WK5-Pharmacology Flashcards
What is the main issue we address in medication management for CV patients?
Addressing neurohormonal and haemodynamic response.
e.g. when CO falls = decreased perfusion of vital organs (inc. kidney)
- response - compensatory hormones release (angiotensin/adrenaline)
What are ACE inhibitors?
“-prils”
Common names: perindopril (Coversyl), Ramipril (tritace), fosinopril (monopril), enalopril (renitec), captopril (acenorm), lisniopril (fibsol)
Inhibits conversion of AngT I to AngT II - reduces vasoconstriction, Na+ retention and aldosterone release
Indications: HTN, HF
SE: hypo, dizziness, hyperkalaemia, dry cough
What are ARBs?
Angtiotensin II receptor blocker
Common names: Irbesartan (Avapro), Candesartan (Atacand), Telmisartan (Micardis), eprosartan (teveten)
MOA: blocks binding of AngT II to AngT receptors
- used instead of ACEI? (ACEI SE: dry cough)
- lowers BP, monitors body’s response to low CO
- avail. in combo products
SE: hypo, dizziness, headache, hyperkalaemia
What are BB?
Beta-blockers “lol”
–> limits affect of adrenaline on heart
Common names: Atenolol (Noten), Metoprolol (minax), propranolol (deralin)
Indications: HTN, prevent angina, HF, regulate HR
MOA: block B receptors in heart (bronchi, periphery), reduces workload on heart = reduces O2 decrease in afterload
SE: hypo, diziiness, fatigue, vivid dreams
What are Ca2+ channel blockers?
2 GROUPS
1. dihydropyridines: Amlodipine (norvasc), Lercandipine (Zanidip)
* mainly act on arteriolar SM = reduce periph vasc res and BP
* minimal effect on myocardial cells
- Nondihydropyridine: Diltiazem (cardizem), Verapamil (Anpec)
* act on cardiac/arteriolar/smooth muscle
* decrease cardiac contractility, HR, conduction (verapamil>diltiazem)
Indications: HTN, angina, irregular beat
SE: headache, flushing, fatigue, constipation
What are anti-platelets?
Aspirin (astrix)
Clopidogrel (plavix)
Ticargrelor (brilinta)
Prasugrel (effient)
Indications: POST stent (DAPT) and ACS
AE: bleeding, increased bleeding time, GI irritation
What are cholesterol lowering medicines?
“statins”
Atorvastatin (lipitor)
Rosuvastatin (crestor)
Simvastatin (lipex)
Pravastatin (pravachol)
Fluvastatin (vastin)
MOA: inhibits HMG-CoA reductase enzyme that synthesises cholesterol in liver
* reduces total cholesterol concentration, increase blood cholesterol uptake, decrease LDL and TG, small increase in HDL
* pleiotropic effects (plaques stabilisation, decrease inflam response)
SE: headache, trouble sleeping, myalgia (myopathy, rhabdomyolysis)
What are nitrates?
Glyceryl trinitrate (GTN) - anginine
GTN spray (used in 1st aid for angina)
Indication: prevent/Tx angina
MOA: nitric oxide mediates vasodilation (predom. venodilators) = decrease preload/afterload (decrease venous return to heart)
AE: mainly due to vasodilatory effect (ortho hypotension, headache, flushing, palpitations, fainting)
What are the 4 main meds in the European update to HFrEF guidelines?
- ACE-1/ARNI (AngT neprilysn inhibitor - new med “Entresto”)
- BB
- MRA (magnetic resonance angiography)
- SGLT2i (new med)- block glucose reabsorption into kidney
How if HFrEF managed with medications?
Medication titration
* increased to target dose or max. tolerated dose
ACEI or ARB or ARNI + BB and MRA are titrated
e.g. BB - regular doses until titrated
What are anti-coagulants?
Warfarin (marevan, Coumadin) - Vit K antagonist
NOACS:
Rivaroxaban (Xarelto) and Apixaban (eliquis) = Factor Xa inhib.
Dabigatran (pradaxa) = direct thrombin inhibitor
Indications: AF, prosthetic heart valves (warfarin), prevention/Tx of VTE (DVT, PE)
SE: bleeding (internal/external)
What is cardiac glycoside -digoxin?
indication: AF, atrial flutter, HF
MOA: increase release stored intracellular Ca causing increased myocardial contraction foruce
–> reduces SNS - slows ventricular rate
SE: N&V, blurred vision, bradycardia, arrhythmia, dig toxicity
Ex considerations:
* rest - possible non-specific ST-T wave changes
* possible ST depression
What are antiarrhythmic agents - Class III?
Amiodarone + Sotalol = RHR & ExHR decrease, potential hypo, no effect on Ex capacity
Amiodarone - slows AV and bypass tract conduction/prolongs refracotry period of myocardial tissues + weak BB
Indication: Tx and prophylaxis of serious tachy-arhyth refractory to other Tx e.g. VT, AF and SVT
Sotalol: non-selective BB also prolongs refractory period of atria, vetricles and bypass tract
Indication: Tx/prevention of arrhythmias e.g. atrial, SVT
What are the three drugs that are part of “triple therapy”?
- aspirin
- clopidogrel
- rivaroxaban
All anti-platelets! Decrease blood clot activity
Most Pt’s not on triple therapy for long time! - there is ischaemic vs bleeding risk!!
~1 month, drop a drug (usually aspirin)
- not >6M, drop to 1 anti-platelet drug
What are NSAIDs?
Anti-inflam Meds
Cause:
- Na+/fluid retention
-HTN
-increased workload on heart
- renal impairment
Ibuprofen - neurofen
Diclofenac - voltaren
Naproxen - aleve naprosyn
Indomethacin - arthrexin, indocid
Celecoxib - celebrex
Meloxicam - mobic
What is the mechanism of NSAIDs?
- ACE inhibitor dilates efferent arteriole + reduced GFR
- diuretics reduce plasma volume and GFR
- NSAIDs constrict blood flow into glomerulus via afferent arteriole and reduce GFR
This leads to renal failure –> filtration rate and effectiveness reduces
What are alternatives to NSAIDS?
Paracetamol (500mg x 2) max 8/day
Panadol Osteo SR (66mg x 2) max. 6/day
Panadeine/forte + coloxyl and senna
Oxycodone (immediate/slow release)
Buprenoprhine patches
Try to avoid opioids in the beginning
Consider co-morbidities and cause of pain
How do cardiac meds affect Ex?
- Ex capacity - decrease?
- med titration affects Ex tolerance
- ACEI, BB, digoxin, nitrates - improve functional capacity in long-term
- dose increases of meds can cause transient decrease in Ex tolerance
- temporary decrease in Ex intensity/duration may be needed for Sx of dizziness, dyspnoea and fatigue
What are the similarities and differences with COPD and asthma?
Both chronic inflam. disease involving small airways and reduce airflow
COPD
* reduced airflow not fully reversible
* usually progressive
* abnormal response of lung to noxious particles/gas
Asthma
* variable airflow obstruction that is often reversible
* hyperresponsiveness, bronchoconstriction
* episodes of wheezing, SOB, chest tightness, coughing (esp. morning/night)
20% of people with COPD have asthma
Asthma&COPD overlap
What are the key aspects of COPD management?
- cease smoking
- pharmocotherapy (technique and adherence!)
- pulmonary rehab
- action plan
- self-management
- comorbidities
- nutrition
- vaccination
What are the main groups for COPD and Asthma?
Main goal: bronchodilate!
2 Categories:
- beta agonists - stimulates Beta2 adrenoceptors
- SABA = short acting. Salbutamol (ventolin), terbutaline (bricanyl)
- LABA = long acting
Eformoterol (Oxis)
Salmeterol (serevent) - Muscarlinic Antagonist - relax smooth muscle
- SAMA - short acting
Ipratroplum (atrovent)
- LAMA = long acting
Tiotroplum (spiriva)
Glycopyrronium (seebri)
What are the Tx steps for COPD?
- Short Acting bronchodilators - use when needed
- long acting bronchodilator (beta agonist or muscarinic antagonist - used regularly
- beta agonist + muscarinic - used regularly
- Add inhald corticosteroid - used regularly
What are the Tx steps for asthma?
- As needed SABA only
- low-dose regular preventer (+SABA when needed)
- low-dose combination regular preventer (+reliever as needed)
- higher-dose combination regular preventer (+reliever as needed)
- add-on specialised Tx
