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Pharm II > Lecture II-IV > Flashcards

Lecture II-IV Flashcards

1
Q

Alpha 1

A

Tissue:

  • Vascular Smooth Muscle
  • Pupillary dilator muscle
  • Pilomotor smooth muscle

Actions: Contracts causing

  • Increased Vascular resistance
  • Mydriasis (Dilation)
  • Erects hair
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2
Q

Alpha 2

A

Tissue:

  • Adrenergic and Cholinergic Nerve terminals
  • Platelets
  • Some vascular smooth muscle

Actions:

  • Inhibits NT release
  • Stimulates Platelet Aggregation
  • Contracts some vascular smooth muscle
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3
Q

Beta 1

A

Tissue:

  • Heart
  • Juxtaglomerular Cells

Actions:

  • Stimulates HR and Increases Contractility
  • Stimulates Renin release (renin increases BP)
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4
Q

Beta 2

A

Tissue:

  • Respiratory, uterine, and vascular smooth muscle
  • Liver
  • Pancreatic B Cells
  • Voluntary muscle

Actions:

  • Relaxes
  • Increases glycogenolysis
  • Stimulates insulin release
  • Causes tremor
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5
Q

Beta 3

A

Tissue:
*Fat Cells

Actions
*Stimulates Lipolysis

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6
Q

Alpha 1 Receptor Signaling

A

Coupled to Phospholipase C via G-alpha-q protein to increase IP3/DAG. IP3 receptor activated by IP3 and that causes release of stored calclium, increasing the cytoplasmic calcium.

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7
Q

Alpha 2 Receptor Signaling

A

Negatively coupled to Adenylyl Cyclase via G-alpha-i subunit that inhibits the formation of cAMP, reducing activation of PKA. This causes a decrease in NT release due to decreased calcium influx which is needed for the vesicles to dock via SNAREs.

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8
Q

Beta 1 Receptor Signaling

A

Coupled to G-alpha-s causing an increase in cAMP. cAMP activates PKA and phosphorylates Calcium channels, increasing calcium in the cell causing faster depolarization and increased contraction by increasing calcium storage.

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9
Q

Beta 2 Receptor Signaling

A

Coupled to adenylyl cyclase via G-alpha-s protein, increasing cAMP. cAMP activates PKA that phosphorylates and inactivates myosin light chain kinase (MLCK- normally this light chain kinase phosphorylates the myosin light chain causing an increase in actin and myosin cross bridge formation causing contraction). Phosphorylation of MLCK by PKA reduces the affinity of MLCK for Ca-calmodulin that results in the reduced activity of the enzyme so can’t phosphorylate myosin light chain.

In Beta 2- PKA Inactivates MLCK causing muscle relaxation. In Alpha 2 receptors- PKA is inhibited so it can activate MLCK causing muscle contraction.

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10
Q

Epinephrine

A

alpha 1, alpha 2, beta 1, beta 2 agonist

Effects:

  • CV: B2 decreases diastolic BP, B1 increases HR and CO, A1 increases vasoconstriction
  • Bronchiole Effect: B2- bronchodilation, A1- decreases bronchiole secretions

Toxicity: Arrhythmias

Therapeutic Uses: Anaphylaxix, Cardiac Arrest, Bronchospasms

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11
Q

Norepinephrine

A

alpha 1, alpha 2, beta 1

Effects:

*CV: A1 increases vasoconstriction (increase in TPR and diastolic BP), B1 increases HR and CO- ALL OF THIS CAUSES A BAROREFLEX THAT DECREASES THE HR.

Toxicity: Ischemia

Therapeutic Uses: Vasodilatory shock

Contraindications: Pre-existing excessive vasoconstriction and ischemia

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12
Q

Dopamine

A

D1 receptors at low affinities, B1 and alpha receptors

Effects:
*CV: D1 decreases TPR, B1 increases HR and CO increases systolic BP, Alpha receptors lead to increased BP and TPR

Toxicity: Hypotension in low doses, ischemia in high doses

Therapeutic uses: Hypotension due to low C.O. during cardiogenic shock

Contraindications: Uncorrected Arrhythmias

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13
Q

Dobutamine

A

B1 selective agonist

Effects:
*CV: Increases HR and CO

Toxicity: Hypotension due to B2, Arrhythmia due to B1

Therapeutic Uses: Short-term for CHF or cardiogenic shock

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14
Q

Isoproterenol

A

B1, B2

Effects:
*CV: Decreases TPR (B2), Increases CO (B1), Small decrease in MAP (B2), Bronchodilation (B2)

Toxicity: Tachyarrhythmias

Indications: Bradycardia

Contraindications: Angina w/arrhythmias

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15
Q

Terbutaline & Albuterol

A

B2

Effects:

  • Bonchodilation
  • Uterine Relaxation

Toxicity: Tachycardia (B1), Muscle Tremor (B2), Tolerance (B2)

Therapeutic Use: Bronchospasm or chronic obstruction of airways

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16
Q

Phenylephrine

A

A1

Effects:

  • Increases TRP and MAP
  • Decrease HR (Baroreflex)
  • Pupillary dilation
  • Decrease secretions

Toxicity: Hypertension

Therapeutic Use: Hypotension during anesthesia SV tachycardia

17
Q

Clonidine

A

A2

Effects:
*Increase in BP (Peripheral effect)
*Reduced BP (central effect) because crosses the BBB and there it reduces Vasoconstriction
MAINLY DECREASES BP

Toxicity:
Dry mouth, Hypertensive crisis (After acute withdrawl when the receptors become hypersensitive)

Therapeutic Uses: Hypertension due to sympathetic activation

18
Q

Amphetamine, Methamphetamine, Methylphenidate, Ephedrine, Pseudoephedrine, Tyramine

A

Effects:

  • Increase TPR and BP (A1+A2)
  • Increase HR & CO, increasing systolic BP (B1)
  • CNS Stimulant (increased NE)
  • Anorexia (increased DA)

Toxicity: Tachycardia (B1)

Therapeutic Uses: ADD, Narcolepsi, Nasal congestion

Contraindications: Rx w/MAO inhibitors within 2 weeks.

19
Q

Propranolol, Nadolol, Timolol

A

Non-selective Beta Blockers (Potentially harmful to patients with respiratory disease)

Effects:

  • Reduced Heart rate, contractility, renin release, vasoconstriction
  • Bronchoconstriction

Therapeutic Use:

  • Hypertension
  • Angina
  • Glaucoma (aqueous humor produced by B1)
  • Heart failure
  • Arrhythmia

Toxicity:

  • Bronchospasm
  • Hypoglycemia (Decrease in response to epi)
  • Bradycardia
20
Q

Atenalol, Metroprolol

A

Cardioselective Beta Blockers

Effects:

  • Reduced Heart rate, contractility, renin release, vasoconstriction
  • Bronchoconstriction

Therapeutic use:

  • Hypertension
  • Angina
  • Arrhythmia

Toxicity:
*depression, insomnia, hypotension, bradycardia

Contraindications:

  • Cardiogenic shock
  • Heart block
21
Q

Pindolol

A

Partial Agonists (Good for when hypertension is due to high sympathetic output)

Effects:

  • Reduced Heart rate, contractility, renin release, vasoconstriction
  • Bronchoconstriction

Therapeutic Use:
*Hypertension in those who are less tolerant of bradycardia

Toxicity:
*Bronchospasms, hypoglycemia, bradycardia

Contraindications:

  • Asthma
  • heart blocks
22
Q

Phentolamine

A

Non-selective alpha receptor antagonist (Reversible)

Effects: Inhibits vasoconstriction, increased inotropy and chronotropy due to blockade of pre-synaptic alpha-2 receptor (increase release of NE), Vasodilatory effect of EPI

Therapeutic uses: dermal necrosis

Toxicity:
Prolonged hypotension, reflex tachycardia, nasal congestions

23
Q

Phenoxybenzamine

A

Non-selective alpha receptor antagonist (irreversible)

Effects: Inhibits vasoconstriction, increased inotropy and chronotropy due to blockade of pre-synaptic alpha-2 receptor (increase release of NE), Vasodilatory effect of EPI

Therapeutic uses: dermal necrosis

Toxicity:
Prolonged hypotension, reflex tachycardia, nasal congestions

24
Q

Prazosin, doxazosin, terazosin

A

Selective A1 receptor blockers

Effects:

  • Inhibit vasoconstriction
  • Less cardiac stimulation than non-selective since A2 receptors are preserved

Therapeutic uses: Hypertension, benign prostatic hyperplasia

Pharm II (10 decks)

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