DRUGS CHEAT SHEET

CARDIO

CLASS GENERAL/TRADE NAME

MECHANISM INDICATIONS SIDE EFFECTS/DRUG INTERACTIONS/PRECAUTIONS

ANTI-HYPERTENSIVEβ-Blocker (β-Blocker for the LOLs)

Propanolol (Non-selective)

Atenolol (Selective)

Metoprolol

Block B1-adrenegic receptor Decrease sympathetic activity Decrease intracellular cAMP Muscle relaxation REDUCE INOTROPY

First line prescription for myocardial infarction

Contraindications:- Asthmatic patients

Side effects:- Bronchoconstriction - Increase risk of

diabetes - Peripheral vascular

disease/cold extremities

- Mask hypoglycaemia (atenolol preferred)

- Nightmares/dreams (propranolol)

- Heart block in combination with verapamil

Ca2+ channel blocker Verapamil Diltiazem

Heart:Block Ca2+ channel No influx of extracellular calcium No calcium release from SR Reduce contractility REDUCE INOTROPY & CHRONOTROPY

Peripherals:Decrease Ca2+ influx in peripheral smooth muscles Vasodilation

- ACEI+CCB - diabetes

- Beta blocker + dihydropyridine - CHF

Contraindications:- Patients on B-blocker

cannot be prescribed with verapamil

- Negative inotropy drugnot to be used in heat failure!

Side effects:- Flushing and peripheral

oedema (dihydropyridines)

- Heart block/heart failure

(verapamil/diltiazem) A2RA (Angiotensin 2 receptor antagonist)

Losartan Valsartan

Block angiotensin 2 receptor in RAAS:

- Decrease BV - Decrease BP

*refer to ACE inhibitor below

Prescribed to patients with coughing with ACE-inhibitor use

- Headache, dizziness- Rashes- Angio oedema- Photosensitivity- Hyperkalaemia

(aldosterone inhibition)- Hypotension (on first

dose)ACE inhibitor Trandolapril

Captopril- Stop RAAS (refer to

diagram below)- Inhibit the

conversion of bradykinin to inactive bradykinin Vasodilation Decrease TPR Decrease afterload Decrease cardiac workload (CO) Decrease BP

First line prescription in:- Myocardial

infarction- Hypertension- Heart failure- <65 years old

( Lack of diabetes)

- Diabetes with proteinuria

- Coughing- Rash/angioedema - Hyperkalaemia - First-dose hypotension- Headache, dizziness,

fatigue, nausea.

Diuretics Loop diuretics Furosemide

- Acts on Na/K/2Cl cotransporter at Loop of Henley

- Inhibit the reuptake of Na from tubule

- Water follow salt

- Hypokalaemia

Thiazide (Metalazone, caffeine)

- Acts on Na/Cl at distal convotuled tubule

- Hypokalaemia

K-sparing Spironolactone/

Aldectone

- Inhibit Na/K antiport at cortical collecting tubule

Aldactone:

- Hyperkalaemia

- Inhibit aldosteroneANTI-PLATELETS

Aspirin - Inhibit COX1 pathway irreversibly

- Reduce thromboxane A2

- Also reduce prostacyclin which inhibit platelet aggregation but the production of TXA2 takes longer time to recover and thus, the anti-platelet effects of aspirin outweigh this effect.

- Arrhythmia- Heart and valve

replacement surgery

Contraindications:- Pregnancy

Side effects: Always give together

clopidogrel/dipyridamole

Bleeding Asthma

Warfarin Vitamin K antagonist inhibit reduction of vitamin K (reduction as in reduce dlm REDox) inhibit activation of clotting factors (2, 7, 9, 10)

- Blood coagulation problems (DVT, PE)

- Atherosclerosis/ MI

- Stroke- Atrial fibrillation - Refer to

indication for aspirin

Contraindications: - Pregnancy

Side effetcs:- Bleeding &

haemorrhage- Warfarin necrosis in

patients with protein C deficiency (thrombosis with skin necrosis and gangrene)

- OsteoporosisCHOLESTEROL CONTROL

Statin HMG-CoA reductase inhibitor

Lipitor Simvastatin

HMG-CoA reductase inhibitorreduction in mevanolate levels. Normal mechanism; HMG-CoAmevanolate

- High risk for hypercholesterolaemia (family history, weight, age)

Side effects- Hepatic damage- Myalgia- Myopathy - Muscle cramps

(by the action of HMG-CoA reductase)cholesterol

Fibrates PPar-alpha receptor agonistincrease beta oxidation in the liver (beta oxidation converts fatty acidacetyl-CoA)lower fatty acidAlso; PPar-alpha receptor agonist increase lipoprotein lipase(1) increase breakdown of LDL, (2) increase breakdown of triglyceride, (3) increase reuptake of LDL (reuptake of LDLdecrease LDL in blood)

Side effects- GI disturbance- Myopathy (increase

when taken with statin)- Cholestatic jaundice- Gallstone formation

Ezetimibe Decrease absorption of cholesterol from duodenum (does not affect triglyceride and fat soluble vitamin)

Also; increase hepatic uptake of LDL decrease of LDL in blood

Side effects- Steatorrhoea - Fatigue- Headache - Hepatitis - Raised LFT- Myalgia - Rashes- Myopathy

ANTI-ARRHYTHMIA

I Na+ channel blocker Quinidine (prokinamide, disopyramide)

Indications:- Ventricular arrhythmia - WPW (just

prokinamide)- Recurrent AF

*kene letak sini sbb diagram besaq sangat

IIβ-blocker Propanolol Atenolol

Bind to B-receptor in cellinhibit sympathetic

- Refer to atas aku dah malas dah

Side effects pun same paham paham je la

Metoprolol actionreduce firing rate of SA nodereduce heart rate

nk type ni woi

IIIK+ channel blocker Amiodarone Dronedarone

Hyperpolarisation prolongs QT interval

- Tachycardia without sinus rhythm

- VT/VF in acute MI

Side effects:- Torsade des pointes

IVCa2+ channel blocker

Verapamil Diltiazem

Block voltage-sensitive calcium channel (L-type calcium channel)inhibit Ca2+ entry caused by depolarizationslows down AP conduction from SA to AVslows down HR

- Reentrant SVT- PSVT- AF

Precautions:- NEVER EVER GIVE to

people with VT!- If given via

IVhypotensionSide effect:

- Heart block V Adenosine, Digitalis, Magnesium

Adenosine Cause hyperpolarisation more time needed to reach threshold (1) slows HR, (2) regulate the firing of SA node, (3)slows down conduction through AV node

Also; decrease cAMPdecrease in inward pacemaker current and the inward calcium currentslows down SA firing rate and also AV node conductionslows HR

- Torsade des pointes

- SVT- PSVT- Reentrant SVT

Side effects:- Confusion - Headache- Bronchoconstrriction- Flushing

Digitalis Enhance vagal tone decrease sympathetic decrease frequency of transmission between SA

Supraventricular reentrant arrhythmia

Contraindications:- Not to be given to pt

with renal failure Side effects:

Node and AV node increase refractory period in AV node reduces ventricular rate

- Nausea- Vomiting- Arrhythmia- Confusion- Toxic effects: digitalis

induced arrhythmia through (1) less –ve resting potential, (2) decrease action potential duration, (3) entrance automaticity

Magnesium Nil Digitalis induced arrhythmia patients

Nil

POSITIVE INOTROPIC Cardiac glycosides Digitalis

(Digoxin)Inhibition of Na+/K+ exchange channel increase Na+ in myocytes decrease Na+/Ca2+ exchange via Na+/Ca2+

antiport increase Ca2+ increase inotropy/contractility

Ditto

Sympathomimetics Catecholamine (adrenaline, noradrenaline, dopamine)

Dobutamine PDE-3 inhibitor (phosphodiaterase-3 inhibitor)

Enoximoxone

ANALGESICOpiods Morphine

(Loperamide)Bind to opioid receptors at CNS block ascending pathway of perception block pain perception

Given to patients with angina when pain not improved with nitrates

Opioid also present in GI system and thus, drugs may cause GI disturbance

VASODILATOR

Organic nitrates GTN (under-the-tongue nitrate/ sublingual)

Anginine

GTN denitrated into NO (active metabolite that causes vasodilation) GTP is converted into cGMP cause muscle relaxation

Given sublingually as to escape first pass metabolism

- Unstable angina

PDE -5 inhibitor (phosphodiaterase-5 inhibitor)

Sildenafil Inihibit cGMP breakdown in cells relaxation enhance vasodilation and oxygenation

Ca2+ channel blocker Dihydropyridine (amlodipine, felodipine)

Peripherals:Decrease Ca2+ influx in peripheral smooth muscles Vasodilation

RAAS

ANGIOTENSIN 1

THIRST

ANGIOTENSINOGEN

VASOCONSTRICTION

ACE

ANGIOTENSIN 2

RENIN

ALDOSTERONE ADH SNS (INC.)

Released when:

Reduced renal perfusion, decrease CO2, increase sympathetic

Inhibit by ACE INHIBITOR

Released by lungs and kidneys

RESPI

CLASS GENERAL/TRADE NAME MECHANISM INDICATIONS SIDE EFFECTS/DRUG INTERACTIONS/PRECAUTIONS

BRONCHODILATORS

Beta-agonists - Short acting B-agonist (Salbutamol, Terbutalin)

- Long acting B-agonist (Salmeterol, Formoterol)

B-agonist bind to B-receptor increase in CAMP increase in intracellular PKA phosphorylation of myosin light chain kinase inhibit muscle contraction

Increase mucus clearance (mechanism unknown)

- Asthma (SABA & LABA)

- COPD (LABA)

Contraindications:

- Patients with cardiovascular disease

Side effects:

- Tremors (due to stimulation of peripheral smooth muscle)

- Tachycardia

- Tolerance

- anxiety

Muscarinic receptor anatgonist

- Short acting (Ipratropium bromide)

Normal fx:

Acetylcholine bind to M3 receptor Activate phospholipase C Increase in IP3 Increase in intracellular CA2+ muscle contraction

*block Ach from binding to M3

- Asthma - Dry mouth

- Throat irritation

receptors

- Long acting (Tiotropium bromide)

Dissociate from M1 to M3 more slowly than M2.

- COPD

Leukotriene antagonist

Zafirlucast, Montelukast Blocks the conversion of leukotriene C4 to leukotriene D4 Decrease in concentration of leukotriene D4 Decrease in inflammation

- Add on therapy to inhaled corticosteroid when LABA is not tolerated

- For frequent intermittent asthma, aspirin-induced and eosinophilic asthma

Methylxanthine Theophylline Normal fx:

Inhibit

ATP CAMP AMP

Thiophylline: Inhibit the conversion of CAMP to AMP increase in CAMP muscle relaxation

ANTI-INFLAMMATORY

Corticosteroids Inhaled: Glucocorticoids: - Asthmatic pt Inhaled:

Fluticasone, Budesonide, Beclomethosone

Oral:

Prednisolone

Bind to the glucocortocoid promoting elements (GRE) in the promoter region of the specific gene to alter the gene production of protein that inhibit inflammation (lipocortin) block arachidonic acid pathway at membrane phospholipid reduce inflammation.

- COPD pt - Voice change

Oral:

- Cushing’s syndrome

- Weight gain

- Puffy face

- Hypertension

- Glaucoma

- Cataract

Cromones Chromoglycate, Nedocromil Inhibit mast cells degranulation inhibit the release of histamine

*Mechanism is not fully understood

- Any airway inflammatory disease

ANTIBIOTICS

Cell wall synthesis inhibitor

B-lactams (Penicillin, Vancomycin)

- Bactericidal

Interfere with the sysnthesis of the bacterial cell wall inhibit the transpeptidases that cross-link the peptide chains attached to the backbone of the peptidoglycan weaken the cell wall leads to bacterial lysis bacterial death

Tolerance:

Normal: Penicillin binds to

- Pneumonia

- Vancomycin is used for patients who are resistant to penicillin (because it is a glycopeptides antibiotic and not a B-lactam)

- Metronidazole is used for patients

Contraindications:

- Allergy/ hypersensitivity

bacterial cell wall inactivation of inhibition of autolytic enzyme lysis of cell wall

Abnormal:

- Inactivation by B-lactamase production of B-lactamase is the major mechanism of resistance to the B-lactam B-lactamase cleaves predominantly penicillin, cephalosporins or both production may be encoded within the bacterial chromosome / gene may be acquired on plasmids or transposon

- Defective autolytic enzyme Bacteria is not lysed even in the presence of drugs

- Alteration of active site of target receptor in bacterial cell wall Unable to bind

who are allergic to B-lactams

- Decrease penetration to the target site gram negative provides good barrier to the penetration of B-lactams antibiotics to the target PBP (Penicillin binding protein) Usually must pass through hydrophilic protein channels in the outer membrane of the gram negative bacilli to reach periplasmic space

DNA synthesis inhibitor

Folate affectors (sulfonamides)

Disrupt folic acid synthesis:

Protein synthesis Macrolides (Erythromycin, Clarithromycin,

Block 50s subunit of ribosome which then inhibit bacterial

- Hypersensitivity

inhibitor azithromycin) protein synthesis - Rashes

- GI disturbance

- Fungal growth

- Fever

Tetracyclines Block 30s subunit of ribosomes which inhibit bacterial protein

- Dizziness

- GI distress

- Photosensitivity

- Skin and mucus pigmentation

- Oral, rectal and genital fungal growth

Topoisomerase inhibitor

TAK FOFULER Disrupt gene transcription by affecting the unfolding process

Anti protozoal drugs Metronidazole Active against anaerobic bacteria and amoebas organisms will reduce metronidazole to its active form intracellulary reduced drug then binds to DNA causingstrand breakage, dissolution of helix formation and overall degradation of the DNA

For those allergic to penicillin

EMERGENCY

Analgesics - ABCDEF management of pneumonia

- COPD

Anti- Biotics Penicillin

CPAP Positive pressure oxygen via nasal prongs

- Blue bloaters is contraindicated for 100% O2 monitor patient’s consciousness discontinued and put on 21% oxygen via mask

Drain Draining fluid in pulmonary oedema

- Physiotherapist

- Diuretics

Extra air Increase O2

Fluid Intravenous fluid Dehydration decrease BP to restore/ maintain BP

ANTI-MUCOLYTIC

Mucolytic agent Acetylcysteine Mechanism is not fully understood

- Any disease with hypersecretion

- Asthma

- COPD

HAEM

CLASS GENERAL/TRADE NAME MECHANISM INDICATIONS SIDE EFFECTS/DRUG INTERACTIONS/PRECAUTIONS

DNA DAMAGING

Alkylating agents - It interferes with DNA synthesis by breaking the cross-link of the DNA strands.

- It affects the cross-link by covalently binding alkyl groups to DNA strands.

Anti-metabolites - Pyrimidine antagonist

- Purine antagonist

- Arabinosides

- Inhibit nucleic acid synthesis

Folic acid antagonist Refer kat atas

DNA REPAIR INHIBITORS

Epipodophyllotoxins Topoisomerase inhibitor

It can inhibit either:- Topoisomerase I:

irinotecan & topotecan - Topoisomerase II:

etoposide

Topoisomerase I:

- Used in lung, colon, ovary and cervix cancer

Topoisomerase II:

- Used in wide range of cancers

Cytotoxic antibiotics - Intercalate adjoining - Used in

nucleotide pairs in the same DNA strands

- Inihibit topoisomerase II DNA repair

haemotological and solid cancer

ANTI-TUBULIN

Vinca alkaloids - Bind to tubulin microtubule formation

- Must never be given intratecally (into spinal theca)

- Associated with neurotoxicity due to their anti-microtubule effect

Taxanes - Bind to tubulin dimmers prevent assembly into microtubules

- Used in many cancers including ovarian, breast and lung cancer

Patients should be premedicated with steroids, H1 and H2 histamine antagonists prior to treatmen

Can cause neurotoxicity and hypersensitivity reactions