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YEAR 3 - SEMESTER 1 > DRUGS > Flashcards

DRUGS Flashcards

ACEi ARBs Beta-blockers Diuretics

1
Q

What is the mechanism of action, indications, and contraindications of GTN?

A

MOA: Venodilation.
Reduces venous return to the heart, reducing preload and myocardial oxygen requirement

INDICATIONS: stable angina, heart failure associated with acute MI (infusion)

CONTRAINDICATIONS: hypotension, hypovolemia, raised ICP

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2
Q

List 3 common adverse effects of GTN

A 
Headache
Flushing
Palpitations 
Orthostatic hypotension
Fainting
Peripheral oedema
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3
Q

What is the mechanism of action, indication, and contraindication of ACE inhibitors?

A

MOA: Prevents the conversion of angiotensin I to II, inhibiting the vasoconstrictive, sodium retention, and aldosterone-releasing effects of ang II. Also inhibits bradykinin breakdown (bradykinin is a vasodilator).

INDICATIONS:

  • Hypertension
  • HFrEF
  • Diabetic nephropathy
  • Prevention of progressive renal failure in patients w/>1g per day of proteinuria
  • Post-MI

CONTRAINDICATIONS:

  • Hx of intolerance
  • Hx of hereditary or idiopathic angioedema (rare, but serious)
  • Pregnancy
  • Renal Artery Stenosis to all functioning kidneys
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4
Q

What are the RELATIVE contraindications of ACE inhibitors?

A
  • Hypotension (<90mmHg)
  • Hyperkalemia (K>6): can cause arrhythmias, death
  • Renal impairment
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5
Q

What causes the ACE inhibitor-induced cough?

A

ACE inhibitors prevent the breakdown of bradykinin.

Bradykinin accumulation can cause cough (in 5-10%) due to pro-inflammatory peptides and local release of histamine.

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6
Q

How does GTN dosage differ for angina and acute decompensated HF?

A

GTN dosage for ADHF is much higher. At this dosage, it dilates the arteries as well as the veins.

This decreases the afterload so the heart doesn’t have to pump against as much resistance.

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7
Q

FOR PATIENTS ON ACE INHIBITORS:

When GFR relies heavily on the _______ arteriole, renal impairment is more common.

A

When GFR relies heavily on the EFFERENT arteriole, renal dysfunction is more common.

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8
Q

Give 2 examples of diseases in which GFR relies heavily on the efferent arteriole.

A
  • Elderly
  • Dehydrated
  • Renovascular disease
  • Pre-existing renal dysfunction (less nephrons, so each carries a greater load)
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9
Q

How are ACE inhibitors and ARBs cleared?

A

Renally

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10
Q

When are angiotensin receptor antagonists used?

A

When ACEi are contraindicated (e.g. angioedema) OR there is an ACEi-induced cough

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11
Q

Why don’t Angiotensin receptor antagonists cause coughing?

A

Don’t act on bradykinin

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12
Q

Why are Angiotensin II receptor antagonists/blockers NOT first-line?

A

In some indications, they are less effective than ACEi and less proven

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13
Q

Angiotensin receptor antagonists end in …?

A

-sartan

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14
Q

Describe the mechanism of action, indications, and absolute contraindications of beta-blockers.

A

MOA: blocks beta-receptors (heart, lung, eye, kidney, liver, brain, pancreas, bronchi, etc.), thus preventing them from being activated by adrenaline and noradrenaline.
Can be selective and non-selective. They are competitive ANTAGONISTS.

Reduces HR, BP, and contractility.

INDICATIONS:

  • HTN
  • Heart failure/HFrEF
  • Angina
  • Tachyarrhythmias
  • MI

ABSOLUTE CONTRAINDICATIONS:

  • Hypotension
  • Bradycardia
  • Uncontrolled HF
  • 2nd or 3rd degree AV Block
  • Severe or poorly-controlled REVERSIBLE airway disease (e.g. asthma)

Basically, whenever the cardiovascular effects are undesirable

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15
Q

How does the MOA differ between SELECTIVE and NON-SELECTIVE beta-blockers?

A

SELECTIVE beta-blockers only block beta-1 receptors

NON-SELECTIVE blocks both beta-1 and beta-2

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16
Q

List 3 common adverse effects of beta-blockers

A
  • Bradycardia
  • Hypotension
  • Orthostatic Hypotension
  • Transient worsening of HF (when first commenced)
  • Nausea
    etc.
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17
Q

Why do beta-blockers need to be used with caution in diabetics?

A

Can mask symptoms of hypoglycaemia

the hypogylcaemia is the issue, NOT the beta-blocker

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18
Q

Why are diuretics less useful in LEFT-sided heart failure?

A

There doesn’t tend to be fluid overload, so there is less need for them. More useful in RHF when you have things like peripheral oedema and fluid overload.

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19
Q

What is the MOA of beta-lactam antibiotics? (Drug class: penicillins)

A

MOA: interfere with bacterial cell wall growth

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20
Q

Why are anti-staph agents used in place of standard penicillins (e.g. penicillin G, V)?

A

Most staphylococcal infections are resistant to standard penicillins

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21
Q

Name an example of an anti-staph penicillin

A

Flucloxacillin

(note: when talking about methicillin-resistant staphylococcus aureus/MRSA, it refers to a bug that responds to flucloxacillin)

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22
Q

When are empiric antibiotics recommended in IE?

A

For haemodynamically unstable patients.

Targeted antibiotics are recommended for everyone.

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23
Q

What is the difference between immunologically and non-immunologically mediated reactions caused by penicillin?

A

NON-IMMUNOLOGICAL REACTIONS/INTOLERANCES: diarrhoea, headache, vomiting

IMMUNOLOGICALLY-MEDIATED: allergies (e.g. SJS, TENS, immediate hypersensitivity)

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24
Q

Does re-exposure to penicillin in someone who is allergic cause a better or worse reaction?

A

WORSE

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25
Q

How are aminoglycosides administered? Why?

A

Injection or topical

They are not bioavailable orally

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26
Q

How are aminoglycosides cleared?

A

100% renally

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27
Q

What type of infections are aminoglycosides used for? Give an example of an aminoglycoside.

A

Serious gram-negative infections

E.g. gentamycin (most commonly-used)

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28
Q

List 3 adverse effects of aminoglycosides

A

Hearing loss
Ataxia
Renal dysfunction

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29
Q

What types of infections is vancomycin (glycopeptide) used for?

A

Gram-positives resistant to penicillin
and anaerobes

IS EFFECTIVE AGAINST MRSA

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30
Q

What similarities are shared by aminoglycosides and vancomycin?

A

Both renally-cleared

Both not absorbed orally (IV administration)

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31
Q

What is vancomycin useful for? Why is its use restricted?

A

MRSA

To reduce pressure for vancomycin-resistant staph aureus

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32
Q

What is the drug class of vancomycin?

A

Glycopeptide

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33
Q

How do beta-blockers help with left-sided ventricular failure?

A

Block SNS action on beta-1 receptors in the AV Node –> slows HR –> increases time in diastole –> increases ventricular filling time –> increased preload –> greater stretching of actin and myosin filaments (Starling forces) –> greater contractility –> improved LVEF

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34
Q

Compare furosemide and spironolactone for CHF, taking into account:

  1. MOA
  2. Contraindications
  3. Adverse effects (especially on electrolytes)
A

FUROSEMIDE (loop diuretic)
1. MOA: inhibits Na+ and Cl- reabsorption in the ascending LOH, which is responsible for ~20% of Na+ reabsorption

  1. Contraindications/Precautions: allergy, gout, severe sodium and volume depletion
  2. Adverse effects (especially on electrolytes): hyponatraemia, hypokalaemia, hypomagnesaemia, hypochloraemia, hypocalcaemia, gout, orthostatic hypotension, dehydration

SPIRONOLACTONE (aldosterone antagonist):
1. MOA: inhibits Na+ absorption in the distal tubule by antagonising aldosterone, increasing Na+ and water excretion and decreasing K+ excretion.

  1. Contraindications/precautions: renal failure, debilitated patients with cardiopulmonary disease or uncontrolled diabetes, prostate cancer, cirrhosis
  2. Adverse effects (especially on electrolytes): hYPERKALEMIA, hyponatremia, weakness, headache

LOOP diuretics are very powerful. Aldosterone antagonists less so.

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35
Q

What do NSAIDs do to the afferent arteriole?

A

NSAIDs that cause COX-1 and COX-2 inhibition can reduce renal blood flow by constricting the afferent arteriole.

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36
Q

What organisms is gentamicin used for?

A

Gram-negative

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37
Q

What organisms is metronidazole used for?

A

Anaerobes

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38
Q

Which aspects should be included in a penicillin ‘allergy’ history?

A
  • What they reacted to
  • What type of reaction it was: GIT, cardiovascular, rash/urticaria, swelling, seizure, dizziness, headache, etc.
  • How long after the treatment did it start?
  • How long ago did they have this reaction?
  • How was the reaction treated?
  • What other antibiotics have they had since? (e.g. cephalosporins)
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39
Q

What would a penicillin INTOLERANCE look like?

Not actually an allergy

A

GIT: nausea, vomiting, diarrhoea
Neurological: dizziness, headache, confusion

Other, e.g. thrush in women

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40
Q

Give 3 examples of low-risk reactions to penicillin

A
  • Unknown reaction >10 years ago
  • Childhood exanthem (details unclear and no severe features or hospitalisation)
  • Diffuse or localised rash with no other symptoms AND occurring >24hrs later AND >10 years ago
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41
Q

Give 3 examples of HIGH-risk reactions to penicillin

A
  • IgE-mediated hypersensitivity: urticaria, angioedema, swelling of the mouth and throat, distress, collapse, death
  • Any history of diffuse rash a short time after starting the medication (e.g. within 2 hours)
  • Diffuse or localised rash that was DELAYED, BUT within the last 10 years
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42
Q

What reaction would you get upon re-exposure to penicillins after a previous high-risk reaction?

A

Possibly the same rash but worse, and with anaphylaxis

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43
Q

Outline the approach to antibiotic prescription in someone who was previously had a high-risk reaction to penicillin.

A

Choose a non-beta lactam antibiotic

Don’t use cephalosporins due to cross-reactivity risk

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44
Q

State the following information for PENICILLINS:

  • Mechanism of action
  • Why does resistance develop?
  • Bioavailability
  • Clearance
  • Spectrum of action
A

MECHANISM OF ACTION: interferes with bacterial cell wall growth

RESISTANCE: due to beta-lactamase, modification of penicillin binding protein, no access to PBP, efflux pump

BIOAVAILABILITY: good oral bioavailability, but varies between benzyl penicillin (15%) and amoxicillin (80%)

CLEARANCE: Renal (generally)

SPECTRUM OF ACTION: very narrow to very wide

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45
Q

Which patient groups tend to develop renal impairment when using ACEi?

A

Anyone can, but the risk is HIGHEST in those whose GFR depends on the EFFERENT arteriole.

  • Elderly
  • Kidney disease (less nephrons, so heavier filtration load on each nephron)
  • Those with renovascular disease
  • Dehydrated
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46
Q

What should be monitored in patients taking ACEi?

A

Within 1-2 weeks of commencement, or before dose changes, the following should be evaluated:

  • Potassium
  • Renal function
  • BP
  • Side effects: cough, angioedema (may not be recognised by the patient as related to their meds)
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47
Q

When are ARBs used?

A

When there are contraindications (e.g. angioedema)

When ACEi aren’t tolerated (e.g. cough is very annoying)

They don’t act on bradykinin and hence won’t cause these side effects

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48
Q

Why are ACEi preferred over ARBs?

A

ARBs are less effective than ACEi for some indications

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49
Q

What should be monitored in patients taking ARBs?

A

Within 1-2 weeks of commencement, or before dose changes, the following should be evaluated:

  • Potassium
  • Renal function
  • BP

i.e. same as ACEi but minus the side effects

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50
Q

Can ACEi and ARBs be stopped without taper?

A

YES

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51
Q

Why is amiodarone so widely-sued?

A

Can be used to supraventricular and ventricular arrhythmias

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52
Q

Outline the de-prescribing pathway for beta-blockers and why it must be done gradually

A

May need to reduce dose 2 weeks at a time over a period of 6-8 weeks (especially if they’ve been on it for years)

Weaning off slowly prevents the recurrence of angina & tachyarrhythmias

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53
Q

What is the mechanism of action of calcium channel blockers?

A

Blocks the effect of calcium channels on cell membranes. This results in:

  • Vascular smooth muscle: Arteriolar relaxation
  • Myocardium: reduces force of contractility
  • Cardiac conduction: reduces HR

i.e. it opposes the normal physiological effects of calcium influx

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54
Q

Why do calcium channel blockers come in a sustained release tablet?

A

Most have a short half-life

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55
Q

What do calcium channel blockers end in?

A

Depends on the class:

Dihydropyridines end in ‘-ine’ (e.g. felodipine, amlodipine)

Non-dihydropyridines are verapamil and diltiazem

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56
Q

How many different classes of calcium channel blockers exist?

A

3 classes:

Dihydropyridines (selective for peripheral vascular tissue)

Diltiazem

Non-dihydropyridines (selective for myocardium)

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57
Q

What are the indications for calcium channel blockers?

A

Hypertension

Angina

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58
Q

What are the side effects of calcium channel blockers and how does this relate to their MOA?

A

Dihydropyridines are selective for peripheral vascular tissue. They have a more profound vasodilatory effect and can cause side effects such as ankle swelling.

Non-dihydropyridines can cause constipation (especially verapamil) and bradycardia.

Common adverse effects: nausea, flushing, dizziness, headache, hypotension.

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59
Q

Can calcium channel blockers be stopped suddenly?

A

YES

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60
Q

Penicillins such as penicillin G (benzyl penicillin) and penicillin V (phenoxylmethyl penicillin) are used for what type of organisms?

A

Gram-positive

61
Q

Narrow-spectrum anti-staph penicillins are used for which organisms?

Give some examples of these drugs.

What do you need to monitor for these drugs?

A

Staphylococcal infections

Individual drug examples: flucloxacillin, methicillin

Monitoring: chronic liver disease, liver dysfunction - do LFTs

62
Q

Why are anti-staph agents used in place of standard penicillins (e.g. penicillin G and V)

A

Most staphylococcal organisms are resistant to standard penicillins

63
Q

Moderate-spectrum penicillins are used for which organisms?

Give some examples of these drugs.

A

Broader spectrum of activity, including against Gram-negatives (e.g. haemophilus).

Commonly-used in respiratory infections.

Individual drug examples: amoxycillin, ampicillin

64
Q

Moderate-spectrum drugs such as amoxicillin have a high risk of what when given during some viral infections (e.g. EBV)?

A

High risk of RASH

65
Q

What additional mechanism of action is present in broad-spectrum penicillins?

A

Beta-lactam PLUS beta-lactamase inhibitor

66
Q

Give an example of a beta-lactamase inhibitor

A

Clavulanate

Tazobactam

Sulbactam

67
Q

Give an example of a broad-spectrum penicillin regime

A

Amoxicillin + clavulanate

Beta-lactam PLUS beta-lactamase inhibitor

68
Q

Give an example of a broad-spectrum penicillin regime that has anti-pseudomonas activity

A

Piperacillin, ticarcillin, carbenicillin +/- clavulanate, tazobactam

69
Q

There is a higher risk of which side effects when using broad-spectrum penicillin regimes?

Why?

A

Diarrhoea

Hepatotoxicity

Thrush

Addition of beta-lactamase activity puts you at higher risk

70
Q

BROAD-spectrum penicillins are used for which organisms?

A

Bacteria with beta-lactamase

(Beta-lactamases are enzymes produced by bacteria that provide multi-resistance to β-lactam antibiotics such as penicillins, cephalosporins)

71
Q

What is the MOA of cephalosporins?

A

They are beta-lactams (similar to penicillins) - hence the risk of cross-reaction if someone has a penicillin allergy

Interfere with bacterial cell wall peptidoglycan synthesis by binding to penicillin-binding proteins, eventually leading to cell lysis and death; bactericidal.

72
Q

Do cephalosporins have a narrower or broader spectrum of action than penicillins?

A

Broader

73
Q

Why are cephalosporins rarely the first drug of choice?

A

Cephalosporins are linked to greater prevalence of infections caused by MRSA and VRE (vancomycin-resistant enterococci), multi resistant Gram-negative organisms, and C. Diff

74
Q

How are cephalosporins classified?

A

First, second, third, and fourth generation.

Ranges from Gram-positive cover to more Gram-negative cover (later generations = more Gram-negative cover)

Note: second-generation ones aren’t used as much

75
Q

Fourth-generation cephalosporins also cover…?

A

Fourth-generation cephalosporins also cover pseudomonas

E.g. Cefepime

76
Q

First-generation cephalosporins are mostly used for…?

A

1st gen: Skin and soft tissue infections (including staph)

(for children or where there is a reaction to penicillin that is not an immediate hypersensitivity)

But again we’d rather not use cephalosporins if we can avoid it

77
Q

Third-generation cephalosporins are mostly used for…?

A

Serious enteric infections

Gonorrhoea (due to penicillin resistance)

Empirical meningitis

78
Q

Can cephalosporins be given for severe penicillin skin reactions such as SJS, DRESS, and TENs?

A

Yes because they do not cross-react, but it’s very difficult to get a good history of the reaction so we just tend to avoid cephalosporins in practice.

If someone gives you a very good Hx of SJS, you can safely give cephalosporin.

79
Q

Can cephalosporins be given for IgE-mediated immediate hypersensitivity reactions such as urticaria, angioedema, SOB, anaphylaxis, hypotension?

A

NO - re-exposure to penicillins results in similar reaction or worse.

5-10% risk of cross-reactivity.

Don’t give cephalosporins.

80
Q

Can cephalosporins be given for patients who developed a RASH but WITHOUT signs of an IgE-mediated immediate hypersensitivity reaction?

A

YES

Re-exposure only results in a rash in about 5-10% of cases, and tends not to progress to worse states.

Similar cephalosporin cross-reactivity to those with the penicillin rash, so rate is actually quite small (5-10% of the 5-10%)

Often the rash was due to drug-virus interactions (e.g. EBV) or excipients in the 70s

81
Q

Aminoglycosides can cause ototoxicity (and hence ataxia) and renal toxicity. Which are these are IRREVERSIBLE?

A

OTOTOXICITY: irreversible

NEPHROTOXICITY: reversible

82
Q

How are aminoglycosides used in order to maximise safety?

A

Short-term single treatment is safe. For longer-term use, adjust the dose according to blood levels.

Safest is when it is given in infrequent pulses.

83
Q

What are aminoglycosides used for?

What needs to be monitored?

A

Aminoglycosides are used for:

  • Serious gram-negative infections
  • Synergy for infective endocarditis

Monitoring:

  • Audiometry
  • Renal function
  • Drug concentration
84
Q

What is the MOA of metronidazole?

To which drug class does metronidazole belong?

What needs to be communicated to patients taking metronidazole?

A

MOA of metronidazole: inhibits DNA synthesis. It is what we’re thinking about when there’s anaerobic organisms.

Class: nitroimidazole

Communication: GI effects, metal taste, YOU CAN’T DRINK ALCOHOL OTHERWISE YOU’LL FEEL VERY HUNGOVER!!! (need to be off alcohol up until 2 days AFTER you stop taking the medication)

85
Q

What is the MOA of macrolides? Give some examples of macrolides.

What organisms are they used for?

What needs to be communicated to patients taking macrolides?

A

MOA: inhibits bacterial protein synthesis.

Bacteriostatic; inhibit bacterial protein synthesis by binding to the 50S ribosomal subunit. They also have immunomodulatory and anti-inflammatory effects.

Organisms: A FUCKING LOT (mainly Gram-positives, some Gram-negatives, atypical respiratory organisms, chlamydia) . Gram-negatives: for H. Pylori, H. influenzas. Also for those with penicillin allergies.

Drug examples: azithromycin, erythromycin, Clarithromycin

Communication/monitoring: GI effects (esp. nausea and vomiting w/erythromycin), drug interactions

86
Q

What is the MOA of quinolones? Give some examples of quinolones.

What are they used for?

What needs to be monitored/communicated?

A

MOA: inhibits bacterial DNA synthesis (bactericidal)

Drug examples: 
Ciprofloxacin
Moxifloxacin
Norfloxacin
Ofloxacin

Use: broad-spectrum, great drugs with great penetration. Only really when other antibiotics aren’t indicated (e.g. penicillin allergy or renal impairment in aminoglycosides)

Monitoring/communication: really depends on the drug. e.g. ciprofloxacin can cause tendon rupture, moxifloxacin QT prolongation.

87
Q

Why are quinolones used sparingly?

A

They are broad-spectrum. Can incur resistance.

88
Q

What is the MOA of lincosamides? Give some examples of lincosamides.

What are they used for?

What needs to be monitored/communicated?

A

MOA: Bacteriostatic; inhibit protein synthesis by binding to the 50S ribosomal subunit.

Drug examples:
Clindamycin
Lincomycin

Use: gram-positives, anaerobes in the case of penicillin allergy

Monitoring/communication: mild-severe diarrhoea (dose-dependent), pseudomembranous colitis

89
Q

What class of drug does vancomycin belong to?

What is vancomycin effective against?

What is it used for?

A

Class: glycopeptide

Effective against: gram-positives, anaerobes

Used for: severely-resistant gram-positive infections (E.g. MRSA)

Use is highly-restricted to reduce pressure for Vancomycin-Resistant staph aureus

90
Q

What are the side effects of vancomycin?

What should be monitored?

A

Side effects: hearing impairment, red man syndrome if given quickly

Monitor: renal function, drug concentration

91
Q

What is the MOA of tetracyclines? Give some examples.

What are they used for?

What should be communicated?

A

MOA: inhibits bacterial protein synthesis (Bacteriostatic)

Drug examples:
Demeclocycline
Doxycycline
Minocycline
Tetracycline

Uses: quite specific, non widely-used (acne, malaria prophylaxis)

Communication: discolours teeth permanently, need to be careful in pregnancy, lactation, and for children

92
Q

How does aspirin inhibit platelet aggregation?

A

Aspirin targets COX-1, which converts arachidonic acid into prostaglandin H2.

Without prostaglandin H2, thromboxane A2 (which stimulates platelet aggregation and activation) is not produced.

https://www.youtube.com/watch?v=eZBtQ0rDnG4

93
Q

The primary goal of treating arrhythmias arising from above or within the AV node is to…?

A

The primary goal of treating arrhythmias arising from above or within the AV node is to REDUCE CONDUCTION across the AV node in an attempt to control the heart rate to within normal ranges.

94
Q

What is the mechanism of action of loop diuretics? Why are they so potent?

A

Acts on the luminal Na+/K+/2Cl- co-transporter in the ascending LOH;

this site accounts for retention of approximately 20% of filtered sodium; therefore, these are potent diuretics. There is a dose-related effect.

95
Q

Name the most commonly-prescribed loop diuretic

A

Furosemide

96
Q

What are the indications for prescribing FUROSEMIDE?

A

Oedematous states, e.g. heart failure, nephrotic syndrome, renal impairment

97
Q

What should be COMMUNICATED to patients taking loop diuretics (e.g. furosemide)?

A

Dramatic diuresis; loop diuretics are very effective and a short duration of action (4-6 hours).

This may results in incontinence, nocturia, polyuria, postural hypotension.

98
Q

What should be MONITORED in patients taking loop diuretics (e.g. furosemide)?

A

Electrolytes; loop diuretics can cause decreased K+, H+, Mg2+, and Ca2+. You can get a hypokalemic alkalosis.

Renal function

Weight

99
Q

What is the mechanism of action of thiazide diuretics?

A

Acts on the luminal part of the Na+/K+/2Cl- co-transporter in the DCT.

100
Q

Why do thiazide diuretics have less of an effect than loop diuretics?

A

There is a diuretic ceiling; at a certain point, there is a limit to the level of efficacy you get (unlike loop diuretics, which have a dose-dependent effect).

101
Q

What are the indications for prescribing THIAZIDES?

A

Mildly oedematous states

Hypertension (due to their added vascular effects)

102
Q

Name the most commonly-prescribed thiazide.

A

Hydrochlorothiazide

103
Q

Outline the suitability issues of thiazide diuretics (4).

A

Allergy to thiazides

Hyponatremia

Gout (can be exacerbated by thiazides)

Postural hypotension (they lower your blood pressure in addition to intravascular volume)

104
Q

What should be MONITORED in patients taking thiazide diuretics (e.g. hydrochlorothiazide)?

A

Postural hypotension

Electrolytes: lowered Na+, K+, H+. Can get hypokalemic alkalosis. (electrolyte levels very dependent on dosage - these effects are much less common at the doses we prescribe today)

Renal function

Weight

105
Q

What is the mechanism of action of spironolactone (an aldosterone antagonist)?

A

Inhibit sodium absorption in the distal tubule by antagonising aldosterone, increasing sodium and water excretion and reducing potassium excretion; they are weak diuretics.

106
Q

Name the potassium-sparing diuretics

A

Spironolactone / mineralocorticoid antagonists / aldosterone antagonists

107
Q

When is spironolactone (aldosterone antagonist) indicated?

A

Oedematous states driven by increased aldosterone levels (e.g. heart failure, nephrotic syndrome, chronic liver disease)

108
Q

What are the suitability issues surrounding spironolactone?

A

Renal impairment

Hyperkalemia

(because they are potassium-sparing, they can be problematic in patients with existing renal failure as these patients tend to already retain potassium)

109
Q

What should be COMMUNICATED to patients commencing spironolactone?

A

Possibility of gynaecomastia

The need for regular potassium checks

110
Q

What should be MONITORED in patients commencing spironolactone?

A

ELECTROLYTES (ESPECIALLY POTASSIUM!! THEY ARE THE ONLY DIURETICS THAT RAISE K+)
Other electrolytes: lowered Na+ and H+.

Renal function

Weight

111
Q

When are potassium-sparing diuretics such as amiloride and triamterene (which can come in combination with thiazides) used?

A

They are used with loop and thiazide diuretics to counteract the issue of hypokalaemia (since they are potassium-sparing)

Don’t really have much of a diuretic effect and you would very rarely use them by themselves

112
Q

When would you choose RATE over rhythm control in AF?

A

RATE CONTROL: for when the patient is asymptomatic and have normal left ventricular function. Focuses on controlling ventricular rate whilst leaving the patient in AF rhythm.

113
Q

When would you choose RHYTHM over rate control in AF?

A

RHYTHM CONTROL: for when the patient is highly symptomatic or has left ventricular dysfunction secondary to atrial fibrillation

114
Q

What is the difference between rate and rhythm control in AF?

A

RATE CONTROL = control ventricular rate to improve haemodynamic status and reduce symptoms

RHYTHM CONTROL = restoring and maintaining sinus rhythm

115
Q

Name a rate-control drug used for AF

A

Beta-blockers (e.g. atenolol, metoprolol)

116
Q

Name 2 rhythm-control drugs used for AF and the situations they would be suited to

A

Flecainide (normal LV function, no CHD)

Amiodarone (LV dysfunction, CHD)

117
Q

Acute treatment of SVT?

A

Adenosine

118
Q

What are the indications for Cabergoline?

A
  • Parkinson’s disease
  • Prolactinomas / Hyperprolactinaemia
  • Lactation suppression
119
Q

What is the mechanism of action of Cabergoline?

A

Stimulates dopamine receptors, causing prolactin inhibition, which results in:

  • Reduced size of prolactinomas
  • Decreased growth hormone in people with acromegaly
120
Q

Name 3 common adverse effects of Cabergoline

A
  • Cardiac fibrosis
  • GIT effects: NV, abdo pain, constipation
  • Headache

https://amhonline-amh-net-au.proxy.library.adelaide.edu.au/chapters/neurological-drugs/drugs-parkinsonism/dopamine-agonists/cabergoline

121
Q

Name the 2 main drug groups for ACUTE treatment of migraines

A

Nonopioid analgesics (try this first)

Triptans

122
Q

How many days per month should the non-opioid analgesic vs. the triptans be taken for in order to prevent medications overuse headaches?

A

NON-OPIOID ANALGESICS: <15 days per month

TRIPTANS: <10 per month

123
Q

When should migraine prophylaxis be considered?

A

When patients need acute migraine treatment on > 2-4 days per month

124
Q

Name 2 non-opioid analgesics that can be used for acute migraine management

A

Aspirin

Ibuprofen

125
Q

When is heparin used?

A

After surgery, on patients who are at high risk of clotting.

Heparin (inhibits factor IIa and Xa) is an anticoagulant that is readily and easily reversible in emergencies (with Protamine sulphate).

126
Q

Why does warfarin require frequent monitoring and dose adjustments?

A

Highly dependent on vitamin K intake, absorption, and metabolism. Variations in vitamin K levels will affect dosing.

127
Q

Name 3 drug classes that can be used for migraine PROPHYLAXIS

A
  • Beta blockers
  • Calcium channel blockers
  • Tricyclic antidepressants
  • Topiramate (anticonvulsant)
128
Q

Outline the progression of pharmacological approach to migraine management

A
  1. Lifestyle measures + non-opioid analgesics
  2. Triptans
  3. Migraine PROPHYLAXIS (considered when patients need acute migraine treatment on >2-4 days per month)
129
Q

Dexamethasone:

  1. MOA
  2. Indications
  3. Precautions
  4. Side effects (short and long-term)
A
  1. MOA: glucocorticoid (e.g. gluconeogenesis, proteolysis, lipolysis, suppression of inflammation and immune responses) and mineralocorticoid (sodium & water retention) effects
  2. Indications: cerebral oedema, chemotherapy-induced NV, acute asthma, etc.
  3. Precautions: breastfeeding, infection, children
  4. Side effects (short and long-term)

SHORT-TERM: adrenal suppression, infection, sodium and water retention, oedema, HTN, hypokalaemia, hypokalaemia, delayed wound healing, skin atrophy, bruising, acne

LONG-TERM: osteonecrosis of the femoral and humeral heads, fat redistribution, muscle wasting, weight gain

130
Q

Sodium valproate MOA & indications

A

MOA: prevents repetitive neuronal discharge by blocking voltage‑ and use-dependent sodium channels. Other actions include enhancement of GABA, inhibition of glutamate and blockade of T-type calcium channels.

Indications: primary generalised epilepsy, simple and complex focal seizures, bipolar disorder

131
Q

Adrenaline as an ionotrope

A 
Indications: 
- Cardiac arrest
- Acute HF and cardiogenic shock
- Anaphylactic reactions
-
132
Q

Aciclovir MOA, indications, adverse effects

A

MOA: inhibit viral DNA polymerase and DNA synthesis.

INDICATIONS: HSV, shingles (VZV reactivation)

ADVERSE EFFECTS: NV, diarrhoea, hallucinations, encephalopathy

133
Q

Levetiracetam

A

.

134
Q

.

A

.

135
Q

.

A

.

136
Q

.

A

.

137
Q

.

A

.

138
Q

.

A

.

139
Q

.

A

.

140
Q

What is the mechanism of action, indication, and contraindications of BENZODIAZEPINES?

A

MOA: binds to GABA(A) receptors in the neuronal cell membrane to potentiate GABA, the major inhibitory neurotransmitter in the CNS. This results in more inhibition.

INDICATIONS: MANY (seizures, anxiety, insomnia, agitation, alcohol withdrawal, muscle spasms)

CONTRAINDICATIONS: CNS depression, respiratory depression, severe hepatic impairment

141
Q

What do benzodiazepines end in?

A

-pam

142
Q

What must be taken into consideration when comparing benzodiazepine choice?

A

LENGTH OF ACTION

Some have a half-life of <6 hours (e.g. midazolam) whilst others >24 hours (e.g. diazepam)

143
Q

Discuss 3 benzodiazepine PRECAUTIONS for certain patient groups

A
  1. Taking Benzos alongside opioids (or other CNS depressants) required careful monitoring as they can cause coma & death.
  2. Elderly patients are more likely to fall, be confused, have ataxia and memory impairment, etc.
  3. Dependence
144
Q

Name 4 important adverse effects of benzodiazepines

A

COMMON: drowsiness, oversedation, dizziness, ataxia, vision impairment, dependence/tolerance (even if used short-term).

INFREQUENT (but important): anterograde amnesia (difficulty forming new memories after using the drug)

145
Q

NEVER WRITE A 6-MONTH PRESCRIPTION FOR BENZODIAZEPINES DURING THE FIRST ENCOUNTER

A

.

146
Q

To which class of drugs does enoxaparin belong?

A

Heparin

147
Q

What is the MOA, indications, precautions, and contraindications of ENOXAPARIN?

A

MOA: inactivates clotting factors IIa (thrombin) and Xa by binding to antithrombin III.

INDICATIONS:

  • VTE prophylaxis in surgical and high-risk patients
  • VTE
  • STEMI, nSTEMI, unstable angina

ACCEPTED: PE, ACS, DIC

PRECAUTIONS:

  • High and low weights
  • CrCl <30ml/min
  • Renal impairment

CONTRAINDICATIONS:

  • Active bleeding
  • Severe thrombocytopenia
  • Severe hepatic impairment or disease (including oesophageal varies)

https://amhonline-amh-net-au.proxy.library.adelaide.edu.au/chapters/blood-electrolytes/anticoagulants/heparins/enoxaparin

148
Q

Valvular AF should be anti-coagulated using?

A

WARFARIN

YEAR 3 - SEMESTER 1 (15 decks)

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