibody
Anti-Ro antibody
Antibody to gastric parietal cells
Autoimmune hepatitis Coeliac disease Pernicious anaemia Dermatitis herpetiformis Primary biliary cirrhosis
Pernicious anaemia
Anti-smooth muscle antibody
Autoimmune hepatitis Coeliac disease Pernicious anaemia Dermatitis herpetiformis Primary biliary cirrhosis
Autoimmune hepatitis
Anti-endomysial antibody
Autoimmune hepatitis Coeliac disease Pernicious anaemia Dermatitis herpetiformis Primary biliary cirrhosis
Coeliac disease/Dermatitis herpetiformis
Anti-tissue transglutaminase antibody
Autoimmune hepatitis Coeliac disease Pernicious anaemia Dermatitis herpetiformis Primary biliary cirrhosis
Coeliac disease/Dermatitis herpetiformis
Anti-mitochondrial antibody
Autoimmune hepatitis Coeliac disease Pernicious anaemia Dermatitis herpetiformis Primary biliary cirrhosis
Primary biliary cirrhosis
Mediated predominantly by antibodies which usually form after the transplantation
Hyperacute rejection
Acute cellular rejection
Acute vascular rejection
Chronic allograft rejection
Acute vascular rejection
Both immunological and non-immunological mechanisms contribute
Hyperacute rejection
Acute cellular rejection
Acute vascular rejection
Chronic allograft rejection
Chronic allograft rejection
Due to presence of pre-formed antibodies
Hyperacute rejection
Acute cellular rejection
Acute vascular rejection
Chronic allograft rejection
Hyperacute rejection
Mediated by activation of CD4 T cells which provide help for a CD8 T cell and B cell response and occurs within 1-4 weeks
Hyperacute rejection
Acute cellular rejection
Acute vascular rejection
Chronic allograft rejection
Acute cellular rejection
42 year old lady develops pruritis, rash, hypotension and difficulty breathing. She has received an intra-articular injection of hydrocortisone and lignocaine 10 minutes previously
Physical urticaria Type IV hypersensitivity to latex Allergic rhinitis Anaphylaxis C1 inhibitor deficiency
Anaphylaxis
16 year old develops itchy red wheals on her skin whenever she goes running. Symptoms tend to be worse in the summer
Physical urticaria Type IV hypersensitivity to latex Allergic rhinitis Anaphylaxis C1 inhibitor deficiency
Physical urticaria
36 year old lady presents with swelling of face and tongue following dental surgery. There is a family history of similar reactions – both her mother and sister are affected.
Physical urticaria Type IV hypersensitivity to latex Allergic rhinitis Anaphylaxis C1 inhibitor deficiency
C1 inhibitor deficiency
14 year old presents with nasal irritation and discharge during the summer months. The symptoms are relieved by over the counter anti-histamines
Physical urticaria Type IV hypersensitivity to latex Allergic rhinitis Anaphylaxis C1 inhibitor deficiency
Allergic rhinitis
25 year old junior doctor develops pruritic/blistering rash on hands within two weeks of starting placement on surgical firm
Physical urticaria
Type IV hypersensitivity to latex
Allergic rhinitis
Anaphylaxis
C1 inhibitor deficiency
Type IV hypersensitivity to latex
A 58 year old pharmacist presents with a 3 month history of skin itching associated with lethargy and loss of energy.
Physical examination is normal, but liver function tests reveal:
Total bilirubin = 36umol/l (0-17umol/l)
ALT = 28U/l (0-31U/l)
Alkaline phosphatase 420U/l (30-130)
- anti-acetyl choline receptor antibody
- anti-adrenal cortex antibody
- antibody to double stranded DNA
- anti-centromere antibody
- anti-TTG antibody
- anti-intrinsic factor antibody
- anti-mitochondrial antibody
- anti-neutrophil cytoplasmic antibody
- anti-RNP antibody
- anti-smooth muscle antibody
- anti-mitochondrial antibody
A 56 year old prison officer presents with a history of recurrent nose bleeds, haemoptysis and joint pain associated with profound lethargy.
On examination, he has crackles in his upper left lung field, and a cavitating left lung lesion is demonstrated on chest radiography.
Urine dipstick is positive for protein and blood.
- anti-acetyl choline receptor antibody
- anti-adrenal cortex antibody
- antibody to double stranded DNA
- anti-centromere antibody
- anti-TTG antibody
- anti-intrinsic factor antibody
- anti-mitochondrial antibody
- anti-neutrophil cytoplasmic antibody
- anti-RNP antibody
- anti-smooth muscle antibody
- anti-neutrophil cytoplasmic antibody
A 22 year old woman presents with joint pain and fatigue. She has an intermittent, skin-sensitive rash, and also complains of mouth ulcers. Physical examination is otherwise normal.
Urine dipstick is positive ++ protein and ++ blood.
Full blood count shows a normocytic normochromic anaemia.
- anti-acetyl choline receptor antibody
- anti-adrenal cortex antibody
- antibody to double stranded DNA
- anti-centromere antibody
- anti-TTG antibody
- anti-intrinsic factor antibody
- anti-mitochondrial antibody
- anti-neutrophil cytoplasmic antibody
- anti-RNP antibody
- anti-smooth muscle antibody
- antibody to double stranded DNA
A 30 year old plumber attends his GP complaining of feeling tired all the time. He has type I diabetes, which is currently well controlled, and a history of irritable bowel syndrome. A full blood count shows a microcytic hypochromic anaemia, and iron studies confirm iron deficiency. Vitamin D levels are within the insufficient range.
- anti-acetyl choline receptor antibody
- anti-adrenal cortex antibody
- antibody to double stranded DNA
- anti-centromere antibody
- anti-TTG antibody
- anti-intrinsic factor antibody
- anti-mitochondrial antibody
- anti-neutrophil cytoplasmic antibody
- anti-RNP antibody
- anti-smooth muscle antibody
- anti-TTG antibody
A 44 year old builder presents with a history of fingers intermittently becoming very cold and white with recent development of a gangrenous tip of his finger. The skin over his fingers feels ‘tight’ and you note telangectasia on his hands.
- anti-acetyl choline receptor antibody
- anti-adrenal cortex antibody
- antibody to double stranded DNA
- anti-centromere antibody
- anti-TTG antibody
- anti-intrinsic factor antibody
- anti-mitochondrial antibody
- anti-neutrophil cytoplasmic antibody
- anti-RNP antibody
- anti-smooth muscle antibody
- anti-centromere antibody
A 19 year old student presents with a chronic, extremely itchy rash consisting of papules and vesicles which is distributed symmetrically over the extensor surfaces of her elbows, legs and buttocks. You suspect dermatitis herpetiformis.
- anti-acetyl choline receptor antibody
- anti-adrenal cortex antibody
- antibody to double stranded DNA
- anti-centromere antibody
- anti-TTG antibody
- anti-intrinsic factor antibody
- anti-mitochondrial antibody
- anti-neutrophil cytoplasmic antibody
- anti-RNP antibody
- anti-smooth muscle antibody
- anti-intrinsic factor antibody
- A. Is mediated by Toll like receptors which recognise pathogen associated molecular patterns
- Oxidative killing
- Pathogen recognition
- Opsonisation
- Non-oxidative killing
Pathogen recognition
- B. May be mediated by antibodies, complement components or acute phase proteins and facilitates phagocytosis
- Oxidative killing
- Pathogen recognition
- Opsonisation
- Non-oxidative killing
Opsonisation
- C. Describes killing mediated by reactive oxygen species generated by action of the NADPH oxidase complex
- Oxidative killing
- Pathogen recognition
- Opsonisation
- Non-oxidative killing
Oxidative killing
- D. May be mediated by bacteriocidal enzymes such as lysozyme
- Oxidative killing
- Pathogen recognition
- Opsonisation
- Non-oxidative killing
Non-oxidative killing
- Derived from monocytes and resident in peripheral tissues
Neutrophils
Natural Killer Cells
Dendritic cells
Macrophages
Macrophages
- Polymorphonuclear cells capable of phagocytosing pathogens and killing by oxidative and non-oxidative mechanisms
Neutrophils
Natural Killer Cells
Dendritic cells
Macrophages
Neutrophils
- Lymphocytes that express inhibitory receptors capable of recognising HLA class I molecules and have cytotoxic capacity
Neutrophils
Natural Killer Cells
Dendritic cells
Macrophages
Natural Killer Cells
- Immature cells are adapted for pathogen recognition and uptake whilst mature cells are adapted for antigen presentation to prime T cells
Neutrophils
Natural Killer Cells
Dendritic cells
Macrophages
Dendritic cells
Express receptors that recognise peptides usually derived from intracellular proteins and expressed on HLA class I molecules
Th1 cells
CD8 T cells
T follicular helper (Tfh) cells
T regulatory cells
CD8 T cells
Subset of lymphocytes that express Foxp3 and CD25
Th1 cells
CD8 T cells
T follicular helper (Tfh) cells
T regulatory cells
T regulatory cells
Subset of cells that express CD4 and secrete IFN gamma and IL-2
Th1 cells
CD8 T cells
T follicular helper (Tfh) cells
T regulatory cells
Th1 cells
Play an important role in promoting germinal centre reactions and differentiation of B cells into IgG and IgA secreting plasma cells
Th1 cells
CD8 T cells
T follicular helper (Tfh) cells
T regulatory cells
T follicular helper (Tfh) cells
Exist within the bone marrow and develop from haematopoietic stem cells
Pre-B cells
IgA
IgG secreting plasma cells
IgM secreting plasma cells
Pre-B cells
Cell dependent on the presence of CD4 T cell help for generation.
Pre-B cells
IgA
IgG secreting plasma cells
IgM secreting plasma cells
IgG secreting plasma cells
Are generated rapidly following antigen recognition and are not dependent on CD4 T cell help
Pre-B cells
IgA
IgG secreting plasma cells
IgM secreting plasma cells
IgM secreting plasma cells
Divalent antibody present within mucous which helps provide a constitutive barrier to infection
Pre-B cells
IgA
IgG secreting plasma cells
IgM secreting plasma cells
IgA
Area within secondary lymphoid tissue where B cells proliferate and undergo affinity maturation and isotope switching
Primary lymphoid organs
Thoracic duct
Thymus
Germinal centre
Germinal centre
Include both the bone marrow and thymus; sites of B and T cell development
Primary lymphoid organs
Thoracic duct
Thymus
Germinal centre
Primary lymphoid organs
Carries lymphocytes from lymph nodes back to the blood circulation
Primary lymphoid organs
Thoracic duct
Thymus
Germinal centre
Thoracic duct
Site of deletion of T cells with inappropriately high or low affinity for HLA molecules and of maturation of T cells into CD4+ or CD8+ cells
Primary lymphoid organs
Thoracic duct
Thymus
Germinal centre
Thymus
Binding of immune complexes to this protein triggers the classical pathway of complement activation
C3
C1
C9
MBL
C1
Cleavage of this protein may be triggered via the classical, MBL or alternative pathways
C3
C1
C9
MBL
C3
Binds to microbial surface carbohydrates to activate the complement cascade in an immune complex independent manner
C3
C1
C9
MBL
MBL
Part of the final common pathway resulting in the generation of the membrane attack complex
C3
C1
C9
MBL
C9
Polymorphonuclear cell capable of phagocytosing pathogens
Neutrophil
Type of cell derived from monocytes and are resident in peripheral tissues
Macrophage
Type of lymphocyte that expresses FOXP3 and CD25
TH1
Divalent antibody present in mucus; provides constitutive barrier to infection
IgA
Binding of immune complexes to this protein triggers the classical pathway of complement
C1
Monoclonal antibody that prevents osteoporosis by inhibiting RANKL. Can be used in pts on long-term steroids
Denosumab
Mycophenolate
Reversibly inhibits guanine synthesis (de novo pathway of purine synthesis)
Used to prevent transplant rejection, esp renal
Can also be a steroid sparing agent in authoimmune diseases
CTLA4-immunoglobulin fusion protein sometimes used in RA when anti-TNF doesn’t work
Abatacept
Drug used in autoimmune disorders (e.g. SLE) when body develops end-organ resistance to corticosteroids and DMARDS fail
Cyclophosphamide
TNF alpha inhibitor for severe RA, when DMARDS fail
Infliximab
Patients in this immune modulating drug require regular monitoring of retina
Hydroxychloroquine
First-line DMARD for RA
Methotrexate
What drug would you prescribe for RA pt who has recently developed vasculitis and requires a strong immunosuppressant
Cyclophoshamide
Immunosuppressive drug for RA that requires washout before a woman can conceive
Leflunomide
Biological DMARD in RA treatment
Infliximab
t(9;22)
Phildelphia chromosome.
Seen in 95% CML, 25-30% ALL
Diagnosis–Fatigue, anemia, lymphocytosis, painless LAD, smudge cells on blood film.
CLL
Diagnosis–Fatigue, night sweats, weight loss, anemia, leukocytosis, splenomegaly, Philedelphia chromosome.
CML
Diagnosis–Anemia, fever, weight loss, splenomegaly, pancytopenia, irregularly-shaped cels with filament-like cytoplasmic projections on blood film
Hairy cell leukemia
Pallor, HSM, anemia, leukocytosis, thrombocytopenia. Blast cells and Auer rods on blood film
AML
Most likely diagnosis-young boy with Down’s, pallor, tachycardia, petechiae, testicular enlargement. Anemia, thrombocytopenia, leukocytosis, blast cells.
ALL
Pt with this disease possesses homozygous isoform of ApoE, ApoE2/E2
Familial dysbetalipoproteinemia (type III)
Type of primary hypercholesterolemia which involves mutation of ATP-binding cassette transporters G5, G8
Phytosterolemia
AD form of primary hypercholesterolemia which can be caused by gain of function mutation of proprotein convertase subtilisi/kexin type 9 (PCSK9) gene
Familial hypercholesterolemia (type I)
AD mutation of ApoB gene could lead to this condition
Hypobetalipoproteinemia
A condition which results from dysregulated lipoprotein metabolism leading to cholesterol deposition in arterial wall
Atherosclerosis
Lipoprotein found in VLDL and chylomicrons; activates lipoprotein lipase in capillaries
ApoC
Main lipoprotein of LDL and chylomicrons. Leads to heart disease if deficient
ApoB
Binds to LDL receptor to promote degradation. Loss of function leads to low LDL levels
PCSK9
Class of apolipoprotein produced by astrocytes in CNS. Polymorphisms of this are associated with Parkinson’s and Alzheimer’s.
ApoE
Major lipoprotein in HDL. Mutation can lead to paradoxical drop in HDL concentration and reduction in atheroma in animal models
ApoA1
Dx: 25 year old man presents with jaundice, fever, RUQ pain
Ascennding cholangitis
Dx: 25 yr old man presents with 3 yr hx occasional episodes mild jaundice, worse with chest infection. Mild unconjugated hyperbilirubinemia, normal liver biopsy
Gilberts.
Dx: 45 year old lady with mildly elevated serum bili, normal ALP and AST, anemia. No urinary bili present
Hemolytic jaundice
60 year old diabetic pt presents with localized back pain, fever, malaise, swelling at site of pain. CRP raised.
Septic Arthritis Prosthetic joint infection Hematogenous osteomyelitis Brodie's abscess Vertebral osteomyelitis Cellulitis Spinal cord neoplasm Gout Acute osteomyelitis Chronic osteomyelitis
Vertebral osteomyelitis
29 year old pt presents with 1 wk painful, red, swollen, restricted knee join. Raised CRP, WCC >50,000/mm3. Causative agent S aureus. Pt is an IV drug abuser
Septic Arthritis Prosthetic joint infection Hematogenous osteomyelitis Brodie's abscess Vertebral osteomyelitis Cellulitis Spinal cord neoplasm Gout Acute osteomyelitis Chronic osteomyelitis
Septic arthritis
Young pt presents with sudden fever, bone pain, swelling, restricted movement in elbow joint three weeks after injury
Septic Arthritis Prosthetic joint infection Hematogenous osteomyelitis Brodie's abscess Vertebral osteomyelitis Cellulitis Spinal cord neoplasm Gout Acute osteomyelitis Chronic osteomyelitis
Acute osteomyelitis
Pt presents 1/12 after bilateral arthroplasty. Claims joints “haven’t felt right:. Fever, leaking wounds, pain. S aureus isolated
Septic Arthritis Prosthetic joint infection Hematogenous osteomyelitis Brodie's abscess Vertebral osteomyelitis Cellulitis Spinal cord neoplasm Gout Acute osteomyelitis Chronic osteomyelitis
Prosthetic joint infection
Suddent onset excruciating pain in left MTP joint, Swelling and high inflamm.
Septic Arthritis Prosthetic joint infection Hematogenous osteomyelitis Brodie's abscess Vertebral osteomyelitis Cellulitis Spinal cord neoplasm Gout Acute osteomyelitis Chronic osteomyelitis
Gout
48 yr old woman, BMI 28, presents with 3/52 history of painful L knee and lethargy. O/E, joint is edematous and hot. She is pyrexial, has reduced range of movement.
Further questioning-has had intra-articular steroid injections for her RA a month previously.
Septic arthritis
Investigations- septic arthritis of joint
Blood culture and synovial fluid aspirate
69 year old man recovering in ward following sx for L2/3 disc herniation and spinal canal compression. Op went well, but pt now has a temperature and complaining of bad back and a pain in his leg. What diagnostic test is most sensitive in helping your dx?
Blood culture and synovial fluid aspirate CT MRI Open biopsy Plain XR
MRI
Whta causative organism do you suspect in previous pt (L2/3 herniation man)
S. aureus
81 year old woman with type I DM presents in A&E 4/52 post-bilateral hip replacement sx. She is in pain, not mobilizing, complaining that hips never felt right after sx.
WCC 20x10^9/L
CRP 156
Pelvic XR shows areas of lysis around acetabular component of both joints and joint aspirate reveals 6700 WC/mL.
What do you suspect?
Prosthetic joint infection
Most common causative organism in septic arthritis
S. Aureus
