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Nursing Level 2 > Patho Midterm One > Flashcards

Patho Midterm One Flashcards

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1
Q

Describe the pacemaker potential. How are pace maker potentials produced

A

Pace maker potential is the gradual DP from -60mV and Na slowly enters the cardiac cell

As the pacemaker potential reaches the threshold, it stimulates Ca channels to open which cause DP

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2
Q

Describe action potentials? How do they relate to heartbeats

A

Occurs when the threshhold is crossed (-40mV)

Causes depolarization (DP) - Ca channels open

Once at a max point, K channels open, causing repolarization until the potential drops to -60mV again

Pacemaker potential starts over again

Each DP causes one heart beat

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3
Q

What is tetanus? How is it prevented?

A

Tetanus is prolonged contraction due to repeated stimulation of the heart muscle

Prevented by the repolarization phase

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4
Q

What is the absolute refractory period?

A

A period of time which the heart muscle cannot be stimulated. Maintained by Calcuim channels being open. Allows the heart to fill properly

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5
Q

What is the cardiac conduction system pathway?

A

SA node in the R atrium stimulates the AV node

Activates the bundle of HIS in the septum

Traevls through the bundle branches in the lower septum into the Purkinje fibres in the ventricles

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6
Q

Describe what happens in the different stages of the ECG

A

P: SA node fires
Atrial Filling (DP)
. Atria Contract (atrial systole)

QRS: AV node fires. Ventricles begin to fill (DP). Atria relax (RP). Ventricles contract.

T: Ventricles relax (RP)

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7
Q

How do valves operate>

A

Flaps of connective tissue that close due to the changes of pressure in the atrium and ventricles. They are anchored by the chordae tendonae to prevent backflow

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8
Q

What are the two normal heart sounds. When do they occur

A

S1: lubb. Louder and longer. Due to closing of the AV valves because ventricles are contracting

S2: Dubb. Closure of the semilunar valves. Ventricles are relaxing causing the Vp < Ap

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9
Q

Where would you place your stethescope to listen to the different heart sounds?

A

Semilunar valves: 2-3ribs

AV: 5-6th ribes

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10
Q

What is Cardiac Output

A

CO = SV x HR

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11
Q

What is stroke volume?

A

SV = EDV - ESV

Governed by Contractilty , preload and afterload

To increase SV, you want to increase EDV and minimizeESV

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12
Q

What is preload? How does increasing preload affect SV?

A

Amound of tension in the ventricles due to the stretch of myocardium.

Increasing preload increases contraction strength

An increase in preload increases SV

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13
Q

What is Contractility? How does it affect SV?

A

The strength of the contraction of the heart

Increased contractiliy increased SV

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14
Q

What is afterload? How is it related to SV?

A

Afterload is the pressure that the heart has to exert to overcome the pressure in the arteries.

Affected by elasticity of vessel, periphery size

Inversly proportional to SV

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15
Q

What is ejection fraction? What does it tell us?

A

EJ = SV / EDV x100%

Fraction of blood that ejected from heart every heartbeat. Measure of how well the valves are working, not if the heart is getting an adequate amount of O2

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16
Q

What is blood pressure? What factors affect it?

A

BP = CO x TPR

CO:

Blood Volume: Increased Na/ H20 absorption, Renin, aldosterone

Cardiac: bpm, volume / beat

TPR:

Blood viscosity (RBCs, albumin)

Vessel radius( influenced by vasomotor tone)

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17
Q

What is vasomotor tone? How does it increase/ decrease?

A

If the sympathetic nervous system is activated, epinephrine is released, causing vasoconstriction.

Walls thicken increasing the PVR - strong tone

When SNS stimulation deceases, smooth muscle relaxes, dilating the vessel, decreasing PVR - weak tone

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18
Q

What is flow? How is it influenced?

A

Flow = volume/ time (mm3/s)

velocity x cross section

Influenced by viscosity of blood, vessel elasticity and vessel radium

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19
Q

How does local control influence BP?

A
  1. Lactic acid (wastes) cause vasodilation
  2. Vasoactive substances (histamines) cause vasodilation
  3. Angiogenesis can increase blood flow to the area
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20
Q

How does neural control affect blood pressure? What are the two pathways?

A

Changes in BP are noted in the baroreceptors (aortic arch, carotoid sinuses and aortic sinus)

ie. If the BP is increased, the arteries stretch and this is detected by the baroreceptors. They activate the cardio-inhibitory center and inhibit the vasomotor center

  1. Cardioinhibitory center- increases vagal tone which decreases HR
  2. Vasomotor - Reduces sympathetic tone which reduces vasomotor tone which causes vasodilation
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21
Q

What hormones control BP?

A

angiotensinogenigenfloats around in the blood stream. When BP drops,Reninis released from the kidneys which converts angiotensinogen toangiotensin I. As Angiotensin I passes through the lungs, ACE converts it toangiotensin II which is a powerful vasocontrictor.

Angiotensin II stimulates the adrenal cortex to release aldosterone which promotes Na and water retention in the kidnets

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22
Q

How is venous return promoted?

A
  1. Venous muscles contract, causing some pressure
  2. Gravity drains the head and neck
  3. Skeletal muscles in the limbs pump blood with movement
  4. Inhalation causes the thoracic cavity to expand, decreasing blood pressure and sucking blood up
  5. Cardiac suction of the atrial space
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23
Q

What factors promote capillary volume and flow

A
  1. Hydrostatic pressure mores fluid, nutrients and O2 from capillaries to the tissue bed
  2. As nutrients are removed, plasma proteins in capillary pull wastes and CO2 back into the capillary - Colloid osmotic pressure
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24
Q

What is the largest cause of cardiac disease?

A

Atherosclerosis

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25
Q

How does artherosclerosis form

A
  1. Trauma to endothelium allows fat cells to get underneath
  2. WBCs follow and try to get rid of them, oxidizing them into foam cells
  3. WBCs release growth factors which cause a plaque to form in the vessel
  4. Plaque blocks the artery
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26
Q

What are chylomicrons? How do they help with cholesterol?

A

Liproprotein particles that transport lipids from the GI tract to the blood to the liver

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27
Q

What are risk factors of atherosclerosis? What are protective factor/s

A

Risk factors that cannot be changed: age, gender, heredity, lack of LDL receptors

Risk factors that can be changed: Diet, obesity, DM II, HTN, increased clotting factors, smoking

Protective factors: estrogen, exercise

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28
Q

What are HDL and LDL cholesterol? Which are good and bad

A

LDLs are bad proteins because they lack the lipoproteins to attach to receptors, so instead they float around in the blood stream. They can also deliver fat to the body

HDLs have a lot of proteins in the surface and therefore bind easily. They go to tissues and pick up lipids

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29
Q

What is the difference between stable and unstable plaques?

A

Stable: have thick fibrous caps over the core and only partially block the vessels. Don’t tend to form clots of emboli

Unstable: Only have thin, fibrous caps which can rupture. Rupture can form a clot and fully occlude the artery or may break free and become an embolus

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30
Q

What are syndromes of Coronary Heart disease?

A

Angina, acute coronaty syndrome (MI and unstable angina), chronic ischemic disease, sudden cardiac death

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31
Q

What is coronary heart disease?

A

Occlusion of the coronary arteries

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32
Q

What can ischemia of the coronary arteries cause?

A
  • Angina
  • Heart attack
  • Cardiac arrythmias
  • conduction deficits
  • heart failure
  • suddent death
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33
Q

When does angina occure? What does it feel like? How can you help treat it?

A

Angina occurs when there is too much demand on the heart and not enough supply of oxygen to the heart muscles

Feels like heartburn or a squeezing pain in the middle of the chest

Increase supply by applying O2

Decrease demand by resting, decreasing anxiety, medications to decrease HR

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34
Q

What are the different types of angina?

A
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35
Q

What are the functions of the plural fluid in the cavity?

A

Reduces friction

Creates a pressure gradient between the atmosphere and the lungs

Compartmentalized infections inside and outside of the lung

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36
Q

WHat is generally considered the upper and lower Resp tract?

A

Upper: nasal cavity, pharynx, oral cavity, larynx

Lower: Bronchi, broncioles and alveoli

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37
Q

What is the function of the upper resp tract?

A

Humidify and filter incoming air

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38
Q

How are foreign particles trapped when entering the resp center?

A

The tracheobronchial epithelium contains goblet cells which produce mucus which trap foreign particles such as dust

Ciliated cells conduct particles back up to the pharynx

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39
Q

What is the bronchial tree? What is it composed of?

A

23 orders of bronchioles which end in alveoli

Line by epithelium, walls are cartiledge (keeps airway open) and smooth muscle (controls airway conductance)

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40
Q

What is conductance?

A

The flow of air

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41
Q

What are the different cell types found in the respiritory membrane?

A

Type I alveolar cells - simple squamous epithelium

Type II - cuboidal cells which produce surfactant

Alveolar macrophages - engulf foreign particles

Capillary endothelium

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42
Q

What are the stages”normal respiritory function”

A
  1. alveolar ventilation - air is drawn into lungs
  2. Alveolar perfusion - cappillaries surround alveoli
  3. Alveolar-capillary diffusion - air leaves alveoli and enters capillaries
  4. Gas transport to the rest of the body

Changes in any of these can cause respiritory failure

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43
Q

What is compliance? What is it dependent on?

A

:How easily the lungs are inflated

Dependent on presence of elastin (stretch) and collagen (prevents over stretching), water content, and surface tension

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44
Q

How does surfactant reduce surface tension?

A

Surfactant breaks down the hydrogen bonds connecting H2O molecules to each other, therefore reducing the surface tension and making it easier for the alveoli to expand

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45
Q

What factors affect alveolar - capillary diffusion

A
  1. Permeability of epithelium (thickness)
  2. Surface area (more SA, more area for diffusion to occur)
  3. Concentration gradient of gas (> gradient = better diffusion)
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46
Q

What is lung ventilation? What does it depend on?

A

The act of driving air in and out of the lungs

Depends on the action of the respiritory muscles (chest compliance) and lung compliance

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47
Q

A man’s lungs were damaged during a fire due to smoke inhalation. The damage destroyed some of his surfactant. What happened to his lung compliance? Why was he given positive pressure ventilation?

A

Compliance is decreased because surfactant is destroyed

Positive pressure aid room will help force air into the lungs

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48
Q

What are the primary respiritory muscles?

A

Diaphragm, external intercostal muscles

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49
Q

When are the accessory muscles used? What are the accessory muscles for inhalation and exhalation?

A

For forced or deep breathing

Inhalation: Scalene, sternocleidomastoid

Exhalation: internal intercostal, abdomonial muscles

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50
Q

What is tidal volume?

A

Air inhaled and exhaled in one quiet breath. Difficult to get an accurate measure

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51
Q

What is residual volume?

A

The air that remains in the lungs after maximum expirarion. Keeps alveoli inflated (1L)

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52
Q

What is vital capacity?

A

The amount of air that can be exhaled with maxiumum effort after maxium inspiration

Measure the amound of air that can pass through the lungs

Assess strength of thoracic muscles & pulmonary function

53
Q

What is forced expiratory volume?

A

% of vital capacity exhaled over time

Health adult ~75-85%

COPD ~ 60-65%

54
Q

What is the minute respiritory volume?

A

Tidal volume x respiritory rate

Rest = 6L/min

Max = 125-175L/m

55
Q

How is O2 transported in blood? What is the normal PaO2?

A

some is dissolved (PO2 = >80mm Hg)

Most is bound to hemoglobin

56
Q

What is the normal PaCO2?

A

35-45mm Hg

57
Q

What occurs as you exhale?

A

Exhaling removed CO2 from blood which reduces carbonic acid (H2CO3) and raises your blood pH

58
Q

How do central chemoreceptors work?

A

Measure the PCO2 and pH in the cerebrospinal fluid

Increases resps when PCO2 increases or ph decreases (stimulated the breathing center in the medulla oblongata)

59
Q

How do peripheral chemoreceptors work?

A

They measure the PO2 in arterial blood (aorta, carotoid arterties)

Increase respirations when PO2 <60mmHg

More sensitive

60
Q

You are caring for a patient with chronically high PCO2. He is being given lowe flow O2 and c/o needing more O2, so you turn up his O2.

When you check on him later, he is unconcious and not breathing.

What happened?

A

Pt has chronic increased PCO2 therefore his central chemoreceptors have been de-sensitized and no longer recognizes having high PCO2.

By increasing the O2, the peripheral chemoreceptors register that the pt is getting enough O2 therefore the resps don’t increase or decrease.

61
Q

How does a peanut allergy cause cardiovascular shock?

What would you measure.

How would you treat it

A

Histamines are released which cause vasodilation.

The decrease in peripheral causes blood pooling in the body which decreases the blood to the heart (CO decreases)

Measure BP

Stop histamine release c anti histamines. Epinephrine activates CNS causing vasoconstriction

62
Q

What is repiritory failure?

A

inability to deliver adequate O2 to the body

63
Q

What are causes of respiritory fialure

A

Hypoventilation - hypercapnia, hypoxia

Impaired diffusion - hypoxemia but not hypercapnia

Pleural disorders

64
Q

Why does impaired diffifusion cause hypoxemia but not hypercapnia?

A

Thickening of the alveoli causes the inability for O2 and CO2 to pass through the endothelium

That causes hypoxia. However, excess build up of CO2 in the blood causes it to be converved to HCO3 which can excreted by the kidney

65
Q

What are causes of hypoventilation?

A

Depression of repiritory center dt brain injury, blood clot, tumor

Dieases of the respiritory nerves or muscles - polio, MS, myesthenia gravis

Thoracic cage disorders (scoliosis, kyphosis)

66
Q

What can cause impaired diffusion?

A

Interstitial lung disease

ARDS

Pumonary edema

Pneumonia

67
Q

What is hypoxemia? What are S&S?

A

When PO2 <60mmHg

Agitation,combative behaviour, euphoria, impaired judgement, convulsions, delirium, stupor & coma

Hypotension and bradycardia dt the heart not receiving enough O2

Results in SNS activation (short term solution)

68
Q

What is hypercapnia? What can it cause?

A

When PCO2 is >50mmHg

Causes increased RR (central chemoreceptors triggered), decreased nerve firing (dt elevation of blood acidity) - disorientation, coma, & decreased muscle contraction

69
Q

What is plueral effusion?

A

When fluid builds up in the lungs. Severity depends amount of effusion and type.

Can be seroius, pus, lymph or blood

70
Q

Hydrothorax,

empyema,

chylothorax

Hemothorax

A

serous fluid

pus

lymph

blood

71
Q

What is pneumothorax? What categories are there?

A

Puncturing of the pleural cavity causing collapse of lung on damaged side

  1. Spontaneous - air filled blister on lung ruptures
  2. Traumatic - chest injury
72
Q

What are the two types of traumatic pneumothorax?

A

Open: air enters the wound on inhalation and exits on exhalation

Tension: Air enters on inhalation but cannot exit on exhalation. Very painful on injured side. Makes ventillation diffifult dt less room. Extra air needs to be exacuated from thoracic cage

73
Q

What are clinical features of pneumothorax?

A

Tracheal shift to the non injured side dt boyancy and being pushed

Cardiac compression

lung deflation

Decreased breath sounds to injured side

Area of density on a radiograph

74
Q

What are obstructive diseases? What are some examples?

A

Disorders which decrease the conductance of air to the lungs

(Asthma, COPD)

75
Q

What are restrictive disorders? What are some examples?

A

Disorders which affect the capacity of the lungs

dt. chest wall changes, pleural effusions or parenchymal changes

76
Q
A
77
Q

What are the different types of angina? How are they treated?

A

Stable - a fixed occlusion (stenosis). Pain occurs when O2 demand for heart is increased. Relieved with rest

Unstable: thromboemboli leads to MI. Tx c anti coagulants

Variant: Coronary artery spasms block blood flow. Usually in young males who use drugs. Tx c calcium channel blockers

78
Q

S&S of an acute MI

A

Chest pain - severe burning or crushing sensation

SNS response - GI distress, N&V, tachycardia, vasoconstriction, anxiety, restlesness, doom

Hypotension and shock - weakness in arms and legs

79
Q

Where do the majority of MIs occur

A

20% in the left circumflex artery (supplied by LCA)

50% in the LT anterior descending artery (supplied by LCA)

30% in RCA (posterior infarction)

80
Q

Why do Lt sided coronary arterial vessels experience 70% of MIs?

A

More pressure is experienced by the LCA. Greater risk of injury which leads to atherosclerosis

81
Q

What is the pathogenesis of Acute Coronary syndrome

A

Plaque is broken down

Tissue thromboplastim is exposed

Platelet aggregates to area, forming a clot

thrombus is formed

acute ischema

82
Q

What are complications of an acute MI?

A

Heart failure

Cardiogenic shock (heart is so damged that it cannot pump blood to the other organs)

Pericarditis (dt rupture)

Thromboemboli dt stagnation of blood in ventricles dt ineffective pumping

Rupture of heart

Ventricular aneurysm

83
Q

What are the common outcomes of an MI 1 day after the infarct?

A

Death (20%)

Arrythmia

84
Q

What are the common outcomes of an MI one week after the infarct?

A

Arrythmias (90%)

CHF (60%)

Shock (12%)

Rupture (1%)

85
Q

What are the common outcomes of an MI one year after the infarct?

A

CHF (70%)

Arrythmia (20%)

Aneurysm (10%)

Thromboemboli (10%)

86
Q

What are the common outcomes of an MI ten years after the infarct?

A

CHF(70%)

Recurring infarcts

Arrythmias

Only about 30% are still alive

87
Q

What are serum cardiac markers of acute coronary syndrome? Why are these markers used?

A

Incraese in Myoglobin, creatinine kinase (makes ATP), triponin

Cell death releases these proteins into the bloodstream

88
Q

How would each of the following affect BP?

  1. Vasodilation
  2. Decreased stretching of baroreceptors
  3. Hypoxemia
  4. Inhibiting ACE
  5. Beta blockers
  6. Aplha 2 agonist
  7. Calcium channel blockers
A
  1. Decrease
  2. Increase
  3. increase
  4. decrease
  5. decrease
  6. increase (causes constriction)
  7. decrease
89
Q

What is primary and secondary HTN?

A

Primary (essential): No identifiable cause. High Na suspected to be related. Most come 90-95%

Secondary: dt pheochromocytoma, adrenal cortex adenomas, atherosclerosis

90
Q

What is Stage 1,2 &3 HTN?

A
  1. Stage 1: 140-159/90-99
  2. Stage 2: 160-179/100-109
  3. Stage 3: >180/110
91
Q

What are complications of HTN?

A

Cardiac hypertrophy (Lt ventricle)

Nephrosclerosis: changes in glomeruli and blood vessels

Retinopathy - hemorrhages lead to blindness

Encephalopathy - rupture of aneruysms

92
Q

What is the difference between hyaline and malignant nephrosclerosis?

A

Hyaline: scar tissue forms over the glomeruli in the afferent arterioles

Malignant: Changes occur in the kidney which activates the renin - angiotensin - aldosterone system causing a cycle of elevated BP. Tiny hemorrhages in the renal cortex

93
Q

What is heart failure? What causes it?

A

Inability to effectively pump the blood delivered to the heart to the rest of the body.

MI, cardiomyopathy

94
Q

How is systolic dysfunction different from diastolic dysfunction?

A

Systolic dysfunction: low ejection graction dt poor contractility. Often associated with MI, ischemia & cardiomyopathy

diastolic dysfunction: Near normal ejection fraction. Dt poor or slow relaxation . Often associated with aging bc of decreased elasticity

95
Q

What are the effects of Lt sided heart failure?

A

Backwards: Back up of blood in the lungs. Results in crackles, infection, laboured breathing. Often results in rt sided failure

Forward: decreased CO leading to decreased perfusion

96
Q

What are the effects of Rt. sided heart failure?

A

Backwards: Jugular vein distension, GI tract congestion (N&V, anorexia), edema

Forwards: Low cardiac output dt decreased contractility, decreased blood carrying O2 in lungs

97
Q

Mr. M has heart failure. He c/o severe SOB and has fluid in his lungs. He has tachycardia, increased diastolic BP and says that he feels weak and anxious.

Which are dt the SNS?

Which side is failing

A

SNS: anxiousness, increased BP, tachycardia, anxiety

Side: Lt ventricular

98
Q

What is pericarditis? What are clinical manifestations?

A

Inflammation of the pericardium (covering around the heart).

Causes pain dt prostaglandins

Exudate (serous - pericardial effusion), fibrinous (adhesions decreasing expansibility)

ECG changes (changes in QRS wave)

99
Q

What are the consequences of pericardial effusion?

A

Restricts heart expansion

Lt side can’t accept enough blood which decreases CO, which decreases BP leading to shock

Rt side can’t accept enough blood, causing edema, jugular distension, increases venous pressure

100
Q

What are examples of myocardial disorders? Do they result in systolic or diastolic disorders?

A

Ventricles are hypertrophic, can’t fill properly - DD

Ventricles are too stiff to stretch - DD

Ventricles are too weak to pump blood - SD

101
Q

What is hypertrophic cardiomyopathy?

A

Genetic disorder in which defects in actin and myosin make the cells weak. The heart has to work harder to pump blood to the body. Causes the muscles to hypertrphy. Heart requires more O2 to fxn properly, making the person more prone to heart failure.

102
Q

What are the types of valve defects?

A

Stenosis

Regurgitation

103
Q

What are the effects of Aortic valve stenosis and regurgitation?

A

Stenosis: Ventricular hypertrophy b/c heart has to pump harder to get blood into aorta

Regurgitation: Ventricle dialates to accomodate the backflow of the blood. Decreases contractility which decreases CO

104
Q

What are the effects of Mitral valve stenosis and regurgitation?

A

Stenosis: dialation of the atria. Could cause pulmonary congestion

Regurgitation: dialation of the atria. Could cause pulmonary congestion

105
Q

What is cardiogenic shock?

A

Occurs when the heart fails to pump blood adequately.

Decreased CO decreases BP, causing SNS response causing vasoconstriction which increases the workload of the heart

106
Q

What is distributive shock? What causes it?

A

When the BV dialate and there is not enough blood in the circulatory system to fill it

blood flow decreases, less blood is brought to the heart and less is pumped to the body

DT decreased SNS activity dt injury to brain or spine, anesthetics, insulin shock, emotions

Vasodilators in blood (histamines, sepsis)

Vessel damage dt severe hypovolemia

107
Q

What is systemic inflammatory response syndrome?

A

aka Septic shock

Vasodilation dt imflammatory mediators

108
Q

What are examples of obstructive airway disorders?

A

Bronchial asthma

Chronic bronchitis, emphysema, bronchietasis, cystic fibrosis

109
Q

What differences are there between extrathoracic & intrathoracic airway problems in children?

A

Extrathoracic - prolonged inspiration, inspirational stridor. Body walll does not move c inspiration

Intrathoracic: Prolonged expiration c wheezing. Rib cage moves but air doesn’t leave lungs

110
Q

What are upper and lower obstructive disorders in children?

A

Upper = croup, epiglottits

Lower - acute bronchiolitis

111
Q

What is croup? How does it present? How do you treat?

A

Occurs mostly in young chldren. Occurs 3 mos - 3 years

Brought about by influenze or other viral infections

S&SL hoarsness, brassy cough, fever, resp stridor, ctanosis, pallow

Tx c cold air

112
Q

How does Epiglottitis presesnt?

A

SImilar to croup

113
Q

What are the causes of asthma?

A

Extrinsic: dt allergic reaction

Intrinsic: exercise, cold, physical factors, physhological stress, chemical irritants, aspirin, age

114
Q

What is the pathogenesis of Extrinsic asthma?

A

Dt Type 1 hypersensitivity. May be genetic. Parents often have ecxema

Allergin is inhaled and enter the endothelium of airways

Mast cells from the connective tissues interact with the allergin and IgE.

IgE attaches to the mast cell and acts as a receptor for the allergin.

The mast cells contain histamine, and when the allergin contacts IgE, histamine is released.

Changes happen to the cell wall - airway thckens, increase mucous production

115
Q

What histology changes occur in bonchials during asthma?

A

Mucus in lumen

Inflammation & basement membrane thickening

Enlarged mucous glands

Smooth muscle hyperplasia

116
Q

How is Asthma controlled?

A

antihistamines, bronchodialators (Ventolin), managing environment, cortico-steroids

117
Q

How do corticosteroids work against asthma? What is the risk of using improperly

A

Increase synthesis of beta receptors which boosts the effects of beta agonists

Overuse can break down bronchial endothelium which can lead to thrusth

Can lead to down regulation of B receptors

118
Q

How do you treat intrinsic asthma?

A

Bronchodilators, antiocholinergics to prevent vagal reflex

119
Q

How does COPD onset? What is the pathophysiology?

A

Onsets gradual changes in the airway to decrease conductance.

Muscus glad hypertrophy, loss of alveoli tissue of loss of eleasticity

120
Q

What is the pathophysiology of emphysema? What is the Etiology?

A

Foreign particles entering the alveoli cause an influx of WBCs, especially neutrophils

Neutrophils try to digest particles with tripsin. However, tripsin can damage damage to alveoli endothelium which reduces elasticity.

Can be a genetic disease dt lack of antitripsin which inactivates tripsin

Smokers are also at high risk

121
Q

What is radial traction?

A

stretching ability of parenchyma

122
Q

What happens when radial traction decreaes?

A

Lose the ability to get rid of stale air in the lungs. Requires more effort to get rid of air. Strong accessory muscles

123
Q

What is the difference between centrilobular and panacinar emphysema

A

Centrilobular - bronchioles are enlarged. Less dangerous than panacinar

Panacinar - Alveoli + broncioles expanded.

124
Q

S&S of emphysema?

A

Barrel chest, pursed lip breathing

Good color, warm (no hypoxia)

125
Q

What is chronic bronchitis?

A

Persistent cough of six mos over a two year period. Increased mucous secretions causing a productive cough

Hypoxic

126
Q

What are the differences between blue bloaters and pink puffers?

A

Pink Puffers - Increased RR, dyspnea, increased temp dt increased metabolic needs, use of accessory muscles. Breath better upright

Blue bloaters: Cyanosis and polycythemia, cor pumonae

127
Q

What is cor pulmonae

A

increased work load causing rt sided heart failure

128
Q
A

Nursing Level 2 (6 decks)

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