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Exam prep! > Endo + Diabetes, Urinary, Infection + MSK finals flashcards!!! > Flashcards

Endo + Diabetes, Urinary, Infection + MSK finals flashcards!!!

1
Q

GFR would increase if:

a. There is afferent arteriole constriction
b. There is efferent arteriole constriction
c. There is an increase in tissue pressure in Bowman’s capsule
d. There is an increased release of renin from the JG cells
e. There is an obstruction of the ureters

A

b. There is efferent arteriole constriction

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2
Q
  1. How would drinking a large amount of water affect osmolarity and volume of the ECF?

a. Decreased osmolarity and increased volume
b. Both would increase
c. No change in osmolarity and increased volume
d. No change in either
e. Greater increase in ECF volume than ICF volume

A

a. Decreased osmolarity and increased volume

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3
Q
  1. Anti-Diuretic Hormone (ADH):

a. Is produced by the anterior pituitary
b. Inserts aquaporins into all parts of the kidney tubule
c. Causes the hypertonic medullary gradient to be established
d. Is released in response to cellular dehydration
e. Is released in response to increased plasma urea

A

d. Is released in response to cellular dehydration

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4
Q
  1. If Drug A’s clearance is greater than inulin clearance, then which of the following would be true of Drug A?

a. net reabsorption
b. no reabsorption
c. no secretion
d. net secretion
e. reabsorbed and secreted

A

d. net secretion

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5
Q
  1. The following acid/base values were obtained:
    pH = 7.25, [HCO3-] = 12mmoles/l, Pco2 = 3.3kPa (25mmHg)

a. They are indicative of a respiratory acidosis
b. The reduction in Pco2 is a result of under-breathing
c. The subject has probably been taking bicarbonate of soda
d. It could be related to impaired renal function
e. The subject may have been vomiting very badly

A

d. It could be related to impaired renal function

(ROME: Respiratory = Opposite (pcO2), Metabolic = Equal (HCO3-))

(Normal PCO2 = 35-45mmHg or 4.7-6kPa, Normal HCO3- = 22-29mmol/L)

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6
Q
  1. The following acid/ base values were obtained:
    pH = 7.45, [HCO3-] = 12mmoles/l, Pco2 = 2.7kPa (20mmHg)

a. The subject is clearly very unwell
b. The subject is likely to have spent a long time at altitude
c. The subject needs bicarbonate
d. The subject is unlikely to be hypoxic
e. This is typical of a metabolic alkalosis

A

b. The subject is likely to have spent a long time at altitude

(ROME: Respiratory = Opposite (pcO2), Metabolic = Equal (HCO3-))

(Normal PCO2 = 35-45mmHg or 4.7-6kPa, Normal HCO3- = 22-29mmol/L)

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7
Q
  1. The following acid/base values were obtained:
    pH = 7.28, [HCO3-] = 36mmoles/l, Pco2 = 8kPa (60mmHg)

a. This is typical of an acute respiratory acidosis.
b. The subject will be excreting large amounts of bicarbonate ions
c. The subject will be excreting large amount of ammonium ions
d. The plasma potassium level is likely to be decreased
e. He has a metabolic alkalosis because of the raised bicarbonate

A

c. The subject will be excreting large amount of ammonium ions

(the lower the pH -> (the more H+ ions present) -> the more NH3 present as NH4+)

(ROME: Respiratory = Opposite (pcO2), Metabolic = Equal (HCO3-))

(Normal PCO2 = 35-45mmHg or 4.7-6kPa, Normal HCO3- = 22-29mmol/L)

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8
Q
  1. The following acid/base values were obtained:
    pH =7.50, [HCO3-] = 45mmoles/l, Pco2 = 8kPa (60mmHg)

a. This may be the result of bad diarrhoea
b. The subject will be excreting bicarbonate ions
c. The subject will be excreting ammonium ions
d. The plasma potassium level is likely to be increased
e. The subject has a respiratory acidosis because of the raised Pco2

A

b. The subject will be excreting bicarbonate ions

(the higher the pH -> (the less H+ ions present) -> the more HCO3- is excreted)

(ROME: Respiratory = Opposite (pcO2), Metabolic = Equal (HCO3-))

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9
Q
  1. The following values were made for an elderly female diabetic patient’s creatinine clearance:
    24hr urine volume 1.44l, serum creatinine concentration 100μmol/L, urine creatinine concentration 6.6mmoles/L.

a. Clinical features of renal impairment would be expected.
b. Serum creatinine alone indicates impaired renal function.
c. Serum potassium should be measured urgently
d. The data suggest there may be renal impairment.
e. There is reason to suspect an incomplete renal collection.

A

d. The data suggest there may be renal impairment.

(- normal serum creatinine:
Men = 59 - 104 µmol/L
Women = 45 - 84 µmol/L

  • normal urine creatinine:
    Men = 7 - 14 mmol/L
    Women = 6 - 13 mmol/L)
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10
Q
  1. A patient with lung cancer develops the syndrome of inappropriate ADH secretion. Which of the following values for Na+ concentration might be expected to be seen?

a. 140mmol/L
b. 145mmol/L
c. 150mmol/L
d. 138mmol/L
e. 128mmol/L

A

e. 128mmol/L

normal Na+ = 135-145mmol/L

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11
Q
  1. Which of the following are classed as loop diuretics?

a. Furosemide
b. Spironolactone
c. Bendroflumethiazide
d. Mannitol
e. Amiloride

A

a. Furosemide

(Spironolactone = mineralocorticoid receptor antagonist

  • Bendroflumethazide = thiazide diuretic
  • Mannitol = osmotic diuretic
  • Amiloride = eNaC inhibitor)
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12
Q

What is the mechanism action of Spironolactone?

A
  • Mineralocorticoid receptor antagonist
  • Blocks Na+-K+ exchanger in the DCT
  • K+-sparing!!
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13
Q

What is the mechanism action of Bendroflumethiazide?

A
  • Thiazide diuretic
  • Blocks Na+-Cl- co-transporter in DCT
  • Increases Na+ and Cl- secretion
  • (NOT K+-SPARING!! - bc blocks a channel proximal in the DCT, therefore increasing the amount of Na+ going to the distal part of the DCT, therefore increasing Na+-K+ exchange and K+ loss…)
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14
Q

What is the mechanism action of Mannitol?

A
  • Osmotic diuretic

- PCT + descending limb of LoH

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15
Q

What is the mechanism of action of Amiloride?

A
  • Blocks eNaCs (Na+ channels) in DCT
  • Prevents reabsorption of Na+ and K+ loss
  • K+ sparing!!
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16
Q

What is the mechanism of action of Furosemide?

A
  • Blocks Na+-K+-Cl- co-transporter
  • in the ascending limb of LoH
  • (NOT K+-SPARING)
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17
Q

What is the mechanism of action of ADH?

What triggers its release?

Where is it released from?

A
  • Stimulates water reabsorption in the Collecting Duct -> increases the insertion of aquaporins into the membranes of the collecting duct (nephron)
  • Triggered during states of increased plasma osmolality (hyperosmolality)
  • increased blood osmotic pressure triggers osmoreceptors in the hypothalamus -> (increases thirst response and) stimulates the release of ADH from the posterior pituitary (by nerve impulses through nerve plexus!!)
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18
Q

Which diuretics are K+-sparing?

A
  • SEAT*
  • Aldosterone antagonists/MRAs = Spironolactone, Eplerenone
  • Direct ENaC inhibitors = Amiloride, Triamterene
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19
Q
  1. A 6 year old child presents with swelling of his face and legs. His serum albumin concentration is 18g/l (normal 37-42) and his mother notices that his urine is frothy. What is the most likely diagnosis?

a. Ig-A glomerulonephritis
b. Minimal change disease
c. Focal and segmental glomerulonephritis
d. Membraneous nephropathy
e. Lupus nephritis

A

b. Minimal change disease

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20
Q
  1. A 23 year old woman complains of flank pain, dysuria and frequency of micturition. She has taken ibuprofen for the pain. Her urinalysis shows protein, nitrites and blood. What is the likely diagnosis?

a. Acute pyelonephritis
b. Cystitis
c. Chronic pyelonephritis
d. Reflux nephropathy
e. Analgaesic nephropathy

A

a. Acute pyelonephritis

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21
Q
  1. A 40 year old man was found to have asymptomatic proteinuria and microscopic haematuria during routine employment-related examination. His BP was found to be 160/100mmHg and serum creatinine 170micromol/l (normal 86-116). He has no urinary symptoms. What is the next most important investigation?

a. Chest X-ray
b. Echocardiogram
c. Intravenous urogram
d. Ultrasound of the urinary tract
e. Renal biopsy

A

d. Ultrasound of the urinary tract

(assesses full urinary tract for problems: upper urinary tract = kidneys + ureters, lower urinary tract = bladder + urethra)

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22
Q
  1. A 60 year old man has stage 5 CKD with a serum creatinine of 500 umol/l, (normal 88-116). Which of the following is likely to be present?

a. High serum calcium
b. Low serum phosphate
c. High serum phosphate
d. Normal serum calcium
e. Normal serum phosphate

A

c. High serum phosphate
* inability to remove phosphate in CKD*
* nb. hyperphosphataemia causes hypocalcaemia due to increased binding of Ca2+*

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23
Q

What are the stages of CKD?

A
  • 5 Stages!!*
  • Stage 1: with normal or high GFR -> GFR > 90 mL/min)
  • Stage 2: Mild CKD -> GFR = 60-89 mL/min
  • Stage 3A: Moderate CKD -> GFR = 45-59 mL/min
  • Stage 3B: Moderate CKD -> GFR = 30-44 mL/min
  • Stage 4: Severe CKD -> GFR = 15-29 mL/min
  • Stage 5: End Stage CKD -> GFR <15 mL/min
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24
Q
  1. A 60 year old man has stage 5 CKD with a serum creatinine of 500 umol/l, (normal 88-116). Which of the following is likely to be present?

a. Low serum calcium
b. Normal serum calcium
c. Low serum phosphate
d. Normal serum calcium
e. High serum calcium

A

a. Low serum calcium

  • inability to remove phosphate in CKD -> hyperphosphataemia causes hypocalcaemia due to increased binding of Ca2+*
  • also: reduction in Calcitriol formation, leads to reduced Ca2+ absorption in the intestines*
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25
Q
  1. Patients with renal failure are often anaemic. What is the best treatment for their anaemia?

a. Oral iron therapy
b. Intravenous iron
c. Vitamin B12
d. Erythropoietin
e. Blood transfusion

A

d. Erythropoietin

kidneys make erythropoeitin -> increases RBC formation

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26
Q
  1. For an uncomplicated urinary infection which of the following organism is the most likely cause?

a. Staphylococcus aureus
b. Klebsiella sp
c. Pseudomonas aeruginosa
d. Candida albicans
e. Escherichia coli

A

e. Escherichia coli

* MSU + Urinalysis: single organism present in high concentration (≥ 10^5 CFU/ml)*

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27
Q

What type of bacteria causes UTI from kidney stones?

A

Proteus spp.

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28
Q
  1. A 70 year old man complains of poor stream of urine, nocturia and post-micturition dribbling.
    Which of the following is the most likely cause?

a. Diabetic neuropathy
b. Urinary tract infection
c. Chronic kidney disease
d. Prostatic hypertrophy
e. Bladder cancer

A

d. Prostatic hypertrophy

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29
Q
  1. A 60 year old man presents with tiredness and malaise. Routine investigations reveal a raised serum creatinine and an estimated GFR of 35ml/min. Which of the following stages of CKD is he in?

a. Stage 1
b. Stage 2
c. Stage 3
d. Stage 4
e. Stage 5

A

c. Stage 3

    • Stage 3A: Moderate CKD -> GFR = 45-59 mL/min
  • Stage 3B: Moderate CKD -> GFR = 30-44 mL/min*
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30
Q
  1. The commonest urological malignancy in patients with painless frank haematuria is:

a. kidney cancer
b. testicular cancer
c. bladder cancer
d. penile cancer
e. prostate cancer

A

c. bladder cancer

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31
Q

What is the most-likely differential of painful frank haematuria?

A
  • UTI

- Urinary calculi (stones)

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32
Q
  1. What is the commonest type of renal tract stones in adults?

a. calcium phosphate
b. calcium oxalate
c. cystine
d. magnesium ammonium phosphate
e. uric acid

A

b. calcium oxalate

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33
Q
  1. What is the commonest mode of presentation for patients with a renal or ureteric stone?

a. loin pain radiating to the flank and/or groin
b. frank haematuria
c. urinary tract infection
d. lower urinary tract symptoms
e. acute urinary retention

A

a. loin pain radiating to the flank and/or groin

* painful frank haematuria = UTI or urinary tract stones!!*

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34
Q
  1. What are the features of acute urinary retention?

a. painful inability to void with a palpable or percussible bladder
b. slow stream of micturition with terminal dribbling and frequency
c. painless condition with a palpable or percussible bladder
d. dysuria with frank haematuria
e. bladder pain which is worse when the bladder is full and relieved by voiding

A

a. painful inability to void with a palpable or percussible bladder

(b = LUTS
c = chronic urinary retention
d = UTI, kidney stone
e = interstitial cystitis (inflammation of the bladder)*
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35
Q
  1. The following antibiotics are generally suitable for empirical treatment of complicated urinary traction infections except:

a. Vancomycin
b. Ciprofloxacin
c. Ceftriaxone
d. Gentamicin
e. Co-amoxiclav

A

a. Vancomycin
* vanc is usually only used for staph aureus, and c. diff -> it is v unusual for staph aureus to cause UTI (it is usually caused by E. coli -> ciprofloxacin!!)*

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36
Q
  1. A patient with hypothyroidism would demonstrate which of the following symptoms:
A.	Exopthalmos
B.	Increased heart rate
C. 	Heat intolerance 
D. 	Increased protein catabolism
E. 	Lethargy
A

E. Lethargy

all the rest = hyPERthyroidism

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37
Q
  1. Goitre is a common symptom of thyroid dysfunction and can be present in both hypo- and hyper- thyroidism. However it would not be present in which of the following thyroid pathologies?
A.	Primary hypothyroidism
B.	Secondary hypothyroidism
C.	Primary hyperthyroidism
D.	Secondary hyperthyroidism
E.	Graves disease
A

B. Secondary hypothyroidism

  • Goitre is caused by overstimulation of the thyroid gland -> causes hypertrophy
  • primary hypothyroidism = lack of T3 and T4 -> causes increased TSH from anterior pituitary (ie. due to autoimmunity, iodine-deficiency)
  • hyperthyroidism = increased activity of the thyroid gland (ie. due to abs mimicking TSH (grave’s/primary), adenoma (most common cause of primary hyperthyroidism) or TSH-secreting tumour (secondary) = GOITRE
  • secondary hypothyroidism = lack of TSH, and therefore a reduction in the stimulation of the thyroid gland = NO goitre!!*
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38
Q
  1. A decrease in circulating cortisol levels would result in which of the following physiological responses:

A. Enhanced gluconeogenesis in the liver.
B. Hypotension
C. Decreased ACTH secretion from the anterior pituitary
D. Elevated fatty acid levels in the plasma
E. Suppression the immune system

A

B. Hypotension

all the others are caused by increased cortisol secretion -> lack of cortisol can be caused by addison’s

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39
Q
  1. A person with primary hypercortisolism would demonstrate:
A. 	Depressed ACTH correct, due to enhanced negative feedback from cortisol
B. 	Elevated CRH 
C. 	Hypotension 
D. 	Hypoglycaemia 
E. 	Increased bone density
A

A. Depressed ACTH

due to negative feedback

*B = unlikely due to negative feedback from cortisol
C = no bc cortisol causes hypertension occurs due to permissive effect of cortisol on noradrenaline α1 adrenoceptors
D = no bc hyperglycaemia is an effect of cortisol secretion due to gluconeogenic action on liver
E =  no bc cortisol stimulates bone resorption so osteoporosis is more likely*
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40
Q
  1. Chronic glucocorticoid therapy is associated with which of the following:

A. Enhanced cortisol release from the adrenal glands
B. Enhanced ACTH release from the anterior pituitary
C. Enhanced CRH release from the hypothalamus
D. Adrenal insufficiency
E. Adrenal hypertrophy

A

D. Adrenal insufficiency

excess glucocorticoid therapy (ie. pred, hydrocortisone) on a chronic basis increases negative feedback on CRH and ACTH, which results in hypo-secretion of cortisol when it is suddenly withdrawn, hence why u need to slowly taper off the dose!!

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41
Q
  1. Which of the following will elevate free calcium levels in plasma?
A. 	Alkalosis 
B. 	Activation of osteoblasts 
C. 	Increased phosphate excretion at the kidney
D. 	Calcitonin 
E. 	All of the above
A

C. Increased phosphate excretion at the kidney

causes reduced Ca2+ in the blood as there is less being complexed with phosphate in bone -> nb. PTH increases phosphate excretion to increase Ca2+ levels!!

*A = no bc loss of H+ frees up binding sites for Ca++ on plasma proteins
B = no bc osteoBlasts Build Bone and use Ca++ in doing so
D = calcitonin is a hormone that reduces plasma calcium levels (made by thyroid gland)
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42
Q

What secretes Calcitonin?

What is it’s functions of Calcitonin?

A
  • Thyroid gland
  • It’s function is to REDUCE plasma Ca2+!*
  • inhibits osteoclast activity
  • inhibits reabsorption of Ca2+ at the renal tubules
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43
Q
  1. Regarding Growth Hormone which of the following is correct:

A. It is also known as somatostatin
B. It is also known as somatomedin
C. It is a steroid hormone
D. Levels in adults are at their highest during REM sleep
E. It is relatively insignificant in terms of foetal and neonatal growth

A

E. It is relatively insignificant in terms of foetal and neonatal growth

*A = no bc GH = somatoTROPIN, somatoSTATIN = GHIH
B = somatomedin C = IGF-1
C = it is a peptide hormone
D = it is highest during delta sleep and lowest during REM sleep 
E = yep, bc it is more important during the months following birth (thyroid hormone and insulin are more important hormones during foetal + neonatal growth)*
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44
Q

What stage of sleep is growth hormone highest and lowest in?

A
  • Highest = Delta sleep

- Lowest = REM sleep

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45
Q

What structure releases GHRH or GHIH?

What is the function of each?

A
  • Hypothalamus!!

- acts on the Anterior Pituitary to increase or decrease GH (respectively)!

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46
Q
  1. The adrenal zona glomerulosa secretes which hormone:
A. 	Testosterone
B.	Progesterone
C. 	Aldosterone
D. 	Cortisol 
E. 	Epinephrine/adrenaline
A

C. Aldosterone

*A = Zona reticularis 
B = Zona reticularis
D = Zona fasiculata
E = Adrenal medulla*
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47
Q
  1. Which of the following responses would you expect following insulin release:
A. 	Hepatic gluconeogenesis
B.	Increased ketone formation
C. 	Increased uptake of glucose by the brain
D. 	Adipose lipolysis
E. 	Stimulation of Na+/K+ ATPase
A

E. Stimulation of Na+/K+ ATPase

function of insulin is to DECREASE BG levels!!

(-> remember, SGLT-1 uses secondary active transport from the sodium gradient created by the Na+-K+-ATPase to bring glucose into cells, so insulin would like that!

  • C = Brain is an obligatory glucose utiliser so does not require insulin for glucose uptake*
  • A, B and D are actions of glucagon*
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48
Q
  1. Which of the following is not a Glucose Counter Regulatory Hormone:
A. Thyroid hormone
B. Epinephrine (adrenaline)
C. Glucagon
D. Cortisol
E. Growth hormone
A

A. Thyroid hormone

  • While TH stimulates gluconeogenesis, TH stimulates futile metabolic cycles that consume the glucose as well so blood glucose does not rise significantly.*
  • all the rest RAISE BG levels*
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49
Q
  1. A 26 year old man is diagnosed with Type 1 diabetes. He works offshore on a ‘2 week on 3 week off’ rota. He drives a car. He has just got married and his wife is expecting their first child. What information should he receive shortly after diagnosis?

A. He should be told he cannot drive.
B He may be able to work off-shore depending on his employer and where he is going.
C He is likely to pass on his diabetes to his child.
D He should be advised to stop drinking any alcohol.
E He should be told he is unlikely to ever have any hypos (hypoglycaemic episodes) if he monitors his blood glucose regularly.

A

B He may be able to work off-shore depending on his employer and where he is going.

*A = Important to take lifestyle of pt. on board and consider their employment and home circumstances -> what kind of vehicle does he drive? Does he hold a normal driver's license and what are the DVLA regulations?
B = There is not an automatic ban on working off shore if you have Type 1 Diabetes but you need to involve your Occupational Health team/employer
C = There is a risk offspring can develop Type 1 DM but not ‘likely’.
D = Alcohol within guidance limits but not to stop alcohol at all. Aware of risk of hypoglycaemia and alcohol. 
E = Patients to achieve good control will experience hypos.
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50
Q
  1. An 80 year old lady who is keen to stay healthy and well comes to see you in clinic. She has been having daily episodes of sweating and palpitations and been feeling hungry. She has had type 2 diabetes for 30 years and is on Metformin 1g bd and Glipizide 5mg bd. Her renal function has deteriorated but her GFR is 50 with a creatinine of 88. Her HbA1c is 51mmol/mol.
    During one of the episodes she checked her blood glucose and found that it was 3.0mmol/l.
    What action should be taken initially with regard to her management?
A. 	Stop metformin
B. 	Stop Glipizide
C. 	Check blood glucose more regularly
D. 	Repeat HbA1c
E. 	Request a holter monitor
A

B. Stop Glipizide

Normal GFR = 60 or higher
Normal Creatinine = 52-92mmol/l
Upper limit of HbA1c = 48 mmol/mol
Normal BG = 4 - 5.4 (when fasting) and up to 7.8 (2hrs after meals)

Glipizide should be stopped as she is having daily hypos and sulphonylureas can cause hypoglycaemia. This is the biggest risk to her safety and her blood glucose levels appear to be reasonably well controlled and the aim of treating her diabetes is to keep her well and safe.

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51
Q
  1. 53 year old man diagnosed with T2 Diabetes Mellitus 6 months ago. He has lost 1 stone in weight his BMI is 28 and HbA1c is 75 mmol/mol (9%). What is the next appropriate medication in his management?
A. 	Insulin
B.	Thiazolidinedione (e.g. pioglitazone)
C. 	Sulphonylurea (e.g. glimepiride)
D. 	Biguanide (e.g. Metformin)
E. 	DPP IV inhibitor (e.g. Sitagliptin)
A

D. Biguanide (e.g. Metformin)

  • Upper limit of HbA1c = 48 mmol/mol*
  • Important to be aware of the algorithms for the management of T2 Diabetes -> Sign 154*
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52
Q

What is the treatment algorithm for Type 2 DM?

A
  • Step 1 = lifestyle advice +/- monotherapy (metformin) (consider 3 months lifestyle change first)
  • > target HbA1c = 53 mmol/mol
  • > remember pt needs normal renal function for metformin (stop metformin treatment if eGFR is <30ml/min/1.73m2)
  • if not reaching target, then…*
  • Stage 2 = add Sulphonylurea (ie. glipizide); or if hypos a concern (ie. due to driving, occupational hazards or falling frequently/risk of falls) thiazolidinedione (ie. pioglitazone -> if no congestive heart failure) or DPP-IV inhibitor (ie. gliptin -> if weight gain was a concern)
  • Stage 3 = triple therapy: thiazolidinedione or DPP-IV inhibitor or injectable insulin or GLP-1 agonist (ie. semaglutide, if obese, desire to lose weight - it is associated with weight loss)
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53
Q

At which eGFR should you stop/not prescribe Metformin for Type 2 DM?

A

30 ml/minute/ 1.73m2

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54
Q

What are the contra-indications for Thiazolidinediones? (ie. pioglitazone)

A
  • Congestive HF

- Obese (BMI >30) (bc it causes weight gain)

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55
Q

Which diabetes drug class is associated with weight loss?

A

GLP-1 agonist (ie. semaglutide)

used in obese (BMI >30) and in those with a desire to lose weight, usually <10yrs from diagnosis

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56
Q
  1. Which symptom below is NOT typical of hypoglycaemia?
A. 	Headache
B.	Itch
C.	Poor concentration
D. 	Sweating 
E. 	Irritability
A

B. Itch

other symptoms include: feeling anxious, trembling or shaking, tingling of lips, hunger, going pale, palpitations

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57
Q
  1. 32 year old patient with T1 Diabetes Mellitus is reviewed at the diabetes clinic. His blood sugar is 3.2 mmol/l and he tells you he is feeling well. What is the best course of action next?
A.	Administer IM glucagon
B.	Send him home for lunch
C.	Give 200ml fresh orange juice
D. 	Give digestive biscuit
E.	Administer his lunchtime insulin
A

C. Give 200ml fresh orange juice

mans is having a hypo:
Normal BG = 4 - 5.4 (when fasting) and up to 7.8 (2hrs after meals))

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58
Q
  1. 25 year old with Type 1 Diabetes Mellitus presents with vomiting and diarrhoea. BP 80/54 and Respiratory Rate is 24 breath/min. Which test is least important for immediate management?
A.	Blood Glucose
B.	pH
C.	Urine/Blood Ketones
D.	Electrolytes
E.	Liver function tests
A

E. Liver function tests

  • DKA protocol: BG, ketones, pH (acid-base balance), U+Es (for electrolytes)*
  • LFTs are important, but not for acute emergency settings: only used if pt. is jaundiced or self-poisoned with paracetamol (clotting screen in self-poisoning lets u know the synthetic function of the liver in the scenario of self-poisoning*
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59
Q

Why are K+ levels high in a DKA?

A
  • NORMAL K+ = 3.6-5.2mmol/L*
  • Insulin stimulates Na+-K+ pump -> this allows SGLT-1 transporter to work as it uses the sodium gradient created by the Na+-K+ pump to allow the co-transport of sodium and glucose into the body
  • This is obvs not working in DKA
  • K+ is not shifted into cells and out of the body, and therefore stays in the interstitial space and causes hyperkalaemia
  • hence the need to monitor electrolytes (U+Es) in DKA!!*
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60
Q
  1. 23 year old man diagnosed with hyperthyroidism and has been commenced on carbimazole. What do you need to counsel him regarding?
A.	Neutropenia
B.	Fertility
C.	Metallic taste in mouth
D.	Renal Function
E.	Discoloration of Urine
A

A. Neutropenia

Neutropoenia and agranulocytosis -> due to carbimazole-induced bone marrow suppression -> needs to be stopped if pt reports symptoms and signs suggestive of infection (esp. SORE THROAT) -> a WBC count also needs to be performed in the scenario of infection -> carbimazole should be stopped if any clinical or lab evidence of neutropoenia

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61
Q
  1. A man with a large prolactinoma complains of impaired vision.
    What is the most likely pattern of visual field loss to be found on clinical confrontation?
A.	Homonymous hemianopia
B.	Bitemporal hemianopia
C.	Total loss of vision in one eye
D.	Homonymous quadrantanopia
E.	Nasal hemianopia
A

B. Bitemporal hemianopia

pituitary adenoma -> impinges on nasal fibres of both optic nerve which cross over just above the pituitary gland -> loss of temporal half of both visual fields!!

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62
Q
  1. 38 year old lady presents feeling tired and dizzy. She is tanned and her investigations show Na 123 (low) K 5.6 (high). Thyroid function tests are normal and calcium is normal. Her cortisol 50 (low). What is her diagnosis?
A.	Hyperparathyroidism
B.	Addison’s Disease
C.	Cushing’s Disease
D.	Grave’s Disease
E.	Conn’s Syndrome
A

B. Addison’s Disease

-> low cortisol and aldosterone

  • normal Na+ = 135-145mmol/L*
  • normal K+ = 3.6-5.2mmol/L*
*A = Hyperparathyroidism causes hypercalcaemia
C = Cushings is an excess of cortisol 
D = Grave’s disease is autoimmune thyrotoxicosis.
E = Conn’s syndrome is excess aldosteronism*
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63
Q

What are the clinical features of Hyperparathyroidism?

A

Hypercalcaemia!

  • Bones
  • Stones
  • Abdominal moans
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64
Q

What are the clinical features of Conn’s syndrome

A
  • Excess aldosteronism!!*
  • Hypokalaemia
  • Hypernatraemia
  • Hypertension
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65
Q
  1. All the conditions below are well recognised causes of secondary diabetes except one. Which condition is not a recognised cause of secondary diabetes?
A.	Acromegaly
B.	Haemochromatosis
C.	Addison’s Disease
D.	Cushing’s Disease
E.	Chronic Pancreatitis
A

C. Addison’s Disease

  • > causes low cortisol and aldosterone, so not associated with hyperglycaemia which u would see in Type 2 DM
  • > actually causes isseues with hyPOglycaemia

When pt’s present with Type 2 DM, always think could this be due to secondary diabetes?
A = GH excess -> monitor IGF-1
B = iron deposits in the pancreas -> bronzed diabetes -> deranged LFTs and iron overload (ferritin levels), can require testosterone replacement in men too
C = hypercortisolism = body habitus, moon face, buffalo hump, thin arms and legs, central obesity
E = has ongoing acute episodes renders the pancreas insufficient -> pain in epigastrium that spreads to the back, malabsorption, steatorrhoea, weight loss -> can require creon too to help absorption of food

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66
Q

What are the typical features of Acromegaly?

A
  • GH excess*
  • Enlarged hands and feet - change in ring or shoe size
  • Enlarged facial features - teeth, nose and jaw getting larger (spaced teeth)
  • Sleep Apnoea (tiredness/difficulty sleeping)
  • Carpal Tunnel syndrome (compressed nerve causing numbness and weakness in hand)
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67
Q

What is the diagnostic test for acromegaly?

A
  • IGF-1 test
  • OGTT
  • > (GH causes hyperglycaemia)
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68
Q

What are the clinical features of cushing’s?

A
  • Hypercortisolism*
  • Body habitus
  • Moon face (+ red and puffy)
  • Buffalo hump
  • Thin arms and legs
  • Central obesity
  • Striae
  • Easy bruising
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69
Q

What is the diagnostic test for Cushing’s?

A
  • 24-hr urine cortisol test
  • > loss of diurnal variation of cushing’s
  • To differentiate between endogenous and ectopic ACTH release
  • low-dose Dexamethasone suppression test
  • > should suppress ACTH, if not then probs due to ectopic cause
  • IPSS (inferior petrosal sinus sampling)
  • > gold-standard
  • > differentiates where the source of the ACTH is coming from by sampling the venous blood
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70
Q

What primary screening diagnostic test would you do for diabetes?

A

Random BG test

(>11 = diagnostic)

this in conjunction with primary diabetic symptoms will make ur diagnosis of diabetes, may need a fasting BG if pt. if presents w no symptoms to confirm diagnosis

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71
Q

What investigations would you do for a prompt diagnosis of diabetes in an acute presentation?

A
  • Capillary BG test
  • Urinalysis (glucose and ketones)
  • Blood ketones
  • to rule out DKA if presenting w symptoms in the clinic*
  • if pt. starts vomiting and appears unwell then REFER FOR DKA!!*
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72
Q

What is important in the initial management of Type 1 Diabetes?

A
  • Review by the diabetes multi-disciplinary team in the local hospital
  • Education especially diet (carbohydrate) and lifestyle
  • Insulin – administration, technique and dose
  • Home blood sugar and ketone testing
  • Hypoglycaemia management
  • if pt. appears well and is not vomiting or anything, if this is the case then REFER ASAP (after taking capillary BG)!!*
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73
Q

What are the identifying clinical features of Paget’s disease?

A
  • Old man
  • Bone pain
  • Raised ALP (alkaline phosphatase)
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74
Q

Which ribs are the kidneys behind?

A

Ribs 11 + 12

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75
Q

What is the Mirel scoring system used for and what are its parameters for “high risk”?

A
  • Assesses the need for prophylactic fixation in pts with metastatic bone tumours (due to increased risk of pathological fracture)
  • High risk of pathological fracture = score of 9 or greater: Peritrochanteric, Lytic, More than 2/3 width of bone involved, Aggravated by function
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76
Q

What is the gold-standard for measuring renal plasma flow?

A

(ie. in renal artery stenosis)

PAH clearance

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77
Q

What is the gold-standard for measuring GFR?

A

inulin clearance

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78
Q

When should you offer bisphosphonates for prevention of fragility fractures?

A
  • 10-yr fragility fracture risk score (Q-fracture (preferred) or FRAX -> ppl at high risk should be offered DXA scan
  • > 50 w a history of fragility fractures OR <40 with a major risk factor for fragility fractures -> offer DXA scan straight away w no need for risk scoring
  • If DXA shows BMD T score of < -2.5 SD = offer bisphosphonates (if no C.I) (give HRT if pre-menopausal young woman)
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79
Q

Which nerve palsy causes foot drop?

Damage to which structure causes this nerve palsy?

What dermatome levels is it composed of?

A
  • Common peroneal nerve palsy
  • Fibular neck fracture
  • L4-S2
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80
Q

Which nerve palsy causes claw hand?

Damage to which structure causes this nerve palsy?

What dermatome levels is it composed of?

A
  • Ulnar nerve palsy (also causes hyper-extended wrist)
  • Damage to medial epicondyle
  • C8, T1
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81
Q

Which nerve palsy causes carpal tunnel syndrome?

Damage to which structure causes this nerve palsy?

What dermatome levels is it composed of?

A
  • Median nerve
  • Wrist
  • C6-C8
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82
Q

Damage to which dermatomal levels causes Erb’s palsy (waiter’s tip)?

What is the characteristic sign seen in this condition?

A
  • C5-C6 (upper trunk of brachial plexus)

- arm hangs by side, internally rotated, hyper-extended wrist

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83
Q

Which nerve palsy causes wrist drop?

Damage to which structure causes this nerve palsy?

What dermatome levels is it composed of?

A
  • Radial nerve
  • Humeral mid-shaft fracture
  • C6 - C8
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84
Q

What are the most important hip abductor muscles?

A

Gluteus medius and minimus

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85
Q

What is the action of Gluteus maximus?

A
  • Main hip extensor

- External rotator

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86
Q

What does an L1 dermatome radiculopathy present with?

A
  • Reduced sensation across the inguinal area

- Reduced power in hip flexion

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87
Q

What does an L2 dermatome radiculopathy present with?

A
  • Loss of sensation across the anterior mid-thigh

- Reduced hip flexion

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88
Q

What does an L3 dermatome radiculopathy present with?

A
  • Loss of sensation over the distal anterior thigh

- Reduced power in hip flexion, and knee extension

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89
Q

What does an L4 dermatome radiculopathy present with?

A
  • Loss of sensation over the medial lower leg
  • Reduced knee extension + dorsiflexion
  • Reduced patellar reflex.
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90
Q

What does an L5 dermatome radiculopathy present with?

A
  • Weakness of hip abduction
  • Foot drop
  • (no specific reflex lost)
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91
Q

What does an S1 dermatome radiculopathy present with?

A

Numbness down the back of the leg into the outside or bottom of the foot.

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92
Q

During a hip examination, John, a 68-year-old male, is found to have a positive trendelenburg’s sign. When he stands on only his left leg, his right pelvis drops.

What muscles and nerve is affected in John?

A
  • LEFT gluteus medius and minimus
  • Superior gluteal nerve

(the LHS is not abducting and able to support the weight of the normal leg so it dips on the normal side (RHS))

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93
Q

What are the main side-effects of SGLT-2 inhibitors?

A
  • Dapagliflozin*
  • works in the PCT to prevent sodium and glucose co-transport + reabsorption*
  • Urinary and Genital infections (secondary to glycosuria): UTIs, yeast infections, Fournier’s gangrene
  • normoglycaemic Ketoacidosis
  • hypoglycaemia
  • hypotension
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94
Q

What are the identifying features of Lupus Nephritis?

A
  • urine dipstick = first line for diagnosis! -> shows proteinuria*
  • Non-specific symptoms: fatigue, arthralgia
  • more common in Women
  • Malar rash, Lymphadenopathy, discoid rash
  • histological appearance = VI different types of GN (WHO classification)
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95
Q

What are the identifying features of Acute Interstitial Nephritis ?

A
  • presents w proteinuria -> check bloods for serum creatinine!!*
  • AKI -> often due to drugs (ie. NSAIDs, allopurinol)
  • Fever and Arthralgia
  • histology = marked interstitial oedema and interstitial infiltrate between tubules
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96
Q

What are the identifying features of Anti-GBM disease (Goodpasture’s syndrome)?

A
  • presents w proteinuria -> check bloods for anti-GBM antibodies*
  • type of Vasculitis
  • Pulmonary haemorrhage
  • rapidly progressing GN
  • more common in Men
  • linear IgG deposits in the BM
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97
Q

What are the identifying features of Diabetic Nephropathy?

A
  • urine dipstick = first-line (albumin-creatinine ratio) -> raised = problematic*
  • urinary frequency
  • peripheral oedema
  • loss of appetite
  • may also be asymptomatic and picked up on screening
  • Histology = thickening of the glomerular basement membrane and mesangial matrix expansion
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98
Q

What is the arterial supply to the Adrenal glands?

Where do these vessels originate from?

A
  • Superior suprarenal artery -> Inferior Phrenic Artery
  • Middle suprarenal artery -> Aorta
  • Inferior suprarenal artery -> Renal Artery
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99
Q

Where do the Adrenal veins drain into?

A
  • RHS = IVC

- LHS = Left Renal Vein

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100
Q

What are the contents of the Antecubital Fossa from lateral to medial?

A
  • Really Need Beer To Be At My Nicest*
  • Radial Nerve
  • Biceps Tendon
  • Brachial Artery
  • Median Nerve
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101
Q

What are the superficial forearm muscles (from medial to lateral)

What do they all attach to?

A
  • F, PL, F, PT*
  • Flexor Carpi Ulnaris, Palmaris Longus, Flexor Carpi Radialis, Pronator Teres
  • nb. FDS = INTERMEDIATE forearm flexor, hence not included!*
  • Medial epicondyle of humerus
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102
Q

What nerve innervates superficial forearm flexors?

A

Median nerve

apart from Flexor Carpi Ulnaris and medial 1/2 of FDP = ulnar nerve!

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103
Q

Which enzyme is deficient in Congenital Adrenal Hyperplasia?

What are the implications of this?

A
  • 21-Hydroxylase
  • lack of Aldosterone and Cortisol production (and resultant hypoglycemia, low BP, dehydration), and ambiguous genitalia (due to increased testosterone production) -> lack of this enzyme results in compensatory Adrenal Hyperplasia to increase production of hormones it is unable to make
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104
Q

What is first line investigation for suspected Bladder cancer?

What is used for staging?

A
  • painless visible (macroscopic) haematuria!!!*
  • Flexible cystoscopy + biopsy
  • MRI pelvis (local spread), CT (distant spread)
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105
Q

What is the RIFLE Criteria for AKI?

A
  • Risk: increased creatinine 50-100% or U.O <0.5/ml/kg/hr for >6hrs
  • Injury: increased creatinine 100-200% or U.O <0.5/ml/kg/hr for >12hrs
  • Failure: increased creatinine >200% or >4mg/dL, or U.O <0.3/ml/kg/hr or anuria for >12hrs
  • Loss of function: need for Dialysis for >4 weeks
  • End-Stage Renal disease: Need for Dialysis for >3 months
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106
Q

What is the definition of Oliguria and Anuria?

A
  • Oliguria = urine output <400ml/day in adults OR <0.5ml/kg/hr in 24hrs
  • Anuria = complete lack of urine output
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107
Q

What is the Gleason score?

A

Used for grading Prostate cancer (5 stages)

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108
Q

How do you diagnose Prostate cancer?

What is used for staging?

A
  • History: Asymptomatic, LUTS (nocturia, hesitancy, poor stream, terminal dribbling, or obstruction), weight loss, +/-bone pain (mets)
  • DRE: hard, irregular prostate
  • Bloods: increased PSA (used for monitoring!)
  • Imaging (gold-standard): TRUS-guided biopsy
  • Staging: pelvic MRI
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109
Q

What is the most common male cancer?

A

Prostate cancer

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110
Q

What is the identifying clinical features of a rotator cuff injury?

A
  • Pain on abduction:
    (rotator cuff tear = first 60 degrees,
    shoulder/subacromial impingement = between 60-120 degrees)
  • Tenderness over anterior acromion
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111
Q

Which LNs are implicated in bladder cancer?

A

External and internal iliac LNs

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112
Q

What are the most common infections post-renal transplant?

A
  • CMV (first 4-6 weeks)

- EBV (>6 months)

113
Q

What are the key clinical features of spinal stenosis?

A
  • Pain is worse walking downhill, and better on walking uphill, takes a while to get better w rest
  • Sciatica
  • Neck pain (Cervical spine), or back pain (Lumbar spine)
114
Q

What are the clinical features of an inferior gluteal nerve palsy?

A
  • Gluteus maximus denervation*
  • impaired hip extension + lateral rotation
  • difficulty in rising from seated to standing position, climbing stairs
  • lurching gait
115
Q

What are the clinical features of a superior gluteal nerve palsy?

A
  • Gluteus medius, minimus + tensor fasciae latae muscle denervation*
  • impaired hip abduction
  • no sensory loss
  • may be due to: misplaced IM injection, hip surgery, pelvic fracture, posterior hip dislocation
  • positive Trendelenburg sign (!!!) (hip moves down on the opposite side of the injury)
116
Q

What are the clinical features of an tibial nerve palsy?

A
  • posterior compartment of leg*
  • impaired foot plantarflexion and inversion
  • sensory loss to sole of foot
  • not commonly injured as deep and well protected:
    popliteral lacerations, posterior knee dislocation
117
Q

What are the clinical features of an obturator nerve palsy?

A
  • medial compartment of the thigh*
  • impaired hip adduction
  • sensory loss to medial thigh
  • may be due to: anterior hip dislocation
118
Q

What are the clinical features of a common peroneal/fibular nerve palsy?

A

anterior and lateral compartments of the leg

  • impaired foot dorsiflexion and eversion
    Extensor hallucis longus
  • sensory loss to dorsum of the foot and the lower lateral part of the leg
  • injury often occurs at the neck of the fibula, tightly applied lower limb plaster cast
  • Injury causes Foot drop (!!!)
119
Q

What should you be aware of when prescribing Methotrexate?

A
  • Mucositis: inflamed gut and/or mouth
  • Myelosuppression
  • Pneumonitis
  • Pulmonary fibrosis
  • Liver fibrosis (hepatotoxic)
  • C.I during pregnancy!!! (Teratogenic) -> need to avoid pregnancy/use contraception for at least 6 months after treatment
120
Q

What nerve injury causes “sign of benediction” and what muscle is implicated?

A
  • Median nerve

- FDS - flexes the MCPs and PIPs

121
Q

What is the difference in terms of flexion and nerve innervation between FDS + FDP?

A
  • FDS = innervated by median nerve = flexes MCPs and PIPs of fingers 2-5
  • FDP = innervated by ulnar (medial 4+5) and median nerve (lateral 2+3) = flexes MCPs and IPs of fingers 2-5
122
Q

What are the boundaries of the adductor canal?

What does it contain?

A
  • Anteromedial (Roof): Sartorius
  • Posterior: Adductor Magnus, Adductor Longus
  • Lateral: Vastus medialis
  • Contents = Saphenous vein, artery and nerve
123
Q

Which pts should be assessed using FRAX or QFracture scoring system?

A
  • All men >75, all women >65
  • younger pts in the presence of risk factors: prev. fragility fracture, frequent or current use of glucorticoids (ie. pred or hydrocortisone), history of falls, FH of hip fracture, other causes of 2ndary osteoporosis, Low BMI (<18.5), smoking, alcohol intake >14 units/week
124
Q

What is the first-line treatment of scabies?

A
  • Perthmethrin 5% cream

- + clean bedding of affected persons

125
Q

What are the deep 6 lateral rotator muscles?

What are they all innervated by?

A

P-GO-GO-Q (top to bottom)

  • Piriformis, Gemellus Superior, Obturator Internus, Gemellus Inferior, Obturator Externus (covered), Quadratus Femoris
  • Sacral Plexus (L4-S2), except obturator externus which is Lumbar plexus
126
Q

What are the key features of Sjögren’s syndrome?

A
  • Female - 40-50y/o
  • dry eyes and mouth, parotid gland enlargement nb. large cheeks!!, systemic upset: fatigue, fever, myalgia, arthralgia, dry skin
  • Diagnosis = blood test: anti-Ro (SSA), anti-La (SSB) antibodies
127
Q

Which structures pass behind the medial malleolus?

A

Tom, Dick and Very Nervous Harry

  • Tibialis posterior
  • flexor Digitorum longus
  • posterior tibial Artery
  • posterior tibial Vein
  • tibial Nerve
  • flexor Hallucis longus
128
Q

What is the underlying pathology in Graves?

A

Autoimmune disease whereby antibodies to the thyroid stimulating hormone (TSH) receptor prolong stimulation -> increased thyroid hormone production from the thyroid gland (hyperthyroidism!)

129
Q

What are the key features of Erysipelas?

A
  • Elderly patient with lowered immunity (diabetes mellitus)
  • with an elevated, well-demarcated, painful rash
  • caused by S. pyogenes
  • treated by Flucloxacillin
130
Q

What is the gold-standard imaging for renal colic?

A

painful haematuria!! -> sudden onset of flank pain radiating laterally to the abdomen and/or to the groin

CT KUB!!

131
Q

What are the key clinical features of Ankylosing Spondylitis?

A
  • HLA-B27
  • Typically males between 20-30y/o -> typically presents w lower back pain and stiffness of insidious onset
  • diagnosis = x-ray findings (Sacroillitis) + one additional clinical feature: at least 3 months of lower back pain that gets better with exercise and doesn’t improve with rest (nocturnal pain, usually worse in the morning), limited movement in your lower back (lumbar spine -> positive Schober’s test), limited chest expansion compared with what is expected for age and sex
132
Q

What are the key clinical features of Osteogenesis Imperfecta?

A
  • Due to defects in Type 1 collagen
  • A child with multiple fractures, deafness and blue sclera (+ also dental problems) = osteogenesis imperfecta
  • adjusted calcium, phosphate, pTH, and ALP results are usually normal
133
Q

What are the key clinical features in Minimal change disease?

A
  • Nephrotic picture: protein (albumin) in the urine, oedema, hypoalbuminaemia
  • CHILDREN
134
Q

What are the key clinical features of Focal segmental glomerulosclerosis (FSGS)?

A
  • Nephrotic picture: protein (albumin) in the urine, oedema, hypoalbuminaemia
  • ADULTS
135
Q

What are the key clinical features of IgA nephropathy?

A
  • Nephritic picture: cellular casts, haematuria
  • during or shortly after URTI
  • confirmation of diagnosis = Kidney biopsy!!
136
Q

What are the key clinical features of Post-streptococcal GN?

A
  • Nephritic picture: cellular casts, haematuria

- a couple of weeks after a streptococcal infection (ie. pharyngitis)

137
Q

What is the difference between a Monteggia and a Galeazzi fracture?

A
  • GRIMUS -> Galleazzi = Radius, Inferior; Monteggia = Ulna, Superior*
  • Monteggia fracture = proximal ulnar dislocation -> superior ulnar dislocation (a = proximal in the alphabet, so proximal fracture)
  • Galeazzi fracture = distal radial dislocation -> inferior dislocation of distal radioulnar joint (z = distal in the alphabet, so distal fracture)
138
Q

What are the key clinical features for Rheumatoid Arthritis?

A
  • Symmetric arthritis in 3+ joints, sparing the DIP joints
  • Morning stiffness lasting >30 minutes -> symptoms improve with exercise/weight bearing as the day progresses
  • Can be diagnosed based on clinical features with support from serological testing (positive ACPA or RF)
  • X-ray may reveal periarticular osteopenia, marginal bony erosions, and joint space narrowing
  • Biopsy of the rheumatoid nodules showing cholesterol deposits is pathognomonic for RA.
139
Q

What are the key clinical features for Reactive Arthritis?

A
  • Characterised by a triad of conjunctivitis, urethritis, and arthritis, with patients often also having diarrhoea
  • usually develops 2-4 weeks after a genitourinary (GU) or gastrointestinal (GI) infection
  • Patients can also develop keratoderma blennorhagicum (hyperkeratotic vesicles on the palms and soles).
140
Q

What are the key clinical features for Septic Arthritis?

A
  • Classically presents as a single red, swollen, and painful joint, with fever
  • Invasion of the synovial membrane which produces a yellow, turbid synovial fluid with high neutrophils.
  • This is most commonly found with infection by Staphylococcus aureus
  • Joint aspiration BEFORE initiating antibiotics!!
141
Q

What are the key clinical features for Osteoarthritis?

A
  • Shorter duration of morning stiffness (<30 minutes), or not there in the mornings - worsens with exercise/weight bearing throughout the day
  • due to cartilage loss
  • Features of OA on x-ray include loss of joint space, osteophytes, subchondral sclerosis and subchondral cysts.
142
Q

What are the key clinical features for Psoriatic Arthritis?

A
  • Usually occurs in patients with a history of psoriasis, although joint symptoms may precede skin involvement
  • Can be symmetric or asymmetric: usually affects the DIP joints (spares MCP joints, unlike RA)
  • swelling in one or more joints
  • feels worse when you get up after a rest and lasts longer than 30 minutes.
  • It is associated with ‘sausage’ digits (dactylitis) and nail changes (pitting), enthesitis, eye disease (conjunctivitis, anterior uveitis)
  • seronegative spondyloarthropathy (males): back stiffness, sacroiliitis, atlanto-axial joint involvement
  • X-ray classically depicts a ‘pencil-in-cup’ deformity.
143
Q

What are the key clinical features of acute compartment syndrome?

A
  • severe pain shortly after having a cast applied!! - doesn’t respond to morphine
  • REMOVE CAST FIRST - then notify the orthopaedic surgeon and theatre team for EMERGENCY FASCIOTOMY
  • If chronic exertional compartment syndrome: 5 P’s (pain, pallor, pulseless, paraesthesia, paralysis -> gold standard for diagnosis is compartment pressure testing (>40mmHg = diagnostic)
144
Q

How to treat a hypoglycaemic episode?

A
  • usually below 4mmol/l*
  • If alert: quick-acting oral glucose (ie. glucogel, sweeties, orange juice)
  • If unconscious or unable to swallow: I/M or S/C glucagon
145
Q

What is the first line investigation for Conn’s syndrome?

What would be the next investigation and why would you do it?

Then what would you do and why?

What is the treatment?

A
  • Raised BP, hypernatraemia, hypokalaemia*
  • Renin-Aldosterone ratio -> Aldosterone raised and Renin low bc of negative feedback
  • To differentiate between a unilateral adenoma and a bilateral adrenal hyperplasion: High resolution CT Abdomen - if that is inconclusive: AVS sampling
  • Treatment: Unilateral adrenal adenoma: surgery, bilateral adrenal hyperplasia: aldosterone antagonist e.g. spironolactone
146
Q

What is the first line investigation for Conn’s syndrome?

What would be the next investigation and why would you do it?

Then what would you do and why?

What is the treatment?

A
  • Raised BP, hypernatraemia, hypokalaemia*
  • Renin-Aldosterone ratio -> Aldosterone raised and Renin low bc of negative feedback
  • To differentiate between a unilateral adenoma and a bilateral adrenal hyperplasion: High resolution CT Abdomen - if that is inconclusive: AVS sampling
  • Treatment: Unilateral adrenal adenoma: surgery, Bilateral adrenal hyperplasia: aldosterone antagonist e.g. spironolactone
147
Q

What is the first line investigation for Conn’s syndrome?

What would be the next investigation and why would you do it?

Then what would you do and why?

What is the treatment?

A
  • Raised BP, hypernatraemia, hypokalaemia*
  • First-line = Renin-Aldosterone ratio -> Aldosterone raised and Renin low bc of negative feedback
  • To differentiate between a unilateral adenoma and a bilateral adrenal hyperplasia: High resolution CT Abdomen - if that is inconclusive: AVS sampling
  • Treatment: Unilateral adrenal adenoma: surgery (most common cause), Bilateral adrenal hyperplasia: aldosterone antagonist e.g. spironolactone
148
Q

What are the clinical features of Pseudogout vs. Gout?

How do you make a diagnosis of Pseudogout vs. Gout?

How are they both treated?

A
  • CLINICAL FEATURES:
  • > Both: intermittent sudden episodes of painful, warm and red joints with swelling - usually affecting one joint
  • > Pseudogout: >60, hx of hyperparathyroidism or haemachromatosis, commonly affects knee, then wrist
  • > Gout: hx of kidney disease, family history, obesity, alcohol intake and certain medications, typically lasts 3-7 days: starts w big toe
  • DIAGNOSIS (diagnosis is usually clinical, but if in doubt or worry of septic arthritis): Arthrocentesis + Light microscopy
  • > Pseudogout: calcium pyrophosphate dihydrate crystal deposition -> weakly-positively birefringent rhomboid-shaped crystals
  • > Gout: uric acid crystal deposition -> negatively-birefringent needle-shaped crystals
  • TREATMENT: acute = NSAIDs, colchicine, pred; long-term prevention (if severe or repeated attacks) = Allopurinol, Febuxostat
149
Q

Which muscles form the Pes Ansinerus?

A
  • Medial thigh insertion*
  • STG*
  • Sartorius
  • Gracilis
  • Semitendinosus
150
Q

What are the key features of De Quervain’s Tenosynovitis?

A
  • Typically affects females 30-50y/o
  • Affects Extensor pollicis brevis and abductor pollicis longus tendons
  • Pain on radial side of wrist - worse on thumb abduction
  • Positive Finklestein test
  • Treatment = conservative (heat or ice to affected area, analgesia (NSAIDs), thumb splint)
151
Q

Describe the classification of Growth Plate fractures

A
  • Uses Sam-Harris system*
  • Type I = Fracture through the physis only (x-ray often normal)
  • Type II = Fracture through the physis and metaphysis (most common)
  • Type III = Fracture through the physis and epiphyisis to include the joint
  • Type IV = Fracture involving the physis, metaphysis and epiphysis
  • Type V = Crush injury involving the physis (x-ray may resemble type I, and appear normal) (uncommon)
152
Q

Describe the classification of Growth Plate fractures

A
  • Uses Sam-Harris system*
  • Type I = Fracture through the physis only (x-ray often normal)
  • Type II = Fracture through the physis and metaphysis (most common)
  • Type III = Fracture through the physis and epiphyisis to include the joint
  • Type IV = Fracture involving the physis, metaphysis and epiphysis
  • Type V = Crush injury involving the physis (x-ray may resemble type I, and appear normal) (uncommon)
153
Q

What are causes of a raised PSA (that is not prostate cancer)?

A
  • BPH
  • Prostatitis, UTI (NICE recommend to postpone the PSA test for at least 1 month after treatment)
  • Ejaculation (ideally not in the previous 48 hours)
  • Vigorous exercise (ideally not in the previous 48 hours)
  • Urinary retention
  • Instrumentation of the urinary tract (ie. catheter, cytoscopy, irrigation)
154
Q

What is 1st line treatment of BPH?

A

Alpha blockers! (Doxazosin)

155
Q

What is the most common cause of hydronephrosis in the newborn?

A
  • Unilateral = PUJ obstruction + VUR

- Bilateral = posterior urethral valves

156
Q

What are the key features of Membranous GN?

A
  • presents with Nephrotic syndrome (proteinuria)
  • idioptahic: due to antiphospholipase A2 antibodies
  • Renal Biopsy: thickened basement membrane, sub-epithelial spikes
  • Treatment: ACEIs or ARBs
157
Q

How do you diagnose Prostate cancer?

A
  • DRE and PSA testing
  • then TRUS + biopsy
  • MRI/CT and bone scan for staging
158
Q

What scoring system is used for determining prognosis of prostate cancer?

A

Gleason score

(two grades awarded: 1 for most dominant grade (on scale of 1-5) and 2 for second most dominant grade (scale 1-5). The two added together give the Gleason score. Where 2 is best prognosis and 10 the worst - nb. a score of 4 and 3 = 7 has a worse prognosis than 3 + 4 = 7)

159
Q

Which zone of the prostate is most affected by cancer?

A

Peripheral zone

largest part of prostate gland - causes 80% of cancers

160
Q

Why does inadequate insulin cause hyperkalaemia?

A

Bc insulin activates the Na+/K+ pump (glucose requires secondary active transport to get into cells)

Therefore if there is no insulin, then there is a reduction in the Na+/K+ pump and hyperkalaemia

161
Q

What are the blood test results for primary, secondary and tertiary hyperparathyroidism?

A
  • Primary = high PTH, high Ca2+, low phosphate -> usually due to parathyroid adenoma
  • Secondary = high PTH, low or normal Ca2+, elevated phosphate, low Vit D -> usually due to chronic renal failure (kidneys cannot excrete phosphate)
  • Tertiary = normal or high Ca2+, elevated PTH, decreased or normal phosphate, normal or decreased Vit D, raised ALP -> usually occurs due to secondary hyperparathyrodism (due to chronic renal failure) occurring for a long period of time, and parathyroid glands hypertrophy to try to raise Ca2+ levels (leading to chronically elevated PTH)
162
Q

What are the key characteristics of a Colle’s Fracture?

A
  • Classically, a fall onto an outstretched hand
  • XR shows: dinner fork deformity
  • Fracture of distal radius with posterior displacement of distal fragment
163
Q

What drugs should be stopped in AKI?

A
  • NSAIDs (ie. aspirin, ibruprofen, naproxen)
  • Aminoglycosides (ie. gentamicin)
  • ACEIs
  • Diuretics
  • Metformin
  • Lithium
  • Digoxin
164
Q

What are the diagnostic tests for suspected AKI?

A
  • U+Es: (creatinine (!!!), Na+, K+, urea)
  • Clinical Features:
  • > a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
  • > a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
  • > a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults
  • Urinalysis
  • Renal US (if no cause for deterioration is found and pt. is at risk of urinary tract obstruction)
165
Q

What are the pre-renal, intrinsic, and post-renal causes of AKI?

A
  • Pre-renal: loss of blood flow to kidneys
  • > Hypovolaemia secondary to D+V
  • > Renal artery stenosis
  • Intrinsic:
  • > GN
  • > ATN
  • > AIN
  • > Rhabdomyolysis
  • > TLS
  • Post-renal:
  • > kidney stone in ureter or bladder
  • > BPH
  • > external compression of ureter
166
Q

What is the treatment of AKI?

A
  • Involves fluid resuscitation, avoidance of nephrotoxic medications and contrast media exposure, and correction of electrolyte imbalances*
  • Stop precipitating drugs!!: NSAIDs (ie. aspirin, ibruprofen, naproxen), Aminoglycosides (ie. gentamicin), ACEIs, Diuretics, Metformin, Lithium, Digoxin
  • Stabilisation of the cardiac membrane: IV calcium gluconate
  • Short-term shift in K+ from extracellular to intracellular fluid compartment:
  • > combined insulin/dextrose infusion
  • > nebulised salbutamol
  • Removal of K+ from the body: Calcium resonium (orally or enema), Loop diuretics, Dialysis
167
Q

Key Features of Thyroid cancer:

  • Papillary?
  • Follicular?
  • Medullary?
  • Anaplastic?
  • Lymphoma?
A
  • Papillary 70% (MOST COMMON) Often young females - excellent prognosis
  • Follicular 20%
  • Medullary 5% Cancer of parafollicular (C) cells, secrete calcitonin, part of MEN-2
  • Anaplastic 1% Not responsive to treatment, can cause pressure symptoms
  • Lymphoma Rare Associated with Hashimoto’s thyroiditis
168
Q

Why does Addison’s cause metabolic acidosis?

A
  • Bc Addisons causes a decrease in Na+ (low bp) and increase in K+
  • Hyperkalaemia and high H+ levels seem to go hand-in-hand with each other -> (bc Na+ is exchanged with both K+ and H++ out of the body, so if it is low, then both K+ and H+ would be high bc they’re not being exhanged) -> metabolic acidosis
169
Q

What splits up the Sciatic foramen?

What are the contents of the Greater and the Lesser Sciatic foramen?

A
  • Piriformis
  • Greater Sciatic foramen = Superior Gluteal Vein, Artery and Nerve
  • Lesser Sciatic foramen = Inferior Gluteal Artery and Vein, Sciatic Nerve
170
Q

How to differentiate between OA and RA?

A
  • OA = morning stiffness <30 mins, gets worse w activity, unilateral symptoms, affecting mainly weight-bearing joints, PIP + DIP joints, more common in the elderly, equal incidence between the sexes
  • RA = morning stiffness >30 mins, improves w activity, bilateral symmetric symptoms in 3+ joints, affects MCP + PIP joints (spares the DIP joints!!), possible systemic features (ie. raynaud’s), occurs in adults of all ages, incidence mainly in females
171
Q

Which cancers are implicated in the hereditary condition MEN2?

A
  • Multiple Endocrine Neoplasia 2*
  • Medullary thyroid cancer
  • Parathyroid tumour
  • Phaeochromocytoma
172
Q

Which test is used to assess the rupture of the collateral ligaments of the knee?

A

Drawer test

173
Q

Where do gonadal (testicular and ovarian) veins drain into?

A
  • Left = Left renal vein

- Right = IVC

174
Q

Which is the most sensitive diagnostic test for diagnosing SLE?

A

ANA test (blood test)

175
Q

What type of Hypersensitivity reaction is SLE?

A

Type 3 HS

Immune-Complex mediated

176
Q

Where is the majority of filtered water re-absorbed in the nephron?

A

PCT (70%)

177
Q

What is the first line treatment of DKA?

A
  • IV fluid replacement
  • followed by IV insulin
  • patients who normally take long-acting insulin should continue their usual dose(s) throughout treatment.
178
Q

What is the first line treatment of DKA?

A
  • IV fluid replacement (!!!)
  • followed by IV insulin (!!!)
  • patients who normally take long-acting insulin should continue their usual dose(s) throughout treatment.
179
Q

What is the first line treatment of DKA?

A
  • IV fluid replacement (!!!)
  • followed by IV insulin (!!!)
  • patients who normally take long-acting insulin should continue their usual dose(s) throughout treatment.
180
Q

What is the difference between MEN type I and type II?

A
  • Type I = 3 Ps: Parathyroid (hyperparathyroidism), Pituitary, Pancreas
  • Type II = 2 Ps: Medullary thyroid cancer, Parathyroid, Phaeochromocytoma
181
Q

What is the difference between MEN type I and type II?

A
  • Type I = 3 Ps: Parathyroid (hyperparathyroidism), Pituitary, Pancreas
  • Type II = 2 Ps: Medullary thyroid cancer, Parathyroid, Phaeochromocytoma
182
Q

When would u give meds for HT?

What would u give first line?

A
  • BP of >140/90 on 2 occasions
    (double-check BP if it is >140/90 in clinic)
  • <55 of any family origin or Type 2 diabetic: ACEIs or ARBs
  • > 55 or Black: CCBs
183
Q

Which ligament is most likely damaged in ankle sprains?

A
  • Anterior Talofibular ligament (ATFL) -> “Always Tears First”
  • resists inversion, so therefore pt. presents with inversion injuries
184
Q

What effect do NSAIDs have on the Kidneys?

A
  • inhibit COX-1 and COX-2 enzymes -> reducing prostaglandin production
  • prostaglandins are responsible for afferent arteriole vasodilation and increasing GFR
  • therefore, NSAIDs block afferent arteriole vasodilation and decrease renal blood flow and GFR
185
Q

What is the most common causative organism in Osteomyelitis?

What about in sickle-cell anaemia?

A
  • Staph Aureus

- Salmonella

186
Q

What is the first line management of Osteomyelitis?

A
  • Bone aspiration/biopsy THEN

- IV abx

187
Q

What type of HS reactions are responsible for renal graft failure?

  • hyperacute (early acute)? (minutes to hours)
  • acute graft failure (<6 months) (late acute)?
A
  • Type 2 HS: antibodies against graft

- Type 4 HS: cytotoxic T-cell mediated (or CMV-mediated)

188
Q

Muscles of the Foot:

Muscle, Origin, Insertion, Nerve supply, Action

A
  • Abductor hallucis:
  • Medial side of the calcaneus, flexor retinaculum, plantar aponeurosis
  • Medial side of the base of the proximal phalanx Medial plantar nerve
  • Abducts the great toe
  • Flexor digitorum brevis:
  • Medial process of the calcaneus, plantar aponeurosis
  • Via 4 tendons into the middle phalanges of the lateral 4 toes.
  • Medial plantar nerve
  • Flexes all the joints of the lateral 4 toes except for the interphalangeal joint.
  • Abductor digit minimi:
  • From the tubercle of the calcaneus and from the plantar aponeurosis
  • Together with flexor digit minimi brevis into the lateral side of the base of the proximal phalanx of the little toe
  • Lateral plantar nerve
  • Abducts the little toe at the metatarsophalangeal joint
  • Flexor hallucis brevis:
  • From the medial side of the plantar surface of the cuboid bone, from the adjacent part of the lateral cuneiform bone and from the tendon of tibialis posterior.
  • Into the proximal phalanx of the great toe, the tendon contains a sesamoid bone
  • Medial plantar nerve
  • Flexes the metatarsophalangeal joint of the great toe.
  • Adductor hallucis:
  • Arises from two heads.
  • The oblique head arises from the sheath of the peroneus longus tendon, and from the plantar surfaces of the bases of the 2nd, 3rd and 4th metatarsal bones.
  • The transverse head arises from the plantar surface of the lateral 4 metatarsophalangeal joints and from the deep transverse metatarsal ligament. Lateral side of the base of the proximal phalanx of the great toe.
  • Lateral plantar nerve
  • Adducts the great toe towards the second toe. Helps maintain the transverse arch of the foot.
  • Extensor digitorum brevis
  • On the dorsal surface of the foot from the upper surface of the calcaneus and its associated fascia
  • Via four thin tendons which run forward and medially to be inserted into the medial four toes. The lateral three tendons join with hoods of extensor digitorum longus.
  • Deep peroneal
  • Extend the metatarsophalangeal joint of the medial four toes. It is unable to extend the interphalangeal joint without the assistance of the lumbrical muscles.
189
Q

Arches of the Foot

A

2 longitudinal arches, 1 transverse arch:

  • Longitudinal arches:
  • > Medial: longitudinal arch is higher on the medial than on the lateral side. The posterior part of the calcaneum forms a posterior pillar to support the arch. The anterior pillar of the medial arch is composed of the navicular bone, the three cuneiforms and the medial three metatarsal bones.
  • > Lateral: The lateral part of this structure passes via the cuboid bone and the lateral two metatarsal bones. The medial part of this structure is more important. The head of the talus marks the summit of this arch, located between the sustentaculum tali and the navicular bone.
  • Transverse arch: The transverse arch is situated on the anterior part of the tarsus and the posterior part of the metatarsus. The cuneiforms and metatarsal bases narrow inferiorly, which contributes to the shape of the arch.
190
Q

What would a patient’s water deprivation test show before and after being given Desmopressin if they had a …

  • Cranial DI?
  • Nephrogenic DI?
A
  • Cranial DI: low urine osmolality before desmopressin, high urine osmolality after desmopressin
  • Nephrogenic DI: low plasma osmolality before and after desmopressin
191
Q

What is the clearance of a substance at the Kidneys dependent on?

A

It’s diffusivity across the basement membrane and it’s tubular secretion/reabsorption

192
Q

What are the key clinical features of Frozen shoulder/Adhesive Capsuliits?

A
  • Most common in middle-aged females, diabetics
  • Features typically develop over days
  • External rotation is affected more than internal rotation or abduction
  • Both active and passive movement is affected
  • Patients typically have a painful freezing phase, an adhesive phase and a recovery phase
  • Bilateral in up to 20% of patient
  • The episode typically lasts between 6 months and 2 years
  • Treatment = conservative (NSAIDs, physiotherapy, oral corticosteroids and intra-articular corticosteroids)
193
Q

What is Sheehan’s syndrome?

A

Global Hypopituitarism present after childbirth
(agalactorrhoea (prolactin), amenorrhoea (lack of FSH, LH (gonadotropins), cold intolerance, constipation, (thyroid hormones) weight loss (steroid hormones)

194
Q

What is the first line treatment for Carpal Tunnel syndrome?

A

Conservative treatment

Wrist splints (at night), physical therapy, and/or corticosteroid injections

195
Q

What are the clinical features of Carpal Tunnel syndrome?

A
  • Pain + parasthesia in the distribution of the median nerve
  • Thenar eminence muscle wasting
  • Difficulty in performing tasks (ie. buttoning shirt, opening jars)
  • Pain relieved by hanging arm over the side of the bed
  • Phalen test + Tinel’s test positive
196
Q

Causes of Hypercalcaemia

A

CHIMPANZEES

C alcium supplementation
H yperparathyroidism
I atrogentic (Drugs: Thiazides -> remember, decreasing Na+ causes increased Ca2+ and vice-versa!)
M ilk Alkali syndrome
P aget disease of the bone
A cromegaly and Addison's Disease
N eoplasia
Z olinger-Ellison Syndrome (MEN Type I)
E xcessive Vitamin D
E xcessive Vitamin A
S arcoidosis
197
Q

Physiological actions of commonly used diuretics:

Site of action, Diuretic, Carrier or Channel inhibited, % of filtered Na+ excreted

A
  • Ascending limb of LoH -> Frusemide -> Na+/K+ 2Cl - carrier -> Up to 25%
  • DCT -> Thiazides -> Na+Cl- carrier -> Between 3 and 5%
  • > Cortical collecting tubule -> Spironolactone -> Na+/K+ ATP ase pump -> Between 1 and 2%
198
Q

What should you suspect if you see:

  1. red cell casts
  2. needle-shaped crystals
  3. rhomboid-shaped crystals

… on urine microscopy?

A
  1. Nephritic syndrome
  2. Gout
  3. Pseudogout
199
Q

THIS IS UR DAILY REMINDER TO REMEMBER THE DIFFERENCE BETWEEN CARPAL TUNNEL + CUBITAL TUNNEL SYNDROME!!!!

A
  • Carpal Tunnel = Median Nerve palsy

- CUBITAL Tunnel = Ulnar Nerve palsy (nb. CLAW HAND as well!!)

200
Q

What scoring system is used for?

A
  • BPH

- If it is =/>8 -> give alpha blockers!! (ie. tamsulosin, alfuzosin)

201
Q

What are the clinical features of SLE?

A
  • anti-ds DNA antibodies (ANA antibodies)
  • Photosensitivity
  • Malar or discoid rash
  • Pancytopenia,
  • Pleuritis
  • Nephritis
202
Q

What are the clinical features of Limited Systemic Sclerosis?

A
  • Anti-centromere antibodies (ANA antibodies)
  • CREST*
  • Calcinosis -> Ca2+ deposits in the skin
  • Raynaud’s
  • Esophageal dysfunction
  • Sclerodactyly
  • Telangiectasias
203
Q

What are the clinical features of autoimmune vaculitis?

(Granulomatosis with polyangiitis (wegener’s), eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome), microscopic polyangiitis)

A
  • proteinuria + red cell casts on urinalysis…*
  • ANCA antibodies: cANCA (wegener’s), pANCA (churg-strauss, microscopic polyangiitis) (!!!)
  • Renal impairment:
    caused by immune complex glomerulonephritis → raised creatinine, haematuria and proteinuria
  • Respiratory symptoms:
    dyspnoea
    haemoptysiis
  • Systemic symptoms:
    fatigue
    weight loss
    fever
  • Vasculitic (purpuric) rash
  • ENT symptoms:
    sinusitis
204
Q

Paediatric Orthopaedics

Diagnosis Mode of presentation Treatment Radiology

A

Developmental dysplasia of the hip Usually diagnosed in infancy by screening tests. May be bilateral, when disease is unilateral there may be leg length inequality. As disease progresses child may limp and then early onset arthritis. More common in extended breech babies. Splints and harnesses or traction. In later years osteotomy and hip realignment procedures may be needed. In arthritis a joint replacement may be needed. However, this is best deferred if possible as it will almost certainly require revision Initially no obvious change on plain films and USS gives best resolution until 3 months of age. On plain films Shentons line should form a smooth arc

Perthes Disease Hip pain (may be referred to the knee) usually occurring between 5 and 12 years of age. Bilateral disease in 20%. Remove pressure from joint to allow normal development. Physiotherapy. Usually self-limiting if diagnosed and treated promptly. X-rays will show flattened femoral head. Eventually in untreated cases the femoral head will fragment.

Slipped upper femoral epiphysis Typically seen in obese male adolescents. Pain is often referred to the knee. Limitation to internal rotation is usually seen. Knee pain is usually present 2 months prior to hip slipping. Bilateral in 20%. Bed rest and non-weight bearing. Aim to avoid avascular necrosis. If severe slippage or risk of it occurring then percutaneous pinning of the hip may be required. X-rays will show the femoral head displaced and falling inferolaterally (like a melting ice cream cone) The Southwick angle gives indication of disease severity

205
Q

Which type of collagen is primarily affected by Osteogenesis Imperfecta?

A

Type 1 collagen

206
Q

What are the commonest causes of hypercalcaemia in hospitalised and non-hospitalised pts?

A
  • Hospitalised: primary hyperparathyroidism
  • Non-hospitalised: metastatic malignancy (PTHrP ie. squamous cell carcinoma of the Lung, Breast, Renal, and Multiple Myeloma)
207
Q

What are the commonest causes of hypercalcaemia in hospitalised and non-hospitalised pts?

A
  • Hospitalised: primary hyperparathyroidism
  • Non-hospitalised: metastatic malignancy (PTHrP ie. squamous cell carcinoma of the Lung, Breast, Renal, and Multiple Myeloma)
208
Q

Which cancers commonly metastasise to the bone?

A
  • Breast
  • Prostate
  • Lung
  • Kidney
  • Thyroid
209
Q

What is the primary ketone body found in DKA?

A

Acetoacetate

210
Q

An 8-year-old boy presents to the GP following 7 days of diarrhoea which his mother mentions has been bloody since yesterday. He has abdominal pain and he is passing scant urine. His mother mentions that she has noticed several bruises but doesn’t recall any trauma. What is the most like causative organism?

A

E. Coli!!!

This is Haemolytic Uraemic Syndrome (HUS) -> produces a triad of haemolytic anaemia, thrombocytopaenia and AKI that may lead to renal failure.

211
Q

What is the first line treatment for Acromegaly?

A

Trans-sphenoidal surgery

212
Q

What are the key clinical features of Fibromyalgia?

A
  • Woman
  • between 30-50 y/o
  • Chronic pain in multiple sites - (11/18 sites)
  • lethargy, cognitive impairment: ‘fibro fog’, sleep disturbance, headaches, dizziness
213
Q

What diagnosis causes muddy brown casts on urine microscopy?

A

Acute tubular necrosis

214
Q

Which hormones drive growth through

  1. infancy? (birth-2 y/o)
  2. childhood? (3-11 y/o)
  3. puberty? (12-18)
A
  1. insulin and nutrition
    (nb. poorly-controlled diabetes during pregnancy will result in over-production of insulin by the foetus and therefore the child will be large (macrocosmic) when it comes out)
  2. GH and Thyroid hormones (lake of maternal thyroid hormones results in infantile features (+ developmental delay of foetus), and suppressed growth regardless of GH status)
  3. GH + Sex steroids
215
Q

What is the role of the Macula Densa?

A
  • Present at the point where the thick ascending limb of the Loop of Henle meets the DCT
  • Acts as chemoreceptors -> detects the conc. of NaCl (which reflects BP) and adjusts GFR accordingly
  • > afferent arteriole vasoconstriction (ATP, adenosine) to reduce GFR in low BP states,
  • > or afferent arteriole vasodilation (NO) to increase GFR in high BP states
216
Q

What is the role of the Juxtaglomerular cells?

A
  • Found in the walls of the afferent arteriole

- Acts as baroreceptors to detect changes in BP and can secrete Renin

217
Q

What does increased specific gravity mean?

A

Conc. of the urine is high

218
Q

Where are the receptors for thyroid hormones?

A

In the nucleus

even though they are peptide hormones lmao -> they ACT as a steroid!

219
Q

Which muscles does the axillary nerve innervate?

A

Teres minor + Deltoid

220
Q

Which fascia contains the thyroid gland?

A

Pretracheal fascia

221
Q

Key clinical features:

hand disease

A

Dupuytren’s contracture, more common in older male, affects palmar fascia mainly of 4th and 5th finger. As it progresses, nodules and cord develop in the palmar fascia resulting in flexion at MCP + PIP joints - most commonly affects ring finger, little finger - manual labourers, Men

Trigger finger causes stiffness, pain and locking sensation when flexing or therefore difficulty extending it.

Ganglion cyst also known as bible cyst is usually found in the dorsal and volar aspect of the wrist and is usually soft in nature. Many cysts disappear on its own.

Flexor tendon rupture is usually due to trauma to the flexor tendon such as sports injury. It is usually acute in nature and results in acute loss of flexion in the affected finger. It usually requires surgery.

222
Q

What are the most common complications of RA?

A
  • Carpal Tunnel syndrome
  • due to widespread inflammation*
  • Lungs: pleurisy, pulmonary fibrosis
  • Heart – Pericarditis
  • Eyes – Scleritis, Sjögren’s syndrome
  • Blood vessels – Vasculitis
  • permanent joint damage, joint deformities
  • CVD
  • Cervical myelopathy
223
Q

What is the most common cause of death in RA?

A

CVD (Atherosclerosis)

224
Q

Which cancer is associated with Paget’s?

A

Osteosarcoma

225
Q

MSK - Paeds

A
  • Development dysplasia of the hip
    Often picked up on newborn examination
    Barlow’s test, Ortolani’s test are positive
    Unequal skin folds/leg length
  • Transient synovitis (irritable hip
    Typical age group = 2-10 years
    Acute hip pain associated with viral infection
    Commonest cause of hip pain in children
  • Perthes disease
    Perthes disease is a degenerative condition affecting the hip joints of children, typically between the ages of 4-8 years. It is due to avascular necrosis of the femoral head
    Perthes disease is 5 times more common in boys. Around 10% of cases are bilateral
    Features
    hip pain: develops progressively over a few weeks
    limp
    stiffness and reduced range of hip movement
    x-ray: early changes include widening of joint space, later changes include decreased femoral head size/flattening
  • Slipped upper femoral epiphysis
    Typical age group = 10-15 years
    More common in obese children and boys
    Displacement of the femoral head epiphysis postero-inferiorly
    Bilateral slip in 20% of cases
    May present acutely following trauma or more commonly with chronic, persistent symptoms
    Features
    knee or distal thigh pain is common
    loss of internal rotation of the leg in flexion
  • Juvenile idiopathic arthritis (JIA) Preferred to the older term juvenile chronic arthritis, describes arthritis occurring in someone who is less than 16 years old that lasts for more than three months. Pauciarticular JIA refers to cases where 4 or less joints are affected. It accounts for around 60% of cases of JIA
    Features of pauciarticular JIA
    joint pain and swelling: usually medium sized joints e.g. knees, ankles, elbows
    limp
    ANA may be positive in JIA - associated with anterior uveitis
  • Septic arthritis
    Acute hip pain associated with systemic upset e.g. pyrexia. Inability/severe limitation of affected joint
226
Q

Which test is the gold-standard for directly measuring renal function?

A

inulin clearance

estimates creatinine clearance/GFR

227
Q

Key clinical features of cystinuria

A
  • Recurrent kidney stones from childhood
  • Positive family history for nephrolithiasis
  • Sodium nitroprusside test positive
228
Q

What is the difference between GLUT2 and GLUT4 transporters?

A
  • GLUT 2 = insulin-independent -> found in Pancreatic beta-islet cells, Liver, Brain, Kidneys
  • GLUT 4 = insulin dependent -> adipose tissue and skeletal muscle
229
Q

What are the effects of strenuous exercise on blood glucose levels?

A
  • Early drop: due to increased glucose uptake in the muscle via GLUT-2 (which is independent of insulin)
  • Occasional rise: high-intensity sport causes release of adrenaline and cortisol which can cause blood glucose to rise temporarily, particularly during competitive sport
  • Late drop: uses muscle and liver glycogen which then is replaced over the next few hours
230
Q

What are the effects of Angiotensin II on GFR?

A
  • it maintains GFR (by increasing it) -> increases filtration fraction (even if plasma blood flow is low)
  • by vasoconstricting the efferent arteriole of the glomerulus
231
Q

Why does alcohol cause increased urinary frequency?

A

Because it suppresses ADH release from the posterior pituitary

232
Q

What are the common neoplastic syndromes of RCC?

A
  • Polycythaemia (due to erythropoeitin release)

- Hypercalcaemia (due to PTH release)

233
Q

What are anti-TPO antibodies associated with?

A

Hashimoto’s thyroiditis

234
Q

What is the principal side-effects of SGLT-2 inhibitors?

A

The gliflozins, such as empagliflozin or dapagliflozin

Recurrent UTIs

(they inhibit renal re-absorption of glucose)

235
Q

What histological finding is present in Minimal Change disease?

A

Fusion of podocytes and effacement of foot processes

236
Q

What are the key characteristics of Adhesive Capsulitis?

A
  • Reduced shoulder movements - both actively and passively

- External rotation is affected more than internal rotation or abduction.

237
Q

What are they key clinical features of Heberden’s nodes?

How do you differentiate them between Rheumatoid nodules?

A
  • OA
  • On the DIP joints (outer Hebrides -> Heberden’s nodes)
  • Asymmetrical
  • Mono or pauci-articular
  • RA = symmetrical and polyarticular
238
Q

What is the difference between Seminomas and Teratomas?

A
  • Seminomas = >40 y/o

- Teratomas = <40 y/o

239
Q

What is the normal passage of blood through the Glomerulus?

A

Afferent arteriole -> glomerular capillary bed -> efferent arteriole -> peritubular capillaries and medullary vasa recta

240
Q

What cells secrete Glucagon?

What is the function of Glucagon?

What increases and decreases its secretion?

A
  • Source: Alpha cells of the Pancreas
  • Function: Glycogenolysis, Gluconeogenesis, Lipolysis
  • Increases = hypoglycaemia, stresses, increased catecholamines + SNS stimulation, increased plasma AAs
  • Decreases = hyperglycaemia, insulin, somatostatin, increased FFAs and keto acids
241
Q

Which zone of the prostate is affected by BPH?

What about prostate cancer?

A
  • BPH = Transitional zone

- Prostate cancer = Peripheral zone

242
Q

Which serum electrolyte should you check in hypocalcaemia which is refractory to treatment with calcium and vitamin D supplementation?

A

Magnesium

Hypomagnesaemia may cause hypocalcaemia which will not be corrected until you correct the magnesium levels!

243
Q

What causes Rickets?

A
  • Reduced Vit D
    (nb. malnourished pts)
  • causes excessive non-mineralised osteoid
    (need Ca2+ for mineralisation)
244
Q

What type of joint is the wrist joint?

A

Synovial condyloid

245
Q

Treatment of hip fractures

A

-> Intracapsular hip fracture
- Undisplaced Fracture:
internal fixation, or hemiarthroplasty if unfit.
- Displaced Fracture:
NICE recommend replacement arthroplasty (total hip replacement or hemiarthroplasty) to all patients with a displaced intracapsular hip fracture
total hip replacement is favoured to hemiarthroplasty if patients:
were able to walk independently out of doors with no more than the use of a stick and
are not cognitively impaired and
are medically fit for anaesthesia and the procedure.

-> Extracapsular hip fracture:
Management
stable intertrochanteric fractures: dynamic hip screw
if reverse oblique, transverse or subtrochanteric fractures: intramedullary device

246
Q

MOA Diabetes drugs

A

Sitagliptin is an inhibitor of the enzyme dipeptidyl-peptidase 4 (DPP-4). As such, it prevents DPP-4 from catalysing the breakdown of naturally occurring incretins, potentiating their ability to stimulate insulin release.

Activate peroxisome proliferator-activated receptor gamma (PPAR-γ) to increase insulin sensitivity is incorrect. This is the mechanism by which thiazolidinediones such as pioglitazone reduce blood glucose.

Decrease blood glucose by inhibiting renal glucose re-uptake via sodium-glucose co-transporter 2( SGLT2) is incorrect. This describes the mechanism of action of SGLT2 inhibitors such as dapagliflozin.

Mimic incretins by binding to GLP-1 receptors and stimulating insulin release is incorrect. This is how GLP-1 receptor agonists such as exenatide promote insulin release and lower blood glucose.

Trigger the closure of ATP-sensitive K+ channels, stimulating insulin exocytosis is incorrect as this is the mechanism of action of sulfonylureas such as glibenclamide, rather than DPP-4 inhibitors.

247
Q

Which bone is affected in a Boxer fracture?

A

5th Metacarpal

occurs after punching a wall/hard surface

248
Q

Flexor tendon injury common cause

A

Prying apart frozen hamburgers

249
Q

Thyroid disease

A

This patient presented with a one-month history of the signs and symptoms the most consistent with a clinical diagnosis of hypothyroidism. She had low mood, weight gain, round puffy face and a low heart rate and blood pressure. The most common cause of clinical hypothyroidism in the developed world is Hashimoto’s thyroiditis.

1: This characterizes Hashimoto’s thyroiditis. This is an autoimmune condition more common women and is certain populations (Japanese). It usually presents in the elderly and is associated with HLA-DR3, 4 and 5 polymorphisms.
2: This will be present in subacute thyroiditis (De Quervain’s thyroiditis). This is usually a painful condition, often occurs following a viral infection and is more common in women. It can also be accompanied by a sore throat. The patient can present with hyperthyroidism in the early phase of the disease and then progress to hypothyroidism.
3: This describes a thyroid condition known as Riedel’s thyroiditis. Patients with this condition present with hypothyroidism and on examination have a hard, non-tender, asymmetric mass fixed to the underlying tissue in the thyroid region. Patients are often investigation for a possible thyroid malignancy due to the characteristics of the mass.
4: This will be present in multinodular goitres. These can be nontoxic or toxic. A toxic multinodular goitre functions autonomously in producing thyroid hormones and therefore produces signs and symptoms of hyperthyroidism.
5: This pathology is characteristic of papillary carcinoma of the thyroid. It is the most common carcinoma of the thyroid and has the best prognosis compared to the other types which are follicular, medullary and anaplastic.

250
Q

What percentage of patients with a raised PSA level (relative to their age) do not have prostate cancer?

A

75%

251
Q

Body fluid volumes:

Compartment -> Volume in litres -> Percentage of total volume

A
  • 70 Kg male = 42 L water (60% of total body weight)*
  • Intracellular -> 28 L -> 60-65%
  • Extracellular -> 14 L -> 35-40%
  • Plasma -> 3 L -> 5%
  • Interstitial -> 10 L -> 24%
  • Transcellular -> 1 L -> 3%
252
Q

What is the normal angle between the femoral neck and the femoral shaft?

A

130 degrees

any changes to this angle may occur due to a disease or pathology and should be investigated

253
Q

What humeral structure articulates with the head of the radius and the head of the ulna?

A
  • Radius = Capitulum

- Ulna = Trochlea

254
Q

What are anti-Jo-1 antibodies associated with?

A

Dermatomyositosis

  • (also seen: muscle weakness, muscle pains and a skin rash (heliotropic: purple))
255
Q

What position would the leg be in a posterior dislocation?

What about an anterior dislocation?

A
  • Leg is INTERNALLY ROTATED with posterior hip dislocation

- but EXTERNALLY ROTATED with anterior hip dislocations

256
Q

Risk factors for Rheumatoid Arthritis

A
  • Peak onset 30-50 yrs (but can occur in all ages)
  • More common in Females (3:1)
  • Native American
  • Associated with HLA-DR4
257
Q

Which blood vessel mainly supplies the femoral head?

A

Medial and lateral femoral circumflex arteries

branches of profunda femoris

258
Q

Which virus is most implicated in viral warts?

A

HPV

259
Q

What are the different Type 2DM medications?

A 
sulphonylureas
metformin
alpha-glucosidase inhibitors (acarbose)
glitazones
insulin
260
Q

Which bacteria causes staghorn calculi?

A

Proteus Miribalis

261
Q

What is the Z score?

How do u interpret results?

A
  • The Z score is a comparison of a person’s bone density with that of an average person of the same age, sex, and ethnic background
  • > -1.0 = normal
    -1.0 to -2.5 = osteopaenia
    < -2.5 = osteoporosis
262
Q

What is the first line treatment of scabies

A

excoriation marks, burrows, ink test

Permethrin 5%

263
Q

Histological findings kidney disease

A
  1. Glomerular hypertrophy will be seen in acute post-streptococcal glomerulonephritis.
  2. In IgA nephropathy, there is a proliferation of the mesangial cells.
  3. Deposits of immune complex in the mesangial cells are present in IgA nephropathy but can only be seen with electron microscopy.
  4. Thickening of the glomerular basement membrane occurs in diabetic nephropathy or membranous nephropathy, which are both types of nephrotic syndrome.
  5. In diabetic nephropathy, there is an expansion of the mesangial matrix.
264
Q

What are the characteristic radiological findings for Calcium Oxalate stones?

A

Envelope-shaped crystals

265
Q

How do you prevent lipodystrophy (as a side-effect of Insulin)?

A
  • typically presents as atrophy/lumps of subcutaneous fat
  • can be prevented by rotating the injection site
  • may cause eractic insulin absorption
266
Q

Where is Renin, ACE and Angiotensinogen released from?

A
  • Renin = JG cells of Kidneys
  • ACE = Lungs
  • Angiotensinogen = Liver
267
Q

What are the associations with Hashimoto’s?

A
  • anti-TPO antibodies
  • firm, non-tender goiter
  • other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo
  • MALT lymphoma
268
Q

Which test is used to confirm the diagnosis of Addison’s?

A

A short synacthen test

synthetic ACTH

269
Q

Which tests confirm a diagnosis of Cushing’s?

A
  • 24-hour urinary free-cortisol test (!!)

- Low-dose dexamethasone suppression test

270
Q

What are the effects of PTH on Vit D to increase Ca2+ levels?

A

PTH increases the activity of 1-α-hydroxylase enzyme, which converts 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol, the active form of vitamin D (at the Kidneys) -> increases Ca2+ absorption in the intestines

271
Q

What are the histological findings for diabetic nephropathy?

A

Kimmelstiel-Wilson lesions (!!!)

nodular glomerulosclerosis

272
Q

What percentage of men with a raised PSA have prostate cancer?

A

25% (1 in 4)

273
Q

What condition is associated with Giant Cell Arteritis?

A

Polymyalgia Rheumatica

274
Q

Anti-diabetic drugs mechanisms of action

A
  • Biguanides
    e. g. Metformin
  • Increase peripheral insulin sensitivity and hepatic glucose uptake.
    Sulfonylureas
    e.g. Gliclazide
  • Depolarise islet cells in the pancreas increasing insulin release.
    Thiazolidinediones
    e.g. Pioglitazone
  • Increase peripheral insulin sensitivity.
    SGLT2 Inhibitors
    e.g. Dapgliflozin
  • Increase urinary glucose loss.
    DPP4-Inhibitors
    e.g. Sitagliptin
  • Inhibit GLP1 breakdown.
    GLP1 Analogues
    e.g. Exenatide
    Increase insulin secretion and sensitivity.
  • Intestinal Alpha-Glucosidase Inhibitors
    e.g. Acarbose
    Delay intestinal carbohydrate absorption
275
Q

What is the treatment for Cellulitis and Erysipelas?

A

IV benzylpenicillin and fluclox

clindamycin if penicillin allergy

276
Q

What is the treatment of Minimal Change disease?

A

Give steroids!!

277
Q

Clinical features of Nephrotic syndrome

A
  • Systemic Disease:
    Diabetes Mellitus (Glomerulosclerosis)
    Systemic Lupus Erythematosus (Membranous)
    Amyloidosis
  • Minimal Change Glomerulonephritis
    Associated with upper respiratory tract infection
    Biopsy: normal light microscopy, fusion of podocytes on electron microscope
    Treat with steroids
    1% go on to have end-stage renal failure
  • Membranous nephropathy
    Associated with cancers (Lung, Colon Breast), inflammatory conditions (SLE, thyroid disease), infections (Hepatitis B) and drugs (Penicillamine and Gold)
    Biopsy: subepithelial immune complex deposits
    40% have spontaneous remission
  • Focal segmental glomerulosclerosis
    More common in Afro-caribbean population
    Associated with Berger’s disease, sickle cell, HIV
    Biopsy: focal scarring, IgM deposition
    Treat with steroids or cylophosphamide/ciclosporin
    30-50% progress to end stage renal failure

-Membranoproliferative/Mesangiocapillary
Less common
May present as both nephrotic or nephritic
Associated with Hepatitis B, Hepatitis C and Endocarditis
50% progress to End-Stage Renal Failure

278
Q

How does Macula Densa control GFR in times of high Renal Blood Flow (RBF)?

A
  • Increased RBF (due to increased BP) means there is an increase in water and Na+ coming to the Macula Densa and increased GFR is happening
  • Therefore, to prevent this excess GFR from happening, the Macula Densa will vasoconstrict the afferent arterioles so that GFR will decrease and return back to normal
  • it’s role is to essentially maintain GFR within normal limits, independent of BP (it works even in an isolated kidney!*
279
Q

What are the indications for surgery and surgical management of Dupuytren’s contractures?

A

Indications for surgery:

  • Functional impairment
  • MCP joint contracture > 30 degrees
  • Any PIP contracture
  • Rapidly progressive disease

Surgical management:
- Fasciectomy with Z-shaped scar

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