Crozer- medicine Flashcards
reasons for post op fever
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
Tx of post op fever
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
When do fever peaks occur
4-8pm
What part of brain regulates the body temp
hypothalamus
What is malignant hyperthermia
SE of general anesthesia- tachycardia, htn, acid base and electrolyte abnormalitis, musclee rigidity, hyperthermia
tx for malignant hyperthermia
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
if risk of malignant hyperthermia suspected what preop test may be performed
CPK- elevated in 79% of patients w malignant hyperthermia
whats mechanism of action for local anesthetics
block NA channel and conduction of action potentials along sensory nerves
whats toxic dose of lidociane
300 mg plain
500 mg w epi
whats toxic dose of bupicacaine (marcine)
175 mg plain
225 mg w epi
how can you convert percentage to mg/ml
1% =10mg/mL
SE of lidocaine and bupivacaine associated w systemic exposure
CNS effect- excitation (dizzy, blurred vision, tremor, seizures) followed by depression (resp and LOC)
Cardio effect- hypotension, bradycardia, arrhythmias, cardiac arrest
what helps revese local anesthetic- induced Cardiovascular collapse
IV fat emulsion
is there a risk with intraarticular injections of bupivacaine
chondrocyte death by prolonged exposure
what age group should bupivicaine be avoided
less than 12
how are amides (lidocaine and bupivacaine) metabolized
liver
how are esters (novocain and cocaine) metabolized
plasma pseudocholinesterase
whats the only local anesthetic w vasoconstriction
cocaine
can local anesthetic cross placental barrier
Yes
what does MAC stand for
monitored anesthesia care
what anesthesia can’t be given to patients w egg shell injury
propofol (diprivan)
pain management w codeine allergy
stadol, toradol, talwin, ultram, darvon, davocet, demerol, nubain
first choice oral pain med
darvocet N 100 one tab PO q4-6h prn pain
First choice for non-narcotic oral
tramadol (ultram) 50 mg one to two tabs PO q4-6 h prn pain. max 400 mg per day
first choice non-narcotic IV
Toradol 30-60 mg IV
2 non narcotic analgesics
ketoralac (toradol), tramadol (ultram)
What schedule are the following? Percocet Vicodin Tylenol 3 Darvocet
Percocet- 2 high potential for abuse- narcotic script
Vicodin-3 moderate
Tylenol 3- 3 moderate
Darvocet -4- low potential
Percocet 5/325?
oxycodone/acetaminophen 5mg/325 mg
1-2 tabs PO q 4-6 hr prn pain
Roxicet
oxycodone/acetaminophen (5mg/325mg/5mL)
essentially liquid form of percoet thats good for peds
difference btwn percocet and percodan
percocet has 325 mg of acetaminophen and percodan has 325 mg ASA
Vicodin 5/500
hydrocodone/acetaminophen (5mg/500mg) 1-2 tabs PO q4-6h
Tylenol 3
codeine/acetaminophen (30-300mg) 1-2 tabs PO q4-6h
Darvocet N 100
propoxyphene/acetaminophen (100mg/650 mg) 1 tab PO q4H PRN pain
ultram
tramadol 50 mg 1-2 tabs PO q 4-6 prn pain
toradol
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
Darvon
propoxyphene 1 tab PO q4h prn pain
OxyCotin
oxycodone extended release
Morphine sulphate
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
MS Contin
morphine sulfate extended release (15-30 mg) 1 tab PO q 8-12 h prn pain
dilaudid
hydromorphone
2-8 mg PO q 3-4 h prn severe pain
1-4 mg IV q 4-6h prn severe pain
VERY strong
Demerol
meperidine- ;lots of side effects
Acetaminophen therapeutic effects
analgesic, anti pyretic
max dose of acetaminophen
4g
Therapeutic effects are seen w most NSAID
analgesic, anti pyretic, anti inflam
what path do NSAIDS work on
COX
most common SE of NSAIDS
GI issues
only cox 2 inhibitor?
celecoxib
NAIDS only have anti inflam effect
indomethacin, tolmetin
do NSAIDS decrease joint destruction
no. only decrease inflammation
Do NSAIDS affect bone healing
NSAIDS and cox 2 inhibitors inhibit bone healing via anti inflammatory effects
what NSAID doesn’t inhibit platelet aggregation
cox 4, celebrex
only IV NSAID
ketorolac (toradol)
what NSAID least nephrotoxicity
celebrex, relafen, lodine
effect of NSAID on asthma?
increase sym of asthma
Safest NSAID for pt with asthma
diclofenac ketoprofen
which NSAID tx collagen vascular disease
ibuprofen, sulindac, tolmetin
Which nsaid is not renally cleared
indomethacin, sulindac
cardiovascular effect of nsaids
vasoconstrict and increase blood pressure
Which nsaid has least cv effect
diclofenac ketoprofen
which nsaid most hepatotoxic
ibuprofen, naproxen, diclofenac
what should be given for indomethacin overdose
benadryl
what is arthrotec
diclofenac/misoprostol, NSAID which protects stomach
whats anti inflammatory dose of ibuprofen
1200-3200 mg/day
what NSAID works on lipoxygenase and cyclooxygenase?
ketoprofen and diclofenac
what is difference btwn cataflam and voltaren
Cataflam is diclofenac potassium and has an immediate release
Voltaren is diclofenac sodium and has a delayed release
what are the only pro drugs for nsaids
nabumetone and sulindac
whats only nonacidic nsaid
nabumetone
which nsaids have fewer pulm problems
ketoprofen and diclofenac
once a day nsaids
celecoxib (Celebrex), piroxicam (Feldene), oxaprozin (Daypro), nabumetone (Relafen),
what drugs do NSAID interact with?
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
whats cause of acute arterial occlusion
Embolism – detached thrombus, air, fat, or tumor
Thrombus – occlusion of vessel by plaque or thickened wall
Extrinsic occlusion – traumatic, blunt, penetrating
triad of PE
dyspnea, chest pain, hemoptysis (tachycardia is common)
tests ordered to diagnose PE
chest xray, ventrilation perfusion scan, pulm angiography
virchos triad
risk of DVT
- venous stasis
- endothelial wall damage
- hypercoagulability
risk factor for DVT
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)
how to diagnose DVT clinically
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
tests to diagnose DVT
Doppler ultrasound
Venogram
D-Dimer
treatments for DVT
Thrombolytic agents
Heparin 5000 Units IV bolus, then 1000 Units IV q1h and monitor PTT
how to dose heparin for periop DVT prophylaxis
5000 units SC 2h prior to surgery
5000 units SC q12h until patient ambulates
half life of heparin
1.5 hours
how does heparin work
Intrinsic pathway
Potentiates antithrombin III 100-fold, which inhibits the serine protease in the clotting cascade
hows heparin reversed
protamine sulfate 1mg/100 units
whats enoxaparin (lovenox)
low molecular wt heparin
how to dose lovenox for periop DVT prophylaxis
30 mg SC q12 h for 7-10 days
half life of lovenox
4.5 hours
advantage of lovenox vs heparin
Advantages – Lovenox has longer plasma half-life with significant anticoagulation in trough
Disadvantages – increased post-op complications when used with spinal/epidural anesthesia
how to check for lovenox
no test
how to reverse lovenox
Factor 7
how to dose coumadin
5-10 mg PO daily for 3-4 days than INR
whats half life of coumadin
20-60 h
how long before Coumadin therapeutic
3-5 days
how does Coumadin work
extrinsic pathway, interferes w factor 2,7,9,10
hows Coumadin reversed
vit K fresh frozen plasma
what are normal and abnormal INR values
normal=1
intense anticoagulation 2-3
what levels of heparin and Coumadin for DVT/anticoagulation prophylaxis
heparin= 2-3 times normal PTT Coumadin= 2 times normal INR
what nonpharmacologic measures are used for periop DVT prophylaxis
Early ambulation – most important
TEDs – thromboembolic deterrent stockings
SCDs – sequential compression devices
surgical tx for pt w prior DVTs or recurrent PE? and where?
greenfield filter- in ivc below renal veins
whats pletal
cilostazol
whats trental
pentoxifylline
whats indication for pletal or trental
intermittent claudication
whats CRPS
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
CRPS type 1
(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
CRPS type 2
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
Stages of CRPS
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
radiographic findings of CRPS
Periarticular, mottled, irregular bony demineralization (30-60% of cases) and cortical thinning
bone scan findings of CRPS
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
Tx of CRPS
Anti-inflammatory drugs Antidepressant drugs Local peripheral nerve blocks Paravertebral sympathetic ganglion blocks Physical therapy
signs of hypoglycemia
Nervousness, tachycardia, diaphoresis, nausea, headache, confusion, tremor, seizures, coma
function of biguanide
antihyperglycemic
what are only FDA drugs for diabetic neuropathy
duloxetine (Cymbalta)
pregabalin (lyrica)
clinical findings of OA
pain relieved w rest
stiffness aggravated w activity
crepitus w motion
asymmetric joint swelling
radiographic findings of OA
asymmetric joint space narrowing
broad/flat articular surfaces
osteophytes at joint margin
subchondral sclerosis
stages of gout
- Asymptomatic hyperuricemia
- Acute gouty arthritis
- Intercritical gout
- Chronic tophaceous gout
clinical findings of gout
Asymmetrical, monoarticular arthritis Sudden onset of red, hot, and swollen joint Excruciating pain with acute attack Tophaceous deposits Most commonly affects 1st MPJ
Radiographic findings of gout
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
Lab test for gout
Uric acid – males >7 mg/dL, females >6 mg/dL, though may be normal during attack
Synovial fluid analysis provides a more accurate diagnosis
What is a martini sign?
Histology showing a PMNC engulfing a crystal
if gout suspected, what should specimen be sent in?
one in formaldehyde (dissolves tophi), one in alcohol(doesn’t dissolve)
tx acute gout
colchicine, NSAIDS-indomethacin, corticosteroids, ACTH
tx chronic gout
colchicine, allopurinol, uricosurics (probenecid, sulfinpyrazone)
dose of colchicine? max dose?
0.6 mg PO q 1h until symptoms resolve, GI side effects, or max dose of 6 mg reached
can allopurinol, probenecid or sulfinpyrazone be used for acute gout
no may cause initial hyperuremia
how to determine overproducer or underexcretor? which more common?
24 hr urinalysis, underexcretor
med for overproducer? underexcretor?
allopurinol
probenecid
