Crozer- medicine Flashcards

1
Q

reasons for post op fever

A
Wind (12-24 h)Atelectasis (from muscle relaxers), Post-op hyperthermia
Water (~24 h)UTI
Walk (~48 h) DVT, PE
Wound (~72 h)Post-op infection
Wonder drug (anytime)Drug fever
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2
Q

Tx of post op fever

A

Wind- Encourage incentive spirometer, Chest x-ray
Water-Straight catheter, Urine analysis (UA) with Gram stain, culture and sensitivity, Treat with antibiotics if necessary
Walk-Heparin or Lovenox protocol, Use SCDs, TEDs, or get patient out of bed
Wound- X-ray, Gram stain, culture and sensitivity, blood cultures, Begin antibiotic
Wonder drug-D/C drug,Give reversal drug if necessary

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3
Q

When do fever peaks occur

A

4-8pm

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4
Q

What part of brain regulates the body temp

A

hypothalamus

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5
Q

What is malignant hyperthermia

A

SE of general anesthesia- tachycardia, htn, acid base and electrolyte abnormalitis, musclee rigidity, hyperthermia

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6
Q

tx for malignant hyperthermia

A

dantrolene (muscle relax) 2.5 mg/kg IV x 1, than 1 mg/kg IV rapid push q6h until sym subside or max dose of 10mg/kg

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7
Q

if risk of malignant hyperthermia suspected what preop test may be performed

A

CPK- elevated in 79% of patients w malignant hyperthermia

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8
Q

whats mechanism of action for local anesthetics

A

block NA channel and conduction of action potentials along sensory nerves

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9
Q

whats toxic dose of lidociane

A

300 mg plain

500 mg w epi

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10
Q

whats toxic dose of bupicacaine (marcine)

A

175 mg plain

225 mg w epi

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11
Q

how can you convert percentage to mg/ml

A

1% =10mg/mL

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12
Q

SE of lidocaine and bupivacaine associated w systemic exposure

A

CNS effect- excitation (dizzy, blurred vision, tremor, seizures) followed by depression (resp and LOC)
Cardio effect- hypotension, bradycardia, arrhythmias, cardiac arrest

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13
Q

what helps revese local anesthetic- induced Cardiovascular collapse

A

IV fat emulsion

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14
Q

is there a risk with intraarticular injections of bupivacaine

A

chondrocyte death by prolonged exposure

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15
Q

what age group should bupivicaine be avoided

A

less than 12

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16
Q

how are amides (lidocaine and bupivacaine) metabolized

A

liver

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17
Q

how are esters (novocain and cocaine) metabolized

A

plasma pseudocholinesterase

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18
Q

whats the only local anesthetic w vasoconstriction

A

cocaine

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19
Q

can local anesthetic cross placental barrier

A

Yes

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20
Q

what does MAC stand for

A

monitored anesthesia care

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21
Q

what anesthesia can’t be given to patients w egg shell injury

A

propofol (diprivan)

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22
Q

pain management w codeine allergy

A

stadol, toradol, talwin, ultram, darvon, davocet, demerol, nubain

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23
Q

first choice oral pain med

A

darvocet N 100 one tab PO q4-6h prn pain

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24
Q

First choice for non-narcotic oral

A

tramadol (ultram) 50 mg one to two tabs PO q4-6 h prn pain. max 400 mg per day

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25
Q

first choice non-narcotic IV

A

Toradol 30-60 mg IV

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26
Q

2 non narcotic analgesics

A

ketoralac (toradol), tramadol (ultram)

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27
Q
What schedule are the following?
Percocet
Vicodin
Tylenol 3
Darvocet
A

Percocet- 2 high potential for abuse- narcotic script
Vicodin-3 moderate
Tylenol 3- 3 moderate
Darvocet -4- low potential

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28
Q

Percocet 5/325?

A

oxycodone/acetaminophen 5mg/325 mg

1-2 tabs PO q 4-6 hr prn pain

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29
Q

Roxicet

A

oxycodone/acetaminophen (5mg/325mg/5mL)

essentially liquid form of percoet thats good for peds

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30
Q

difference btwn percocet and percodan

A

percocet has 325 mg of acetaminophen and percodan has 325 mg ASA

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31
Q

Vicodin 5/500

A

hydrocodone/acetaminophen (5mg/500mg) 1-2 tabs PO q4-6h

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32
Q

Tylenol 3

A

codeine/acetaminophen (30-300mg) 1-2 tabs PO q4-6h

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33
Q

Darvocet N 100

A

propoxyphene/acetaminophen (100mg/650 mg) 1 tab PO q4H PRN pain

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34
Q

ultram

A

tramadol 50 mg 1-2 tabs PO q 4-6 prn pain

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35
Q

toradol

A

ketorolac 10 mg
30 mg IV q6h
1 tab PO q4-6 h prn pain
an NSAID not be used mora than 5 days due to side effects

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36
Q

Darvon

A

propoxyphene 1 tab PO q4h prn pain

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37
Q

OxyCotin

A

oxycodone extended release

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38
Q

Morphine sulphate

A

2-4 mg IV q 2-6 h prn mod severe pain.
for very painful dressing change or bedside debridement
2 mg IV one dose

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39
Q

MS Contin

A

morphine sulfate extended release (15-30 mg) 1 tab PO q 8-12 h prn pain

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40
Q

dilaudid

A

hydromorphone
2-8 mg PO q 3-4 h prn severe pain
1-4 mg IV q 4-6h prn severe pain
VERY strong

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41
Q

Demerol

A

meperidine- ;lots of side effects

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42
Q

Acetaminophen therapeutic effects

A

analgesic, anti pyretic

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43
Q

max dose of acetaminophen

A

4g

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44
Q

Therapeutic effects are seen w most NSAID

A

analgesic, anti pyretic, anti inflam

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45
Q

what path do NSAIDS work on

A

COX

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46
Q

most common SE of NSAIDS

A

GI issues

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47
Q

only cox 2 inhibitor?

A

celecoxib

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48
Q

NAIDS only have anti inflam effect

A

indomethacin, tolmetin

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49
Q

do NSAIDS decrease joint destruction

A

no. only decrease inflammation

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50
Q

Do NSAIDS affect bone healing

A

NSAIDS and cox 2 inhibitors inhibit bone healing via anti inflammatory effects

51
Q

what NSAID doesn’t inhibit platelet aggregation

A

cox 4, celebrex

52
Q

only IV NSAID

A

ketorolac (toradol)

53
Q

what NSAID least nephrotoxicity

A

celebrex, relafen, lodine

54
Q

effect of NSAID on asthma?

A

increase sym of asthma

55
Q

Safest NSAID for pt with asthma

A

diclofenac ketoprofen

56
Q

which NSAID tx collagen vascular disease

A

ibuprofen, sulindac, tolmetin

57
Q

Which nsaid is not renally cleared

A

indomethacin, sulindac

58
Q

cardiovascular effect of nsaids

A

vasoconstrict and increase blood pressure

59
Q

Which nsaid has least cv effect

A

diclofenac ketoprofen

60
Q

which nsaid most hepatotoxic

A

ibuprofen, naproxen, diclofenac

61
Q

what should be given for indomethacin overdose

A

benadryl

62
Q

what is arthrotec

A

diclofenac/misoprostol, NSAID which protects stomach

63
Q

whats anti inflammatory dose of ibuprofen

A

1200-3200 mg/day

64
Q

what NSAID works on lipoxygenase and cyclooxygenase?

A

ketoprofen and diclofenac

65
Q

what is difference btwn cataflam and voltaren

A

Cataflam is diclofenac potassium and has an immediate release
Voltaren is diclofenac sodium and has a delayed release

66
Q

what are the only pro drugs for nsaids

A

nabumetone and sulindac

67
Q

whats only nonacidic nsaid

A

nabumetone

68
Q

which nsaids have fewer pulm problems

A

ketoprofen and diclofenac

69
Q

once a day nsaids

A

celecoxib (Celebrex), piroxicam (Feldene), oxaprozin (Daypro), nabumetone (Relafen),

70
Q

what drugs do NSAID interact with?

A

Coumadin – increases action of Coumadin
Sulfonylureas – increases action of sulfonylureas
Corticosteroids – increases GI risk
Anti-epileptics – increases anti-epileptic toxicity
Antihypertensives – antagonizes antihypertensive meds
Digoxin – increases digoxin’s effect
Methotrexate – decreases methotrexate’s clearance
Lithium – decreases lithium’s clearance
Probenecid – increases concentration of NSADs

71
Q

whats cause of acute arterial occlusion

A

Embolism – detached thrombus, air, fat, or tumor
Thrombus – occlusion of vessel by plaque or thickened wall
Extrinsic occlusion – traumatic, blunt, penetrating

72
Q

triad of PE

A

dyspnea, chest pain, hemoptysis (tachycardia is common)

73
Q

tests ordered to diagnose PE

A

chest xray, ventrilation perfusion scan, pulm angiography

74
Q

virchos triad

A

risk of DVT

  1. venous stasis
  2. endothelial wall damage
  3. hypercoagulability
75
Q

risk factor for DVT

A
I – immobilization
A – arrhythmia
M – MI (past history)
C – coagulable states
L – longevity (old age)
O – obesity
T – tumor
T – trauma
T – tobacco
E – estrogen
D – DVT (past history)
76
Q

how to diagnose DVT clinically

A

Pain, heat, swelling, erythema of unilateral limb
Positive Pratt sign – squeezing of posterior calf causes pain
Positive Homan sign – abrupt dorsiflexion of foot causes calf pain
Pulmonary embolism

77
Q

tests to diagnose DVT

A

Doppler ultrasound
Venogram
D-Dimer

78
Q

treatments for DVT

A

Thrombolytic agents

Heparin 5000 Units IV bolus, then 1000 Units IV q1h and monitor PTT

79
Q

how to dose heparin for periop DVT prophylaxis

A

5000 units SC 2h prior to surgery

5000 units SC q12h until patient ambulates

80
Q

half life of heparin

A

1.5 hours

81
Q

how does heparin work

A

Intrinsic pathway

Potentiates antithrombin III 100-fold, which inhibits the serine protease in the clotting cascade

82
Q

hows heparin reversed

A

protamine sulfate 1mg/100 units

83
Q

whats enoxaparin (lovenox)

A

low molecular wt heparin

84
Q

how to dose lovenox for periop DVT prophylaxis

A

30 mg SC q12 h for 7-10 days

85
Q

half life of lovenox

A

4.5 hours

86
Q

advantage of lovenox vs heparin

A

Advantages – Lovenox has longer plasma half-life with significant anticoagulation in trough
Disadvantages – increased post-op complications when used with spinal/epidural anesthesia

87
Q

how to check for lovenox

A

no test

88
Q

how to reverse lovenox

A

Factor 7

89
Q

how to dose coumadin

A

5-10 mg PO daily for 3-4 days than INR

90
Q

whats half life of coumadin

A

20-60 h

91
Q

how long before Coumadin therapeutic

A

3-5 days

92
Q

how does Coumadin work

A

extrinsic pathway, interferes w factor 2,7,9,10

93
Q

hows Coumadin reversed

A

vit K fresh frozen plasma

94
Q

what are normal and abnormal INR values

A

normal=1

intense anticoagulation 2-3

95
Q

what levels of heparin and Coumadin for DVT/anticoagulation prophylaxis

A
heparin= 2-3 times normal PTT
Coumadin= 2 times normal INR
96
Q

what nonpharmacologic measures are used for periop DVT prophylaxis

A

Early ambulation – most important
TEDs – thromboembolic deterrent stockings
SCDs – sequential compression devices

97
Q

surgical tx for pt w prior DVTs or recurrent PE? and where?

A

greenfield filter- in ivc below renal veins

98
Q

whats pletal

A

cilostazol

99
Q

whats trental

A

pentoxifylline

100
Q

whats indication for pletal or trental

A

intermittent claudication

101
Q

whats CRPS

A

Complex regional pain syndrome (previously known as RSD – reflex sympathetic dystrophy) is
a progressive disease of the autonomic nervous system causing constant, extreme pain that is out
of proportion to the original injury

102
Q

CRPS type 1

A

(reflex sympathetic dystrophy)
 Nerve injury cannot be immediately identified
 Spontaneous pain not limited to single nerve distribution
 Abnormal response in sympathetic nervous system
 Abnormal reflex leading to vasomotor instability and pain

103
Q

CRPS type 2

A

Causalgia
Distinct, “major” nerve injury has occurred
o Trauma
o Peripheral nerve injury
o Drugs – anti-TB, barbiturates, cyclosporine
 Continued pain not necessarily limited to injured nerve distribution

104
Q

Stages of CRPS

A

Acute – early (0 to 8-20 weeks)
 Constant pain out of proportion (intense burning)
 Possible edema, muscle wasting
 Hyperhidrosis
 Pain increased by light touch, movement, emotion
2. Dystrophic – mid (2-6 months, possibly up to 1 year)
 Increased edema that is indurated (brawny edema)
 Constant pain by any stimulus
 Skin is cool pale and discolored
 X-ray shows diffuse osteoporosis
3. Atrophic – late (over 6-12 months)
 Intractable pain spreads proximally to involve entire limb
 Decreased dermal blood flow causing cool, thin shiny skin
 Fat pat atrophy
 Joint stiffen, may proceed to ankylosis

105
Q

radiographic findings of CRPS

A

Periarticular, mottled, irregular bony demineralization (30-60% of cases) and cortical thinning

106
Q

bone scan findings of CRPS

A

The 3-phase bone scan has sensitivity of 96% and specificity of 98%. A normal scan does not
exclude the diagnosis. The findings of the bone scan are based on the phase.
1. Acute- Increased flow and blood pool activity in the affected extremity, Increased activity particularly in a periarticular distribution on delayed images
2. Dystrophic- Flow and blood pool abnormalities begin to normalize, Increased activity on delayed images persists
3. Atrophic-Flow and blood pool activity can be normal or decreased (in about 1/3 of patients), Normal or decreased activity is commonly seen on delayed images, however,
persistent increased delayed activity has been reported (up to 40%), Decreased flow in advanced stages may be related to disuse, which is a common
feature of post-hemiplegic CRPS

107
Q

Tx of CRPS

A
Anti-inflammatory drugs
Antidepressant drugs
Local peripheral nerve blocks
Paravertebral sympathetic ganglion blocks
Physical therapy
108
Q

signs of hypoglycemia

A

Nervousness, tachycardia, diaphoresis, nausea, headache, confusion, tremor, seizures, coma

109
Q

function of biguanide

A

antihyperglycemic

110
Q

what are only FDA drugs for diabetic neuropathy

A

duloxetine (Cymbalta)

pregabalin (lyrica)

111
Q

clinical findings of OA

A

pain relieved w rest
stiffness aggravated w activity
crepitus w motion
asymmetric joint swelling

112
Q

radiographic findings of OA

A

asymmetric joint space narrowing
broad/flat articular surfaces
osteophytes at joint margin
subchondral sclerosis

113
Q

stages of gout

A
  1. Asymptomatic hyperuricemia
  2. Acute gouty arthritis
  3. Intercritical gout
  4. Chronic tophaceous gout
114
Q

clinical findings of gout

A
Asymmetrical, monoarticular arthritis
Sudden onset of red, hot, and swollen joint
Excruciating pain with acute attack
Tophaceous deposits
Most commonly affects 1st MPJ
115
Q

Radiographic findings of gout

A

appear late in the disease after multiple attacks
Bone lysis in acute stages
Periarticular swelling with preserved joint space
Tophi at joint margins
Rat bite – punched-out, periarticular erosions
Cloud sign – tophaceous material
Martel sign – periarticular overhanging shelves of bone

116
Q

Lab test for gout

A

Uric acid – males >7 mg/dL, females >6 mg/dL, though may be normal during attack
Synovial fluid analysis provides a more accurate diagnosis

117
Q

What is a martini sign?

A

Histology showing a PMNC engulfing a crystal

118
Q

if gout suspected, what should specimen be sent in?

A

one in formaldehyde (dissolves tophi), one in alcohol(doesn’t dissolve)

119
Q

tx acute gout

A

colchicine, NSAIDS-indomethacin, corticosteroids, ACTH

120
Q

tx chronic gout

A

colchicine, allopurinol, uricosurics (probenecid, sulfinpyrazone)

121
Q

dose of colchicine? max dose?

A

0.6 mg PO q 1h until symptoms resolve, GI side effects, or max dose of 6 mg reached

122
Q

can allopurinol, probenecid or sulfinpyrazone be used for acute gout

A

no may cause initial hyperuremia

123
Q

how to determine overproducer or underexcretor? which more common?

A

24 hr urinalysis, underexcretor

124
Q

med for overproducer? underexcretor?

A

allopurinol

probenecid