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Respiratory and Kidney > Respiratory > Flashcards

Respiratory Flashcards

1
Q

pleural fluid

A

negative pressure making the lung stick to chest wall

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2
Q

pleurisy

A

inflammation of pleural cavity, sharp pain worse on inspiration

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3
Q

visceral pleura

A

insensitive to pain, relay stretch sensation only

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4
Q

cause of pleurisy

A

viral infections, pulmonary embolism, myocardial infarction, pneumothorax, pericarditis, pneumonia

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5
Q

airway geometry

A

divides 23 times, exchange only in last 4 generations (alveolar ducts and alveoli)

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6
Q

compliance definition

A

delta volume over delta pressure

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7
Q

hydrostatic pressure

A

relative to barometric pressure, cm of water above atmospheric

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8
Q

pleural pressure

A

subatmospheric, mouth is open and lungs are held inflated by difference in pressure

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9
Q

elastic recoil forces

A

inward for lungs, outward for chest, equal and opposite at FRC

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10
Q

functional residual capacity

A

amount of gas present in lungs when mouth is open and respiratory muscles are relaxed

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11
Q

source of lung elastic recoil

A

lung tissue elastic from collagen and elastin, surface tension forces (surface tension main contributor to lung recoil)

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12
Q

surface tension

A

from cohesive forces between liquid molecules

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13
Q

surface tension on alveolus

A

surface tension forces tend to collapse it, towards the center

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14
Q

shunt

A

vascular pathway in which there is no gas exchange

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15
Q

pulmonary surfactant

A

90% phospholipids and 10% proteins, secreted by alveoli type II cells, mostly dipamitoyl phosphatidyl choline

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16
Q

surface tension and pulmonary surfactant

A

more concentrated the surfactant is, more the surface tension is lowered

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17
Q

ARDS

A

reduced production of surfactant or increased destruction of surfactant

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18
Q

IRDS

A

high level of collapse, administer surfactant using bronchoscope, grunting noises, acts like a shunt

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19
Q

inhalation

A

active process, diaphragm, external intercostal muscles (lift the ribs when they contract)

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20
Q

accessory muscles

A

shoulder girdle, used in exercise, coughing, sneezing, COPD and emphysema

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21
Q

tripod position

A

assumed by people in respiratory distress, optimizes mechanics of respiration by utilizing accessory muscles of neck and upper chest

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22
Q

exhalation

A

passive process, diaphragm relaxes, volume decreases, alveolar pressure becomes positive

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23
Q

forced exhalation

A

contract internal intercostals, contract abdominal muscles (push guts into the diaphragm)

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24
Q

Boyle’s Law

A

pressure inverse to volume

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25
Q

transmural pressure

A

palv-ppl

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26
Q

begin inhalation transmural pressure

A

transmural greater than recoil so lung begins to expand, alveoli increase in size and decrease in pressure

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27
Q

end inhalation transmural pressure

A

forces are balanced, flow is zero

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28
Q

chest flail

A

chest wall caves in, moves in the opposite manner, cannot generate sufficiently low intrapleural pressure during inhalation, mechanical ventilation with positive pressure

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29
Q

pneumothorax-tension vs non-tension

A

shift of mediastinum away from pneumothorax
tension-more air in pleural cavity with each breath
non-tension-not as dangerous

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30
Q

atelactasis

A

no air entering pleural caivty, mediastinal shift to side of collapse

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31
Q

spontaneous pneumothorax

A

without blunt force

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32
Q

primary spontaneous pneumothorax

A

without any existing lung pathology

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33
Q

secondary spontaneous pneumothorax

A

arising due to lung disease

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34
Q

traumatic pneumothorax

A

blunt force trauma

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35
Q

iatrogenic pneumothroax

A

trauma due to medical procedure

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36
Q

treatment of pneumothorax

A

needle aspiration or insertion of one-way chest tube

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37
Q

specific compliance

A

normalizes compliance value to the total lung capacity

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38
Q

measurement of compliance

A

spirometry

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39
Q

total compliance

A

from lung and chest wall, 1/total=1/chest+1/lung

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40
Q

lung compliance measurement

A

esophageal balloon

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41
Q

alveolar simplification

A

tissue destruction due to increased breakdown of structural proteins, happens in emphysema

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42
Q

Emphysema morphological

A

alveolar simplification increases compliance, increases FRC, gas transfer diminished

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43
Q

centrilobar emphysema

A

central portion of secondary pulmonary lobules, superior parts of lung, exposure to chemicals and smoking

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44
Q

panacinar emphysema

A

uniformly destroys alveolus, mainly lower half of lungs. alpha 1 antitrypsin and Ritalin induced emphysema

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45
Q

decrease in compliance

A

fibrosis-more difficult to inflate, loss of surfactant

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46
Q

increase in compliance

A

emphysema, loss of elastic fibers, age, easier to inflate

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47
Q

airways resistance

A

should be in greatest in small airways but decreased by parallel arrangement, greatest airway resistance is in the largest airways

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48
Q

silent zone

A

low airway flow velocity and low airway resistance, applies to small airways

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49
Q

expansile forces

A

positive alveolar and negative pleural keep airway open

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50
Q

dynamic compression

A

pressure outside is greater than the pressure inside, collapsing more likely in forced exhalation because pleural pressure becomes positive

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51
Q

Bernoulli’s effect on airway

A

faster airflow=lower pressure, lower pressure promotes collapse

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52
Q

cartilaginous rings

A

prevent collapse caused by high flow rates

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53
Q

airway in emphysema

A

loss of radial traction
loss of tissue
high velocity, low pressure

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54
Q

asthma

A

edema of wall
mucus narrowing airway
high velocity, low pressure

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55
Q

tethering

A

resist collapse better, loss in emphysema patients

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56
Q

tidal volume

A

volume of air inspired or expired with each breath

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57
Q

dead space

A

aire which a person breathes but is not used for gas exchange (fills respiratory passages like the nose, pharynx, and trachea)

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58
Q

residual volume

A

amount of air in lungs which cannot be exhaled or pushed out of lungs

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59
Q

total lung capacity

A

volume of air in the lungs after a maximal inspiratory effort

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60
Q

forced vital capacity

A

amount of air that can be exhaled as quickly during a forced exhalation

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61
Q

forced expiratory volume in 1 second

A

amount exhaled in first second, should be 80% of FVC

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62
Q

functional residual capacity

A

volume of air in lung when lung and chest wall have equal recoil force

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63
Q

lung capacity

A

sum of two or more volumes

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64
Q

direct measure of spirometry

A

TV, FVC, FEV1, FEF

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65
Q

not measured on spirometry

A

RV, FRC, TLC

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66
Q

measure of FRC

A

helium dilution test, COPD use box body plethysmography

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67
Q

FRC supine

A

lesser, body contents pushing into chest

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68
Q

FRC and RV with age

A

increase (softer)

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69
Q

obesity and pregnancy on FRC

A

decrease FRC

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70
Q

kyphoscoliosis

A

abnormal curvature of spine, decrease FRC

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71
Q

emphysema

A

increase FRC, barrel chest syndrome

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72
Q

obstructive diseases

A 
emphysema
asthma
bronchitis
cystic fibrosis
COPD
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73
Q

restrictive disease

A 
pulmonary fibrosis
sarcoidosis
silicosis
asbestosis
Wegener's granulomatosis
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74
Q

FEV1 and FEF 25-75

A

lower in patient with obstructive pulmonary disease

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75
Q

FEV/FVC

A

increased in restrictive

decreased in obstructive

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76
Q

slope PEF curve

A

decreased in obstructive

increased in restrictive

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77
Q

flow loop obstructive

A

shift to left (larger volumes)

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78
Q

flow loop restrictive

A

shift to right (smaller volumes)

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79
Q

flow loop high airway resistance

A

no change in volumes

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80
Q

variable intrathoracic lesion

A

tumor of lower trachea, inside the thoracic cage, problem with expiration

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81
Q

variable extrathoracic lesion

A

vocal cord paralysis, fat deposits, outside thoracic cage, airway compressed on inspiration

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82
Q

fixed obstructions

A

foreign bodies or scarring, affect both inspiration and expiration

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83
Q

methacholine challenge test

A

concentrations of methacholine increase, decline in 20%, if less than 8 hyperactive airways

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84
Q

problems with methacholine challenge

A

COPD or allergic rhinitis test positive, asthma with anti-inflammatory will test negative, asthma triggered by specific agents may test positive

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85
Q

DLCO

A

depends on area available for exchange and thickness of the alveolar capillary membrane
measure of conductance

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86
Q

Henry’s law

A

amount of gas dissolved in fluids depends on their solubility coefficients and partial pressures

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87
Q

flow of gases

A

always move down partial pressure gradients

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88
Q

compartments of O2

A

dissolved (insolube)-contributes to partial pressure

bound to hemoglobin-does not contribute to partial pressure

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89
Q

Hb

A

bind 4 O2 molecules, acts as buffer (tissue PO2 only changes a bit from large drop in PO2)

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90
Q

alveolar movement of O2

A

moves from alveolus into capillary and then binds to Hb

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91
Q

tissue movement of O2

A

dissolved oxygen into tissue, lowers PO2 and causes Hb to release O2

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92
Q

O2 content

A

total amount of O2 in blood, dissolved plus bound to Hb

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93
Q

arterial to venous

A

drops 5%

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94
Q

anemia

A

PaO2 normal, PvO2 low, extraction is difficult

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95
Q

CO poisoning

A

reduces O2 transport, PaCO=0, reduces O2 transport, unloading of O2 can only happen when PO2 is very low

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96
Q

carboxyhemoglobin

A

cherry red in color, CO poisoning cherry red skin

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97
Q

therapy for CO poisoning

A

95% O2 or pure O2

95% stimulates respiratory centers in brain

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98
Q

O2 capacity

A

maximal amount of oxygen Hb is capable of carrying
decreased-anemia, CO poisoning
increased-polycythemia

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99
Q

pulse oximeter

A

measures saturation of Hb (650 red and 900 blue), does not tell how much Hb and what it is saturated with (not helpful with CO poisoning or anemia)

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100
Q

arterial blood gas

A

tells pulmonary function, venous does not

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101
Q

P50

A

partial pressure of oxygen when Hb is 50% saturated

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102
Q

shift to right

A

H increase
temperature increase
PCO2 high
increase 2,3 DPG

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103
Q

erythropoesis

A

increased blood volume and increased viscosity of blood create increase in workload (polycythemia)

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104
Q

transport of CO2

A

dissolved
as bicarbonate
bound to hemoglobin (carbamino)

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105
Q

diffusion of CO2

A

diffuses faster, requires less of a pressure gradient

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106
Q

CO2 in lungs

A

Cl moves out and CO2 moves in

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107
Q

CO2 in tissue

A

Cl moves in and CO2 moves out

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108
Q

carbamino transport

A

only 5%, fast reaction

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109
Q

Haldane effect

A

PO2 is low and affinity of Hb for CO2 increases, aids in loading of RBCs with CO2

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110
Q

CO2 and partial pressure

A

linear, no saturation kinetics

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111
Q

defense mechanism of lung

A

macrophages released

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112
Q

air conditioning

A

nasal mucosa and nasal turbinates heat and humidify air

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113
Q

olfaction

A

detect odors

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114
Q

filtration

A

particles removed by nose, cilia lining moves others up (mucociliatory escalator)

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115
Q

immotile cilia syndrome

A

scarring and inflammation

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116
Q

blood filter

A

can trap clots, bubbles, fat cells

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117
Q

blood reservoir

A

blood is expelled from pulmonary circulation to systemic

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118
Q

metabolism of circulating substances

A

E1, E2, F2 alpha removed from lungs, A1, A2, I2 are unaffected

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119
Q

bronchial circulation

A

2% of CO, drains into pulmonary veins, shunt

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120
Q

pulmonary circulation

A

represents total cardiac output

121
Q

characteristics of pulmonary circulation

A

small, low resistance, soft and distensible, low resistance and low pressures

122
Q

zone 1

A

not perfused (A>a>v)

123
Q

zone 2

A

intermittently at systolic pressure (a>A>v)

124
Q

zone 3

A

always perfused (a>v>A)

125
Q

resistance in lung

A

resistance decreases as you go to the bottom of the lung, perfusion greatest at bottom of lung

126
Q

hemorrhage and general anesthesia

A

high amounts of zone 1

127
Q

exercise

A

increase in zone 2 and zone 3

128
Q

PEEP

A

zone 1, can lead to right heart failure

129
Q

alveolar hypoxia

A

smooth muscle contracts in low PO2 to try to V/W mismatch

130
Q

recruitment

A

passive, blood into unperfused capillaries

131
Q

distension

A

stretching of existing pulmonary capillaries

132
Q

alveolar vessels

A

high volume, high resistance

low volume, low resistance

133
Q

extra-alveolar vessels

A

high volume, low resistance
low volume, high resistance
radial traction helps keep it open

134
Q

mechanical ventilation

A

PVR elevated, high resistance, leads to right heart failure

135
Q

pulmonary angiography

A

into pulmonary artery, monitored by X rays, Xenon is insolube

136
Q

V/Q scan

A

albumin microaggregates with Tc or I, gamma rays, few capillaries=dark

137
Q

pulmonary edema

A

results in impaired gas exchange

138
Q

hydrostatic edema

A

caused by increased capillary pressure
no change in Kf and sigma
usually occurs in left heart failure (ex. mitral stenosis), shows Kerly B lines

139
Q

permeability edema

A

increase in permeability of vessel wall, wall is more porous, principal in ARDS, Kf can change because of bacterial toxins

140
Q

ARDS

A

persistent lung inflammation and increased capillary permeability, diffuse alveolar damage and pulmonary edema

141
Q

high altitude pulmonary edema

A

atmospheric PO2 is low, leads to low alveolar PO2, vasoconstriction due to hypoxia, leaking across membranes

142
Q

rate of diffusion

A

highly impacted by changes of partial pressure

143
Q

factors governing gas exchange

A

gradient in partial pressure
thickness and properties of membrane
surface area of alveolus

144
Q

perfusion limitation

A

gas diffuses through the membrane and equilibriates quickly, O2, CO2, N2O

145
Q

diffusion limited

A

PaCO=0, ability of membrane to transfer CO by diffusion is low

146
Q

DLCO

A

measure how well a patient’s lungs exchange gases, measurement of conductance

147
Q

decrease DLCO

A

obstructive (decrease area)
restrictive (increase thickness)
pulmonary edema-increase tension
embolus, edema, tumors, sarcoidosis, lupus, anemia, pregnancy, alveolar proteinosis, smokers, lung resection, pulmonary hypertension

148
Q

no change in DLCO

A

bronchitis
myasthemia gravis
chest wall deformities
asthma

149
Q

increase in DLCO

A

supine, exercise, polycythemia, asthma, hemorrhage, left to right shunt, obesity

150
Q

ventilation distribution

A

higher at the bottom of the lung

151
Q

compliance distribution

A

higher at the bottom of the lung

152
Q

oxygen consumption and CO2 production

A

250 for O2 and 200 for CO2

153
Q

alveolar ventilation

A

takes into consideration dead space

154
Q

anatomical dead space

A

large airways

155
Q

physiological dead space

A

alveoli that are ventilated but not perfused

156
Q

Bohr’s assumption

A

CO2 in atmosphere is negligible, CO2 expired comes from alveoli (alveoli that are ventilated and perfused)

157
Q

hyperventilation

A

decreases PACO2

158
Q

hypoventialtion

A

increases PACO2

159
Q

alveolar ventilation proportions

A

proportional to metabolic rate, inverse to CO2

160
Q

central chemoreceptors

A

located in brainstem, sensitive to CO2 in brain interstitium, can adapt

161
Q

peripheral chemoreceptors

A

cannot adapt, neck region, most sensitive to PO2 (also H and PCO2), located in carotid and aortic bodies

162
Q

Blood brain barrier

A

permeable to CO2, poorly permeable to H or HCO3

163
Q

buffering capacity of CSF

A

low, lacks hemoglobin, low HCO3, low protein levels

164
Q

amplification of respiration

A

adding hypoxia, hypercapnia, and acidosis all work together to amplify respiration

165
Q

supplemental O2 in lung disease

A

ventilation dependent on hypoxia, giving O2 to patient can depress ventilation

166
Q

phrenic nerve

A

C3-C5, controls muscles of inspiration, FRC most near normal if damaged phrenic nerve

167
Q

dorsal respiratory groups

A

inspiratory neurons, responsible for basic rhythm of breathing

168
Q

ventral respiratory groups

A

inspiratory and expiratory, controls upper airways

169
Q

apneustic

A

pons, stimulates VRG and DRG, if cut will hold inspiration

170
Q

pneumotaxic center

A

pons, prevents apneuistic, enhances and fine tines rhythmicity of breathing

171
Q

congenital central hypoventilation syndrome

A

central pattern generator is inoperative, insensitive to chemoreceptors, no automatic control but voluntary breathing is intact, danger at night when they sleep (permanent tracheostomy)

172
Q

increase in respiratory drive

A

cocaine, amphetamines, caffeine

173
Q

decrease in respiratory drive

A

cerebral edema, intracerebral abnormality, acute poliomyelitis, ingestion of alcohol, opiates, benzo, barbituates, anesthetics

174
Q

body temperature on ventilation

A

deep hypothermia depresses ventilation
fever increases ventilation
painful stimuli increase ventilation and panic

175
Q

cheyne-stokes breathing

A

gradual increase in volume and frequency of breathing, PCO2 changes in advance of PCO2 in respiratory neurons, corresponds to brain PCO2

176
Q

Biots respiration

A

hyperapnea, meningitis patients, deep long pauses

177
Q

Kussuads

A

deep movements, drive high and more frequent, diabetic ketoacidosis

178
Q

obstructive sleep apnea

A

inspiratory process is intact

179
Q

central sleep apnea

A

signal from thoracic fades

180
Q

high pressure environments

A

treatment of gaseous gangrene (wound healing)
SCUBA
caissons for bridges

181
Q

increase in pressure

A

1 atmosphere every 10 meters

182
Q

compression on descent

A

mask squueze
ear drum rupture
middle ear squeeze

183
Q

expansion on ascent

A

pneumothorax, dissection of mediastinum, gas emboli, exhale continuously when going to surface to avoid

184
Q

oxygen toxicity

A

too much can cause alveolar and endothelial membrane damage, due to peroxide and oxygen radical interactions (normal air at 6 ATA can cause seizures in 5-10 minutes)

185
Q

nitrogen toxicity

A

acts the same way as alcohol, the bends if rise too rapid-bubbles

186
Q

hypoxia of high altitude

A

peripheral chemoreceptors sense hypoxia, increase ventilation

187
Q

acute adjustments

A

acute increase in ventilation due to peripheral chemoreceptors

188
Q

acclimation to altitude

A

hyperventilation, increased hematocrit, increased capillary growth, plasma volume decrease (reduced water intake)

189
Q

acute mountain sickness

A

greater than 8000 feet, experience headaches, insomnia, weakness, associated with fluid retention, treated with diuretic

190
Q

high altitude cerebral edema

A

ataxia, swelling causes brain ischemia and herniation

191
Q

high altitude pulmonary edema

A

most serious, highest mortality, most commonly seen in athletic young males

192
Q

ideal V/Q ratio

A

0.8

193
Q

shunt

A

ventilation but not perfused

194
Q

A-a gradient

A

bigger the gradient, poorer the exchange, normal between 5 a and 15

195
Q

V/Q top of the lung

A

over ventilated and contribute to dead space (high at the top)

196
Q

V/Q bottom of the lung

A

shunt like exchange (low at the bottom)

197
Q

lung transplant outcomes

A

successful in fibrosis, in emphysema single lung transplant didnt help because air went to the bad lung (higher recoil in new lung vs high compliance in old lung)

198
Q

V/Q to partial pressures

A

inverse to PaCO2

direct to PaO2

199
Q

treatment for right heart failure

A

nitric oxide reverses hypoxic pulmonary vasoconstriction, selectively dilates ventilated blood vessels

200
Q

nitroprusside

A

increases blood flow to all lung segments, including those that are not well ventilated

201
Q

right to left shunt

A

leaves left atrium without being oxygenated

202
Q

absolute intrapulmonary shunts

A

true shunts

203
Q

low V/Q mismatch

A

hypoxemia
increased A-a gradient
hypercapnia

204
Q

compensation mechanism for V/Q mismatch

A

alveolar hypoxia leading to smooth muscle contraction

stimulation of ventilation

205
Q

result of compensation of V/Q mismatch

A

normalizes carbon dioxide

does not normalize oxygen

206
Q

limit of ventilation

A 
emphysema
bronchitis
asthma
restrictive disease
pneumonia is a classic shunt
207
Q

A-a gradient contributions

A

gravity causing V/Q mismatch
shunts
increases with age due to wear and tear
smaller in supine position

208
Q

diagnosing a shunt

A

100% oxygen, if PaO2 increases drastically it is a low V/Q mismatch

209
Q

causes of hypoxemia

A 
air with low PO2
hypoventilation
shunts
low V/Q mismatch
diffusion problem
210
Q

high V/Q ratios

A

pulmonary emboli, top of the lung

211
Q

pulmonary embolus

A

high V/Q, local inflammation which then destroys surfactant and alters capillary permeability that causes combination of low and high V/Q mismatches

212
Q

pulmonary embolism ventilation

A

increase in ventilation, work harder to breathe leading to low V/Q

213
Q

contents of perinephric spaces

A

kidneys, adrenal glands, proximal ureters, perirenal fat

214
Q

contents of anterior pararenal space

A

pancreas (except tail), second and third part of duodenum, aorta, inferior vena cava, ascending and descending colon

215
Q

intravenous pyelogram

A

replaced by CT

216
Q

pyelonephritis

A

striated nephrogram-alternating stripes or wedges of opacified and nonopacified parenchyma caused by nonhomogeneous edema

217
Q

renal cysts

A

ubiquitous, easily recognized but complicated cysts are more difficult to assess in terms of a benign or malignant lesion

218
Q

chest imaging modalities

A

plain radiography
computed tomography
magnetic resonance imaging

219
Q

technique

A

AP-at bedside
PA-preferred
lateral

220
Q

level of inspiration

A

10th rib posteriorly

221
Q

penetration

A

lower thoracic vertebrae should be visible, bronchial and vascular structures behind the heart should be seen

222
Q

rotation

A

spinous processes should be at the medial end of the clavicles

223
Q

angulation

A

if beam is angled toward head, lordotic view results

clavicles above the level of the ribs

224
Q

hilum

A

Right anterior

left superior

225
Q

pleura

A

should not be visible

226
Q

fissures of lung

A

minor is seen on PA

major is seen on lateral

227
Q

right hemidiaphragm

A

higher due to presence of liver

228
Q

left bumps of mediastinum

A

aortic arch
pulmonary trunk
left ventricle

229
Q

retrosternal

A

RV

230
Q

right side

A

right atrium

231
Q

airspace opacity

A

alveoli are filled with dense material

232
Q

silhouette sign

A

airspace opacity resulting in loss of lung-mediastinum or lung-diaphragm interface

233
Q

interstitial opacities

A

thin linear or reticular opacities

234
Q

patterns of pneumonia

A

lobar-pneumococcal
lobular-staphyloccocal
interstitial-viral, mycoplasma

235
Q

atelectasis

A

collapse of lung, post operative due to mucus plugging, mediastinum shifts toward opposite side due to contralateral hyperinflated lung

236
Q

transudative

A

low protein

237
Q

exudative

A

high protein

238
Q

diagnosing pulmonary embolism

A

CTA

239
Q

lung masses

A

solitary-primary lung carcinoma

multiple bilateral masses-metastatic disease

240
Q

renal capsule

A

fibrous capsule that can be stripped off the surface of the kidney

241
Q

renal cortex

A

outer zone of kidney

242
Q

renal medulla

A

inner zone of kidney consisting of pyramids and columns

243
Q

renal sinus

A

space within the kidney that is occupied by the renal pelvis, calices, vessels, nerves, fat

244
Q

renal papilla

A

apex of renal pyramid where urine is excreted into the minor calyx

245
Q

minor calyx

A

receives urine at the papilla, several minor calyces combine to form major calyx

246
Q

major calyx

A

formed by union of minor calyces, combine to form the renal pelvis

247
Q

renal pelvis

A

funnel shaped superior end of the ureter that lies within the renal sinus

248
Q

ureter

A

muscular duct that carriers urine from the kidney to the urinary bladder

249
Q

risks for hypertension

A

coronary artery disease, congestive heart failure, stroke

highest correlation is with stroke

250
Q

normal

A
251
Q

pre hypertension

A

120-139/80-89

252
Q

stage 1

A

140-159/90-99

treat with mono drugs

253
Q

stage 2

A

> 160/>100

treat with combo drugs

254
Q

benefits of lowering blood pressure

A

prevents strokes better than MI

255
Q

compelling indications

A 
heart failure
diabetes with proteinuria
Coronary artery disease (prior MI)
chronic renal insufficiency
CVA
256
Q

Guyton model

A

altered renal set point necessary to maintain hypertension

257
Q

renovascular hypertension

A

arteriograms remain gold standard

stenosis causes one to sense low BP and secrete renin

258
Q

hyperaldosteronism

A

nonstimulatable renin and nonsuppressable aldosterone
hypokalemia in face of ACE inhibitor is red flag
stimulate renin with diuretic and suppress aldo with volume expansion

259
Q

pheochromocytoma

A

autonomous production of vasoconstrictors (epinephrine and norepinephrine)

260
Q

hypertension in CRF

A

significant renin stimulation, inhibitor of sodium pump

261
Q

essential hypertension

A

genetics

environmental-stress, alcohol, dietary salt, smoking, sedentary

262
Q

causes of hypertension

A

primary (essential) more common than secondary

263
Q

malignant hypertension

A

medical emergency, acute vascular injury in context of HTN, found on retinal examination

264
Q

secondary hypertension

A

early, without family history, severe or difficult to control

265
Q

types of renovascualr hypertension

A

fibromuscular dysplasia-young, female, familial

266
Q

atheromatous

A

older, correlates with PVD

267
Q

grading of fundoscopic exam

A

I-narrowing
II-AV nicking
III-hemorrhages or exudate
IV-papilledema

268
Q

risk factors for atherosclerosis

A 
smoking
dyslipidemia
>60
male or postmenopausal female
family history
269
Q

uncompicated hypertension

A

diuretics

270
Q

diabetes

A

ACE inhibitors or ARB

271
Q

myocardial infarction

A

beta blocker

272
Q

systolic heart failure

A

ACE inhibitors or ARB

273
Q

pulmonary responses to exercise

A

increased ventilation and improved V/Q matching

274
Q

cardiovascular responses to exercise

A

increase in cardiac output and redistribution of blood flow

important in determining maximum O2 consumption

275
Q

VO2 max

A

highest rate of O2 consumption that can be achieved during maximal exercise

276
Q

plateau in VO2

A

primary criterion that indicates VO2 max has been reached

277
Q

determinants of VO2 max

A

genetics is major determinant, training, peaks at 18 and then declines, females lower (gap decreases with training)

278
Q

O2 uptake

A

increases linearly until plateau

279
Q

minute ventilation

A

increases linearly until disproportionate increase at ventilatory threshold

280
Q

arterial CO2

A

constant until ventilatory threshold is reached, metabolic acidosis triggers increase in ventialtion that causes PaCO2 to drop

281
Q

arterial pH

A

constant until ventilatory threshold where acidosis occurs

282
Q

PaO2

A

relatively constant during exercise

283
Q

initial increase in ventilation

A

mediated by central command mechanism, delayed responses are mediated by mechanical and chemical signals arising from skeletal muscles and cardiovascualr reflexes

284
Q

autonomic nervous system activation

A

mechanoreceptors and chemoreceptors, feed forward mechanism in anticipation of exercise (decreases vagal output and increases sympathetic output), net result is increase in force and rate of contraction

285
Q

mechanical mechanisms

A

muscle pump activity, respiratory activity to enhance blood flow and venous return

286
Q

metabolic mechanisms

A

vasodilator metabolites for contracting muscles

287
Q

cardiac output from exercise

A

increases due to increase in heart rate and stroke volume

288
Q

heart rate

A

increases in direct proportion to exercise intensity

289
Q

stroke volume

A

moderate increases but plateaus, maintained by pumping muscles, larger inspirations, venoconstriction and arterial vasodilation, sympatheric stimulation, lusitropy, atrial kick, declines when those mechanisms cannot keep up

290
Q

systemic vascular resistance

A

decreases as intensity increases due to vasodilation

291
Q

systolic blood pressure

A

increases progressively, pulse pressure also increases

292
Q

mean arterial pressure

A

increases less than would be expected because CO increases and SVR decreases

293
Q

blood pressure and HR

A

usually inverse but arterial baroreceptor reflex is operating at higher set point so it does not fire to slow HR

294
Q

blood flow to skeletal muscles

A

net effect of widespread sympathetic stimulation is shunting of blood flow from inactive tissues to actively contracting muscles

295
Q

blood flow to skin

A

increased due to vasodialtion sensed by hypothalamus, if it is too intense then sympathetic will divert it away

296
Q

blood flow to kidney and splanchnic circulation

A

decreases due to sympathetic activity

297
Q

changes in cardiac vascular function curves

A

increases equilibrium point where both increase (due to decrease in SVR and increase in CO)

298
Q

training

A

increases O2 delivery and O2 extraction, increases maximal stroke volume does not change heart rate), extraction improved by increased capillary proliferation and increased density to decrease diffusion barrier, increased mitochondria, increased plasma compartment (sports anemia)

299
Q

factors to training

A

genetic component

Respiratory and Kidney (2 decks)

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