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LPN to RN > N211 -Health Differences Across the Life Span 1 > Flashcards

N211 -Health Differences Across the Life Span 1 Flashcards

1
Q

HTN

A

28-31% adults in US

of this , 90-95% PRIMARY HTN (unidentified cause)

remaining 5-10% SECONDARY HTN (identified cause)

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2
Q

Identified Causes for HTN

A

-narrowing renal arteries, renal parenchymal dis, hyperaldosteronism (mineralocorticoid HTN), Pregnancy, coarctation of aorta, certain meds

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3
Q

ETOH and HTN linked to

A

UP triglycerides, sugars, weight gain, LDLs, cardiac function

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4
Q

Dx someone with HTN elevation on one round. Must have average of

A

2 or more contacts w health care provider

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5
Q

Normal BP

A

<120/<80

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6
Q

Pre HTN

A

120-139/80-89

PIH (pregnancy induced HTN usually resolves after placenta expelled)

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7
Q

Stage 1

A

140-159 / 90-99

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8
Q

Stage 2

A

160 up / 100 up

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9
Q

Stage 1 TX

A

Medication, MD until stable

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10
Q

Stage 2 Tx

A

doctor and workups

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11
Q

?250 - 400

A

Moderate Cardio Vas dis.

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12
Q

UnTx HTN

A

.UP workload to heart
.thickening of arterial wall
. etc

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13
Q

HTN Emergency

A

BP 180/120

.pressure in head

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14
Q

HTN Crisis Tx.

Short lived meds (minutes - 4hrs)

A

Nitroglycerin (Nitro-Bid)
Socium Nitroprusside (nipride or nitropress)
nicardipine hydrocholoride (cardene)
enalaprilat (vasotec)

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15
Q

Vasodilator: Fendolopam

A

Fendoldopam (Corlopam)

1.action

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16
Q

Alpha Adrenergic Clocker

A

WORK DIRECTLY ON BLOOD VESSELS

keeps hormone from tightening muscles and walls. counter epi and nor epi.

SE: V/N/D, urinary freq, cardio vascular collaps

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17
Q

Alpha Adrenergic Clocker

A

WORK DIRECTLY ON BLOOD VESSELS

keeps hormone from tightening muscles and walls. counter epi and nor epi.

SE: V/N/D, urinary freq, cardio vascular collaps

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18
Q

Beta Adrenergic Blocker

COREG

ALPHA and BETA

A

Dry Cough - BAD, change meds

Slow transition to get used to

SE: cardiovascular. can worsen ss. not for newly HTN patients Not first line drug.

Contracindicated in Heart failure, COPD and ?

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19
Q

Beta Adrenergic Blocker: Inderol

A

Propanolol

for Stage Fright, BP control,

slows HR, reduces cardiac output, fatigue, bizarre dreams

SE bradycardia, insomnia, fatigue,

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20
Q

Calcium Chan Blocker

A

Diltiazem

Inhibit calcium ion influx and reduce after load.

inhibit na, inhibit water.

Procardia: CHF, resistant Angina,

Some people chew to get emergency fast effects. not for normal pt as it can bottom out pressure fast.

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21
Q

Beta Adrenergic Blocker

A

Lopressor, Corguard, Inderol, Toprolol

slow HR. they get breathless, can’t excercise on this drug.

decrease contractions and AV signal,

SE bradycardia, insomnia, fatigue, bad dreams, sex dysf, LO HDL, GI probs, LO BP, depresson

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22
Q

ACE Inhibitors

A

Angio 1 - 2.

lowers resistanece of peripheral vascular syste =less risistance

SS proteinurea, dry cough, hyperkalemia, renal damage

Catapress
Aldamet
diminish periphera outflow from brain. brain action to neurons.

dose at bedtime. monitor 30-90min for syncopy

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23
Q

Diuretics

A

Thiazides

pulling fluid from extra vascular to intra vascular spaces to rebalance lo plasma.

affect smooth muscle.

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24
Q

Burn patients

A

hi K levels. As they stabilize, K drawn back into cells.

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25
Q

Loop Diuretics

A

can cause volume depletion . NOT first line. After Thiazines tried.

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26
Q

K sparing Diurents

A

can cause Hyper Kalemia.

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27
Q

Vasodialiators

Hydralazine

A

Hydralazine (Apresoline)

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28
Q

DASH Diet

A

reduce cholestoerol in blood

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29
Q

Chart textbook P15

A

MAKE CARDS

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30
Q

PTT (partial prothrombin time)

A

eficacy of Heparin

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31
Q

PT(C) (prothrombin time)

A

Efficacy of Coumadin

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32
Q

when we have a venus problem, DO NOT add heat

A

it will increase circulation. If arterial problem, yes warm. you want blood to go down to extremeties. in venous, the blood is pooling and we need to elevate legs to help move up blood.

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33
Q

intermitent caudicatoin

A

when person walks, not enough blood flow to legs. sever pain, heavy , sharp.

they stand still , then it goes away, then it starts again when they walk

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34
Q

Abdominal Aortic Aneurysm

A

-asymptomatic

Watch for
clotting
emboli
rx for clotting

SS:
Abdominal pain, low back pain, feel heart beat

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35
Q

Assessing AAA

A

Bruit, swooshing over consicted artery.

Pain: abdominal/loabdomin

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36
Q

Calcium Channel Blockers

A

Tx Angina, HBP

affect movement of ca in cells of heart

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37
Q

Digoxin/Linoxin

A

stronger heart contraction

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38
Q

Beta Blockers

A

Control catacholoamines

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39
Q

Beta Blockers

A

Control catacholoamines

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40
Q

Digoxin Antagonist

A

digoxinase ?

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41
Q

Hyperkalemia Antagonist

A

Kayexalate

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42
Q

Heparin

A

protamin sulfate

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43
Q

Coumadin antagonist

A

vit k

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44
Q

Pulse Pressure

A

diff between top and bottom

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45
Q

Pump Problems

A

cardiomyopathy

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46
Q

Cardiogenic shock

A

loss of hearts ability to pump enough blood to heart

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47
Q

hypovolemic shock

A

loss of large amount of blood or fluid

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48
Q

Distributive Shock

A

loss of vascular tone causing decreased peripheral resistance, larger vascular bed, result in hypovolemia

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49
Q

Class 3

A

9/6/18

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50
Q

Problems of intake and supply of O2

A

.

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51
Q

beta blockers

Inderol?

A

non selective vs selective

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52
Q

classic angina comes from

A

exertion or stress

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53
Q

unstable angina pre infarction

A

frequent times daily with increasing severity

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54
Q

classic dysrythmias result from

A

hypoxia and hypercapnia

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55
Q

Digitalis preps effective in treating

A

CHF

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56
Q

cardiac glycoside aka

A

dig glycoside

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57
Q

digitalis

A

allows heart to work less but beat stronger

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58
Q

strted from page 24

A

review ABG

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59
Q

Sudden hypercapnia causes

A

.UP Pulse, resp, BP
.Mental cloud

see rest

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60
Q

Acute Respiratory Acidosis

A

inadequate excretion of CO2 w inadequate vent

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61
Q

Chronic Resp Acidosis

A

occurs w pulmonary diiseases

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62
Q

Nursing Interventions

A

.lo flo O2

.monitor consiousnee, abg, ekg for dysrythmias

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63
Q

SLIDE 9

A

HCO3 is Bicarb not H2CO3

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64
Q

when you rae chronically aciic, hi CO2

A

body become used to it. It’s stops becoming the hi CO2 that makes the breath, but the lo O2 levels.

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65
Q

go over respiratory vs metabolism

A

k

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66
Q

Respiratory Alkalosis

A

Carbonic Acid deficit

.body loses CO2, decrease in acid, increases ph level
.occurs w hyperventilation, leads to loo CO2
……

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67
Q

Causes

A

.

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68
Q

SS

A

.

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69
Q

.

A

.

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70
Q

.

A

.

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71
Q

.

A

.

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72
Q

Nursing Intervention

A

.tx underlying cause

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73
Q

Metabolic Acidosis

A

.ABG
.lo bicarb
.lo ph

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74
Q

Metabolic Alkalosis

A

.hi ph > 7.45
.hi plasma bicarb (HCO3 > 26)
.paCO2 INC as lungs attempt to compensate for excess bicarb by retaining CO2

compensate by blowing it off

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75
Q

Acidotic complication

A

.peripheral vasodilation and decrease cardiac output w Ph drops to <7.0
.chronic metabilic acidosis usually seen wtih chronic renal failure
.closemonits K leves. hypokalemia

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76
Q

LOOK at old ABG slides

A

look at old ABG slides

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77
Q

metabolic acidosis

A

.see P57 in book
. lo bicarb
.hyperkalemia

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78
Q

SEE pg 57 in book

A

MAKE SLIDES

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79
Q

Adult Respiratory Failure

A

Slide 97

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80
Q

pg 61

A

beta antagonist

corticosteroids

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81
Q

Atropine

A

drying secretions

…….

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82
Q

PNA clsassification

A 
community
hospita
incompromised host
aspiration pna
?
?
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83
Q

ended at laryngeal obstructino

A

slide 182

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84
Q

Factors Causing Hypertension

A

.INcreased Sympathetic stimulation
.UP blood volume d.t increased renal reabsorption of Na+, CL- and H2o retention
.UP activity of RAAS system, caused expansion of extracellular fluid volume. causing systemic vascular resistance
.Dysfx of vascular endothelium causing decreased vasodilation of arterioles
.resistance to Insulin

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85
Q

most gastric cancers are

A

adenocarcinomas

will go through stomach and into other organs

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86
Q

most gastric cancers are

A

adenocarcinomas

will go through stomach and into other organs

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87
Q

Ovarian Ca SS

88
Q

to take the ovaria

89
Q

Capoten

A

Captopril

ACE inhibitor

90
Q

Lotensin

A

Benazepril

91
Q

Zestril

A

Lisinopril

92
Q

Aldactone

A

Spironolactone

ARB - Aldosterone Receptor Blocker

93
Q

Cozaar

A

Losartin

ARB

94
Q

what does epinephrine do?

A

vasoconstrict

95
Q

Lopressor

A

Metaprolol

Beta Blocker

96
Q

Tenormin

A

Atenolol

BB

97
Q

Norvasc

A

Amlodipine

CCB

98
Q

Plendil

A

Felodipine

CCB

99
Q

Procardia

A

Nifedipine

100
Q

Catapres

A

Clonidine

Central Alpha 2 agonist

101
Q

Coreg

A

Carvedilol

alpha and BB

102
Q

Apresoline

A

Hydralazine (direct vasodilator) helps body loose excess water by releasing excess salt

103
Q

Esidrix

A

Hyrochlorothiazide

Diuretic

104
Q

Prinzide

A

Lisinopril / HCTZ

(Lisinopril/HCTZ) {=Thiazide diuretic and ACE inhibitor} causes the blood vessels to loosen and dilate. This decreases the strain on the arterial walls. Therefore, the speed and pressure inside the artery walls decreases {=Vasodilators}

105
Q

Prinzide

A

Lisinopril / HCTZ

(Lisinopril/HCTZ) {=Thiazide diuretic and ACE inhibitor} causes the blood vessels to loosen and dilate. This decreases the strain on the arterial walls. Therefore, the speed and pressure inside the artery walls decreases {=Vasodilators}

106
Q

Systolic heart failure

A

most common

alteration in ventricular contractoin

107
Q

Diastolic heart failure

A

stiff noncompliant heart muscle

108
Q

Type of Heart Failure determined by EF

A

Ejection Fraction, vol blood ejected w each contraction of ventricular volume (normal 55-65%)

determines Systolic or Diastolic heart
failure

HF = low EF

109
Q

Left Sided HF

A

Pulmonary Edema

SS: dyspnea, wet lung, cough, fatigue, tachy, anxiety, restlessness, confusion, paroxysmal nocturnal dyspnea (sudden attacks at nght), orthopnea (diff breathing lying down)

Frothy pink sputum = severe Pulm Edema

Dominant feature of heart failure is decreased tissue
perfusion to kidney, brain, and GI system

110
Q

Right Sided HF

A

Peripheral Edema

SS: peripheral edema, weight gain, distended neck vain, anorexia, nausea, nocturia, weakness

111
Q

HF

A 
.decreased cardiac output
.impaired urinary elim d/t decreased perfusion
.activity intolerance
.anxiety
.ineffective tissue perfusion

Tx: restrict Na, to reduce salt and water retention, reducing vascular volume

.assess/monitor q4hrs
.assess/mon apical hr
.assess for hypoxia (restlessness, tachy, chest pain)
.auscultate lungs for pulmon edema (crackles/wet sounds)
.admin O2

112
Q

HF Interentions

A

.observe ss of edema (daily weight, monitor i&O, measure abdom girth, observe ankles/fingers for swelling.
.elevate HOB to assist w breathing and limit Na intake.
.check apical HR before Digitalis, HOLD if <60.
.diuretics in AM
.periods of rest after activity

113
Q

Cardiomyopathy, 3 types

A

Disease of myocardium

  1. Dilated (most common)
    • Causes diffuse cellular necrosis and fibrosis
    • Leads to decreased contractility (systolic failure)
  2. Hypertrophic (rare)
    • A chronic disorder in which the heart muscle becomes abnormally
    thick.
  3. Restrictive cardiomyopathies lead to decreased
    distensibility and ventricular filling (diastolic failure)
114
Q

HF NURSING DX

A

• Altered cardiac and peripheral circulation related to
decreased cardiac output
• Ineffective tissue perfusion from altered circulation
• Anxiety related to lack of knowledge and fear of the
unknown
• Activity intolerance related to decreased cardiac
output

115
Q

PAC

A

Preatrial Contraction

normal electrophysiological phenomenon

frequent PACs may cause palpitations, or sense of “skipping a beat”

can trigger afib, aflutter etc.

116
Q

Atrial Fibrillation (Afib)

A

Electrocardiogram
– Chaotic activity from the AV node
– No true P wave visible
– Irregular ventricular rhythm

TX:
– Anticoagulant therapy due to risk of stroke
– Antidysrhythmic drugs
– Cardioversion to treat atrial dysrhythmia
– Ablation of atria

117
Q

Preventricular Contraction

A

Ectopic firing

118
Q

Ventricular Tachycardia

A

Electrocardiogram
– Wide bizarre QRS
– Pulse erratic and with impaired cardiac output
Treatment:
– Synchronized cardioversion if pulse present
– If no pulse, treat as ventricular fibrillation
– Antidysrhythmics

119
Q

Ventricular Fibrillation

A 
Cardiac Emergency
Electrocardiogram
– Irregular undulations of varyious amplitudes from coarse
to fine
– No cardiac output
Treatment:
– CPR
– Defibrillation as quickly as possible
– Antidysrhythmic drugs
120
Q

Myocardial Infaction

A

Part of myocardium permanently destroyed

• Caused by reduced blood
flow in coronary artery
• Due to rupture of
atherosclerotic plaque
• Subsequent occlusion of
artery by thrombus
121
Q

ACS, Acute Coronary Symdrome

A

Unstable Angina: plaque rupture, but artery not completely occluded

or also

• Vasospasm (sudden
narrowing)
• Decreased oxygen supply
(from acute blood loss,
anemia, or low BP)
• Increased demand for 02
(rapid heart rate,
thyrotoxicosis, or ingestion
of cocaine)
122
Q

Cardiac Markers for Dx and MI

A
  1. Troponin (cTc1 and cTnT) – will be evident 3-4 hours after a
    heart attack, peak in 12-16 hrs and stay elevated for 2 – 3
    weeks
  2. Myoglobin (Mb) can elevate in other conditions; troponin
    level is taken to confirm MI (1-3 hrs and peaks in 12 hrs)
  3. Creatine kinase (CK), an enzyme found in heart muscle cells
    and other cells of the body, so a more specific level of
    elevation in cardiac cell must be obtained (peaks in 24 hrs)
123
Q

3 Cardiac Markers for MI

A
  1. Troponin, 3-4 hrs after attack
  2. Myoglobin
  3. Creatine Kinase
124
Q

Electrocardiogram

A

note dysrhythmias, changes in T wave and SG segment and presence of Q wave

125
Q

Echocardiogram

A

to assess cardiac muscular function and valves

126
Q

Types of Schock

A

Cardiogenic: loss of heart ability to pump

Hypovolemic: loss of blood

Distributive: loss of vascular tone

127
Q

Cardiogenic Shock SS

A

.sinus tachycardia, weak, thready pulse, tachypnea
.S3 and S4 heart sound
.hypotension
.Oliguria (<30ml/hr)

NI: NPO, reduce risk of aspiration
.admin/monitor fluids to avoid fluid overload
.admin 02 to maximize cardiac
.mon pulmonary and renal fx
.monitor intra-aortic balloon pump (IABP)
.Digitalis
.Vasoconstriction agents
.dopamine
128
Q

Iron Deficiency Anemia

A

MEN: Normal 13-31 Umole/L

WOMEN: 11-29 umole/L

129
Q

Megaloblastic Anemia

A

.caused by deficiencies of Vit B12 or Folic Acid
.changes in bone marrow, peripheral blood
.abnormally large Erythrocytes called Megaloblastic red cells

SS: weakness, listlessness, fatigue

NI: DO NOT admin RBC transfusion because body w compensate and go into fluid overload.

130
Q

Low Hemoglobin

A

heart compensates by pumping faster/harder to deliver more blood to hypoxic tissue

SS: tachy, palpitation, dyspnea, dizzy, orthopnea, exertional dyspnea

131
Q

Sickle Cell Disease

A

.inherited Autosomal Recessive disorder of HgB
.African/eastern mediterranean descent
.after 6 mos age
.hemoglobin S replace all or part of normal HgB, causes RBCs to sickle w O2 is released into tissue

132
Q

Sickle Cell Anemia

A

if both parents have sickle cell train, children may inheri 2 abnormal HbS genes and w have sickle cell anemia, most severe form of disease

133
Q

Sickle Cell Anemia SS

A

.bone marrow expand in childhood, compensate to offset anemia

.anemia (7-10 g/dL)
.jaundice
.enlarged facial bones and skull
.tachy, enlarged heart, murmurs

134
Q

Hand-Foot Syndrome

A

swollen hands

135
Q

Sickle Cell Crisis

A
  1. Sickle cell crisis: tissue hypoxia and necrosis in tissue or organ
  2. Aplastic crisis: infec w human parvovirus
  3. Sequestration crisis: other organs pool sickled cells

Most kids with SC will have a Splenic Infarction by age 10 and it becomes non functional (liver and lungs in adults)

136
Q

Splenic infaction

A

a condition in which oxygen supply to the spleen is interrupted, leading to partial or complete infarction (tissue death due to oxygen shortage) in the organ. Splenic infarction occurs when the splenic artery or one of its branches are occluded, for example by a blood clot.

137
Q

Acute Chest Syndrome

A

Rapid decrease in hemoglobin, fever, tachi, bilateral inflitrates
.mimics infection but are infarctions withing pulmonary

Image result for acute chest syndromethorax.bmj.com

138
Q

Pulmonary HTN

A

sequel to sickle cell disease

139
Q

4 Sickle Cell Txs

A 
.Bone Marrow Trans
.Hydroxyurea: (Hydrea):
chemotherapy
agent – increases
hemoglobin F levels
and decreased
formation of sickled
cells
.Arginine: antisickling
properties;
used in combination
with Hydrea to
manage pulmonary
hypertension
.Long-term RBC transfusions
140
Q

Sickle Cell NI’s

A

manage pain, swollen joints, elevate extremities
.relaxation
.manage infection
.promote coping skills

141
Q

Chronic myeloproliferative disorder

A 
• Increased RBCs
• .Leukocytosis
• Thrombocytosis
• Increased hemoglobin concentration
• Occurs between ages 40-60 in males of Jewish ancestry
(mortality high if not treated)
142
Q

Polycythemia SS & TX

A 
SS:
• Clubbing of digits
• Dizziness
• Headache
• Hypertension
• Ruddy cyanosis of nose
• Thrombosis of smaller
vessels
• Visual disturbances
Tx:
• Phlebotomy
• Chemotherapy
• Myelosuppressive drugs
• Anti-gout agents
(Allopurinol)
• Replace fluid volume lost
during procedure
143
Q

Polycythemia SS & TX

A 
SS:
• Clubbing of digits
• Dizziness
• Headache
• Hypertension
• Ruddy cyanosis of nose
• Thrombosis of smaller
vessels
• Visual disturbances
Tx:
• Phlebotomy
• Chemotherapy
• Myelosuppressive drugs
• Anti-gout agents
(Allopurinol)
• Replace fluid volume lost
during procedure
144
Q

Idiopathic Thrombocytopenic Purpura (ITP)

A

Auto Immune

.Idiopathic

SS:
– Too few platelets
– Bruising, petechiae, and internal
bleeding

TX:
– Steroids
– Immune globulins
– Splenectomy

145
Q

Thrombocytopenio: Low Platelet Count

A

.lo platelet production in marrow
.up destruction of platelets
.up consumption of platelets

SS: .<20K/mm3 petechiae
.nasal/gum bleeding
.hi menstrual bleed
.monitor dental and Sx.

Tx:
.teach avoid substance that lo platelet fx. (i.e. otc meds, herbs, supplements etoh)
.inform med providors

146
Q

Disseminated Intravascular Coagulation (DIV)

A

massive amt of tiny clots form in microcirculatotion

triggered by: trauma, sepsis, shock, ca, abruptio placentae, toxins, allerg reactions

Initially normal clotting time, then as the many clots forming use u the plateletes and clotting factors, coag time starts to fail.

PARADOXICAL result of up clotting is bleeding

147
Q

DIC more

A

pt bleed from mucous membranes, venipuncture site, gi, urinary tract

148
Q

Hemophelia

A

bleeding disorder, males

contracted by x-linked recessive chromosome (mother carrier)

normla factor activity 50-200%, Hemophelia 0-25%

Dx: PTT prolonged, factor VIII assays <25% of normal factor

149
Q

class 2, pg 80

150
Q

AICD:Automatic Implanted Cardioverter Defibrillator:

A

A
device that detects and terminates life-threatening
episodes of ventricular tachycardia (VT) or fibrillation
(VF)

151
Q

Pacemaker

A

an electronic
instrument that supplies
electrical stimuli to the heart
muscle

152
Q

Intra-Aortic Balloon Pump (IABP)

A

.facilitate UP myocardial O2 supply

.LO myocardial O2 demand

153
Q

IABP Compmlications

A 
Transient loss of
peripheral pulse
Limb ischemia;
compartment
syndrome
Thromboembolism;
cardiac tamponade
Compartment
syndrome
Aortic dissection
Local vascular injury—
false aneurysm,
hematoma, bleeding
from the wound
Infection
Balloon rupture (can
cause gas embolus) or
balloon entrapment
Hematological
changes, i.e.,
thrombocytopenia
Malpositioning causing
cerebral or renal
compromise
154
Q

IABP NI

A

.monitor pulmonary pressure
.treat arrhythmias. >106
.monitor HgB and Hct for anemia
.monitor complication of cardiogenic shock
.monitor for impending renal compromise <30cc/hr

155
Q

Intracoronary Stent

A

stent placed in artery to maintain patency.

156
Q

Stent complication

A 
.bleeding/hematoma
.weak pulse distal to insertion site
.pseudoaneurysm and arteriovenous fistula
.retroperitoneal bleeding
.acute renal failure
157
Q

Normal ABGs

A

pH 7.35 – 7.45 Kids 7.36 – 7.44
PCO2 34 – 45 mmHg (ACID)
PO2 80 – 100 mmHg
HCO3 21 – 28 mEq/L (BASE)

158
Q

Respiratory Acidosis

A

response to HYPOventilation

  1. pH < 7.53
  2. PaCO2 > 45mmHg
  3. UP CO2, UP Carbonic Acid
  4. Hyperkalemia

COMPENSATION:
.UP respirations to blow off CO2
.Bicarb UP to compensate

Med Tx:
Calcium, Insulin, glucose, NaO2, Dialysis

159
Q

Acidosis SS

A

h/a, sleepiness, confusion, loc, coma, sob, cough, seizure, weakness, diarrhea, arrhythmia, up hr, N/V

160
Q

Causes of Resp Acidosis

A

Hypoventilation

.severe pna, ards, impairment of resp muscles, pulmonary edema, aspiration of foreign object, atelectasis, pneumothorax, od sedatives, sleep apnea, non therapeutic O2, COPD pts

161
Q

COPD and Chronic Hypercapnia

A

COPD pts gradually accumulate CO2 over time, may not develop hypercapnia d/t compensatory renal changes.

162
Q

Respiratory Alkalosis

A

Carbon Acid deficit

lo CO2, decrease in acid, UP pH >7.45, PaCO2 < 38mmhg

.HYPERventilation, LO CO2

.Lo Carbonic Acid

163
Q

Causes of Respiratory Alkalosis

A 
.extreme anxiety
. blow off excess CO2
.Hypoxemia
.Gram Neg bacteremia
.salicylate intox, ventilator settings
164
Q

SS of Respiratory Alkalosis

A

ha, sleepy, confusion, loc, coma, sob, cough, arrhythmia, up hr, seizures, weakness, n/v/d, light headed, stupor, coma, hand tremor, parestesia, twitching, spasms,

165
Q

Respiratory Alkalosos

A

Dx:
.UP Ph >7.45
.

166
Q

continue on Pg 25

167
Q

Adult Respiratory Failure (ARF)

A

sudden, life threat

deterioration of gas exchange of O2 for CO2 in lungs

can not keep up w rate of O2 consumption and CO2 production

CONDITION not a disease.

any disease w disorder of nerves, spinal cord, muscles or neuromuscular junction involved in respiration

Muscular dystrophy, myasthenia gravis, poliomyelitis,
ALS (amyotrophic lateral sclerosis, Guillain-Barre
syndrome, and cervical spinal cord injuries

168
Q

Chronic Respiratory Failure (CRF)

A

CRF is a deterioration in the gas exchange function of the
lung, which develops insidiously, OR has persisted for a long
period after an episode of ARF

169
Q

Acute Respiratory Distress Syndrome

A

severe form of acute lung injury

Major cause of death: non pulmonary multiple system organ failure

170
Q

Suctioning

A

.apply suction ONLY when REMOVING catheter, gently rotating while withdraw

.NO more than 10-15sec, 3-4 times

.O2 1-2 min before and after suction

171
Q

O2 Administration

A

Nasal Cannula, Simple face mask, non rebreather mask, partial rebreather mask, , venturi mask

172
Q

PNA risks

A

pt w

.alteration in LOC
.LO/NO gag reflex
.immobile

Raise head of bed when feeding.

173
Q

PNA

A

Inflammation of lower resp track.

Bacterial, Viral, Fungal (rare), Chemical

174
Q

Types of PNA

A

.community acquired
. hospital acquired
.PNA in immunocompromised host
.aspiration pna

175
Q

CAP

A

Community Aquired PNA

.reside naturally in upper resp tract, then colonizes.
.causes lobar or bronchopneumonia
. after recent resp illness

176
Q

PNA SS

A 
Streptoccal (pneumococcal) PNA: 
.sudden onset of chills
.rapid fever (101-105)
.patient severely ill
.tachypnea (25-45bmp)
.UP plulse
177
Q

VAP

A

Ventilator Assisted PNA

178
Q

VAP SS

A 
.bradycardia (viral)
.mycoplasma infection
.legionella organim
.may URI, Mucopurulent sputum
.h/a, lo fever, pleuritic pain, myalgia, rash, pharyngitis

.SEVERE: flushed cheeks,

OLDER adults: .lethargy, confusion, anorexia, rapid hr
.pain/dullness during percussion over affected lung area
.bronchial breath sounds, crackles

Xray: infiltrates w consolidation or pleural effusion

179
Q

PNA NIs

A 
.monitor abx
.deep breathing q 2hrs
.humidity to loosen secretions
.suction airway PRN
.up to 3L/day fluid
.encourage flu shot
180
Q

Chronic Bronchitis

A 
.chronic sputum w cough production on daily basis for min of 3 mos - 1yr
.chronic hypoxemia
. UP mucous
.UP bronchial wall thickness
.
181
Q

Blue bloater

A 
chronic bronchitis
.excessive mucous
.airway obstruction
.hypoxia
.residual lung volume UP
182
Q

Pink Puffer

A 
emphysema
.hyperventilation
.muscle wasting
.weight loss
.less hypoxia, work neck and chest muscles
183
Q

Tripod Position

A

sitting in chair, hands on knees (tripod)

184
Q

TB

A

infection w Mycobacterium Tuberculosis bacteria
.AIRBORNE
.after initial exposure, bacteria encapsulates (form GHON lesion)
.bac dormant until later when ss appear.

185
Q

TB SS

A 
.asymptomatic
.fever, night sweats
.anorexia
.malaise
.cough, sputum
.dyspnea, pleuritic chest pain
.cavitation or calcification per Xray
.positive sputum culture
186
Q

TB Skin Test

A

Bacillus Calmette Guerin (BCG) vaccine test w be positive

positive = induratio 10mm or greater in 48-72hrs

187
Q

TB NIs

A 
• Risk for infection
• Ineffective Airway Clearance
• Activity Intolerance
• Anxiety
• Imbalanced nutrition: less than
body requirements
• Impaired Gas Exchange
• Knowledge deficit
188
Q

TB Interventions

A 
.H, isolation
.cough into tissue and dispose immediately in to special basket
.meds for 9-12mos
.hand washing
.report ss of deteriorating/hemorrhage
.collect sputum culture
.return to work after 3 neg cultures
189
Q

Cystic Fibrosis

A

.Autosomal recessive disease, cause dysfx of exocrine gland
.tenacious mucus production, obstructs vital structures
.lung insufficiency
.pancreatic insuff
.UP los of Na+ and Cl- in sweat

190
Q

Cystic Fibrosis SS

A

usually dx in white infant or child

.meconium ileus at birth (10-20%)
.chronic resp infection
.pulmonary congestion
.steatorrhea (fatty stool)
.foul smelling stool
.LO growth and weight
.skin salty when kissed
191
Q

Cystic Fibrosis NIs

A

.monitor respiration
.IV abx
.pancreatic enzymes
.fat soluble vits A, D, E, K in water soluble form
.nebulizer and O2 tx
.percussion and postural drainage
.DIET: HI cal, HI protein, MOD/HI fat, MOD/LO carbs

child needs 150% of usual calorie intake for normal growth and dev.

192
Q

Sleep Apnea

A

sleeping, loud snoring, breathing cessation for 10sec or longer
.awaken abruptly w loud snort as O2 level drops
.5-several hundred events per night.
.HI risk for CAD, cerebrovascular disease, premature death
.repeated apneic events cause hypoxia and hypercapnia
.daytime sleepiness and fatigue

193
Q

Types of Sleep Apnea

A

Central and Obstructive

194
Q

Obstructive Sleep Apnea

A

most common
.reduced diameter of upper airway or reduced upper airway muscle tone

TX: nasal CPAP or BiPAP w supplemental O2 for severe hypoxia and hypercapnia

.weight loss recommended for obese
.no ETOH and sedatives

195
Q

Central Sleep Apnea

A

simultaneous suspension of both airflow and respiratory mvmt

Sx:
– Uvulopalatopharyngoplasty to correct obstruction
– Tracheostomy to bypass obstruction for respiratory failure
or life-threatening dysrhythmias; unplugged during sleep

NI:
.avoid ETOH and respiratory suppressive drugs
.weight loss
.notify re potential daytime sleepiness

196
Q

Sleep Apnea MEDS

A

• Modafinil (Provigil) to reduce daytime sleepiness
• Protriptyline (Triptil) HS to increase respiratory drive;
improve upper airway muscle tone
• Patient may require nasal continuous positive airway
pressure (CPAP)

197
Q

Childhood Upper Airway Disorders

A 
.Croup
.Epiglottis
tis
.Laryngotracheobronchitis
.Spasmodic Laryngitis
.Tracheitis
198
Q

Epiglottitis

A

infection of epiglottis. caused by H. Influenzae type B

SS:
.sudden onset
.restlessness
.hi fever
.dysphagia
.drooling
.muffled voice
.child assumes upright position w chin out and tongue protruding
199
Q

Epiglottitis

A

• Epiglottis cherry red, swollen and edematous and
can obstruct airway
• Secretions pool in pharynx and larynx above
epiglottis
• Child has sore throat and unable to swallow
• Can have airway obstruction within 2-6 hours
• Hib vaccine has reduced incidence

200
Q

Bronchiolitis

A

RSV, Respiratory Syncytial Virus

.young infants
. HIGHLY contagious
.thick secretions
.paroxysmal coughing, nasal flaring, prolonged expiratory phase, wheezing, rales
.deteriorates to rapid, shallow respiration

201
Q

Bronchitis NIs

A 
.upright position
.intubation/Trach
.IV abx
.NPR, I7o
.antipyretics, cotiscosteroids to decrease edema
.manage sore throat pain
202
Q

Croup in kids

A

Laryngotracehobronchitis

203
Q

Laryngotracheobrochitis

A

viral infection

inflammation, edema and narrowing of larynx, trachea and bronchi
.3mos - 8yrs
.most common croup syndrome
.inspiratory stridor and suprasternal retractions upon inhalation (barking cough)

204
Q

Tonsilitis ss

A 
sore throat
fever
snoring
diff swallow
enlarged adenoids cause mouth breathing, head colds, earaches
205
Q

SARS

A

Severe Acute Respiratory Syndrome

206
Q

SARS

A

.discovered asia, 2/2003
.RESPIRATORY, droplet
.spread by contaminated surfaces then touching mucous membranes

207
Q

SARS SS

A 
.HI fever
.H/a
body aches
.mild respiratory ss
. 10-20% have diarrhea
.after 2-7 days, dry cough
208
Q

SARS Contaigion

A 
• More contagious when
symptoms present
• Most contagious during
second week of illness
• Limit contact until ten days
after fever no longer
present and respiratory
symptoms improved
• Treatment same as CAP
209
Q

Nursing Process

A

ADPIE

Assess
Dx
Planning
Implementation
Evaluation
210
Q

Leading Cause death for MEN

A

Lung, Prostrate, Colorectal

211
Q

Leading Cause death for WOMEN

A

Lung, Breast, Colorectal

212
Q

Cell membrane of malignant cells contain

A

proteins tha develop over tikme called “tumor-specific antigens” i.e. prostate-specific antigen (psa)

213
Q

Malignant Cells

A

.grow and divind w glucose, O2

.mali`gnant cells us ANEROBIC metabolism

214
Q

Malignant cells attatch to endothelium and

A

attract fibrin, platelets and clotting factors to seal off from immune system.

Endothelium retracts, mal cells secret LYSOSOMAL ENZYME tha destroys body sys and allow implantation

215
Q

Angiogenesis

A

development of new capillaries from host tissue by release of growth factors and enzymes
such as vascular endothelial growth factor (VEGF)

.These proteins rapidly stimulate formation of new
blood vessels that help malignant cells obtain
nutrients and oxygen
• Through vascular network, the tumor emboli enter
systemic circulation and travel to distant sites.
Therapies target VEGF or its receptors.

216
Q

Carcinogenesis

A

malignant transformation

.Imitation: chemicals, physical factors, biologic agents, escape normal enzymatic mechanisms
and alter genetic structure of cellular DNA

.Promotion: repeated exposure to promoting agents (co-carcinogens) causes expression of
abnormal or mutant genetics information (different latency periods)

.Progression: • cells that changed during imitation and promotion invade adjacent tissues and
metastasize

LPN to RN (13 decks)

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