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Adults 2 > Final Exam > Flashcards

Final Exam Flashcards

1
Q

meningitis

A

infection of the meninges contacted through blood stream; crosses through blood stream

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2
Q

manifestations of meningitis

A

nuchal rigidity, positive kernigs signs, brodzinskis sign

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3
Q

diagnosing meningitis

A

CT scan/MRI, lumbar puncture for bacterial culture and gram staining of CSF

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4
Q

CSF aspiration during meningitis

A

cloudy, low glucose, high protein, high WBC

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5
Q

preventative treatment of meningitis

A

meningococcal vaccine during high school and college, prophylaxis treatment when in contact with rifampin or ciprofloxacin w/in 24 hours

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6
Q

management of meningitis

A

antibiotics like vancomycin and cephalosporin, steroids, fluids, seizure precautions with phenytoin

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7
Q

nursing management of meningitis

A

neuro checks, VS, IOs, labs, daily weights, electrolytes, infection prevention, seizure precautions, pressure ulcer precautions, pneumonia, pt/family education

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8
Q

brain abscess

A

collection of infectious material within brain tissue; want to prevent otitis media and rhinosinusitis from progressing

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9
Q

findings of brain abscess

A

headache that is worse in the morning, fever, vomiting, signs of increased ICP

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10
Q

diagnosing brain abscess

A

MRI and CT scan

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11
Q

nursing management of brain abscess

A

neuro assessment, meds like antibiotics and steroids, supportive care

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12
Q

3 types of traumatic brain injry

A

concussion- mild; contusion- moderate to severe; diffuse axonal injury- severe

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13
Q

concussion

A

mild TBI; sudden trauma induced alteration at alert state; may or may not lose consciousness; small fx, bleed, or swelling may or may not occur

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14
Q

contusion

A

moderate to severe TBI; bruising of the brain; LOC with stupor and confusion; injury may be present at site of injury or at opposite side; damage to cortex; larger contusions may need to be surgically removed

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15
Q

diffuse axonal injury

A

severe TBI; deceleration injury with differential movement of brain and skull causing axonal shearing; high mortality rate; immediate onset with no lucid interval; posturing

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16
Q

decorticate posturing

A

damage to corticospinal tract (cortex lesion); interrupts pathway between brain and spinal cord; rigid extended legs, pointed and turned in toes, arms bent toward center of body, curled wrists and balled hands against chest

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17
Q

decerebrate posturing

A

severe injury to the brain at the level of brain stem; poor prognosis; rigid extended legs, pointed and turned in toes, flexed wrists, curled fingers, straight tense arms parallel to body

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18
Q

brain death

A

absence of brainstem reflexes and apnea; irreversible condition; coma is different due to distinguishable presence of brain stem response such as spontaneous breathing and reflexes

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19
Q

spinal shock

A

occurs immediately after injury (24hrs-6 weeks following); complete but temporary loss of motor function, sensation, and autonomic activity; brain unable to transmit signals to muscle and organs

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20
Q

treatment of spinal shock

A

spinal stabilization, maintain ABCs, PT, OT

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21
Q

clinical manifestations of spinal shock

A

flaccid paralysis, clonus is fist sign, no DTR, low visceral and somatic sensations, anhidrosis, paralytic ileus

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22
Q

cushings triad

A

HTN/widened pulse pressures, bradycardia, irregular breathing pattern; sign of brain injury

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23
Q

neurogenic shock

A

acute injury to brain, cervical, or thoracic spine; causes distributive shock d/t loss of autonomic nervous system and control of blood vessel

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24
Q

patho of neurogenic shock

A

loss of SNS tone, massive vasodilation and venous pooling, hypotension, low perfusion, cell death; occurs 30 minutes up to 6 weeks after injury

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25
Q

clinical manifestations of neurogenic shock

A

hypotension, bradycardia, poikilothermia (irregular temp), anhidrosis

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26
Q

treatment of neurogenic shock

A

spinal stabilization, vasopressors, atropine, pacemaker

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27
Q

mitral and aortic valve stenosis

A

valves do not completely open reducing blood flow through valve; thickened and stenotic valve leaflets

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28
Q

mitral and aortic valve regurgitation

A

valves do not completely close causing backflow of blood through valve

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29
Q

effects of mitral valve stenosis

A

reduced cardiac output; rising pressure in left atrium; left atrium hypertrophy and pulmonary congestion

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30
Q

effects of aortic valve stenosis

A

left ventricle hypertrophys

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31
Q

effects of mitral valve regurgitation

A

allows blood from left ventricle to left atria; reduced cardiac output; hypertrophy of left ventricle d/t pumping harder

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32
Q

mitral valve prolapse

A

part of one or both valve leaflets collapse back into the left atrium

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33
Q

symptoms of mitral valve prolapse

A

palpitations, chest pain, fatigue, dizziness, shortness of breath

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34
Q

types of valve repairs

A

valvuloplasty- valve repair and reconstruction done minimally invasive; commissurotomy- repair to stenosed mitral valve, fused commissures are incised

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35
Q

types of valve replacements

A

prosthetics consist of mechanical- long term disability, risk for thrombi/emboli, risk for infection, require lifelong antibx; biologic- durability <10yrs; homograft- human but limited availability; all procedures done if valvuloplasty cannot be done

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36
Q

cardiac tamponade

A

compression on the heart due to excessive fluid in pericardium; auscultate at PMI; treat with pericardiocentesis

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37
Q

assessment of valve disorders

A

decreased cardiac output and decreased cerebral perfusion; syncope with exertion; pulmonary edema; dyspnea; tachypnea; tachycardia; chest pain

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38
Q

diagnosing valvular disorders

A

TEE, echocardiogram, murmur auscultated d/t turbulent blood flow

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39
Q

treatment of valvular disorders

A

want NSR and avoid AFib; control HR with BB and CCB; valve repair

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40
Q

treatment of Afib

A

amiodarone and cardioversion

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41
Q

treatment of HF

A

diuretics and sodium restriction

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42
Q

heart failure

A

aka dilated cardiomyopathy; prone to dysrhythmias, valve dysfunction; causes sns stimulation to increase BP and narrow arteries and increase workload

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43
Q

signs and symptoms of dilated/HF

A

SOB on exertion, fatigue, weakness, cough while lying, orthopnea, chest pain, cardiomegaly, fluid retention, nausea. palpitations, syncope with exertion, S3 heart sound

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44
Q

diagnosing HF

A

echo to visualize and calculate ejection fraction, EKG, stress test, CXR, MRI, CT scan, cardiac cath lab, B natriuretic peptide (BNP)

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45
Q

treating HF

A

diet- sodium restriction; telemetry- monitor rhythms; meds like anticoagulants and antiplatelets; biventricular pacing; surgery

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46
Q

anticoagulants used for cardiac treatments

A

apixaban (eliquis), warfarin, rivaroxaban (xarelto)

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47
Q

antiplatelets used for cardiac treatments

A

aspirin, clopidogrel (plavix)

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48
Q

order of electrodes

A

salt pepper meat lettuce tomato; white pt top right, black pt top left, brown in middle sternum, green pt bottom right, red pt bottom left

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49
Q

electrical conduction system within heart

A

SA node is primary pacemaker and initiates atrial contraction, travels to AV node which is backup pacemaker and acts to depolarize atria and slow impulse, then atrial contraction begins and conduction travels to heart apex, then travels to bundle of his and bundle branches, then travels to purkinje fibers and through ventricular myocardium, causing ventricular contraction

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50
Q

moving from negative to positive (top to bottom)

A

causes positive deflections on 12 lead

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51
Q

P wave

A

atrial contraction (depolarization)

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52
Q

PR interval

A

from beginning of P wave to beginning of QRS; should be 0.12-0.2 sec

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53
Q

PR segment

A

from end of P wave to beginning of QRS complex; movement of electrical activity from atria to ventricles; impulse is held in AV node leading to isoelectric line

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54
Q

QRS complex

A

ventricular contraction (depolarization); should be 0.06-0.12 sec

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55
Q

ST segment

A

end of S wave to beginning of T; time between ventricular depolarization and repolarization

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56
Q

T wave

A

ventricular relaxation (repolarization)

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57
Q

QT interval

A

from beginning of QRS to end of T wave; time from beginning of ventricular contraction until ventricular repolarization; should be <0.4 sec

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58
Q

TP interval

A

end of t wave to beginning of P wave; ventricles are relaxing and filling

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59
Q

absolute refractory period

A

time where tissue cannot conduct any electrical impulse; QRS to T

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60
Q

EKG measurements

A

each box is 0.04s, each big box is 0.2 s, 5 large boxes is 1s, each strip is 6s

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61
Q

method of interpreting EKG

A
  1. measure the rate; 2. examine R-R interval to see if regular or irregular; 3. examine the p wave (constant, one for every QRS, upright); 4. measure PR interval; 5. is P wave followed by QRS; 6. Examine and measure QRS complex (wide or short); 7. measure QT interval; 8. identify the rhythm
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62
Q

sinus bradycardia

A

less than 60 bpm, regular R-R, upright regular and matching P wave; P wave precedes QRS

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63
Q

treatment for sinus bradycardia

A

speed up heart; atropine 0.5mg, dopamine, pacemaker

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64
Q

types of pacemakers

A

temporary- transcutaneous, transvenous, epicardial; permanent- pacemaker, implantable cardioverter defribrillator, biventricular pacemaker

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65
Q

atrial pacemaker spikes and ventricle pacemaker spike

A

atrial PM pacer spike occurs before P wave; ventricle pacer spike occurs before QRS (QRS will be wider if paced and that is normal)

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66
Q

sinus tachycardia

A

rate > 100 and <140; R-R interval is regular; P wave is regular upright and matching; P wave precedes QRS

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67
Q

treating sinus tachycardia

A

fluids, O2, fever, pain, rest; meds like beta blockers (metoprolol)

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68
Q

atrial fibrillation

A

irregular R-R interval; P wave is undistinguishable; unable to calculate PR interval; cannot identify if P wave precedes each QRS; QT interval cannot be determined

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69
Q

concern/problem with atrial fibrillation

A

loss of atrial kick which causes hypotension and blood stasis

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70
Q

atrial fibrillation RVR

A

rate greater than 110

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71
Q

treating atrial fibrillation

A

beta blockers, calcium channel blockers, digoxin, amiodarone (not as commonly used); all used to slow conduction from SA to AV node

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72
Q

atrial flutter

A

regular R-R interval; P wave cannot be distinguished but can see flutter “sawtooth”; cannot calculate PR interval; cannot identify if P wave precedes each QRS; QT interval cannot be determined

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73
Q

concern with atrial flutter

A

loss of atrial kick and blood stasis; not as bad as Afib; one spot of atria is misfiring

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74
Q

supraventricular tachycardia

A

rate is > 140; regular R-R interval; unable to identify P wave; cannot calculate PR interval; cannot identify if P wave precedes each QRS; unable to identify QT interval; fast and skinny; cannot distinguish between P and T waves

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75
Q

treating SVT

A

want to convert and slow; vagal maneuver, carotid massage, medications or cardioversion; adenosine

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76
Q

adenosine

A

1st line therapy for SVT when vagal does not work; given rapidly over 1-2 sec; temporarily inhibits AV node conduction and blocks to reset HR

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77
Q

ventricular tachycardia

A

extremely widened QRS; R-R interval is regular; P wave is undistinguishable; no PR interval; P wave does not precede each QRS; unmeasurable QT interval

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78
Q

cardiac tamponade on EKG

A

crescendo then decrescendo then crescendo; types of Vtach; treat with magnesium and peridcardial centesis

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79
Q

treating Vtach

A

stable with pulse- O2 therapy, antiarrhythmics like amiodarone, synchronized cardioversion; unstable without pulse- CPR, ACLS protocol for defib., possible intervention, drug therapy like epi vaso and amiodarone

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80
Q

ventricular fibrillation

A

complete loss of contraction; R-R interval is undeterminable; no p wave; PR interval is not calculable; P wave does not precede each QRS; no QT interval;

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81
Q

treating ventricular fibrillation

A

defibrillate; meds like epi and amiodarone

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82
Q

asystole

A

complete cessation of hear electrical impulses in heart; pt is pulseless and unconscious; treat with CPR and meds (no defib)

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83
Q

pulseless electrical activity

A

electrical activity shown on EKG but no pulse present; need to reverse underlying cause; treat with CPR and epinephrine

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84
Q

etiology of PEA

A

H’s and T’s; hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypoglycemia, toxins, tamponade, tension pneumo, thrombosis, trauma

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85
Q

premature ventricular contraction

A

can be completely normal; 3 in a row is considered Vtach; can be electrical or actual contraction; does not add to cardiac output; treat by monitoring and if frequent notify physician

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86
Q

elective cardioversion

A

admin electrical current synchronized with patients heart rhythm; ised to treat SVT, AF, Aflutter, Vtach with pulse that is med resistant; 50-150 joules x3

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87
Q

R on T phenomenon

A

administering cardioversion on T wave tat can cause and lead to lethal arrhythmias

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88
Q

digoxin

A

+ inotropic effect to increase squeeze; - dromotropic effect that slows impulses in AV node; - chronotropic effect causing to beat slower

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88
Q

mechanical circulatory support for HF

A

ventricular assist device, intra-aortic balloon pump

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89
Q

acute respiratory distress syndrome

A

severe form of respiratory failure; rapidly progressive hypoxemia; alveolar capillary injury; damage to endothelia lining of alveolar membrane increasing permeability; plasma and proteins leak from capillaries into interstitial spaces and alveoli that causes damage, reduces lung compliance, lung volume, and normal gas exchange; most fatal within 24-48 hrs

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90
Q

common etiology of ARDS

A

aspiration of gastric contents, pneumonia, covid, shock of any etiology, sepsis

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91
Q

manifestations of acute respiratory distress syndrome

A

hypoxia that does not improve with O2 (hallmark), tachypnea, increasing dyspnea, hyperventilation, resp. distress, no adventitious lung sounds, tachycardia, HTN, restlessness/anxiety, chest Xray resemble pulmonary edema, BNP to distinguish from pulmonary edema, visible bilateral infiltrates

92
Q

why prone positioning/rotoprone for ARDS

A

improve oxygenation, increase end-expiratory lung volume, improve bronchial drainage, improve functional residual capacity, improve gas exchange

93
Q

obstructive sleep apnea

A

upper airway obstruction causing decreased ventilation and gas exchange, intermittent breathing

94
Q

clinical manifestations of OSA

A

snoring/snorting, apneic events, gasping, recurrent waking and sleep disruption, choking, excessive daytime sleepiness, workplace or car accidents, decreased cognitive functioning, retention and performance compromise; partners identify signs and symptoms

95
Q

risk factors for OSA

A

obesity, DMII, HF, pulmonary HTN, large neck circumeference

96
Q

diagnosing OSA

A

health history with sleep study

97
Q

treating OSA

A

lifestyle modifications, CPAP, surgery as needed

98
Q

pulmonary embolism

A

clot in pulmonary artery or branch; embolism can be fat, air, thrombus, amniotic, or septic; size determines severity; causes increased vascular resistance and increased pulmonary arterial pressure

99
Q

risk factor for developing PE

A

vrichows triad- venous stasis, hypercoagulative state (pregnant or COPD), endothelial damage (HTN or DM); DVT

100
Q

saddle PE

A

form clot at biforkation of lungs blocking blood flow

101
Q

clot busting drug

A

alteplase

102
Q

clot preventing drug

A

warfarin

103
Q

manifestations of PE

A

sudden dyspnea, pleuritic chest pain, anxiety, tachycardia, cough, diaphoresis, hemoptysis, syncope, impending doom, petechiae

104
Q

diagnosing PE

A

elevated D-dimer, EKG, chest xray, ABG, spiral CT or VQ scan, pulmonary arteriogram

105
Q

Prevention of PE

A

active leg exercises, mobility with pt, early ambulation, anticoag therapy, SCDs

106
Q

treatment of PE

A

measures to improve respiratory and vascular status like O2 therapy, ECG monitoring, IV access; anticoag therapy like heparin or warfarin, thrombolytic therapy like streptokinase and alteplase; surgical intervention like embolectomy

107
Q

pulmonary HTN

A

mean pressure >25mmHg and pulmonary capillary wedge pressure > 5mmHG; can be idiopathic or d/t existing cardiac/pulmonary disease; more frequent in women; often fatal within 5 yrs

108
Q

manifestations of pulmonary HTN

A

dyspnea, substernal chest pain (non cardiac), weakness, fatigue, syncope, signs of right sided HF

109
Q

diagnostic testing for pulmonary HTN

A

chest xray, pulmonary function tests, ECG and echo, cardiac cath with measurement of right heart pressures

110
Q

manag,ent of pulmonary HTN

A

supplemental O2 therapy, central venous access for prostanoids; meds like CB, phosphodiesterase inhibitor, prostanoids, lung transplant

111
Q

prostanoids use for pulmonary HTN

A

active lipid mediators thar regulate inflammatory response

112
Q

phosphodiesterase inhibitor use for pulmonary HTN

A

cause blood vessels to relax and widen, improve circulation, lower BP

113
Q

pneumothorax

A

partial or complete collapse of lung due to positive pressure in pleural space; can be hemothorax, tension pneumo, or pneumo

114
Q

hemothorax

A

blood in pleural space that collapses lung, d/t trauma or post op

115
Q

tension pneumothorax

A

emergency situation with increasing positive pressure in pleural space that can displace lungs and heart; can be open or closed; will see TD d/t shifting mediastinum; can put pressure on vena cava and decrease blood return

116
Q

treatment of pneumothorax

A

chest tube or dart in 2nd intercostal space to open up lung opening lung to intubate

117
Q

diagnosing pneumothorax

A

presentation and assessment; related history, chest xray, ABG, respiratory acidosis due to decrease in PaO2 and increase in PaCO2

118
Q

chest tube

A

breath changes aka tidaling is normal; should be no bubbling in water-seal chamber and if there is there could be an air leak

119
Q

chest tube removal

A

suction is discontinued and set to water seal for 6-24 hours prior, cxr prior, lungs re-expanded and pleural drainage is complete, pre medicate and educate, remove sutures, have pt exhale and then remove, occlusive dressing over wound, pleura self heals, offer NSAIDs

120
Q

chest tube occlusive dressing around tube

A

do not remove, if disconnected then place end in sterile water for seal; subcutaneous emphysema/crepitus aka air into subcutaneous tissue- inspect and palate at insertion site, report immediately to HCP

121
Q

PaCO2

A

35-45; regulated by the lungs

122
Q

HCO3

A

22-26; regulated by the kidneys

123
Q

PaO2

A

80-100; regulated by the lungs

124
Q

method of evaluating ABGs

A
  1. check pH for acidotic or alkalotic; 2. evaluate PaCO2; 3. Assess HCO3; 4. check PaO2 and O2 for hypoxemia and impaired oxygenation
125
Q

normal ABG values

A

pH- 7.35-7.45; CO2- 35-45; HCO3- 22-26

126
Q

ROME Method for ABG

A

Respiratory opposite- pH and CO2; Metabolic equal- pH and HCO3

127
Q

uncompensated ABG values

A

pH is out of range but CO2 or HCO23 is in range

128
Q

partially compensated ABG values

A

CO2, HCO3, and pH all out of range

129
Q

fully compensated ABG values

A

pH is in range

130
Q

respiratory compensation

A

body can partially compensate for metabolic imbalances by adjusting ventilation

131
Q

metabolic compensation

A

respiratory imbalances can be compensated through changes in bicarbonate levels

132
Q

respiratory acidosis

A

pH < 7.35 and CO2 > 45; lungs retaining too much CO2 and kidneys excrete hydrogen and retain bicarb; pt unable to breath out CO2 and require intubation

133
Q

signs and symptoms of respiratory acidosis

A

increased respiratory rate, restlessness, confusion, headache, sleepy/coma

134
Q

interventions for respiratory acidosis

A

administer O2, semi-fowlers, turn cough deep breath, pneumonia requiring increase in fluids; intubate if CO2 > 50

135
Q

respiratory alkalosis

A

pH > 7.45 and CO2 < 35; lungs are losing too much CO2; kidneys excrete excess bicarb and retain hyhdrogen

136
Q

signs and symptoms of respiratory alkalosis

A

increase heart rate, confused and tired, tetany, EKG changes, + chvosteks sign

137
Q

pre-renal AKI

A

due to reduction in blood flow to the kidney; hypoperfusion and decreased O2

138
Q

causes of prerenal AKI

A

hypovolemia from bleeding, hypotension, vasoconstriction, renal artery stenosis, inadequate cardiac output

139
Q

intra-renal AKI

A

intrarenal failure is due to damage to the filtering structures in the kidney; aka acute tubular necrosis

140
Q

causes of intra-renal AKI

A

acute tubular necrosis, nephrotic medications like NSAIDs, CT contrast, antibx ending in -mysin; diagnosed with creatinine >1.3; treat by removing underlying cause

141
Q

acute tubular necrosis

A

destroyed tubular segment of the nephron causing uremia and renal failure; blood flow to kidney is disrupted

142
Q

causes of acute tubular necrosis

A

ischemic injury, nephrotoxic injury, blood transfusion reaction, rhabdomyolysis, hypotension, major surgery, septic shock

143
Q

post-renal AKI

A

renal blockage after the kidneys blocking outflow of urine causing increased pressure in kidneys that limit filtration ability

144
Q

causes of obstruction to urine outflow

A

upper- renal calculi, tumors; lower- BPH, urethral strictures, occluded catheter; functional- neurogenic, spinal cord disease

145
Q

diagnosing post renal AKI

A

xray to look for calculi/hydronephrosis, ultrasound to look for obstruction, CT without dye to check for obstruction and view renal perfusion

146
Q

treating post renal AKI

A

remove underlying cause if possible, IV hydration, supportive measures

147
Q

indications for temporary dialysis

A

volume overload that is unresponsive to diuretics, hyperkalemia, metabolic acidosis, progressive azotemia (BUN > 100); options are intermittent dialysis, continuous renal replacement therapy, peritoneal dialysis

148
Q

end stage renal disease

A

GFR < 15; stage 5 CKD

149
Q

risk factors for CKD

A

diabetes; HTN- nephrosclerosis, ACE/ARBs, glomerulonephritis

150
Q

etiology of CKD

A

metabolic disorders, renal vascular disorders, immunologic disorders like lupus, infection like UTI or pyelonephritis, primary tubular disorders, urinary tract obstruction, congenital disorders like PKD, most frequently caused by DM and HTN

151
Q

signs and symptoms of ESRD

A

decreased UOP, proteinuria and hematuria, lethargy, altered LOC/confusion, seizures, HTN, fluid volume excess, HF, anorexia, N/V, uremic fetor, metallic taste, impaired immune and inflammatory respone, uremic frost, pruritus, anemia, increased bleeding, prolonged bleeding, amenorrhea, ED, decreased libido

152
Q

lab vales for ESRD

A

increased BUN, increased creatinine, increased K, increased Mg, decreased calcium, increased phosphate

153
Q

indications for dialysis

A

ESRD- GFR < 5-10, BUN > 80-100, creatinine > 8; metabolic acidosis, poisonings to clear drugs/toxins, fluid volume excess in anuric pt; hyperkalemia unresponsive to therapy; AKI

154
Q

central venous line access for dialysis

A

acute but temporary, use subclavian, internal jugular, or femoreal; cons- thrombosis, hematoma, not enough blood flow

155
Q

AV fistula vascular access for hemodialysis

A

rapid flow that is surgically created, 2-3 months to mature and last 3 years; pros- last long, not prone to infection, excellent blood flow, can shower, less likely to have clots; cons- need to mature, need direct needles into skin

156
Q

AV graft vascular access

A

inadequate blood vessel, 2-5 weeks to mature; pros- excellent blood flow, take shower after healing; cons- less time than fistula, more prone to infection, 2 weeks before use, clotting

157
Q

pt education for fistula care

A

do- lanolin for dry skin, check bruit frequently, report bleeding/oozing of patch, medic alert bracelet, hold pressure for 20 min after removal of access; dont- no blood draws IVs or BP, no tight clothing or jewelry, do not lift heavy items, do not bump, do not itch/pick at scabs

158
Q

hemodialysis

A

remove blood from patient and filter through dialysis membrane and return filtered blood to patient; outpatient 2-3 times per week at home; may clot,risk for infection; requires anticoag and BP sufficient to tolerate approx 1 pint of blood out of circulation at one time; hypotension and blood loss may occur; most efficient form of dialysis; dialysate formulated to pt specific need

159
Q

contraindications to hemodialysis

A

inability to be anticoagulated, severe cardiac disease, hemodynamic instability

160
Q

peritoneal dialysis

A

dialysate solution warmed to body temperature and infused into peritoneum; equilibration occurs across peritoneal membrane then solution is drained; heparin may be added to dialysate to prevent clot formation; want light yellow drainage; need bag to below insertion

161
Q

complications

A

infection like peritonitis, bowel or bladder perforation, bleeding

162
Q

methods of peritoneal dialysis

A

intermittent- dialysis is 3-5 weeks for 8-12 hours via automatic cycler machine; continuous; continuous- dialysate infused into peritoneum, dwells for 4-5 hours then drained; cyclic continuous- combines intermittent night time cycling with day time ambulatory dialysis

163
Q

contraindications to peritoneal dialysis

A

severe obesity, COPD, less efficient, catheter can clog and be displaced

164
Q

continuous renal replacement therapy

A

hemodynamically unstable patients; slow continuous microfiltration; need A line for accurate readings of pressure prior to CRRT

165
Q

types of UTI

A

pyelonephritis (kidney infection), uretitis, cystitis, urethritis, prostatitis

166
Q

signs and symptoms of UTI

A

frequent urination, painful urgent, burning; dark red milky or cloudy urine; foul smelling urine; pain in flank region; pressure in pelvic area; fever, fatigue, altered mental status; confusion in older adult

167
Q

interventions for UTI

A

simple- trimethoprim/sulfamethazine, nitrofurantoin; complex- ciprofloxacin (can cause tendon rupture); pyridium analgesic for pain and spasms

168
Q

renal calculi

A

can occur in renal tract (renal pelvic or calices), risk for development when increased stone component; predisposed if dehydrated, infection obesity, exercise

169
Q

four types of kidney stones

A

calcium (oxalate and phosphate)- associated with increased calcium levels; magnesium ammonium phosphate (struvite)- associated with UTI; uric acid stones- related to uric acid levels; cystine stones- seen in cysturia

170
Q

signs and symptoms

A

N/V; flank pain that may radiate to groin, testicles, abdominal pain; sharp sudden severe pain; hematuria, dysuria, urinary frequency

171
Q

diagnosing kidney stone

A

US, IVP, renal stone analysis, KUB scan, serum calcium oxalate and uric acid

172
Q

etiology of renal calculi

A

infection, urinary stasis/retention, immobility, dehydration, increased uric acid, increased urinary oxalate

173
Q

treatment of renal calculi

A

calculi <4mm have 80% chance of passing with vigorous hydration, removal of stone via lithotripsy or nephrolithotomy, determine composition of stone, dietary consult, med treatment with analgesics diuretics and thiazides

174
Q

thiazide effects on renal calculi

A

decrease calcium excretion in urine

175
Q

leukemia

A

cancer of blood and blood forming organs; usually leukocytes; immature blast stage where cells cant mature and divide rapidly; drains the resources in bone marrow

176
Q

signs and symptoms of leukemia

A

low RBC, low Hgb, low Hct, low platelets, bruising, bone pain, intermittent fever with no other findings

177
Q

complications with leukemia

A

neutropenia, anemia, bleeding, DIC, fungal infections, tumor lysis syndrome

178
Q

treatment of leukemia

A

chemotherapy, hematopoietic stem cell transplant, supportive care

179
Q

goals for pt with leukemia

A

absence of complications and pain, attainment and maintenance of adequate nutrition, ability to proved self care and cope with diagnosis; understanding of disease

180
Q

multiple myeloma

A

plasma cell cancer (b lymphocyte); bone marrow and skeleton tumors; malignant plasma cells penetrate BM forming tumors

181
Q

signs and symptoms of multiple myeloma

A

bone pain in spine and chest; pain and numbness in legs; fatigue; weight loss; osteoporosis; bone fractures; renal impairment

182
Q

complications with multiple myeloma

A

infection, brittle bones, enamia, kidney failure, hypercalcemia

183
Q

treatment for multiple myeloma

A

HSCT, chemo, bisphosphonates, radiation; rarely cured but can manage pain

184
Q

lymphoma

A

neoplasm of lymphoid origin; hodgkins and non-hodgkins

185
Q

hodgkins lymphoma

A

single node; reed sternberg cells; epstein barr virus; genetic (20-30s); environmental

186
Q

non hodgkins lymphoma

A

lymph tissue infiltrated with malignant cells; lymphadenopathy; chromosomal translocation; infections; environmental; AIDS; chemotherapy; radiation

187
Q

clinical manifestations of lymphoma

A

swollen lymph nodes in axilla, neck, groin; weight loss; fever; night sweats

188
Q

treatment of lymphoma

A

chemo, radiation, HSCT, NHL: immunotherapy

189
Q

polycythemia vera

A

bone marrow is hypercellular; increased blood cell mass and viscocity;

190
Q

manifestations of polycythemia vera

A

initially asymptomatic; CNS- headache, dizziness, TIA; CV- angina, claudication, SOB, HTN; fatigue, night sweats; ABD- early satiety, abdominal pain

191
Q

complications with polycythemia vera

A

CVA, MI, bleeding risk from dysfunctional platelets

192
Q

diagnosing polycythemia vera

A

elevated erythrocytes, leukocytes, platelets, HGB and HCT

193
Q

CML

A

philadelphia cells; mutation in myeloid stem cells causing uncontrolled proliferation; failure of B cell

194
Q

AML

A

defect in stem cell that differentiates into myeloid cells like monocytes, granulocytes, erythrocytes, platelets; peak incidence in 60s

195
Q

ALL

A

uncontrolled proliferation of lymphoid cells from stem cell; young children mostly affected; peak incidence is 4 yrs; boys affected more often

196
Q

prior to blood transfusion

A

type and cross match; explain procedure; informed consent; atleast 20 gauge IV; hospital policy and procedure with IV pump; label and compare to order; double nurse witness

197
Q

sickle cell anemia

A

shortened red blood cell life due to hemolysis; sickled shape; blocks arteries; geneticcompl

198
Q

complications with sickle cell anemia

A

stroke, hypoxia/ischemia; dehydration; MI; kidney disease; substance abuse; HF

199
Q

bleeding disorders

A

thrombocytopenia, immune thrombocytopenic purpura, platelet defects, hemophilia, von willebrand

200
Q

thrombocytopenia

A

deficient # of platelets causing bleeding into tissues; all coagulation factors are present and normal

201
Q

signs and symptoms of thrombocytopenia

A

bleeding, petechiae, ecchymosis, epistaxis, bleeding gums

202
Q

HIT

A

heparin induced thrombocytopenia; fall in platelet count; risk for clots; need to stop heparin and switch to another anticoag

203
Q

disseminated intravascular coagulation

A

altered hemostasis mechanism; massive clotting in microcirculation; all clotting factors are consumed and causes profuse bleeding

204
Q

signs and symptoms of DIC

A

petechiae, hematuria, melena, epistaxis

205
Q

anemia

A

lower than normal Hgb and fewer circulating erythrocytes; microcytic, normocytic,, macrocytic, sickle cell

206
Q

microcytic anemia

A

decrease RBC production, MCV <80; iron deficiency; smaller pale RBCs

207
Q

normocytic anemia

A

MCV- 80-100; increased reticulocyte count- hemolytic anemia/hemorrhage/sickle cell; decreased reticulocyte count- bone marrow suppression, chronic disease

208
Q

macrocytic anemia

A

MCV >100; megaloblastic- Vit B12 deficiency, folate deficiency; non-megaloblastic- alcohol

209
Q

classic signs of anemia

A

pallor, fatigue, dyspnea on exertion, dizziness

210
Q

interventions for anemia

A

balance physical activity and rest, adequate nutrition and hydration, med compliance, monitor VS, supportive therapy, complication management of HF parasthesia and confusion

211
Q

do not take iron with…

A

calcium; take with vit c and fruit juice on empty stomach

212
Q

acute hemolytic reaction

A

fever, chills, jaundice, flank pain, chest pain, heat feeling along vein, impending doom; fatal reaction risk increases if >100mL transfused

213
Q

preoperative phase

A

decision is made and ends with pt on OR bed

214
Q

intraoperative phase

A

patient OR bed and ends with admission to PACU

215
Q

postoperative phase

A

begins with admission of pt to PACU and ends with follow up

216
Q

intervention for thermal burns

A

remove charred clothing, saline or water to cool tissues, fluffed gauze in between fingers and toes individually

217
Q

chemical brun intervention

A

remove by brushing or flushing with water, remove any clothing, neutralizing agents not recommended, tissue destruction for up to 72 hrs

218
Q

acid vs alkaline burns

A

acid- protein denaturation and necrosis, short-lived and local; alkaline burns are far worse and cause progressive liquefaction necrosis with deeper tissue penetration and prolonged effect

219
Q

electrical burn intervention

A

remove electrical current before touching, cell rupture, iceberg effects, bone fracture, identify entrance and exit, compartment syndrome

220
Q

rule of 9s

A

entire head/neck is 9% (4.5 front and back); entire torso is 36* (18 front and back), entire right arm is 9% (4.5 front and back), entire left arm is 9% (4.5 front and back), entire right leg is 18% (9 front and back), entire left leg is 18% (9 front and back), groin is 1%

221
Q

systemic burns

A

20% TBSA in adults and >10% in children

222
Q

inhalation injury

A

damage to respiratory system due to breathing in smoke, thermal or chemical; deterioration in severely burned pt; need to be intubate

223
Q

signs and symptoms of inhalation injury

A

charred burned or bright red lips, burn to head neck or face, wheezing, change in voice, difficulty breathing, singed nose hairs or eye brows, dark mucus

224
Q

fluid resuscitation formula

A

weight in kg x %TBSA x 4mL; first half given over 8 hours, second half given over 16 hours; only for TBSA >20%

225
Q

green triage

A

able to walk; victim with relatively minor injuries; status unlikely to deteriorate over days; may be able to assist in own care; “walking wounded”

226
Q

yellow triage

A

unable to walk, spontaneous breathing, RR <30, radial pulse present or capillary refill <2, mental status able to obey commands; transport can be delayed; serious and potentially life-threatening injuries but status not expected to deteriorate significantly over several hours

227
Q

red triage

A

unable to walk, spontaneous airway absent but recurs with airway repositioning, respiratory rate >30, radial pulse absent or capillary refill >2 sec, mental status does not obey commands; victim can be helped by immediate intervention and transport; requires medical attention within 60 minutes for survival; compromise to ABCs

228
Q

black triage

A

unable to walk, no spontaneous breathing even with airway adjustment; victim unlikely to survive given severity of injuries or level of available care, palliative care and pain relief should be provided

Adults 2 (7 decks)

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