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ACUTE TEST 1 Flashcards

1
Q

HOW MANY DAYS SUPPLY FOR SCHEDULE 2

A

7

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1
Q

SCRIPT AUTHORITY

A

Need a DEA# to prescribe controlled substances

No psychotropic medications may be prescribed for children under age 18 years (Except by PMHNP)

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2
Q

APRN MAY NOT PRESCRIBE IN WHAT LOCATION

A

PAIN MANAGEMENT CLINIC

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3
Q

BSN MSN OR DOCTORATE FOR PRESCRIBING CONTROLLED SUBSTANCES

A

MASTERS OR DOCTORATE

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4
Q

HOW MANY HOURS OF CEU

A

3 FOR SAFE EFFECTIVE PRESCRIBING OF CONTROLLED SUBSTANCES REQUIRED BIENNIALLY WHEN YOU RENEW YOUR APRN LICENSE

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5
Q

CHRONIC PAIN

A

Greater than 3 months
Continuous or episodic
Effects quality of life
Non narcotic preparations are suggested

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5
Q

ACUTE PAIN

A

Less than one month of tissue damage. Should be healed within a month and requiring only temporary pain treatment

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6
Q

SUBACUTE

A

1-3 months. Could be unresolved acute pain. Can evolve into chronic pain

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7
Q

INTERVENTIONAL TECHNIQUES FOR CHRONIC PAIN

A
  • Injections
  • Spinal fusions
  • Percutaneous disc compression
  • Radiofrequency rizotemy
  • Neuromodulatory therapy
  • Vertobroplasty
  • Kyphoplasty
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8
Q

MORPHINE specifically regarding excretion

A
  • Renal insufficiency will make the morphine active metabolite stick around and cause further respiratory depression. Can continue to over sedate the patient
  • Renal failure pt with crea cl less than 10 ml/min we lower the dose.
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9
Q

take into consideration when prescirbing pain medications

A

social determinants of healh

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9
Q

MAJOR SIDE EFFECTS OF OPIODS

A

 Respiratory Depression
 Cardiovascular Effects
 Intestinal Motility
 Nausea and Vomiting
 Sedation
 Hypotension
 Dependence and withdrawal
  intracranial pressure

** dec brain stem respiratory impaired gut motility paralytic ileus; methotrexate to reverse the gut very expensive; can cause vasodilation blood pressure goes down but then can cause increase intracranial pressure as fluid shifts

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10
Q

state of FL APRN need ______ to do prescriptive authority

A

Need a collaborative practice agreement

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11
Q

opioid use and overuse is tied to

A

social determinant of health and inequalitities

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12
Q

difference between visceral and somatic pain

A

visceral-cannot pin point versus somatic you can

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13
Q

visceral pain

A

involving organs/ diffuse/ originates from blood vessels and internal organs

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14
Q

somatic pain

A

bone muscle or tendon/ you can pinpoint; no nerves** neuropathic pain is separate

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15
Q

opioids for neuorpathic pain?

A

should not use, use non-opioids

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16
Q

non pharmacologic tx for pain

A

hot and cold therapy ; patient education therapeutic neuroscience education; coping skill training; tens; acuputure; mindful meditiation

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17
Q

the main components of the WHO guidelines for cancer pain

A

initiation of pain relief (non and opioid); maintenance of pain relief (opioids); adjuvant medicines for cancer pain (steroids) and the management of pain related to bone metastases (biphosphonates and radiotherpay)

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18
Q

oral medicines for cancer pain

A

preferred to parental adminstration

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19
Q

cancer pain by the clock

A

analgesics should be given on a regular basis by the clock rather than by demand

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20
Q

dosage of analgesic for cancer pain

A

for the individual, determined on an individual basis

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21
Q

morphine has a _____release

A

histamine release why we see hypotension and pruritus

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22
Q

box warning for nsaids

A

severe stomach bleeding; higher chances if you are 60 or older, have stomach ulcers or bleeding problems, take blood thinners (anticoagulants) or steroid drugs; take other drugs containing prescription or nonprescription NSAIDs (aspirin, ibuprofen, naproxen, or others); have three or more alcoholic drinks every day while using the product or take more or for a longer time than directed

cardiac patient inc risk for heart failure and stroke

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23
Q

this drug is contraindicated in post op CABG and can cause bleeding and MI

A

toradol = ketorolac

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24
Q

not an NSAID

A

tylenol acetaminophen

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25
Q

acetaminophen

A

antipyretic, reliev emild pain and discomfort; greater analgesic effects when combined with opioids vs highers doses alone

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26
Q

toxic level of acetaminophen

A

4g/day other patients***

potential metabolism liver <2g/day**

hepatotoxicity

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27
Q

acetaminophen is excreted

A

renally

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28
Q

aspirin

A

antiplatelet

cox1 is found within platelets and promotes platelet aggregation

aspirin inhibits cox1

leads to a decreased risk for MI and stroke

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28
Q

tramadol

A

caution seziure disorder
seritonin syndrome*** multimodal taking sari,ssri,tca and or mai; when combined antidepressant can cause seritonin sysndrome

reduce dose for renal impairment

less respiratory depression

weak mu agonist
weak opiod

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29
Q

approved in 2010

A

IV acetaminophen; intended for short term tx of pain or fever post op if unable to tolerate PO

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30
Q

signs and syndrome of seritonin syndrome

A

shivers

shivering
hyperreflexia/myoclonus
increased temp >41 degree
vital sign instability (high hr/high rr, low bp)
encephalopathy
restless
sweating/diaphoretic

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31
Q

ketaomine

A

weird hallucinations and less respiratory depression

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32
Q

methadone MSYK why give

A

not a first line

nonopioid

you should know neuropathic pain, cancer pain, pain refractory to other opioids, intolerance of other opioids, and opioid use disorder

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33
Q

if you are in an outpatient clinic (MSYK) working in neuro trauma and your patient goes home with pain and prescriibnng on some level of opioid pain medication the recommnedation is to

A

prescribe them Narcan in case they overdose

lower the risk of opioid overdose

especially if other people in the family can get into the medicine cabinet it is prescribed so it is in the house and teach how to use it

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34
Q

all states have access to ______ laws

A

naloxone OD;

prescriptive laws

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35
Q

benzo withdrawl can cause

A

seizures

to avoid convert to longer acting agent to taper slwoly

signs: insomnia, anxiety, autonomic instability

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36
Q

RASS SCALE

A

sedation

+4 combative
+3 very agitated
+2agittated
+1 restless
0 alert and calm
-1drowsy
-2light sedation
-3moderstae
-4deep
-5unarousable

optimal zero***

37
Q

CAM ICU

A

delirious

38
Q

reversal for benzo

A

iv flumazenil (romazicon) its the benzo antagonist but it can also cause seizures

39
Q

gaba agonist activity; high lipid solubility allows to cross the blood brain barrier rapidly

A

propofol

40
Q

propofol why is it great?

A

sedate because hypermetabolic; traumatic brain injury; rapid onset and short duration, requires the use of mechanical ventilation; preferred when rapid awakening is important; neuro surgery, traumatic; recommendation for refractory status epileptics

41
Q

side effects of prop

A

urine can turn green

Brady; hypotension

prop infusion syndrome causes inc in triglycerides; metabolic acidosis; rhabdo

42
Q

precedex is

A

anxiolytic, hypnotic, antishivering and analgesic sparing properties; no respiratory depression and cooperative sedation

no resp. depression

43
Q

precedex works on…

A

centrally activity highly selective alpha 2 agents; 8x more selective than clonidine

44
Q

______ pretty clean drug for patients having delirium

A

precedex

45
Q

upgraded statements for BIS monitoring is used when?

A

best suited for sedative titration during deep sedation or neuromuscular blockade

0-100

pulse ox for the brain

45
Q

precedex side effects

A

brady and hypotension but most commonly brady

45
Q

ABCDEF

A

multiapproach

45
Q

SCCM recommends suggest using either: ____ and or ____ over benzos

A

prop or precedex

46
Q

haldol is a ______ blocker

A

dopamine

47
Q

box warning of haldol

A

dementia related use increased death

48
Q

caution when using haldol for what type of patients

A

cardiac due to QT prolongation

49
Q

preferred agent for the treatment of delirium

A

vitamin H= haldol

50
Q

adverse effects of haldol

A

QT prolongation turns into torsades or vfib (>490)

q6h around the clock recommended dosaging

51
Q

PADIS

A

pain, agitation, delirium, immobility and sleep

52
Q

suggestion using ____ over ______ sedation

A

light>deep

53
Q

risk calculator primary prevention

A

they have not had a stroke its prevention

54
Q

age 40-75 y and LDL >70-<190 wihtout diabetes 10 year ASCVD risk precent begin risk discussion

A

5-7/5% borderline risk

**risk discussion if risk enhancers present then risk discussion regarding moderate intensity statin therapy

*** you start to talk about a statin

55
Q

risk enhancers are ________ in ascvd

A

family hx of premature; persistent elevated ldl; CKD persistent elevated triglycerides

56
Q

you really start to talking about a statin around

A

> 7.5-20% intermediate risk; to prevent stroke

57
Q

> 20%

A
58
Q

high risk scary patients that could have a stroke

A
  • ldl>190 no risk assessment go start to a statin

-DM and age 40-75 start a moderate intensity statin

-DM and age 40-75y risk assessment **

59
Q

> 75 years and they have never had a heart attack or stroke

A

leave her alone clinical assessment and risk discussion not immediate start a statin

60
Q

once they have had a stroke

A

a statin

61
Q

everyone with a ASCVD

A

get a statin

62
Q

statins

A

first line

affect the metabolic pathway that produces cholesterol the mainstays of the treatment; we know work very well with minimum side effect profile

they all have -statin at the end of it

63
Q

if not controlled with a high dose statin the next choice

A

zetia (ezetimibe)

64
Q

after zetia we could use

A

PCSK9

65
Q

differentials for chest pain

A

aortic dissection-back pain

acute MI

acute coronary ischemia

cardiac tamponade

respiratory: pe, tension pnuemo, esophageal rupture

66
Q

TROPONIN

A

signals muscle injury

If they are having a true cardiac event do a series of them

at least two in a row 4-6 hours apart and they will spike when having a true cardiac injury

67
Q

anemia

A

check a CBC could be an MI

check their platelets

68
Q

door to needle ideal

A

90 minutes but can be up to 12 hours

69
Q

PRINZMETAL ANGINA

A

SPASM

PCI- radial or fem injecting a dye and checking the branches

CCB

69
Q

STABLE ANGINA

A

STABLE-REST OR NITRO can resolve it

And usually PROVOKEd BY STRESS

70
Q

unstable angina

A

ACS**

71
Q

non modifiable risk factors for CAD

A

AGE GENDER RACE HEREDITY

MENOPAUSE LOSE THAT ESTROGEN PROTECTOR FROM CHLOESTROL

72
Q

ST ELEVATION MI STEMI

A

TISSUE WILL DIE IF NO INTERVENTION TO OPEN UP

73
Q

NSTE-ACS

A

ACS** WITH POSITIVE TROP NO ST ELEVA

EKG COULD BE NORMLA OR INVERTED T WAVES

NOT INFARCTION

74
Q

MODIFIABLE RISK FACTORS FOR CAD

A

dm2, hyperlipidemia, smoking, obesity, oral contraceptives, increased stress, htn

75
Q

PE signs and symptoms findings of ACS

A

nausea vomiting, diaphoresis, cool, clammy skin, chest pain usually substernal; in MI not relieved by NITRO; dyspnea and feeling of impending doom

76
Q

classical MI EKG

A

ST elevation > 1mm in contiguous leads; new LBBB

And q wave greater than 0.04 sec duration

77
Q

pericarditis in EKG

A

diffuse ST segment elevation; PR segment depression

78
Q

after we had the heart attack ______ prevention

A

secondary; trying to prevent a second heart attack after we had an event

79
Q

msyk why to have a PCI/PTCA indications

A

Door to needle goal is 90 minutes but can do between less than 12 hours, ecg changes with st depression or elevation and a new LBBB, evolving MI take me to pci to possibly stent or if high risk mi stemi only they use the fibronilytics, unstable angina go to cath lab to diagnosis, lesions characteristics and adequate ventricular function and collateral circulation

symptoms onsent <12 h and a pci is feasible- then go; symptoms onset >12 hours and patient in cardiogenis shock or failure and pci feasible yes- pci; no cabg

90 minutes

for a year you have to put the patient on dual antiplatelet therapy

80
Q

class 1 indications for CABG

A

left main >50%

proximal lad and proximal circuflex >70 %

3 vessels disease in asymptomatic patient in those with mild or stable angina

3 vessel with poor LV function

1-2 vessel and a large area in high-risk area in patients with stable angina

> 70% proximal LAD stenosis with either EF< 50% or demonstrable ischemia on noninvasive testing

81
Q

new LBBB

A

could be considered a stemi and a chest pain could be ACS

82
Q

medical tx for ACS

A

dual antiplatelet

BB

nitrates (nitroglycerine- open the coronaries)

ace inhibitors

statin

CCB (hypertensive and no signs of heart failure)

83
Q

allergy to aspirin

A

use clopidogrel

84
Q

clopidogrel

A

P2y12 inhibitor

Approved for patients with unstable angina

stemi need a load of 600 and then 75 x 12 months

nstemi 300mg load and then 75 daily with aspirin 75-325

for a recent MI stroke or PVD 75 daily and can give if there is an allergy to aspirin

85
Q

for a stemi a load of ?

A

clopidogrel; 600mg loading dose followed by 75mg daily x12 months

86
Q

antiplatelet high-risk patients with refractory UA/NSTE-ACS

A

GP 2b3a antagonist: reopro, integrillin, aggrastat to totally block the atction

87
Q

beta blockers

A

hx of MI

reduce mortality

improve perfusion and oxygen use

antianginal benefits

need to have a decent EF

not in shock state

88
Q

morphine in ACS

A

acute anginal symptoms reduce myocardial oxygen consumption with vasodilation; initial dose around 4mg IV; IV narcotic effective for relief of anginal symptoms

IV Narcotic effective for relief of anginal symptoms.
Give for chest pain refractory to Nitroglycerine

89
Q

fibrinolytic therapy is for?

A

busting the clot stemi only not indicated for UA/NSTEMI-ACS

Proper pt selection critical.
Diagnosed MI clinically and by ECG and ST segment elevation and bundle branch block on ECG have the best outcomes.
Greatest benefit for thrombolytic therapy when it is given early within 6 hours after symptomatic onset of acute MI.

90
Q

adverse effects of BB

A

Bronchospasm
Postural hypotension
Claudication
Depression
Potential masking of hypoglycemia
Abrupt withdrawal
Angina
MI
Arrhythmias

91
Q

Chest pain and symptomatic arrival to the hospital the ER staff should do a ______ within ______ minutes

A

ECG within 10 minutes

NP (6 decks)

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