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patho > exam 3 > Flashcards

exam 3 Flashcards

1
Q

endothelial cells

A

hyper/hypotension

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2
Q

lumen

A

diameter of a blood vessel

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3
Q

endothelium

A

controls vascular function, platelet function, platelet adhesion, blood clotting, modulation of flow, vascular resistance, regulation of immune and inflammatory responses

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4
Q

Systole

A

-contraction
-BP rises
-left ventricle contracts

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5
Q

diastole

A

-relaxation
-BP falls
-the heart relaxes

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6
Q

systolic pressure

A

-less than 120 mm Hg in adults
-rapid upstroke occurs during LV contraction

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7
Q

diastolic pressure

A

less than 80 mm Hg
-lowest pressure

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8
Q

mean arterial pressure (MAP)

A

-average pressure in arterial system during ventricular contraction and relaxation
-indicator of tissue perfusion
-est 90-100 mm HG in adults

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9
Q

vagal stimulation- neuro

A

bradycardia

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10
Q

sympathetic stimulation-nuero

A

tachycardia

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11
Q

baroreceptors-nuero

A

-pressure sensitive receptors located in walls of blood vessels
-carotid and aortic baroreceptors effects changes in heart rate, contraction, and vascular tone

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12
Q

blood pressure regulation: Humoral

A

-RAAS
-Vasopressin (ADH)
-epinephrine-norepinephrine

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13
Q

systolic and diastolic actions

A
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13
Q

disorders of systemic arterial blood flow

A

disease of the arterial system affects the body function by impairing blood flow
-the effect of impaired blood flow on the body depends on the structures involved and the extent of the altered flow

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13
Q

ischemia!

A

reduction in arterial flow to a level that is insufficient to meet the oxygen demands of the tissues

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14
Q

infarction!

A

an area of ischemic necrosis in an organ produced by occulusion of its aterial blood supply or its venous drainage

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14
Q

hyperlipidemia

A

elevated levels of lipids in the blood
-cholesterol, triglycerides, phospolipids)

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14
Q

dyslipidemia

A

condition of imbalance of lipid components of the blood

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15
Q

VLDL

A

very low density lipoprotein
carries large amounts of triglycerides

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16
Q

low density lipoprotein (LDL)!

A

-atherogenic (forms plaques in intima layer of arteries)
-carry cholesterol to the peripheral tissues
-“bad” cholesterol

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17
Q

High-density Lipoprotein (HDL)!

A

-protective
-remove cholesterol from the tissues and carry it back to the liver for disposal
-cardioprotective because it carries cholesterol away from artery walls to be excreted
-“good” cholesterol

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18
Q

primary dyslipidemia

A

genetic basis

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19
Q

secondary dyslipidemia

A

dietary, obesity, type II diabetes
-other factors

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20
Q

metabolic syndrome

A

-elevated fasting blood glucose
-elevated BP
-elevated waist circumference
-dyslipidemia

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21
Q

atherosclerosis

A

formation of fibrofatty lesions in intimal lining of large and medium sized arteries

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22
Q

major risk factor of atherosclerosis

A

hypercholesterolemia (elevations of LDL)
-other risk factors: smoking, obesity, hypertension, diabetes

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23
Q

modifiable atherosclerosis!

A

hypercholesterolemia
-lifestyle changes
-diet

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23
Q

nonmodifiable atherosclerosis!

A

age, family history, male sex, genetics, post-menopause

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24
Q

fatty streaks: artherosclerosis

A

thin, flat yellow intimal discolorations that progressively enlarge

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25
Q

fibrous atheromatous plaque:artherosclerosis

A

the accumulation of intracellular and lipids, proliferation of vascular smooth muscle cells, and formation of scar tissue

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26
Q

complicated lesion: artherosclerosis

A

contains hemorrhage, ulceration, and scar tissue deposits

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27
Q

lesions with atherosclerosis

A

as lesion increase in size, lumen of the artery decreases (the artery constricts)

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28
Q

developmental stages of atherosclerosis

A

endothelial cell injury, migration of inflammatory cells,lipid accumulation and SMS proliferation, plaque structure

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29
Q

endothelial cell injury

A

endothelial injury occurs and then the monocytes and platelets adhere

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30
Q

migration of inflammatory cells

A

inflammatory cells initiate atherosclerotic lesions and then monocytes transform into macrophages which engulf lipoproteins and cause “foam cells”

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31
Q

lipid accumulation and smooth muscle cell proliferation

A

progressive accumulation of foam cells leads to lesion progression leading to migration of SMCs and foam cells die leading to necrotic debris in the vascular wall

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32
Q

plaque structure

A

aggregation of SMCs macrophages, leukocytes, collagen forms a fibrous cap (the shoulder)

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33
Q

plaque structure!

A

rupture, ulceration, or erosion of an unstable of vulnerable fibrous cap leads to hemorrhage into the plaque or thrombotic occlusion

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34
Q

atherlosclerosis clinical manifestations

A

-narrowing of the vessel (the lumen) and production of ischemia
-sudden vessel obstruction due to plaque hemorrhage or rupture
-thrombosis andn formation of emboli resulting from damage to the vessel endothelium
-aneurysm formation due to weakening of the vessel wall

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35
Q

atherosclerosis complications

A

larger vessels= complications are thrombus formation and weakening of the vessel wall
-medium sized arteries (coronary and cerebral) = ischemia and infarction due to vessel occlusion is more common
-arteries supply the heart, brain, kidneys, and lower extremeties and small intestine are most frequently involved

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36
Q

aneurysm

A

-abnormal localized dilation of a blood vessel that occurs in arteries and veins, most commonly in the aorta
-classified according to cause, location, anatomic features

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37
Q

aneuysm etiology

A

congenital, trauma, infection, atherosclerosis

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38
Q

aortic aneurysm etiology

A

ascending, aortic arch, descending, thoracoabdominal aorta, or abominal aorta
-elevated lipids, HTN, smoking

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39
Q

aortic aneurysm clinical manifestations of a thoracic !

A

back, neck pain, hoarseness, brassy cough

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40
Q

aortic aneurysm clinical manifestations of a abdominal !

A

pulsating mass, mid abdominal or lumbar discomfort or back pain, may impinge on renal, iliac, or vertebral arteries that supply the spinal cord!

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41
Q

aortic dissection

A

acute, life threatening
-hemorrhage into vessel wall with longitudinal tearing of the vessel wall

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42
Q

aortic dissection etiology

A

hypertension, degeneration of medial layer of vessel wall leading to changes in elastic and smooth muscle layers

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43
Q

Aortic dissection clinical manifestations

A

excruciating pain from tearing, anterior chest, back, elevated BP (will become unatainable in one or both arms as the dissection disrupts arterial flow to arms), syncope, paralysis, heart failure

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44
Q

acute arterial occlusion etiology/patho

A

sudden event that interrupts arterial flow
-result of embolus or thombus

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45
Q

arterial occlusion :emboli

A

atrial fibrillation, ischemic heart disease
-fat, amniotic, air emboli
-emboli lodge in bifurcation of major arteries

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46
Q

acute aortic occlusion manifestations

A

pallor, pain, pulselessness, paresthesia, paralysis, polar

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47
Q

atherosclerotic occlusive disease (peripheral artery disease) etiology

A

common in lower extremity vessels (femoral, popiteal)
-advanced age
-cigarette smoking, diabetes

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48
Q

atherosclerotic occlusive disease (peripheral artery disease) manifestations

A

gradual s/s, intermittent claudications (pain w walking)- calf pain because highest oxygen consumption
-vague aaching/numbness
-atrophic changes
-weak pedal pulses
-ischemic pain at rest, ulceration, gangrene, necrosis

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49
Q

thromboembolism

A

venous thrombosis: presense of thrombus in vein and inflammation

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50
Q

thromboembolism etiology

A

stasis of blood- immobilization, venous pooling
-hypercoagulability, factor V leiden, BCP, smoking, cancer
-vessel wall injury- trauma, surgery, infection/inflammation

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51
Q

thromboembolism manifestations

A

pain, swelling (calf, posterial, tibial) deep muscle tenderness, inflammation
-asymptomatic

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52
Q

chronic venous insufficiency

A

persisent venous hypertension on the structure and function of the venous system of the lower extremities

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53
Q

chronic venous insuffienciey etiology

A

prolonged standing, incompetent valves, DVT, inflammation, endothelial dysfunction

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54
Q

chronic venous insufficiency manifestations

A

tissue congestion, edema, impaired tissue nutrition, skin atrophy, brown pigmentation, stasis dermatisis (thin, shiny, bluish brown, irregulary pigmented skin)

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55
Q

stages of chronic venous disease

A

C1- spider veins
c2- varicose
c3- swelling
c4- skin changes
c5-6- venous ulceration

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56
Q

disorders of BP regulation

A

-BP must be closely regualted throught the body to ensure adequate perfusion of body tissues adn to prevent damange to blood vessels

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57
Q

low BP

A

tissues dont receive sufficient blood flow to ensure delivery of nutrients and oxygen and removal of cellular wastes- hypoxic ischemia

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58
Q

high BP

A

can damage endothelial tissue, increasing likelihood of both atherosclerotic vascular disease and vascular ruptures

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59
Q

hypertension

A

sustained condition of elevation of the BP within arterial circuit

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60
Q

hypertension etiology

A

primary (essential) HTN: clinical presence of HTN without evidence of specifc causitive condition
secondary HTN: caused by medical condition such as renal failure

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61
Q

primary HTN risk factors/etiology non modifiable

A

age, gender, race, fam history, genetics

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62
Q

primary HTN etiology modifiable

A

dietary, dyslipidemia, tobacco, alcohol consumption, fitness, obesity, Blood glucose diabetes, OSA

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63
Q

secondary HTN: risk factors

A

erythropoietin, renal HTN/disease, disorders of adrenal cortical hormones, oral contraceptive use, cocaine, amphetamines

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64
Q

clinical consequences of HTN

A

HTN increses the workload of the left ventricle, increasing the pressure against which heart must pump as it ejects blood

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65
Q

clinical consequences of HTN on organs

A

heart- angima, AMI, heart failure
brain- stroke
kidney- chronic disease
eye- blindness

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66
Q

normal BP

A

less than 120 and less than 80

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67
Q

elevated BP

A

120-129 and less than 80

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68
Q

stage 1 HTN

A

130-139 or 80-90

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69
Q

stage 2 HTN

A

over 140 or over 90

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70
Q

chapter 27

A
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71
Q

disorders of the pericardium
pericarditis

A

inflammation of the pericardium causes severe pain

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72
Q

pericardial sac

A

double layered serous membrane that isolates the heart from other thoracic structures
-barrier to infection

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73
Q

two layers of pericardium

A

1) visceral pericardium (thin)
2) parietal pericardium (fibrous, outer)

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74
Q

two layers separated by potential space

A

pericardial cavity (NML: 50 mL serous fluid)- lubricates, prevents friction

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75
Q

inflammation

A

viral, bacterial, rheumatic fever, uremia, AMI, cardiac surgery

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76
Q

neoplastic disease

A

breast cancer, lung cancer

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77
Q

congenital (from birth)

A

cysts

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78
Q

acute pericarditis etiology

A

viral most common, bacterial, uremia

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79
Q

acute pericarditisis patho

A

inflammation of pericardium, increased capillary permeability

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80
Q

manifestations of acute pericarditis

A

Triad of symptoms: sharp chest pain that radiates to shoulders, neck, back pain (gets worse with deep breathing, positional- releief when sitting up)
-pericardial friction rub
-ECG changes

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81
Q

pericardial effusion

A

-accumulation of fluid in pericardial cavity
-result from infection or inflammation
-small effusion: minimal symptoms
-increases intercardiac pressures

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81
Q

tamonade manifestions

A

-Becks triad!:
muffled heart sounds, jugular venous distention, narrowed pulse pressure (hypotension)

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82
Q

pericardial tamponade

A

compression of the heart due to infections, neoplasms, and bleeding into pericardial sac

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83
Q

coronary artery

A

supplies blood to the heart

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84
Q

coronary artery disease

A

heart disease caused by impaired coronary blood flow

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85
Q

CAD etiology

A

atherosclerosis which causes myocardial infarction, cardiac irrythmias, conduction defects, heart failure, and sudden death

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86
Q

CAD risk factors

A

smoking, elevated BP, elevated serum toal and LDL cholesterol, low HDL, diabetes, age, obesity, inactivity

87
Q

assessment of coronary blood flow

A

12 lead ECG
excercise stress training
echocardiograph
cardiac MRI/CT
cardiac catheterization

87
Q

determinants mv02

A

heart rate, left ventricular contractility, myocardial wall stress (SBP)
-as heart rate goes up, myocardial oxygen consumption and demand increases

88
Q

pathogenesis of CAD

A

atherosclerosis (most common)
-chronic ischemic heart disease
-acute coronary syndrome

89
Q

chronic ischemic heart disease

A

recurrent, transient, myocardial ischemia (intermittent, not permanent)
stable agina: results from narrowing of artery lumen

90
Q

acute coronary syndrome

A

unstable angina, myocardial infarction
near permanent

91
Q

atherosclerotic lesions: fixed/stable plaque

A

obstructs blood flow
-implicated in stable angina

92
Q

atherosclerotic lesions: unstable plaque

A

-worse
-high risk plaque- abrupt changes-ruptures-causes platelt adhesion and thrombus formation
-implicated in unstable angina
-trigger event: emotion distress, physical activity

93
Q

thrombus and vessel occlusion

A

thrombosis after plaque distribution: lipid core provides stimulus for platelet aggregation and thrombus formation
-thrombin and fibrin deposition

94
Q

chronic ischemia heart disease

A

myocardial ischemia occurs when the ability of the coronary arteries to supply blood is inadequate to meet the metabolic demands of the heart
-atherosclerosis vs vasospasm

95
Q

types of CIHD

A

chronic stable angina
variant/vasospastic angina

96
Q

stable angina

A

-fixed coronary obstruction (stable!)
-angina precipitated by situations that increase the workload of the heart
-relieved within minutes by rest or NTG

97
Q

stable angina: angina pectoris !

A

-constricting/squeezing
-precordial/substernal pain
-may radiate to left shoulder, jaw, and arm

98
Q

variant/prinzmetal angina

A

endothelial dysfunction, hyperactive SNS, defects in handling of calcium
-occurs during rest or with minimal exercise
-occurs nocturnally

99
Q

acute coronary syndrome is an umbrella term for

A

unstable angina, non-ST segment elevation (non-Q wave), and ST-segment elevation (Q wave)

100
Q

unstable angina (USA)
nonST segment MI (NSTEMI)
patho- 5stages

A

-unstable plaque ruptures/nonobstructive thrombosis
-obstruction/spasm occurs
-severe narrowing of coronary lumen
-decreased oxygen supply

101
Q

unstable angina (USA)
nonST segment MI (NSTEMI)
patho- 5stages

A

subendocardial (NSTEMI) infarcts involve 1/3 to 1/2 of ventricular wall (severerly narrowed but patent arteries)

102
Q

unstable angina (USA)
nonST segment MI (NSTEMI)
three clinical features

A

-occurs at rest lasting move then 20 minutes if not interrupted by NTG
-severe pain, new onset
-more severe, prolonged, or frequent then previously experienced

103
Q

ST-segment elevation MI (STEMI)

A

-ischemic death of myocardial tissue
-complete coronary occlusion
-area of infarction determined by coronary artery affect and by its distribution of blood flow, duration of occlusion, metabolic needs, collateral circulation

104
Q

STEMI patho

A

transmural stemi infarcts: involve full thickeness of ventricular wall (obstruction of single artery)
-aerobic- anaerobic metabolism:unable to sustain normal function
-loss of contractile function within 60 seconds
reversibile changes if blood flow restored- after 20-40 minutes of severe ischemia is irreversible the pump fails
-ventricular remodeling occurs

105
Q

STEMI/ Acute corornary syndrome manifestations

A

-abrupt onset
-someones sitting on my chest
-severe crushing, constricting, suffocatnig
-radiation to left arm, neck, jaw
-STEMI progression from NSTEMI
-prolonged, no relief from resting
-GI/ N/V
-fatigue
-pale, cool, moist skin
-impending doom
-sudden death within an hour (fatal arrythmia)

106
Q

ECG changes NSTEMI

A

non-stemi= no st wave
-st segment depression
-may be transient st segment elevation

107
Q

ECG changes STEMI

A

-st segment elevation
-t wave inversion
-Q wave (goes down)

108
Q

diagnosis ACS

A

-ECG first time sensitive
-troponin 1 (Tn1) and troponin 2 (TnT): MORE SPECIFIC (increase withing three hours)
-creatinine kinase MB (CK-MB)- less specific-found in muscle cells (4-8 hours)
-coronary angiography, stress testing

109
Q

infection endocarditis

A

potentially life threatening

110
Q

infectious endocarditis patho

A

colonization or invasion of the heart valves and endocardium
-formation of bulky, friable vegetations, and destruction of underlying cardiac tissues
-septic emboli: carried by the blood stream- initiate infection or ischemia in remote tissues

111
Q

infectious endocardititis etiology

A

staphylococcal infections

112
Q

portal of entries that the organism gains access to the circulatory system

A

valvular disease, prosthetic valves, congential heart defects provides an environment conducive to bacteria growth
-oral lesions, dental procedures

113
Q

infectious endocarditis; manifestations

A

fever, chills, petechiae, splinter hemorrhages, cough

114
Q

function of heart valves

A

promote directional flow of blood through the chambers of the heart

115
Q

etiology of valvular disorders

A

-congenital
-trauma
-ischemic damage
-degenerative changes
-inflammation

116
Q

mechanical disruptions: stenosis

A

-narrowing of the valve opening– valves do not open properly (gets stuck)
-increasing resistance to blood flow through the valve

117
Q

mechanical disruptions: regurgitation

A

-distortion of the valve– valve does not close properly
-permits backward flow to occur when the valve should be closed

118
Q

mitral valve

A

left atrium to the left ventricle
-paroxysmal nocturnal dyspnea, orthopnea, DOE, CP, fatigue

119
Q

mitral valve stenosis

A

-incomplete opening of mitral valve during diastole
-left atrial distention, impaired ventricle filling
-etiology: rheumatoid heart disease

120
Q

mitral valve regurgitation

A

-incomplete closure
-LF stroke volume- 1/2 goes foward 1/2 goes backward back into lungs
-etiology: rheumatoid heart disease

121
Q

mitral valve prolapse

A

floppy valve which balloon back into left atrium during systole

122
Q

aortic valve stenosis etiology

A

-congenital valve malformation, acquired calcification “wear and tear”

123
Q

aortic valve stenosis patho

A

-increases restitance to ejection of blood from LV into aorta
-calcification develops gradually– LV has time to adapt
-LV wall becoming thicker– obstruction to forward flow

124
Q

aortic valve stenosis manifestations

A

severe obstruction causes progressive pressure overload–increased heart workload–signs of heart failure

125
Q

aortic valve regurgitation patho

A

result of an incompetent valve that allows blood to flow back into LV during diastole
-LV must increase its stroke volume to include blood entering from the lungs as well as that leaking back through the regurgitant valve

126
Q

aortic valve regurgitation etiology

A

IE, trauma, aortic distention

127
Q

aortic valve regurgitation manifestions

A

dyspnea, orthopnea, abnormal drop is diastolic pressure leads to decreased perfusion

128
Q

heart failure

A

complex syndrome
-related to functional or structural disorder of the heart– manifestations of low cardiac output and pulmonary or systemic congestion (if blood cant get back into the LA, can go back into the lungs)

129
Q

function of the heart pertaining to heart failure

A

move deoxygenation blood from the venous system through the right heart into the pulmonary circulation
-move oxygenated blood from the pulmonary circulation through the left heart and into atrial circulation

130
Q

heart failure etiology

A

-coronary artery disease, hypertension, dilated cardiomyopathy, valvular heart disease

131
Q

cardiac output – how to find

A

cardiac output (amount of blood ejected by ventricle per min)= HR (balance between SNS and PNS) x stroke volume (amount of blood ejected each heart beat)

132
Q

preload

A

volume of blood in the ventricle at teh end of disastole
-volume of blood stretching the heart muscle at the end of diastole–determined by venous return to the heart

133
Q

afterload

A

the amount of resistance that the ventricle must overcome in order to eject blood out of the heart
-peripheral vascular resitance
-ventricular wall tension

134
Q

myocardial contractility (inotropy- heart ability to contract)

A

the contractile performance of the heart
-contractility increases cardiac output independent of preload and afterload
-requires ATP and calcium

135
Q

ejection fraction (EF)

A

should be between 55-70%
determines systolic vs. diastolic dysfunction

136
Q

systolic dysfunction

A

decrease in myocardial contractility
-decreased EF less than 40%
-ischemic heart disease
-valvular disorder
-HTN
-weak LV cannot pump blood forward

137
Q

diastolic dysfunction

A

EF is preserved
-contraction is normal but ventricular relaxation is impaired
-pericardial effusion, HCM (increase wall thickness)
-aging
-less filling of blood in LV

138
Q

right sided heart failure etiology

A

Left ventricle failure pulmonary hypertension, pulmonary embolus

139
Q

right sided heart failure patho

A

inability to move deoxygenated blood from systemic circulation into pulmonary circulation– then to left side–reduction of LV cardiac output
-increased ventricular end diastolic, right atrial, and systemic venous pressure

140
Q

right sided heart failure manifestions

A

edema, hepatomegaly, jugular venous distention, abnominal pain, anorexia

141
Q

left sided heart failure (ventricular dysfunction)

A

-hypertension, AMI
-patho: impaired movement of blood from low pressure pulmonary circulation into high pressure arterial side of system circulation
-decrease in cardaic output, blood occumulated in left ventricle, LA, and pulmonary circulation

142
Q

left sided heart failure manifestations

A

-pulmonary edema (nocturnally), pulmonary symptoms

143
Q

frank-staling mechanism

A

increased preload–increased stretch–increase in force of contraction

144
Q

SNS

A

catecholamines elevated, stimulated HR and cardiac contractility

145
Q

RAAS

A

recognizes reduced renal blood from from low CO leading to increased sodium and water retention

146
Q

natriuretic peptides

A

potent diurectic hormones (anp and BNP)

147
Q

acute heart failure syndromes

A

-gradual or rapid changes in heart failure signs and symptoms resulting in need for urgent therapy
-worsening dysfunction that respond to treatment
-new onset from a precipitating event (large AMI)
-worsending end stage heart failure

148
Q

clinical manifestations AHFS

A

-respiratory: dyspnea, orthopnea, PND, chronic dry nonproductive cough, bronchospasm, cheney stokes
-fatigue, weakness, confusion
-fluid retention, edema, nocturia, oliguria, ascites, pleural effusion
-cachexia, malnutrition
-cyanosis,
-arrythmia, sudden cardiac death

149
Q

clinical manifestations AHFS: pulmonary edema

A

-gasping for air, cyanosis, frothy/pink sputum, crackles

150
Q

ventilation

A

involves the movement of atmospheric air to the alveoli for provision of oxygen and removal of carbon diox

151
Q

adequate oxygenation adn removal of c02 depends on

A

-adequate circulation of blood through pulmonary blood vessels
-appropriate contact between ventilated alveoli and perfused capillaries of pulmonary circulation
-ventilation and perfusion!!

152
Q

gas exchange

A

-takes place within the lungs
-involves exchange of 02 and c02 between air in the alveoli and the blood in pulmonary capillaries

153
Q

causes of acute respiratory failure: hypoxemic

A

-COPD
-severe pneumonia
-atelectasis
(retaining c02)

154
Q

causes of acute respiratory failure: hypercapnic/hypoxic

A

-upper airway obstruction (laryngospasm)
-weak/paraylsis respiratory muscles
-chest wall injury

155
Q

respiratory failure

A

failure in gas exchange due to heart or lung failure or both
-occurs in conditions that impair ventilation, causes a mismatches ventilation and perfusionor impaired gas diffusion
-faulure of oxygenation or failure or eliminating c02
! two types: hypoxemic
hypercapnic/hypoxic

156
Q

hypoxemic respiratory failure

A

Pa02 less than 50mm Hg
hypoxia- pa02 less than 95 m Hg

157
Q

hypoxemia results from

A

inadequate oxygen in air, disorder of respiratory system, dysfunction of neurological system, alterations in circulatory function

158
Q

mechanisms by which hypoxia occurs

A

hypoventilation, impaired diffusion of gases, inadequate circulation of blood through the pulmonary capillaries, mismatching of ventilation and perfusion

159
Q

hypoxemic heart failure

A

-tissues with the greatest need are the brain, lungs, and heart
if oxygen falls below critical level (50mm) anaerobic metabolism occurs and then releases lactic acid that causes METABOLIC ACIDOSIS

160
Q

hypoxemic respiratory failure: mismatch of ventilation and perfusoin

A

lungs ventilated but not perfused and vice versa

161
Q

hypoxemic respiratory failure: impaired diffusion

A

gas exchange between alveolar air and pulmonary blood impeded

162
Q

mild hypoxemia

A

slight impaired mental status, vasoconstriction, tachycardia

163
Q

chronic hypoxemia

A

increased RBC’s, clubbing, cyanosis, pulmonary vasoconstriction

164
Q

hypercapnia

A

pc02 (carbon dioxide) greater than 50mm Hg

165
Q

hypercapnia etiology

A

hypoventilation in hypercapnia without hypoxemia
-mismatching of ventilation and perfusion (hypercapnia and hypoxemia)

166
Q

hypercapnia: four factors contribute

A

-alterations in carbon dioxide production
-disturbance in gas excahnge function of the lungs
-abnormalities in function of teh chest wall and respiratory muscles
-changes in neural control of respiration

167
Q

hypecapnia manifestations

A

decreased Ph (RESPIRATORY ACIDOSIS: pH below 7.35, pac02 above 45)
-vasodilation of blood vessels (brain)
-depression of CNS function

168
Q

work of breathing

A

-shortness of breath, dyspnea, tachypnea/bradypnea, tachycardia, diaphoresis, cyanosis, use of accessory muscles, pursed lip breathing, abdominal breathing

169
Q

disorders of lung inflation

A

obstruction of airway, lung compression, lung collapse

170
Q

pleural effusion

A

abnormal collection of fluid within the pleural cavity that compresses lung tissue and inhibits lung inflation

171
Q

pleural effusion patho

A

-rate of fluid formation exceeds rate of removal
-fluid accumulated within the pleural space (parietal/visceral pleura)

172
Q

etiology hydrothorax

A

-heart failure, renal/liver failure, malignancy

173
Q

pleural effusion: fluid

A

transudative: cirrhosis, CHF, nephrotic syndrome
exudative: bacterial/viral pneumonia, pulmonary infarction, malignancies

174
Q

pleural effusion

A

-pleuritic chest pain, dullness/flatness to percussion, diminished breath sounds to effects area, hypoxemia
thoracentesis: releives pressure on lungs and provides for fluid analysis

175
Q

hemothorax patho

A

blood in pleural cavity

176
Q

hemothorax etiology

A

chest injury, complicaion of chest surgery, rupture of great vessel (aortic aneurysm)

177
Q

hemothorax manifestations

A

alteration in oxygenation, venilation, respiratory effort, signs of blood loss, tachycardia

178
Q

pneumothorax patho

A

presence of air in the pleural space causing partial or full collapse

179
Q

pneumothorax etiology

A

primary spontaneous: bleb, smoking
secondary spontaneous: underlying patho process in the lung like TB, pneumonia, CF
traumatic: penetrating/non penetrating wound (GSW, Rib)
tension: intrapleural pressure exceeds atmospheric pressure causing buildup of air within pleural cavity that compresses lung, shifts mediastinum to opposite side of chest, compression of vena cava (life threatening)
- decreased cardiac output!

180
Q

atelectasis

A

incomplete expansion of a lung or portion of lung

180
Q

acelectasis etiology

A

airway obstruction, lung compression, loss of pulmonary surfactant
-narcotics, anestesia, post-surgical pateint, malignancy

181
Q

atelectasis manifestations

A

retractions, decreased breath sounds

182
Q

obstructive airway disorders

A

-caused by disorders that limit expiratory airflow
-asthma, obstructive airway disorders, emphysema, chronic bronchitis

183
Q

obstructive airway disorders

A

-acute and chronic
-contraction of smooth muscle layer controls diameter of airways
-PNS stimulation=bronchial constriction
-SNS stimulation= bronchial dilation

184
Q

asthma

A

-chronic disorder of airways that causes episodic:
- airway obstruction, bronchial hyperresponsiveness, airway inflammation, reversible, symptom free between attacks, airway remodelings

185
Q

asthma patho

A

-exaggerated hyperresponsiveness to a variety of stimuli
-IgE mediated (eosinophils, mast cells)
-TNF-a and IL 4 and IL5– amplification of airway inflammation
-eosinophils generate inflammatory enzymes and release leukotrienes causing incresed mucous secretion– obstruction and further release of histamine from mast cells
-chronic inflammation: leads to airway remodelling
-short acting B2 adrenergic agonist relaxes bronchial smooth muscle

186
Q

asthma genetic and environmental

A

allergens, exercise, aspirin, emotional, hormones (premenstrual), weather

187
Q

manifestatiton of asthma

A

-wheezing
-prolonged expiration
-use of accessory muscles
-chest tightness
-distant or absent breath sounds
-able to speak only one to two words

188
Q

refractory asthma

A

-persistant bronchoconstriction despite attempts to treat the attack with varous medication
-high medications requirements
-increased risk for fatal or near fatal asthma

189
Q

COPD

A

chronic and recurrent obstruction of airflow in pulmonary airways
-accompanied by inflammatory responses
-leading cause of M and M
-is a combo of chronic bronchitis and emphysema

190
Q

copd risk factors

A

tobacco, genetics (alpha 1 deficiency), hyperresponsive airway

191
Q

COPD patho

A

obstruction of airflow- ventilation/perfusion mismatch
-inflammation and fibrosis of bronchial wall
-hypersecretion of mucous
-loss of elastic lung fibers and alveolar tissue
-loss of elastic fibers impairs expiratory flow rate increasing air trapping and airway collapse
(think decrease expiration = higher c02)

192
Q

emphysema patho

A

loss of elasticity, abnormal enlargement of airspace distal to terminal bronchioles, destruction of alveolar walls
-over-distention of alveoli with air trapping–hyperinflation of lungs
-hyperreactive airways- leads to broncho constriction

193
Q

chronic bronchitis patho

A

airway obstruction of the major and small airways
-increse in goblet cells– hypersecretion of mucus in large airways-results in mucous plugging
-Diagnosis: cough for 3 months out of the year for 2 consecutive years

194
Q

COPD manifestations

A

fatigue, exercise intolerance, cough w sputum, shortness of breath, frequent infection, respiratory failire, air hunger, tripod, hypoxemia/hypercapnia

195
Q

emphysema

A

-no cyanosis
-pursed lip puffer breathing
-prolonged exhaling
-barrel shaped chest
-diaphragm pushed downward
-PINK PUFFER

196
Q

chronic bronchitis manifestations

A

cyanosis
-fluid retention from right sided heart failure
BLUE BLOATER

197
Q

disorders of pulmonary circulation

A

blood moves through the pulmonary capillaries– oxygen content increases and c02 decreases
-dependent on ventilation (gas exchange) and perfussion (blood flow)

198
Q

pulmonary embolism

A

develops when blood borne substance lodges in a branch of the pulmonary artery and obstructs blood flow
-thrombus, air, fat, amniotic fluid
-thromboemboli occur from deep vein thrombosis which lodge in pulmonary blood vessel as they move from right heart to pulmonary circulation

199
Q

pulmonary embolism patho

A

-obstruction of pulmonary blood flow–bronchoconstriction, impaired gas exchange, wasted ventilation, loss of alveolar surfactant

200
Q

pulmonary embolism complication

A

pulmonary hypertension, right heart failure

201
Q

pulmonary embolism etiology

A

VIRchows triad: venous stasis (immobility, chf), venous endothelial injury (trauma, surgery), and hypercoagulability states (protein C deficiency, cancer, BCP, pregnancy)

202
Q

pulmonary embolism manifestations

A

-depends on size and location
-dyspnea, chest pain, tachypnea
-pleuritic pain change changes w respiration
-moderate hypoxemia wo c02 retention
-apprehension
-blood streaks sputum

203
Q

massive emboli

A

-sudden collapse, hypotension, JVD
-often fatal
-D-dimer, helical chest CT, lower limb ultrasound, ventilation-perfusion scans, pulmonary angioangraphy

204
Q

Acute respiratory distress syndrome

A

-most severe form of acute lung injury
-severity is measured by pa02/fi02 (how much oxygen on) = P/F ratio

205
Q

ARDS etiology

A

A: aspiration(drowning, gastric)
I:infection (sepsis)
D: drugs (coke, smoke, raditation)
S: shock/trauma (burns, embolism)

206
Q

adult respiratory distress syndrome

A

-rapid onset of respiratory distress (12-18 hours)
-increase in RR
signs of respiratory failure
-Marked hypoxemia- refractory to treatment decreaed PF ratio
-bilateral infiltrated in tje absence of cardiac failure
-noncompliant lung (stiff lungs) difficult to ventilate

207
Q

respiratory defense mechanisms

A

-glottic and cough reflexes
-mucociliary blanket
-phagocytic and bacterialcidial action of alveolar macrophages
-immune defenses

208
Q

pneumonia

A

inflammation of the parenchymal structures of the lung in the lower respiratory trac (alveoli, bronchioles)

209
Q

pneumonia etiologic agents

A

infections: psuedomonas, candida, other fungi
non infectious: inhalation of fumes, aspiration of gastric contents
-consider immune status of pt

210
Q

pneumonia setting classification

A

-community acquired
-hospital acquired

211
Q

pneumonia agent class

A

-typical
-atypical

212
Q

pneumonia distribution class

A

-lobar: consolidation of a part of all of a lung lobe
-bronchopneumonia: patchy consolidation involving more than one lobe

213
Q

typical pneumonia agent

A

-bacteria cause inflammation and exudates of fluid into air filled alveoli

214
Q

atypical pnuemonia agent

A

-viral/mycoplasma that involves intersititum of the lung
-less striking symptoms
-lac of purulent sputum
-NO alveolar inflitration

215
Q

community acquired pneumonia

A

-infections from organisms found in the community rather than in hospital/nursing home
-infection that begins outside of the hospital or is diagnosed within 48 hours of admission
-no residence in LTC facility for 14 days or more
-s.pneumoniae, H.infleunza, mycoplasma, legonella, RSV

216
Q

hospital acquired

A

lower respiratory tract infection that was not present or incubating on admission
-infections occuring after 48 hours of admission
-2nd most common hospital acquired infection
-most are bacterial: P. aeruginosa, S.aureus, Klebsiella

217
Q

acute bacterial/typical pneumonia

A

-lung below main bronchi normally sterile
-microorganism enter air passages during ventilation/aspiration
-loss of cough reflex, damage to ciliated endothelium, impaired immune defenses predispose to colonization and infection-diabetes, smoking, antibiotics that alter normal flora
-pneumococcal pneumonia- gram positive- spleen plays a major role in elimination of the organism
-legionnaire disease (gram negative)-infection occurs when water that contains pathogen is aerosolized into droplets and is inhaled

218
Q

primary atypical pneumonia

A

etiologic agents: M. pneumoniae( mycoplasma infections), influenza, RSV
-patchy involvement of the lung
-moderate sputum
-moderate leukocytosis
-no alveolar infiltrates
-cough?dry and hacking

219
Q

tuberculosis

A

worlds foremost cause of death from a single infectious agent
-M.tuberculosis (rod shaped, aerobic bacteria)
-outer waxy capsure that makes them resistant to destruction
-can persis in old necrotic and calcified lesions adn remain capable of reinitiating growth
-referred to as acid fast bacilli
-strict aerobes that thrive in oxygen rich environment
-airborne, droplet nuclei

220
Q

TB

A

caseating necrosis and cavitation resulting from hypersensitivity immune response
-macrophages are the primary cell infected- they cannot kill the organism but they initiate a cell-mediated immune response that eventually contains the infection
-in patients with intact cell-mediated immunity a granulomatous lesion (Ghon focus) develops caseous cheese like

221
Q

TB manifestations

A

inhaled droplet nuclei with contain tubercle bacillus
-latet TB -cannot transmit no symtoms
-fever, weight loss, fatigue, night sweats, blond-tinged sputum (rusty)

patho (5 decks)

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