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Final MB Part II - Short Answer Questions > 100 Cases Questions I > Flashcards

100 Cases Questions I Flashcards

1
Q

What is the most common type of lung cancer?

A

Adenocarcinoma

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2
Q

Which type of lung cancer is most heavily associated with a strong history of smoking?

A

Squamous cell carcinoma

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3
Q

How do the results of the LHRH test differ in the non-pubertal and pubertal state? (2)

A
  • FSH Predominance; if the FSH level rises more than LH following LHRH administration then the patient is unlikely to be undergoing puberty<br></br>- LH Predominance;if the LH level rises more than FSH following LHRH administration then the patient is likely to be undergoing puberty
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4
Q

Outline the triad of features associated with immune (idiopathic) thrombocytopaenic purpura (ITP)? (3)

A
  • Petechiae and/or bruising
  • Epistaxis
  • Thrombocytopaenia
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5
Q

Outline the main differentials for a patient presenting with polydipsia and polyuria? (4)

A
  • Diabetes mellitus
  • Diabetes insipidus
  • Primary polydipsia
  • Hypercalcaemia
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6
Q

Outline the key investigations required to differentiate the main causes of polydipsia and polyuria? (4)

A
  • Blood glucose monitoring; random glucose, fasting glucose, HbA1c<br></br>- Urinalysis; glucose, specific gravity, urine osmolality<br></br>- Fluid deprivation test; restrict fluid for 8 hours and measure urine osmolality, administer desmopressin<br></br>- Corrected serum Ca2+; to account for variation in serum albumin concentrations
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7
Q

What is the equation used to estimate serum osmolality?

A

Serum osmolality = 2 x [Na+] + [urea] + [glucose]

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8
Q

Why do we need to calculate the corrected serum calcium when investigating potential hypocalcaemia?

A
  • Most of the calcium in the body is bound to albumin
  • Therefore when albumin levels are low, the measured serum calcium will also appear low
  • Similarly in cases of hyperalbuminaemia the measured serum calcium may appear elevated
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9
Q

How can you differentiate glomerular and non-glomerular causes of microscopic (non-visible) haematuria?

A

Glomerular causes of microscopic (non-visible) haematuria will have a concomitant proteinuria whereas non-glomerular causes will not

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10
Q

Outline the main types of microscopic (non-visible) haematuria? (3)

A
  • Glomerular; associated with damage at the level of the nephron (glomerulus)
  • Post-glomerular; associated with damage to the urinary tract at the level of whole organ (kidney, ureter, bladder, urethra)
  • Other; excess anticoagulation, march haematuria (repetitive impacts on the body, particularly the feet, causing haemolysis)
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11
Q

Outline the gold-standard investigation for a patient presenting with painless haematuria?

A

Flexible cystoscopy

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12
Q

Outline the main red flag symptom associated with bladder cancer?

A

Painless haematuria

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13
Q

Outline the main types of hyponatraemia in terms of plasma osmolality and the underlying mechanism? (3)

A
  • Hypertonic hypernatraemia; solutes in the extracellular fluid draw water out from cells and thus dilute the sodium concentration
  • Isotonic hypernatraemia; due to retention of an isosmotic fluid in the extracellular fluid compartment
  • Hypotonic hyponatraemia; caused by solute loss, volume expansion or volume contraction
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14
Q

Outline thepathognomonic features associated with nephritic and nephrotic syndrome? (2)

A
  • Nephritic syndrome; haematuria, hypertension, uraemia and renal failure<br></br>- Nephrotic syndrome; proteinuria, hypoalbuminaemia, oedema and hyperlipidaemia
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15
Q

What is the most common cause of nephrotic syndrome in children?

A

Minimal change disease (MCD)

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16
Q

Outline the two main aetiologies of nephrotic syndrome? (2)

A
  • Primary glomerular disorders; minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous glomerulopathy (MN)<br></br>- Systemic diseases affecting the kidneys; systemic lupus erythematosus (SLE), diabetes mellitus (DM), amyloidosis, drugs
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17
Q

What key feature in the history of a child with nephrotic syndrome raises the suspicion of minimal change disease (MCD)?

A

A recent upper respiratory tract infection (URTI)

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18
Q

Outline the treatment of minimal change disease (MCD) in children?

A

Corticosteroids; most children make a full recovery with normal renal function

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19
Q

Outline the blood test results consistent with a haemolytic anaemia?

A

Normocytic anaemia with a raised LDH and raised bilirubin (haemoglobin breakdown product)

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20
Q

What is the most common complication of systemic lupus erythematosus (SLE)?

A

Lupus nephritis; a glomerulonephritis caused by a type III hypersensitivity reaction

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21
Q

What is the purpose of screening tests?

A

To identify individuals at increased risk of developing a disease so that they may undergo further testing to investigate the diagnosis

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22
Q

Outline the main criteria needed in order to develop a screening test for a disease? (2)

A
  • Condition must be an important but treatable health problem
  • Must be identifiable at a early stage
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23
Q

Outline the current reccommendations for prostate cancer screening in the UK?

A

There is no current prostate cancer screening programme in the UK

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24
Q

What is the most common cause of a fasting hypoglycaemia?

A

Insulinoma; a benign insulin-secreting tumour of the pancreatic β cells

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25
Q

Which key investigation is needed when considering a diagnosis of insulinoma?

A

Supervised Fast<br></br>- Plasma glucose concentrations<br></br>- Serum insulin measurements<br></br>- C-peptide levels

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26
Q

Outline Whipple’s triad for confirmed episodes of hypoglycaemia?

A
  • Hypoglycaemic symptoms associated with fasting or exercise<br></br>- Confirmed hypoglycaemia during symptomics attacks<br></br>- Reversal of symptoms with glucose administration
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27
Q

Outline the classification and causes of jaundice? (3)

A
  • Pre-hepatic; autoimmune haemolytic anaemia (AIHA), sickle cell disease (SCD), hereditary spherocytosis, iatrogenic (metallic heart valves)<br></br>- Hepatic;<br></br> • Congenital; Gilbert’s syndrome, Crigler-Najjar syndrome, Dubin-Johnson syndrome<br></br> • Acquired; autoimmune hepatitis, viral hepatitis, alcohol-related liver disease, primary biliary cirrhosis/cholangitis (PBC), drugs (halothane, paracetamol)<br></br>- Post-hepatic; biliary strictures, gallstones, malignancy (pancreatic, HCC, cholangiocarcinoma), primary sclerosis cholangitis (PSC), pancreatic pseudocytsts
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28
Q

What is the most common form of overdose in the UK?

A

Paracetamol overdose

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29
Q

What is the mechanism by which paracetamol overdose causes toxicity? (2)

A
  • Depletion of glutathione stores in attempt to detoxify NAPQI metabolite of paracetamol
  • Leads to increased levels of reactive oxygen species (ROS) which can damage the liver
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30
Q

Why do paracetamol levels need to be measured between 4-16 hours after taking an overdose? (2)

A
  • Before 4 hours the levels may be falsely reduced due to imcomplete absorption in that time<br></br>- After 16 hours the levels may be falsely elevated due to the resultant liver injury
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31
Q

Outline the treatment of paracetamol overdose depending on the time at presentation? (4)

A
  • Within 1 hour of overdose; give activated charcoal<br></br>- Between 4-6 hours; if plasma paracetamol levels above threshold, give 3 infusions of N-acetylcysteine (NAC) plus IV fluid replacement<br></br>- Unknown time of overdose; give 3 infusions of N-acetylcysteine (NAC) plus IV fluid replacement<br></br>- Staggered overdose (>1 hr duration); give 3 infusions of N-acetylcysteine (NAC) plus IV fluid replacement
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32
Q

Outline the main aetiologies of hypercalcaemia? (5)

A

MIDGE;

  • Malignancy-associated; squamous cell lung cancers (SCCs), osteolytic metastases
  • Iatrogenic; thiazide diuretics, lithium
  • Vitamin-D related; granulomatous disease, excess vitamin D intake
  • Genetic; familial hypocalciuric hypercalcaemia, Gitelman syndrome
  • Endocrine; primary, secondary or tertiary hyperparathyroidism and thyrotoxicosis
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33
Q

Outline the main classes of management in primary hyperparathyroidism? (3)

A
  • Conservative; fluid rehydration and observation<br></br>- Medical; bisphosphonates, cinacalcet (inhibits PTH release)<br></br>- Surgical; parathyroidectomy
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34
Q

Outline the criteria for parathyroidectomy in patients with primary hyperparathyroidism? (2)

A
  • Symptomatic patients<br></br>- Asymptomatic patients with ≥ 1 of the following;<br></br> • Young; age < 50 years<br></br> • Renal failure; eGFR < 60<br></br> • Reduced bone density; T score ≤ -2.5<br></br> • Serum calcium; ≥ 0.25 mM above normal range
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35
Q

Outline the Rotterdam criteria used in the diagnosis of polycystic ovarian syndrome (PCOS)? (3)

A

≥ 2 of the following;

  • Infrequent ovulation (oligomenorrhoea) OR no ovulation (amenorrhoea)
  • Clinical or biochemical signs of hyperandrogenism (e.g. hirsutism) OR elevated levels of total or free testosterone
  • Polycystic ovaries as seen on ultrasound OR an increased ovarian volume
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36
Q

Outline the pathophysiology behind a goitre?

A

Hyperstimulation of the thyroid follicular cells by thyroid stimulating hormone (TSH) which results in hypertrophy

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37
Q

Outline the potential causes of a raised TSH with normal fT4 levels? (2)

A
  • Subclinical or compensated hypothyroidism<br></br>- Treated hyperthyroidism
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38
Q

What important test should be carried out in all patients diagnosed with a subclinical hypothyroidism?

A

Measure serum antibodies for thyroid peroxidase (anti-TPO antibodies) as this is indicative of Hashimoto’s thyroiditis which will often progress to clinical hypothyroidism

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39
Q

Outline the argument for treating subclinical hypothyroidism?

A

Subclinical hypothyroidism can lead to impaired cardiovascular function and increased LDL levels which raises a patients cardiovascular risk

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40
Q

Outline the differentials diagnoses for a patient presenting with joint pain affecting multiple joints (polyarthropathy)? (6)

A

ROSC-DV;

  • Rheumatoid arthritis (RA)
  • Osteoarthritis (OA)
  • Seronegative arthropathies; reactive arthritis, ankylosing spondylitis, reactive arthritis, enteropathic arthritis
  • Crystal arthropathies; gout, pseudogout
  • Systemic diseases; systemic lupus erythematosus, systemic sclerosis, CREST
  • Viral arthropathies: HSP etc.
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41
Q

Which diagnostic test has the greatest sensitivity and specificity for rheumatoid arthritis (RA)?

A

Anti-CCP antibodies; sensitivity 65-85%, specificity >95%

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42
Q

What is the significance of a raised anion gap on a background of metabolic acidosis?

A

This implies the presence of increased levels of an unknown anionthat is likely to be contributing to the acidaemia

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43
Q

Outline the most common causes of a raised anion gap metabolic acidosis? (5)

A
  • Ketoacidosis; diabetic, alcoholic
  • Lactic acidosis; tissue hypoxia, drugs
  • Exogenous acids; salicylates
  • Uraemic acidosis; renal failure
  • Inherited organic acidoses; accumulation of organic acids
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44
Q

What is the most common cause of a bacterial meningitis in a homeless individual who drinks excess alcohol?

A

<i>Streptococcus pneumoniae</i>

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45
Q

Outline the most common conditions associated with primary immunodeficiency? (4)

A
  • Common variable immunodeficiency (CVID)
  • X-linked agammaglobulinaemia (XLA)
  • Subjective Ig subclass deficiency (SISD)
  • Hyper-IgM syndrome (HIMS)
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46
Q

What is the most common condition causing primary immunodeficiency?

A

Common variable immunodeficiency (CVID)

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47
Q

Outline the set of investigations used in suspected immunodeficiency? (4)

A
  • FBC; to check for a reduced white blood cell count<br></br>- Protein electrophoresis; complement or β2-microglobulin deficiency<br></br>- Serum immunoglobulins; to identify immunoglobulin deficiency<br></br>- HIV testing; to indentify a common secondary cause of immunodeficiency
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48
Q

Broadly speaking, outline the two possible causes of a metabolic acidosis with normal anion gap? (2)

A
  • Increased H+ retention/decreased H+ excretion<br></br>- Increased HCO3- loss/usage
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49
Q

What is the significance of a metabolic acidosis with normal anion gap?

A

It suggests a disturbance in the endogenous acid-base (H+/HCO3-) balance

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50
Q

Outline the most common causes of hyperchloraemic metabolic acidosis? (3)

A
  • Diarrhoea; leading to excess HCO3- loss from the GI tract
  • Renal tubular acidosis (RTA) type I; causes decreased H+ excretion in the urine
  • Fluid therapy; large volumes of normal 0.9% saline used in resuscitation and/or maintenance
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51
Q

Outline the main types of renal tubular acidosis (RTA)? (4)

A
  • RTA Type I; distal RTA caused by impaired H+ secretion associated with nephrolithiasis
  • RTA Type II; proximal RTA caused by a failure of HCO3- reasborption leading to HCO3-loss
  • RTA Type III; hyperkalaemic RTA where increased K+ secretion as a compensatory mechanism is linked with the increased H+reabsorption
  • RTA Type IV; the most common cause of renal tubular acidosis and is due to an aldosterone deficiency
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52
Q

Why is renal tubular acidosis (RTA) associated with nephrolithiasis?

A

Acidosis causes increased reabsorption of citrate in the proximal tubule which predisposes renal stone formation

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53
Q

Outline the major microvascular complications of T2DM? (3)

A
  • Nephropathy; microalbuminaemia due to vessel damage predisposes to CKD<br></br>- Neuropathy; sensory and autonomic neuropathy of particular significance in the development of diabetic foot ulcers<br></br>- Retinopathy; ischaemia triggers VEGF release and formation of new vessels that are weak and friable
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54
Q

Outline the major macrovascular complication of T2DM?

A

Atherosclerosis; which increases cardiovascular risk factors for ACS/CVA

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55
Q

Alongside tests to establish blood glucose levels, which bedside test can be used to aid in the investigation of a potential diagnosis of T2DM?

A

Urine dipstick; to look for glucose, ketones and/or protein in the urine

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56
Q

Outline the most reliable variable used to differentiate pre-renal, renal and post-renal causes of acute kidney injury (AKI)?

A

Urea:creatinine ratio (Ur:Cr)<br></br>- Pre-Renal; Ur:Cr > 100:1<br></br>- Renal; Ur:Cr < 40:1<br></br>- Post-Renal; Ur:Cr 40-100:1

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57
Q

Outline the definition of a laboratory diagnosis of tumour lysis syndrome (TLS)? (2)

A
  • ≥ 2 metabolic disturbances in <br></br> • Uric acid<br></br> • Potassium<br></br> • Phosphate <br></br> • Calcium<br></br>- Occuring from 3-days prior to 7-days after receiving anti-cancer therapy
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58
Q

Outline the definition of a clinical diagnosis of tumour lysis syndrome (TLS)? (4)

A
  • Confirmed laboratory diagnosis PLUS ≥ 1 of
    •Serum creatinine; > 1.5 upper limit normal
    • Cardiac arrhythmias/sudden death
    • Seizures
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59
Q

Outline the two potential categories of causes of ambiguous genitalia? (2)

A
  • Viralisation of XX; most commonly CAH due to mutation in 21-hydroxylase<br></br>- Underviralisation of XY; most commonly due to a 5α-reductase deficiency
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60
Q

Outline the key investigations that make up routine ante-natal care? (6)

A
  • 8-11+6 weeks; booking visit<br></br>- 12 weeks; dating scan<br></br>- 12-13+6 weeks; combined test (nuchal scan plus PAPP-A)<br></br>- 14 weeks; quadruple test if unable to have combined test (too late booking to be accurate)<br></br>- 18-20+6 weeks; anomaly scan, assess growth and amniotic fluid<br></br>- 28 weeks; routine care, first dose of anti-RhD if indicated
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61
Q

Why is vitamin K given given to neonates immediately after birth?

A
  • Vitamin K is needed by the VKORC1 enzyme as a cofactor for the synthesis of a number of clotting factors
  • However, vitamin K cannot cross the placenta during development and, before birth, the fetal gut microbiome lacks the bacteria that make vitamin K
  • This means that newborn babies are deficient in vitamin K which may lead to haemorrhagic disease of the newborn (HDN) due to decreased clotting factor synthesis
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62
Q

Outline the first-line tests that can be used to establish a diagnosis of Cushings syndrome? (4)

A
  • Low-dose dexamethasone suppression test<br></br>- 24-hour urinary cortisol collection<br></br>- Midnight serum cortisol levels<br></br>- Dexamethasone-CRH sucession test
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63
Q

Which test is used first line to establish the cause of a patient’s Cushing syndrome and how can it be interpreted?

A

Plasma ACTH Levels<br></br>- Low/undetectable levels; indicates an ACTH-independant cause and hence most likely due to excess production of cortisol by the adrenal glands<br></br>- Raised/normal levels; suggestive of an ACTH-dependant cause either coming from the pituitary or an ectopic source of ACTH

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64
Q

Outline the diagnostic test used in an ACTH-independant Cushing’s syndrome?

A

CT adrenal gland; possible MRI/PET-CT if CT alone inconclusive

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65
Q

Outline the third-line investigation used in patients with an ACTH-dependant Cushings syndrome and how this may be interpreted?

A

High Dose Dexamethasone Suppression Test<br></br>- ACTH suppressed; pituitary source indentified, most likely a pituitary adenoma (Cushings disease)<br></br>- ACTH unsuppressed; ectopic source more likely, most likely a SCLC

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66
Q

Outline the secondary causes of hypertension? (4)

A

ROPE

  • Renal disease; renal artery stenosis (RAS), renin-producing tumours, Liddle’s syndrome, pseudohypoaldosteronism
  • Obesity; obstructive sleep apnoea
  • Pregnancy; pre-eclampsia/gestational hypertension
  • Endocrine; phaeochromocytoma, Conn’s syndrome, Cushings syndrome, acromegaly
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67
Q

Outline the stages of investigation in Conn’s syndrome (primary hyperaldosteronism)? (3)

A
  • Screening testing; aldosterone-renin ratio (ARR); plasma aldosterone concentration (PAC)<br></br>- Confirmatory testing; oral sodium loading test, saline infusion test, captopril challenge test, fludrocortisone suppression test<br></br>- Causative testing; adrenal venous sampling, CT adrenal glands
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68
Q

What is the typical value of the aldosterone-renin ratio (ARR) in patients with primary hyperaldosteronism (Conn’s syndrome)?

A

Aldosterone-renin ratio (ARR) > 2000:1

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69
Q

What is the link between H+and K+ in terms of the way they are handled by the body?

A
  • Broadly speaking H+and K+travel in opposite directions across the cell<br></br>- Hence when correcting a metabolic alkalosis, H+is taken up and K+is lost which can result in hypokalaemia<br></br>- Similarly non-K+-sparring diuretics can cause metabolic acidosis as they promote K+excretion meaning that H+uptake is increased
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70
Q

Broadly speaking, what are the three main mechanisms by which hypokalaemia can develop? (3)

A
  • Reduced K+intake
  • Increased K+loss/excretion
  • Transcellular K+shift
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71
Q

Outline the most common causes of a transcellular K+ shifts resulting in hypokalaemia? (3)

A
  • Insulin; stimulates glucose uptake which increases [ATP] and hence the activity of the Na+/K+ATPase
  • β2AR agonists; stimulate adenylate cyclase which increases [cAMP] and in-turn the activity of the Na+/K+ATPase
  • Alkalosis; triggers compensatory mechanisms for H+reabsorption in the kidney which occurs at the expense of K+secretion and excretion
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72
Q

Outline the most common causes of extra-renal K+loss? (3)

A
  • Vomiting; results in H+loss and subsequent alkalosis which promotes H+reabsorption in the kidney in exchange for K+excretion<br></br>- Sweating; K+is lost in the sweat hence excess sweating can be sufficient to cause hypokalamia<br></br>- Dialysis; removal of K+during dialysis can be sufficient to cause hypokalamia
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73
Q

Outline the most common causes of hypokalaemia due to renal loss of K+? (4)

A
  • Diuretics; non-K+-sparring diuretics such as loop diuretics, thiazide diuretics and osmotic diuretics<br></br>- Hypomagnesaemia; magnesium deficiency impairs Na+/K+ATPase function which decreases cellular uptake of K+<br></br>- Hyperaldosteronism; aldosterone promotes Na+reabsorption in exchange for K+excretion<br></br>- Renal tubular acidosis; RTA can cause renal failure and K+loss in the urine
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74
Q

Outline the ECG changes associated with hypokalaemia? (4)

A

<div>ECG features<br></br>- U waves<br></br>- Small or absent T waves<br></br>- Prolonged PR interval<br></br>- ST depression</div>

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75
Q

Outline the two subtypes of hypogonadism based on the position of the lesion amongst the HPG axis? (2)

A
  • Primary hypogonadism; due to intrinsic problems with the gonads (ovaries/testes)<br></br>- Secondary hypogonadism; mainly due to pituitary disease or hypothalamic dysfunction
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76
Q

Outline the main aetiologies of primary hypogonadism in males? (2)

A
  • Congenital; Klinefelter’s, testicular agenesis, 5α-reductase deficiency
  • Acquired; mumps/orchtitis, bilateral testicular injury/torsion, chemo/radiotherapy
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77
Q

What is the most common type of pituitary adenoma?

A

Prolactinoma

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78
Q

How can you differentiate primary hypogonadism from secondary hypogonadism?

A

Measure gonadotrophin (LH/FSH) levels<br></br>- Primary hypogonadism; hypergonadotropic hypogonadism due to loss of negative feedback via sex hormones<br></br>- Secondary hypogonadism; hypogonadotropic hypogonadism due to decreased GnRH and/or LH/FSH release

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79
Q

Outline the symptoms of a prolactinoma in men and women? (2)

A
  • Men; loss of libido, erectile dysfunction, gynaecomastia

- Women; amenorrhoea, galactorrhoea, infertility

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80
Q

What is the most common cause of familial hypercholesterolaemia?

A

Mutations in the LDL receptor (LDL-R) which decrease cholesterol clearance from the blood stream

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81
Q

Outline the main features of familial hypercholesterolaemia? (4)

A
  • Hypercholesterolaemia<br></br>- Hyperlipidaemia<br></br>- Early-onset vascular disease; diabetes, hypertension ect.<br></br>- Tendon xanthomas; pathognomonic
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82
Q

Outline the main complications associated with bone marrow transplantation? (3)

A
  • Infection; due to reduced WCC from immunosuppressant medications
  • Bleeding; due to reduced platelet counts associated seen in patients undergoing bone marrow transplantation
  • Graft versus host disease (GvHD); due to allogeneic (donor) T-lymphocytes reacting to host (recipient) HLA antigens
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83
Q

Outline the pathognomonic feature of graft versus host disease (GvHD) secondary to bone marrow transplantation?

A

Erythematous rash that develops on the palms of the hand or soles of the feet 10-30 days after transplantation that may progress to cause desquamation

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84
Q

What is the most common type of bladder cancer?

A

Urothelial cell carcinoma (transitional cell carcinoma)

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85
Q

What is the most common type of prostate cancer?

A

Adenocarcinoma

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86
Q

What is the most common type of kidney cancer?

A

Renal cell carcinoma (RCC)

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87
Q

What is the most common subtype of renal cell carcinoma (RCC)?

A

Clear cell carcinoma

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88
Q

What is the most common type of testicular cancer?

A

Germ cell tumours

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89
Q

What is the most common type of testicular germ cell tumour?

A

Seminoma

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90
Q

What is the specific definition of a Colles’ fracture?

A

Fracture of the distal radius with dorsal displacement of the distal fragment

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91
Q

What are the classical examples of fragility fractures? (3)

A
  • Colles’ fracture of the distal radius<br></br>- Fractured neck of the femur<br></br>- Vertebral body fracture
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92
Q

Outline the causes of secondary osteoporosis? (4)

A

ENDO<br></br>- Endocrine; thyrotoxicosis, Cushing’s syndrome, hyperparathyroidism<br></br>- Nutritional; vitamin D deficiency, malabsorption (coeliac disease)<br></br>- Drugs; steroids, aromatase inhibitors, tamoxifen<br></br>- Other; multiple myeloma, osteogenesis imperfecta, rheumatoid arthritis (RA)

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93
Q

Outline the threshold needed for diagnosis of osteoporosis on DEXA scan?

A

T-score ≤ -2.5; meaning that bone density is more than 2.5x less than what it should be

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94
Q

What is the most common cause of osteoporosis?

A

Primary osteoporosis is the most common form and occurs predominantly in post-menopausal women due to the reduction in oestrogen levels

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95
Q

Outline the management of osteoporosis? (5)

A

<div>BCDEF</div>

<div>- Bisphosphonates<br></br></div>

  • Calcium<br></br>- Vitamin D<br></br>- Education<div>- Fall prevention</div>
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96
Q

Outline the main complications of solid organ transplantation? (4)

A
  • Operative complications; anastomotic leaks, bleeding ect.<br></br>- Infection; especially CMV<br></br>- Rejection; hyperacute, acute or chronic<br></br>- B-lymphocyte transformation; lymphoproliferation either due to EBV reactivation in the host or introduction of EBV-positive tissue from the donor
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97
Q

What is the most common cause of a subacute stridor?

A

Laryngomalacia; soft and floppy laryngeal cartilage, with an abnormal epiglottis and/or arytenoid cartilages

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98
Q

What is the most common cause of respiratory distress in a child with laryngomalacia?

A

Intercurrent upper respiratory tract infections (URTIs) can cause exacerbation oflaryngomalacia

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99
Q

Which investigation is used to confirm a diagnosis oflaryngomalacia?

A

Flexible laryngoscopy; usually carried out by ENT surgeons as an outpatient appointment

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100
Q

What is the most common cause of an acute stridor?

A

<div>Laryngotracheobronchitis (croup); most commonly caused by the parainfluenza virus</div>

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101
Q

Outline the main differential diagnoses in an acute stridor? (4)

A
  • Laryngotracheobronchitis (croup)
  • Inhaled foreign body
  • Anaphylaxis
  • Epiglottitis
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102
Q

Outline the management steps used in the treatment of croup? (4)

A
  • First-line; oral dexamethasone<br></br>- Second-line; nebulised budesonide<br></br>- Third-line; nebulised adrenaline<br></br>- Fourth-line; intubation and ventilation
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103
Q

Which medication can be given prophylactically to infants at high-risk of bronchiolitis?

A

Palivizumab; an anti-RSV monoclonal antibody

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104
Q

Outline the classic signs and symptoms of cystic fibrosis in children? (3)

A
  • Recurrent chest infections
  • Fingernail clubbing
  • Bulky offensive stools (malabsorption)
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105
Q

What is the most common cause of nailclubbing in children in the UK?

A

Cystic fibrosis

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106
Q

How does the presentation of cystic fibrosis differ in different ages during childhood? (3)

A
  • Neonatal; merconium ileus, intestinal atresia<br></br>- Infant; failure to thrive, malabsorption<br></br>- Toddlers/children; recurrent chest infections, difficult asthma, diabetes
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107
Q

Outline the tests carried out in the diagnosis of cystic fibrosis? (3)

A
  • Neonatal screening; Guthrie card measuring immunoreactive trypsinogen (IRT)<br></br>- Confirmatory genetic testing; CFTR sequencing<br></br>- Chloride sweat test; if diagnostic uncertainty
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108
Q

What is the most common cause of an acute deterioration of chronic asthma in paediatric patients?

A

Poor adherence to home treatment and/or poor inhaler technique

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109
Q

Outline the two main subtypes of a persistent wheeze in children? (2)

A
  • Episodic Viral Wheeze (EVW); wheeze associated with an upper respiratory tract infection (URTI)
  • Multiple Trigger Wheeze; (MTW); wheeze associated with allergens, viral infections and exercise
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110
Q

Outline the management of preschool episodic viral-induced wheezing?

A
  • Management of acute flare-ups; management resembles treatment of acute asthma<br></br>- No need for prophylactic therapy
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111
Q

Outline the management of preschool multiple trigger wheezing (MTW)?

A
  • Management of acute flare-ups<br></br>- Prophylactic therapy; trial of LRTA or ICS
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112
Q

Which additional differential is important to consider in paediatric patients presenting with abdominal pain?

A

Lower lobe pneumonia; due to poor ability of patients to localise pain

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113
Q

When are the childhoodpneumococcal vaccinations against <i>Steptococcus pneumoniae</i>serotypes given? (2)

A
  • 3 months

- 1 year

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114
Q

What is the most common cause of chest pain in children?

A

Idiopathic chest pain

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115
Q

Why are there few congenital cyanotic heart conditions that present on the first day of life?

A

<div>- Because the ductus arteriosus remains open at this stage, flow through it is reversed due to the decrease in pressure in the pulmonary arteries <br></br>- This acts to maintain pulmonary blood flow as blood flows from the aorta into the pulmonary arteries, allowing for sufficient oxygenation</div>

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116
Q

What is the most common cardiac cause of cyanosis in the newborn?

A

Transposition of the great arteries (TGA)

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117
Q

Which investigations are useful in diagnosing transposition of the great arteries (TGA)? (2)

A
  • Chest X-ray; may shown ‘egg-on-string’ appearance plus narrowing of the superior mediastinum
  • Hyperoxia test; exposure to 90-100% oxygen fails to trigger a rise in the PaO2
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118
Q

Outline the management of transposition of the great arteries (TGA)? (3)

A
  • Prostaglandin infusion; to maintain the ductus arteriosus<br></br>- Correction of any metabolic acidosis; these may have arised due to hypoxia<br></br>- Surgical correction; balloon atrial septostomy, arterial switch
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119
Q

Outline the most common congenital cardiac lesions presenting with neonatal collapse? (4)

A
  • Severe aortic coarctation
  • Aortic arch interruption
  • Critical aortic stenosis
  • Hypoplastic left heart syndrome
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120
Q

Outline the classification used for the differential diagnoses of a collapsed neonate? (7)

A
  • Infection; group B Streptococcus (GBS), herpes simplex virus (HSV)<br></br>- Cardiogenic; hypoplastic left heart syndrome (HLHS), supraventricular tachycardia (SVT)<br></br>- Hypovolaemic; dehydration, bleeding<br></br>- Neurogenic; meningitis, subdural haemotoma (‘shaken-baby’)<br></br>- Pulmonary disorder; congenital diaphragmatic hernia (late presentation)<br></br>- Metabolic; propionic acidaemia, methylmalonic acidaemia<br></br>- Endocrine; panhypopituitarism
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121
Q

What is the most common pathological arrhythmia seen in childhood?

A

Supraventricular tachycardia (SVT)

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122
Q

What is the typical heart rate in a supraventricular tachycardia (SVT)?

A

200-300 beats/min

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123
Q

Where is the most common location in the GI tract forintussusception to occur?

A

Ileocolic; terminal ileum (intussusceptum) invaginates into the colon (intussuscipiens)

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124
Q

What is the most common type of endometrial cancer?

A

Endometrioid; the most common type of endometrial cancer which is seen in up to 80% of cases.

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125
Q

What is the most common type of ovarian cancer?

A

Serous; epithelial ovarian cancers are the most common type, of which the serous subtype occurs in 60-70% of cases.

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126
Q

Which imaging modalities are preferred for investigating upper vs lower urinary tract causes of haematuria? (2)

A
  • Upper urinary tract; CT urogram<br></br>- Lower urinary tract; flexible cystoscopy
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127
Q

Outline the normal range of kidney size seen on ultrasound scanning?

A

10 - 12 cm in length

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128
Q

Why can patients with chronic kidney disease (CKD) have hyperphosphataemia with hypocalcaemia and a raised alkaline phosphatase (ALP)? (3)

A
  • Hyperphosphataemia; due to reduced renal elimination ofPO42-
  • Hypocalcaemia; due to reduced renal production ofactivated vitamin-D (calcitriol)
  • Elevated ALP; due to compensatory bone resorption to restore serum [Ca2+]
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129
Q

Which equation can be used to estimate glomerular filtration rate (eGFR)?

A

eGFR Equation

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130
Q

Outline the main causes of chronic kidney disease (CKD)? (6)

A
  • Hypertension<br></br>- Diabetes mellitus<br></br>- Glomerulonephritis<br></br>- Renovascular disease<br></br>- Chronic obstruction/interstitial nephritis<br></br>- Hereditary/cystic renal disease
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131
Q

What kind of anaemia is associated with chronic kidney disease (CKD)?

A

Normocytic anaemia; due to reduced production of erythropoeitin (EPO) by the damaged kidneys

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132
Q

Which symptom/sign associated with Addison’s disease classically presents first?

A

Hyperpigmentation; particularly in the palmar creases, around the nipple areolae and in scar tissue

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133
Q

What is the most common cause of primary adrenal insufficiency (Addison’s disease) in the UK?

A

Autoimmune adrenalitis; often seen in patients with history of autoimmune disease, most often T1DM and/or coeliac disease

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134
Q

Outline the main investigation used to diagnose adrenal insufficiency?

A

Short synthacten test; administration of synthetic ACTH (synthacten) measure cortisol at 0, 30 and 60 minutes

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135
Q

Outline the investigation used differentiate primary adrenalinsufficiency (Addison’s disease) from secondary/tertiary adrenal insufficiency?

A

Plasma ACTH<br></br>- Elevated; indicates a primary adrenal insufficiency (Addison’s disease) due to lack of feedback suppression via cortisol<br></br>- Low/normal; indicates a secondary/tertiary adrenal insufficiency

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136
Q

What abnormality may be seen in the ECG of a patient with aortic dissection?

A

ST elevation in anterior (V1-V4) and lateral leads (I, aVL, V5, V6) indicative of myocardial ischaemia

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137
Q

Outline the most common complications associated with Marfan’s syndrome? (3)

A

<div>- Mitral valve prolapse</div>

  • Spontaneous pneumothorax<br></br>- Aortic dissection
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138
Q

Which features raise the suspicion of a hereditary breast cancer syndrome? (5)

A

OBAMA;<br></br>- Onset < 50 years<br></br>- Bilateral breast cancers<br></br>- Ashkenazi Jewish ancestry<br></br>- Male breast cancer<br></br>- Associated cancers; ovarian, peritoneal, fallopian tube

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139
Q

Outline the risk of breast and ovarian cancer in patients with BRCA1 and BRCA2 mutations? (2)

A

BRCA1<br></br>- Breast cancer; 80% lifetime risk<br></br>- Ovarian cancer; 40% lifetime risk<br></br><br></br>BRCA2<br></br>- Breast cancer; 40% lifetime risk<br></br>- Ovarian cancer; 10% lifetime risk

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140
Q

Outline the most common causes of seizures in a neonate (< 28 days)? (4)

A
  • Hypoxic ischaemic encephalopathy (HIE)<br></br>- Intracranial haemorrhage (ICH)<br></br>- CNS infections; meningitis<br></br>- Metabolic disorders; hypoparathyroidism
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141
Q

What is the most common cause of hypocalcaemia?

A

Hypoalbuminaemia

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142
Q

Outline the features of tetralogy of fallot (ToF)? (4)

A
  • Overriding aorta<br></br>- Pulmonary stenosis<br></br>- Right ventricular hypertrophy<br></br>- Ventricular septal defect (VSD)
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143
Q

Outline the two most common diseases associated with congenital cardiac defects? (2)

A
  • Down syndrome; trisomy 21<br></br>- DiGeorge syndrome; 22q11 deletion
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144
Q

Outline the three main ways that a diagnosis of HIV may be confirmed? (3)

A
  • Genetically; nucleic acid amplification test (NAAT/PCR)<br></br>- Serologically; detection of p24 antigen (capsid protein)<br></br>- Immunologically; detection of a low CD4+T cell population
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145
Q

How long does it take for HIV antibodies to be detectable in the serum?

A

4-8 weeks

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146
Q

What is the most common cause of a ‘funny turn’ in a teenager?

A

Neurally mediated (vasovagal) syncope

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147
Q

Outline the paediatric definition of overweight and obese? (2)

A
  • Overweight; a BMI above the 91st centile

- Obese; a BMI above the 98th centile

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148
Q

Outline the UK definition of precocious puberty in males and females? (2)

A
  • Females; puberty commencing before the age of 8 years<br></br>- Males; puberty commencing before the age of 9 years
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149
Q

What is the first sign of puberty in males and females? (2)

A
  • Males; enlargement of the testes<br></br>- Females; development of the breasts
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150
Q

Outline the investigations used in cases of suspected precocious puberty? (4)

A
  • LH-releasing hormone (LHRH) test; administration of a GnRH agonist<br></br>- Wrist X-ray bone aging<br></br>- Pelvic ultrasound; in females<br></br>- Cranial MRI; in males
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151
Q

What is the most common cause of precocious puberty in females?

A

Usually idiopathic or familial and follows normal sequence of puberty

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152
Q

What is the most common cause of precocious puberty in males?

A

Cranial lesion

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153
Q

Outline the treatment of precocious puberty? (2)

A
  • Monthly injections of an LHRH analogue (GnRH agonist) until the age of 11 years<br></br>- Treatment of the underlying cause if identified (i.e. cranial lesion)
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154
Q

What is the main down-side of not treating precocious puberty?

A

<div>Significant risk of premature fusion of the epiphyses resulting in a short adult height and subsequent psychosocial implications</div>

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155
Q

Why is rheumatic heart disease in adulthood often associated with history of unexplained fever and joint pain in childhood?

A
  • Fever and joint pain in childhood raises the suspicion of a rheumatic fever which is a common cause of rheumatic heart disease
  • This is an infection cause by group A (β-haemolytic)<i>Streptococci </i>most commonly<i>Streptococcus pyogenes</i>
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156
Q

What causes rheumatic heart disease to develop secondary to rheumatic fever?

A

Rheumatic heart disease is a type II hypersensitivity reaction caused by antibody cross-reactivity between between the M protein of group A <i>Streptococcus</i> and cardiac tropomyosin

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157
Q

Which valve is most commonly affected in rheumatic heart disease and why? Which murmurs are often associated with it? (2)

A
  • The mitral valve is most commonly affected due to it being the valve with the greatest pressure gradient across it<br></br>- This results in mitral regurgitation (MR) in the early stages of the disease followed by mitral stenosis (MS)
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158
Q

Which two murmurs are most commonly seen in rheumatic heart disease? (2)

A
  • Mitral stenosis; mid-diastolic murmur heard best at the apex<br></br>- Aortic regurgitation; early diastolic murmur heard best at end expiration at left sternal edge
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159
Q

Which histopathological findings are pathognomonic of rheumatic heart disease?

A

Aschoff bodies; granulomas found within the all three layers of the heart but predominantly in myocardium and contain giant cells (mainly macrophages) that can develop into Anitschkow cells

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160
Q

Which type of hypersensitivity reaction is seen in rheumatic heart disease?

A

Type II (antibody-mediated cytotoxic) hypersensitivity

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161
Q

What is the definition of sudden cardiac death?

A

Sudden cardiac death; death occuring within 1-hour of the onset of cardiac symptoms

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162
Q

Outline the most common causes of sudden cardiac death in young people and middle-aged/older people? (2)

A
  • Young people; hypertrophic obstructive cardiomyopathy (HOCM)<br></br>- Middle-aged/older people; ischaemic heart disease (IHD) +/- myocardial infection (MI)
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163
Q

What is the most common mechanism by which sudden cardiac death occurs?

A

Fatal arrhythmia triggered by irritability of the myocardium

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164
Q

Outline the main complications of myocardial infarction? (6)

A

THREAD

  • Tamponade; due to heart muscle/septal rupture
  • Heart failure; caused oedema
  • Regurgitation of heart valves; due to rupture of papillary muscles
  • Embolism; stroke and mesenteric ischaemia
  • Arrhythmia and aneurysm
  • Dressler’s syndrome; post-MI pericarditis
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165
Q

What is meant byconstitutional delay of growth and puberty (CDGP)?

A

Constitutional delay in growth and puberty (CDGP)isa condition in which children experience delayed puberty compared to their peers of similar age associated with a delay in the pubertal growth spurt

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166
Q

Why does the growth spurt in males occur later than in females? (2)

A
  • Females enter puberty, on average, early in their adolescence<br></br>- Testosterone is a poor growth promoter in low concentrations, unlike oestrogen in females
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167
Q

What is the threshold tesicular volume that is thought to indicate the transition into puberty?

A

4 mL

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168
Q

What is the most common cause of virilised female genitalia?

A

Congenital adrenal hyperplasia (CAH) due to a 21-hydroxylase (21-OH) deficiency

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169
Q

Outline the definition of an abdominal aortic aneurysm (AAA)?

A

An infrarenal aortic diameter that is ≥ 3 cmand involves all three layers of the arterial wall

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170
Q

Outline the threshold size of an abdominal aortic aneurysm sufficient for endovascular aneurysm repair (EVAR) surgery?

A

≥ 5.5 cm

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171
Q

Outline the management of abdominal aortic aneurysm (AAA) depending on the size of the aneurysm? (3)

A
  • ≥ 5.5 cm; elective endovascular aneurysm repair (EVAR)<br></br>- 4.4cm - 5.5 cm; 3-monthly abdominal ultrasound scans<br></br>- < 4.4 cm; 12-monthly abdominal ultrasound scans
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172
Q

Why do ruptured abdominal aortic aneurysm (AAAs) commonly present as back and flank pain?

A

Abdominal aorta is retroperitoneal

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173
Q

Outline the risk factors for abdominal aortic aneurysms (AAAs)? (5)

A

<div>- Atherosclerosis<br></br></div>

  • Male sex<br></br>- Obesity<div>- Smoking<br></br>- Hypertension<br></br></div>
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174
Q

Outline the screening programme currently used in the UK for abdominal aortic aneurysms (AAA)?

A

A single abdominal ultrasound for <br></br>- Males ≥ 65<br></br>-Females ≥ 70 who have not already had abdominal imaging with any one of;<br></br> • COPD<br></br> • Vascular disease<br></br> • Positive family history<br></br> • Hyperlipidaemia<br></br> • Hypertension<br></br> • Smoking history

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175
Q

Outline the two cardinal features of chronic obstructive pulmonary disease (COPD)? (2)

A
  • Chronic bronchitis; a chronic productive cough for at least 3 months over two consecutive years
  • Emphysema; abnormal airspace enlargement distal to the terminal bronchioles with evidence of destruction of the alveolar wall
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176
Q

Outline the most common complications of chronic obstructive pulmonary disease (COPD)? (4)

A

<div>- Infective exacerbations; reccurent chest infections</div>

  • Respiratory failure; usually type 2 respiratory failure due to CO2 retention<br></br>- Cor pulmomale; right-sided heart failure caused by pulmonary hypertension<br></br>- Pneumothorax; secondary pneumothoraces
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177
Q

Outline the classification of lung cancers?

A
  • Non-small cell lung cancer (NSCLC); 80%<br></br>• Squamous cell carcinoma<br></br>• Adenocarcinoma<br></br>- Small cell lung cancer (SCLC); 20%
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178
Q

How does the management of non-small cell (NSCLC) and small cell lung cancer (SCLC) differ?

A
  • Surgery is offered first-line for non-small celllung cancers (NSCLCs)
  • Chemoradiotherapy is only treatment choice for small celllung cancers (SCLCs)
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179
Q

Why is gynaecomastia common in pubertal males?

A

<div>Gynaecomastia can be common in pubertal males due to a decreased ratio of testosterone to oestrogen levels</div>

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180
Q

Outline the investigations that may be used in a case of pubertal gynaecomastia? (2)

A
  • Serum gonadotropins; LH and FSH<br></br>- Serum sex hormones; testosterone and oestrogen
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181
Q

What feature of pubertal gynaecomastia in a male would raise the suspicion of a prolactinoma?

A

Galatorrhoea alongside the features of gynaecomastia

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182
Q

What is the most common cause of rickets?

A

Secondary to inadequate sun exposure coupled with poor nutrition

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183
Q

Outline the most common clinical signs of rickets? (4)

A
  • Bow-legs<br></br>- Swollen wrists<br></br>- Frontal bossing<br></br>- Ricket rosary (prominent costochondral junctions)
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184
Q

Which kind of anaemia is classically seen in iron deficiency?

A

Microcytic hypochromic anaemia with low ferritinand a raised total iron binding coefficient (TIBC)

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185
Q

Which kind of anaemia is most commonly associated with rickets?

A

Iron deficiency anaemia (IDA) as rickets often arises due to poor diet which is a common association with IDA

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186
Q

Outline the classical symptoms associated with anti-GBM disease (Goodpasture’s syndrome)? (2)

A
  • Haematuria<br></br>- Haemoptysis
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187
Q

Outline the main organ systems classically affected by anti-GBM disease (Goodpasture’s syndrome)? (2)

A
  • Renal; glomerulonephritis (nephritic syndrome)<br></br>- Pulmonary; haemorrhage (haemoptysis)
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188
Q

Outline the main diagnostic tests that can be used in anti-GBM disease (Goodpasture’s syndrome)? (2)

A
  • Anti-glomerular basement membrane (anti-GBM) antibody test; ELISA looking for anti-GBM
  • Renal biopsy; light microscopy may show crescentic glomerulonephritis
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189
Q

Which type of hypersensitivity reaction is seen in anti-GBM disease (Goodpasture’s syndrome)?

A

Type II hypersensitivity (antibody mediated)

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190
Q

To which antigen are the antibodies seen in anti-GBM (Goodpastures syndrome) directed against?

A

IgG antibodies are directed against the non-collagenous domain (NCI) of the α3 chain of collagen IV

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191
Q

Outline the main treatment approaches used in anti-GBM disease (Goodpasture’s syndrome)? (2)

A
  • Plasmapheresis;removal of the patients plasma replacing it with human albumin solution (HAS) in order toremove circulating autoantibodies
  • Immunosuppression; usuallysteroidscombined withcyclophosphamide
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192
Q

Which two investigations can be diagnostic for multiple sclerosis? (2)

A
  • Contrast-enhanced MRI head; enhancing lesions in the periventricular areas
  • CSF electrophoresis; oligoclonal immunoglobulin G bands
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193
Q

Where in the brain are demylinating lesions associated with multiple sclerosis (MS) most commonly found?

A

In the periventricular areas particularly the white matter tracts

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194
Q

Outline the type of visual loss associated with multiple sclerosis?

A

Usually unilateral (monocular) painful visual loss associated with diplopia indicative of optic neuritis

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195
Q

Which imaging modalities can be used to distinguish vascular dementia from Alzheimer’s disease? (2)

A
  • Single photon emission computed tomography (SPECT); can show evidence of metabolic activity inkeeping with vascular dementia<br></br>- Positron emission tomography (PET); can show evidence of metabolic activity inkeeping with vascular dementia
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196
Q

Outline the features of dementia with Lewy bodies (DLB)? (4)

A
  • Progressive cognitive decline<br></br>- Visual hallucinations<br></br>- Rapid eye movement sleep (REM) disturbances<br></br>- Parkinsonism; bradykinesia, rigidity, tremor
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197
Q

What is the difference between dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD)?

A
  • Dementia with Lewy bodies (DLB) is a tau-(τ)-opathy defined as the onset of cognitive decline within 1 year of a diagnosis of parkinsonism
  • Parkinson’s disease dementia (PDD)is an α-synucleinopathy defined by the onset of cognitive decline at least 1 year after a diagnosis of parkinsonism
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198
Q

Outline the macroscopic features seen in the brains of patients with Alzheimer’s disease? (2)

A
  • Cortical atrophy; characterised by atrophy of sulci and widening of gyri<br></br>- Dilation of the ventricles; secondary to parenchymal loss
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199
Q

What is the most common cause of hyperthyroidism in children and adolescents?

A

Graves’ disease

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200
Q

Outline the typical age of presentation for infants with pyloric stenosis?

A

Between 2-8 weeks

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201
Q

Outline the typical acid-base disorder associated with pyloric stenosis?

A

Hypokalaemic metabolic alkalosis with increased base excesss

202
Q

Why is hypokalaemia classically associated with persistent vomiting? (2)

A
  • The kidneys attempt to reabsorb H+from the tubular fluid to compensate for that that is being lost in the vomit<br></br>- This occurs in exchange for K+ secretion into the tubular fluid
203
Q

Outline the most common differential diagnoses for non-bilious vomiting in an infant? (7)

A
  • Pyloric stenosis
  • Gastro-oesophageal reflux disease (GORD)
  • Gastritis
  • Urinary tract infection (UTI)
  • Overfeeding
  • Cow’s milk protein allergy/intolerance
  • Tracheo-oesophageal fistula
204
Q

Outline the definitive treatment used in pyloric stenosis?

A

Pyloromyotomy; either open (Ramsted’s pyloromyotomy) or laparoscopic

205
Q

Outline the peak age range for a presentation of intussusception?

A

3 months to 3 years

206
Q

Which biochemical finding is classically associated with dehydration?

A

Raised urea

207
Q

Which imaging modality is preferred when investigating a diagnosis of intussusception?

A

Abdominal ultrasound

208
Q

Outline the management of intussusception? (3)

A
  • Drip & suck; as with any other case of bowel obstruction, fluids to correct dehydration and NG tube to decompress the stomach<br></br>- Intravenous antibiotics; penicillin, gentamicin and metronidazole due to risk of perforation or sepsis<br></br>- Pneumatic reduction; this utilises air to resolve the intussusception and is carried out under fluoroscopic guidance
209
Q

Outline the main differentials for rectal bleeding in a child? (9)

A
  • Gastroenteritis<br></br>- Anal fissure<br></br>- Intussusception<br></br>- Cow’s milk protein allergy/intolerance<br></br>- Meckel’s diverticulum<br></br>- Inflammatory bowel disease<br></br>- Polyps<br></br>- Clotting abnormalities<br></br>- Sexual abuse
210
Q

What is the pathophysiological difference between bilious and non-bilious vomiting? (2)

A
  • Non-bilious vomiting occurs where there is an obstruction proximal to the duodenum
  • Bilious vomiting occurs where there is an an obstruction distal to the duodenum
211
Q

Outline the two main aetiological factors that predispose to peptic ulceration? (2)

A
  • Gastric acid hypersecretion<br></br>- Damage to the mucosal barrier
212
Q

How can cholecystitis be differentiated from biliary colic (cholelithiasis)? (3)

A

Cholecystitis;

  • More likely to present with a fever in addition to the RUQ pain, nausea and vomiting
  • More likely to present with elevated inflammatory markers, systemic malaise and peritoneal irritation
  • Pain is more often constant and severe whereas in biliary colic it tends to be transient
213
Q

What is the link between biliary colic due to cholelithiasis and acute cholecystitis?

A

Repeated episodes of biliary colic due to cholelithiasiscan cause acute cholecystitis due to inflammation of the gallbladder wall

214
Q

Outline the aetiology of coeliac disease?

A

Coeliac disease is caused by a sensitivity to the protein component of gluten which is known as gliadin

215
Q

What is the gold-standard investigation required for a diagnosis of coeliac disease and what would it show?

A

Duodenal/jejunal biopsy; showing villous atrophy and blunting, crypt hyperterophy and intraepithelial lymphocytosis

216
Q

Which autoantibodies are associated with coeliac disease? (2)

A
  • Anti-endomysial antibodies<br></br>- Anti-tissue transglutaminase (TTG) antibodies
217
Q

What key features differentiate inflammatory bowel disease (IBD) fromirritable bowel syndrome (IBS)? (3)

A

Irritable bowel syndrome (IBS)

  • Does not lead to weight loss
  • No associated fevers
  • Normal blood results

Inflammatory bowel disease (IBD)

  • Weight loss is a common feature
  • Associated with fevers
  • Abnormal blood results
218
Q

Why is it important to examine the anus in cases of suspected Crohn’s disease?

A

<div>Perianal disease such as skin tags, abscess and fistulae are present in 45% of patients</div>

219
Q

Why is it that patients with inflammatory bowel disease (IBD) often have low albumin?

A

<div>Due to malabsorption of protein and subsequent protein loss in the stool</div>

220
Q

Outline the typical anaemia seen in patients with inflammatory bowel disease (IBD)?

A

Iron deficiency anaemia (IDA); microcytic anaemia with low ferritin

221
Q

What are the implications of inflammatory bowel disease (IBD) on growth and development?

A

<div>Growth failure (e.g. dropping centiles, small for age) and delayed puberty are common</div>

222
Q

Outline the most common extra-intestinal manifestations of Crohn’s disease? (3)

A
  • Arthritis; typically affecting the large joints which occurs in around 10% of cases<br></br>- Erythema nodosum/pyoderma gangrenosum<br></br>- Episcleritis/uveitis; all patients require ophthalmic examination
223
Q

Outline the essential investigations for a child with suspected inflammatory bowel disease (IBD)? (3)

A
  • Colonoscopy; with colonic and terminal ileal biopsies
  • Upper gastrointestinal endoscopy; upper tract disease can be present in Crohn’s disease
  • Faecal calprotectin;sensitive marker for inflammation in the gastrointestinal tract
224
Q

Outline the fluid volume given over 24 hours for paediatric patients with dehydration? (2)

A
  • No signs of shock; 50 mL kg-1 per 24 hours<br></br>- Signs of shock; 100 mL kg-1per 24 hours
225
Q

What is the most common cause of acute onset diarrhoea in children?

A

Viral gastroenteritis; norovirus, adenoviruses, rotavirus

226
Q

Outline the broad classes of aetiologies that can cause bloody diarrhoea in adults? (2)

A
  • Infectious; bacterial, viral or protozoal

Non-infectious; inflammatory bowel disease (IBD), ischaemic bowel disease, diverticular disease, polyps, haemorrhoids

227
Q

What is the major long-term complication of inflammatory bowel disease (IBD)?

A

Increased risk of colorectal cancer due to long-standing chronic inflammation

228
Q

Outine the differences in presentation of right and left-sided colorectal tumours? (2)

A
  • Right-sided tumours often present later often only with signs of anaemia, these tumours are often large due to the space available in the caecum<br></br>- Left-sided tumours present much earlier due to presence of fresh bleeding/mucus visible in the stool alongside associated rectal pain
229
Q

Which staging system is now commonly used to grade a variety of tumours pathologically?

A

TNM Staging

  • Tumour size
  • Nodal involvement
  • Metastases
230
Q

Outline the most common causes of pancreatitis? (2)

A
  • Alcohol excess<br></br>- Gallstones (cholelithiasis)
231
Q

Outline the key differentials for epigastric (foregut) pain? (6)

A
  • Pancreatitis<br></br>- Gastritis<br></br>- Peptic ulcer disease (PUD)<br></br>- Cholelithiasis<br></br>- Cholecystitis<br></br>- Hepatitis
232
Q

Which two features are needed for a diagnosis of pancreatitis? (2)

A
  • Severe epigastric pain<br></br>- Markedly elevated serum amylase or serum lipase
233
Q

Outline the pathophysiology of pancreatitis?

A

Inappropriate activation of pancreatic pro-enzymes and leakage into the parenchyma resulting in inflammation

234
Q

How can chronic pancreatitis be differentiated from acute pancreatitis aside from the duration of symptoms?

A
  • Acute pancreatitis; histology is needed to see atrophy and fibrosis
  • Chronic pancreatitis; chronic inflammation results in calcification which can be seen on a CT abdomen
235
Q

Outline the triad of features associated with appendicitis? (3)

A
  • RIF pain
  • Vomiting
  • Low-grade fever
236
Q

Outline the main complication associated with acute appendicitis?

A

Perforation and subsequent peritonitis

237
Q

What is meant by chronic abdominal pain of childhood/recurrent abdmoinal pain (RAP)?

A

<div>Chronic abdominal pain of childhood or recurrent abdominal pain (RAP) is a benign, very common but potentially debilitating condition characterised by recurrent episodes of abdominal pain with no clear organic cause. Hence it is a diagnosis of exclusion with the commonest cause being psychosomatic</div>

238
Q

What is the most common cause of constipation in children?

A

Functional constipation; associated with faecal masses in the lower abdomen

239
Q

Outline the management of constipation in children? (3)

A
  • First-line; dietary advice, hydration ect.<br></br>- Second-line; osmotic laxative such as Movicol<br></br>- Third-line; add stimulant laxative such as Senna
240
Q

What is the widely-used definition of failure to thrive in children under 2-years of age?

A

<div>A current weight, or rate of weight gain, that is significantly below what is normal for a child of that age and sex</div>

241
Q

What is the most common cause of a failure to thrive?

A

Poor nutrient intake

242
Q

Which test is vital to carry out alongside a tissue-transglutaminase (anti-TTG) when suspecting coeliac disease and why?

A

<div>Serum immunoglobulin A (IgA); anti-TTG is an IgA antibody and hence a concurrent IgA deficiency may mask the diagnosis and produce a false negative diagnosis of coeliac disease</div>

243
Q

What kind of antibody is the anti-tissue transglutaminase (anti-TTG) antibody?

A

IgA

244
Q

Which specific antibodies can be tested for when investigating a patient for coeliac disease? (2)

A
  • Anti-tissue transglutaminase (anti-TTG)<br></br>- Anti-endomysial antibody (EMA)
245
Q

Outline the examination findings consistent with ‘cerebellar signs’? (6)

A

DANISH<br></br>- Disdiachokinesia<br></br>- Ataxia<br></br>- Nystagmus<br></br>- Intention tremor<br></br>- Slurred speech<br></br>- Hypotonia

246
Q

Why should caution be exercised when considering giving steroids to patients with malignancies, particularly haematological malignancies?

A

Steroid administration can promote development of tumour lysis syndrome (TLS)

247
Q

Broadly speaking, how can you distinguish between liver or bone-related causes of a raised ALP?

A

Serum γGT

  • Raised γGT and raised ALP; indicates hepatic release of ALP
  • Normal γGT and raised ALP; suggests bone (or placental) release of ALP
248
Q

What is the most common cause of an isolated hyperbilirubinaemia?

A

Gilbert syndrome; due to a mutation in the promoter region of the uridine diphosphoglucuronate-glucuronosyltransferase 1A1 (UGT1A1) gene

249
Q

Outline the triad of biochemical features associated with alcoholic hepatitis? (3)

A
  • Raised transaminases (AST & ALT)
  • AST/ALT ratio > 1.5:1
  • Raised γ-GT
250
Q

Outline the spectrum of conditions covered by the term alcohol-related liver disease (ArLD)? (3)

A
  • Alcoholic fatty liver<br></br>- Alcoholic hepatitis<br></br>- Alcoholic liver cirrhosis
251
Q

Which stages of alcohol-related liver disease (ArLD) are reversible?

A

Alcoholic fatty liver disease and alcoholic hepatitis are reversible

252
Q

What is the main pathological finding in patients with alcoholic fatty liver and alcoholic hepatitis?

A

Centrilobular fatty infiltration into hepatocytes

253
Q

Describe the pathophysiology of ascites in alcohol-related liver disease? (2)

A
  • Cirrhosis and scarring of the liver leads to portal hypertension which increases capillary hydrostatic pressure forcing fluid out into the tissues<br></br>- Hypoalbuminaemia due to the reduced synthetic function of the liver reduces the oncotic pressure for fluid reabsorption from the tissues
254
Q

Describe the macroscopic appearance of the liver in patients with cirrhosis?

A

Often will be shrunken and nodular due to the fibrosis

255
Q

What type of ascitic fluid is associated with alcohol-related liver disease (ArLD)?

A

Trasudative; high protein content due to portal hypertension and hypoalbuminaemia

256
Q

How can you differentiate exudative and transudative ascites? (4)

A
  • Calculate the serum ascitic albumin gradient(SAAG)<br></br>- SAAG = [serum albumin] - [ascitic fluid albumin]<br></br> •> 1.1 g dL-1; transudative<br></br> • < 1.1 g dL-1; exudative
257
Q

Broadly speaking, what is the pathophysiology behind the specific problems seen in cystic fibrosis? (2)

A
  • Loss of function of the cystic fibrosis transmembrane conductance regulator (CFTR) protein decreases Cl- efflux into the lumen of the airways/ducts
  • This decreases the amount of water present in secretions which increases the viscosity and hence causes blockages and failure to clear pathogens
258
Q

What is the significance of renal casts detected in the urine?

A

Presence of casts indicates renal parenchymal damage

259
Q

Outline the main types of urinary casts and what they may indicate? (3)

A
  • Leukocytic casts; indicate infection of the renal parenchyma<br></br>- Tubular casts; indicates glomerulonephritis (nephritic syndrome)<br></br>- Granular casts; indicate chronic parenchymal pathology (chronic pyelonephritis)
260
Q

Which chronic condition can be associated with a predisposition to pyelonephritis?

A

Non-insulin dependant diabetes mellitus (NIDDM)/type 2 diabetes mellitus (T2DM)

261
Q

Outline the two cardinal features of pyelonephritis? (2)

A
  • Fever<br></br>- Loin pain
262
Q

Outline the classical appearance of the kidneys in patients with chronic pyelonephritis?

A

Asymmetrically contracted kidneys with unilateral coarse scarring

263
Q

Which features in the history may enable you to differentiate pre and post-hepatic causes of jaundice?

A

Stool and urine pigmentation<br></br>- Pre-hepatic jaundice; normally pigmented stools and urine<br></br>- Post-hepatic jaundice; pale stools, dark urine

264
Q

What is the most common cause of acute hepatitis in older children and adults?

A

Hepatitis A

265
Q

What is the most common cause of a swelling in the groin of a child?

A

Lymph node; small, mobile and lie inferolaterally in the groin

266
Q

Which single group of paediatric patients have a 30% risk of developing and inguinal hernia?

A

Pre-term infants; especially those with very low birth weight

267
Q

What is the most common cause of an inguinal hernia in a child?

A

Failure of obliteration of the processus vaginalis

268
Q

Which two conditions are associated with a failure processus vaginalis obliteration? (2)

A
  • Hydrocoele; due to a failure of obliteration of the distal end of the processus vaginalis
  • Inguinal hernia; due to a failure of obliteration of the proximal end of the processus vaginalis
269
Q

Outline the management of inguinal hernias in infants?

A

<div>In young babies (< 6 months), the hernia should be operated on within 2-weeks of presentation, as there is a high risk (50%) of strangulation.</div>

270
Q

Outline the difference in presentations of a urinary tract infections (UTI) in infants and older children? (2)

A
  • Infants; fever, vomiting, lethargy, irritability and poor feeding<br></br>- Older children; frequency, dysuria, abdominal or loin pain and fever
271
Q

When is a urinary tract ultrasound indicated in children with urinary tract infections (UTIs)? (2)

A
  • Infants < 6 months of age

- Children > 6 months with severe, atypical and/or recurrent UTIs

272
Q

What is the threshold for conducting urinalysis in children?

A

Any unwell and febrile child should have urinalysis performed

273
Q

Outline the most common causes of haematuria in children? (3)

A
  • Urinary tract infections (UTIs)<br></br>- Post-Streptococcal Glomerulonephritis (PSGN)<br></br>- Henoch-Schönlein purpura (HSP)
274
Q

Which conditions are associated with group A (β-haemolytic) Streptococci, most notably <i>Streptococcus pyogenes</i>? (6)

A
  • Rheumatic fever/rheumatic heart disease<br></br>- Upper respiratory tract infections (URTIs); ‘Strep throat’<br></br>- Necrotising fasciitis<br></br>- Scarlett fever<br></br>-Post-streptococcal glomerulonephritis<br></br>- Impetigo
275
Q

Which two tests will be particularly useful in diagnosing post-streptococcal glomerulonephritis? (2)

A
  • Anti-streptolysin O titre (ASOT); raised in post-streptococcal glomerulonephritis<br></br>- C3 and C4 levels; C3 will be reduced in post-streptococcal glomerulonephritis
276
Q

Outline the classical presentation of post-streptococcal glomerulonephritis (PSGN)?

A

A child with visible haematuria +/-acute severe nephritic syndrome presenting 7-14 days after a recent upper respiratory tract infection (URTI)

277
Q

Which two specific nephritic syndromes can occur following an upper respiratory tract infection (URTI)? (2)

A
  • Post-streptococcal glomerulonephritis<br></br>- IgA nephropathy
278
Q

Briefly describe the pathophysiology of post-streptococcal glomerulonephritis (PSGN)?

A

A nephritic syndrome caused by a type III hypersensitivity reaction mediated by immune complex deposition (mainly IgG, IgM and C3) in the glomeruli

279
Q

What is the most common cause of nephritic syndrome in children?

A

Post-streptococcalglomerulonephritis (PSGN)

280
Q

How can you differentiate post-streptococcal glomerulonephritis (PSGN) from IgA nephropathy? (3)

A

Post-Streptococcal Glomerulonephritis (PSGN)<br></br>- Low complement C3 and C4 levels<br></br>- Main symptom is proteinuria (although haematuria can occur)<br></br>- Longer interval between URTI and the onset of renal problems

281
Q

Outline the main investigations that should be carried out in a patient with nephrotic syndrome? (6)

A
  • Cholesterol and triglyceride levels; elevated in nephrotic syndrome
  • Anti-streptolysin O titre (ASOT); ; investigate potential post-streptococcal disease
  • C3/C4 levels; investigate potential post-streptococcal disease
  • Antinuclear antibody (ANA); may be positive in vasculitides such as systemic lupus erythematosus (SLE)
  • Viral serology; HBV, VZV and measles virus
  • Blood cultures; if febrile
  • Urine; microscopy, culture and sensitivity (MC&S), spot urine protein:creatinine ratio
282
Q

Broadly speaking, ouline the management of nephrotic syndrome in children?

A

High dose oral steroids;around 90% of cases respond, although there is a 70% chance of relapse

283
Q

What is the most widely-used threshold value for prostate specific antigen (PSA) that warrants further investigation?

A

A PSA ≥ 4 ng mL-1 should raise suspicion

284
Q

Which test is required in addition to serum PSA and a digital rectal examination (DRE) to investigate potential prostate cancer?

A

Biopsy; either transrectal or transperineal core biopsies

285
Q

Outline how the Gleason score is calculated for patients with prostate cancer?

A

Gleason Score = [most predominant grading pattern] + [most advanced grading pattern]

286
Q

Where do the majority of aggressive prostate cancers most commonly spread to?

A

Lumbar vertebrae

287
Q

Outline the managment of prostate cancer in regards to its Gleason score? (3)

A
  • ≤ 6; active surveillance<br></br>- 7; radical prostatectomy +/- radical radiotherapy<br></br>- 8-10; radical prostatectomy and radical radiotherapy
288
Q

Outline the specific testicular tumour markers and the specific type of tumour they are associated with? (3)

A
  • Serum LDH; elevated in seminomas<br></br>- Serum AFP; elevated in yolk-sac tumours<br></br>- Serum β-hCG; elevated in choriocarcinoma
289
Q

Why is it that multiple testicular tumour markers are often elevated in the same patient?

A

Testicular tumours frequently occur in mixed forms with multiple different subtypes of tumours present at once

290
Q

What percentage of testicular tumours are malignant?

A

Around 95%

291
Q

Outline the two broad classes of testicular tumours and their relative severity? (2)

A

Germ cell tumours (95%); malignant

- Non-germ cell tumours; (5%); often benign

292
Q

Outline the subtypes of testicular germ cell tumours? (2)

A
  • Seminomas; classical, spermatocytic, anaplastic
  • Non-seminomatous germ cell tumours (NSGCT)
    • Embryonal carcinoma
    • Yolk sac tumours
    • Choriocarcinoma
    • Teratoma
293
Q

What are the most common benign tumours that affect females?

A

Uterine fibroids (leiomyomas)

294
Q

Which type of uterine fibroids are most commonly associated with infertility?

A

Submucosal fibroids; these are located immediately beneath the endometrium where they may distort the uterine cavity

295
Q

What is the most common type of cervical cancer?

A

Squamous cell carcinoma (SCC); accounts for around 85%

296
Q

What is the definition of nocturnal enuresis?

A

<div>Involuntary voiding of urine during sleep at least 3 times per week in a child aged 5 years or older</div>

297
Q

Outline the three main aetiologies behind primary nocturnal enuresis? (3)

A
  • Lack of arousal from sleep
  • Bladder instability/low functional bladder capacity
  • Nocturnal polyuria; due to low vasopressin (ADH)
298
Q

What is the definition of secondary nocturnal enuresis?

A

Nocturnal enuresis following a ≥ 6 month period of dryness

299
Q

Outline the most common causes of secondary enuresis? (4)

A
  • Constipation<br></br>- Urinary tract infection (UTI)<br></br>- Diabetes mellitus<br></br>- Psychosocial stresses
300
Q

Which two aspects of the history are vital to obtain in a patient with nocturnal enuresis? (2)

A
  • Presence of daytime symptoms; urgency, frequency, dysuria or wetting
  • Primary or secondary; was there a ≥ 6 month interval of dryness
301
Q

What is the most common cause of hypertension in a pubertal child?

A

Essential (idiopathic) hypertension most common in the context of obesity

302
Q

What is the most common cause of hypertension in a pre-pubertal child?

A

Renal disease; renal artery stenosis, glomerulonephritis

303
Q

Which additional differentials should be considered in the case of a child with a fever who has recently returned from abroad? (3)

A
  • Malaria; returning from a malaria-endemic area is malaria until proven otherwise<br></br>- Dengue fever; caused by the dengue virus<br></br>- Typhoid fever; caused by <i>Salmonella typhi</i>
304
Q

Which common full blood count (FBC) abnormality can be associated with malaria?

A

Thrombocytopenia

305
Q

Outline the diagnostic criteria in Kawasaki disease? (6)

A
  • Fever for ≥ 5 days PLUS<br></br>- ≥ 4 of the following<br></br>• Non-purulent conjunctivitis<br></br>• Cervical lymphadenopathy<br></br>• Skin rash<br></br>• Erythema of the oral and pharyngeal mucosae<br></br>• Erythema of the hands and feet followed by desquamation
306
Q

Outline the main aetiologies of a prolonged fever in a child (lasting > 7 days)? (4)

A
  • Infection; tuberculosis, HIV, Kawasaki disease<br></br>- Malignancy; lymphoma, leukaemia, renal tumours<br></br>- Autoimmune disease; juvenile idiopathic arthritis (JIA)<br></br>- Miscellaneous; inflammatory bowel disease (IBD), drugs
307
Q

What is the main complication associated with Kawasaki disease?

A

Coronary artery aneurysms

308
Q

Outline the management of Kawasaki disease? (2)

A
  • High dose oral aspirin for 2 weeks or until afebrile, then lower dose for 6-8 weeks<br></br>- 1 dose of intravenous immunoglobulin within 10 days of onset of symptoms
309
Q

Outline the causes of a primary immunodeficiency? (6)

A
  • Antibody (immunoglobulin) deficiency
  • Complement deficiency
  • Cellular immune deficiency
  • Innate immune system defects
  • Neutropenia
  • Chronic granulomatous disease
310
Q

Outline the causes of a secondary immunodeficiency? (6)

A
  • HIV<br></br>- Immunosuppressive drugs<br></br>- Malnutrition<br></br>- Hyposplenism<br></br>- Cystic fibrosis<br></br>- Anatomical abnormalities; skull base defect, fistulae ect.
311
Q

What is the gold-standard diagnostic test used in patients with tuberculosis?

A

<div>Histopathological confirmation of mycobacteria from a positive sputum smear or culture</div>

312
Q

Outline the two tests that can be carried out to investigate prior exposure to tuberculosis? (2)

A
  • Tuberculin skin test (Mantoux test); intradermal injection of tuberculin protein triggers a type IV delayed hypersensitivity reaction that causes skin thickening
  • Interferon gamma release assay (IGRA); blood test to quantify IFNγ release from TH1 cells in response to mycobacteria antigens in an attempt to activate M1 macrophages
313
Q

Outline the management of active tuberculosis? (4)

A

RIPE

  • Rifampicin; for 6 months
  • Isoniazid; for 6 months
  • Pyrazinamide; for 2 months
  • Ethambutol; for 2 months
314
Q

Why is pyridoxine given alonside isoniazid in patients undergoing treatment for tuberculosis?

A

Isoniazid can cause peripheral neuropathy (tingling in the hands and feet), pyridoxineis a vitamin B6 analogue that acts to prevent this

315
Q

What is the difference between active and latent tuberculosis? (2)

A
  • Active tuberculosis; infection with tuberculosis that causes disease<br></br>- Latent tuberculosis; infection with tuberculosis that does not cause disease
316
Q

Outline the dignostic criteria for sepsis in a child? (7)

A

<div>- Suspected or proven infection AND <br></br>- At least 2 of the following</div>

<div> • Altered mental state/reduced GCS</div>

<div> • Fever or hypothermia</div>

<div> • Inappropriate tachycardia</div>

<div> • Inappropriate tachypnoea</div>

<div> • Prolonged capillary refill time</div>

<div> • Abnormal white cell count</div>

317
Q

Outline the definition of septic shock in a child?

A

<div>Sepsis with hypoperfusion despite appropriate (e.g. ≥30 mL kg-1) fluid therapy</div>

318
Q

Outline the breast screening programme in the UK? (2)

A
  • Most patients; mammogram (X-ray) or breast ultrasound every 3 years from age 50-71
  • Family history of breast or ovarian cancer; mammogram (X-ray) or breast ultrasound every 3 years from age 40
319
Q

Which breast cancer screening tests are preferred for younger versus old women and why? (2)

A
  • Younger women; breast ultrasound is preffered as they have more glandular tissue which is better picked up by USS<br></br>- Older women; mammography is preffered as the breast contains more fatty tissue and is less dense
320
Q

Which investigation is considered the standard for assessing a suspicious breast lump?

A

Core biopsy

321
Q

Which investigation is considered the standard for assessing an axillary lymph node in cases of suspected breast cancer?

A

Fine needle aspiration (FNA) with ultrasound-guided biopsy

322
Q

Broadly speaking what are the two main histological classifications of breast cancer? (2)

A
  • In situ carcinoma

- Invasive (infiltrating) carcinoma

323
Q

What is the most common type of breast cancer?

A

Invasive ductal carcinoma; accounts for around 75% of breast cancer cases

324
Q

Roughly speaking, what is the 10-year disease-free survival rate of breast cancer with lymph node involvement?

A

Between 70-80%

325
Q

What are the three main aetiologies associated with granulomatous disease? (3)

A
  • Infectious; mycobacteria, cryptococccus, histoplasma
  • Foreign bodies; suture material, surgical prosthetics
  • Inflammatory; Crohn’s disease, sarcoidosis
326
Q

Which three organisms are most commonly associated with granulomatous inflammation? (3)

A

<div>MHC;</div>

  • Mycobacteria<br></br>- Histoplasma<br></br>- Cryptococcus
327
Q

Which special stains can be used to identify mycobacteria? (2)

A
  • Ziehl-Neelsen; acid-fast bacili (AFB)

- Auramine stain; quicker turnaround

328
Q

Which special stain can be used to identify fungal pathogens?

A

Silver stain

329
Q

Why is serum angiotensin converting enzyme (ACE) elevated in sarcoidosis?

A

Epithelioid cells contained within the granulomata are modified macrophages that express the ACE enzyme

330
Q

Why can serum calcium become elevated in patients with sarcoidosis?

A

Sarcoidal macrophages (epithelioid cells) express 1α-hydroxylase which increases the generation of activated vitamin D (calcitriol) which in turn promotes calcium reabsorption in the gut as well as increased bone turnover

331
Q

What is the first-line investigation used in patients with palpable lymph nodes?

A

Fine needle aspiration (FNA)

332
Q

Which feature in the growth of a melanoma indicates the acquisition of metastatic properties?

A

Switch from radial (horizontal) growth to vertical growth causing the lesion to become raised

333
Q

Outline the classical appearance of scabes excoriations?

A

Burrows, papules, andvesiclesaffecting palms, soles, axilla and scalp

334
Q

Outline the pathognomonic features of scabies?

A

Thread-like, linear burrows, typically in the finger webs and wrists

335
Q

Which medication is often used to treat scabies infestations?

A

Permethrin; a type I synthetic pyrethroid that prevents deactivation of voltage-gated Na+ channels resulting in excitotoxicity of the <i>Sarcoptes scabiei </i>mite

336
Q

What causes eczema herpeticum?

A

Infection of eczematous skin with herpes simplex virus (HSV)

337
Q

Which organism is most commonly associated with an acute deterioration of eczema?

A

<i>Staphylococcus aureus</i>

338
Q

What is the most common cause of blistering skin lesions present at birth?

A

Epidermolysis bullosa

339
Q

Outline the differences between bullous impetigo and staphylococcal scalded-skin syndrome (SSSS)? (2)

A
  • Bullous impetigo is the localised presentation of a <i>Staphylococcal</i> infection whereas staphylococcal scalded-skin syndrome (SSSS) is a systemic presentation
  • <i>Staphylococcus aureus</i> can be cultured from bullous impetigo lesions but SSSS is mediated by exfoliative toxins and thus skin swabs are often sterile
340
Q

Outline the first-line treatment of an umbilical granuloma?

A

<div>Cauterisation using a silver nitrate stick</div>

341
Q

Which age group is most commonly affected by Henoch–Schönlein purpura (HSP)?

A

Children 4-7 years of age

342
Q

Briefly describe the pathophysiology of Henoch-Schönlein purpura (HSP)?

A

Leukocytoclastic vasculitis(LCV) affecting the small blood vessels caused by the deposition of IgA immune complexes within the basement membrane of blood vessels that can activate complement and other inflammatory pathways.

343
Q

Outline the cardinal symptoms of Henoch-Schönlein purpura (HSP)? (4)

A
  • Palpable purpura; often withsymmetrical distribution over the lower limbs
  • Abdominal pain
  • Renal involvement; commonly proteinuria and haematuria
  • Joint pain and/or inflammation
344
Q

What is the most common systemic vasculitis in children?

A

<div>Henoch–Schönlein purpura (HSP)</div>

345
Q

Which specific condition are children with Henoch–Schönlein purpura (HSP) particularly at risk of?

A

Intussusception; hence an abdominal ultrasound is required +/- surgical review

346
Q

How long after a diagnosis of Henoch–Schönlein purpura (HSP) should children be followed up for?

A

Patients should be followed up for upto 12 months as renal complications may occur up to this time point

347
Q

What is the threshold for a diagnosis of low birth weight in a neonate?

A

Any neonate < 2.5 kg (5 lbs 8 oz) is considered to be of low birth weight

348
Q

How may you differentiate an upper gastrointestinal bleed (UGIB) from a lower gastrointestinal bleed (LGIB)?

A

Upper gastrointestinal bleeds (UGIB) often cause an elevated urea due to the digestion of blood as it passes through the digestive tract

349
Q

What is the difference between the anaemia seen in an upper gastrointestinal bleed (UGIB) compared to an anaemia due to haemolysis?

A
  • Upper gastrointestinal bleeds (UGIB) cause a normocytic anaemia with raised urea<br></br>- Anaemia secondary to haemolysis causes a normocytic anaemia with raised bilirubin
350
Q

What is the most common eletrolyte abnormality that causes nausea and vomiting in oncology patients?

A

Hypercalcaemia

351
Q

Outline the difference between acute and chronic blood loss in terms of the type of anaemia? (2)

A
  • Acute blood loss; normochromic normocyticanaemia<br></br>- Chronic blood loss; hypochromic microcytic anaemia
352
Q

What are the most common causes of iron-deficiency anaemia (IDA) in men and women? (2)

A
  • Men; chronic gastrointestinal blood loss<br></br>- Women; menorrhagia
353
Q

Why might ferritin levels be normal in a patient with iron-deficiency anaemia (IDA)?

A

Because ferritin is an acute phase reactant, it may be falsely elevated in acute inflammation and/or infection

354
Q

What is the most commonly usedthreshold haemoglobin concentration needed for a transfusion to be indicated?

A

Hb < 80 g dL-1

355
Q

What one aspect of a patients blood work is the most reliable indication of iron-deficiency anaemia (IDA)?

A

Elevated transferrin levels; upregulated in an attempt to compensate for decrease iron levels

356
Q

Outline the specific causes of a lymphocytosis (elevated lymphocyte count)? (5)

A
  • Infections<br></br>- Chronic lymphocytic leukaemia (CLL)<br></br>- Acute lymphoblastic leukaemia (ALL)<br></br>- Non-Hodgkin’s lymphoma (NHL)<br></br>- Thyrotoxicosis
357
Q

What is the most common form of leukaemia in the Western World?

A

Chronic lymphocytic leukaemia (CLL)

358
Q

Outline the classical immunophenotypic profile indicative of chronic lymphocytic leukaemia (CLL)?

A

CD5, CD20 and CD23 positive

359
Q

Which abnormal cell type seen in a blood film is classicaly associated with chronic lymphocytic leukaemia (CLL)?

A

Smudge/smear cells; cell remnants that arise during slide preparation due to the abnormally fragile lymphocytes seen in CLL

360
Q

What is the threshold value of a lymphocytosis needed for a diagnosis of chronic lymphocytic leukaemia (CLL)?

A

Lymphocytes > 5 x 109 L-1

361
Q

What is the most common presentation associated with a diagnosis of chronic lymphocytic leukaemia (CLL)?

A

Incidental finding in a completely asymptomatic patient

362
Q

What complication is commonly associated with chronic lymphocytic leukaemia (CLL)?

A

Autoimmune haemolytic anaemia; due to lymphocyte production of antibodies against red blood cells

363
Q

Which staging system is used to stratify patients with chronic lymphocytic leukaemia (CLL)?

A

Binet Staging<br></br>- Binet A;< 3 lymphoid sites<br></br>- Binet B;≥ 3 lymphoid sites<br></br>- Binet C; anaemia and/or thrombocytopaenia

364
Q

Which biochemical abnormality is commonly associated with an atypical pneumonia caused by <i>Legionella pneumophilia</i>?

A

Hyponatraemia; due to associated SIADH and inappropriate secretion of antidiuretic hormone (ADH) as a result of the infection

365
Q

Why can leukaemias cause a pancytopaenia?

A

<div>An arrest in the maturation process keeps cells in their early non-functioning stage where they begin to divide rapidly and occupy more space in the bone marrow which disturpts normal haemopoiesis</div>

366
Q

Which kind of anaemia is associated with acute leukaemias (AML/ALL)?

A

Macrocytic anaemia due to the increased size of blast cells

367
Q

Outline the threshold values for platelet transfusion in the bleeding and non-bleeding patient? (2)

A
  • Not bleeding; < 20 x 109 L-1<br></br>- Bleeding; < 50 x 109L-1<br></br>
368
Q

Outline the difference between a blast cell and a lymphocyte as seen on blood film analysis? (2)

A

Blast cells are bigger than lymphocytes and tend to have a greater nucleus-to-cytoplasm ratio than lymphocytes

369
Q

Outline the specific serious complication associated with acute leukaemias?

A

Neutropenic sepsis; this is a medical emergency requiring immediate antibiotics

370
Q

Which specific conditions can be associated with disseminated intravascular coagulation (DIC)? (5)

A

STOMP<br></br>- Sepsis<br></br>- Trauma; head injury, burns, fat emboli<br></br>- Obstetric complications; placental abruption, pre-eclampsia<br></br>- Malignancy<br></br>- Pancreatitis

371
Q

Outline the typical blood test result features seen in disseminated intravascular coagulation (DIC)? (6)

A
  • Thrombocytopaenia (low platelets)<br></br>- Decreased fibrinogen<br></br>- Increased prothrombin time (PT)<br></br>- Increased activated partial thromboplastin time (APTT)<br></br>- Increased D-Dimer (fibrinogen breakdown product)<br></br>- Haemolytic anaemia; normocytic anaemia with a raised LDH and raised bilirubin
372
Q

Outline the treatment of disseminated intravascular coagulation (DIC)? (2)

A
  • Blood product replacement<br></br>- Treat the underlying cause
373
Q

Which two specific organ dysfunctions are the most common precipitants of disseminated intravascular coagulation (DIC)? (2)

A
  • Renal failure; leads to impaired platelet function

- Liver failure; leads to decreased clotting factor synthesis

374
Q

What is the definition of polycythaemia?

A

Erythrocytosis with high haematocrit plus high packed cell volume (PCV)

375
Q

Outline the clinical features of polycythaemia rubra vera (PRV)? (4)

A

PEST

  • Polycythaemia
  • Erythrocytosis
  • Splenomegaly
  • Thrombocytosis
376
Q

Which myeloid lineages are classically expanded in polycythaemia rubra vera (PRV)? (3)

A

<div>PEN</div>

<div>- Platelets<br></br></div>

  • Erythrocytes (RBCs)<br></br>- Neutrophils
377
Q

What is the most common cause of polycythaemia rubra vera (PRV)?

A

V617F mutation in JAK2 which allows EPO-independent erythropoiesis

378
Q

Outline the typical symptoms associated with polycythaemia rubra vera (PRV)? (2)

A
  • Neurological symptoms; headache and blurred vision<br></br>- Itching; due to histamine release
379
Q

Outline the main-stay treatment used in polycythaemia rubra vera (PRV)?

A

Venesection; blood letting to remove excess myeloid cells

380
Q

Broadly speaking, what are the two main aetiologies of a pancytopaenia? (2)

A
  • Bone marrow failure

- Bone marrow infiltration

381
Q

Outline the investigations required for a patient with pancytopaenia? (6)

A
  • Blood film<br></br>- Red cell indices; MCV, MCH, haematocrit<br></br>- Reticulocytes<br></br>- Viral titres; hepatitis viruses, EBV and parvovirus<br></br>- Chromosome breakage analysis (CBA)<br></br>- Bone marrow aspirate and trephine (BMAT)
382
Q

Which specific malignant conditions can cause bone marrow infiltration and subsequently lead to pancytopaenia? (5)

A
  • Leukaemia
  • Lymphoma
  • Neuroblastoma
  • Myelofibrosis
  • Myelodysplasia
383
Q

Outline the most important risks to be aware of in a patient with pancytopaenia? (2)

A
  • Infection; due to suppressed white cell count<br></br>- Bleeding; due to reduced platelet count
384
Q

What is the main risk associated with multiple platelet transfusions?

A

Alloimmunisation; development of anti-platelet antibodies that trigger transfusion reactions and diminish the increment in platelet count

385
Q

Outline the management options for patients with aplastic anaemia? (2)

A
  • Bone marrow transplant; HLA-matched sibling donor<br></br>- Immunosuppression; anti-thymocyte globulin (ATG) and ciclosporin
386
Q

Outline the differentials of a purpuric rash in child? (7)

A
  • Immune (idiopathic) thrombocytopaenia purpura (ITP)<br></br>- Infection; meningococcal septicaemia<br></br>- Vasculitides; Henoch-Schönlein purpura (HSP)<br></br>- Vomiting or coughing; in distribution of SVC<br></br>- Trauma; if localised only<br></br>- Clotting disorders; haemophilia, von Willebrand disease<br></br>- Drugs; steroids
387
Q

What is the most serious complication associated with immune (idiopathic) thrombocytopaenia purpura (ITP)?

A

Intracranial haemorrhage (ICH); although the incidence of this is 0.1-0.5%

388
Q

Outline the management of immune (idiopathic) thrombocytopaenia purpura (ITP)? (2)

A
  • Most patients; supportive management<br></br>- Prednisolone; if mucous membrane bleeding and/or extensive cutaneous symptoms
389
Q

Which bacterial infections are patients with hyposplenism particularly susceptible to? (3)

A

Encapsulated bacteria (NHS)

  • <i>Neisseria meningitidis</i>
  • <i>Haemophilus influenzae</i>
  • <i>Streptococcus pneumoniae</i></i></i>
390
Q

Outline the management of patients with hyposplenism? (2)

A
  • One-off pneumococcal vaccination<br></br>- Regular penicillin V (phenoxymethylpenicillin) prophylaxis
391
Q

Outline the main complications associated with sickle cell disease? (3)

A
  • Hyposplenism<br></br>- Sickle cell crises<br></br>- Stroke
392
Q

What is the most common cause of strokes in children?

A

Sickle cell disease

393
Q

What is the most common cause of an abdominal mass in children?

A

Constipation due to faeces; characteristically craggy, mobile and in the lower abdomen

394
Q

Which two malignancies are most commonly associated with an abdominal masses in children? (2)

A
  • Wilm’s tumour (nephroblastoma)

- Neuroblastoma

395
Q

Outline the median age at presentation of a Wilm’s tumour in a child?

A

Between 3 and 4 years of age; earlier if bilateral

396
Q

Which congenital syndromes are associated with an increased risk of development of a Wilms’ tumour? (2)

A
  • WAGR Syndrome; Wilms’ tumour, aniridia, genitourinary abnormalities and retardation
  • Beckwith-Wiedemann syndrome; mutations at 11p15.5 causing a hemihypertrophy, macroglossia and visceromegaly
397
Q

What is a neuroblastoma?

A

<div>An embryonal cancer of the peripheral sympathetic nervous system</div>

398
Q

What are the most common locations for a neuroblastoma to develop? (2)

A
  • Adrenal glands<br></br>- Retroperitoneal sympathetic ganglia
399
Q

Which biochemical tests can be used to differentiate neuroblastoma from a Wilms’ tumour?

A

Neuroblastoma is associated with elevated urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels

400
Q

How does the prognosis of Wilms’ tumours and neuroblastomas differ? (2)

A

<div>- Wilms' tumours; have an excellent prognosis with patients with stage 1-3 tumours having an overall cure rate of 88-98%<br></br></div>

  • Neuroblastoma; often presents late with symptoms of metastatic spread, such as fever, bone pain, irritability and weight loss<br></br>
401
Q

Outline the threshold needed for a diagnosis of hypetension in a child?

A

Any blood pressure ≥ 95th centile adjusted for age, sex and height

402
Q

What is the most common site of a space-occupying lesion in a the brain of a child?

A

Posterior cranial fossa; 2/3rds of brain tumours

403
Q

Outline the symptoms of raised intracranial pressure (ICP) in a child?

A

Neck pain, rubbing of head in distress, nausea and vomiting

404
Q

Which organisms most commonly cause bacterial meningitis in adults? (3)

A

NHS<br></br>- <i>Neisseria meningitidis</i><br></br>- <i>Haemophilus influenzae</i><br></br>- <i>Streptococcus pneumoniae</i>

405
Q

Which organisms most commonly cause bacterial meningitis in infants? (3)

A

BabyBEL<br></br>- Group B <i>Streptococci</i><br></br>- <i>Escherichia coli</i><br></br>- <i>Listeria monocytogenes</i>

406
Q

What type of anaemia is often found in sickle cell disease (SCD)?

A

Chronic haemolytic anaemia; microcytic anaemia with raised bilirubin due to red cell lysis

407
Q

What is the most common symptom of vaso-occlusive crises in sickle cell disease (SCD)?

A

Bone pain

408
Q

Which single long-term complication is important to consider in patients with sickle cell disease (SCD)?

A

Cerebrovascular accident (CVA); strokes are more common and may be silent in children

409
Q

Outline the pathophysiology of immune (idiopathic) thrombocytopaenia purpura (ITP)?

A

Autoantibodies against the glycoprotein IIb/IIIa or Ib-V-IX complex on the surface of the megakaryocytes in the bone marrow leads to their opsonisation and degradation resulting in decreased platelet generation and thus subsequent thrombocytopaenia

410
Q

Outline the difference in the appearance of blood films from patients acute and chronic phase leukaemia? (2)

A
  • Chronic phase leukaemias exhibit the presence of all developmental stages of the affected lineage<br></br>- Acute phase leukaemias predominantly consist of blast cells of the affected lineage
411
Q

Which conditions make up the myeloproliferative neoplasia (MPN) group? (4)

A
  • Primary myelofibrosis (PMF)<br></br>- Essential thrombocytosis (ET)<br></br>- Polycythaemia rubra vera (PRV)<br></br>- Chronic myeloid leukaemia (CML)
412
Q

What causes the BCR-ABL fusion gene seen in ≥ 95% of cases of chronic myeloid leukaemia (CML)?

A

Philadelphia chromosome; a translocation between chromosomes 9 and 22

413
Q

Which features of a full blood count (FBC) suggest a chronic myeloid leukaemia (CML) over an infective process? (2)

A
  • Persistent unexplained neutrophilia

- Normal inflammatory markers e.g. CRP

414
Q

Outline the potential aetiologies of enlarged lymph nodes? (2)

A
  • Infection; EBV, myobacteria, toxoplasma<br></br>- Malignancy; lymphoma, leukaemia
415
Q

What is the definition of enlarged lymph nodes? (2)

A
  • Cervical/axillary lymph nodes ≥ 1cm in diameter<br></br>- Inguinal lymph nodes ≥ 1.5 cm in diameter
416
Q

How may bacterial and viral infective causes of enlarged lymph nodes be distinguished? (2)

A
  • Bacterial infections; tender, warm and erythematous<br></br>- Viral infections; tender but not warm or erythematous
417
Q

How may inflammatory lymph nodes be distinguished from those occuring as a result of malignancy? (2)

A
  • Inflammatory lymph nodes; painful, softer and more motile

- Malignancy-associated lymph nodes; non-tender, firmer and non-motile

418
Q

Which organisms are the most common cause of cervical lymphadenitis in children?

A

Gram positive cocci; most commonly <i>Staphylococcal</i> and <i>Streptococcal</i> species

419
Q

Outline the X-ray features consistent with osteosarcoma? (4)

A
  • Bone destruction
  • Gross swelling
  • Elevation of the periosteum with creation of Codman’s triangle
  • ‘Sunray’ spicules of new bone visible in the muscle and subcutaneous tissues
420
Q

Which organism is most commonly associated with chorioamionitis?

A

Group B Streptococcus; usually <i>Streptococcus agalactiae</i>

421
Q

Outline the main aetiologies that may underlie a lymphocytosis (elevated lymphocyte count)? (3)

A
  • Infection; acute or chronic
  • Malignancy; leukaemia, lymphoma
  • Endocrine; thyrotoxicosis
422
Q

Which medications are classically associated with hypercalcaemia? (2)

A
  • Thiazide diuretics

- Lithium

423
Q

What is the most common cause of death in children with cancer in remission who are undergoing treatment?

A

Infection

424
Q

Which features can increase the risk of infection in patients with cancer? (5)

A
  • Neutropaenia; immunosuppression due to chemotherapy<br></br>- Mucositis; inflammation of the gastrointestinal tract as a result of chemo and radiotherapy<br></br>- Indwelling central lines; allows easy portal of entry for skin commensals<br></br>- Frequent hospital admissions; exposure to nocosomial infections<br></br>- Poor nutrition; resulting in secondary immunodeficiency
425
Q

Which symptoms can suggest mucositis in patients undergoing treatment for cancer?

A

Abdominal pain and diarrhoea

426
Q

What is the most common childhood leukaemia?

A

Acute lymphoblastic leukaemia (ALL); accounts for > 80% of cases

427
Q

What causes the hepatosplenomegaly sometimes seen in patients with haematological malignancies?

A

Extramedullary haematopoeisis occuring in the liver and spleen due to invasion/failure of the bone marrow

428
Q

Which two specific conditions are associated with endometriosis? (2)

A
  • Adenomyosis; specific deposits of endometrial tissue within the myometrium of the uterus
  • Endometriomas; ovarian cysts frequently referred to as ‘chocolate cysts’ due to the appearance of the containedmenstrual blood
429
Q

What is the main complication associated with a slipped upper femoral epiphysis (SUFE)?

A

Avascular necrosis of the femoral head

430
Q

Which radiological finding is consistent with a diagnosis of slipped upper femoral epiphysis (SUFE)?

A

Trethowan’s Sign;theline of Kleinpassing above the femoral head

431
Q

Which imaging modality is used to diagnose a slipped upper femoral epiphysis (SUFE)?

A

Hip X-ray with lateral or frog leg view as well as an anteroposterior view

432
Q

Which two initial blood test abnormaities may point towards a diagnosis of hereditary haemochromatosis? (2)

A
  • Derranged LFTs<br></br>- Elevated serum ferritin
433
Q

Which single test is most useful in determining if a patient is suffering from iron overload?

A

Transferrin saturation; should be < 50% in healthy adults, if increased indicates iron overload

434
Q

Which coagulation cascade pathway and clotting factors are implicated in a prolonged activated partial thromboplastin time (APTT)?

A

A prolonged APTT indicates a problem with any of the intrinsic pathway factors (VIII, IX, XI and XII)

435
Q

Which coagulation cascade pathway and clotting factors are implicated in a prolonged prothrombin time (PT)?

A

A prolonged PT indicates a problem with any of the extrinsic pathway factors (II, V, VII and X)

436
Q

How do the sites of bleeding differ between haemophilia and von Willebrand’s disease?

A
  • Haemophilia tends to present early in life with haemarthroses (bleeding into the joint spaces)
  • von Willebrand’s disease tends to present later in the second to third decades of life with mucosal bleeding (epistaxis, bleeding gums ect.)
437
Q

Outline the pathophysiology of acquired haemophilia?

A

Autoantibodies against clotting factor VIII

438
Q

Outline the main causes of acquired haemophilia? (5)

A
  • Autoimmune; SLE<br></br>- Lymphoproliferative disoders<br></br>- Malignancy<br></br>- Infection<br></br>- Idiopathic
439
Q

Outline the management of acquired haemophilia B? (2)

A
  • Coagulation cascade bypass; activated prothrombin complex concentrate or recombinant factor VIIa<br></br>- Immunosuppression; corticosteroids, cyclophosphamide, azathioprine or rituximab
440
Q

What are the two main differentials to consider in a child with joint pain with signs of infection? (2)

A
  • Septic arthritis<br></br>- Osteomyelitis
441
Q

Outline the major complication associated with delaying antibiotics in the treatment of septic arthritis/osteomyelitis in children?

A

<div>Delay in treatment of osteomyelitis or septic arthritis can cause significant long-term effects on the growth and function of the affected limb, particularly if the growth plate is involved</div>

442
Q

What is the most common site affected by osteomyelitis or septic arthritis?

A

Legs

443
Q

Which organism is most commonly associated with osteomyelitis or septic arthritis?

A

<i>Staphylococcus aureus</i>

444
Q

Outline the classification of juvenile idiopathic arthritis (JIA)? (2)

A

<div>- Polyarticular JIA; ≥ 5 joints affected in the first 6 months of onset of symptoms<br></br>- Oligo(pauci)articular JIA; < 5 joints affected in the first 6 months of onset of symptoms</div>

445
Q

What is the most common type of juvenile idiopathic arthritis (JIA)?

A

Oligoarticular juvenile idiopathic arthritis; polyarthropathy affecting < 5 joints

446
Q

Outline the threshold requirements for a diagnosis of juvenile idiopathic arthritis (JIA)?

A

<div>≥ 6 continuous weeks of arthritis with exclusion of other causes</div>

447
Q

What systemic condition is commonly associated with juvenile idiopathic arthritis (JIA)?

A

Still’s disease; also known as systemic juvenile idiopathic arthritisthat presents with systemic features such as salmon-pink rash associated with polyarticular joint pain and fever

448
Q

Which specific complication are patients with oligoarticular juvenile idiopathic arthritis (JIA) particularly at increased risk of?

A

Chronic anterior uveitis; requires formal ophthalmology screening and regular review

449
Q

What is the definition of a scoliosis?

A

Abnormality of spinal alignment in the coronal plane

450
Q

What test can be used to differentiate between a structural and postural scoliosis?

A

Forward-bend test; get patient to bend forward and touch their toes, postural scoliosis will disappear whereas a structural scoliosis will persist

451
Q

Outline the most common causes of cerebral palsy? (6)

A
  • Pre-term birth<br></br>- Hypoxic ischaemic encephalopathy<br></br>- Congenital birth defects<br></br>- Kernicterus<br></br>- Traumatic brain injury<br></br>- Infections
452
Q

What thorough investigation is required in patients with a structural scoliosis?

A

Neurological examination; scoliosis can cause neurological deficits due to impingment of nerves and the spinal cord

453
Q

Which group of patients are at increased risk of their structural scoliosis progressing to cause early joint disease and cardiorespiratory compromise?

A

Pre-menarchal females

454
Q

Outline the typical features of oligoarticular juvenile idiopathic arthritis (JIA)? (3)

A

<div>- Polyarthropathy affecting < 5 separate joints</div>

  • Typically affects the knees and ankles (less often the elbows or a single finger joint)<br></br>- Occurs in young children < 6 years, particularly girls
455
Q

Which immunological test is most likely to be positive in patients with juvenile idiopathic arthritis (JIA)?

A

Anti-nuclear antibodies (ANA)

456
Q

Why are haptoglobin levels low in patients with haemolysis?

A

Haptoglobins are produced by the liver and bind free haemoglobin in the circulation that is release as a result of haemolysis

457
Q

Outline the features suggestive of microangiopathic haemolytic anaemia (MAHA)? (3)

A
  • Haemolytic anaemia; normocytic anaemia with raised LDH and bilirubin
  • Thrombocytopaenia; confirmed via blood film analysis
  • Increased red cell fragments (schistocytes)
458
Q

Outline the features of thrombotic thrombocytopaenic purpura (TTP)? (5)

A
  • Purpuric rash<br></br>- Thrombocytopaenia<br></br>- Microangiopathic haemolytic anaemia<br></br>- Fever<br></br>- Neurological deficits
459
Q

Outline the pathophysiology of thrombotic thrombocytopaenic purpura (TTP)?

A
  • Either a deficiency in the ADAMTS-13 enzyme, or widespread endothelial activation leads an inability of the enzyme to appropriately regulate the size of von Willebrand factor (vWF) polymers
  • This leads to the generation of prothrombotic vWF polymers that trigger widespread platelet activation and thrombi formation in various organs
460
Q

Outline the management of thrombotic thrombocytopaenic purpura (TTP)?

A

Plasma exchange; as soon as possible as TTP is a medical emergency

461
Q

What kind of anaemia is often associated with a <i>Mycoplasma pneumoniae</i> atypical pneumonia?

A

Autoimmune haemolytic anaemia; normocytic anaemia with raised bilirubin and LDH

462
Q

Which two conditions are commonly associated with ‘B symptoms’ i.e. fever, night sweats, weight loss, lethargy and lymphadenopathy? (2)

A
  • Tuberculosis<br></br>- Lymphoma
463
Q

Outline the main investigations required in suspected cases of lymphoma? (2)

A
  • Lymph node biopsy; fine needle aspiration, mediastinoscopy ect.<br></br>- Bone marrow biopsy; for staging and rule out bone marrow infiltration
464
Q

Outline the top differentials of a thrombocyopaenia in pregnancy? (2)

A
  • Gestational thrombocytopaenia; benign condition<br></br>- Haemolysis, Elevated Liver enzymes, Low Platelets (HELLP) Syndrome; medical/obstetric emergency
465
Q

Outline main the blood tests that make up a haemolysis screen? (5)

A
  • Lactate dehydroganse (LDH)
  • Reticulocyte count
  • Direct antiglobulin test/direct Coomb’s test (DAT/DCT)
  • Haptoglobins
  • Bilirubin
466
Q

Outline the threshold platelet count for platelet transfusion in pregnancy?

A

Platelet count > 80 x 109 L-1may be sufficient for platelet transfusion, especially if epidural anaesthesia is forseen

467
Q

Outline the investigations indicated for a neonate born with congenital bruising? (2)

A
  • Anti-HPA1a and anti-HPA5b antibodies; investigating for neonatal alloimmune thrombocytopaenia (NAIT)<br></br>- Transcranial ultrasound scan; investigating for potential intracranial or intraventricular haemorrages (IVH)
468
Q

Outline the pathophysiology of neonatal alloimmune thrombocytopaenia (NAIT)? (3)

A
  • Mother develops antibodies against human platelet antigens (HPA) which she does not express <br></br>- These IgG antibodies can cross the placenta and bind to HPA antigens expressed by the fetus that have been inherited from the father<br></br>- This causes opsonisation and degradation of platelets thus causing thrombocytopaenia
469
Q

Outline the two main subtypes of autoimmune haemolytic anaemia? (2)

A
  • Warm autoimmune haemolytic anaemia<br></br>- Cold autoimmune haemolytic anaemia
470
Q

What is the most common form of autoimmune haemolytic anaemia?

A

Warm autoimmune haemolytic anaemia

471
Q

Why can patients with autoimmune haemolytic anaemia present with splenomegaly? (2)

A
  • The spleen is often the predominant site of haemolysis in autoimmune haemolytic anaemia
  • Macrophages in the spleen express Fcreceptors which bind to the antibodies bound to the surface of the red blood cells
472
Q

What kind of anaemia is associated with a chronic autoimmune haemolytic anaemia?

A

Macrocytic anaemia; due to the increased reticulocytes in peripheral blood which are larger than RBCs

473
Q

Which diseases are often associated with an autoimmune haemolytic anaemia? (2)

A
  • Systemic lupus erythematosus (SLE)<br></br>- Lymphoproliferative disorders (lymphoma)
474
Q

What is the most common precipitant of an autoimmune haemolytic anaemia?

A

Infection

475
Q

Outline the aetiology of monoclonal gammopathy of undetermined significance (MGUS)?

A

Monoclonal gammopathy of undetermined significance (MGUS) occurs due to an overproliferation of a clone of mature B-lymphocytes (plasma cells) that produce an excessive amount of the kappa (κ) light chain (paraprotein) component of the IgG antibody

476
Q

Outline the key complication associated with monoclonal gammopathy of undetermined significance (MGUS)?

A

Progression to multiple myeloma

477
Q

Outline the key investigation findings associated with multiple myeloma? (5)

A
  • Monoclonal IgG bands > 20 g L-1; seen on serum electrophoresis<br></br>- Pancytopaenia; due to bone marrow infiltration and suppression of haematopoeisis<br></br>- > 10% plasma cells; identified on bone marrow biopsy<br></br>- Bence-Jones protein positive; κ or λ IgG light chains detected in the urine<br></br>- Boney lytic lesions; due to bone marrow infiltration
478
Q

Outline the blood film features associated with myelodysplasia? (3)

A
  • Thrombocytopaenia
  • Neutropaenia
  • Abnormal neutrophils; hypogranulated, bilobed nuclei (pseudo-pelger)
479
Q

Which specific group of patients are at increased risk of developing myelodysplasia (MDS)?

A

Patients with previous exposure to cytotoxic medications and/or radiotherapy; found in 15% of patients with MDS

480
Q

Outline the amount of fluid used for resuscitation in paediatrics?

A

20 mL kg-1of 0.9% NaCl (normal saline)

481
Q

Outline the main contraindications to lumbar puncture? (7)

A
  • Papilloedema<br></br>- Pupillary dilatation<br></br>- GCS < 13<br></br>- Hypetension with bradycardia<br></br>- Widespeard purpuric rash<br></br>- Thrombocytopaenia and/or clotting disorder<br></br>- Focal neurological signs
482
Q

Which investigation should be carried out immediately in all children preseting with seizures?

A

Blood glucose; hypoglycaemia is a common cause

483
Q

What is the most common precipitant of siezures in children?

A

Fever; secondary to infection can reduce the threshold for siezures in healthy children and those successfully being managed with anti-epileptics

484
Q

Which family of viruses most commonly associated with meningoencephalitis?

A

Enteroviruses; account for ≥ 80% of cases

485
Q

Which specific medications should be commenced following the taking of blood cultures in patients with meningoencephalitis? (3)

A
  • Ceftriaxone; broad-spectrum antibiotic<br></br>- Aciclovir; to cover for HSV-1 viral meningoencephalitis<br></br>- Macrolide; usually clarithromycin to cover for <i>Mycoplasma pneumoniae</i>
486
Q

How can electroencephalograms (EEGs) be useful in investigating meningoencephalitis? (2)

A
  • Most cases; can show slow wave activity without focal features<br></br>- HSV-1 cases; focal features indicating temporal lobe involvement
487
Q

Which of the viral meningoencephalitis-causing viruses has the worst prognosis?

A

Herpex simplex virus-1 (HSV-1); severe sequelae of the infection are common and morbidity/mortality is high

488
Q

Outline the differential diagnoses of a coma in children? (6)

A
  • Hypoxic ischaemic encephalopathy (HIE)<br></br>- Epileptic siezure/postictal state<br></br>- Trauma; IVH, cerebral oedema<br></br>- Infections; meningitis, encephalitis, cerebral abscess<br></br>- Metabolic; hypoglycaemia, DKA, renal/hepatic failure<br></br>- Poisoning<br></br>- Vascular lesions; stroke
489
Q

What is the most likely cause of a subdural haemorrhage in children under 1 year of age?

A

Non-accidental injury (NAI); either through shaking of the baby or a direct impact

490
Q

Which AVPU score equates to a GCS of 8 and is therefore the threshold for consideration of airway support?

A

P - patient responds to pain

491
Q

Which neurological deficit scoring system is more commonly used in paediatrics?

A

AVPU;Alert, Voice, Pain, Unresponsive

492
Q

Outline the management of raised intracranial pressure (ICP) in an infant? (3)

A
  • Sit the infant at 30°<br></br>- Fluid restrict; to 2/3rds maintenance<br></br>- Intubation and ventilation; maintain pCO2 4-4.5 kPa
493
Q

What is the most important differential diagnosis to exlcude in young males with a delay in gross motor skills?

A

Duchenne muscular dystrophy (DMD)

494
Q

Which first line invesitgation can be used in patient with suspected Duchenne muscular dystrophy (DMD)?

A

Creatinine kinase (CK); extremely elevated levels are suggestive of DMD

495
Q

Outline the main aetiologies of delayed walking? (4)

A
  • Generalised developmental delay; fragile X syndrome (FXS), Down syndrome
  • Neuromscular disease; cerebral palsy, Duchenne muscular dystrophy
  • Musculoskeletal; congenital dislocation of the hip, developmental dysplasia of the hip (DDH)
  • Idiopathic ‘normal’ late walker; majority of cases
496
Q

Outline thesystemic inflammatory response syndrome (SIRS) criteria that may be used to inform a diagnosis of sepsis? (4)

A

<div>Presence of ≥2 of the following:</div>

  • Temperature: > 38.0ºC or < 36.0ºC<br></br>- Heart rate: > 90/min<br></br>- Respiratory rate: > 20/min<br></br>- White cell count: > 12 x109/L or < 4 x109/L
497
Q

Which genes are most commonly associated with familial hypercholesterolaemia? (3)

A
  • LDL receptor (LDLR)
  • Apolipoprotein B (ApoB)
  • Proprotein convertase subtilisin/Kexin Type 9 (PCSK9)
498
Q

Which specialised blood test can be used to inform whether a patient is likely to be suffering from pre-eclampsia (PET)?

A

sFlt-1/PlGF ratio

  • Placental growth factor (PlGF); decreased levels in pre-eclampsia
  • FMS-like tyrosine kinase-1 (sFlt-1); increased levels in pre-eclampsia
499
Q

Outline the structure of a standard histopathology report? (5)

A
  • Patient demographics
  • Clinical details
  • Macroscopic description
  • Microscopic description
  • Conclusion
500
Q

Outline the pathophysiology of pre-eclampsia? (2)

A
  • Incomplete extra villous trophoblastic (EVT) invasion of spiral arteries leads to impaired vasodilation leads to high resistance in the spiral arteries
  • This in turn results in reduced uteroplacental blood flow which can predispose to intrauterine growth restriction (IUGR) and fetal demise

Final MB Part II - Short Answer Questions (3 decks)

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