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Clin Lab Med > Drug managment > Flashcards

Drug managment Flashcards

1
Q

Digoxin.. how does it circulate through the body? Metabolism, and half life?

A

20-30% Dig bound to alb
80% excreted unchanged by kidneys
20% metabolized by liver
serum 1/2 life: 36-38 hr

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2
Q

when does digoxin peak after oral dose and what is the therapeutic range

A

Oral dose, digoxin peaks in 30-90min, declines till plateau after 6-8 hr
*don’t draw blood till after this 6-8 hr
Range: 0.5-2 ug/100mL

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3
Q

Do you use loading dose with Dig?

A

Yes, if need earlier effect (unlike warfarin)

start with 0.25-0.5mg STAT then give 0.25mg every 6-8 hr till total of 1-1.5mg given

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4
Q

what is the maintenance dose with dig

A

0.125-0.25mg/d

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5
Q

IV vs oral for digoxin and onset of action

A

IV: dig onset in 15-30min
oral: w/in 2 hr

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6
Q

how does reduced renal function affect digoxin levels

A

ELEVATES (reduces excretion).. may increase 1/2 life from 36 hr to 5 days
*amt of dig depends on pt.. some pt can have adequate dig effect w/ below normal blood level

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7
Q

frequency of Dig toxicity and predisposing factors?

A

May occur in 5-15% of pt

Risk: electrolyte abn (esp low K), drug interaction, hypoxemia, hypoTH, renal insuff, volume depletion

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8
Q

Cardiac SE of dig are. Other SE??

A

PVC, AV block ,Vtach, **PAT WITH BLOCK
Other: anorexia, N/V, diarrhea (which can make hypoK worse)
*altered mental status, agitation, vision color changes

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9
Q

tx for dig toxicity

A

depends on clinical feature and blood level:
- dc drug
- ensure adequate K
- cardiac monitoring
- correct exacerbating factors
- antiarrhythmic meds if needed
- avoid cardioversion except as last resort
DIGIFAB for life threatening when no other available
*40mg vial = 0.6 mg dig

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10
Q

What is Dilantin (phenytoin)

A

commonly used anticonvulsant (usually 300 mg/d)

*occasionally used as anti-arrhythmic

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11
Q

How safe is Dilantin (phenytoin), what is the therapeutic range and how do you determine adequacy of next dose

A

Narrow therapeutic window
excess is toxic
THERAPEUTIC range: 10-20ug/mL
*draw blood before next dose to get levels
*also, if toxic sx present, get drug levels during sx or peak levels

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12
Q

How does Dilantin/phenytoin circulate throughout the body. How is it metabolized?

A

90% bound to serum pro
70%** METABOLIZED IN LIVER
5% excreted unchanged in kidney

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13
Q

when do you get peak levels of Dilantin

A

4-8 hr after oral dose or 15 min after IV

Serum half life 24 hr, steady state achieved 4-6 days after starting

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14
Q

what is the key to phenytoin pharmacology

A

dose response curve is not linear, small increases may result in very large increase in serum level

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15
Q

what are common SE of phenytoin/Dilantin

A

RASH (morbilliform or sever exfoliative)
LETHARGY
MEGALOblastic anemia (responds to folic acid)
Benign Lymphoid hyperplasia
GINGIVAL HYPERTROPHY (also in “dipine” CCB)
HIRSUTISM

rash, tired, big anemia, gingiva, LAD, Hairy

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16
Q

what would be an excessive phenytoin blood level and what clinical findings might indicate this

A

> 20 ug/mL = pheny toxic
findings:
lethargy, nystagmus/tremor, ataxia, reduced coordination, dizzy, slurred speech
*LOTS OF NEURO SX with pheny toxic

17
Q

A pt comes in lethargic, ataxic, slurring speech and losing balance. You find out they have blood level of 21 ug/mL of phenytoin. How do you treat their phenytoin toxicity

A

NO ANTIDOTE :( poor pheny

supportive care, follow blood levels, hemodialysis possibly

18
Q

what percent of pt with AMI don’t even have classic chest pain? what about nondx ECG of pt who actually end up having an AMI

A

1/4 pt don’t have chest pain

1/2 have nondx ECG

19
Q

Acute Coronary syndrome consists of

A
  1. unstable Angina
  2. STEMI (AMI)
  3. NSTEMI (AMI)
20
Q

what are classifcations for unstable angina

A
  1. min exertion or at rest >10min or 20min
  2. New onset (past 4-6 wk) and severe (limits PA)
  3. Worse than previously (crescendo pattern)
    - more sever, more prolonged, more frequent
21
Q

what are descriptions for noncardiac chest pain

A

Pleuritic - sharp, knife like, hurt when cough or breath
Mid to lower abdomen
discomfort localized with one finger
discomfort reproduced by mvmt of palpation
constant pain lasting for days
Fleeting pain lasting sec
pain radiating to legs or above mandible

22
Q

what are the cardiac enzymes

A

CK-MB
Troponin more sensitive and specific
*if normal ecg and CK-MB but elevated troponin, may still indicate MI

23
Q

Criteria for MI

A

rise and fall of cardiac enzyme PLUS

a) ischemic sx
b) new Q wave
c) ECG changes: ST elevation or depression
d) imaging evidence of new loss of viable myocardium or new regional wall motion abn

24
Q

the line bw UA and MI…

A

UA: sx but no enzyme or EKG indications
MI: assumed if troponin and/or CK-MB are elevated

25
Q

Troponin.. what is it

A

troponin I and T are cardiac reg proteins that control CALCIUM MEDIATED interaction of ACTIN and Myocin

  • preferred marked for dx of myocardial injury
  • increase 3-4 hr after MI, Peak 10-24, decrease after 5-14 days
26
Q

ranges for troponin

A

1.5 MI

increase 3-4 hr after MI, peak 10-24 hr, fade after 5-14 d

27
Q

CK MB

A

released with any muscle or brain tissue injury (not as specific as troponin)
3 serum isoenzymes: MM (muscle), MB (heart), BB (brain)
MB may also be small amt in SI, tongue, uterus, prostate

28
Q

Normal CK-MB

Blood levels and timing?

A

<5

increase 3-6 hr after MI, peak 18-28, decrease around 2 days

29
Q

Sensitiviy CK-MB

A

50% single measurement
95% serial
>95% senstivity and specificty for MI when measured w/in 24-36 hr of onset of chest pain
ORDER 3 serial (every 6 hr)

30
Q

How should you treat STEMI

A

a) MONA

b) initiation of reperfusion tx
- -> PCI or Fibrinolysis (PCI safer, Fibrinolysis risk bleeding) *if pt will be catheterized, NO THROMBOLYTICs

c) Anticoagulation to prevent rethrombosis (antiplt or anticoag med)
d) Bblocker (prevent recurrent ischemia and arrhythmia (CONTRindicated: CHF, bradycardia, HB, reactive airway dz, cardiogenic shock)

31
Q

Tx UA and NSTEMI

A 
MONA
no fibrinolysis
yes anticoag
yes BBlocker
*consult cardiologist (PCI vs MED tx)
32
Q

summary, go to tx UA and NSTEMI

A

anticoag, cardiac consult

33
Q

KEY.. STEMI tx

A

PCI or fibrinolysis
ASA
Cardio consult

34
Q

Key UA and NSTEMI

A

Anticoag, ASA, consult

35
Q

ASA… why important

A

used for STEMI, UA, NSTEMI

36
Q

Who to assess for Chol

A

a) health pt no risk, age 20-70: check lipid/BP/evidence DM every 4-6 yr

37
Q

Pt not on chol lowering meds with LDL 70-190, you can estimate what

A

the 10 yr CV risk using calculator

38
Q

what 4 groups benefit from statins

*note: ASCVD = arthersclerotic cardiovascular disease

A
  1. clinical ASCVD
  2. LDL?190
  3. age 40-75 w/ DM, and LDL bw 70-190
  4. Pt w/o clinical ASCVD or DM with est 10yr CV risk of ASCVD >7.5%

Clin Lab Med (6 decks)

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