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Make a Medic Finals Deck > PSA Passmed Stuff > Flashcards

PSA Passmed Stuff Flashcards

1
Q

Malignancy causing SIADH

A

Small cell lung cancer
(also: pancreas +prostate)

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2
Q

4 Neurological causes of SIADH

A

Stroke
SAH
SDH
Meningitis/ encephalitis/ abscess

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3
Q

2 Infectious causes of SIADH

A

TB
Pneumonia

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4
Q

6 Drug causes of SIADH

A

Sulfonylureas
SSRIs
TCAs
Carbamezapine
Vincristine
Cyclophosphamide

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5
Q

Which sulfonylureas cause SIADH?

A

Glimepiride
Glipizide

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6
Q

2 other causes of SIADH

A

Positive end-expiratory pressure (PEEP)
Porphyrias

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7
Q

What are the investigations for SIADH?

A

Urine osmolality: HIGH
Serum osmolality: LOW
(inappropriate as kidneys should dilute urine when serum osmolality is low)
Urine sodium: HIGH (due to action of ADH on renal tubules)

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8
Q

Describe management of SIADH

A

Correct slowly to avoid precipitating central pontine myelinolysis
Fluid restriction
Demeclocycline: reduces responsiveness of the collecting tubule cells to ADH

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9
Q

In which patients requiring fluid should glucose be avoided?

A

Stroke patients (non-hypoglycaemic)
Due to increased risk cerebral oedema
Prescribe normal saline if rehydration required

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10
Q

What are the maintenance fluid requirements?

A

25-30 ml/kg/day of water
+
~1 mmol/kg/day of potassium, sodium + chloride
+
~50-100 g/day of glucose to limit starvation ketosis

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11
Q

Describe maintenance fluid requirements for an 80kg patient

A

2L water
80 mmol potassium

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12
Q

Describe the electrolyte contents of 0.9% saline

A

Na+: 154 mmol
Cl-: 154 mmol

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13
Q

What does 5% glucose contain?

A

50g glucose

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14
Q

Describe the contents of Hartmann’s solution

A

Na+: 131
Cl-: 111
K+: 5
HCO3-: 29

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15
Q

What is the risk of using large volumes 0.9% saline?

A

Hyperchloraemic metabolic acidosis

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16
Q

In which patients should Hartmann’s not be used? Why?

A

Hyperkalaemic patients
Hartmann’s contains potassium

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17
Q

List 6 drugs that can cause impaired glucose tolerance

A

Diuretics
Steroids
Immunosuppressants
Interferon-alpha
Nicotinic acid
Antipsychotics

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18
Q

Which diuretics are cause impaired glucose tolerance?

A

Thiazides
Furosemide (less common)

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19
Q

Which drug can cause slight impairment of glucose tolerance?

A

B-blockers
Also use with caution in diabetics as can interfere with metabolic + autonomic responses to hypoglycaemia

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20
Q

Name 2 Immunosuppressants that cause impaired glucose tolerance

A

Tacrolimus
Ciclosporin

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21
Q

List 5 drugs that may cause urinary retention

A

TCAs e.g. amitriptyline
Anticholinergics e.g. antipsychotics, antihistamines
Opioids
NSAIDs
Disopyramide

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22
Q

List 5 drugs that can cause lung fibrosis

A

Amiodarone
Cytotoxic agents: busulphan, bleomycin
Anti-rheumatoid drugs: methotrexate, sulfasalazine
Nitrofurantoin
Ergot-derived dopamine receptor agonists (bromocriptine, cabergoline)

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23
Q

List 3 significant adverse effects which patients should be warned about when starting Allopurinol

A

Severe cutaneous adverse reaction (SCAR)
Drug reaction with eosinophilia + systemic symptoms (DRESS)
Stevens-Johnson syndrome

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24
Q

List 3 ethnic groups at higher risk of dermatological reactions of Allopurinol

A

Chinese
Korean
Thai

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25
Q

Name 3 drugs that interact with Allopurinol

A

Azathioprine
Cyclophosphamide
Theophylline

26
Q

Describe the interaction between Allopurinol and Azathioprine

A

Xanthine oxidase is responsible for metabolism of 6-mercaptopurine (metabolite of Azathioprine)

Thus, Allopurinol leads to high levels of 6-mercaptopurine

A much reduced dose (e.g. 25%) must therefore be used if the combination can’t be avoided

27
Q

Describe the interaction between Allopurinol and Cyclophosphamide

A

Allopurinol reduces renal clearance, therefore may cause marrow toxicity

28
Q

Describe the interaction between Allopurinol and Theophylline

A

Allopurinol causes an increase in plasma conc. of theophylline by inhibiting its breakdown

29
Q

Aspirin potentiates which 3 drugs/ classes

A

Oral hypoglycaemics
Warfarin
Steroids

30
Q

Why should Aspirin be avoided in children? What is the exception to this?

A

Risk of Reye’s syndrome

Kawasaki: benefits outweigh risk

31
Q

Name 2 non-dihydropyridine CCBs

A

Verapamil: highly negatively inotropic
Diltiazem: less negatively inotropic

32
Q

Name 2 dihydropyridine CCBs

A

Amlodipine
Nifedipine
Felodipine

33
Q

What are the indications of Verapamil?

A

Angina
HTN
Arrhythmias

34
Q

Name 3 contraindications to verapamil

A

Heart failure
Bradycardia
Hypotension

35
Q

List 2 side effects of Verapamil

A

Flushing
Constipation

36
Q

What drug should not be given with Verapamil? Why?

A

DONT give with b-blockers
May cause heart block

37
Q

Name 2 indications for Diltiazem

A

Angina
HTN

38
Q

List 3 contraindications to Diltiazem

A

Hypotension
Bradycardia
Heart failure

39
Q

Name 2 side effects of Diltiazem

A

Constipation
GI discomfort

40
Q

List 3 indications for dihydropyridine CCBs

A

HTN
Angina
Raynauds

41
Q

Which CCBs do not result in worsening of heart failure?

A

Dihydropyridine CCBs
Affect peripheral vascular smooth muscle more than myocardium

42
Q

List 3 side effects of dihydropyridines

A

Flushing
Headache
Ankle swelling

43
Q

What effect may be seen with shorter acting dihydropyridines? Give an example drug

A

Nifedipine
Cause peripheral vasodilation which may result in reflex tachycardia

44
Q

List 5 indications for Ciclosporin

A

Following organ transplantation
RhA
Psoriasis (direct effect on keratinocytes as well as modulating T cell function)
UC
Pure red cell aplasia

45
Q

What is Ciclosporin?

A

Immunosuppressant
Calcineurin inhibitor

46
Q

What organs can be adversely affected with Ciclosporin use?

A

Nephrotoxicity
Hepatotoxicity

47
Q

List 3 adverse abnormalities in the blood caused by cyclosporin

A

Hyperkalaemia
Impaired glucose tolerance
Hyperlipidaemia

48
Q

List 6 adverse clinical features of Ciclosporin use

A

Fluid retention
HTN
Hypertrichosis (excess hair)
Gingival hyperplasia
Tremor
Increased susceptibility to severe infection

49
Q

What drug can increase the concentration of ciclosporin?

A

Cannabidoil

50
Q

What is Digoxin?

A

Cardiac glycoside
Mainly used for rate control in AF Mx

51
Q

What properties allow use of Digoxin in heart failure? What is the effect of this?

A

Positive inotropic properties
Improves Sx but not mortality

52
Q

What is the MOA of digoxin?

A

Decreases conduction through the AV node which slows the ventricular rate in AF + flutter

increases force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump.

Also stimulates vagus nerve

53
Q

If Digoxin toxicity is suspected when should plasma concentration be measured?

A

Within 8-12h of last dose

54
Q

List 6 symptoms of Digoxin toxicity

A

Malaise
Lethargy
N+V
Anorexia
Confusion
Yellow-green vision

55
Q

Give 2 clinical signs of Digoxin toxicity

A

Arrhythmias (e.g. AV block, bradycardia)
Gynaecomastia

56
Q

What is the classic precipitant to Digoxin toxicity?

A

Hypokalaemia
Digoxin normally binds to the ATPase pump on the same site as K+ Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects

57
Q

List 7 drugs associated with Digoxin toxicity

A

Amiodarone
Quinidine
Verapamil
Diltiazem
Spironolactone
Ciclosporin
Drugs that cause hypokalaemia e.g. Thiazides + loop diuretics

58
Q

Describe management of Digoxin toxicity

A

Digibind: Digoxin-specific antibody Fab fragments
Correct arrhythmias
Monitor potassium

59
Q

What is the class of Gentamicin? Describe its pharmacokinetics

A

Aminoglycoside
Poorly lipid soluble, thus given parentally or topically

60
Q

Name 2 adverse effects of gentamicin

A

Ototoxicity
Nephrotoxicity

61
Q

Give a contraindication to Gentamicin

A

Myasthenia Gravis

62
Q

Describe dosing of Gentamicin

A

Peak (1h after admin) + trough levels (just before next dose) are measured

High peak: decrease dose

High trough: increase interval between doses

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