Cardiovascular pharmacology

Question 1

what is a sympathomimetid drug? how does it operate?

Answer 1

1. sympathomimetic
   
   1. mimics functions of the SNS by stimulating adrenoceptors
      
      1. direct
         
         1. ​bind directly to the receptor
      2. indirect
         
         1. ​stimulate the release/block reuptake of NE

Question 2

what is a sympatholytic druug?

Answer 2

sympatholytic- interrupts function of the SNS by blocking adrenoreceptors

Question 3

define the receptors

Answer 3

• A1
  
  • vasoconstriction
  • peripheral resistance
  • arterioles
    
    • skin
    • mucous membranes
    • viscera
• A2
  
  • inhibition of NE release
  • presynaptic membranes
    
    • pancrease- insulin release
• B1
  
  • tachycardia
    
    • myocardial contraction increase(inotropy)
    • release of renin
    • lipolysis
  • heart
  • kidneys
• B2
  
  • vasodilation
  • peripheral resistance decrease
  • vascular smooth muscle

Question 4

what do B-adrenergic receptors

1. have ahigh affinity for?
2. activate?

Answer 4

1. all b-ar’s have a high affinity for isoproterenol
2. all couple G proteins
   
   1. increase cAMP
   2. phosphorylate protein

Question 5

what are the categories of sympathomimetic drugs?

Answer 5

• direct acting drugs
  
  • bind directly to one or more of the adrenergic receptors
    
    • selective or non selective

Question 6

describe the receptors in the vasculature. How does the relationship work?

Answer 6

1. A1 and B2 are in the vasculature
2. relationship
   
   1. B2
      
      1. have a high affinity for epinephrine
      2. are in lower concentration on the cell membrane compared to a1
      3. when epinephrine is in low concentration= b2 are active= vasodilation
   2. A1
      
      1. have a low affinity for epinephrine
      2. are in higher concentration on the cell membran compared to b2
      3. when epinephrine is in HIGH concentration=a1 overwhelm b2 signal=vasoconstriction

Question 7

what happens to TPR in low dose epinephrine?

Answer 7

TPR decreases. B2 receptors are activated , causing vasodilation

drop in diastolic and systolic.

exact opposit for the activation of a1

Question 8

epinephrine

1. type of adrenergic agonist?
2. receptors/physiological action
3. therapeutic use
4. pharmacokinetics
5. adverse effects
   
   1. consider diabetics

Answer 8

1. CV system
   
   1. direct acting non selective
2. receptors/PHYSIOLOGICAL ACTION
   
   1. a1- HIGH DOSE
      
      1. constrict arterioles in
         
         1. skin,
         2. mucous membranes,
         3. viscera
         4. skeletal muscle
   2. b1-HIGH DOSE
      
      1. inotrope, chronotrope, dromotrope
      2. renin release
   3. b2-LOW DOSE
      
      1. dilate vessels
         
         1. liver
         2. skeletal muscle
3. therapeutic uses
   
   1. emerency treatment of bronchospasm
      
      1. acute asthma attack
      2. anaphylatic shock
   2. vasoconstrictive agent in surgery
4. pharmacokinetics
   
   1. rapid onset of action, quickly degraded (MAO,COMT)
   2. iften administered IM in emergency
   3. IV proveds most rapid effect
5. adverse
   
   1. CNSeffects: fear, anxiety, tension, tremor
   2. may triggerarythmia
   3. need to adjust insulin dose in diabetics

Question 9

norepinephrine

1. physiological action
2. therapeutic use
3. adverse effects

Answer 9

1. physiological actions
   
   1. a1
      
      1. constrict arterioles in
         
         1. skin
         2. muscous membranes
         3. viscera
         4. skeletal muscle
   2. b2 agonist= weak
   3. b1=opposes affect
      
      1. this is because of the reflex bradycardia (M2), increased blood pressure triggers a vagal response = decreasing diastole
2. therapeutic uses
   
   1. treatment of shock- increases blood pressure
3. adverse affects
   
   1. anxiety, fear, tension, tremor
   2. potent vasoconstrictor
      
      1. not to be used in asthmatics!!!!
      2. blanching and sloughing of skin along vein may occur

Question 10

clonidine

1. function
2. therpeutic use

Answer 10

1. acts centrally to decrease sympathetic outflow from the CNS by activating a2 receptors
   
   1. direct acting selective adrenergic agonist
2. treatment of
   
   1. hypertension
   2. withdrawl symptoms

Question 11

1. what are some uses for adrenergic receptor antagonists,
2. differen terminologies
3. group considerations

Answer 11

1. general use
   
   1. prevent activation by endogenous catecholamines
   2. primary uses is in cardiovascular disease
2. terminology
   
   1. sympatholytic agents
   2. “blockers” (beta blocker, alpha blocker)
3. group considerations for a1 blockers
   
   1. blocking a1 receptors
      
      1. leads to dexreased sympathetic tone and drop in perihperal resistance
   2. induction of a reflex tachycardia
   3. response is determined by sympathetic tone in patient

Question 12

prazosin

1. function
2. mechanism
3. use
4. adverse affects

Answer 12

1. function
   
   1. selective a1 equillibrium competative antagonist
2. mech
   
   1. decrease TPR w/o signigicant effects on cardiac output
3. use
   
   1. hypertension
   2. benign prostatic hyperplasia
4. adverse effects
   
   1. orthostatic hypotension- occurs with first dose
   2. sexual dysfunction
      
      1. no ejaculation- a1 receptors allow for ejaculation
   3. potential for additive antihypertensive effect with sildenafil or nitrates

Question 13

propranolol

1. function
2. uses
3. adverse affects

Answer 13

1. function
   
   1. act as nonselective b1 receptor antagonist
   2. decrease cardiac output
      
      1. negative
         
         1. chronotrpic
         2. inotropic
         3. dromotropic
   3. attenuate HR during stress and exercise
   4. decrease
      
      1. renin
      2. angiotensin
      3. aldosterone
      4. cardiac output
2. uses
   
   1. hypertension
      
      1. decrease TPR
3. adverse
   
   1. bronchoconstriction
   2. limited cardiac output = limited amount of exercise and physical activity a person can commit to. hit a wall with how much exertion is allowed
   3. CNS effects
      
      1. depression, dizziness, fatigue, short term memory loss

Question 14

what are the three ways drugs affect hemostasis and thrombosis? give examples to know

Answer 14

1. blood coagulation (fibrin formation)
   
   1. rivaroxaban( factor xa inhibitor)
2. platlet function
   
   1. abciximab
3. fibrin removal

Question 15

rivaroxaban

1. mech
2. adverse
   
   1. toxicity
3. use
4. antidote

Answer 15

1. mecha
   
   1. specific factor Xa inhibitor
2. adverse
   
   1. toxicity
      
      1. bleeding
      2. neuraxial anesthesia or spinal puncture
         
         1. boxed warning
            
            1. epidural or spinal hematoma
               
               1. long term pralysis
      3. pregnancy category C
   2. increased plasma concentration with moderatte renal or hepatic dysfunction
3. uses
   
   1. prevention of deep vein thrombosis post surgery
4. antidote
   
   1. recominanat factor X-threatening or uncontrolled bleeding
   2. warning of thromboembolic and ischemic eventt
      
      1. for reversal due tto lifer

Question 16

abciximab

1. mechanism
2. uses
3. adverse

Answer 16

1. mech-antiplatlet agent
   
   1. prevent intteraction of glycoprotein 2B/3A to fibrinogen or vWF
      
      1. this prevents interaction with foreign surfaces (endothelium) andother plattlets
   2. prevents platlet aggregation due ttoany agonist
2. use
   
   1. acute coronary syndrome
3. adverse
   
   1. bleeding