pharm exam 2 Flashcards
Blocking adrenergic receptors are useful in treating
Hypertension –> causing vasodilation by blocking α1 receptors
Raynaud’s –>reduce symptoms by preventing α mediated vasoconstriction in fingers and toes
BPH –> reduced contraction of smooth muscle
Adverse effects:
-vasodilation from blockade of alpha receptors can also result in
–Reflex tachycardia
–Ortho hypotension: more pronounced with venous dilation
–Nasal congestion
–Inhibition of ejaculation
Alpha receptors
Used to treat HTN & BPH
HTN meds: OSIN alpha blocker
Prazosin : only effect for HTN - No action on smooth muscle of prostrate
Doxazosin: help with S/S of BPH too
Terazosin: help with S/S of BPH too
BPH meds:
-Tamsulosin
-Alfuzosin
-Sildosin*
Action
-Selective blockade of α1 receptors on arterioles and veins
Relaxes smooth muscle of bladder and prostate
BPH meds: selective for α1 on smooth muscle, weak action on vascular α1 receptors
Alpha adrenergic blockers
end in OSIN
sexual dysfunction
side effects
-Orthostatic hypotension
-1st dose effect –> syncope (esp if risk for fall or on blood thinner
-Reflex tachycardia
-Nasal congestion
-Headache
-*Sexual dysfunction
NM:
-Start low and increase slow until desired dose
-Give 1st dose at bedtime to prevent syncope
-Don’t drive after taking 1st dose until they know how to respond to drug
-Education for male patients
Alpha adrenergic blockers Tamsulosin* Alfuzosin Sildosin* Prazosin * Doxazosin Terazosin
Arteriole Dilation -decreases afterload -reduced workload of the heart -increased cardiac output and tissue perfusion Adverse effects of arteriole dilation -Reflex Tachycardia* -Increased blood volume* -↓ BP decreases renal perfusion --> activate RAAS --> increases Na+ & H2O reabsorption -seen with prolonged use
Venous dilation
-Venous Dilation
reduces preload: less blood return to heart
-decreased cardiac workload
-decreased cardiac output and tissue perfusion
Adverse effects of venous dilation:
-Reflex tachycardia*
-Orthostatic Hypotension*
-Sudden drop in BP with position changes from pooling of blood in peripheral veins
-fall risk
-decrease cerebral blood flood
-for managing angina (like nitro) : 2 types = hydralazine and sodium nitroprusside
Direct vasodilators
Don’t work with alpha or beta receptors, but same therapeutic effect (dilate vessels)
2 ways they work: arterial dilation venous dilation or both
Activate RAAS with long-term use
Action: -Selective dilation of arterioles thru direct action on vascular smooth muscle →drop in peripheral resistance & BP Side effects -Reflex tachycardia* -Headache -Dizziness -Weakness -Fatigue -Severe hypotension -SLE-like syndrome NM: - Monitor response -Give in smallest dose -Tolerance develops with prolonged use so want to limit use
Hydralazine
direct vasodilator for venous dilation
decrease in systemic vascular resistance
often PRN or system <160-180 or given IV
Action:
-Arteriolar & venous dilation with minimal reflex tachycardia
-**drug of choice for HTN emergencies
side effects:
- Severe hypotension
-RAAS activation –> drop BP too quickly
-Cyanide poisoning (rare and if one has liver impairment) & Thiocyanate toxicity (prolonged >3 days)
NM:
- Continuous BP monitoring with art line or NIBP
-Careful titration q 3-5 minutes
-Max rate is 10mcg/kg/min
Sodium nitroprusside
direct vasodilator
only give IV and for HTN emergency
effects are almost immediate
if drop too fast you activate RAAS
*art line is ideal for continuous BP monitoring but isn’t always possible
Activates α2 receptors in the CNS and brainstem (not in peripheral)
Signals adequate norepinephrine is available so synthesis of NE is decreased
Results in decreased action of the sympathetic nervous system
-Vasodilation
-Decreased HR & CO
central acting alpha-agonist
Clonidine and Methyldopa
acts as antagonist but activates signals only in brain
Action/use: -HTN*: PO or transdermal Other Uses -Severe pain: via epidural -ADHD -Opioid withdrawal Adverse effects: -Drowsiness and dry mouth -Xerostomia Less Common S/E -Depression (with pts with hx of depression – can exacerbate that) -Vivid dreams or nightmares Impotence NM: -Used for resistance HTN -Sudden discontinuation rebound hypertension, tachycardia, and sweating -High doses can cause euphoria, sedation, hallucinations (useful during opioid withdrawal) Potent - drops BP a lot so that's why it's not used as a 1st line drug -To manage hospital or short term management or resistant patient for HTN *can't suddenly stop r/t rebound HTN
Clonidine
central acting alpha-agonist
indication:
- 1st choice for HTN during pregnancy r/t vasodilates but doesn’t effect HR or CO (want that for placenta)
-No effect on HR or CO
-Rarely seen used for HTN today
side effects:
-+ Coomb’s Test (looks for antibodies attack against RBC – doesn’t mean they will develop hemolytic anemia though. If positive, continue monitor RBC, H/C, and for hem anemia)
-Hemolytic Anemia
-Hepatotoxicity: cause liver necrosis/hepatitis so draw LFT – watch for jaundice/dark urine/fatigue/anorexia/ abd distention/discomfort, N/V
NM:
-Teach & monitor for s/s of hemolytic anemia
-RBC count
-Teach & monitor for s/s of liver impairment
-Periodic monitoring of LFT’s
Methyldopa
central acting alpha-agonist
older med not used as much
-β1: reduces heart rate, reduces force of contraction, and reduced velocity of impulse conduction through the atrioventricular (AV) node
-β1: suppress release of renin by blocking receptors on juxtaglomerular cells in the kidney which reduces angiotensin II mediated vasoconstriction and aldosterone mediated volume expansion
Adverse effects:
-BI = bradycardia, induce or worsening HF, AV heart block, mask symptoms of hypoglycemia
-B2 = bronchoconstriction, hypoglycemia
beta receptors
review if we don’t remember
Action:
-Delays repolarization by blocking K+ channels
-Used for dysrhythmias only NOT HTN
Important info:
-Will cause bronchoconstriction
-Do not use with verapamil or diltiazem (these CCB have the same action & effect)
For severe a fib, a flutter, v tach - not selective so causes bronchoconstriction, low BS, so don’t use for asthma pts or diabetics
Sotalol non-selective B2 and B2
beta blcokers
Indications:
-Used for SVT, a flutter and a fib
Important info:
-Short half-life (9m) and must be given IV infusion
-Need telemetry monitoring & continuous BP
Unique Side Effects
-Hypotension
-Monitor for excessive ↓in CO
Only for dysrhythmias - only IV r/t short half life - effects wear off once stopped
esmolol**
selective B1
beta blocker
- A neurodegenerative disorder of the extrapyramidal system
- Degeneration of neurons that supply dopamine
- Characterized by dyskinesia and bradykinesia*
- Chronic & progressive
- No cure for motor symptoms
- Goal of drug therapy
- Maintain functional mobility
- Prolong quality of life
- Neurons were worried about supply dopamine and these neurons start to get destroyed in brain but we don’t now why
- Proper function of straitum requires a balance between dopamine and acetylcholine (ACh)
- Dopamine inhibits neurons that release GABA
- ACh excite neurons that release GABA
- ACh release is unopposed
- Excessive release of GABA
- Causes dyskinesia & bradykinesia
Parkinson’s disease
- Drug selection and dosages determined by level of disability with ADL’s & work
- Age of patient (younger – try to delay use of levodopa/carbidopa)
Dopaminergic agents -Dopamine Replacement -Dopamine Agonists -COMT Inhibitors -MAO-B Inhibitors -Dopamine Releasers Anticholinergic agents -Central acting -Block muscarinic receptors in striatum
med selection and drug classifications for parkinson’s
-Most effective medication available
-Can cross the blood-brain barrier
-Full effects seen after several months
-Always combined with carbidopa - carbidopa doesn’t work on own
-Symptoms well controlled for first 2 years
-Return to pretreatment state at end of 5 years
MOI
-Increases dopamine synthesis – giving pt chemical form of dopamine
-Converted to dopamine once in the brain
-Helps to restore a proper balance between dopamine and ACh
-Given orally
-Rapidly absorbed from small intestine
-Food delays absorption – take 2 hours before or after meals
-High-protein meals reduce effectiveness
pseudoparkinson’s)
Levodopa/Carbidopa
Dopamine replacement
Acute loss of effect
- Gradual loss or “wearing off”
- -Indicates drug levels are sub-therapeutic
- Minimize ‘wearing off’
- -Give more often
- -Add another med
- –Prolong half-life of levodopa
- –Direct-acting dopamine agonist
- -Don’t take with food or high-protein
- Abrupt loss or “on-off”
- -Not related to drug levels
- -“off” times are expected to increase over course of treatment
for wear off avoid empty stomach
for on off avoid high protein
loss of effect phenomena with
levodopa/carbidopa
dopamine receptor
Affects about 80% within 1 year of beginning
Annoying vs disabling
Dyskinesias can be managed in three ways
-Reduce dosage of levodopa
-Treat with Amantadine to decrease severity
-Surgery and electrical stimulation
-Repetitive tick, pill rolling, involuntary movement
Dyskinesia
Most common s/e of levodopa/carbidopa
Side effects
-Dyskinesia*
-Nausea & Vomiting *
-Orthostatic Hypotension*
-Psychosis*
-Insomnia
-Nightmares
-Dark body fluids in sweat/urine
-Malignant Melanoma (so won’t prescribe if hx of it or take more precautions) (benefit vs risk)
NM
-N/V: manage with lower dose, give with food (but can delay absorption)
-Orthostatic hypotension: common in early treatment, increase intake of Salt and Water, low dose alpha-adrenergic agonist, concern r/t risk for falls with elderly
-Psychosis: affects 20%, visual hallucinations, paranoid idention, put on 2nd generation (Clozapine and Quetiapine) not 1st (Haldol) r/t s/e block dopamine receptors and can induce
levodopa/carbidopa
dopamine receptor
