Path Flashcards

Question 1

Q

A gram negative intracellular diplococcus that causes meningitis

Answer

A

Neisseria or Neisseria Meningitidis

Question 2

Q

A gram positive diplococcus that causes pneumonia

Answer

A

Pneumococcus or streptococcus pneumoniae

Question 3

Q

A gram positive organism that grows in bunches and causes abscesses

Answer

A

Staphylococcus Aureus

Staphylococcus comes from the greek, and means ‘grape-cluster berry’

Question 4

Q

The organism that causes tetanus

Answer

A

Clostridium tetanae

Clostridium species tend to be soil dwelling and form spores. This includes the causative organisms of Botulinum toxin, Gas gangrene and tetanus.

Question 5

Q

A gram negative rod that commonly causes urinary tract infections

Answer

A

E-coli

The most common enteric bacterium that causes pathology.

Question 6

Q

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

Answer

A

galactocoele

this is caused by a proteinaceous blockage of the lactiferous duct and the accumulation of milk, producing a cyst.

The milk within the cyst is sterile and there is no point of ingress for bacteria so they don’t become infected. It will resolve when lactation ceases. A simple needle drainage won’t resolve the cyst as the plug remains and milk will continue to be produced.

If management is needed then the cyst should be surgically excised.

Question 7

Q

Infection of the breast that occurs during lactation

duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating
adenoma

Answer

A

mastitis

the suffix ‘-itis’ tells you that of the options this is the only infective/inflammatory process.

The symptoms include a red, swollen area of the breast that is often tender. There can also be nipple discharge, sometimes streaked with blood, a firm tender lump, or a burning pain in the breast.

Question 8

Q

Occurs in males with liver disease

duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating
adenoma

Answer

A

gynaecomastia

Due to build up of oestrogen seen in liver disease, results in development of breasts.

Question 9

Q

Occurs in the presence of a high prolactin

duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating
adenoma

Answer

A

galactorrhoea

Galactorrhoea is the abnormal prodction of milk, as opossed to lactation which is physiological.

It is often seen with pituitary tumours such as prolactinomas.

Question 10

Q

The commonest benign tumour of the female breast

duct ectasia
mammary duct ectasia
fibroadenoma
mastitis
fibrocystic change
galactocoele
galactorrhoea
gynaecomastia
intraductal papilloma
lactating
adenoma

Answer

A

fibroadenoma

A fibroadenoma is a benign lump of the female breast, it is colloquially known as a ‘breast mouse’. They are well defined and very mobile within the tissue, this distinguishes them from malignant lumps. They tend to be solitary and found in women of childbearing age.

Question 11

Q

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

Answer

A

Intestinal fistula

There is an increased loss of bicarbonate if there is an intestianal fistula

Question 12

Q

Causes increased H+ production

Diabetic ketoacidosis
Intestinal fistula
Metabolic acidosis
Metabolic alkalosis
Poor lung perfusion
Pyloric stenosis
Renal failure
Respiratory acidosis
Respiratory alkalosis

Answer

A

Diabetic ketoacidosis

In diabetic ketoacidosis there is an ionic shift due to the accumulation of ketones in the body. this leads to a shift of potassium into the intracellular compartment. THis in turn increases the H+ production to mantain the ionic gap.

Question 13

Q

Causes increased H+ loss

Diabetic ketoacidosis
Intestinal fistula
Metabolic acidosis
Metabolic alkalosis
Poor lung perfusion
Pyloric stenosis
Renal failure
Respiratory acidosis
Respiratory alkalosis

Answer

A

Pyloric stenosis

In pyloric stenosis there is a delay in emptying the stomach contents and there is an increase in vomiting, this is the source of lost H+ ions.

Question 14

Q

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

Answer

A

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.

Question 15

Q

Can be compensated by hypoventilation

Diabetic ketoacidosis
Intestinal fistula
Metabolic acidosis
Metabolic alkalosis
Poor lung perfusion
Pyloric stenosis
Renal failure
Respiratory acidosis
Respiratory alkalosis

Answer

A

Metabolic alkalosis

Also although hypoventilation would compensate for a metabolic alkalosis, that effect is minimised in humans by hypoxia.

Question 16

Q

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

Answer

A

a. Metabolic Alkalosis

This is by definiton a metabolic acidosis.

Question 17

Q

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

Answer

A

a. Respiratory Alkalosis

In true EMQ style this young woman is having a panic attack due to the broken ankle and is hyperventilating. This is resulting in the off-gassing of her CO2 resulting in a respritory alkolosis.

Question 18

Q

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

Answer

A

a. Metabolic Alkalosis

The patient has an alkalotic pH with a high bicarbonate. She has a degree of hypercapnia, but not enough to compensate.

In this case we see that this patient is having symptoms of metabolic alkolosis, with the parastesia and poor balance. It is likely that in EMQ land this fashion model has been frequently vomitinf.

Question 19

Q

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

Answer

A

a. Metabolic Acidosis with Respiratory Compensation

This case demonstrates only a partial compensation, she is still acidotic at pH7.30

Question 20

Q

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

Answer

A

a. Metabolic acidosis with respiratory compensation

He’s been huffing so much glue he’s put himself in metabolic acidosis. This is due to the metabolism of the volitaile compounds leading to increased secretion of sodium and potassium in the urine.

His Kussmaul breathing is a physiologic response to blow off more CO2, but it hasn’t come close to correcting this acidosis.

Question 21

Q

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

A

Answer: 1. COPD 2. Pneumonia 3. Pulmonary embolism 4. Tension pneumothorax 5. Hyperventilation

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.

Question 22

Q

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

Answer

A

a. Metabolic Alkalosis

He’s been eating antacid tablets like sweeties

We see an alkalotic pH combined with a normal CO2, combined with the history, and we know it’s metabolic with no compensation.

Question 23

Q

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

Answer

A

a. Type II Respiratory Failure

The pH here is normal but there is a low O2 and high CO2, which is a type II respiratory failure, by definition.

Question 24

Q

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

Answer

A

a. Metabolic Acidosis

Sodium Bicarbonate is going to make the blood more alkali, as such it could only plausibly be a treatment for acidosis, respiratory acidosi is caused by hypoventialtion, the treatment for which is ventilation support.

Metabolic acidosis is caused by increased H+ ions or increased loss of bicarbonate ions, so it stands to reason that it is treated with IV bicarbonate.

Question 25

Q

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

Answer

A

a. Compensated Metabolic Acidosis

We know that a Salicylate poisining causes a metabolic acidosis, but in this case the blood gas shows a normal pH and a low CO2, we also have the observation that she is breathing heavily. This is therefore a compensated metabolic acidosis.

Question 26

Q

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

Answer

A

a. Respiratory Acidosis

We see here an acidic pH with a high CO2.

Guillain-Barre can affect the muscles of respiration, as we see here. This has resulted in hypoventilation and an accumulation of CO2.

Question 27

Q

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

Answer

A

a. Benzylpenicillin

What is being described here is the classic chancre ulcer that is the harbinger of primary syphilis infection. The microscopy describes the causative organism of Treponema pallidum.

Syphilis is simply treated with a single dose of IM Benzylpenicillin

Question 28

Q

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

Answer

A

a. Vancomycin

Vancomycin is recommended for use on gram-positve bacteria where resistance to penicillins is known or suspected.

Question 29

Q

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

Answer

A

a. Orally

C.difficile is an infection of the digestive system so the most effective method of administration is into the digestive system. IV administration would be more effective if this were an organism presenting as a bacteraemia.

Question 30

Q

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

Answer

A

a. Chloramphenicol

Grey baby syndrome occurs due to insufficient enzyme activity and kidney excretion of the drug in neonates. This allows Chloamphenicol to build up to toxic levels, resulting in the life threatening Grey baby syndrome.

Question 31

Q

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

Answer

A

a. Rifampicin

Question 32

Q

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

Answer

A

a. Primary hyperaldosteronism

Here we have a patient with hypernatremia and hypokalemia, these two abnormalities point towards hyperaldosteronism. The only other syndrome in the list of options is Cushing’s, which would result in hyperglycaemia but with no other electrolyte disturbances.

It is importatnt ot remember that aldosterone is produced in response to the renin-angiotensin system. If there was a tumour secreting renin, or there was excess renin secretion due to renal artery stenosis, then this would be secondary hyperaldosteronism. In this case we are told that the renin levels are appropriately low, so there must be a tumour secreting aldosterone, this is therefore primary hyperaldosteronism.

Question 33

Q

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

Answer

A

a. Secondary adrenal insufficiency

Here we have a hyponatremia and a hyperkalemia, which is suggestive of glucocorticoid deficiency. The fact that she has undergone a short synACTHen test just confirms that. The test shows that the adrenals are able to pump out cortisol to a normal level (morning cortisol should be 138–635nmol/l).

Therefore the problem is not the adrenal cortex, it must be an issue woth ACTH production at the pituitary, this is therefore a secondarly adrenal insufficiency.

Question 34

Q

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

Answer

A

a. Adrenal tumour causing Cushing’s syndrome

Here we have a patient with excess cortisl, following administeration of an exogenous corticosteroid the levels of ACTH are found to be negligible, but in spite of this there is still a high level of cortisol. This tells you that there is a pathological source of cortisol that is outside the phisiological axis. This is an adrenal tumour secreting cortisol.

Question 35

Q

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

Answer

A

a. Ectopic ACTH causing Cushing’s syndrome

Here we have a patient with an excess of cortisol, in this case the supression test does not reduce the levels of ACTH. This tells you that there is a pathological source of ACTH that is flogging the adrenals. Hence, this is an ectopic ACTH source causing the Cushing’s syndrome.

Question 36

Q

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

Answer

A

a. Adrenal medulla

Here we have a patient with entirely normal blood results who is experiencing hypertensive episodes. This is your hint that it is that typical Imperial pathology condition; a phaeochromocytoma. As such is has to be in the adrenal medulla, the site of adrenaline synthesis.

Question 37

Q

What is the first line of treatment in phaeochromocytomas?

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
*

Answer

A

a. Alpha blockade

You need to block the effects of the adrenaline secreting tumour before attempting to remove it. it is likely that the disturbance of the tumour during surgery will cause a huge surge of adrenaline. In terms of alpha and beta blockade, both are needed, but alpha is needed first.

I always remember this as alpha being before beta in the greek alphabet!

Anyway, if the alpha blockade isn’t done first then there is a serious risk that the patient will have an uncontrollable hypertensive episode during surgery. And that, is a bad idea…

Question 38

Q

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.

What is the diagnosis?

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

Answer

A

a. Conn’s syndrome

This is a primary hyperaldosteronism, it is being driven by an aldosterone secreting tumour, and so is known as Conn’s syndrome.

If this was being driven by excessive renin it would be a secondary hyperaldosteronism.

Question 39

Q

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.

Conn’s syndrome
Phaeochromocytoma
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

Answer

A

a. Phaeochromocytoma

The episodic nature of these ‘panic attacks’ combined with the hypertension and high levels of catecholamines tells you that htis is a tumour secreting catecholamines. It is thus, a Phaeo.

Question 40

Q

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 ?

Conn’s syndrome
Phaeochromocytoma
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

Answer

A

a. 24 hour ambulatory blood pressure

There doesn’t appear to be an endocrine cause for this gentleman’s hypertension. The glucose is right on the uper range for a random, it might indicate a glucose tolerance issue, but that doesn’t explain the hypertension. As such he really needs further measuring of his BP with ambulatory monitoring.

Question 41

Q

Which part of the adrenal cortex produces glucocorticoids in response to the Adrenocorticotrophic hormone ? (ACTH)

Conn’s syndrome
Phaeochromocytoma
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

Answer

A

a. Zona fasciculata

The adrenal cortex is made up of 3 layers, which moving from superficial to deep are as follows:

Zona Glomerulosa - produces mineralcorticoids (aldosterone)

Zona Fasiculata - produces glucocorticoids (Steroids)

Zona Reticularis - produces androgens (testosterone precursors)

Question 42

Q

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

Answer

A

a. Type I hypersensitivity

Here you need to recognise that this is an anaphylatic reaction to the wasp sting. This is a hypersensitivity caused by an IgE response leading to a massive mast cell degranulation. This is a type I hypersensitivity.

Question 43

Q

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

Answer

A

Hayfever

This is pretty basic, this is a reaction to pollen leading to the typical presentation of hayfever we see here.

Question 44

Q

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

Answer

A

a. C1 inhibitor deficiency

This deficiency is involved in hereditary angioedema, which results in unchecked activation of the complement system in response to minimul trauma. It causes the facial swelling and reccuring abdominal pain we see here.

Question 45

Q

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

Answer

A

a. Dermatitis herpetiformis

Irish girl with weight loss, diarrhoea and abdominal pain basically screams coeliac disease. The blistering rash on the elbows and knees is a complication of coeliac and is termed Dermatitis herpetiformis. The causal mechanism is unknown.

Question 46

Q

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

Answer

A

a. Contact dermatitis

The rash apears on the hands after gardening makes it likely that he is being exposed to a chemical or perhaps he is wearing gloves containing latex. Contact dermatitis seems likely here. It is a delayed T-cell mediated reaction.

Question 47

Q

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?

Adrenalineb-Defensin
Complement C3
Contrast medium
Corticosteroids
Diluent
Filaggrin
Histamine
IgA
IgE
IgG
Mast cell (serum) tryptase
Noradrenaline
Peanuts
Penicillin

Answer

A

a. IgE

As tempting as it is to simply answer ‘peanuts’ here, this is a case of an urticarial reaction to peanuts. This is a type I hypersensitivity reaction and so is mediated by IgE.

Question 48

Q

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?

Adrenalineb-Defensin
Complement C3
Contrast medium
Corticosteroids
Diluent
Filaggrin
Histamine
IgA
IgE
IgG
Mast cell (serum) tryptase
Noradrenaline
Peanuts
Penicillin

Answer

A

a. Histamine

Your positive control needs to produce a reaction in the skin, as such the only compound you know will produce an urticarial reaction is histamine.

Question 49

Q

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?

Adrenalineb-Defensin
Complement C3
Contrast medium
Corticosteroids
Diluent
Filaggrin
Histamine
IgA
IgE
IgG
Mast cell (serum) tryptase
Noradrenaline
Peanuts
Penicillin

Answer

A

a. Mast cell (serum) tryptase

Tryptase is the most abundant chemical in mast cells, it can be used as a marker for assaying the level of mast cell activation .

Question 50

Q

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?

Adrenalineb-Defensin
Complement C3
Contrast medium
Corticosteroids
Diluent
Filaggrin
Histamine
IgA
IgE
IgG
Mast cell (serum) tryptase
Noradrenaline
Peanuts
Penicillin

Answer

A

a. Filaggrin

Filaggrin is a component of the lipid membrane that is part of the stratum corneum. Mutations in the gene coding for this protein lead to a loss of integrity of the skin’s barrier function. This in turn leads to the drying of the skin seen in eczema.

Question 51

Q

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?

Adrenalineb-Defensin
Complement C3
Contrast medium
Corticosteroids
Diluent
Filaggrin
Histamine
IgA
IgE
IgG
Mast cell (serum) tryptase
Noradrenaline
Peanuts
Penicillin

Answer

A

a. Contrast medium

I love the line about the several hour long coffee break. This patient has kidney stones so has been sent for contrast imaging to see the number and site of the stones.

Knowing this it seems obvious that he is having an adverse reaction to the contrast.

Question 52

Q

First line treatment for mild to moderate C. Difficile

Amoxicillin
Ceftriaxone
Chloramphenicol
Ethambutol
Erythromycin
Flucloxacillin
Gentamicin
Isoniazid
Metranidazole
Pyrazinamide
Rifampicin
Vancomycin

Answer

A

a. Metronidazole

Just need to memorise this

Question 53

Q

Treatment of infections resistant to penicillin e.g. MRSA

Amoxicillin
Ceftriaxone
Chloramphenicol
Ethambutol
Erythromycin
Flucloxacillin
Gentamicin
Isoniazid
Metranidazole
Pyrazinamide
Rifampicin
Vancomycin

Answer

A

a. Vancomycin

Vancomycin is the standard treatment for resistant gram-positives

Question 54

Q

May cause deafness an unwanted side effect

Amoxicillin
Ceftriaxone
Chloramphenicol
Ethambutol
Erythromycin
Flucloxacillin
Gentamicin
Isoniazid
Metranidazole
Pyrazinamide
Rifampicin
Vancomycin

Answer

A

a. Gentamicin

Causes ototoxicity and nephrotoxicity (all of the aminoglycosides do), the sensory-neuro deafness is permanent.

Confusingly Erythromycin causes a temporary deafness also.

Question 55

Q

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

Answer

A

a. Chloramphenicol

you just have to learn this as the second line treatment for meningitis.

Can’t give it to baby’s though, they go grey and get very sick (grey baby syndrome).

Question 56

Q

Treatment of TB but may cause optic neuritis.

Amoxicillin
Ceftriaxone
Chloramphenicol
Ethambutol
Erythromycin
Flucloxacillin
Gentamicin
Isoniazid
Metranidazole
Pyrazinamide
Rifampicin
Vancomycin

Answer

A

Ethambutol

The first line treatment for TB uses four drugs, I remember them by the mnemonic RIPE: Rifampicin, Isoniazid, Pyrazinamide, Ethambutol

Of these four Ethanbutol is asociated with optic neuritis.

Rifampicin - Hepatotoxicity

Isoniazid - Hepatotoxicity and peripheral neuropathy

Pyrazinamide - Hepatotoxicity and hyperuricaemia

Question 57

Q

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

Answer

A

a. Tetracyclines

They cause bone and teeth problems in the developing fetus. I always remember by tetra sounds a little like terato as in teratogenic…

Question 58

Q

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

Answer

A

Cefuroxime

Cephalosporins are a class of beta lactam antibiotic. the second generation includes Cefuroxime

Question 59

Q

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
*

Answer

A

Macrolides

one to remember

Question 60

Q

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
*

Answer

A

Tazocin

this is a combination of Piperacillin (a penicillin) and Tazobactam (a beta lactamase inhibitor). It is given IV and is used for ITU cases as it is broad spectrum and has good activity against Psudomonas, which is a real sucker for colonising lines.

Question 61

Q

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
*

Answer

A

a. 3 days

nice and quick

Question 62

Q

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

Answer

A

a. Oral Acyclovir

This child is afflicted by the herpes simplex virus, he isn;t massively unwell so IV isn’t needed. Oral acyclovir is the drug of choice here.

Question 63

Q

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

Answer

A

a. IV Gancyclovir

This infant is showing signs of congenital cytomegalovirus, this can cause a variety of complications including;

low birth weight, microcephaly, seizures, petechial rash moderate hepatosplenomegaly (with jaundice).

There can also be complications within the first few years of life that may include hearing loss, vision impairment, and varying degrees of mental retardation.

The treatment here is Gancyclovir

Question 64

Q

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

Answer

A

a. Antiretroviral Therapy

This child is unfortunately displaying signs of HIV seroconversion, this normally occurs in the first weeks or months after exposure to the HIV virus before going into a latent stage, so I’m not entirely sue why this is happening in a 2 year old.

Regardless, he needs antiretrovirals. The evidence now is that if the antiretrovirals are started early there is no reduction in life expectancy due to HIV.

Answer 65

A

a. Symptomatic treatment and reassurance

This seems to be Chicken pox, there is no need to treat. The risk here is that if the infected child has been around pregnant women (who have never had the virus) thier unborn children are at risk from congenital VZV infection.

But there is nothing here to take us down that line of thought.

Answer 66

A

Oseltamivir

This is a case of influenza, Oseltamivir (brand name Tamiflu) is a neurominidase inhibitor and so prevents reproduction of the influenza virus. It is given to this patient because of thier young age they are a high risk group for influenza and there is a need to treat.

Answer 67

A

Right Posterior Inferior Cerebellar Artery (PICA) Occlusion

PICA occlusion is also known as lateral medullary syndrome.

This is an infarction of the medulla, part of the brainstem, it causes the typical features we see here; Contralateral sensory deficits of the trunk and extremities combined with ipsilateral sensory deficits affecting the face and cranial nerves.

Diagnostically with this syndrome we see loss of nociception and temprature sensation on the contralateral side of the body but ipsilateral side of the face.

There is also ataxia if the cerebellum is affected, and a Horner’s syndrome if the hypothalamospinal fibers are damaged, as this disrupts sympathetic relay.

Answer 68

A

Watershed infarction

Watershed infarcts are cortical infarcts caused by prolonged periods of low perfusion, common in patients with a history of cardiovascular disease.

This pattern of loss affecting the visual cortex and only the proximal limbs is not consistent with a stroke, the history of cardiovascular risks gives you the clue here.

Answer 69

A

Left Middle Cerebral Occlusion

Here we have a right sided loss so the infarct must be in the left hemisphere. The aphasia is due to damage to Broca’s (non-fluent aphasia) or Wernicke’s (fluent aphasia) area, this confirms this as being a middle cerebral occlusion. of the different territories to be affected, the middle cerebral artery is the most common area.

This is a very helpful website for stroke syndromes;

http://www.neuroanatomy.ca/stroke_model/mca_info.html

Answer 70

A

Right Posterior Cerebral Occlusion

The damage to the occipital lobe in this case is causing the left homonymous hemianopsia. This infarct has involved the deeper branch of the posterior artery also, this has damaged the internal capsule and thalamus leading to disruptin of sensory fibres running in this tract, leading to the sensory loss seen here.

good website for explaining stroke syndromes;

http://www.neuroanatomy.ca/stroke_model/pca_info.html

Answer 71

A

Chronic subdural haemorrhage

Chronic sub-durals are iso-dense or hypo-dense on CT, compared to acute sub-durals which are hyper-dense.

the reasoning behind this is that a fresh bleed is, obviously, fresh blood. This contains iron within the haemoglobin and so attenuates the radiation being hyper-dense. As time passes the haemoglobin is broken down and the osmotic draw of the haematoma makes the space closer in density to the brain parenchyma, and eventually similar to water.

Answer 72

A

5000

This question seems a bit pointless

Answer 73

A

70

CLL is a disease that primarily affects the elderly

Answer 74

A

Allogenic stem cell transplantation

CML treatment if with biologics (such as imatinib) as a first line, here we see our patient as become resistant to those. In that case we need to look at giving this patient the potentially curative option of an allogenic stem cell transplant, the patient is young and there is no reason to think he is anything other than healthy aprart from the CML.

Answer 75

A

Donor lymphocyte infusion

Answer 76

A

Allogenic stem cell transplantation

Answer 77

A

Imatinib

Imatinib is the first line treatment for CML, which this is as there is a Philadelphia chromosome.

Answer 78

A

Dosatinib

Dosatinib is the second line biologic treatment for CML after Imatinib

Answer 79

A

Imatinib

The translocation here, t(9,22) is the philadelphia chromosome, a translocation closely linked to CML. The first line treatment for CML is imatinib, which gives a normal life expectency in treatment receptive cases, even without the use of chemo or radiotherapy.

Answer 80

A

Dosatinib

Dosatinib is the second line treatment for CML after Imatinib.

Answer 81

A

Allogeneic stem cell transplantation

Here we have a CML patient who has become very symptomatic, treatment at this stage should be with a SCT as opossed to a biologic.

Answer 82

A

Donor lymphocyte infusion

Answer 83

A

Allogeneic stem cell transplantation

Imatinib and dosatinib are the tyrosine kinase inhibitors in question here. The next step is to go for an allogenic SCT.

Answer 84

A

B Cold Autoimmune HA

The direct coombs test tells us that this is an autoimmune haemolytic anaemia, The prescence of IgM confirms this as the Cold subtype.

Conversely the warm typre is mediated by IgG, or rarely IgA.

Answer 85

A

N Sickle Cell disease

this is a case of classic EMQ patterns, the african boy with painful hands is hinting at sickle cell diseae, the disease can be excacerbated by the cold, as we see here. The presentation of dactylitis and a chest crisis is typical of an attack.

Answer 86

A

F Hereditary spherocytosis

Hereditory spherocytosis causes the symptoms we see here, jaundice as an infant, spenomegaly (due to increased RBC turn over), ulcers (due to occlusions) and anaemia. The family history also helps to establish that this is hereditary.

The blood results are also showing us speherocytes, these are spherical red blood cells and not a biconcave disc. This explains why they lack the central pallor (they are thickest in the middle, completely opposite to normal RBCs). they are generally hyperchromic because they are thicker so less light penetrates under microscopy.

Answer 87

A

D G6PD deficiency

G6PD deficiency is an x-linked recessive condition that causes haemolysis when the affected person is exposed to certain drugs (such as antimalarials), foods (fava beans) or diseases (hepatitis viruses).

It is particularly common in mediterranean and african populations.

Heinz bodies are inclusions of denatured haemoglobin within red blood cells, the haemoglobin is denatured due to oxidative stress.

Bite cells are red blood cells with a missing section of cell mambrane, this is removed in the spleen due to oxidative damage of the membrane.

Both of these blood film findings are charachteristic of G6PD deficiency.

Answer 88

A

I Malaria

Rigors are caused by malaria (or a profound bacterimia), as a general rule.

Generally this history is very sugesstive of malaria.

Answer 89

A

B Drug induced/Iatrogenic

There’s not a lot to go on here, the woman is showing signs of haemolysis, it is autoimmune and she is on medication. So drug induced fits.

Answer 90

A

M Warm Type AIHA

Answer 91

A

H Microangiopathic haemolytic anaemia (MAHA)

We have a picture of a woman with a pelvic/abdominal mass, given the amenorrhea this is likely a pregnancy…

Factor in the hypertension and haemolysis and it looks like HELLP syndrome, which includes a microangiopathic haemolytic anaemia.

Answer 92

A

E Hereditary spherocytosis

Howell-jolly bodies - inclusions of nuclear remnants in red blood cells

Poikilocytosis - any abnormal red cell morphology

Both of these are suggestive of sphereocytosis, the osmotic fragility test is diagnostic for hereditary sphereocytosis.

Answer 93

A

C Glucose-6-phosphate deficiency

He’s from the right geographical area, and hes just started on a vegatarian diet, presumably heavy on the fava beans.

Answer 94

A

Lymphocyte adhesion deficiency

this is a primary immunodeficiency where the lymphocytes do not correctly adhere to the endothelial wall and then migrate to the site of infection.

This leads to the frequent infections seen, but the lack of lymphocyte migration means that there is no formation of pus, hence the lack of abscess formation.

Answer 95

A

Chronic granulomatous disease

in this (usually) X-linked condition there is a congenital defect with phagocytes, this means that they lack a type of NADPH used to create reactive oxygen species, this reduces the ability to engage in oxidative killing.

The dihydrorhodamine test is used to asses the level of reactive oxygen coumpounds, it is abnormal because there is a deficiency.

Answer 96

A

Kostmann syndrome

This syndrome is a severe congenital neutropenia, it responds well to treatment with granulocyte colony-stimulating factor.

Answer 97

A

IFN gamma receptor deficiency

interferon gamma is an important cytokine in the activation of macrophages and plays a key role in dealing with viruses and mycobacteria. The loss of the receptor makes these patients more prone to mycobacterial infection.

It also helps to know that we can test for TB infection with the interferon gamma release assay.

Answer 98

A

• X-linked SCID

Here we have a case of an immunodeficiency affecting both the T cells and the B cells, there is also the loss of two classes of antibody. This is by definition a severe combined immuno deficiency.

Answer 99

A

• IFN gamma receptor deficiency

interferon gamma is responsible for activating macrophages to target viruses and bacteria (particularly mycobacteria). This infection with an atypical mycobacterium screams IFN gamma receptor deficiency.

Answer 100

A

• DiGeorge’s syndrome

The abnormal facial features combined with cardiac and aortic abnormalities are strongly sugestive of DiGeorges syndrome.

it is charecterised by reduced T-cellnumbers due to thymic aplasia

Answer 101

A

• Bare lymphocyte syndrome type II

In this condition there is a loss of the MHC class II. Without that there can be no antigen presentation to helper T-cells so they are absent. There is also no class switching of antibodies to produce IgG.

Answer 102

A

• Common variable immunodeficiency

Common variable immunodeficiency is charecterised by hypogammaglobulinemia, this lack of antibodies is why they are particularly prone to bacterial infections.

Bronchiectasis often develps due to reccurent respiratory infections, especially when left underttreated.

This condition also has links to a host of autoimmune conditions, such as hypothroidism, SLE, psoriasis, vitiligo, rheumatoid arthritis and autoimmune haemolytic anemia.

Answer 103

A

• X linked hyper IgM syndrome due to CD40ligand mutation

The clue here is that this is a hyper IgM condition, the description of the case specifically says high IgM

Answer 104

A

• Bruton’s X linked hypogammaglobulinaemia

Bruton’s is a severe congenital agloblinaemia, we see it here presenting in an infant with reccurent respiratory infections.

Answer 105

A

• IgA deficiency

Kind of self-explanatory

Answer 106

A

• C3 deficiency with presence of a nephritic factor

Nephritc factor gives it away here

Answer 107

A

• C9 deficiency

Loss of the late stage complement stages (C5-9) leaves the person very vulnerable to meningococcal infections.

The loss of C1, C2, and C4 is associated with autoimmune disease.

Answer 108

A

• C1q deficiency

The loss of C1, C2, and C4 is associated with autoimmune disease, such as SLE.

Loss of the late stage complement stages (C5-9) leaves the person very vulnerable to meningococcal infections.

Answer 109

A

• MBL deficiency

Deficiencies in the components of the mannose binding lectin pathway are relatively common (around 10% of the population, more in certain ethnicities). most people are asymptomatic, but with immune supression they can be subject to reccurent infections.

Answer 110

A

• 4. T reg cell

Answer 111

A

• 5. Dendritic cell

Answer 112

A

Neutrophil

Answer 113

A

• 9. Plasma cell

Answer 114

A

• 1. Th17 cell

TH17 cells secrete IL17, the clue is in the number!

Answer 115

A

• 2. Macrophage

Answer 116

A

• 6. CD4+ T cell

Answer 117

A

• 10. CD8 T cells

Answer 118

A

• 3. CCR5

The viral membrane protein GP120 on HIV binds to CCR5 and uses it as a co-receptor.

the 32 amino acid deletion in this protein confers a degree of HIV resistance.

Answer 119

A

• 4. Reverse transcriptase

Producing DNA from RNA goes against the traditional unidirectional transcription, it is made possible by the viral enzyme reverse transcriptase.

Answer 120

A

• 8. CCR7

Answer 121

A

• 9. Macrophages

CD4, along with CCR5 are the cell receptors that guide HIV’s site of infection

Answer 122

A

• 1. Gp120

GP120 is the cell membrane binding protein that binds to CCR5 on immune cells.

Answer 123

A

• 7. Protease inhibitors

Protease is an enzyme that cleaves the origional long amino acid chain into the small number of functional proteins in a mature HIV viron.

Answer 124

A

Familial Mediterranean Fever

The gene, MEFV, is an abbreviation of MeditErranean FeVer. Job done

Answer 125

A

Crohn’s disease

NOD and CARD15 = Crohn’s

Answer 126

A

Ankylosing Spondylitis

Just need to remember that AnkSpond is a HLA associated condition.

Answer 127

A

Rheumatoid arthritis

The immune system often attacks Citrullunated proteins, the role of PAD in autoimmune disease has been seen in rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus and Sjögren’s syndrome.

It has been found that citrullinated proteins occur after smoking.

Answer 128

A

IPEX (immune dysregulation polyendocrinopathy, enteropathy, X linked syndrome)

Foxp3 is a key transcription factor for the regulation of regulatory T-cells. In IPEX this mutation leads to dysfunction of the regulatory T-cells and auto-immunity.

Answer 129

A

Anti-Ro antibody

Anti-Ro and Anti-La are both linked with congenital heart block.

Anti double stranded DNA is diagnostic of SLE, but it is not the cuasative antibody for the congenital heart block.

Answer 130

A

Anti-DNA antibody

Answer 131

A

Anti-RNP antibody

Answer 132

A

Anti-centromere antibody

Answer 133

A

Anti-Ro antibody

Although anti-Ro is seen in SLE also, it is much more common in Sjogren’s.

Answer 134

A

Pernicious anaemia

Gastric parietal cells produce intrinsic factor, which binds B12. If they are destroyed in anauto-immune manner then this leads to pernicious anaemia.

Answer 135

A

Autoimmune hepatitis

both Anti-nuclear and Anti-smoth muscle are classically found

Answer 136

A

Coeliac disease/Dermatitis herpetiformis

Anti endomysial and Anti-transglutaminase antibodies are the tests of choice for Coeliac and it’s assiciated condition, Dermatitis herpetiformis.

Answer 137

A

Coeliac disease/Dermatitis herpetiformis

Anti endomysial and Anti-transglutaminase antibodies are the tests of choice for Coeliac and it’s assiciated condition, Dermatitis herpetiformis.

Answer 138

A

Primary biliary cirrhosis

During this disease there is an autoimmune destruction of the small bile ducts, ducts composed of smooth muscle.

Answer 139

A

Acute vascular rejection

This is clearly an acute reaction so that leaves us two options here.

Of the two, cellular rejection involves the cellular immune system (T-cells) and vascular involves the humoral immune system (antibodies).

Answer 140

A

Chronic allograft rejection

for both the rapid immune system and the slower process of fibrosis to be involved it has to be a chronic rejection.

Answer 141

A

Hyperacute rejection

If there are already pre-formed antibodies then the reaction is going to be very rapid, this has to be a hyper-acute reaction.

Answer 142

A

Acute cellular rejection

This is clearly an acute reaction so that leaves us two options here.

Of the two, cellular rejection involves the cellular immune system (T-cells) and vascular involves the humoral immune system (antibodies).

Answer 143

A

Anaphylaxis

This woman is having a reaction to the lignocaine injection, it is affecting her skin and respiratory system so is anaphylaxis. She is also showing signs of systemic shock, this is an emergency.

Answer 144

A

Physical urticaria

This is the medical term for the wheals described here. It is caused by histamine realease in responce to allergens or physical factors, such as heat, and exercise.

Answer 145

A

C1 inhibitor deficiency

This is an inherited condition where there is angiodema in responce to a minor trauma or enviromental factor.

Answer 146

A

Allergic rhinitis

This is hayfever (allergic rhinitis) it is pretty distinctive.

Answer 147

A

Type IV hypersensitivity to latex

Type IV is contact dermatitis, they even point out it’s to latex. This doctor must have really gotten stuck in as a medical student if they are only just discovering it.

Answer 148

A

anti-mitochondrial antibody

Primary biliary cirrhosis is a condition mainly affecting middle-aged women, and those with other autoimmune diseases. The puritis and LFTs suport this diagnosis. Anti-mitochondrial antibody is the test of choice.

Answer 149

A

anti-neutrophil cytoplasmic antibody

The symptoms theis gentleman is displaying are classic for Granulomatosis with polyangiitis (formerly known as Wegener’s granulomatosis).

cANCA is the test of choice here

Answer 150

A

antibody to double stranded DNA

This is SLE, the test of choice here is anti-dsDNA

Answer 151

A

anti-TTG antibody

Coeliac disease, anti-endomysial or anti-TTG are the tests used for diagniosis.

Answer 152

A

anti-centromere antibody

This is limited cutaneous scleroderma (previously CREST syndrome), he is demonstrating the classic signs of Reynauds, sclerodactyly and Telangiectasia.

The test for this condition is ant-centromere antibody.

Answer 153

A

anti-intrinsic factor antibody

You’ve got me here, this sounds like Coeliac which should be anti-TTG. I have no idea why this is pernicious anaemia.

Answer 154

A

Pathogen recognition

It’s basically given in the question

Answer 155

A

Opsonisation

The process of proteins such as C3b attaching to microbial walls allows phagocytotic cells to attach and engulf the pathogenic organisms.

Answer 156

A

Oxidative killing

its given to you in the question!

Answer 157

A

Non-oxidative killing

enzymatic methods of patogen killing are obviously of the non-oxidative variety.

Answer 158

A

Macrophages

Answer 159

A

Neutrophils

Answer 160

A

Natural Killer Cells

Answer 161

A

Dendritic cells

Answer 162

A

CD8 T cells

CD8 T-cells are heavily involved in triggering apoptosis of cells infected with intracellular pathogens. The MHC class I is expressed on all cells and presents intracellular peptides for recognition by CD8 T-cells. Those cells that have been hijacked and are producing pathogenic proteins are recognised and given apoptotic signals.

Answer 163

A

T regulatory cells

Fop3 is a master regulator for T-cells and is therefore found on T-regulatory cells.

Answer 164

A

Th1 cells

T-helper cells are CD4 positive, that is why HIV (which targets CD4 cells) is so devastating to the immne system

Answer 165

A

T follicular helper (Tfh) cells

The follicular cells reside in the lymphoid tissue and are crucial to the selection and survival of B cells that are producing high-affinity antibodies to encountered pathogens. Follicular cells start life as T-helper cells and then migrate to the lymphoid tissue after exposure to an antigen.

Answer 166

A

Pre-B cells

The starting point of plasma cells

Answer 167

A

IgG secreting plasma cells

IgG is the high affinity antibody that is produced after helper T-cells encounter a specific pathogen, and then migrate to the lymphoid tissue where they become follicular helper T-cells. Once in the lymphoid tissue these T-cells promote B-cells into class switching to produce high-affinity antibodies.

Answer 168

A

IgM secreting plasma cells

IgM is the low affinity antibody and is produced without specific encounters with the antigen and follicular T-cell class switiching of B-cells.

Answer 169

A

IgA

IgA is a dimer, think two y-shaped antibodies end to end. It is the only antibody that can cross the mucus membranes. Loss of function or abcense of this antibody leads to reccurent respiratory or GI infections.

Answer 170

A

Germinal centre

Here T-helper cells that have been exposed to an antigen and have become follicular helper T-cells reside. They facilitate the affinity maturation and class switching of B-cells to produce the high affinity IgG. It’s a bit like a boot camp.

Answer 171

A

Primary lymphoid organs

self explanatory really.

Answer 172

A

Thoracic duct

Answer 173

A

Thymus

The thymus is the site of T-cell development and the elimination of self-targeting T-cells. The agenesis of the Thymus in DiGeorges syndrome is why there are extremely low levels of T-cells in that condition.

Answer 174

A

C1

There are three complement pathways,

The ‘classical’ pathway starts with C1 and antigen-antibody complexes on bacterial surfaces.
The ‘Alternative’ pathway starts with C3 binding to bacteria
The mannose binding - Lectin pathway starts with MBL (mannose binding lectin) attaching to bacterial sugars such as manose.

All of these pathways then arrive at the point were C3 is cleaved into C3a and C3b

Answer 175

A

C3

There are three complement pathways,

The ‘classical’ pathway starts with C1 and antigen-antibody complexes on bacterial surfaces.
The ‘Alternative’ pathway starts with C3 binding to bacteria
The mannose binding - Lectin pathway starts with MBL (mannose binding lectin) attaching to bacterial sugars such as manose.

All of these pathways then arrive at the point were C3 is cleaved into C3a and C3b

Answer 176

A

MBL

There are three complement pathways,

The ‘classical’ pathway starts with C1 and antigen-antibody complexes on bacterial surfaces.
The ‘Alternative’ pathway starts with C3 binding to bacteria
The mannose binding - Lectin pathway starts with MBL (mannose binding lectin) attaching to bacterial sugars such as manose.

All of these pathways then arrive at the point were C3 is cleaved into C3a and C3b

Answer 177

A

C9

C5 to C9 are all involved in forming the membrane attack complex

Answer 178

A

Neutrophil

Answer 179

A

Macrophage

Answer 180

A

Denosumab

Answer 181

A

Reversibly inhibits guanine synthesis (de novo pathway of purine synthesis)Used to prevent transplant rejection, esp renalCan also be a steroid sparing agent in authoimmune diseases

Answer 182

A

Abatacept

Answer 183

A

Cyclophosphamide

Answer 184

A

Infliximab

Answer 185

A

Hydroxychloroquine

Answer 186

A

Methotrexate

Answer 187

A

Cyclophoshamide

Answer 188

A

Leflunomide

Answer 189

A

Infliximab

Answer 190

A

Phildelphia chromosome.Seen in 95% CML, 25-30% ALL

Answer 191

A

CLL

smudge cells are remnants of leukocytes with no identifiable structres. they look like pink/purple smudges funnily enough

Answer 192

A

Hairy cell leukemia

The irregularly shaped cells with the filliments are the hairy cells mentioned.

Answer 193

A

Familial dysbetalipoproteinemia (type III)

Answer 194

A

Phytosterolemia

Answer 195

A

Familial hypercholesterolemia (type I)

Answer 196

A

Hypobetalipoproteinemia

Answer 197

A

Atherosclerosis

Answer 198

A

Ascending cholangitis

Answer 199

A

Gilberts.

This is a condition chaerecterised by isolated elevated levels of unconjugated billirubin. It is episodic and worse in time sof infection.

Answer 200

A

Hemolytic jaundice

Answer 201

A

Vertebral osteomyelitis

this is an infection of the bone within the vertebral body. The history suports this

Answer 202

A

Septic arthritis

S.aureus is commonly introduced to the blood stream i in IV drug users, where it cause several pathologies. It is also the most likely organism for infective endocarditis in IV drug users.

Answer 203

A

Acute osteomyelitis

Answer 204

A

Prosthetic joint infection

This one is clear enough

Answer 205

A

Gout

Classic site for teh first presentation of gout is the first meta-tarsal phalangeal joint, the big toe.

Answer 206

A

Septic arthritis

Answer 207

A

Blood culture and synovial fluid aspirate

Answer 208

A

MRI

The neurological syptoms here dictate that your first step is a spinal MRI.

Answer 209

A

S. aureus

Commonest post operative infective agent.

Answer 210

A

Prosthetic joint infection

Answer 211

A

S. Aureus

Answer 212

A

H. influenza

Answer 213

A

N. gonorrhoeae

Answer 214

A

Mycobacterium tuberculosis

Answer 215

A

Coag negative staph (e.g.staph epidermidis)

Answer 216

A

S. aureus

Answer 217

A

Lyme disease

This bulls-eye rash is erythema migrans, which just screems Lyme disease (Borrelia burgdorferi), a tick bourne bacteria.

Answer 218

A

Brucellosis

Unpasturised milk or contact with cattle in asia/middle east/ africa, think Brucellosis (named after an army doctor, Maj.Gen Sir David Bruce, no less).

Answer 219

A

Q fever

another zoonosis, nothing massively specific about it’s presentation in the initial period. It can have GI and upper respiratory tract symptoms.

It can progress to an atypical pneumonia, and rarely after many months, years or even decades of chronic infection it can cause a endocarditis that is usually fatal if untreated.

Answer 220

A

Psittacosis

Bird keeper is either going to have Psittacosis or cryptococcus, the Leventhal-Cole-Lillie bodies are key to identifying this as psittacosis.

Answer 221

A

Leptospirosis

sewage or mucky river water = leptospirosis (weil’s disease)

Answer 222

A

Cryptococcus

the india ink stain is the giveaway here

Answer 223

A

Hyatid disease

this si a cystic disease caused by the parasitic tapeworm Echinococcus, humans are not the definitive hosts for this pathogen so it forms cysts within the muscle, organs and brain. Really nasty stuff, check ut videos of the cysts being removed, they can be the size of melons.

There is a serious risk of a massive IgE reaction if these cysts rupture

Answer 224

A

Brucellosis

The rose Bengal stain is the key element here.

Unpasturised milk or contact with cattle in asia/middle east/ africa, think Brucellosis (named after an army doctor, Maj.Gen Sir David Bruce, no less).

This guy has been in contact with cattle in eastern eurpe, Brucellosis is less common there but still possible.

Answer 225

A

Lassa fever

This is damn rare, the only chance you have is if you know what ribavarin is used to treat. It is used as an oral preparation for Hep C, the use here as an IV infusion means it is for a viral haemorraghic fever.

I’m not really sure how you could narrow it down from there!

Answer 226

A

Ehrlichiosis

Another obscure one! Erlichosis is a bacterial infection carried by ticks, it classically destroys white blood cells and supresses TNF-alpha. It also causes the liver damage we see here.

Answer 227

A

Rabies

You dont get many clues here!

Answer 228

A

Borreliosis

This is lyme disease, it presents with the classic bulls-eye rash of erythema migrans.

Answer 229

A

Cutaneous larva migrans

This is a cutaneous infection casued by the larvae o parastic nematode worms shed in animal faeces.

Answer 230

A

Brucellosis

Unpasturised milk or contact with cattle in asia/middle east/ africa, think Brucellosis (named after an army doctor, Maj.Gen Sir David Bruce, no less).

Answer 231

A

Yersinia pestis

The black death ladies and gentlemen, likey to be a common presenting complaint during your foundation years.

Answer 232

A

West Nile virus

This question is a bit bogus as there is no mention of travel, and the WN virus doesn’t exist in n.europe.

Answer 233

A

Bubonic plague

the gram-negative coccobacillus here is yersinia pestis

The massive tender inguinal lymph node following tick bites is rather diagnostic of this condition.

Answer 234

A

Dengue fever

Answer 235

A

P. malariae

the rigors and the classic 72 hour fever are the massive clues here.

The stop over in nigeria is her opportuunity for exposure, although in reality you don’t expect malaria transmission in urban areas, so unless her stopover included a trip to a rural area it’s an unlikely scenario.

Answer 236

A

Correct F.

NevirapineResponse Feedback: In 1999, the HIVNET 012 team reported exciting preliminary results that single-dose nevirapine prophylaxis for mother and baby significantly lowered HIV-1 infection risk at 14–16 weeks compared with controls who received short-course zidovudine prophylaxis.

Answer 237

A

Correct K. Interferon-α (alpha)

Answer 238

A

Correct H. Oseltamivir

Answer 239

A

Correct J. Aciclovir triphosphate

Answer 240

A

Correct B. Ribavirin

Answer 241

A

Correct C. Aciclovir monophosphateResponse Feedback: Aciclovir diphosphate and triphosphate are the product of cellular tyrosine kinase, whereas aciclovir monophosphate is the product of viral tyrosine kinase.

Answer 242

A

Correct K. Aciclovir triphosphateResponse Feedback: Aciclovir diphosphate and triphosphate are the product of cellular tyrosine kinase, whereas aciclovir monophosphate is the product of viral tyrosine kinase.

Answer 243

A

Correct A. Cytomegalovirus

Answer 244

A

Correct B. Guanosine

Answer 245

A

Correct J. Varicella-zoster virus

Answer 246

A

Correct F. Interferon

Answer 247

A

Correct K. Foscarnet

Answer 248

A

Correct G. Gancyclovir

Answer 249

A

Correct C. Amantadine

Answer 250

A

Correct M. Aciclovir

Answer 251

A

Correct L. Zidovudine

Answer 252

A

Correct B. Indinavir

Answer 253

A

Correct J. Aciclovir

Answer 254

A

Correct I. Zanamivir

Answer 255

A

Correct M. Human specific immunoglobulin

Answer 256

A

Correct C. S. pneumoniae

Answer 257

A

Correct D. L. pneumophila

Answer 258

A

Correct E. M. pneumoniae

Answer 259

A

Correct J. M. tuberculosis

Answer 260

A

Correct B. C. psittaci

Answer 261

A

Correct E. M. pneumoniae

Answer 262

A

Correct C. MSSA

Answer 263

A

Correct L. MSSA or MRSAResponse Feedback: Q2: influenza is a classic precedent of S. aureus pneumonia. This is because there is transient postviral hypofunction of airway clearance mechanisms e.g. cilia.

Answer 264

A

Correct H. Burkholderia cepacia

Answer 265

A

Correct G. S. pneumoniae

Answer 266

A

Correct D. Chlamydia psittaci

Answer 267

A

Correct B. AnaphylaxisResponse Feedback: With regards to the first question, whilst the anaphylaxis is most likely due to a drug allergy, it is important to note that this is an anaphylactic reaction. The answer ‘drug allergy’ does not emphasise the type of reaction occuring. Note that ambiguous questions will NOT appear on your exam - these questions have been written by students. For a discussion about anaphylaxis vs anaphylactoid reactions see attached file.

Answer 268

A

Correct D. Food allergy

Answer 269

A

Correct J. Allergic Rhinitis

Answer 270

A

Correct E. Chronic Urticaria

Answer 271

A

Correct A. Contact dermatitis

Answer 272

A

Correct H. Mast cell degranulationMast cell degranulation is not IgE mediated.

Answer 273

A

Correct F. C1 inhibitor deficiency

Answer 274

A

Correct J. Coeliac diseaseCoeliac disease is associated with a superficial, blistering skin rash ‘dermatitis herpetiformis’, which is intensely itchy!

Answer 275

A

Correct E. Acute urticaria

Answer 276

A

Correct B. Urticarial vasculitis

Answer 277

A

Correct D. AnaphylaxisThe combination of hypotension, respiratory distress, urticaria and bronchoconstriction is very suggestive of anaphylaxis

Answer 278

A

Correct A. Acute urticariaThis rash is very suggestive of acute urticaria. The temporal association with scuba diving may indicate an allergy to latex (in wet suits).

Answer 279

A

Correct F. Contact hypersensitivityThis rash is typical of contact hypersensitivity. The distribution of the rash suggests that the specific agent is nickel, which used to be a component of the studs of jeans and is commonly found in the metal used in belts.

Answer 280

A

Correct I. Allergic rhinitisThe combination of sneezing, rhinorrhea and loss of smell is very suggestive of allergic rhinitis

Answer 281

A

Correct C. Acute angioedemaThis woman has angioedema of the tongue, without symptoms suggestive of a generalised allergic reaction. Isolated angioedema may be allergic in origin, but 94% of cases angioedema presenting to A&E are drug induced and the majority of these are associated with ACE inhibitors (eg captopril).

Answer 282

A

Correct A. IM adrenaline 1mL of 1:1000The most important treatment of anaphylaxis is adrenaline, which should be given intramuscularly. (Note for final year pharm: 1:1000 means 1mg/mL; 1:10000 means 0.1mg/mL ; 1% means 1g/dL)

Answer 283

A

Correct G. PO antihistaminesSevere acute urticaria is effectively treated with a short course of oral anti-histamines

Answer 284

A

Correct F. None of the aboveContact hypersensitivity should be treated by avoidance of the sensitising agent, in this case nickel

Answer 285

A

Correct G. PO antihistaminesOral antihistamines and intranasal corticosteroids are the mainstay of treatment of mild allergic rhinitis. (As intranasal corticosteroid is not an option available, the “single best” answer here is oral antihistamines.)

Answer 286

A

Correct D. IM adrenaline 0.5 mL of 1:1000Intramuscular adrenalin should be used in patients with severe local angioedema with secondary acute respiratory tract obstruction. However this is not always effective in ACE inhibitor-induced angioedema, and some patients will require intubation. Always stop the causative agent!

Answer 287

A

Correct J. Interferons

Answer 288

A

Correct E. IgA

Answer 289

A

Correct M. Major histocompatability complex class 2

Answer 290

A

Correct K. IL6

Answer 291

A

Correct I. Natural Killer cells

Answer 292

A

Correct M. Major histocompatability complex class 2T helper cells are CD4+ and bind MHC class II ; cytotoxic T cells are CD8+ and bind MHC class I.

Answer 293

A

Correct G. Major histocompatability complex class 1T helper cells are CD4+ and bind MHC class II ; cytotoxic T cells are CD8+ and bind MHC class I.

Answer 294

A

Correct H. IgM

Answer 295

A

Correct L. IgG

Answer 296

A

Correct D. Classical complement pathway

Answer 297

A

Correct E. Neutrophil

Answer 298

A

Correct E. Neutrophil

Answer 299

A

Correct K. Bacterial

Answer 300

A

Correct C. Complemental

Answer 301

A

Correct C. Complement

Answer 302

A

Correct H. IgA

Answer 303

A

Correct C. Neutrophils

Answer 304

A

Correct L. NADPH oxidoase

Answer 305

A

Correct F. C3a

Answer 306

A

Correct M. CH50

Answer 307

A

Correct A. Type II – Antibody mediated

Answer 308

A

Correct H. Type III – Immune complex mediated

Answer 309

A

Correct D. Type IV – T-cell mediated

Answer 310

A

Correct E. Not an autoimmune disease

Answer 311

A

Correct D. Type IV – T-cell mediated

Answer 312

A

Correct A. Type II – Antibody mediated

Answer 313

A

Correct A. Type II – Antibody mediated

Answer 314

A

Correct H. Type III – Immune complex mediated

Answer 315

A

Correct A. Type II – Antibody mediated

Answer 316

A

Correct A. Type II – Antibody mediated

Answer 317

A

Correct G. Anti-DNA antibodyThe rationale for the answer for SLE being anti-DNA antibody rather than ANA is that whilst ANA is very sensitive for SLE, it is not specific. Anti-DNA, in contrast, is highly specific to SLE (~95%).

Answer 318

A

Correct B. c-ANCARemember that c-ANCA matches with Wegener’s Granulomatosis, whilst p-ANCA would match with polyarteritis nodosa

Answer 319

A

Correct F. Anti-CCP antibodyRheumatoid factor is not specific or sensitive to rheumatoid arthritis and is common in the elderly. Anti-CCP is a more specific test for rheumatoid arthritis and a better predictor of an aggressive course.

Answer 320

A

Correct H. Coomb’s test

Answer 321

A

Correct E. Anti-mitochondrial antibody

Answer 322

A

Correct L. Type IV collagenpoorly written question…

Answer 323

A

Correct B. Smooth linear pattern

Answer 324

A

Correct D. Prednisolonebad question

Answer 325

A

Correct I. Lung

Answer 326

A

Duct ectasia

Answer 327

A

Phyllodes tumour

Answer 328

A

Ductal carcinoma in situ

Answer 329

A

Fibrocystic disease (now called fibrocystic breast changes…)

Answer 330

A

Acute mastitis

Answer 331

A

Fibroadenoma

Answer 332

A

Duct ectasia

Answer 333

A

Invasive ductal carcinoma

Answer 334

A

Acute pyogenic mastitis

Answer 335

A

Fat necrosis

Answer 336

A

Sclerosing adenosis

Answer 337

A

Lobular carcinoma in situ

Answer 338

A

Fibroadenoma

Answer 339

A

Breast abscess

Answer 340

A

Duct ectasia

Answer 341

A

Duct papilloma

Answer 342

A

Fibroadenoma

Answer 343

A

Fibrocystic changes

Answer 344

A

EACBD from immediate to late.E – Serious/life threatening arrhythmias (such as ventricular fibrillation) are mostly likely to happen within the first hour after a MI. This is often a cause of sudden deathA – Pericarditis – Transmural MIs can cause fibrinohemorrhagic pericarditis (due to myocardial inflammation) and usually appears 2-3 days after an infarction.C – Myocardial rupture are caused by the lysis of myocardial connective tissue which reaches maximum stage during day 3-7. This causes the infarcted muscles to become soft, friable granulation tissue.B – Dressler syndrome specifically refers to pericarditis that occurs from week 2 to months afterwards which is believed to be caused by autoimmune inflammation of the infarct.D – Ventricular aneurysm is a late complication after a MI (months) caused by the thin wall of the scar tissue of the MI

Answer 345

A

Correct D. 90

Answer 346

A

Correct G. 4

Answer 347

A

Correct B. 290

Answer 348

A

Correct G. 4

Answer 349

A

Correct B. 290

Answer 350

A

Correct D. Wilson’s disease

Answer 351

A

Correct B. Chronic hepatitis B

Answer 352

A

Correct E. Primary biliary cirrhosis

Answer 353

A

Correct G. Hepatitis A

Answer 354

A

Correct C. Budd-Chiari syndrome

Answer 355

A

Correct H. Aspartate transaminase

Answer 356

A

Correct C. Prothrombin timeThe intrinsic pathway is initiated by the activation of the ‘contact factor’ of plasma and can be measured by the APTT test. The extrinsic pathway is initiated by the release of tissue factor and can be measured by the PT test.

Answer 357

A

Correct D. Alkaline phosphatase

Answer 358

A

Correct F. Gamma glutamyl transpeptidase

Answer 359

A

Correct E. Albumin

Answer 360

A

Correct F. Anti-endomysial antibodies(1) Coeliac disease: Anti-endomysial antibodies/ Tissue-transglutaminase antibodies

Answer 361

A

Correct K. Anti-gastric parietal cell antibodies(2) Pernicious anaemia: Anti-intrinsic factor antibodies, and gastric parietal antibodies.

Answer 362

A

Correct G. c-ANCA(3) Wegener’s : Antibody to Proteinase-3 : 3 is the 3rd letter of the alphabet; c-ANCA.

Answer 363

A

Correct M. Osmotic fragility test Spherocytosis: Osmotic fragility test.

Answer 364

A

Correct B. Anti-mitochondrial antibody(5) PBC - AMA E2 subtype of pyruvate dehydrogenase complex

Answer 365

A

Correct I. Anti-GAD(7) Type 1 diabetes: Anti-Glutamic acid decarboxylase antibodies (Anti-GAD).

Answer 366

A

Correct L. Ham’s test(6) Paroxysmal nocturnal haemoglobinuria (PNH): Ham’s test.

Answer 367

A

Correct G. Primary hyperparathyroidism

Answer 368

A

Correct A. Sarcoidosis

Answer 369

A

Correct L. Diabetes mellitus type 1

Answer 370

A

Correct I. Psychogenic polydipsia

Answer 371

A

Correct J. Impaired glucose tolerance

Answer 372

A

Correct D. AlbuminPlasma renin activity also varies with posture - it rises in the upright position. Some people have so-called benign postural and/or exercise-induced albuminuria.

Answer 373

A

Correct G. Creatinine Kinase

Answer 374

A

Correct F. ALP

Answer 375

A

Correct G. Creatinine KinaseThere are 3 main iso-forms of CK.CK-MM: present in muscles.CK-BB: Present in Brain.CK-MB: Present in cardiac muscle.

Answer 376

A

Correct H. Cortisol

Answer 377

A

Correct G. Theophylline

Answer 378

A

Correct B. Poor compliance

Answer 379

A

Correct A. Oxidation by cytochrome P450

Answer 380

A

Correct D. Kidneys

Answer 381

A

Correct J. Rosiglitazone

Answer 382

A

Correct K. DigoxinPossible features of DIGOXIN TOXICITY include:• arrhythmia: the most common arrhythmias are ventricular extrasystoles, ventricular bigeminy / trigeminy and atrial tachycardia with complete heart block• anorexia, nausea and vomiting and occasionally, diarrhoea• confusion especially in the elderly• yellow vision (xanthopsia), blurred vision and photophobia

Answer 383

A

Correct B. Gentamicin

Answer 384

A

Correct N. Digoxin

Answer 385

A

Correct H. Lithium

Answer 386

A

Correct B. Gentamicin

Answer 387

A

Correct I. Heparin - unfractionated

Answer 388

A

Correct I. Cocaine‘In the lectures slides it mentiones EBE and BE as breakdown products of cocaine: what are these?’EME = ecgonine methyl esterBE = benzoylecgonineThey are the two degredation products of cocaine produced by pseudocholinesterases and hydrolysis respectively.

Answer 389

A

Correct O. Ecstasy

Answer 390

A

Correct A. Cyanide

Answer 391

A

Correct F. Paracetamol

Answer 392

A

Correct P. Heroin

Answer 393

A

Correct F. Activated charcoalRemember activated charcoal is NOT helpful in poisoning with: cyanide, iron, ethanol, lithium, acid or alkali, pesticides.

Answer 394

A

Correct I. Haemodialysis

Answer 395

A

Correct D. Glucagon

Answer 396

A

Correct C. Hyperbaric oxygen

Answer 397

A

Correct J. Symptomatic and Supportive treatment

Answer 398

A

Correct I. EcstasyBoth TCA od’s and ecstasy od’s can cause wide dilated pupils.Ecstasy is more likely to lead to agitation and TCA drowsiness.ps…the other question in the stem , points very clearly to TCA overdose (reflexes and widened QRS complexes). Also….remember that ecstasy may induce vasopressin secretion and an SIADH, with hyponatraemia

Answer 399

A

Correct C. Salicylates

Answer 400

A

Correct D. Carbon Monoxide

Answer 401

A

Correct H. Tricyclic antidepressantsBoth TCA od’s and ecstasy od’s can cause wide dilated pupils.Ecstasy is more likely to lead to agitation and TCA drowsiness.ps…the other question in the stem , points very clearly to TCA overdose (reflexes and widened QRS complexes). Also….remember that ecstasy may induce vasopressin secretion and an SIADH, with hyponatraemia

Answer 402

A

Correct F. Organophosphates

Answer 403

A

Correct I. Immunoassay

Answer 404

A

Correct C. Blood sample

Answer 405

A

Correct D. Paracetamol

Answer 406

A

Correct H. Liquid chromotography

Answer 407

A

Correct K. Thin layer chromotography

Answer 408

A

Correct D. Hair

Answer 409

A

Correct B. Morphine

Answer 410

A

Correct E. Toxicology

Answer 411

A

Correct I. Saliva

Answer 412

A

Correct A. THC

Answer 413

A

Correct H. Endothelial cell

Answer 414

A

Correct I. Fibrin

Answer 415

A

Correct M. Tissue plasminogen-activator (t-PA)

Answer 416

A

Correct D. a2 macroglobulin

Answer 417

A

Correct G. Antithrombin III

Answer 418

A

Correct G. Thromboxane A2

Answer 419

A

Correct A. Ehlers-Danlos syndrome

Answer 420

A

Correct K. Vitamin K deficiency

Answer 421

A

Correct F. von Willebrand deficiency

Answer 422

A

Correct M. Autoimmune thrombocytopenic purpura

Answer 423

A

Correct H. Protein S

Answer 424

A

Correct H. Protein S

Answer 425

A

Correct I. Vascular endothelium

Answer 426

A

Correct D. Cyclooxygenase

Answer 427

A

Correct J. Thrombin

Answer 428

A

Correct E. Osler-Weber-Rendu SyndromeA rare autosomal dominant disorder. Alternative name = hereditary haemorrhagic telangiectasia. There is a structural abnormality of the blood vessels, resulting in telangiectases, which are thin walled so are likely to bleed. This leads to haemorrhage and anaemia. It is more common in females, and may not present until later in life. Epistaxis is the commonest presenting symptom. This patient is feeling tired, not just because of her 4 children, but because she also has iron deficiency anaemia.

Answer 429

A

Correct M. Henoch – Schönlein PurpuraAffects children between 2-8yrs old. More common in winter. Usually presents following an upper respiratory tract infection. Rapid onset, with a palpable purpuric rash over the buttocks and legs, as well as symmetrical urticarial plaques, and haemorrhagic bullae. Arthritis of the knee and ankle. Abdominal pain – perhaps due to mesenteric vasculitis. Can have renal involvement – with haematuria/proteinuria. (not idiopathic thrombocytopenic purpura – because it’s not an option here)

Answer 430

A

Correct G. Vitamin K DeficiencyPrevalence of coeliac disease is highest in Saharawi refugees. This patient has coeliac disease, and as a result of malabsorption is losing weight and has loose stools (steatorrhoea), and vitamin K deficiency. The blood results related to vitamin K deficiency.

Answer 431

A

Correct J. Von Willebrand’s DiseaseThe most common hereditary bleeding disorder, affect 1% of the population. vWF is a carrier protein for factor VIII and stabilises it. Mutation is in chromosome 12

Answer 432

A

Correct G. Vitamin K DeficiencyDrugs, such as anticonvulsants, which the mother is likely to be taking as she suffers from epilepsy, as well as isoniazid, rifampicin and anticoagulants, are risk factors for haemorrhagic disease of the newborn – which is what this baby has. This is due to vitamin K deficiency – although rare now in the UK as prophylactic vitamin K is given to newborns.

Answer 433

A

Correct A. Superficial venous thrombosisThrombophlebitis refers to the inflammation of a vein which is thrombosed - you get all the normal signs of inflammation. It can be migratory - migratory thrombophelbitis. Superfical venous thrombosis is what it says on the tin - thrombosis of a superficial vein. This may be associated with thrombophlebitis - ie there is associated inflammation.

Answer 434

A

Correct C. Superior vena caval obstruction

Answer 435

A

Correct J. Postphlebitic syndrome

Answer 436

A

Correct B. Pulmonary embolism

Answer 437

A

Correct F. Deep vein thrombosis

Answer 438

A

Correct L. Unfractionated heparin (UFH)

Answer 439

A

Correct D. Dalteparin (LMWH)

Answer 440

A

Correct K. Prothrombin time (PT)

Answer 441

A

Correct J. APTT

Answer 442

A

Correct A. Warfarin

Answer 443

A

Correct B. Thrombin time (TT)

Answer 444

A

Correct N. Aspirin

Answer 445

A

Correct E. Dipyridamole modified release (MR) and aspirin

Answer 446

A

Correct O. Clopidogrel

Answer 447

A

Correct H. Clopidogrel and aspirin

Answer 448

A

Correct M. 10mg, 10mg, 5mg, measure on 4th day then every 2 days

Answer 449

A

Correct G. 5mg, 5mg, 5mg, 5mg, measure on 5th day, 8th day and then every 4 days

Answer 450

A

Correct A. Warfarin

Answer 451

A

Correct D. Dalteparin (LMWH)

Answer 452

A

Correct A. Warfarin

Answer 453

A

Correct A. Warfarin

Answer 454

A

Correct L. Unfractionated heparin (UFH)

Answer 455

A

Correct D. Dalteparin (LMWH)

Answer 456

A

Correct P. Streptokinase

Answer 457

A

Correct I. Chronic Myelomonocytic AnaemiaWe agree that the case for CMML is nonspecific. The main positive feature is the monocyte count.

Answer 458

A

Correct K. Secondary Sideroblastic Anaemia

Answer 459

A

Correct F. Refractory Cytopaenia with Multilineage DysplasiaTo count as significant, dysplasia must involve at least 10% of cells in a lineage. To count as RCMD, at least 2 MYELOID lineages must be dysplastic, and there must be bi or pancytopenia in the peripheral blood. (This can include anaemia!)

Answer 460

A

Correct B. Refractory Anaemia with excess of Blasts II

Answer 461

A

Correct D. Acute Myeloid Leukaemia

Answer 462

A

Correct H. Acute myeloid leukaemia

Answer 463

A

Correct F. 5q syndrome

Answer 464

A

Correct E. Secondary aplastic anaemia

Answer 465

A

Correct I. Refractory anaemia with an excess of blasts

Answer 466

A

Correct B. Refractory cytopenia with multilineage dysplasia

Answer 467

A

Correct E. Pseudopolycythaemia

Answer 468

A

Correct N. Essential thrombocythaemia

Answer 469

A

Correct I. HaematocritBurning sensation of the hands and feet is denoted by the term ‘erythromelalgia’.

Answer 470

A

Correct H. Imitanib

Answer 471

A

Correct G. Tear drop poikilocytes

Answer 472

A

Correct I. Acute myeloid leukaemia

Answer 473

A

Correct B. Richter’s syndrome

Answer 474

A

Correct E. Tumour-lysis syndrome

Answer 475

A

Correct D. Chronic myeloid leukaemia

Answer 476

A

Correct N. Acute lymphoblastic leukaemia

Answer 477

A

Correct M. Acute lymphocytic leukaemia

Answer 478

A

Correct G. Blast cells

Answer 479

A

Correct L. Down’s syndrome

Answer 480

A

Correct H. Ionising radiation

Answer 481

A

Correct F. Chronic lymphocytic leukaemia

Answer 482

A

Correct D. NeutrophilsCML. Increased mass of turning-over cells generates urate. Q2. CML, blast phase. Transformation tends to be into AML but in 20% is lymphoblastic (ALL). Q3. CLL. Only two chronic B cell leukaemia/lymphomas are CD5+: CLL (CD5+ CD23+) and Mantle Cell Lymphoma (CD5+ CD23-). CLL may be assoc. with Coombs positive AIHA and ITP. The combination is called Evans syndrome. Q4. CML del(11q23): poor prognostic sign in CLL. Tip: Neutrophil alkaline phosphatase is LOW in CML and raised in myeloproliferative disorders and infections. Pelger Huet cells: bilobed neutrophils. Autosomal dominant or AML or MDS (myelodysplastic syndrome)

Answer 483

A

Correct A. Blast cells

Answer 484

A

Correct E. Clonal B lymphocytes

Answer 485

A

Correct G. Chromosome 9;22 translocation