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34 Cards in this Set

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Thiazides

diuretics used for hypertension to lower BP. Inhibits the Na+ and Cl- reabsorption in the kidney. (distal tubule)




usually well tolerated but... hypotension= dizziness, loss of potassium




loss of Na+= loss of water= decrease in BP

Cilazapril

ACE inhibitor. Inhibits angiotensin 1-->2


decrease in production of AGT2= vasodilation, increased Na+ excretion, fewer activation of AT1 and AT2 receptors= decrease in aldosterone (Na retention)




increase in bradykinin concentration. (vasodilator, involved in inflammation) = cough




used for hypertension.




cough, hypotension, rash, angiodema

Losartan

Angiotensin 2 receptor blocker .




Blocks the AT receptors= no bradykinin accumulation= no coughs.




still have positive effects of AT2 receptors.


- vasodilation


- increased Na+ excretion




Used for hypertension


Generally well tolerated

Glyceral Trinitrate (GTN)

Nitrate. breaks down to release nitric oxide (NO)


- NO is a vasodilator


- Causes Vasodilation to coronary arteries which supply the heart.


- Not specific vasodilation




NO--> Guanylate cyclase enzyme activity--> increase in cyclic CGMP levels--> activate CGMP dependent protein kinase--> smooth muscle relaxation




Used for acute angina attacks


effects: hypotension, headaches, dizziness

Propanolol-

Non selective beta blocker.




Reduces sympathetic activity. by being a non selective antagonist for Beta 1 and 2 receptors.




Lipophilic so CAN pass through BBB


Blocks B1 receptors in kidney. (renin release X)


Blocks B1 and 2 receptors in the heart


Blocks B2 receptors in the lungs




Used for: Hypertension, angina and anxiety




Adverse effects: CNS effects, Fatigue and poor exercise tolerance, worse lipid profiles, bronchoconstriction

Metoprolol

Selective Beta Blocker




Selective antagonist for Beta 1 receptors.


Used for: arrythmias-->atrial fibrillation and tachcardia, angina, ypertension




Lipophillic and can pass through BBB




Adverse effects: fatigue, CNS effects, poor exercise tolerance

Atenolol

Selective beta 1 receptor


Used for: arrythmias, angina, hypertension


Hydrophobic so cannot pass through BBB




Adverse effects: Fatigue, poor exercise tolerance

Vepramil and Diltiazem

Non selective Calcium Channel blocker




Blocks L type Voltage gated Calcium channels. (blocks the pores)


- Cardiac and vessel selectivity


- Prevents Ca2+ ions from moving through




Reduce HR, conduction velocity, and heart contraction




Used for: Angina, arrthrias, hypertension




Adverse effects: flushing, GI effects, Hypotension, bradycardia

Nifedipine

Vessel specific selective CCB




Blocks L type voltage gated Ca2+ channels on smooth muscle. (stabilizes inactive channels)




- Vessek sekectivity


- prevents depolarization from occuring


- relaxation of smooth muscle= vasodilation




Does not directly affect HR or contraction




Used for hypertension. (esp elderly with stiff vessels)




Adverse effects: DO NOT USE ALONE WITH ANGINA. causes tachycardia (elevated HR) because BP will decrease, increased force of contraction, Dramatically increase myocardial O2 demand.




Use nifedipine with Beta blockers

Aspirin

Antiplatelet




Inhibits cox 1 at low dose and prevents thromboxane formation= platelet aggregation prevented, reduced recruitment of further platelets, reduced clot formation




At high dose inhibits COX 2 which prevents production of Prostacyclin and promotes dilation




Used for: reducing risk of developing clot, post treatment for angina, stroke. MI




CAN get gastric bleeding

Heparin

Anticoagulant ( IV administration )




Promotes the binding of heparin to AT3+ Factor 10 or + thrombin




both needed for the coagulation cascade. and prevents production of fibrin because fibrinogen--> fibrin needs thrombin. (factor 10 needed to produce prothrombin-->thrombin)




Used for: MI, stroke, deep vein thrombosis


Adverse effects: haemorrhage


Reversal therapy: Protamine sulphate. Heprain binds this instead of AT3

Warfarin

Anticoagulant (oral administration)




Prevents reduction of vitamin K epoxide reductase. (reduced form of VK is the active version)


Prevents Vitamin K from activating clotting factors


Reduces formation of fibrin




Used for: MI, stroke


Adverse effects: Low therapeutic index, risk of hemorrhage


Reversal therapy: Vitamin K administration (slow)


Fresh frozen plasma (fast)

Alteplase

Fibrinolytic




Breaks down the clot after it has formed. Converts plasminogen to plasmin. Plasmin then breaks down the fibrin




Used for: MI, Stroke




If outside therapeutic window: High risk of haemorrhage= excessive bleeding



Indomethacin

Acetic acid NSAID




Potent anti inflammatory agen. Most adverse effects in NSAIDS. because more selectivity for COX 1 (COX 1 produces PGE1,2 and PGI2 which protects against gastric ulcers )




COX 1 inhibited= more gastric side effects

Ibuprofen

Propionic acid NSAID class




Analgesic and anti inflammatory effects. Widely used for inflammatory pain. Weaker than other NSAIDS




Fewer Adverse effects: has reversible binding like aspirin. May have GI disturbances

Diclofenac

Acetic Acid NSAID class


Most potent/ powerful NSAID


Higher affinity for toxins


Powerful analgesic effects= Pain reliever for inflammation




Adverse effects: GI upset, Headache







Paracetamol

Simple analgesics (not considered NSAID)




Weak inhibitor of COX 1 and COX 2


Analgesic and antipyretic


- Pain reliever and prevent fever


- No anti inflammatory effects




Mechanism not fully determined


Irak administration




Quite safe. Large regular intake causes kidney damage



Coxibs

COX 2 Inhibitor




Targets inflammatory COX 2 while maintaining Gastroprotective COX 1


High therapeutic potential for inflammatory condition. Has the same side effects except no GI upset. If take highly potent COX 2 inhibitor= risk of getting heart attack

Corticosteroids (Preventer)

Preventer!! Powerful Anti Inflammatory drug (more than NSAIDS)




Reduces # of airways inflammatory cells and damage to airways epithelium


Reduces Vascular permeability


No immediate effect on bronchodilation




2 Routes of administration


- Orally (prednisolone, Prednisone)- Bone degeneration, fat deposition


- Inhalation(fluticasone) Goes through first pass metabolism in liver. very little in systemic circulation. Reduces Adverse reactions

Leukotriene receptor antagonists

Anti inflammatory drug (preventer)




Binding to Leukotriene GPCR has effects:


- Decreases vascular permeability ( leukotrienes= Inflammatory mediators produced by immune cells


- Vasodilation


- Bronchodilation




Less potent. Gets into systemic circulation much less. Reduces ADR

Lipoxygenase Antagonist

Targets the enzyme upstream

Salbutamol

SABA Beta 2 Agonist




short acting Beta 2 Agonist. Acute inhalation treatment for bronchospasm.




Prevents exercise induced asthma.




Effects: relaxes airways, Bronchodilation. Used as required. lowest dose possible. only lasts 2-5 hours. Not nocturnal




Adverse effects: Skeletal muscle tremor, Increase HR and force of contraction, Dilate peripheral vessels--> BP lowered, reflex tachycardia

Salmetrol

LABA. Long acting B2 agonist


- used for nocturnal asthma


used as a prevention treatment. Also used with inhaled corticosteroids. Better control= Lower dose of corticosteroids.





Muscarinic Antagonists

Atropine, Scopolamine, Hyoscine, Ipratropium




- Blocks effects of parasympathetic NS stimulation of M3 receptor= Causing Bronchoconstriction


- Atropine, Scopolamine and Hyoscine:


30 min to onset, 3-5 hours of duration, given with Beta 2 agonist




All these used for asthma treatment




For ipratropium--> for acute asthma treatment




Adverse effects: Dry mouth, GI motility disorders, Cardiac effects, urinary retention, blurred vision

Theophylline

Methylxanthines




Treatment for COPD and asthma




Phosphodiesterase inhibitor


- Increase smooth muscle relaxation


- Inhibits Phosphodiesterase 4 in lymphocytes and eosinophils


- Improves asthma control




Adenosine receptor antagonists


- Bronchodilation


- May be responsible for toxic

Tubocurarine

Paralytic/ non depolarizing NMJ


- Blocks AcH from binding to receptors. They are competitive inhibitors which blocks the ability of motor neurons to activate muscle


- Prevents depolarization and hence no AP too.




Can be reversed by addition of acetylcholinesterase inhibitor





Suxamethionium

Paralytic/ Cholinergic depolarizing NMJ




- Activates nicotinic acetylcholine receptor. Not hydrolyzed, Causing excessive depolarisation of muscle membranes which deactivate Na+ channels.


- Much stronger and more persistent agonists than acetylcholine


- Used to relax muscles and have anaesthesia effect



Spasmolytics- CNS

Diazepam- Blocks GabA A receptor. Sedation.


Baclofen- Blocks GABA B receptor, GPCR. Sedation but less than baclofen


TIzamidine- Works on alpha 2 adrenoreceptors on motor neurons. drowsy, hypotension dry mouth


Gabapentin- Voltage gated Ca2+ channels. Dizzy, sedation





All these drugs are treatment for neurological conditions: MS, Cerebral palsy, stroke, muscle spasms causing chronic pain. Reduces spasticity and reduces muscle spasms

Spasmolytic- PNS

Dantrolene- Interferes with Ca release--> reduce release from intracellular calcium stores-->interfering with muscle fibres= decrease skeletal muscle strength




Indications: Muscle spasticity , malignant hyperthermia




Adverse effects: Muscle weakness, sedation, rare hepatitis




Botulinum Toxin (BOTOX)


- Blocks release of AcH by slicing SNARE proteins. Snare proteins are necessary for transport of vesicles to the membrane for the release of ACh




Indications:


- Cosmetic purpose


- Painful muscle spasms




Adverse effects:


- Muscle paralysis

Carbidopa

Dopa decarboxylase inhibitor- Cannot pass through BBB. Inhibits conversion of L-dopa to dopamine.


Use when L-dopa alone is producing irregular therapeutic control. Also reduces peripheral side effects of elevated dopamine-->Hypotension, GI discomfort

Apomorphine (dopamine agonist)

Second line treatment. Subcutaneous injection. Prior to L-dopa effect kicking in. antiparkinsons effect approximately 5 min




Short relief but good for rapidly treating. and although less effective it...


- Lasts longer


- lower risk of dyskinesia




Adverse side effects:


- Hallucinations


- Nausea

Selegiline--> Enzyme inhibitor

Monoamine oxidase inhibitor




Specifically binds to B subtype. Reduces the breakdown of dopamine at synapse. Which increases the duration of action of dopamine in brain and increases activity of binding to receptor.




Can be used as monotherapy in the early stages of parkinsons disease

Haloperidol

Typical Antipsychotic




Antagonist for type 2 Dopamine receptors.


Can get parkinson disease like symptoms


Also blocks


- Muscarinic (constipation) , histamine (weight gain, drowsiness) and adrenergic receptors ( decrease BP, Dizzy and drowsy)




Side effects:


- Reduced dopamine receptor activation in prefrontal cortex


- Reduced dopamine activity in nigostriatal pathway

Clozapine

Second generation. Atypical antipsychotic


- Inhibits both D1 and D2 receptor types for dopamine. also blocks serotonin (5- HT) receptors