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Final Flashcards

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1
Q

Emergent triage

A

Respiratory distress
Chest pain
Active hemorrhage
Unstable vital signs

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2
Q

Urgent triage

A

Severe abdominal pain
Displaced/multiple fractures
Complex/multiple soft tissue injuries
Respiratory infection

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3
Q

Non-urgent triage

A

Skin rash
Strains & sprains
Cold
Simple fracture

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4
Q

Exertional heat stroke

A 
Sudden onset
Strenuous physical activity in hot conditions
Change in LOC
Hypotension
Tachycardia 
Tachypnea
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5
Q

Classic heat stroke

A 
Over period of time
Chronic exposure to hot environment
Change in LOC
Hypotension
Tachycardia
Tachypnea
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6
Q

Pit viper envenomation

A

Local necrosis & swelling
Minty, rubbery, metallic taste
Paresthesias of scalp, face, & lips

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7
Q

Antivenom for pit vipers

A

C/I pineapple allergies
4-6 vials 1st 60 min
2 vials every 6 hrs for 18hrs

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8
Q

Antivenom for coral snakes

A

3-6 vials over 2 hrs

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9
Q

Early S/S frostbite

A

White, waxy appearance of skin

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10
Q

Prerenal AKI

A 
Caused by direct damage to kidneys (arrythmias, burns, dehydration, diuretic overuse)
Hypotension
Tachycardia
Decreased urine output
Lethargy
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11
Q

Intrarenal AKI

A 
Caused by nephrotoxins, transfusion reaction
Edema
Oliguria/anuria
Lethargy
NV
Flank pain
Hypertension
Tachycardia
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12
Q

Postrenal AKI

A

Caused by pelvic cancers & stones

S/S same as intrarenal

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13
Q

Onset phase AKI

A

Begins with event & ends with oliguria

Hours to days

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14
Q

Oliguric phase AKI

A

Urine output 100-400mL/24 hrs–does not respond to diuretics
Lasts 1-3 wks
Dyspnea

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15
Q

Diuretic phase AKI

A

Sudden onset 2-6 wks after oliguric
Urine flow increases
Up to 10L/day
Normal kidney tubular function is reestablished

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16
Q

Recovery phase AKI

A

May take up to 12 mos

Kidney function may not return to normal

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17
Q

AKI drug therapy

A 
Fluid challenge
Diuretics
CC blockers
Kayexelate--hyperkalemia
Glucose & insulin
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18
Q

Chronic kidney disease

A

Progressive

Irreversible; kidney function doesn’t recover

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19
Q

Reduced renal reserve

A

No buildup of wastes in blood
Nephrons compensate
No manifestations of kidney dysfunction

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20
Q

Reduced GFR

A

Nephron damage has occurred
Increased dilute UO
Reduced GFR

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21
Q

ESKD

A

Urea & creatinine build up in blood

Kidneys can’t maintain homeostasis

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22
Q

Continuous ambulatory peritoneal dialysis

A

Dialysate infused & remains for specified time

Removed by gravity

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23
Q

Automated peritoneal dialysis

A

Cycling machine

Continuously, intermittently, or at night

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24
Q

Post-dialysis assessment

A 
Hypotension
Headache
Nausea, vomiting
Malaise
Muscle cramps
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25
Q

Dialysis disequilibrium syndrome

A

Rapid decrease in fluid volume & BUN

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26
Q

PE manifestations

A 
Dyspnea/tachypnea
Tachycardia
Chest pain
Dry cough
Distended neck veins
Hypotension
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27
Q

Ventilatory failure extrapulmonary causes

A

Neuro disorders
Spinal cord injuries
CNS dysfunction
Chemical depression

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28
Q

Ventilatory failure intrapulmonary causes

A

COPD, asthma
PE
Pneumothorax
ARDS

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29
Q

Oxygenation failure causes

A

High altitudes
Pneumonia
PE
ARDS

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30
Q

ARDS manifestations

A

Hypoxia even when O2 at 100%
Dyspnea
Pulmonary edema
Whited-out chest xray

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31
Q

Assist-control ventilation

A

Ventilator takes over the work of breathing for the pt

Tidal volume & ventilatory rate preset

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32
Q

SIM ventilation

A

Allows spontaneous breathing at pt’s own rate

Tidal volume & ventilatory rate preset

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33
Q

BiPAP

A

Preset inspiratory pressure & expiratory pressure similary to PEEP

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34
Q

Tidal volume

A

Amount of air received with each breath

7-10

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35
Q

Peak inspiratory pressure (PIP)

A

Highest pressure reached during inspiration

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36
Q

CPAP

A

Positive airway pressure throughout entire respiratory cycle for spontaneously breathing pts
Keep alveoli open during inspiration & prevents collapse during expiration

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37
Q

PEEP

A

Positive pressure exerted during expiratory phase

Prevents atelactasis

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38
Q

Barotrauma

A

Damage to lungs by positive pressure

Pneumothorax

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39
Q

Volutrauma

A

Excess volume delivered to one lung over the other

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40
Q

Thrombotic stroke

A

Atherosclerosis in blood vessel wall

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41
Q

Embolic stroke

A

Emboli break off & travel to cerebral arteries
Common source is heart
Pts with atrial fibrillation

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42
Q

Left hemispheric stroke

A

Aphasia/dysphagia
Alexia
Agraphia
Acalculia

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43
Q

Right hemispheric stroke

A

Visual & spacial awareness
Disoriented to time & place
Personality changes
Poor judgement

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44
Q

Broca’s aphasia

A

Pt understands, but can’t communicate verbally

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45
Q

Wernicke’s aphasia

A

Pt can’t understand spoken & often written word

May be able to speak, but speech is meaningless

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46
Q

Cushing’s triad

A

Severe hypertension
Widened pulse pressure
Bradycardia

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47
Q

Normal ICP

A

10-15 mmHg

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48
Q

Epidural hemorrhage

A

Neurologic emergency

Temporal bone fractures

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49
Q

Subdural hemorrhage

A

Highest mortality rate

Laceration of brain tissue

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50
Q

Intracerebral hemorrhage

A

Brain edema & ICP elevation

Brain stem hemorrhage

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51
Q

Brain herniation

A

Brain tissue may shift & herniate downward in presence of increased ICP

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52
Q

Brain abscess

A

Pus forms in extradural, subdural, or intracerebral areas

Treat with penicillin

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53
Q

Bradycardia tx

A

Atropine 0.5 mg IV up to 3 mg

Monitor for tachycardia

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54
Q

Tachycardia tx

A

Treat cause of tachycardia

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55
Q

PAC

A

Premature P wave
No symptoms
No caffeine

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56
Q

SVT

A

Usually caused by PAC
150-280 BPM
Adenosine 6 mg IV, then 12 mg IV push
Asystole after

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57
Q

A-fib

A

Alcohol excess (holiday heart)
No discernable p waves
Antidysrhythmics–cardizem, amiodarone, beta-blockers, digoxin
Anticoagulants

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58
Q

PVC

A

Wide QRS
Unifocal (all alike) or multifocal (different)
Multifocal more dangerous
Can trigger V-tach or V-fib

59
Q

V-tach

A

Pt may seem fine

Wide QRS

60
Q

Torsade de pointes

A

Twisting–too fast to cardiovert

Mg sulfate IV

61
Q

V-fib

A

Epi–1mg (1:10,000) every 3-5 min
Vaso–50 mg for 1st 2 doses of epi
Ami–300 mg, then 150 IV push

62
Q

1st degree AV block

A

PR >.20 sec

No S/S; no treatment

63
Q

2nd degree AV block type 1

A

PR gets wider & wider & then drops

Atropine

64
Q

2nd degree AV block type 2

A

PR normal & then drops

Cardiac pacing

65
Q

3rd degree AV block

A

P wave & QRS regular, but at different intervals
Cardiac pacing
Atropine

66
Q

Bradycardia tx

A

Atropine 0.5 mg IV up to 3 mg

Monitor for tachycardia

67
Q

Tachycardia tx

A

Treat cause of tachycardia

68
Q

PAC

A

Premature P wave
No symptoms
No caffeine

69
Q

SVT

A

Usually caused by PAC
150-280 BPM
Adenosine 6 mg IV, then 12 mg IV push
Asystole after

70
Q

A-fib

A

Alcohol excess (holiday heart)
No discernable p waves
Antidysrhythmics–cardizem, amiodarone, beta-blockers, digoxin
Anticoagulants

71
Q

PVC

A

Wide QRS
Unifocal (all alike) or multifocal (different)
Multifocal more dangerous
Can trigger V-tach or V-fib

72
Q

V-tach

A

Pt may seem fine

Wide QRS

73
Q

Torsade de pointes

A

Twisting–too fast to cardiovert

Mg sulfate IV

74
Q

V-fib

A

Epi–1mg (1:10,000) every 3-5 min
Vaso–50 mg for 1st 2 doses of epi
Ami–300 mg, then 150 IV push

75
Q

1st degree AV block

A

PR >.20 sec

No S/S; no treatment

76
Q

2nd degree AV block type 1

A

PR gets wider & wider & then drops

Atropine

77
Q

2nd degree AV block type 2

A

PR normal & then drops

Cardiac pacing

78
Q

3rd degree AV block

A

P wave & QRS regular, but at different intervals
Cardiac pacing
Atropine

79
Q

Chronic stable angina

A

Predictable following exertion

Relieved by nitrates & rest

80
Q

Unstable angina EKG

A

Depressed ST
Inverted T-wave
Resolves when pain goes away
At rest or with exertion

81
Q

Variant angina

A

Coronary spasm
Elevated ST
Responds to nitrates

82
Q

New onset angina

A

1st angina symptoms

Increased exertion

83
Q

Pre-infarction angina

A

Occurs in days or weeks before MI

84
Q

Subendocardial

A

Only through subendocardial muscle
NSTEMI
More likely to have STEMI later on

85
Q

Transmural

A

All the way through heart muscle
STEMI
ST elevation in 2 contiguous leads

86
Q

Heart changes in MI

A

Blue & swollen initially
48 hrs gray with yellow streaks
8-10 days granulation tissue
2-3 mos scar tissue

87
Q

Anterior MI

A

L anterior descending artery
ST elevation V1-V4
Tachycardia; 2nd & 3rd degree heart blocks

88
Q

Posterior (lateral) MI

A

Circumflex artery
ST elevation V5 & V6
Sinus arrhythmias

89
Q

Inferior MI

A

Right coronary artery
ST elevation in 2, 3, & aVF
Sinus bradycardia; heart blocks

90
Q

LDL

A

<70 known CAD risk

91
Q

HDL

A

> 40

92
Q

Triglycerides

A

<150 men

93
Q

Metabolic syndrome risk factors

A 
Hypertension
Decreased HDL
High LDL
High triglycerides
Large waist
94
Q

Creatinine Kinase

A

Women 30-135

Men 55-170

95
Q

Cardiac catheterization

A

Determine extent & exact location of MI

Watch for cold extremities

96
Q

Unstable angina/NSTEMI treatement

A 
Glycoprotein inhibitors
Beta-blockers
ACE inhibitors
ARBs
CC blockers
97
Q

Thrombolytics C/I

A 
Abdominal surgery/stroke
Intracranial hemorrhage
Malignant neoplasm
Ischemic stroke w/in 3 mos unless w/in 3 hrs
Closed head injury w/in 3 mos
98
Q

Class 1 heart failure

A

Absent crackles & S3

IV nitrates & diuretics

99
Q

Class 2-3 heart failure

A

More aggressive interventions needed

100
Q

Class 4 heart failure

A 
Cardiogenic shock
Tachycardia
Hypotension
UO <30 ml/hr
Tachypnea
101
Q

Cardiogenic shock tx

A

IV morphine–pain
O2–decrease O2 requirements
Vasopressors–maintain tissue perfusion

102
Q

Intra-aortic balloon pump

A

Inflates during diastole to keep vessel open

103
Q

PTCA

A

Balloon compresses plaque against wall of vessel

Stent is usually inserted

104
Q

CABG

A

Artery bypass
Angina w/ >50% occlusion
Acute MI w/ cardiogenic shock
PTCA not an option

105
Q

Post-CABG hypertension

A

Nitroprusside

Cover tubing with aluminum foil; absorbed in light

106
Q

Cardiac tamponade

A

Sudden cessation of drainage
JVD
Pulsus paradoxus

107
Q

Progression of CABG pt

A

3-6 hrs–ventilator
2 hrs after extubation–pt dangled side of bed
4-8 hrs–pt up to chair
1st day postop–ambulating 25-100 ft 3x/day

108
Q

Mediastinitis

A 
Infection develops 5 days to several wks postop
Fever beyond 4 days postop
Boggy sternum
Redness & swelling of sutures
Increased WBC
109
Q

Initial stage shock

A

MAP decreased <10
Compensatory mechanisms effective
HR & RR increased or slight increase in diastolic BP may be only signs

110
Q

Non-progressive (compensatory) shock

A 
MAP decreased 10-15
Kidney & hormonal compensatory mechanisms kick in 
Acidosis & hyperkalemia
Decreased UO
Stop conditions that cause shock
111
Q

Progressive (intermediate) shock

A

MAP decreased >20
Compensatory mechanisms no longer deliver O2 to vital organs
Feeling of impending doom
Multi-organ failure

112
Q

Irreversible (refractory) shock

A

Therapy can’t save pt’s life even if cause corrected & MAP returns to normal

113
Q

Hypovolemic shock

A

Loss of blood volume
Loss of O2-carrying capacity–loss of RBCs
Hemorrhage/dehydration
Changes in mental status early signs

114
Q

Cardiogenic shock

A

Actual heart muscle is unhealthy

115
Q

Distributive shock

A

Fluid delivered to interstitial tissues & can’t be circulated properly

116
Q

Neurogenic shock

A

Spinal cord injury
Head trauma
Widespread vasodilation

117
Q

Chemical induced distributive shock

A

Anaphylaxis
Sepsis
Capillary leak syndrome

118
Q

Septic inflammatory response (SIRS)

A

Organisms escape local control

Inflammatory response takes over

119
Q

Septic shock tx

A

Vancomycin
Aminoglycosides
Penicillin
Cephalosporins

120
Q

Primary prevention

A

Prevention of initial occurrence of disease or injury
Nutrition counseling
Sex education
Immunizations

121
Q

Secondary prevention

A 
Early detection of disease & treatments with goal of limiting severity & A/E
Screenings
Treatment of STDs
Treatment of TB
Control of communicable diseases
122
Q

Tertiary prevention

A

Maximization of recovery after injury or illness
Rehabilitation
Support groups
Case management

123
Q

School nurse primary prevention

A

Immunization status

Knowledge regarding health issues

124
Q

School nurse secondary prevention

A

Assess illness or injury
Early detection of disease–scoliosis, lice
Detect child abuse or neglect

125
Q

School nurse tertiary prevention

A

Assess children with disabilities

Long-term health needs–diabetes, asthma

126
Q

HIV clinical A

A

Flu-like symptoms

Enlarged lymph nodes

127
Q

HIV clinical B

A

HIV with 1 or more infections

128
Q

HIV clinical C

A

HIV with AIDS

129
Q

HIV 1

A

CD4 at least 500

29%

130
Q

HIV 2

A

CD4 200-499

14-28%

131
Q

HIV 3

A

CD4 <14%

132
Q

Superficial thickness burns

A

Epidermis injured

Heals 3-5 days

133
Q

Superficial partial-thickness burns

A 
Involves entire epidermis
Blister formation
Blanchable
Increased pain (nerve endings exposed)
Heals 10-21 days
134
Q

Deep partial-thickness burns

A 
Deeper into dermis
No blister
May or may not blanch
Decreased pain (nerve endings are damaged)
Heals 3-6 wks
May require skin grafts
135
Q

Full-thickness burns

A 
Destruction of entire epidermis & dermis
Grafting necessary
Hard leathery eschar
No blood supply
Decreased sensation
Healing weeks to months
136
Q

Deep full-thickness burns

A

Extends into fascia & tissues
Damage to bone, muscles, tendons
Excision & grafting

137
Q

Fluid shift after burns

A

Capillary leak syndrom
Hyperkalemia
Hyponatremia
Hemoconcentration

138
Q

Resuscitation/emergent phase

A 
24-48 hrs
ABCs
Head to toe
Cool, cover, carry
Fluid resuscitation--crystalloids
139
Q

Fluid resuscitation

A

4mL/kg/% burned
1st 1/2 over 1st 8 hrs
2nd 1/2 over next 16 hrs

140
Q

Acute phase

A

36-48 hrs–fluid resuscitation finished to wound covered by tissue
Prevent infection–tetanus, antibiotics
Debridement
Silvadene

141
Q

Autograft

A

Skin from burn victim

142
Q

Homograft

A

Cadaver skin

Usually rejected 2-3 wks

143
Q

Heterograft

A

Pig skin

High infection rate–treat with silver nitrate

144
Q

Rehabilitative phase

A

Years-end of life–burn healing to reconstruction complete

Nursing (9 decks)

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