All Medication Chart Flashcards Preview

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Flashcards in All Medication Chart Deck (40)
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1
Q

Albuterol

A

β2-Adrenergic receptor agonists; increase in cAMP

2
Q

Atracurium

A

Intermediate acting NDNMB Compete with acetylcholine (ACh) for binding to nicotinic receptor α subunits, cause receptor antagonism, thus resulting in skeletal muscle relaxation

3
Q

Atropine Sulfate

A

Atropine is a naturally occurring tertiary amine that is capable of inhibiting the activation of muscarinic receptors, Cholinergic blocker, decreased cyclic GMP

4
Q

Calcium Chloride

A

Moderates nerve and muscle performance via action potential excitation threshold regulation

5
Q

Calcium Gluconate

A

In hydrogen fluoride exposures, calcium gluconate provides a source of calcium ions to complex free fluoride ions and prevent or reduce toxicity

6
Q

Droperidol

A

Butyrophenones D2-receptor antagonists.

Black box warning: Prolong QTI

7
Q

Dexamethasone

A

It decreases inflammation by suppression of neutrophil migration, decreased production of inflammatory mediators, and reversal of increased capillary permeability; suppresses normal immune response. Dexamethasone’s mechanism of antiemetic activity is unknown.

8
Q

Ephedrine
Acts on
Releases and inhibits what?
Can you do an infusion?

A

Ephedrine acts primarily on α- and β-receptors But less potent than epinephrine. Releases endogenous norepinephrine from sympathetic neurons and inhibits norepinephrine reuptake, accounting for additional indirect α- and β-receptor effects.

9
Q

Diphenhydramine

A

H1 receptor antagonists

Block Histamine 1 receptors (block Smooth muscle contraction in respiratory and GI tract)

10
Q

Etomidate

A

Causes neuronal hyperpolarization and subsequent depression of the reticular activating system through inhibition of neural signals. Etomidate increases the affinity of GABA receptors for the GABA molecule. B2 and B3 subunits

11
Q

Propofol

A

Sedative-hypnotic agent, Stimulation of γ-aminobutyric acid receptors. Binds to all 5 alpha subunits

12
Q

Ephedrine
Acts on
Releases and inhibits what?
Can you do an infusion?

A

Mixed synthetic non-catecholamines
Ephedrine acts primarily on α- and β-receptors But less potent than epinephrine. Releases endogenous norepinephrine from sympathetic neurons and inhibits norepinephrine reuptake, accounting for additional indirect α- and β-receptor effects.

13
Q

Epinephrine

A

Stimulates alpha-, beta1-, and beta2-adrenergic receptors resulting in relaxation of smooth muscle of the bronchial tree, cardiac stimulation (increasing myocardial oxygen consumption), and dilation of skeletal muscle vasculature; small doses can cause vasodilation via beta2-vascular receptors; large doses may produce constriction of skeletal and vascular smooth muscle

14
Q

Esmolol

A

Class II antiarrhythmic: Competitively blocks response to beta1-adrenergic stimulation with little or no effect of beta2-receptors except at high doses, no intrinsic sympathomimetic activity, no membrane stabilizing activity

15
Q

Diltiazem

A

Diltiazem, the best-known benzothiazepine, has cardiac effects that are somewhat similar to those of verapamil but are not as pronounced. Diltiazem has some effects on the peripheral vasculature, similar to those of the DHPs. It reduces SVR but does not produce the same degree of reflex tachycardia as is seen with the use of the DHPs.

16
Q

Famotidine

A

Competitive inhibition of histamine at H2 receptors of the gastric parietal cells, which inhibits gastric acid secretion

17
Q

Fentanyl

A

Its an opioid Kappa agonists

18
Q

Flumazenil

A

Flumazenil is a specific antagonist of the central nervous system effects of benzodiazepines because it binds with high affinity to specific sites on the GABA-A receptor, where it competitively inhibits the binding of the neurotransmitter GABA to this receptor.

19
Q

Furosemide

A

Primarily inhibits reabsorption of sodium and chloride in the ascending loop of Henle and proximal and distal renal tubules, interfering with the chloride-binding cotransport system, thus causing its natriuretic effect

20
Q

Glucagon

A

Stimulates adenylate cyclase to produce increased cyclic AMP, which promotes hepatic glycogenolysis and gluconeogenesis, causing a raise in blood glucose levels; antihypoglycemic effect requires preexisting hepatic glycogen stores. Extra hepatic effects of glucagon include relaxation of the smooth muscle of the stomach, duodenum, small bowel, and colon.

21
Q

Phenylephrine

A

Direct acting synthetic non-catecholamines

22
Q

Heparin

A

Potentiates the action of antithrombin III and thereby inactivates thrombin (as well as other coagulation factors IXa, Xa, XIa, XIIa, and plasmin) and prevents the conversion of fibrinogen to fibrin; heparin also stimulates release of lipoprotein lipase (lipoprotein lipase hydrolyzes triglycerides to glycerol and free fatty acids)

23
Q

Hydralazine

A

Direct vasodilation of arterioles (with little effect on veins) with decreased systemic resistance

24
Q

Sevoflurane

A

Inhalation anesthetic agents induce anesthesia by depressing brain function via a dose-dependent reversible mechanism that is not fully understood. It is suspected that they potentiate inhibitory signals such as GABA and block excitatory signals throughout the central nervous system (CNS)

25
Q

Ketamine

A

Ketamine is chemically related to phencyclidine (“PCP” or “angel dust”)The properties of ketamine are primarily mediated by noncompetitive antagonism at N-methyl-d-aspartate (NMDA) receptors for glutamate. Glutamate is the most prominent excitatory amino acid in the body.

Ketamine is a nonbarbiturate that is termed a dissociative anesthetic for two reasons. First, the patient appears “dissociated” from the environment. Effective analgesia and sedation often occur with the patient appearing awake, with slow nystagmus, whereas other reflexes remain intact, including corneal, papillary, and gag reflexes, laryngeal tone, and muscle tension. Second, ketamine anesthesia produces an EEG showing that the thalamus is no longer synchronized with, or is “dissociated” from, the limbic system.

26
Q

Ketorolac

A

NSAIDs, inhibit cyclooxygenase (COX)1 and COX2 receptors

27
Q

Labetalol

Beta to alpha blocking ratio

A

MOA of labetalol (act on 4 receptors)
Alpha 1 antagonism–> relaxation of arterial SM and vasodilation causing decrease SVR and BP
Non-selective B2 blockade, decreased HR
B1 blockade decreased BP
it is a PARTIAL AGONIST at Beta 2 receptors, vasodilation

3: 1 for oral
7: 1 for IV

28
Q

Lidocaine

A

Class 1B
Less potent Na+ Channel blocks , they produce little effect on slowing conduction compared to other class I agents.
Improves AV conduction
• Action potential duration and effective refractory period is shortened
BETTER FOR RE-ENTRY TACHYCARDIAS

29
Q

Magnesium Sulfate
GI?
Parentally ?

IV mag?

A

When taken orally, magnesium promotes bowel evacuation by causing osmotic retention of fluid which distends the colon with increased peristaltic activity;

parenterally, magnesium decreases acetylcholine in motor nerve terminals and acts on myocardium by slowing rate of S-A node impulse formation and prolonging conduction time. Magnesium is necessary for the movement of calcium, sodium, and potassium in and out of cells, as well as stabilizing excitable membranes.

Intravenous magnesium may improve pulmonary function in patients with asthma; causes relaxation of bronchial smooth muscle independent of serum magnesium concentration.

30
Q

Methergine

A

Uterine atony and postpartum hemorrhage treatment
Increases the tone, rate and amplitude of contractions on the smooth muscles of the uterus, producing sustained contractions which shortens the third stage of labor and reduces blood loss.

31
Q

Methylene blue

A

Methylene blue, in low concentrations, hastens the conversion of methemoglobin to hemoglobin;
has opposite effect at high concentrations by converting ferrous ion of reduced hemoglobin to ferric ion to form methemoglobin; in cyanide toxicity, it combines with cyanide to form cyanmethemoglobin preventing the interference of cyanide with the cytochrome system

In the treatment of vasoplegia syndrome, methylene blue may be able to restore vascular tone by a direct inhibitory effect on endothelial nitric oxide synthase (eNOS), and probably inducible NOS (iNOS), by oxidation of enzyme-bound ferrous iron.
Methylene blue also blocks the formation of cyclic guanosine monophosphate (cGMP) by inhibiting the guanylate cyclase enzyme through binding to iron in the heme complex and subsequently reducing vasorelaxation

32
Q

Metoclopramide

Does muscarinic antagonists block reglan?

A
  1. Selective cholinergic stimulation of the GI tract by enhancing the response to Ach of tissue in the upper GI tract primarily via 5-HT4 receptor agonists
  2. Dopamine 2 receptor antagonism in the GI tract.

Any muscarinic antagonists will BLOCK the effect of reglan

33
Q

Neostigmine

A

They act indirectly through inhibition of the acetylcholinesterase (AChE) enzyme, which normally metabolizes acetylcholine (ACh) into choline and acetate.

34
Q

Nitroprusside

A

Sodium nitroprusside is a potent, rapid-acting intravenous vasodilator used for the acute management of blood pressure.
Thiocyanate toxicity?

35
Q

Nitrous oxide

A

Nitrous oxide is a weak inhalational anesthetic agent with a minimum alveolar concentration of 104%.

36
Q

Ondansetron

A

5-hydroxytryptamine (Serotonin, 5-HT3) Receptor Antagonists. Bind to receptors in the Chemoreceptor Trigger Zone and the gastrointestinal tract.

37
Q

Pitocin

A

Uterine atony and postpartum hemorrhage treatment
Increases the tone, rate and amplitude of contractions on the smooth muscles of the uterus, producing sustained contractions which shortens the third stage of labor and reduces blood loss.

38
Q

Scopolamine

A

Scopolamine, another belladonna alkaloid, sometimes referred to as hyoscine, has stronger antisalivary actions and much more potent central nervous system effects than does atropine (Table 63.1). It is a strong amnesic that usually also produces sedation.

39
Q

Sodium Bicarbonate

A

Sodium bicarbonate (NaHCO3) is an alkaline inorganic salt that readily dissociates into Na+ and HCO3− ions, whereby the HCO3− ion is the principal buffer in extracellular and interstitial fluid.

40
Q

Rocuronium

A

Blocks acetylcholine from binding to receptors on motor endplate inhibiting depolarization