FUNDAMENTAL: ANTI-INFLAMMATORY DRUGS

Class Drug Example MOA Uses Side Effect Contraindication

Steroid - Glucocorticoid
- Corticosteroid
- Prednisolone
- Hydrocortisone
- Dexamethasone
- Betamethasone
- Triamcinolone
- Methylprednisolone
Glucocorticoid Replacement therapy Cushing syndrome - PU
1. Inhibit leukocyte infiltrate - acute adrenal insufficiency - Round face - DM
2. Interfere with mediators of - chronic adrenal insufficiency - Buffalo hump - HTN
inflammatory response (Addison’s disease) - Truncal obesity - TB
3. Suppress humoral immunity - Congenital adrenal hyperplasia - Thin limbs - HSV keratitis
- CHF renal failure
Corticosteroid Pharmacotherapy Others - Viral & fungal infections
1. Stimulate lipocortins & prevent - RA & Osteoarthritis - Fragile skin, purple striae, - Osteoporosis
synthesis of inflammatory mediators - Rheumatic fever easy bruising, hirsutism - Psychosis
2. Inhibit phospholipase A2 inhibitory - Gout - Hyperglycemia - Seizures
proteins - Hypersensitivity - Muscle weakness
3. Interfere with leukocyte infiltration - Autoimmune - Delayed wound healing
4. Inhibit release of arachidonic acid from - Asthma - Peptic ulceration, bleeding,
phospholipids - Collagen: SLE, Polyarthritis perforation
5. Reducing formation of PG nodosa, Nephrotic syndrome, - Osteoporosis
Glomerulonephritis - GC save - Cataract, glaucoma
Prednisolone life - Growth retardation
1. Limiting vascular capillary dilatation & - Eye: conjunctivitis, keratitis, - Suppression HP-adrenal
permeability retinitis axis: malaise, fever, anorexia,
2. Restrict accumulation of PMNL & - Skin: eczema, dermatitis, nausea, weakness
macrophages. Steven Johnson Syndrome GC
3. Reduce release of vasoactive kinins. save life
4. Reduce inflammatory reactions - Intestinal: UC, CD

Class Drug Example MOA Uses Side Effect Contraindication

NSAIDS - Aspirin (antiplatelet) 1. Inhibit cyclooxygenase enzyme (Cox1 - Osteoarthritis - Dyspepsia - Irritable bowel
(Nonselective) - Ibuprofen & Cox2) - Rheumatoid arthritis - Gastric ulceration/bleeding syndrome
- Ketoprofen 2. Prevent synthesis of prostaglandins - Tennis elbow - Diarrhea - Elderly with GI
- Naproxen and thromboxane. - Headache - Oedema problems
- Meloxicam 3. Reduce inflammation and pain - Migraine - Hypertension - PU (stomach bleeding)
- Acute gout - Nephrotoxicity - Kidney disease
NSAIDS - Celecoxib 1. Inhibit cyclooxygenase enzyme (Cox2) - Dysmenorrhea - Photosensitivity - IBF (CD & UC)
(COX2 - Rofecoxib 2. Prevent synthesis of prostaglandins - Postoperative pain - Risk stroke & MI (except - Transient ischaemic
Inhibitors) - Etoricoxib and thromboxane. - Muscle stiffness (PD) aspirin) attack (except aspirin)
3. Reduce inflammation and pain - Stroke (except aspirin)

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 FUNDAMENTAL: ANTIHISTAMINE & PROSTAGLANDINS

Class Drug Example MOA Uses Side Effect Contraindication

H1 Receptor 1st Generation
Antagonist Antihistamine
- Meclizine
- Hydroxyzine
- Doxylamine H1 receptor antagonist
- Promethazine - Sedation
1. Inhibits histamine action at the receptor
- Clemastine - Allergic - Drowsiness
2. Competes with histamine for binding
- Dimenhydrinate - Insect bite & ivy poisoning - Dry mouth
3. Displace histamine from receptor - Glaucoma
- Diphenhydramine - Antipruritic agent - Blur vision
- Peptic ulcer
- Block runny nose - Light headedness
H1 receptor antagonist - Hypertension
2nd Generation - Preanesthetic medication - Motor incoordination
- Inhibit increased vascular permeability - Bronchial asthma
Antihistamine - Cough suppressant - Urinary hesitancy
- Inhibit allergy bronchoconstriction - COPD
- Loratadine - Labyrinth suppressant (vertigo) - Fatigue and sedation
- Cetirizine - Antihistaminic, anticholinergic, - Alteration bowel movement
H2 receptor antagonist
- Azelastine antiemetic - Diminished alertness and
- Reduce gastric acid production
- Desloratadine concentration

H2 Receptors - Cimetidine
Antagonist - Ranitidine
- Famotidine

Class Drug Example MOA Uses Side Effect Contraindication

Prostaglandins - Misoprostol 1. PG bind to PG receptors (GPCR) - Terminate pregnancy - Hypotension - NSAIDS
- Enoprostil 2. G-Protein Couple Receptors stimulate - Facilitating of labour - Bronchoconstriction - Corticosteroid inhibit
- Dinoprost inositol triphosphate (IP3) and c-AMP - Peptic ulcer: increase mucous - Vomiting and diarrhea Phospholipase A2
- Carboprost pathway production and mucosal BF - Fever and dizziness - Analogues PGE1,
- Beraprost 3. Inhibition of adenyl cyclase via G1 - Prevent platelet aggregation - Flushing PGF2α, PGI2
- Bimatoprost activation - Treat pulmonary hypertension
- Dinoprostone 4. Ca2+ mobilization from G1 leading to: - Treat glaucoma
- Unoprostone vasodilation, reduce BP, reduce acid - Enhance penile erection
secretion, bronchodilation, natriuresis, - Teat bronchial asthma
uterine contraction, increase peristalsis,
increase sensitivity to pain

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 FUNDAMENTAL: ANTIMICROBIAL AGENT

Class Drug Example MOA Uses Side Effect Contraindication

Penicillins Broad Spectrum - Gram +ve aerobes - N&V - Hypersensitivity
- Ampicillin - Gram –ve aerobes - Pruritus - Steven Johnson
- Amoxicillin - Spirochetes - Headache syndrome
- Anaerobe - Leukopenia - Pregnancy and lactation
Narrow Spectrum - Branching gram -ve mother
- Penicillin G
- Penicillin V
- Procaine
- Benzathine

Beta Lactams
- Nafcilin

Class Drug Example Uses Side Effect Contraindication

Cephalosporin 1st Generation - Gram +ve cocci - Hypersensitivity - Hypersensitivity
- Cephalexin - Enterobacteria - GI distress - Premature neonates
1. Bind to penicillin binding protein (PBP)
- Cefazolin - Gram –ve (beta lactam - Pancreatitis - Jaundice (full term
2. Inhibit final transpeptidation.
- Cefadroxil resistance, pseudomonas) - Headache & dizziness neonates)
3. Interfere synthesis of peptidoglycan in
- Methicillin Resistance - Candidal vaginitis
cell wall
2nd Generation Staphylococcus aureus (MRSA) - Rash and flushing
4. Lead to bacterial lysis and death
- Cefuroxime
- Cefprozil
- Cefaclor

3rd Generation
- Ceftriaxone
- Cefixime
- Cefoperazone

4th Generation
- Cefepime
- Cefpirome

5th Generation
- Ceftaroline
- Ceftolazone

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 FUNDAMENTAL: ANTIMICROBIAL AGENT

Class Drug Example MOA Uses Side Effect Contraindication

Carbapenems - Meropenem 1. Bind to penicillin binding protein (PBP) - Broad spectrum (beta lactam - N&V - Hypersensitivity
- Emipenem 2. Inhibit bacterial cell wall synthesis resistance) - Seizures - History of anaphylactic
- Ertapenem 3. Lead to cell wall assembly stop - Gram +ve cocci - Headache reaction
- Doripenem 4. Eventually bacterial cell lysis - Gram –ve bacilli - GI distress
- Anaerobes
Class Drug Example MOA Uses Side Effect Contraindication
Monobactams - Aztreonam 1. Bind to PBP-3 - Against gram –ve bacilli - GI distress Hypersensitivity
2. Inhibit bacterial cell wall synthesis - Intrinsic beta lactamase - Headache
3. Lead to cell wall assembly stop resistance - Vertigo
4. Eventually bacterial cell lysis
5. Highly resistant to hydrolysis by narrow
beta lactamase

Class Drug Example MOA Uses Side Effect Contraindication

Glycopeptide - Vancomycin 1. Bind to D-alanyl-D-alanine of cell wall - Multi drug resistance organism - Nephrotoxicity - Hypersensitivity
- Telavancin precursor - Broad spectrum coverage - Red man syndrome
- Dalbavancin 2. Block glycopeptide polymerisation - Against gram +ve bacteria - Anaphylactic reaction
- Oritavancin 3. Lead to inhibition of cell wall synthesis - MRSA
- Teicoplanin 4. Impairs bacterial cell membrane
permeability
5. Impairs bacterial RNA synthesis

Class Drug Example MOA Uses Side Effect Contraindication

Aminoglycoside - Gentamycin - Severe gram –ve bacilli - N&V - Hypersensitivity
(30S subunit) - Streptomycin infections - Anaemia
- Amikacin - Tuberculosis (TB) - Convulsion
1. Bind to 30S ribosomal subunit - Nephrotoxicity
2. Prevent binding of aminoacyl transfer
Class Drug Example RNA Uses Side Effect Contraindication
Tetracycline - Tetracycline 3. Inhibiting protein synthesis - Atypical bacteria: - GI distress - Hypersensitivity
(30S subunit) - Doxycycline 4. Arresting cell growth mycoplasma, rickettsia, - Photosensitivity
- Minocycline anaplasma, chlamydia, - Deposition in developing
ureaplasma, vibrio cholera bone and teeth
- Superinfection

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 FUNDAMENTAL: ANTIMICROBIAL AGENT

Class Drug Example MOA Uses Side Effect Contraindication

Macrolide - Azithromycin - Atypical pneumonia - Increase intestinal motility - Hypersensitivity
(50S subunit) - Erythromycin - URTI - Acute cholestatic hepatitis
- Clarithromycin - Chlamydia - Eosinophilia
- Gram +ve cocci - Rash
- Neisseria
1. Bind to 50S ribosomal subunit
2. Result in blockage of transpeptidation
Class Drug Example Uses Side Effect Contraindication
3. Therefore preventing peptide bond
Lincosamide - Clindamycin - Anaerobes bacteria - GI distress - Hypersensitivity
formation, ribosome assembly and
(50S subunit) - Lincomycin - Aspiration pneumonia - Clostridium difficile colitis
translation process
- Lung abscess
4. Inhibit protein synthesis

Class Drug Example Uses Side Effect Contraindication

Chloramphenicol - Chloramphenicol - Rickettsia - Dose related anaemia - Hypersensitivity
(50S subunit) - Meningitis due to - Grey baby syndrome
Haemophilus influenzae, - Anaplastic anaemia
Neisseria meningitides,
Streptococcus pneumoniae
Class Drug Example MOA Uses Side Effect Contraindication
Fluoroquinolones - Ciprofloxacin - Gram –ve bacilli in UTI and GI - Seizures - Hypersensitivity
- Levofloxacin infection - Tendinitis
- Gemifloxacin - Genital pathogen - GI distress
1. Inhibits DNA gyrase and
- Enofloxacin - Pseudomonas - Jaundice
topoisomerase
- Pneumonia
2. Interfere with bacterial DNA
- Penicillin resistance
replication, transcription, repair and
- Pneumococci
recombination
3. Thereby inhibit relaxation of
Class Drug Example Uses Side Effect Contraindication
supercoiled DNA
Quinolones - Nalidixic acid - Uncomplicated lower UTI - Nausea and vomiting - Hypersensitivity
4. Lead to breakage of bacterial DNA
- Shigellosis - allergic rash
strand
- Dizziness or vertigo
- Muscular weakness

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 FUNDAMENTAL: ANTIMICROBIAL AGENT

Class Drug Example MOA Uses Side Effect Contraindication

Sulphonamides - Sulfisoxazole 1. Interfere with synthesis of nucleic - Gram +ve bacteria - GI distress - Hypersensitivity
- Sulfamethoxazole acid - Gram –ve bacteria - Acute haemolysis in G6PD - Renal or hepatic
2. Blocking the conversion of P- - Simple UTI - Crystaluria impairment
aminobenzoic acid (PABA) to - Nocardia - Aplastic anaemia - Blood disorders
dihydrofolic acid - Toxoplasmosis - Nephrotoxicity - Porphyria
3. Give bacteriostatic action - Malaria - Pre-hepatic jaundice - SLE
4. Can be bactericidal when low
thymine concentration

Class Drug Example MOA Uses Side Effect Contraindication

Rifamycins - Rifampicin 1. Inhibit bacterial RNA synthesis - Mycobacterium tuberculosis - N&V - Hypersensitivity
(antimycobacterials) - Rifabutin 2. Bind to beta subunit of DNA- - Leprosy - Rash
dependent RNA polymerase - Haemophilus influenzae B - Pruritus
3. Prevent the elongation of RNA - Meningococcal prophylaxis - Hepatitis
4. Lead to bactericidal

Class Drug Example MOA Uses Side Effect Contraindication

DHFR (Dihydrofolate - Trimethoprim 1. Inhibit Dihydrofolate reductase - Recurring UTI - Rash - Hypersensitivity
Reductase) Inhibitors - Pyrimethamine 2. Prevent conversion of dihydrofolate - Respiratory infections - Headache and fever - Megaloblastic anaemia
to tetrahydrofolate - Ear and sinus infections - Bone marrow suppression
3. Interfere synthesis of bacterial - Shigella - Hyperkalaemia
nucleic acid and protein - Salmonella - GI disturbance
4. Lead to bacteriostatic or bactericidal

Class Drug Example MOA Uses Side Effect Contraindication

Nitroimidazoles - Metronidazole - Bacterial vaginosis - Dizziness and headache - Hypersensitivity
- Tinidazole - Trichomoniasis and giardiasis - Peripheral neuropathy - Pregnant and lactation
1. Inhibits bacterial protein synthesis
- Acute necrotising ulcerative - Sensory disturbance mother
2. Interact with bacterial DNA
gingivitis - Abdominal pain
3. Loss of DNA helical structure
- Eradicate helicobacter pylori - Anorexia
4. Breakage of DNA strand
associate PUD - Dark urine
5. Lead to bacterial cell death
- Intestinal and hepatic
amoebiasis

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 FUNDAMENTAL: ANTICANCER AND CHEMOTHERPAY

Goal of cancer treatment? Management of toxicities?

1. Curative, total eradicate of cancer cells 1. Nausea and vomiting – 5HT Antagonist (Ondansetron)
2. Palliative, reduce of symptoms (QOL) 2. Cancer cachexia – Glucocorticoid
3. Adjuvant, reduce chance of recurring 3. Hyperuricemia – Allopurinol
4. Neo-adjuvant, given before surgery to shrink the tumour 4. Hypercalcemia – Alendronate (Bisphosphonate)
5. Bone marrow suppression – Filgrastim or Sargramostim
Combination chemotherapy?
1. Suppression of drug resistance Steroid in cancer treatment?
2. Increased killing of cancer cells 1. Anti-inflammatory
3. Reduced injury to normal cells (no overlapping toxicities) 2. Increase appetite
3. Produce euphoria
General adverse effect of anti-cancer? 4. Increase body weight
1. Bone marrow – leukopenia, thrombocytopenia, anaemia 5. Prevent hypersensitivity reactions
2. GI tract – oral or intestinal ulceration, diarrhea 6. Treatment of hypercalcemia
3. Hair follicle – Alopecia (hair loss) 7. Increase antiemetic (anti-vomiting) effect
4. Gonads – menstrual irregularities, premature menarche, impaired spermatogenesis
5. Wound – impaired wound healing
6. Fetus – Teratogenesis (especially during first trimester)

Class Drug Example MOA Uses Side Effect

Alkylating agents 1. Alkylating agents (carbonium ions) - Lung cancer - Nausea and vomiting
- Cisplatin attack nucleophilic on guanine base. - Ovarian cancer - Nephrotoxicity
- Carboplatin 2. Result in cross linking, abnormal base - Breast cancer - Neurotoxicity
pairing, and cutting of DNA strands - Numbness, tingling and burning
3. Block replication and transcription of sensation
tumour cells - Bone marrow suppression

CCNS (Cell Anthracycline 1. Intercalate between base pairs - ABVD regimen - N&V
Cycle Non- - Doxorubicin 2. Inhibit topoisomerase II - Hodgkin’s lymphoma - Alopecia
Specific) Agents - Epirubicin 3. Generate free radicals - Headache
4. Block DNA and RNA synthesis - BM suppression
5. Cause cutting of strands

Antibiotics
- D-actinomycin
- Mitomycin

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 FUNDAMENTAL: ANTICANCER AND CHEMOTHERPAY

Class Drug Example MOA Uses Side Effect

1. MTX is Folic acid analog that bind with - Breast cancer - Nausea and vomiting
DHFR enzyme - Epidermoid cancer - Hepatotoxicity
2. Interfere with synthesis of tetrahydrofolate - Lung cancer - Kidney failure
3. Interfere with enzymatic processes - Advance stage Non-Hodgkin’s Lymphoma - Folic acid deficiency
4. Inhibit formation of DNA, RNA and key (NHL) - BM suppression
Antimetabolites (S phase) cellular protein during S phase
- Methotrexate 5. Stopping cancer cells
- Fluorouracil
- Fludarabine 1. Fluorouracil is thymidylate synthase inhibitor - Metastatic carcinoma of breast and GI - Nausea and vomiting
2. Block synthesis of pyrimidine thymidine - Carcinoma of ovary, cervix, urinary bladder, - Mucositis
3. Interfere with DNA replication prostate, and pancreas - Diarrhea
4. Lead to shortage of dTMP - oropharyngeal cancer - Hand and foot syndrome
5. Rapidly dividing cancerous cells undergo - Alopecia (hair loss)
thymine-less death - Hyperpigmentation

CCS (Cell Cycle Taxanes (M phase) 1. Interfere with mitotic spindle - Ovarian cancer - N&V
Specific) Agents - Paclitaxel 2.Prevent conversion of microtubule polymer - Breast cancer - Myalgia
- Docetaxel into tubulin monomers (M phase) - NSCLC - Headache
- Ixabelipone 3. Stabilising existing microtubules - Bladder cancer - BM suppression
4. Inhibit their disassembly - Prostate cancer
5. Interfere with G2 mitotic phase - Oesophageal cancer
6. Inhibit tumour cell replication and supresses
cell proliferation

Vinca alkaloids (M phase)

- Vinblastine - GI upset
- ABVD regimen
- Vincristine 1. Block the formation of mitotic spindle - Alopecia
- Hodgkin’s Lymphoma
2. Preventing the assembly of tubulin dimers - Leukopenia
- Non small cell lung cancer (NSCLC)
Podophyllotoxin (G-S phase) into microtubule - Thrombocytopenia
- Bladder cancer
- Etoposide 3. Block polymerization of tumour cell - Sweating
- Testicular cancer
- Teniposide - Muscle cramps

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 FUNDAMENTAL: DRUGS ACTING ON SYMPATHETIC SYSTEM

Sympathomimetic Sympatholytic
Increase insufficient response Reduce sympathetic activity
Stimulatory action Inhibitory action
Agonist Antagonist

SYMPATHOMIMETIC AGENT
Classification of Sympathomimetic Agonist
Direct Acting Indirect Acting
Alpha Agonist Beta Agonist Releasers (amphetamine) Reuptake Inhibitor (cocaine)
- Nonselective (norepinephrine) - Nonselective (isoproterenol)
- Alpha1 selective (phenylephrine) - Beta1 selective (dobutamine)
- Alpha2 (clonidine) - Beta2 selective (albuterol)

Pharmacological actions of catecholamine?

1. All α stimulation except on the GIT
2. All β inhibit except on the heart

α1
- Vasoconstriction
- Increased peripheral resistance
- Increased blood pressure
- Mydriasis (dilatation of pupil)
- Increase closured internal sphincter of
the bladder
Adrenergic Receptors
α2 β1 β2
- Inhibition of norepinephrine release - Tachycardia - Vasodilation
- Inhibition of acetylcholine release - Increased lipolysis - Bronchodilation
- Inhibition of insulin release - Increased myocardial contractility - Increased glucose release
- Increased release of renin - Relaxed uterine smooth muscle
- Increased muscle and liver
glycogenolysis
- Slightly increase peripheral resistance

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 CORRELATION PA, USES AND SE OF EPINEPHRINE

Drugs Site of Action Pharmacological Action Uses Side Effect

Heart - Stimulate at β1 receptor - Cardiac arrest (normal heart) - Ventricular arrhythmias
- Increase HR & FOC - e.g. electric short and drowning - Palpitation, hypertension
- Increase SBP - Cerebral haemorrhage

Blood vessel - Stimulate α1 receptor - Alleviate pulmonary congestion - Tissue necrosis

- Skin and splanchnic VC - Reduce bleeding from small vessel - Severe hypertension
- e.g. tooth extraction - Cerebral haemorrhage
- Ischemia and gangrene

Blood pressure - Increase SBP and CO (β1 receptor) - Shock to increase tissue perfusion - Transient hypertension
- Reduce DBP and PR (β2 receptor) - Except cardiogenic shock - Cerebral haemorrhage
- First choice of anaphylactic shock

Bronchial muscle - Strong β2 agonist - Bronchial asthma - Irritation and coughing

- Dilate bronchioles - Dry mouth and throat
- Headache and flushing

Epinephrine Eye - Stimulate α1 receptor - Induced mydriasis - Glaucoma

- Dilatation of radial muscle of iris - Conjunctiva decongestion

Physiological - Increase BP (α1) - Anaphylactic shock

antagonist - Stimulate HR (β1) - Relieve bronchospasm
histamine - Bronchi dilatation (β2) - Angioedema and mucosa swelling
- Inhibit histamine and SRS-A release from mast cell - Insect sting or allergen

Metabolic effect - Increase liver and skeletal muscle glycogenolysis - Hyperglycemia with DM
- Increase blood glucose (β2) patient
- Reduce insulin secretion (α1)

CNS stimulation - Fear

- Anxiety
- Sweating
- Headache
- Nausea and vomiting

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 SYMPATHOLYTIC AGENTS

Adrenergic Receptor Antagonist

Alpha Blockers Beta Blockers
Nonselective Selective Nonselective Selective Beta-1
- Phentolamine (reversible) Alpha-1 Alpha-2 1st generation 3rd generation 2nd generation 3rd generation
- Phenoxybenzamine (irreversible) - Prazosin - Yohimbine - Propranolol - Carvedilol - Acebutolol - Betaxolol
- Labetalol - Atenolol - Celiprolol

Class
Non selective α blocker
Selective α blocker
l - Prazosin
Non selective β blocker
Drugs PA TU SE
- Phentolamine - Reduction in vascular tone - Presurgical pheochromocytoma - reflex tachycardia
- Phenoxybenzamine - Reduction in arterial and venous pressure - Raynaud phenomenon - Orthostatic HTN
- Erectile dysfunction
- Reduce blood pressure with less - HTN - Postural HTN
- Yohimbine tachycardia reflex - CHF - Syncope
- Relaxing effect in smooth muscle in prostate - Prevent urinary retention (BPH) - Headache and dizziness
- Variant angina
Heart - Arrhythmias - Reduce HR
- Reduce HR - Hypertension (portal HTN) - Heart block
- Reduce FOC - Hyperthyroid - Hypotension
- Reduce SBP - Anxiety and alcohol withdrawal - Hypertension in
pheochromocytoma when use
alone
- Propranolol
Bronchial Smooth Muscle - Bronchial spasm
- Bronchoconstriction - CI in bronchial asthma

Eye - Glaucoma
- Reduce IOP

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 HAEMOPOIETIC & LYMPHOID SYSTEM: DRUGS THERAPY OF MALARIA

Class Drugs MOA TU SE

- Chloroquine (CQ) - Acute attack of CQ sensitive - GI irritation
- Piperaquine falciparum and non-falciparum - Skin rash
- Tetracycline Destroy schizonts or merozoites in the RBC. - Chemoprophylaxis - Headache
- Doxycycline 1. Accumulate in food vacuole of plasmodium - Amoebic live abscess - Skin lesions
- Clindamycin 2. Prevents polymerization of haemoglobin - Retinal damage
3. Breakdown product heme into hemozin - Myocardial depression
4. Intracellular accumulation of heme is toxic to the
- Artesunate parasite - Chloroquine resistant malaria - Nausea & vomiting
- Artemether - Multidrug resistance - Diarrhea
- Dihydroartemisinin plasmodium falciparum

- Quinine 1. Complex with DSDNA - CQ resistant to plasmodium - Haemolytic anaemia

2. Prevent strand separation falciparum - Blackwater fever
Blood Schizonticides
3. Result in block of DNA replication and transcription - Severe complicated falciparum - Intravascular coagulation
to RNA malaria - Impaired hearing
- Nausea and vomiting
- Oedema
- Renal failure
- Mefloquine - Act as blood schizonticides - Prophylaxis for CQ resistance - GI distress
- Skin rashes
- Headache and dizziness
- Seizures

- Antifolate drugs 1. Antimetabolites of PABA - CQ resistance falciparum - GI distress

2. Block folic acid synthesis - Chemoprophylaxis of CQ - Skin rashes
3. By inhibiting dihydropteroate synthase - Kidney damage

Types of therapy
1. Prophylactic
2. Therapeutic (curative)
3. Prevention of transmission

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 HAEMOPOIETIC & LYMPHOID SYSTEM: DRUGS THERAPY OF MALARIA

Class Drugs MOA TU SE

Tissue schizonts - Primaquine Destroys secondary EE stage of tissue schizonts - Prevent relapse malaria - GI distress
1. Form quinolones – quinone metabolites - Prevent transmission of infection - Pruritus
2. Electron transferring redox compound - Headache
3. Act as cellular oxidants - Haemolyses in G6PD

Gametocide - Primaquine Destroy gametocyte in blood - GI irritation

- Chloroquine - Skin rash
- Quinine - Headache
- Retinal damage

Sporonticides - Proguanil Prevent sporogony and multiplication in

- Pyrimethamine mosquito

Drugs prevention malaria in travellers?

Chloroquine & Mefloquine

Multidrug resistance malaria?

Doxycycline, Malarone, Primaquine

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 HAEMOPOIETIC & LYMPHOID SYSTEM: DRUGS TO TREAT ANAEMIA

Class Drugs MOA TU SE

Iron (Ferrous Oral 1. Biosynthesis of heme and heme-containing proteins - Iron deficiency anaemia - N&V
Sulfate) - Ferrous gluconate 2. Include haemoglobin and myoglobin - Microcytic anaemia - Dyspnoea
- Ferrous fumarate 3. Replaces Fe found in HB, myoglobin and enzymes - Dark stool
Parenteral 4. Allow transportation of oxygen via Hb - Dental discoloration
- Iron dextran
- Iron sucrose complex

Iron chelators - Deferoxamine 1. Chelates excess iron - Acute iron poisoning - Hypotension
- Hemochromatosis - Neurotoxicity

Vitamin B12 - Cyanocobalamin 1. Cofactor for enzymatic reactions that form tetrahydrofolate - Vitamin B12 deficiency - CHF
- Hydroxocobalamin 2. Converted to coenzyme B12 - Megaloblastic anaemia - Arthralgia
3. Co-B12 convert methylmalonate to succinate - Pernicious anaemia - Headache
2. Convert homocysteine to methionine - Hydroxocobalamin - Angioedema
3. Promote haematopoiesis

Folic acid - Folic acid - Require for normal DNA synthesis - Folate deficiency - Flushing
- FA converted to tetrahydrofolate by dihydrofolate reductase - Megaloblastic anaemia - Anorexia
- FA is essential for nucleoprotein synthesis - Prevent congenital neural tube - Pruritus
- To maintain erythropoiesis defects - Malaise

Erythrocyte - Epoetin alfa 1. Agonist of erythropoietin receptors expressed by red cell - Anaemia associated with chronic - Hypertension
Stimulating progenitors renal failure - Thrombotic
Agents 2 Stimulate erythroid proliferation and differentiation - HIV Infection - Pure red cells aplasia
3. Induces the release of reticulocyte from the bone marrow - Cancer

Myeloid - Granulocyte colony 1. Stimulates neutrophil progenitor proliferation and - Neutropenia - Bone pain
Growth stimulating factor differentiation - Myelodysplasia - Splenic rupture
Factors - Filgrastim 2. Activates phagocytic activity of mature neutrophils and - Aplastic anaemia
extends their survival - Cytotoxic chemotherapy
3. Mobilizes hematopoietic stem cells

Megakaryocyte - Oprelevkin (IL-11) 1. Activate IL-11 receptors - Secondary prevention - Fatigue

Growth 2. Stimulate growth of multiple lymphoid and myeloid cells, thrombocytopenia - Headache
Factors include megakaryocytes - Cytotoxic chemotherapy - Dizziness
3. Increased number of circulating platelets and neutrophils - Anaemia

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 HAEMOPOIETIC & LYMPHOID SYSTEM: DRUGS ACTING ON BLEEDING AND CLOTTING DISORDERS

Class Drugs MOA TU SE

- Heparin (LMWH) 1. Inhibit coagulation - Treatment of established venous - Haemorrhage
2. Activating antithrombin III thromboembolism - Heparin induced
3. ATIII is a naturally occurring inhibitor of thrombin and - Reduce risk VT in angina and thrombocytopenia
clotting factor IX, Xa, XI, and XII following acute MI - Alopecia
- Osteoporosis
- Hypersensitivity

Anticoagulants
Warfarin 1. Structural analog of vitamin K - Prevent progression venous - Bleeding
2. competitively inhibit Vitamin K epoxide reductase enzyme thrombosis & pulmonary embolism - Fracture tendency
3. Leading to inhibition of synthesis of coagulation factor II, VII, - Prevent arterial thromboembolic - Pruritus
IX and X - Purpura
- Ecchymosis
- Purple toe syndrome

- Aspirin 1. Irreversibly inhibit COX1 - Mild to moderate pain and fever - Thrombocytopenia
2. Resulting in direct inhibition synthesis of prostaglandin and - Rheumatic disorder - Gastric irritation
thromboxane from arachidonic acid - Angina pectoris, MI, AI stroke - Dizziness
3. Inhibit platelet aggregation - Prophylaxis of CVS event - Bronchospasm

- Ticlopidine 1. Inhibit adenosine diphosphate to platelet receptors - Intermittent claudication - Diarrhea

Antiplatelet
2. Impair ADP mediated activation of glycoprotein complex - IHD - hepatitis
3. Prevent fibrinogen binding to platelets - Prevent thrombotic stroke - cholestatic jaundice
4. Inhibit platelet aggregation and prolongs the bleeding time - Prevent subacute stent occlusion - Increase serum
cholesterol level
- TTP
- Aplastic anaemia
Fibrinolytic - Streptokinase 1. Form a complex plasminogen - Acute MI - Abdominal pain
(Thrombolytic) 2. Converts plasminogen to plasmin - Pulmonary thromboembolism - N&V
3. Plasmin break down clots, fibrinogen & other plasma protein - Arteriovenous occlusion - ARF
4. Clots dissolved - Hypotension

Coagulants - Vitamin K 1. Inhibit fibrinolysis - Short term control haemorrhage - Impaired colour vision
- Coagulation Factors 2. Prevent the binding of plasminogen and plasmin to fibrin - Menorrhagia - Anaemia
- Tranexamic Acid 3. Prevent dissolution of haemostatic plug - Hereditary angioedema - N&V
- Haemophilia patient undergo - Fatigue and cramps
dental extraction - Migraine

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 CARDIOVASCULAR SYSTEM: DRUGS USED IN HYPERCHOLESTEROLEMIA

Class Drugs MOA TU SE

HMG-CoA Prodrugs 1. Inhibit HMG-CoA reductase - Reduce LDL level - Increase creatine kinase
Reductase - Lovastatin 2. Reduce concentration of cholesterol within cell - Increase triglyceride - Increase serum aminotransferase
Inhibitors - Simvastatin 3. Low [cholesterol] stimulate synthesis of LDL receptor - Increase HDL level - Rhabdomyolysis
4. Increase number of LDL receptor - Teratogenic
Active Drugs 5. Promote uptake of LDL from blood
- Fluvastatin 6. Low intracellular cholesterol reduce VLDL secretion
- Pravastatin

Bile acid - Cholestyramine 1. Prevent recycling of bile acids - Hypercholesterolemia - Constipation

sequestrants - Colestipol 2. Bile acid-binding resin divert hepatic cholesterol - Relieves pruritus - Impair ADEK renal absorption
- Colesevelam 3. Synthesis of new bile acid (accumulation of bile acid in - Interfere intestinal drug absorption
4. Reduce amount of cholesterol in tightly regulated pool biliary obstruction)
5. Increase removal of LDL in blood

Antilipemic agent - Niacin 1. Inhibit lipolysis in adipose tissue - Lowering cholesterol - Cutaneous flush & pruritus
2. Reduce level of plasma FA and TG - Raising plasma HDL - Nausea and abdominal pain
3. Reduce VLDL concentration in liver - Hyperuricemia and gout
4. Reduce plasma LDL concentration - Hepatotoxicity

Fibrates - Fenofibrate 1. Reduce total plasma triglyceride - Hypertriacyl-glycerolemias - Nausea

- Gemfibrozil 2. Activation of PPAR-alpha and lipoprotein lipase - Type III hyperlipidemia - Lithiasis
3. Reduce production of apoprotein CIII - Myositis
4. Increase synthesis of apoprotein AI, AII and FA - Elevate level of sulfonylureas
transport protein
5. Result in increasing VLDL catabolism and FA oxidation
6 Increase HDL level

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 CARDIOVASCULAR SYSTEM: ANTIHYPERTENSIVE (DRUG THERAPY OF HYPERTENSION)

Class Drugs MOA TU SE

Thiazide 1. Inhibit NA reabsorption in distal tubule - Hypertension - Photosensitivity
- Hydrochlorothiazide 2. Increased excretion of Na, K, Mg, H ions and water - Oedema - Hyperglycemia
3. Promote diuresis - Renal dysfunction
4. Reduce (ECF volume, CO, BP) - Orthostatic hypotension
5. Direct vasodilation, reduce (PR and BP)

Loop Diuretic 1. Inhibit reabsorption of NA and Cl in ascending LoH - Oedema - N&V

- Furosemide 2. Interfere with chloride binding cotransport system - Hypertension - Dehydration
3. Causing Na excretion in urine - Oliguria in renal failure - Muscle spams
Diuretics 4, Promote diuresis - Acute pulmonary oedema - Orthostatic hypotension

K Sparring Diuretic 1. Steroid that resemble aldosterone - Oedema - N&V

- Spironolactone 2. Inhibit aldosterone receptor in DCT - Malignant ascites - Hepatotoxicity
3. Increase excretion of NaCl and water - Diagnose primary hyperaldosteronism - Muscle spasm
4. Maintain K and H ions - Nephrotic syndrome - Hypotension
5. Promote diuresis - CHF with oedema
- Hypertension
- Heart failure

Class Drugs MOA TU SE

Central SL 1. Stimulate central alpha adrenergic receptors - Hypertension - N&V
- Methyldopa 2. Use false receptor (alpha-methylnorepinephrine) - Drowsiness
- Clonidine 3. Reduce sympathetic outflow - Bradycardia
4. Lead to fall in BP - Orthostatic hypotension

Neuronal Blocker 1. Cause depletion of NE, serotonin & catecholamine - Hypertension - Nasal congestion
- Reserpine 2. Result in reduce BP, bradycardia & CNS depression - Chronic psychosis - Abdominal cramps
- Guanethidine 3. Decrease CO and PR lead to hypotensive effect - Bradycardia
Sympatholytic
α1 Receptor Blocker 1. Competitively inhibit postsynaptic α1 adrenoreceptor - Hypertension - Angina
- Prazosin in vascular SM. - Heart failure - Dyspnoea
- Doxazosin 2. Result in vasodilation, decrease TPR and BP - BPH (Raynaud’s syndrome) - Oedema

β Receptor Blocker 1. Competitively block β1 and β2 receptors - Angina pectoris - N&V

- Propranolol 2. Reduce HR, BP, CO & myocardial contractility - Pheochromocytoma - Hallucination
- Atenolol 3. Reduce angiotensin level (reduce renin) - Hypertrophic cardiomyopathy - Hypotension

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 CARDIOVASCULAR SYSTEM: ANTIHYPERTENSIVE (DRUG THERAPY OF HYPERTENSION)

Class Drugs MOA TU SE

Direct 1. Direct vasodilators at arterioles - Hypertension - SLE like syndrome
- Nitroprusside 2. Inhibit Ca release from sarcoplasmic reticulum - CHF - Postural hypotension
- Hydralazine 3. Inhibit myosin phosphorylation in arterial SM - Hypertensive crisis - Tachycardia
- Minoxidil - Anorexia
- Diazoxide

Vasodilators Calcium Chanel Blocker
- Nifedipine (vessel)
- Verapamil (cardiac)
1. Inhibit transmembrane influx of extracellular Ca2+ - Hypertension - Peripheral oedema
2. Inhibit across myocardial and vascular SM layers - Angina pectoris - Heartburn
3. Without changing serum calcium concentrations - Raynaud’s syndrome - Hypotension
4. Result in inhibit of cardiac and vascular SM - Constipation
contraction - Dyspnoea
5. Dilatation of coronary and systemic arteries - Headache

ACE Inhibitors 1. Sulfhydryl contain ACE inhibitor - Hypertension - N&V

- Captopril 2. Inhibit ACE - CHF - Hypotension
3. Prevent conversion of Angiotensin I to II - Post MI - Dyspnoea
4. Increase plasma renin activity - Diabetic nephropathy - Pruritus
5. Reduce aldosterone secretion
6. Promotes sodium and water excretion
Angiotensin
Antagonist ARBs (Angiotensin II) 1. Bind to angiotensin I receptor - Hypertension - N&V
- Irbesartan 2. Block vasoconstriction and aldosterone secreting - Diabetic nephropathy - Fatigue
effect of angiotensin II - Heartburn
3. Inhibit release of aldosterone - Orthostatic hypotension
4. Unable to reabsorb NaCl and water
5. Reduce plasma volume

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 CARDIOVASCULAR SYSTEM: DRUG FOR HEART FAILURE

Class Drugs MOA TU SE

- Digoxin 1. Inhibit Na, K, ATPase - CHF - N&V
2. Increase intracellular Na - Atrial fibrillation - Headache
3. Increase intracellular Ca via Na-Ca exchange carrier mechanism - Slow ventricular rate - Bradycardia
4. Increase myocardial uptake of Ca - Increase sensitivity of AV nodes - Arrhythmias
5. Augments Ca release to myofilaments during excitation - Increase peripheral VR
6. Invoke positive inotropic responses

Therefore stimulate:
Positive - Myocardial contractility
inotropic agent - Increase CO
- Promotes diuresis
- Reduce diastolic pressure
- Increase systemic venous pressure

- Milrinone 1. Increase calcium influx in the heart during action potential - HF - N&V
2. Inhibit phosphodiesterase - Thrombocytopenia
- Liver enzyme change

Beta agonist - Dobutamine 1. Bind at Beta adrenergic receptor - Management of acute HF - Tachycardia
- Dopamine 2. Activates adenyl cyclase to produce cAMP - Tolerance
3. cAMP activate protein kinase - Arrhythmias
4. Phosphorylation of calcium channel - Peripheral vasoconstriction
5. Increase calcium flow into cell
6. Increase FoC of heart muscle

Beta blockers - Propranolol 1. Competitively inhibit beta-1 and beta-2 receptors - CHF - Dizziness
- Atenolol 2. Decrease in heart rate - Bradycardia
- Bisoprolol 3. Myocardial contractility - Bronchospasm
- Metoprolol 4. BP and myocardial oxygen demand - Orthostatic hypotension
- Carvedilol 5. Negative inotropic effect and membrane stabilising activity

Other drugs use?

Diuretics, ACEi, and Vasodilators
**refer to: cardiovascular system: antihypertensive (drug therapy of hypertension)
**inotropic effect: change the force of contraction in heart (+ve ino: strengthen, -ve ino: weaken)

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 CARDIOVASCULAR SYSTEM: ANTI-ARRHYTHMICS

Class Drugs MOA TU SE

Class I – Sodium - Procainamide (IA) 1. Block Na channel - Acute MI - Bradycardia
Channel Blockers 2. Reduce conduction velocity through myocardium - Supraventricular tachyarrhythmia - Myalgia

- Lidocaine (IB) 1. Lidocaine alters signal conduction - Ventricular arrhythmias - Sleepiness

2. Prolong inactivation of fast voltage gated Na channel - Digoxin poisoning - Vomiting
3. Inhibit action potential (AP) propagation - Cardiac catheterization - Pupillary changes
4. Stop generation of AP - Hallucinations

- Flecainide (IC) 1. Block Na channel in the heart - Supraventricular tachycardia - Tachycardia

2. Slowing upstroke cardiac AP - Wolff Parkinson White Syndrome - Dizziness
3. Slowing conduction - Blurred vision
4. Reduce muscle contractility - Chest pain
5. Decrease in ejection fraction

Class II – Beta - Propranolol 1. Competitively inhibit beta-1 and beta-2 receptors - CHF - Dizziness
Blockers 2. Decrease in heart rate - Cardiac arrhythmias - Bradycardia
3. Myocardial contractility - Bronchospasm
4. BP and myocardial oxygen demand
5. Negative inotropic effect
6. Membrane stabilising activity

Class III – Potassium - Amiodarone 1. Inhibit adrenergic stimulation - Ventricular arrhythmias - Hypotension
Channel Blockers 2. Block K channel - Ventricular tachycardia - Fatigue
3. Prolong AP duration - Anorexia
4. Reduce AV conduction - Photosensitivity

Class IV – Calcium - Verapamil 1. Inhibit calcium entry into slow channels during - Supraventricular arrhythmias - Bradycardia
Channel Blockers depolarisation - Angina pectoris - Flushing
2. Relaxes coronary vascular SM - Prophylaxis MI - Fatigue
3. Coronary vasodilation - Hepatotoxicity
4. Increase myocardial oxygen delivery
5. Slow AV node conduction

Prepared by Shafuan Abu Bakar (MSU-MBBS Batch April 2019)

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 CARDIOVASCULAR SYSTEM: ANTI-ARRHYTHMICS

Class Drugs MOA TU SE

Class V - Adenosine 1. Endogenous purine nucleoside - Supraventricular tachycardia - Nausea
2. Stimulate A1 receptors - Myocardial imaging - Headache
3. Slow conduction time through AV nodes - Bradycardia
4. Stimulate A2 receptors - Bronchospasm
5. Produce peripheral and coronary vasodilation
6. Increasing blood flow in normal arteries

Positive Inotropic - Digoxin 1. Inhibit Na, K, ATPase - CHF - N&V

Agent 2. Increase intracellular Na - Atrial fibrillation - Headache
3. Increase intracellular Ca via Na-Ca exchange carrier - Slow ventricular rate - Bradycardia
mechanism - Increase sensitivity of AV nodes - Arrhythmias
4. Increase myocardial uptake of Ca - Increase peripheral VR
5. Augments Ca release to myofilaments during excitation
6. Invoke positive inotropic responses

Therefore stimulate:
- Myocardial contractility
- Increase CO
- Promotes diuresis
- Reduce diastolic pressure
- Increase systemic venous pressure

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