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Patho > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

primary function of the lungs

A

gas exchange

-O2 transported to tissues

-CO2 transported out of body

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2
Q

alveoli

A

-grapelike clusters of air filled sacs

-gas exchange of oxygen and carbon dioxide

-good ventilation

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3
Q

ventilation

A

movement of air into and throughout the lungs (inspiration and expiration)

-needs openings in pulmonary airways

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4
Q

perfusion

A

movement of blood through pulmonary circulation eventually providing oxygen to every part of the body

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5
Q

diffusion

A

-movement gas from high to low concentration

-oxygen diffused out of alveoli into blood

-CO2 diffusion out of blood into alveoli

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6
Q

upper airway structures

A

nasopharynx, oropharynx, laryngopharynx

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7
Q

lower airway structures

A

Larynx

Trachea

Bronchi

Bronchopulmonary segments

Bronchioles

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8
Q

bronchopulmonary segments (right lung)

A

-upper lobe

-middle lobe

-lower lobe

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9
Q

bronchopulmonary segments (left lung)

A

-upper lobe

-lower lobe

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10
Q

right and left main bronchus difference

A

-right is straighter than left

-makes right lung more susceptible to aspiration and intubation

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11
Q

Role of cilia in respiratory tract

A

-push things out airway

-line trachea and bronchi

-defense

-cough reflex

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12
Q

what impairs the function of cilia in respiratory tract

A

-smoking

-increased mucous

-alcohol (ethanol)

-temp changes

-low humidity

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13
Q

accessory muscles of respiration

A

-sternocleidomastoid

-scalene

-trapezius

-pectoralis major

-internal intercostals

-abdominal muscles

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14
Q

when are accessory muscles of respiration active

A

assist the primary muscles when the chest is not expanding or contracting effectively to meet ventilation demands

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15
Q

bronchial artery system

A

Supplies oxygenated blood to lungs and pleura

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16
Q

pulmonary artery system

A

Vast network of capillary that allows for gas exchange

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17
Q

pulmonary artery leaves

A

right ventricle with unoxygenated blood to the lungs

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18
Q

pulmonary vein carries

A

oxygenated blood from lungs back into heart

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19
Q

how is ventilation controlled

A

-medulla oblongota!

-pons

-“respiratory center” of brain moves air throughout lungs to capillaries

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20
Q

proprioreceptors in the muscles

A

-respond to body movement

-stimulated by exercise, respiratory rate and depth increase

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21
Q

stretch receptors in bronchi and bronchioles

A

-dilate alveoli

-prevents overstretch

-neonates

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22
Q

chemoreceptors in the brain respond to changes in

A

CO2 and pH in bloodstream and cause alterations in the rate and depth of respirations

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23
Q

baroreceptors in vascular system respond to changes in

A

blood pressure

-BP decreased, breathe faster

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24
Q

how is perfusion controlled

A

-blood flow to alveoli

-affected by gravity: goes to lowest point

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25
Q

uneven distribution in perfusion

A

-body position: sit upright for even distribution

-exercise

-lung zones

-low volume

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26
Q

factors affecting perfusion

A

-fluid volume within lung

-fluid shifts

-interstitial edema

-alveolar edema

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27
Q

pulmonary capillary network

A

-low pressure system

-wrap alveoli

-normal pressure: 22/8 to 25/8 mm Hg

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28
Q

pulmonary blood flow zone 1

A

minimal perfusion

-apex

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29
Q

pulmonary blood flow zone 2

A

intermittent perfusion

-pulmonary artery

-pulmonary vein

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30
Q

pulmonary blood flow zone 3

A

continual perfusion

-most gas exchange

-base

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31
Q

ventilation/perfusion ratio (V/Q ratio)

A

adequate volume air matched with adequate blood flow

-amount of air reaching the alveoli to the amount of blood reaching the alveoli

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32
Q

normal ventilation (VA)

A

4L/min alveolar air flow

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33
Q

normal perfusion (Q)

A

5L/min capillary blood flow

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34
Q

normal VA/Q ratio

A

0.8

-amount air (min)/ amount blood (min)

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35
Q

high V/Q ratio

A

-#1 cause pulmonary embolism

-ventilated but not perfused

-pulmonary embolus!

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36
Q

low V/Q ratio (hypoxemia)

A

-perfused but not ventilated

-airway constriction

-asthma!

-pneumonia!

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37
Q

shunt V/Q ratio

A

-no gas exchange, oxygen and blood not connecting

-no ventilation

-alveolar collapse

-acute respiratory failure!

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38
Q

how does oxygen get from environment to tissues

A

-dissolved in plasma (PaO2)

-bind to hemoglobin (SaO2)

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39
Q

oxygen binds to hemoglobin (SaO2)

A

-affinity in lungs binds O2 to hemoglobin

-affinity in tissues releases O2 at site

-95-100 hemoglobin should be saturated!

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40
Q

oxyhemoglobin dissociation curve: PaO2

A

partial pressure of oxygen in arterial blood

-80-100 mm/Hg!

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41
Q

oxyhemoglobin dissociation curve: SaO2

A

saturation of hemoglobin with oxygen in arterial blood

-95-100%

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42
Q

what causes right shift of oxyhemoglobin curve

A

-increased hydrogen, decreased pH: acidosis!

-increased Co2!

-increased temp!

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43
Q

what does right shift of oxyhemoglobin curve do to oxygen saturation and availability

A

-enhances O2 release to tissues

-less affinity

-oxygen less tightly bound to hemoglobin

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44
Q

what causes left shift of oxyhemoglobin curve

A

-decreased hydrogen, increased pH: alkalosis!

-decreased Co2!

-decreased temp!

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45
Q

what does left shift of oxyhemoglobin curve do to oxygen saturation and availability

A

-decreases O2 release to tissues

-hemoglobin holds on longer to oxygen

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46
Q

hypoventilation

A

-not enough air in

-insufficient air delivery to alveoli causes inadequate O2 delivery and Co2 removal

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47
Q

hypoventilation causes

A

-medication

-obesity

-pain

-sleep apnea

-paralysis

-pt out of surgery at risk

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48
Q

hyperventilation

A

-breathe too fast

-increased air entering alveoli resulting in hypocapnia (PaCo2 below 35)

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49
Q

hyperventilation causes

A

-hypoxic stimulation

-anxiety

-fear

-fever

-sepsis

-brain stem injury

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50
Q

hypoxia

A

-oxygen at tissue level

-low O2 in tissues

-cant measure

-pale, blue lips and fingernails

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51
Q

hypoxemia

A

-not enough oxygen in bloodstream

-low hemoglobin saturation

-measure with pulse ox (SaO2)

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52
Q

normal PaO2

A

80-100

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53
Q

mild hypoxemia PaO2

A

70-79

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54
Q

moderate hypoxemia PaO2

A

60-69

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55
Q

severe hypoxemia PaO2

A

<60

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56
Q

acute respiratory failure

A

disturbed gas exchange resulting in abnormal blood gas values (ABGs)

-failure of oxygenation (hypoxemia) or failure of ventilation (hypercapnia) or both

-pulmonary system fails to oxygenate the blood or fails to eliminate carbon dioxide

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57
Q

normal ABGs

A

-PaO2: 80-100

-PaCo2: 35-45

-pH: 7.35-7.45

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58
Q

how is acute respiratory failure diagnosed

A

ABGs

-PaO2: < 60 (hypoxemia)

-PaCo2: >50 (hypercapnia)

-pH: < 7.3

CXR

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59
Q

acute respiratory failure general features

A

-headache

-dyspnea

-confusion!

-restlessness/agitation!

-dizziness

-tremors

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60
Q

early signs and symptoms of acute respiratory failure

A

-rapid shallow breathing

-increased inspiratory muscle movement

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61
Q

late signs and symptoms of acute respiratory failure

A

-cyanosis

-nasal flaring

-sternal/intercostal retractions

-cool clammy skin

-dysrhythmias

-decreased capillary refill

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62
Q

acute respiratory failure treatment

A

-ventilatory support

-airway patency

-supportive care (keep all other organ systems functioning)

-nutrition

-pain management

-emotional support

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63
Q

pulmonary hypertension etiology

A

-pulmonary vasculature is high flow, low pressure system

-sustained pulmonary arterial pressure >30 mmHG

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64
Q

primary pulmonary hypertension (PPH) etiology

A

-rapidly progressive/poor prognosis (only live few years)

-no underlying cause just happens

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65
Q

secondary pulmonary hypertension

A

-get from HF or chronic lung disease

-increased pulmonary blood flow (left sided failure)

-increased resistance to blood flow (hypoxic responsive vasoconstriction)

-increased left atrial pressure (aortic stenosis)

-live longer

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66
Q

pulmonary hypertension pathogenesis

A

over time right sided heart failure occurs

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67
Q

pulmonary hypertension signs and symptoms

A

-often asymptomatic until damage is done

-exercise intolerance is first symptom!

-chest pain

-hemoptysis (cough up blood)

-pulmonary edema

-cor pulmonale: right sided heart enlargement/failure

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68
Q

pulmonary hypertension diagnosis

A

-pulmonary artery catheter measurement

-CXR: pulmonary arteries and right ventricle enlargement

-EKG

-echo

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69
Q

pulmonary hypertension treatment

A

-control underlying disease process

-oxygen

-vasodilators/diuretics!

-lung or heart transplant: not common

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70
Q

Virchow’s triad

A

factors that predispose thrombus formation

-venous stasis

-hypercoagulability

-damage to vessel wall

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71
Q

pulmonary venous thromboembolism etiology

A

-blood clot lodges in vascular space

-occludes pulmonary vasculature

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72
Q

pulmonary venous thromboembolism sources

A

-deep veins legs (90%)

-fat emboli

-air emboli

-amniotic fluid: delivery

-foreign material

-septic bodies

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73
Q

pulmonary thromboembolism risk factors

A

-immobility

-trauma

-pregnancy

-cancer

-heart failure

-estrogen use (birth control)

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74
Q

pulmonary thromboembolism pathogenesis

A

-thrombus dislodged from trauma, exercise and muscle action, change in blood flow pattern

-travel to heart and lungs

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75
Q

pulmonary thromboembolism signs and symptoms

A

-restlessness

-anxiety

-sense of “impending doom”

-dyspnea

-tachycardia

-chest pain

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76
Q

pulmonary thromboembolism diagnosis

A

-Va/Q lung scan

-pulmonary arteriography: inject dye into pulmonary artery

-ultrasound lower extremities

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77
Q

pulmonary thromboembolism treatment

A

-prevention: nurses role, range of motion, SCDs

-heparin therapy

-vena cava filter: wire traps clot

-embolectomy: surgically remove embolus

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78
Q

lung cancer etiology

A

-85% smoking

-asbestos exposure

-over age 50

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79
Q

lung cancer four major types

A

-squamous cell

-adenocarcinoma

-large cell

-small cell (oat cell)

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80
Q

lung cancer pathogenesis squamous cell

A

-detected in sputum

-detected early

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81
Q

lung cancer adenocarcinoma and large cell carcinoma pathogenesis

A

metastasize to distant organs

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82
Q

lung cancer small cell carcinoma (oat cell) pathogenesis

A

-rapid growth

-widespread metastasis

-most difficult to treat

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83
Q

lung cancer signs and symptoms intrathoracic

A

lung and airway

-dyspnea

-cough

-increased sputum

-hoarseness

-hemoptysis

-chest pain

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84
Q

lung cancer signs and symptoms extrathoracic

A

non airway

-weight loss

-anemia

-facial/ upper extremity edema: retain fluid, prevents blood flow down body

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85
Q

lung cancer diagnosis

A

-bronchoscopy washings: tube takes out tx

-pleural fluid samples

-biopsy

-CXR

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86
Q

lung cancer treatment

A

surgery, radiation, chemotherapy

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87
Q

asthma etiology

A

-episodic airway obstruction resulting from bronchospasm, increased mucus, mucosal edema, usually reversible with bronchodilators

-inflammatory chemicals from mast cells

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88
Q

Asthma triggers

A

-allergens

-stimuli

-twice as many boys

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89
Q

Intrinsic/Environmental (Non-Allergic) asthma

A

-middle age, poorer prognosis

-precipitated by respiratory infections and exercise

-stress

-pulmonary irritants

-foods

-drugs

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90
Q

Extrinsic/Genetic (Allergic) IgE mediated asthma

A

-begins in childhood

-family history

-sensitivity to specific allergens: pollen, animal dander, dust etc

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91
Q

asthma pathogenesis

A

-mediated by IgE after exposure to specific antigen

-inflammation: bronchospasm, mucosal edema, mucous plug formation, airway remodeling (scarring)

-changes in epithelial cells

-genetic

-seasonal, environmental, occupational factors

-can lead to COPD

92
Q

asthma signs and symptoms

A

-wheezing! airway constriction

-chest tightness

-dyspnea

-cough

93
Q

asthma diagnosis

A

-pulmonary function tests

-ABGs: CO2 and O2 values

-CXR

-sputum exam

94
Q

asthma treatment

A

-avoid triggers

-bronchodilators

-steroids

-oxygen

95
Q

acute bronchitis etiology

A

-acute inflammation of trachea and bronchi from bacterial or viral infection

-smokers, young children, elderly, winter, bacterial infections, smoking

96
Q

acute bronchitis pathogenesis

A

-airway becomes inflamed/narrowed by excessive mucous secretion

-swelling from exudative fluid

97
Q

acute bronchitis signs and symptoms

A

-fever

-cough

-malaise

-sore throat

-post nasal drip

98
Q

acute bronchitis diagnosis

A

-acute cough (symptomology)

-purulent sputum

-elevated WBC

99
Q

acute bronchitis treatment

A

-cough medicine

-self limiting: caused by virus

-antibiotics if bacterial

100
Q

chronic bronchitis- type B COPD etiology

A

combination of chronic bronchitis, emphysema and reactive airway disease (RAD)

-increased mucous production

-chronic cough

-blue bloater: difficulty air in (blue) fluid backs up from edema (bloater) !

101
Q

chronic bronchitis- type B COPD pathogenesis

A

-chronic inflammation of bronchial mucosa

scarring

-mucous plugs

-decrease arterial oxygen, airflow limitation

102
Q

chronic bronchitis- type B COPD signs and symptoms

A

-chronic cough

-barrel chest

-overweight

-excess body fluids

-DOE

-muscle aches

-end stage: right heart failure

103
Q

chronic bronchitis- type B COPD diagnosis

A

-hypersecretion bronchial mucous

-chronic cough

104
Q

chronic bronchitis- type B COPD treatment

A

-prevent flareups

-limit disease progression

-bronchodilators!

-corticosteroids!

105
Q

emphysema- type A COPD etiology

A

destructive changes of alveolar wall without fibrosis or dilation!

-alveolar wall breaks down and loses area to gas exchange

106
Q

emphysema- type A COPD causes

A

-smoking

-air pollution

-occupational hazards

-alpha 1 antitrypsin deficiency (smoking causes)!

107
Q

emphysema- type A COPD pathogenesis

A

-release proteolytic enzymes from inflammatory cells

-smoking inactivates alpha 1 antitrypsin

-breakdown of alveolar walls

108
Q

loss of alveolar wall in emphysema

A

-decreased capillary beds for gas exchange

-less elasticity lung tissue

-decreased air flow

-air trapping in alveoli

109
Q

emphysema- type A COPD signs and symptoms

A

-accessory muscles

-pursed lip breathing!

-leaning forward to breathe

-pink puffer (vasodilated)

-barrel chest

-clubbing

110
Q

emphysema- type A COPD treatment

A

-prevent flareups

-limit disease progression

-bronchodilators!

-corticosteroids!

111
Q

bronchiectasis etiology

A

misshaped alveoli, retain sputum which gets thick and cant cough out

-classified by shape: saccular, cylindrical, fusiform

112
Q

bronchiectasis pathogenesis

A

-dilation bronchioles

-bronchiole wall destruction

-purulent secretions lead to airway obstruction!

113
Q

bronchiectasis signs and symptoms

A

-chronic cough

-copious foul smelling, green or yellow sputum!

-fever

-pallor

-clubbing

114
Q

bronchiectasis treatment

A

Antibiotics

Bronchodilators

Chest physiotherapy

Nutrition

115
Q

cystic fibrosis etiology

A

-autosomal recessive disorder!

-cant retain sodium

-hyperthick mucous secretions

116
Q

cystic fibrosis pathogenesis

A

-CFTR on chromosome 7

-thick secretions plug glands and ducts: pancreas, enzymes break down food which you dont have so youre very thin.

117
Q

cystic fibrosis bronchopulmonary system

A

Airway obstruction

Stasis of secretions

Frequent infections

Atelectesis

Air trapping

118
Q

cystic fibrosis signs and symptoms

A

-violent cough with thick sticky sputum

-recurrent pulmonary infections

-bronchitis

-right sided heart failure (cor pulmonale)

119
Q

cystic fibrosis physical exam signs

A

-clubbing

-dyspnea

-sternal retractions

-hyperresonance

-adventitious breath sounds

-growth rate, weight, head circumference

120
Q

cystic fibrosis treatment

A

-150% caloric intake

-high protein

-replacement pancreatic enzymes

-aggressive management of pulmonary infections: leading cause of death!

121
Q

interstitial lung disease etiology

A

Infiltration of the alveolar walls by cells, fluid, & CT

-scarred lung tx, lungs dont expand and recoil

122
Q

interstitial lung disease pathogenesis

A

-not well understood

-3 pathologic patterns: inflammation, fibrosis, destruction

123
Q

interstitial lung disease signs and symptoms

A

-progressive dyspnea

-non productive cough

124
Q

interstitial lung disease diagnosis

A

-pulmonary functions tests

-honeycomb CXR

125
Q

interstitial lung disease treatment

A

Remove environmental triggers (smoking)

Immunosuppressive therapy

Steroids

Lung transplant in selected patients

126
Q

acute respiratory distress syndrome (ARDS) etiology

A

-damage to alveolar capillary membrane

-hallmark: hypoxemia refractory to increasing levels of supplemental O2, cant get person saturated with oxygen!

127
Q

acute respiratory distress syndrome (ARDS) is associated with

A

-trauma

-shock

-sepsis

128
Q

ARDS memory jogger

A

A-assault to the pulmonary system

R-respiratory distress

D-decreased lung compliance

S-severe respiratory failure

129
Q

acute respiratory distress syndrome (ARDS) pathogenesis

A

widespread inflammation leads to

-pulmonary edema

-atelectasis (collapsing alveoli)

-fibrosis causes lungs to stiffen

130
Q

acute respiratory distress syndrome (ARDS) signs and symptoms

A

-precipitating event 1-2 days prior

-increase HR, RR

-shallow rapid breathing

-crackles, wheezing

CXR changes late!

131
Q

acute respiratory distress syndrome (ARDS) diagnosis

A

-tell tale sign is CXR initially normal but progressing to “whiteout”

132
Q

acute respiratory distress syndrome (ARDS) treatment

A

-high pressure ventilation (PEEP)

-treat underlying cause

-supportive care

133
Q

Common cold/rhinitis etiology

A

viral infection of upper respiratory system

-caused by rhinovirus, parainfluenza virus, respiratory virus, coronavirus, adenovirus

-acquire immunity

-portal of entry: nasal mucosa and conjunctiva

134
Q

Common cold/rhinitis signs and symptoms

A

-increased nasal secretions

-lacrimation

-swelling and redness respiratory tract

-sore throat

-hoarseness

-headache, fever, chills

135
Q

Are antibiotics a good treatment for rhinitis

A

antibiotics are ineffective because its a virus

136
Q

rhinosinusitis/sinusitis etiology

A

-inflammation of paranasal sinuses

-blockage and narrowing of ostia that drain sinuses

137
Q

rhinosinusitis/sinusitis predisposing risks

A

-URI

-nasal polyps

-barotrauma (tissue damage)

-swimming

-abuse nasal sprays

138
Q

rhinosinusitis/sinusitis signs and symptoms

A

facial pain and headaches

139
Q

rhinosinusitis/sinusitis diagnosis and treatment

A

diagnosis: visual inspection and palpation, sinus xray

treatment: antibiotics if bacterial, decongestants, antihistamines, saline sprays, heated mist

140
Q

pneumonia etiology

A

inflammation in alveoli and interstitium of lungs

-occurs as result of: aspiration, inhalation, translocation (microorganisms escapes)!

141
Q

pneumonia classifications

A

-Community acquired vs Hospital acquired

-Bacterial vs atypical vs viral

-Bacterial

-Gram + vs gram -

-Opportunistic in immunocompromised patients

142
Q

pneumonia risk factors

A

elderly, immunocompromised, immobility, chronic illness

143
Q

pneumonia pathophysiology

A

-entry of microbes in lungs then inflammatory response in lungs

144
Q

inflammatory response in lungs with pneumonia

A

-exudate collects and thickens in alveoli and interstitium

-V/Q mismatch

-bacteria produce toxins worsening injury

145
Q

pneumonia signs and symptoms

A

-fever/chills

-crackles

-wheeze

-rales

-cough

-coryza: cold S&S

-headache

-malaise

146
Q

pneumonia diagnosis

A

-CXR

-sputum cultures and gram stain

-increased WBC count

147
Q

pneumonia treatment

A

antibiotics if bacterial, hydration, S&S relief

148
Q

tuberculosis initial infections

A

immunocompromised, malnourished, overcrowded

149
Q

tuberculosis signs and symptoms

A

-low grade fever

-night sweats

-chronic progressively productive cough

^^ tell tale signs

150
Q

tuberculosis pathophysiology

A

-caused by mycobacterium tuberculosis

-airborne

-may affect lungs and lymphatics

-Ghon complexes: hard to get antibiotics through this !

151
Q

tuberculosis diagnosis

A

-3 consecutive am sputum cultures

-CXR

-mantoux (skin test)

152
Q

tuberculosis treatment

A

-multidrug therapy for 9-12 months

-2-4 weeks isolation

-compliance!

153
Q

pleural effusion, pneumothorax, and hemothorax

A

accumulation of fluid or air in the pleural space

154
Q

pleural effusion

A

-collection of fluid or pus in pleural space

-transudative, exudative, empyema

155
Q

pleural effusion type (chylothorax)

A

collection of chylous (lymph fluid) usually associate with local infection

156
Q

pleural effusion type (hemothorax)

A

collection of blood

157
Q

pleural effusion pathophysiology

A

-changes in hydrostatic and oncotic pressure in pleural capillary and intrapleural

-increased pleural membrane permeability

-impaired lymphatic drainage

158
Q

pleural effusion signs and symptoms

A

-may be asymptomatic

-dyspnea

-pain worsens with inspiration

-decreased chest movement, breath sounds and fremitus

159
Q

pleural effusion diagnosis and treatment

A

-thoracentesis: remove fluid

-drains

-fluid analysis

-imaging

160
Q

pneumothorax

A

air in pleural space

161
Q

primary pneumothorax

A

thin, tall

20-40 yo males,

cigarette smokers

Generally occur in the apices (upper 1/3) of the lung as a result of negative pressure created during inspiration.

Smaller airways collapse leaving compressed lung and air space

162
Q

secondary pneumothorax

A

Underlying lung disease leads to weakened small airways which collapse with respirations.

163
Q

traumatic pneumothorax

A

penetrating trauma, air enters pleural space through chest wall collapsing lung

164
Q

tension pneumothorax

A

trapped air in pleural space

-major life threatening complication: mediastinal shift of heart and trachea to contralateral side

165
Q

pneumothorax signs and symptoms

A

-decreased or absent breath sounds

-hyperresonance

-dyspnea

-increased RR with respiratory alkalosis

166
Q

Pneumothroax treatment

A

-chest tube

-pleurodesis

167
Q

hemothorax etiology

A

collection of blood in plural space

168
Q

hemothorax signs and symptoms

A

-decreased or absent breath sounds

-hyperresonance

-dyspnea

-increased RR with respiratory alkalosis

-decreased RBC count!

169
Q

hemothroax treatment

A

chest tube, surgical correction, blood replacement

170
Q

what is pH

A

-reflects hydrogen ion concentration!

-degree of acidity or alkalinity

171
Q

if pH is abnormal

A

cellular function is impaired

-death below 6.9 or above 7.8

172
Q

acid

A

-increase hydrogen, decrease pH

173
Q

alkaline (base)

A

-decrease hydrogen, increase pH

174
Q

type of acid our bodies make during normal cellular metabolism

A

-carbonic acid

-metabolic acid

175
Q

carbonic acid

A

Co2 and H2O make H2CO3 (carbonic acid) , get rid through respiratory system

176
Q

metabolic acid

A

kidney regulated

-becomes lactic acid

-ex: anaerobic metabolism

177
Q

buffers

A

-first line of defense

-immediate

-chemicals control pH

-keeps 20:1 bicarbonate to Co2

178
Q

bicarbonate buffer

A

-most important in extracellular fluid!

-HCO3- (weak base) bicarbonate

-H2CO3 (weak acid) carbonic

179
Q

too much acid in bicarbonate buffer

A

bicarbonate takes up released H and become carbonic acid, excreted through respiratory system

180
Q

too little acid in bicarbonate buffer

A

bicarbonate releases H

181
Q

respiratory system

A

-second line of defense

-Co2 and h20 make carbonic acid (H2CO3)

182
Q

what kind of acid do the lungs excrete

A

carbonic acid and water

183
Q

what is the indicator of lung effectiveness

A

PaCo2

184
Q

what do the lungs do if the Co2 is high?

A

hyperventilate, rate and depth increase and “blow off” CO2

-PaCo2 high means carbonic acid accumulated in blood

185
Q

what do the lungs do if the Co2 is low?

A

hypoventilation, rate and depth decrease

-retain carbonic acid (Co2) because not enough

186
Q

renal system

A

3rd line of defense

-excrete any acid except carbonic acid

-excrete or retain H

-excrete or retain HCo3 (bicarbonate)

187
Q

kidneys excrete H if

A

too acidic (low pH)

188
Q

kidneys retain H if

A

too basic (high pH)

189
Q

kidneys retain HCo3 (bicarbonate) if

A

too acidic

190
Q

kidneys excrete HCo3 (bicarbonate) if

A

too basic

191
Q

what is the indicator of renal effectiveness

A

HCo3 (bicarbonate)

192
Q

how do the lungs compensate for the kidneys?

A

compensate for acid imbalances of metabolic acids

-get rid of or add carbonic acid to balance kidneys metabolic acids

193
Q

how do the kidneys compensate for the lungs?

A

compensate for acid imbalances of carbonic acids

-get rid of or add metabolic acids to balance lungs carbonic acid

194
Q

if compensation has been achieved

A

pH is within 7.35-7.45

195
Q

respiratory acidosis

A

caused by hypoventilation!

-excess carbonic acid (high PaCo2): hypercapnia

196
Q

respiratory acidosis etiology

A

-COPD Pulmonary edema

-Pneumonia

-Airway obstruction

-Underventilation on vent

-Hypoventilation

-Anesthetic, sedatives, narc overdose

-Neuromuscular disorders

-Severe spinal deformities

-CNS depression

-Cardiopulmonary arrest

197
Q

respiratory acidosis clinal manifestations

A

-hypercapnia

-anxiety

-restlessness

-headache

-lethargic

-fatigue

-SOB

-tachypnea

-cough

-dysrhythmias (hyperkalemia)

-advanced: confusion, somnolence. coma

198
Q

what system compensates for respiratory acidosis

A

-increased renal excretion of H and retention of HCO3- (bicarbonate)

199
Q

respiratory acidosis treatment

A

improve ventilation

-oxygen

-bronchodilation

-treat infection

200
Q

respiratory alkalosis

A

hyperventilation!

-carbonic acid deficit (low Co2): hypocapnia

-increased respiratory acid excretion (RR>20)

201
Q

respiratory alkalosis etiology

A

-lung disease with SOB

-overventilation on vent

-acute pain

-anxiety

-prolonged sobbing

-alcohol intoxication

-stimulation of brain stem

202
Q

respiratory alkalosis clinical manifestations

A

-hypocapnia

-increased neuromuscular excitability: hypocalcemia and hypokalemia

-cerebral vasoconstriction

203
Q

what system compensates for respiratory alkalosis

A

-decreased renal excretion of H and increased excretion of HCO3- (bicarbonate)

204
Q

respiratory alkalosis treatment

A

identify underlying trigger

-pain management

-breathe in paper bag

205
Q

metabolic acidosis

A

excess any acid except carbonic acid (H2CO3) or decrease in base or combination of both

206
Q

metabolic acidosis etiology

A

-ketoacidosis

-lactic acidosis

-fistulas

-electrolyte imbalance

-kidney disease

-decreased base: assidosis (diarrhea)

207
Q

metabolic acidosis clinical manifestations

A

-neuromuscular fatigue

-confusion

-drowsiness

-twitching

-respiratory distress

-nausea and vomiting

-hyperkalemia

-tachycardia

208
Q

what system helps compensate for metabolic acidosis

A

respiratory hyperventilation

-increased rate and depth

209
Q

metabolic acidosis treatment

A

correct underlying disorder

210
Q

what potassium imbalance happens with acidosis

A

too much hydrogen causing hyperkalemia

-need to kick out potassium

211
Q

metabolic alkalosis

A

deficit of any acid besides carbonic acid or an increase in base or combination

212
Q

metabolic alkalosis etiology

A

decreased metabolic acid:

-emesis

-gastric suction

-increased renal secretion

-hypokalemia

increased base (bicarbonate):

-antacids

-transfusion

-excess IV sodium bicarbonate

213
Q

metabolic alkalosis clinical manifestations

A

-hypotension

-hypokalemia: muscle spasms and weakness

-hypocalcemia: Chvosteks sign (face twitches with touch), Trousseaus sign (hand twitches with blown up BP cuff)

214
Q

what system helps compensate for metabolic alkalosis

A

respiratory hypoventilation

215
Q

metabolic alkalosis treatment

A

electrolyte and fluid replacement

216
Q

alkalosis causes

A

hypokalemia

217
Q

pH normal range

A

7.35-7.45

218
Q

pH 7.4 or below

A

acidosis

219
Q

pH 7.41 or above

A

alkalosis

220
Q

PaCO2 normal value

A

-35-45 mm/Hg

221
Q

HCO3 (bicarbonate)normal value

A

22-26 mEq/L

222
Q

PaCO2 less than 35 pH

A

alkalosis (base)

223
Q

PaCO2 greater than 45 pH

A

acidosis (acid)

224
Q

HCO3 less than 22 pH

A

acidosis (acid)

225
Q

HCO3 greater than 26 pH

A

alkalosis (base)

Patho (10 decks)

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