Pharm-Post MT

• -drug used to treat mild congestive heart failure
• -decrease NaCl reabsorption in kidneys -> decrease water retention and decrease blood volume -> increase urination
• -decrease BP, pulmonary congestion and peripheral edema
• -Toxicity: decreased K+ (b/c Na+ and K+ channel)

• -ACE inhibitor to treat Congestive Heat Failure
• -decrease angiotensin -> decrease NE and aldsterone (salt and water retention)
• -decrease bradykinin 0> vasodilation
• --> decrease BP
• -Toxicity: severe hypotension, cough, angioedema

• AT1 Antagonist to treat Congestive heart failure
• -bloke AT1 receptor -> vasodilation -> decrease BP
• -Indication: Px who can't tolerate ACE inhibitors
• -Toxicity: severe hypotension

• decrease inflammation and overactive immune system by inhibiting phospholipase A2 and consequently eicosanoid production (decrease neutrophil and monocytes, processing centers, eicosanoids) -> immune compromised and underlying disease is still there
• -used to treat uveitis, allergic conjunctivitis
• -ie. hydrocortisone, prednisone, dexamethasone

• inhibit COX leading to decrease in eicosanoids
• -reliefs pain and tissue damage (inflammation, pain and fever decreased)

• inhibits COX1 and COX2 leading to decrease of prostaglandins (decreases fever) and thromboxanes (increases bleeding)
• -used to decrease pain, fever, inflammation and thrombus formation
• -no tolerance, no dependency, no CNS depression, BUT do NOT use in children (Reye's Syndrome)

• COX-2 inhibitor -> analgesia and decreases inflammation without GI side effects
• -no effect on thromboxane and platelets (no clot formation and no platelet aggregation)
• -toxicity: MI, stroke

• decreases prostaglandin synthesis in CNS
• -toxicity: hepatotoxicity (liver failure)

short-acting glucocorticoid that is used to treat CHRONIC inflammation ie. autoimmune disease

long-acting glucocorticoid that is used to treat very high acute inflammation ie. septic shock, brain edema

• drug for heart failure (Na/K ATPase blocker)
• -increases cardiac contractility
• -use in combo with diuretics and ACEi

• drug for heart failure
• -BB blocker
• -decreases heart rate AND renein release
• -do NOT use in seniors

• drug for heart failure
• -vasodilator
• -releases NO -> smooth muscle contraction and reduces edema and cardiac size

• direct-acting cholinergic receptor agonist -> increases PNS repsonse
• -mimics ACh, resistant to Achase

• indirect acintg reversible AChase inhibitor
• -> increases PNS function
• -treats Myasthenia gravis (reversal of neuromusclar blockage)

• direct-acting muscarinic cholinergic receptor agonist -> increases PNS response
• -mimics ACh
• -causes contraction of ciliary body -> decreases IOP (used for emergency Tx of glaucoma)
• -Toxicity: CNS disturbances, sweating, salivation

• irrevesible indirect acting (covalently phophorylate AChase)
• -causes long-lasting miosis
• -for longer Tx of glaucoma

• indirect acting cholinergic (inactivates AChase) -> contraction of ciliary body
• -can enter CNS -> convulsions
• -Tx for glaucoma, atropine poisoning

• cholinergic anatagonist (competitively binds AChR) -> SNS active
• -long acting mydriasys and cycloglegia
• -toxicity: CNS effects, sweating, salivation, increased HR, hallucinations, delirium, coma

• cholinergic antagonist
• -shorter competitive binding AChR -> SNS active
• -mydriasis and cycloplegia

• selective a1 agonist only
• -vasoconstriction -> increases BP
• -used for mydriasis (without cycloplegia), decreases conj injection and synechiae

• B1 agonist -> SNS
• heart (HR and contractility increase) and kidneys (GFR increases)
• -used for kidney failure

• B2 agonist -> SNS stimulation
• -bronchodilator
• -used for asthma

• Beta blocker
• -decreases AH production -> decreases IOP
• -Tx for glaucoma

• B1 blocker
• -decreases heart contractility, slows conduction
• -Tx for HTN

• non-selective B blocker ->decreases SNS (slows SA node pulse and AV conduction) -> decreases HR, constricts bronchioles, decreases GFR
• -worsens asthma, hypglycemia in DN
• -Tx for HTN, angina, arrhythmia, post-MI

• Na+ channel blocker
• -to treat all types of chronic arrhythmias
• -toxicity: cannot be used with digoxin (a Na/K ATPase inhibito that increases HR) b/c decreases renal clearance

• Na+ channel blocker
• -treat acute ventricular arrhythmias
• -normal HR
• -toxicity: CNS drowsiness, confusion, tremor, convulsions

• K+ channel blockers -> slows repolarization
• -increases refractory period and decrease automaticity of ischemic cells in ventricles
• -Tx for tachyarrhythmias

• Ca2+ chanel blocker
• -decreases contraction (and SA impulse and AV conduction separately)
• -Tx for tachyarrhythmias

• Alleviates Alzheimer disease
• AChase inhibitor
• Side effects: nausea, diarrhea, insomnia, vomitting, cramps, fatigue, appetite loss

• Alleviates Parkinson's Sxs
• MAO-B inhibitor (dopamine metabolism is decreased)
• Side effects: Dyskinesia, hallucinations, hypotension

• Alleviates Parkinson's Sxs
• mimics dopamine, crosses blood brain barrier
• Side effects: dyskinesia, anxiety, psychoses, nausea, vomitting, hypotension

• Alleviates Parkinson's Sxs
• Antimuscarinc drug (decreases cholinergic activity of subtantia nigra -> decreases GABA)
• Side effects: drowsiness, confusion, hallucinations, peripheral side effects

• Typical nueroleptic (Phenothiazine class) used to treat Schizophrenia
• -decreases dopamine levels (increases attn, pleasure and cognition while decreasing hallucinations)
• -Side effects: Parkinsonian Sxs

• Typical nueroleptic (Butyrophenone class) used to treat Schizophrenia-decreases dopamine levels (increases attn, pleasure and cognition while decreasing hallucinations)
• Side effects: Parkinsonian Sxs

• Atypical nueroleptic used to treat
• Schizophrenia-decreases dopamine levels (increases attn, pleasure and  cognition while decreasing hallucinations)
• Side effects: Hypotension, weight gain