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Flashcards in Exam #2 Deck (39):


positive chronotropy is increased heart rate (SA node)



positive inotropy is increased force of contraction (atrial and ventricular cardiac muscle)


pharmacologic antagonist

bind to the same receptor as the agonist

competitive reversible:
- curve shifts right
- surmountable
- Emax stays same, EC50 inc., potency dec.

non-competitive (irreversible)"
- curve shifts down
- non-surmountable
- Emax dec, EC50 and potency stay same


physiologic antagonist

bind to a different receptor that mediates a physiologic response that is opposite to that of activation of the receptor for the agonist


G proteins for specific muscarine receptors

M3 (and M1): Gq = inc. contraction via IP3 and phospholipase C (GI)

M2 (and M2): Gi = dec. contraction via dec. cAMP (Heart)


sweat glands - part of ANS, NT released, and receptor type

part of SNS, but Ach is released to muscarinic receptors - exception
- not important in pharmacotherapy


G proteins for specific adrenergic receptors

a1: Gq = inc. contraction via IP3 and phospholipase C (vascular SM)
a2: Gi = dec. contraction via dec. cAMP (dec. SNS)
b1 and b2: Gs = inc. contraction via inc. cAMP (inc. HR and bronchodilation)


relationship between agonist and antagonist effect and tone

antagonist = effect is proportional to level of tone
- depends on receptor type and quantity
agonist = can overcome tone when use enough
- depends on dose


epinephrine reversal

when epi causes hypotension since patient on an a1 blocker (antagonist) --> excess b2 vasodilation
- treat with an a1 agonist (phenylephrine - Sedated PE)


sensitization to epi-induced hypertension

see excess inc. in HTN since patient is on a non-selective beta blocker --> unopposed epi a1 vasoconstriction



activates a2 receptors
- dec. SNS outflow
- dec. release of Ach from cholinergic (muscarinic) neurons innervating the salivary glands

Treatment: HTN and opioid/alcohol withdrawal sxs

SE: dry mouth
- activates a2 receptors on cholinergic neurons in GI tract
- dec. Ach release from cholinergic neurons innervating salivary glands


beta-1 antagonists

beta-1 selectivity seen at low doses only - push dose can spill over to beta 2 (bad for asthmatic - bronchospasm)


if there is no PNS innervation of the vasculature, how does muscarinic activation (Ach) on muscarinic receptors result in vasodilation?

indirect effect mediated via generation of nitric oxide --> cGMP --> dec. BP


side effects of muscarinic blocking agent (most sensitive to least sensitive)

Exocrine glands: reduced salivary and bronchial secretions → dry mouth

Sweat glands: impaired sweating and direct vasodilation → increased body temperature (“atropine flush” at high doses); most life-threatening result of overdose
• Children are especially susceptible (OD toxicity)

Heart: block of cholinergic slowing of heart rate → tachycardia

Eye: mydriasis and paralysis of accommodation (cycloplegia) → blurred vision, ↑ IOP (block aqueous humor drainage)

Lungs: relaxation of bronchiolar smooth muscle → bronchodilation

Genitourinary tract: relaxation of ureters and bladder wall muscle (detrusor) → urinary retention

Gastrointestinal tract: reduced gastrointestinal motility → constipation; gastric secretions (HCl, pepsin) blocked less effectively than salivary secretions

CNS effects: restlessness, delirium; sedation with scopolamine


lethal injection

Sodium thiopental: IV general anesthetic = unconscious
• Now unavailable in US – benzodiazepines* used

Pancuronium*: neuromuscular blocker = blocks respiration and involuntary muscle movements

Potassium chloride*: Produces complete heart block
• * 2016 – restricted from use in executions by Pfizer


baroreceptor reflex

Activation of baroreceptor (increased arterial pressure increases vessels tension and activates)
• Inhibits sympathetic discharge from medulla: vasodilation, dec. HR (reflex bradycardia)
• Vagus nerve activity increases (PNS) → dec. HR
• Overall: decrease blood pressure

Relaxation of baroreceptor (decreased arterial pressure)
• Disinhibits tonic sympathetic discharge, resulting in SNS-mediated release of NE
o Heart: B1 receptors → reflex tachycardia (inc. HR)
o Blood vessels: α1 receptors → vasoconstriction
• Overall: increase in arterial blood pressure


indirect acting sympathomimetics (adrenergic agonists) vs. indirect acting parasympathomimetics (cholinergic agonists)

Indirect-acting sympathomimetics (adrenergic agonists) act like NE by being uptaken by NET, transported to storage vesicle (VMAT), and displaces endogenous NE which is released into synapse

Indirect acting parasympathominetics (cholinergic agonists) inhibit the enzyme (AchE) the breaks down Ach; thus, prolonging the time Ach is in synapse


substance most associated with the acute bronchospastic response seen in patients with asthma
- target pharmacotherapy



why should NSAIDs be used cautiously in patients with asthma

b/c they inc release of leukotrienes and can cause bronchospastic response


effects of endogenous histamines

vasodilation of arterioles via NO (hypotention / reflex tachycardia)

inc. capillary permeability (edema, urticaria, hives)

contraction of GI smooth muscle and inc. secretions


stimulation of nerve endings (pain, itching)

triple response: wheal and flare

anaphylactic reaction


most effective physiologic antagonist of histamine in smooth muscle

epinephrine and albuterol

Note: antihistamines are pharmacologic antagonists


treatment of acute cough due to the common cold

1st generation antihistamine/decongestant (e.g., diphenhydramine/pseudoephedrine)

Naproxen (tid x 5 days): blocks inflammation that stimulates cough afferents (for pain)

Comments: antitussives mixed results; zinc not recommended; 2nd generation antihistamines ineffective


treatment of cough due to upper airway cough syndrome (postnasal drip)

1st generation antihistamine/decongestant (e.g., diphenhydramine/pseudoephedrine


treatment of dry, non-productive coughs that keep you up at night

anti-tussives (opioids or opioid agonists work at level of cough center


roles of cells in GI tract

parietal cells: pump out H+ via H+/K+ ATPase
epithelial cells: protect GI lining
- prostaglandins dec. H+, inc. HCO3, inc. mucous


why do NSAIDS cause ulcers

they wipe out prostaglandins (cytoprotective)


why treat h. pylori with ABX

to prevent reoccurrence


proton pump inhibitors (PPIs): side effects and DDI

mild: HA, abd pain, nausea, constipation, diarrhea

DDIs: omeprazole may inhibit conversion of anti-platelet drug clipidogreal to active form

Caution: dose reduction in severe hepatic disease


H2 antagonists: side effects and DDI

mild: dizziness, HA, constipation, diarrhea

Cimetidine: CNS dysfunction (slurred speech, confusion), endocrine effects (gynecomastia, galactorrhea, dec. sperm count

DDI: Cimetidine inhibits CYP450 oxidative metabolism, inc. toxicity for many drugs

Caution: dose reduction in impaired renal fx


how do PPIs protect GI tissues

decrease H+ secretion


how to prostaglandins protect GI tissues

dec H+ secretion, inc. HCO3, inc. mucous


properties of antacids

rapidly raise pH of stomach content to 4-5 (above ideal oH of pepsin but below gastrin to prevent rebound acid secretion)

use: pain relief due to peptic ulcerations and acute gastritis (doses titrated to sxs relief)

non-absorpable, long-acting, no undesirable side effects (most have constipation or diarrhea)


which antacids cause constipation and which cause diarrhea

- calcium carbonate
- aluminum hydroxide

- magnesium oxide (Milk of Magnesia)


antacids and DDIs

space drug dosing around antacid dosing to minimize DDIs


treatment of simple constipation

proper diet (high fiber: 20-30 g/day)
exercise (esp. abdominal muscles)
adequate fluids (6-8 8oz glasses / day)


drugs that cause constipation

o Calcium channel blockers (esp. verapamil)
o Opioid analgesics (cause both pain relief and constipation since interact with opioid (mu) receptors)
o Antimuscarinic agents (antispasmodics, overactive bladder agents)
o Drugs with antimuscarinic side effects (tricyclic antidepressants, antipsychotic agents, 1st generation antihistamines, parkinsonian agents)
o Antacids: aluminum and calcium-containing
o Calcium supplements (esp. carbonate)
o Chemotherapeutic vinca alkaloids
o 5HT3 antagonists - not SSRIs (block serotonin)


drugs that cause diarrhea

o Misoprostol: prostaglandin analog stimulates intestinal musculature
o Antibiotics (esp. broad spectrum)
o Muscarinic agonists (SLUDGE)
o Reserpine: sympatholytic agent allows parasympathetic dominance in GI tract
o SSRIs: elevated synaptic 5HT levels stimulates GI motility (inc. serotonin in gut = inc. diarrhea)
o Colchicine (anti-inflammatory for gout)
o Digoxin: parasympathomimetic action (similar to muscarinic excess)
o Magnesium antacids: osmotic laxative actions


opioid analgesic-injuced constipation

Constipation: managed with stool softeners (docusate), stimulant laxatives (bisacodyl - senna), osmotic laxatives (PEG [Miralax®] - milk of magnesia)

Option for patients taking opioids for non-cancer pain that have failed laxative therapy
- Peripherally acting opioid antagonists

Methylnaltrexone (Relistor®): given SC, doesn’t cross BBB
• Expensive ($700 per day)

Naloxegol (Movantik®): new pegylated derivative of naloxone given orally
• Extensive first-pass metabolism - primarily binds opioid receptors in GI tract only
• $10 per day


Second generation anti-histamines

loratadine: Claritin
fexofenadine: Allegra
cetirizine: Zyrtec