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Pharm Block 2 - 2014 > pharm block 2 > Flashcards

pharm block 2 Flashcards

1
Q

prophylaxis

A

treating pts who are not yet infected or have not yet developed disease.

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2
Q

empiric therapy

A

use of antibiotics to tx an infection before the specific causative organism has been identified w/ lab test

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3
Q

definitive therapy

A

use of specific antibiotics based on a previously identified identifying organism

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4
Q

normal flora

A

organisms that live symbiotically on or w/in the human host but rarely cause disease

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5
Q

colonization

A

the process of a newly introduced microorganism that successfully competes w/ normal flora

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6
Q

infection

A

a disease caused by microorganisms, esp those that release toxins or invade body tissue

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7
Q

superinfection

A

a new infection occurring in a pt already having an infection (usually caused by opportunistic microorganisms resistant to the antimicrobial agents used in tx of the first infection)

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8
Q

contamination

A

the introduction of pathogens or infectious material into or on normally clean or sterile objects, spaces, or surfaces

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9
Q

bactericidal

A

capable of killing bacteria

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10
Q

bacteriostatic

A

inhibition or retardation of the growth of bacteria w/out their destruction

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11
Q

Minimum inhibitory concentration (MIC)

A

the lowest concentration antibiotic that inhibits bacterial growth

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12
Q

minimum bactericidal concentration

A

the lowest concentration of antibiotic that kills 99.9% of bacteria

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13
Q

penetration & concentration of abx in CSF is a result of

A

lipid solubility, molecular weight of drug, protein binding of drug

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14
Q

additive combination drug response

A

the response elicited by combined drugs is equal to the combined responses of the individual drugs if they were taken separately (1+1=2)

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15
Q

synergistic combination drug response

A

the response elicited by combined drugs is greater than the combined response of the individual drugs if they were taken separately (1+1=3)

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16
Q

MOA for aminoglycosides

A

ribosomal protein synthesis inhibitor – bactericidal

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17
Q

gentamicin, streptomycin, neomycin are examples of which class of antibiotic?

A

aminoglycosides

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18
Q

what are the 2 subclasses within beta-lactams?

A
  • penicillins

- cephalosporins

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19
Q

MOA of PCNs

A

inhibits cell wall synthesis

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20
Q

MOA of cephalosporins

A

beta lactam binds PCN-binding-proteins and inhibits cell wall synthesis

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21
Q

MOA of nucleoside analogs (antiviral)

A

inhibits DNA polymerase and incorporates into viral DNA

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22
Q

3 drugs to treat headlice/scabies/crabs

A
  1. lindane (all 3 are topical use only)
  2. permethrin
  3. pyrethrins
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23
Q

clinical use for aminoglycoside antibiotics

A

Gram - infections (including pseudomonas)

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24
Q

major PCN spectrum of activity

A

gram +

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25
Q

1st generation cephalosporins (keflex, cefazolin) major spectrum of activity

A

Gram +

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26
Q

2nd generation cephalosporins (cefuroxime, cefaclor) major spectrum of activity

A

mediocre coverage for both Gram + and Gram –

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27
Q

3rd generation cephalosporins (ceftriaxone, cefixime) major spectrum of activity

A

Gram –

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28
Q

4th generation cephalosporins (cefepime) major spectrum of activity

A

good for both Gram + and Gram – (typically used for serious, hospitalized infections)

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29
Q

macrolides (erythromycin, clarithromycin, azithromycin) mech of action

A

inhibition of ribosomal function, therefore, no protein synthesis

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30
Q

macrolide spectrum of activity

A

Gram +

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31
Q

tetracyclines (doxycycline, tetracycline, minocycline) MOA

A

protein synthesis inhibition
(broad spectrum)
(adverse rxns: photosensitivity, tooth discoloration in children)

32
Q

quinolones (ciprofloxican, norfloxican) MOA

A

inhibits DNA replication

33
Q

quinolones spectrum of activity

A

both Gram + and Gram –

34
Q

sulfa drugs (trimethoprim-sulfamethoxazole) MOA

A

inhibits synthesis of bacterial dihydrofolic acid

broad spectrum

35
Q

metronidazole indications & adverse effects

A

ind:treatment of amebic infections
, anaerobic bacteria, parasites.
AE: metallic taste, yeast infections (esp in mouth), dizziness, vertigo

36
Q

mebendazole indications

A

wide spectrum use against nematodes.

37
Q

2 types of corticosteroids

A
  1. glucocorticoids (act similar to cortisol, promotes gluconeogenesis)
  2. mineralcorticoids (similar to aldosterone)
38
Q

physiologic dose of steroid

A

replacement or maintenance dose. The glucocorticoid dose administered to elicit the same effects as natural cortisol production in the body. mimics the diurnal pattern of normal secretion.

39
Q

short term effects of glucocorticoids

A

hyperglycemia, elevated WBC count (due to demargination), GI bleed/ulcers, sodium retention (edema, hypertension CHF), hypokalemia, metabolic acidosis, steroid psychosis

40
Q

long term effects of glucocorticoids

A

HPA axis suppression after 2 wks, cushingoid features, muscle weakness, thinning of skin, osteoporosis, cataracts/glaucoma, decreased immune response, poor wound healing

41
Q

Anticoagulants: MOA

A

diminishes clotting factor actions

42
Q

anticoagulants prototype drug

A

warfarin (oral), heparin (IV)

43
Q

antiplatelets MOA

A

inhibits production of thromboxane

44
Q

antiplatelets prototype drug

A

aspirin

45
Q

diuretic drugs that work on the proximal tubule

A

carbonic anhydrase inhibitors

46
Q

diuretic drugs that work on the loop of Henle

A

loop diuretics, thiazide diuretics, osmotic diuretics

47
Q

diuretic drugs that work on the distal convoluted tubule

A

thiazide diuretics, K+ sparing diuretics

48
Q

volume depletion from diuretic therapy

A

where Na goes, water follows. causes reduced BP, pulmonary & systemic vascular resistance, reduced central venous pressure, and reduced L ventricular end diastolic pressure

49
Q

azotemia from diuretic therapy

A

increase in BUN and SCr due to decrease in renal perfusion & decreased GFR

50
Q

hypokalemia from diuretic therapy

A

2 mechs cause this:

  1. high tubular flow to the cortical collecting ducts, increase delivery of Na to the collective duct & decrease in intravasc vol as a result of salt wasting.
  2. diuretics stimulate aldosterone, so low intravasc vol resulting in hyperaldosteronism & enhanced secretion of aldosterone
51
Q

hyperkalemia from diuretic therapy

A

K sparing diuretics reduce both K & H secretion in the collecting tubules

52
Q

hyperuricemia due to diuretic therapy

A

reduced urate secretion due to competition for organic acid secreting pathway. increase renal reabsorption secondary to plasma vol contraction

53
Q

hyponatremia due to diuretic therapy

A

almost all cases are due to thiazides (not loop diuretics), the ECF vol depletion stimulates ADH, causing impaired water excretion, resulting in hyponatremia

54
Q

hyperglycemia due to diuretic therapy

A

exact mech is unknown - possibly due to decreased insulin secretion, decreased tissue sensitivity to insulin or increased insulin depletion. loop diuretics have less marked effect than thiazides

55
Q

hypomagnesemia due to diuretic therapy

A

approx 70% of the filtered Mg is reabsorbed in the thick ascending limn and 10% in the distal convoluted tubule. inhibition of Na/K/Cl transporter by loop diuretics diminishes the lumen to positive potential required to reabsorb Mg

56
Q

the 3 subclasses of Ca Channel blockers

A
  1. Dihydropyrimidines (nifedipine)
  2. Phenylalkylamines (verpamil)
  3. Benzothiazepines (diltiazem)
57
Q

anesthesia

A

partial or complete loss of sensation, w/ or w/out loss of consciousness, as a result of disease, injury, or admin of anesthetic

58
Q

analgesia

A

absence of normal sense of pain

59
Q

hyperalgesia

A

an excessive sensitivity to pain ; painful stimuli are perceived as more painful

60
Q

hyperesthesia

A

an increased sensitivity to sensory stimuli, such as pain or touch

61
Q

allodynia

A

non painful stimuli are perceived as painful

62
Q

dysthesia

A

unpleasant sensations (ex: “pins/needles” or “ants crawling on skin”)

63
Q

hyperpathia

A

all stimuli (noxious & innocuous) are more intense

64
Q

neuropathic pain

A

nerve pain, usually burning/tingling, or electric-shock like, a type of chronic pain from nerves in CNS getting damaged

65
Q

nociceptive pain

A

most often derived from stimulation of pain receptors. may arise from tissue inflamm, mechanical deformation, ongoing injury, or destruction. Can be visceral (poorly localized, originating from internal organ/cavity), or somatic (well-localized)

66
Q

idiopathic pain

A

pain that has no apparent underlying cause but is extremely real to the pt

67
Q

psychogenic pain

A

somatoform pain disorder is severe enough to disrupt everyday life. pain is like that of a physical disorder, but no physical cause is found

68
Q

physical dependence

A

a state of adaptation that is manifested by a drug class specific withdrawal syndrome that can be produced by abrupt cessation, rapid dose reduction, decreasing blood level of drug, or administration of an antagonist

69
Q

tolerance

A

a state of adaptation in which exposure to a drug induces changes that result in a diminution of one or more of the drug’s effects over time

70
Q

addiction

A

a primary, chronic disease of brain reward, motivation, memory & related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social, &spiritual manifestations

71
Q

peripheral agents (acetominophen) MOA

A

inhibits prostaglandin synthesis in the CNS which makes it antipyretic and analgesic. No effect on inflamm or platelets

72
Q

NSAIDS MOA

A

propionic acid derivatives. irreversibly inhibit COX-1 and COX-2 & inhibit synthesis of prostaglandin precursors but not leukotrienes. Anti-inflamm, analgesic, anti-pyretic, alter platelet function, and prolong bleeding time)

73
Q

Opiods MOA

A

bind specific opiod receptors in CNS to produce effects that mimic the action of endogenous peptide neurotransmitters such as endorphins, enkephalins, and dynorphins

74
Q

Bisophonates (used for bone pain) MOA

A

analogs of pyrophosphate. decrease osteoclastic bone reabsorption

75
Q

neuropathic agens MOA for pain relief

A

all CNS acting drugs act by altering a step in the neurotransmission process either by affecting a presynaptic neuron from releasing neurotransmitters or by blocking a postsynaptic receptor.

76
Q

antidepressant agents MOA for pain relief

A

increases actions of norepinephrine and/or serotonin in the brain by blocking the neurotransmitter reuptake

77
Q

anticonvulsant agents MOA for pain relief

A

block voltage-gated Na+ or Ca+ channels, enhance inhibitory GABA-ergic impulses, interfere w/ excitatory glutamate transmission.
these alter the pain threshold.

Pharm Block 2 - 2014 (1 decks)

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