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Pharmacology > ACS and Heart Failure > Flashcards

ACS and Heart Failure Flashcards

1
Q

MOA of Aspirin

NB: anti platelet effect occurs at low doses and lasts for lifetime of platelet

A

Irreversibly inhibits cox reducing platelet aggregation

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2
Q

Give 3 SEs of Aspirin

A
  • GI irritation, ulcer, haemorrhage
  • bronchospasm
  • tinnitus
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3
Q

2 contraindications of aspirin?

A
  • children <16
  • aspirin sensitivity
  • 3rd trimester pregnancy
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4
Q

What conditions should you have a caution about giving aspirin in?

A
  • peptic ulcer disease

- gout

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5
Q

In ACS prescribe a loading dose of aspirin ___mg, followed by a regular daily dose of ___mg

A

300mg

75mg

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6
Q

Warfarin MOA

A

-inhibits vitamin K epoxide reductase (responsible for synthesis of clotting factors)

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7
Q

2 indications for the use of statins and 3 examples of names of statins

A
  • primary prevention of CV events (MI/stroke) w QRISK >10% 40yrs+
  • secondary prevention of CV events (+lifestyle changes, to prevent events in pts with established CV disease)
  • primary hyperlipidaemia treatment
  • e.g. rosuvastatin, parvastatin, simvastatin, atorvastatin
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8
Q

MOA of statins

A
  • inhibits HMG Co-A reductase decreasing serum cholesterol levels
  • also increases clearance of LDL cholesterol from blood
  • indirectly reduces triglyceride levels, and increase HDL
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9
Q

3 statin SEs?

A
  • headache
  • GI disturbance
  • muscle aches, myopathy
  • rhabdomyalisis (rare)
  • elevated liver enzymes (e.g ALT)
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10
Q

Statin cautions

A
  • hepatic impairment
  • renal impairment - reduce dose
  • avoid pregnancy/breastfeeding
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11
Q

Statins are metabolised by

A

Cytochrome p450 enzymes (so inhibitors of this enzyme reduce the effect of statins)

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12
Q

Give 1 SEs of warfarin use?

A
  • bleeding
  • increased risk w trauma and peptic ulcers
  • OD can —> spontaneous bleeding
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13
Q

2 Warfarin contraindications:

A
  • pt at immediate risk of haemorrhage (trauma, surgery)
  • liver disease
  • 1st trimester pregnancy
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14
Q

What type of medications increase warfarin metabolism therefore lower the therapeutic effect and leave pt at risk of clots?

A

CYP inducers

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15
Q

3 SEs of heparin

A
  • haemorrhage
  • bruising at injection site
  • hyperkalaemia (effects on adrenal aldosterone secretion)
  • heparin induced thrombocytopenia (HIT) - rare immune reaction, low platelet count and thrombosis (!) - more with UFH
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16
Q

Give 2 indications for Heparin (e.g. enoxaparin, dalteparin, UFH, fondaparinux)

A
  • VTE prophylaxis for in-pts, or initial VTE rx until oral anticoagulation is established
  • ACS: LMWH/fondaparinux used with antiplatelets to reduce clot progression/maintain revascularisation
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17
Q

Heparin MOA

A
  • antithrombin inactivates clotting factors IIa and Xa

- heparin enhances this anticoagulant effect of the antithrombin

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18
Q

We know that heparins act by (antithrombin inactivates clotting factors IIa and Xa), heparin enhances this anticoagulant effect of the antithrombin, how does the size of the heparin relate to the specificity UFH vs LMWH?

A
  • UFH: large and small molecules, these promote inactivation of both factor IIa and Xa
  • LMWH: smaller molecules, is more specific for factor Xa

NB: Fondaparinux is a synthetic polysaccharide that mimics the sequence of the binding site of heparin to AT and is very specific for factor Xa

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19
Q

When should you exercise caution in prescribing heparin?

A
  • increased bleeding risk (clotting disorder, severe uncontrolled HT, recent trauma/surgery)
  • withhold before and after an invasive procedure
  • renal impairment
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20
Q

What type of heparin should be used in renal impairment and why? /reduce dose

A
  • UFH should be used

- as LMWH and fondapariux will accumulate so requires a much lower dose/don’t use

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21
Q

In major bleeding, what 2 agents can reverse UFH action but is less effective for LMWH (and no effect on fondaparinux)

A

Protamine

Andexanet

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22
Q

A typical VTE prophylaxis dose is dalteparin ___ UNITS daily, mode of administration is ___, in renal impairment can give ___ ““UNITS “” mode 12-hrly

A
  • 5000 UNITS
  • Subcutaneous (into abdo wall not arm as can –> uncomfortable/disabling bruising)
  • Unfractionated Heparin 5000 UNITS
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23
Q

LMWH and fondaparinux effect is predictable enough to not need monitoring, but UFH when used therepeutically must have the dose titrated against the activated ___ ____ ratio (APTR) with a usual target of ___. FBC, clotting and renal profiles must be checked pre-rx, what 2 blood tests must be monitored in case of HIT?

A
  • Activated partial Thromboplastin Ratio (target 1.5-2.5)

- Platelet count and serum K+

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24
Q

3 indications for the use of ACEi

A
  • HT
  • Chronic HF
  • Ischaemic Heart Disease
  • Diabetic Nephropathy and CKD w proteinuria
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25
Q 
MOA ACEi
(relate to effect on BP, intra-glomerular effect and benefit for HF)
A
  • block ACE so prevent ang I –> ang II conversion
  • ang II is a v.constrictor and stimulates aldosterone secretion
  • blocking ang II reduces TPR (afterload) and lowers BP, also dilates the efferent arteriole so reduces intraglomerular pressure and slows CKD progression
  • lower aldosterone = more sodium and water excreted so lower CVP (preload) good for HF
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26
Q

Give 2 examples of ACEi, and 3 common side effects

A

-ramipril
-lisinopril
-perindopil
SEs: hypotension (esp after 1st dose), persistent dry cough, high K+, worsen renal failure

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27
Q

Explain the following SEs of ACEi:

  • persistent dry cough,
  • high K+,
  • worsen renal failure-esp with renal artery stenosis
A
  • cough: due to increased bradykinin levels-usually inactivated by ACE
  • high K+: as aldosterone levels are lower, potassium retention is promoted
  • worsen renal failure: pt may rely on constriction of efferent glomerular arteriole to maintain GFR
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28
Q

Name 2 contraindications and 2 cautions for the administration of ACE inhibitors:
advice regarding K+?

A

CI: RENAL ARTERY STENOSIS, AKI
Caution: pregnant, breastfeeding, CKD - although can help some, use lower doses and monitor carefully
-avoid prescribing with other potassium elevating drugs unless under specialist

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29
Q

The combination of ACEi with which medication class is associated with a marked increase in risk of nephrotoxicity?

A

NSAIDs

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30
Q

Ramipril daily dose in HF is __mg, for other indications start dose is ___mg.
These are titrated up to a max of __mg daily over weeks according to pts response, SEs and renal function

A
  • 1.25mg HF
  • 2.5mg other indications
  • up to 10mg
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31
Q

Give 3 examples of ADP-receptor antagonist antiplatelet drugs used with aspirin for ACS treatment with aim to prevent/limit __ ___ and reduce subsequent ___

A
  • clopidogrel, ticagrelor, prasugrel
  • limit arterial thrombosis
  • reduce mortality
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32
Q

Other than ACS treatment, give 2 indications for ADP-receptor antagonist antiplatelet drugs.

A
  • prevent coronary artery stent occlusion (+aspirin)

- long term 2dry prevention of thrombotic arterial events in CVD, cerebro-vasc disease and PVD

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33
Q

MOA of ADP-receptor antagonist antiplatelet drugs

A

-prevent platelet aggregation and reduce risk of arterial occlusion by binding irreversibly to ADP-receptors (P2Y12 subtype) on platelet surfaces

34
Q

Name 2 SEs of ADP-receptor antagonist antiplatelet drugs e.g. clopidogrel

A
  • bleeding
  • GI upset: dyspepsia, abdo pain, diarrhoea
  • thrombocytopenia rarely
35
Q

Give 1 CI and 2 cautions in the administration of ADP-receptor antagonist antiplatelet drugs e.g. clopidogrel

A
  • CI: SIGNIF. CTIVE BLEEDING

- Caution: stop 7 days before elective surgery, renal and hepatic impairment

36
Q

Clopidogrel is a pro-drug that requires metabolism to its active form by ____. It’s efficacy can therefore be reduced by ___ ___ such as .. .. ..
What impact does this have on the choice of gastroprotection prescribed?

A
  • hepatic cytochrome p450
  • reduced by CYP inhibitors e.g. omeprazole, ciprofloxacin, erythromycin, some SSRIs…
  • so lansoprazole or pantoprazole PPIs are preferred as are less likely to inhibit clopidogrel’s activation
37
Q

Clopidogrel ACS loading dose and maintenance doses are the same as aspirin, hence:

A
  • 300mg (write in the once-only section of drug chart)

- 75mg daily

38
Q

Give 3 examples of beta blockers and 3 indications for their use

A
  • e.g. bisoprolol, atenolol, propranolol, metoprolol, carvedilol
  • Ischaemic HD
  • chronic HF
  • AF (reduce ventricular rate and maintain sinus rhythm)
  • SVT - to restore sinus rhythm
  • HT if other meds are insufficient/inappropriate
39
Q

B-blocker MOA in relation to IHD, AF and SVT rx

A
  • B1-receptors (found mainly in heart) blockade -> reduced force of contraction and speed of conduction (relieves myocardial ischaemia by reducing cardiac work and O2 demand, increasing myocardial perfusion)
  • In AF/SVT they slow the ventricular rate by prolonging the refractory period of AVN
  • In HT they act in many ways including reducing renin secretion from kidney
40
Q

B blockers common SEs - name 3

A
  • fatigue, cold extremities, headache
  • GI disturbance e.g. nausea
  • sleep disturbance, nightmares
  • impotence in men
41
Q

2x CI and 2 cautions of beta blockers

A

CI: ASTHMA - fatal bronchospasm risk, generally safe in COPD - use b1 selective e.g. bisoprolol
HEART BLOCK
Caution: HF-start low, go slow as can initially impair heart function
Haemodynamic instability, Hepatic failure (reduce dose)

42
Q

B-blockers must not be used with non-____ ___ e.g. diltazem, ___ (except under specialist) as combo can cause __, bradycardia and even ____ (!)

A
  • non-dihydropyridine CCBs e.g. verapamil
  • HF
  • even asystole
43
Q

Alteplase and streptokinase are examples of what class of drugs? When are they indicated (3)

A

Fibrinolytics aka Thrombolytic

  • acute ischaemic stroke (given within 4.5hrs)
  • acute STEMI (given within 12hrs of symptom onset, if not for PCI)
  • massive PE with haemodynamic instability
44
Q

Fibrinolytic drugs e.g. alteplase MOA: catalyses the conversion of ____ to ___ which acts to ___ ……
…

A
  • catalyse conversion of plasminogen to plasmin, which acts to dissolve fibrinous clots and re-canalise occluded vessels
  • this allows reperfusion of affected tissues, limiting tissue infarction/cell death so improves pt outcomes.
45
Q

name 3 common SEs of Fibrinolytic drugs e.g. alteplase and 3 effects that should lead to terminating the therapy (!)

A
  • nausea, vomiting, bruising around injection site, hypotension
  • (!) serious bleeding, allergic reaction, cardiogenic shock, cardiac arrest
46
Q

What is the risky side effects of administering Fibrinolytic drugs e.g. alteplase when reperfusion of infarcted areas occurs in:

  • the heart muscle
  • the brain
A
  • arrhythmias

- cerebral oedema

47
Q

Why is reversal of Fibrinolytic drugs e.g. alteplase upon serious bleeding with anti-fibrinolytics e.g. transexamic acid rarely required?

A

-Fibrinolytic drugs e.g. alteplase have a very short half life

48
Q

CIs to fibrinolytics relate to factors predisposing to bleeding such as: (name 3)
In acute stroke what must be excluded w CT before treatment?
What is a CI to streptokinase use?

A

Bleeding CIs: RECENT HAEMORRHAGE, RECENT TRAUMA/SURGERY, BLEEDING DISORDERS, SEVERE HT, PEPTIC ULCERS

  • must rule out INTRACRANIAL HAEMORRHAGE
  • CI to streptokinase -PREVIOUS TREATMENT (development of anti-streptokinase antibodies can block its effect)
49
Q

Fibrinolytic drugs e.g. alteplase mode of administration is by ____ only, a ___ dose is usually given first followed by an __ _____.

A
  • injection only

- a bolus dose followed by an IV infusion

50
Q

Give 2 e.gs of nitrates and 2 indications

A
  • isosorbide mononitrate, GTN
  • GTN for acute angina associated w ACS
  • long acting e.g. iso mono for PROPHYLAXIS OF ANGINA where a b-blocker/CCB are insuffienct/not tolerated
  • IV nitrates used to treat pulmonary oedema usually along w oxygen and furosemide
51
Q

Nitrates MOA:

  • converted to NO
  • NO leads to increased…
  • venous __ and relaxation of __ __ vessels reduces __ __ and LV ___
  • this reduces __ __ and myocardial __ __, relieving __
  • they can also relieve coronary ___ and ___ collateral vessels improving coronary ____
A
  • NO increases c.GMP synthesis and reduces intracellular Ca2+ in VSMCs –> they relax
  • venous vasodilation, relaxation of venous capacitance vessels reduces cardiac preload and LV filling
  • together this reduces cardiac work and myocardial O2 demand, relieving angina/cardiac failure
  • can relieve coronary vasospasm and dilate collateral vessels improving coronary perfusion

(also causes some relaxation of systemic arterioles so lowers TPR and afterload)

52
Q

3 SEs of nitrates (vasodilator..)

A
  • flushing, headaches, light-headedness
  • hypotension
  • sustained use —> tolerance
53
Q

1 CI of use of nitrates

A
  • SEVERE AORTIC STENOSIS (heart can’t increase CO sufficiently through the narrowed valve area to maintain pressure in the now dilated vasculature
  • HAEMODYNAMIC INSTABILITY (esp. hypotension)
54
Q 
What medication class should not be prescribed with nitrates due to them
Enhancing and prolonging the hypotensive effect
A

PDE inhibitors e.g. sildenafil

55
Q

Use nitrates with caution alongside ____ (may precipitate hypotension)

A

Anti hypertensives

56
Q

GTN half life is approx

A

<5mins

vs isosorbide mononitrate (ISMN) ~5hrs

57
Q

Advice for pts taking GTN for angina relief in terms of when to take and what to do after taking?

A
  • use it before tasks that normally bring on their angina (good preventer rather than terminator)
  • sit down and rest for 5mins after taking it due to postural hypotension risk
58
Q

Give 3 indications for strong opiods e.g. oxycodone, morphine

A
  • rapid relief of acute severe pain
  • relief of chronic pain (high on analgesic ladder)
  • relief of breathlessness in end of life care
  • relief of breathlessness and anxiety in acute pulmonary oedema (+o2, furosemide, nitrates)
59
Q

Strong opiods MOA

A
  • activated mu receptors in CNS, this reduces neuronal excitability and pain transmission
  • in medulla, blunts the response to hypoxia and hypercapnia so reduces resp drive and SOB
  • reduce sympathetic fight/flight activity (in MI/pulmonary oedema, may reduce cardiac work and O2 demand)
60
Q

Name 5 SEs/adverse effects of strong opiods:

A
  • resp. depression
  • euphoria, detachment
  • neurological depression
  • N&V (activate CTZ)
  • constipation (mu receptors in bowel increases SM tone, reduces motility)
  • itching (histamine release in skin)
  • tolerance and dependence risk (apparent on cessation –>withdrawal reaction
61
Q

In what pts should you exercise caution in the administration of strong opiods?

A
  • hepatic failure
  • renal impairment
  • elderly
  • do not give in respiratory failure (exp. palliation specialist)
  • avoid in biliary colic (can cause Sphincter of Oddi spasm, worsening pain)
62
Q

What other class of medications should be avoided when a pt is taking strong opiods?

A

-other sedating drugs (anti-psychotics, benzos, tricyclic antidepressants)

63
Q

Name a useful anti-emetic to prescribe for strong-opiod induced nausea:

A

Metoclopramide

64
Q

Name2 cytochrome P450 inhibitors:

A
  • amiodarone
  • diltazem
  • itraconazole
  • macrolides
  • protease inhibitors
  • grapefruit juice
65
Q

What metabolic abnormality should be checked for before starting treatment with a statin?

A
  • TSH/thyroid status

- as hypothyroidism is a reversible cause of hyperlipidaemia (NB: it also increases the risk of myositis w statins)

66
Q

Furosemide and bumetanide are examples of what class of diuretics? Give 2 indications for their use:

A
  • loop diuretics
  • relief of breathlessness in pulmonary oedema (with nitrates and O2)
  • symptomatic rx of fluid overload in chronic HF
  • symptomatic rx of fluid overload in other oedematous states e.g. due to renal/hepatic disease
67
Q

MOA of loop diuretics:

-where do they act? Which transporter? What effect do they have on blood vessles? How does this help acute HF?

A
  • act mainly on the ascending limb of the loop of Henle
  • inhibit the Na+/K+/2Cl- co-transporter (usually transports all these ions from tube lumen to epithelial cell with water following), inhibiting this has a potent diuretic effect
  • they also cause dilation of capacitance veins (in acute HF this reduces preload so improves contractile function of heart muscle)
68
Q

Name 3 adverse SEs of loop diuretics?

-why do ear related SEs occur? What SEs am I referring to?

A
  • water losses can –> dehydration and hypotension
  • inhibition of Na+/K+/Cl- co-transporter increases urinary loss of these ions so can get low electrolyte state
  • hearing loss and tinnitus at high doses because there is a similar Na+/K+/Cl- co-transporter in the inner ear that regulated endolymph composition
69
Q

Give 2CIs for loop diuretics and 1 caution

A
  • CI: SEVERE DEHYDRATION
  • CI: HYPOVOLAEMIA
  • Caution: pts at risk of hepatic encephalopathy as hypoK+ can cause coma
  • Caution: pts with severe hypokalaemia and/or hyponatraemia
  • Caution: gout (over time, loop diuretics inhibit uric acid secretion so worsens gout)
70
Q

Loop diuretics have the potential to affect drugs that are excreted by the kidneys
-give 2 e.g.s of levels of drugs that may -> toxic due to loop diuretic use?

A
  • lithium levels will be increased (as less will get excreted)
  • digoxin levels may increase (due to diuretic-associated hypokalaemia)
  • aminoglycosides are more nephrotoxic and ototoxic if prescribed alongside loop diuretics
71
Q

40mg of furosemide is the equivalent to __mg Bumetanide

A

1mg

72
Q

Suggest 2 indications for prescribing oxygen

A
  • increase tissue O2 delivery in acute hypoxaemia
  • accelerate reabsorption of pleural gas in pneumothorax
  • reduce carboxyHb half life in CO poisoning
  • LTOT in pts with chronic hypoxaemia
73
Q

2 SEs of giving oxygen

A
  • face mask discomfort
  • dry throat
  • o2 accelerates combustion so is a fire risk if exposed to heat source/flame
74
Q

Name 2 aldosterone antagonists and 2 indications for their use:

A
  • Spironolactone, Eplerenone
  • Ascites and oedema due to liver cirrhosis
  • chronic HF (usually post MI on top of ACEi and B-blocker therapy)
  • primary hyperaldosteronism
75
Q

Aldosterone antagonist MOA

A
  • inhibits effect of aldosterone by competitively binding to the aldosterone receptor
  • this increases sodium and water excretion (no activation of ENaC channels), and more K+ is retained
76
Q

One adverse effect of aldosterone antagonists is ___, which can lead to:
-2 other SEs include

A
  • hyperkalaemia: muscle weakness, arrhythmias and cardiac arrest
  • gynaecomastia
  • liver impairment and jaundice
  • Steven-Johnson’s syndrome -> bullous skin eruption
77
Q

2 CIs for aldosterone antagonist use and 1 caution

A
  • CI: SEVERE RENAL IMPAIRMENT
  • CI: HYPERKALAEMIA
  • CI: ADDISON’S DISEASE
  • CI: POTASSIUM SUPPLEMENTS
  • caution: pregnancy/breastfeeding
78
Q

Losartan, candesartan and irbesartan are what class of drugs? And indicated in what 3 instances?

A
  • angiotensin receptor blockers
  • hypertension
  • chronic heart failure
  • ischaemic heart disease
  • diabetic nephropathy/CKD w proteinuria
79
Q

ARBs block the action of angiotensin II on the AT1 receptor, what effects does this have? (Relate to anti-hypertensive and CKD rx effect)

A

Ang II is a vasoconstrictor and stimulates aldosterone secretion

  • blocking it reduces TPR (after load) which lowers BP
  • less aldosterone so Na+ and water excretion promoted, helps reduce venous return (preload) good for HF
  • it dilated the efferent glomerular arteriole so reduces intraglomerular pressure so slows CKD progression
80
Q

2 SEs of angiotensin receptor blockers

A
  • hypotension (esp after first dose)
  • hyperkalaemia
  • renal failure (esp if renal artery stenosis)
81
Q

Suggest 2pts groups to avoid angiotensin receptor blockers use in as a contraindication and one to exercise caution with:

A

CI: RENAL ARTERY STENOSIS
CI: ACUTE KIDNEY INJURY
Caution: pregnant/breastfeeding, CKD, renal impairment (reduce dose), use with other potassium elevating drugs or NSAIDS

Pharmacology (14 decks)

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