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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
1st generation cephalosporins (keflex, cefazolin) major spectrum of activity
Gram +
26
2nd generation cephalosporins (cefuroxime, cefaclor) major spectrum of activity
mediocre coverage for both Gram + and Gram --
27
3rd generation cephalosporins (ceftriaxone, cefixime) major spectrum of activity
Gram --
28
4th generation cephalosporins (cefepime) major spectrum of activity
good for both Gram + and Gram -- (typically used for serious, hospitalized infections)
29
macrolides (erythromycin, clarithromycin, azithromycin) mech of action
inhibition of ribosomal function, therefore, no protein synthesis
30
macrolide spectrum of activity
Gram +
31
tetracyclines (doxycycline, tetracycline, minocycline) MOA
protein synthesis inhibition (broad spectrum) (adverse rxns: photosensitivity, tooth discoloration in children)
32
quinolones (ciprofloxican, norfloxican) MOA
inhibits DNA replication
33
quinolones spectrum of activity
both Gram + and Gram --
34
sulfa drugs (trimethoprim-sulfamethoxazole) MOA
inhibits synthesis of bacterial dihydrofolic acid | broad spectrum
35
metronidazole indications & adverse effects
ind:treatment of amebic infections , anaerobic bacteria, parasites. AE: metallic taste, yeast infections (esp in mouth), dizziness, vertigo
36
mebendazole indications
wide spectrum use against nematodes.
37
2 types of corticosteroids
1. glucocorticoids (act similar to cortisol, promotes gluconeogenesis) 2. mineralcorticoids (similar to aldosterone)
38
physiologic dose of steroid
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
short term effects of glucocorticoids
hyperglycemia, elevated WBC count (due to demargination), GI bleed/ulcers, sodium retention (edema, hypertension CHF), hypokalemia, metabolic acidosis, steroid psychosis
40
long term effects of glucocorticoids
HPA axis suppression after 2 wks, cushingoid features, muscle weakness, thinning of skin, osteoporosis, cataracts/glaucoma, decreased immune response, poor wound healing
41
Anticoagulants: MOA
diminishes clotting factor actions
42
anticoagulants prototype drug
warfarin (oral), heparin (IV)
43
antiplatelets MOA
inhibits production of thromboxane
44
antiplatelets prototype drug
aspirin
45
diuretic drugs that work on the proximal tubule
carbonic anhydrase inhibitors
46
diuretic drugs that work on the loop of Henle
loop diuretics, thiazide diuretics, osmotic diuretics
47
diuretic drugs that work on the distal convoluted tubule
thiazide diuretics, K+ sparing diuretics
48
volume depletion from diuretic therapy
where Na goes, water follows. causes reduced BP, pulmonary & systemic vascular resistance, reduced central venous pressure, and reduced L ventricular end diastolic pressure
49
azotemia from diuretic therapy
increase in BUN and SCr due to decrease in renal perfusion & decreased GFR
50
hypokalemia from diuretic therapy
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
hyperkalemia from diuretic therapy
K sparing diuretics reduce both K & H secretion in the collecting tubules
52
hyperuricemia due to diuretic therapy
reduced urate secretion due to competition for organic acid secreting pathway. increase renal reabsorption secondary to plasma vol contraction
53
hyponatremia due to diuretic therapy
almost all cases are due to thiazides (not loop diuretics), the ECF vol depletion stimulates ADH, causing impaired water excretion, resulting in hyponatremia
54
hyperglycemia due to diuretic therapy
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
hypomagnesemia due to diuretic therapy
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
the 3 subclasses of Ca Channel blockers
1. Dihydropyrimidines (nifedipine) 2. Phenylalkylamines (verpamil) 3. Benzothiazepines (diltiazem)
57
anesthesia
partial or complete loss of sensation, w/ or w/out loss of consciousness, as a result of disease, injury, or admin of anesthetic
58
analgesia
absence of normal sense of pain
59
hyperalgesia
an excessive sensitivity to pain ; painful stimuli are perceived as more painful
60
hyperesthesia
an increased sensitivity to sensory stimuli, such as pain or touch
61
allodynia
non painful stimuli are perceived as painful
62
dysthesia
unpleasant sensations (ex: "pins/needles" or "ants crawling on skin")
63
hyperpathia
all stimuli (noxious & innocuous) are more intense
64
neuropathic pain
nerve pain, usually burning/tingling, or electric-shock like, a type of chronic pain from nerves in CNS getting damaged
65
nociceptive pain
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
idiopathic pain
pain that has no apparent underlying cause but is extremely real to the pt
67
psychogenic pain
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
physical dependence
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
tolerance
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
addiction
a primary, chronic disease of brain reward, motivation, memory & related circuitry. Dysfunction in these circuits leads to characteristic biological, psychological, social, &spiritual manifestations
71
peripheral agents (acetominophen) MOA
inhibits prostaglandin synthesis in the CNS which makes it antipyretic and analgesic. No effect on inflamm or platelets
72
NSAIDS MOA
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
Opiods MOA
bind specific opiod receptors in CNS to produce effects that mimic the action of endogenous peptide neurotransmitters such as endorphins, enkephalins, and dynorphins
74
Bisophonates (used for bone pain) MOA
analogs of pyrophosphate. decrease osteoclastic bone reabsorption
75
neuropathic agens MOA for pain relief
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
antidepressant agents MOA for pain relief
increases actions of norepinephrine and/or serotonin in the brain by blocking the neurotransmitter reuptake
77
anticonvulsant agents MOA for pain relief
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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