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CardioPulm > Midterm Deck 2 > Flashcards

Midterm Deck 2 Flashcards

1
Q

What are the 2 rules of thumb for acid base compensation in the body

A

It will never get us back to exactly normal, always made by the other system than what caused problem

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2
Q

What parts of the kidney nephron can secrete HCO3 and H+ to regulate pH change

A

Distal convoluted tubule and collecting duct

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3
Q

How do we compensate respiratory alkalosis with the kidneys

A

Reabsorb H+ and excrete HCO3

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4
Q

How do kidneys attempt to fix respiratory acidosis

A

Secrete H+ and reabsorb HCO3

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5
Q

How do we try to fix pH problems with ventilation

A

Increase ventilation to blow off more CO2 and INCREASE pH

Or

Decrease ventilation to retain more CO2 and DECREASE pH

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6
Q

How do we predict an expected HCO3 level for acute respiratory acidosis

A

expected [HCO3]= 24 + ((PaCO2-40)/10)

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7
Q

How do we predict an expected HCO3 level for chronic respiratory acidosis

A

Expected [HCO3]= 24+ 4((PaCO2-40)/10)

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8
Q

How do we predict an expected HCO3 level for acute respiratory alkalosis

A

Expected [HCO3]= 24-2((40-PaCO2)/10)

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9
Q

How do we predict an expected HCO3 level for chronic respiratory alkalosis

A

Expected [HCO3]=24-5((40-PaCO2)/10)

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10
Q

In what range is metabolic acidosis adequately compensated?

A

When Expected PaCO2 = (1.5[HCO3]+8) plus or minus 2

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11
Q

In what range is metabolic alkalosis adequately compensated

A

When the change in PaCO2 = (0.5 to 1) * change in HCO3

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12
Q

What is a normal osmolarity in the body?

A

290 mOsmoles/L and is tightly regulated

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13
Q

What’s the equation to calculate osmolarity?

A

(2*serum Na+) + (BUN/2.8) + (glucose/18)

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14
Q

why would it be advantageous to use echo for cardiac imaging

A

cheap, portable, best view of valve structure and function

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15
Q

at what vertebral level do you find the apex of the lungs

A

T1

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16
Q

at what vertebral level do you find the sternoclavicular joint

A

T2

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17
Q

at what vertebral level do you find the top of the aortic arch

A

T3

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18
Q

at what vertebral level do you find the bifurcation of trachea and sternal angle

A

T4-5

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19
Q

at what vertebral level do you find the top of heart

A

T6

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20
Q

at what vertebral level do you find the diaphragm opening for inferior vena cava

A

T8

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21
Q

at what vertebral level do you find the xiphoid process

A

T9

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22
Q

at what vertebral level do you find the diaphragm opening for esophagus

A

T10

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23
Q

at what vertebral level do you find the diaphragm opening for aorta

A

T12

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24
Q

at what vertebral level do you find the attachment of crura of diaphragm

A

L3

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25
Q

What is more commonly used to view coronal section of anterior axilla: MR or CT

A

CT (unless pt is allergic to contrast) because its a much sharper image and easier to create reconstructions

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26
Q

Which xray view is needed to see oblique fissure of the lung

A

Lateral view

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27
Q

Which X-ray angle is needed to see horizontal fissure

A

Lateral view or PA view

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28
Q

Where. Does the axis. Of the heart project

A

45 degrees anteriorly, 45 degrees left

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29
Q

When using echocardiography + doppler to image the heart, how do we know the direction of blood flow

A

Red is flow toward the transducer (anterior chest wall) and blue is away from the transducer. Yellow is turbulence

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30
Q

What causes a meniscus sign (seen on lung X-ray)

A

Pleural effusion (surface tension of fluid on pleura causes concavity near diaphragm dome)

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31
Q

Term describing: Pleural effusion confined to one or more pockets in pleural space seen in X-ray

A

Loculated

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32
Q

How do you identify interstitial pulmonary edema on X-ray

A

Kelley b lines

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33
Q

The tip of an enteric feeding tube should extend where

A

To upper left quadrant of abdomen (stomach)

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34
Q

Pleural fluid, pneumonia, and atelectasis are all pathologies that appear on imaging as an obstcuration of normal borders (of heart/lung/diaphragm) what do we call this?

A

Silhouette sign

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35
Q

what condition causes destruction of alveoli creating large air spaces and loss of capillaries in the lungs

A

COPD/ emphysema

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36
Q

The body attempts to normalize mismatched V/Q ratios (like those created by emphysema) how?

A
  1. hypoxic vasoconstriction (to correct low V/Q)

2. bronchoconstriction (to correct high V/Q)

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37
Q

Who (capillaries or alveoli) is better at fixing a high V/Q ratio?

A

alveoli (they will bronchoconstrict)

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38
Q

Who (capillaries or alveoli) is better at fixing a low V/Q ratio?

A

capillaries (they will vasoconstrict)

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39
Q

inadequate oxygen available for use by tissues

A

hypoxia

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40
Q

inadequate oxygen in the blood

A

hypoxemia

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41
Q

total absence of oxygen delivered to tissue

A

anoxia

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42
Q

form of hypoxia where PaO2 is below normal because alveolar oxygen is reduced (altitude) OR because blood can’t equilibrate with air (emphysema)

A

hypoxic hypoxia

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43
Q

form of hypoxia where lungs work but blood can’t carry oxygen as well (like with CO binding or low RBC count)

A

anemic hypoxia

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44
Q

form of hypoxia where lungs work and blood can carry oxygen but tissue can’t receive it because heart can’t pump blood to the tissue (or clots)

A

circulatory hypoxia

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45
Q

name a disease which can cause two different forms of hypoxia

A

sickle cell anemia: circulatory hypoxia because the sickle cells don’t do a good job of delivering to tissue and then anemic hypoxia as we start to lose RBCs altogether

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46
Q

form of hypoxia where poison (cyanide) causes tissue to be unable to use oxygen even though the lungs and blood and circulation are working just fine

A

histotoxic hypoxia

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47
Q

what is the direct stimulus for the central chemoreceptors

A

H+ ions in the CSF

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48
Q

what blood gas do the central chemoreceptors tell the rest of the brain about

A

CO2

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49
Q

excess CO2 in the blood

A

hypercapnia

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50
Q

what do peripheral chemoreceptors detect

A

oxygen

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51
Q

who makes CSF

A

choroid plexus

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52
Q

what makes composition of CSF different than ECF or plasma

A

less protein and no cholesterol

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53
Q

how do our central chemoreceptors adjust to hypocapnia?

A

they don’t, the choroid plexus does! (it produces H+ and bicarb then ships the bicarb out with blood and sends H+ to central receptors so they sense a lower pH and think its ok to have less CO2)

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54
Q

what happens with H+ produced by the choroid plexus when it is adjusting CSF contents during hypercapnia

A

it gets deposited in the blood and taken care of by kidneys

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55
Q

what decreases as altitude increases

A

barometric pressure (and thus alveolar O2 pressure)

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56
Q

whats the first response to hypoxia?

A

peripheral chemoreceptors detect it and increase ventilation in response

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57
Q

when we increase ventilation it increases PaO2 and does what else?

A

decreases PaCO2

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58
Q

what does hypoxia do to the kidney

A

causes erythropoietin release (to increase RBC production and thus O2 carrying capacity of blood increases)

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59
Q

for every ___ m below water surface you go on a dive, the barometric pressure increases by ___ atm

A

10 m, 1 atm

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60
Q

what is the barometric pressure at 40 m below sea level

A

[40 m * (1 atm/10m)] due to water + [1 atm] due to air= 5 atm

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61
Q

why is too much oxygen bad

A

formation of superoxide anion and peroxide which are toxic to cells

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62
Q

during ascent from diving, you must keep your glottis open to let air escape the lungs. if you fail to do this what can happen

A

air embolus enters blood stream

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63
Q

as we descend below sea level, the amount of dissolved N in the blood increases. at high concentrations it has similar effects to alcohol on the CNS and this is known as what

A

nitrogen narcosis

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64
Q

if you ascend from a dive too quickly, nitrogen does not have ample time to return to a gas form and escape from the lungs. instead it returns to gas form in the tissue and causes what

A

the bends / decompression sickness (pain, parasthesias, itching, paralysis)

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65
Q

how do we treat decompression sickness

A

hyperbaric chamber forces gas back into solution then we control rate of decompression to allow the N gas to be exhaled

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66
Q

site that generates core timing (frequency) of respiratory rhythm

A

pre-botzinger complex

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67
Q

transition from inspiration to expiration helps determine frequency. what controls this by turning off inspiration?

A

pontine pneumotaxic center

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68
Q

absence of breathing

A

apnea

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69
Q

being stuck in inspiration (due to lesion in pontine pneumotaxic center)

A

apneusis

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70
Q

Where does phrenic. Nerve get 95% of its premotor innervation

A

Dorsal respiratory group

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71
Q

What are the two function of ventral respiratory group

A

Rostral part- inspiratory muscles

Caudal part- expiratory muscles

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72
Q

Who controls depth of breathing

A

DRG, VRG

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73
Q

Pontine damage would lead to increased CO2, decreased. O2 and eventually death because of what condition

A

Apneusis

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74
Q

Medullary or spinal damage would lead to increased CO2, decreased. O2 and eventually death because of what condition

A

Apnea

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75
Q

Chemoreceptors increase their firing under what conditions

A

Increased CO2 or H+

Decreased O2

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76
Q

Where do we find peripheral chemoreceptors

A

Carotid and aorta

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77
Q

Central chemoreceptors respond to what stimuli

A

H+ created in CSF after CO2 enters the brain

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78
Q

Which kind of chemoreceptors are faster at responding

A

Peripheral

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79
Q

How do. We keep. Track of our lung volume

A

Slowly adapting Pulmonary stretch receptors in the airways send signal to brain via vagus n (terminate. Inspiration)

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80
Q

When in life are slow-adapting pulmonary stretch receptors important for controlling respiration

A

Infancy, adults during exercise

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81
Q

Where do you. Find rapidly. Adapting pulmonary. Stretch receptors

A

Airways

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82
Q

What causes a response in rapidly adapting pulmonary stretch receptors of the airways

A

Irritation, foreign bodies, stretch

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83
Q

After the vagus nerve carries rapid adapting pulmonary stretch receptor signal to brain, what does brain tell body to do?

A

Cough

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84
Q

Who can detect pulmonary edema

A

J receptors

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85
Q

Where do you find j receptors

A

Near blood vessels of alveoli

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86
Q

What is the effect of J receptors after vagus takes their message to the brain

A

Cough and tachypnea

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87
Q

Protective reflexes that override the normal respiratory control system

A

J receptors and Rapidly adapting pulmonary stretch receptors

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88
Q

What brain. Structure can. Bypass medullary center completely and send input directly to muscles of respiration

A

Cortex

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89
Q

A. Measure of stretchability of the lungs (due to elastic fibers)

A

Compliance

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90
Q

When is compliance of the lung at its highest (stretchable lung that is easily inflated)

A

In normal breathing range

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91
Q

Why is there hysteresis between inspiration and expiration (hysteresis) in terms of their volume and pressure changes

A

Surfactant is not evenly distributed (randomly positioned moving apart during. Inspiration and. Back together. A. Different way during expiration)

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92
Q

How do. You calculate compliance

A

Change in volume/ change in pressure

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93
Q

What two structures combine their volume and pressure forces to make up the respiratory mechanics curve

A

Lungs (wanna shrink) and rib cage (wanna expand)

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94
Q

The elastic recoil of the lungs and that of the rib cage exactly balance each other out at what value

A

Functional residual capacity

95
Q

why is the balance point (on a volume versus airway pressure graph) for the rib cage so much higher than for the lungs

A

because of expanding forces of joints and muscle attached to rib cage

96
Q

in a normal person what is the FEV1/FVC ratio? (the air exhaled forcefully in the first second versus the vital capacity)

A

80%

97
Q

who would have a reduced FEV1/FVC ratio (below 70%)

A

obstructive disorder (emphysema or asthma)

98
Q

when the absolute values of FEV1 and FVC are both reduced to the same extent what type of dysfunction is present (lungs can’t expand but they can recoil very easily)

A

restrictive disease (fibrosis)

99
Q

explain alveolar interdependence

A

you would think that alveoli would collapse completely during exhalation but since they share walls they are all recoiling in opposite directions, so they stay open

100
Q

why must the lungs “do work”

A

to overcome elastic recoil, overcome resistance to airflow

101
Q

Whats teh most common rib fracture

A

Middle ribs fracture just anterior to costal angle

102
Q

What type of joint is manubriosternal

A

Symphysis

103
Q

What type. Of joint is xiphisternal

A

Synchondrosis

104
Q

What type of joint is sternocostal junction for rib 1? Ribs 2-7?

A

1: synchondrosis

2-7: synovial planar

105
Q

Rib dislocation occurs at what joint

A

Sternocostal

106
Q

Rib separation occurs at what joint

A

Costochondral

107
Q

Insert hypodermic needle through intercostal space to obtain fluid sample or drain fluid from pleural cavity

A

Thoracentesis

108
Q

Insertion of tube to remove large amounts of air/ fluid/ blood from pleural cavity (5th or 6th space)

A

Chest tube insertion

109
Q

Insert horoscope into pleural cavity through small incision for visualizing/ biopsying pleural cavity contents

A

Thoroscopy

110
Q

Nerves that can be involved in lung cancer

A

Phrenic, vagus, recurrent laryngeal

111
Q

Removal of lung

A

Pneumonectomy

112
Q

Procedure used to remove a specific bronchopulmonary segment (segmentectomy)

A

Lung resection

113
Q

Widespread narrowing of airways produced by contraction of smooth muscle,, edema of mucosa and. Mucus in lumen of bronchi

A

Bronchial asthma

114
Q

What separates superior form inferior mediastinum

A

Sternal angle

115
Q

What specific cavity does the heart lie in

A

Middle inferior mediastinum

116
Q

Lack of blood flow to myocardium as a result of coronary artery blockage

A

MI

117
Q

Buildup of lipids on internal walls of coronary arteries decreasing lumen size increasing likelihood of embolus or plug blocking vessel

A

Coronary atherosclerosis

118
Q

Pain originating in the heart producing strangling pain of chest: usually result of narrow or obstructed coronary arteries that produces ischemia of myocardium

A

Angina pectoris

119
Q

The fetus ductus arteriosus shunted blood in which direction

A

From pulmonary trunk to aorta to bypass nonfunctional lung (right to left)

120
Q

Where do we insert catheter for cardiac visualization of R heart and pulmonary arteries

A

Femoral v

121
Q

Atrial contraction

A

Diastole

122
Q

Ventricles contract

A

Systole

123
Q

Irregular twitching of atrial cardiac muscle fibers causing ventricles to respond at irregular intervals (circulatory usually remains fine)

A

Atrial fibrillation

124
Q

Rapid irregular ventricle twitch which renders heart unable to pump blood: requires defibrillation

A

Ventricular fibrillation

125
Q

Cardiac referred pain occurs where due to sharing spinal ganglion with other sensory fibers

A

Upper limb and superior lateral chest wall

126
Q

Space that allows surgeons to access area posterior to aorta and pulmonary trunk to clamp or insert tubes of bypass machine

A

Transverse pericardial sinus

127
Q

Pericarditis of pericardium can can lead to pericardial friction rub and what happens when left untreated

A

Pericardium can calcify

128
Q

Accumulation of fluid or pus in periardial sac that can compresses heart

A

Pericardial fusion

129
Q

Heart compression

A

Cardiac tamponade

130
Q

Cardiac tamponade can be received by what procedure

A

Pericardiocentesis

131
Q

When a small balloon is. Inserted to increase lumen size of coronary artery

A

Coronary angioplasty

132
Q

When blood clot, fat globule, or air bubble obstructs pulmonary artery

A

Pulmonary embolism

133
Q

How does the sympathetic nervous system indirectly decrease secretion through non-sweat glands

A

Vasoconstriction

134
Q

lung buds begin to develop when in development

A

week 4

135
Q

lungs derive from which germ layer

A

endoderm (they out pouch from foregut)

136
Q

appearing on the floor of the caudal end of the anterior foregut is a median outgrowth called the __ to start lung development

A

laryngeotracheal groove

137
Q

the laryngeotracheal groove at the end of week 4 protrudes to form a pouch called what

A

lung bud (laryngeotracheal diverticulum)

138
Q

fusion of folds coming from laryngeotracheal diverticulum occurs in week 5 to create what

A

tracheoesophageal septum

139
Q

ventral to the tracheoesophageal septum we find what structures

A

laryngeotracheal tube

140
Q

dorsal to the tracheoesophageal septum we find what

A

pharynx and esophagus

141
Q

the epithelium and glands of the trachea are derived from what embryonic tissue

A

endoderm

142
Q

the pulmonary epithelium of trachea is derived from what embryonic tissue

A

endoderm

143
Q

smooth muscle, connective tissue, and cartilage of the trachea are derived from what embryonic tissue

A

splanchnic mesenchyme

144
Q

lung buds split into ____ during week 5

A

primary bronchial buds

145
Q

primary bronchial buds branch into __ during week 6

A

lobar (secondary) bronchi

146
Q

lobar bronchi branch into ___ during week 7

A

tertiary bronchi

147
Q

how many tertiary bronchi form in the left lung? right lung?

A

left: 9
right: 10

148
Q

who (demographically) has the best chance of surviving premature birth based on lung development

A

african american females

149
Q

what stage of lung development occurs wk 5-17? can premature birth be viable in this stage?

A 
pseudoglandular
no survival (no alveolar-capillary membrane has formed)
150
Q

what stage of lung development occurs wk 16-25? can premature birth be viable in this stage?

A

canalicular

some can survive after minimum 21 weeks (vascularization has occurred)

151
Q

what stage of lung development occurs wk 24- birth? can premature birth be viable in this stage?

A

terminal sac

YES they will survive (they have I and II pneumocytes now)

152
Q

what are Type I pneumocytes

A

squamous epithelium where gas exchange occurs

153
Q

what are Type II Pneumocytes

A

secretory epithelium that create surfactant

154
Q

when do I and II pneumocytes show up in lung development

A

during terminal sac stage (wk 24- birth)

155
Q

when do alveoli fully mature (develop functional alveolocapillary membrane)

A

alveolar stage (from 32 wk- 8 years)

156
Q

what happens in utero to cause aspiration of amniotic fluid (to help lung development)

A

fetal breathing movements (FBM)

157
Q

what kind of pressure pushes amniotic fluid that has been aspirated up to the nose and mouth or into circulation and lymphatics so that the newborn lungs can begin to breath air

A

on the fetal thorax during vaginal delivery

158
Q

why is oligohydramnios bad for lung development

A

not enough fluid to help lungs expand/ develop = pulmonary hypoplasia

159
Q

baby born with low lung volumes, tachypnea, nasal flaring, suprasternal retractions, cyanosis, with ground glass appearance on CXR probably has what

A

respiratory distress syndrome (hyaline membrane disease)

–lack of surfactant

160
Q

which stage of lung development went wrong in a kid born with respiratory distress syndrome

A

they lack surfactant- terminal sac stage

161
Q

polyhydramnios coupled with baby secretions (drool, choke, cough, gag, inability to feed) indicates what

A

esophageal atresia

162
Q

whats the most common defect of the tracheoesophageal septum

A

tracheoesophageal fistula (esophagus ends in blind pouch superiorly and a lower segment originates above bifurcation of trachea)

163
Q

what might provide a honeycomb appearance on X-ray of a newborn child

A

congenital lung cyst (fluid or air filled)

164
Q

diffusing capacity of the lung can be reduced by anemia: true or false

A

true

165
Q

measuring TLC is needed to confirm restrictive disease: true or fasle

A

true

166
Q

air trapping leads to increase in RV: true or false

A

true

167
Q

decreased FEV1/FVC ratio is consistent with what kind of problem

A

obstructive

168
Q

what condition minimizes ability of blood to accept gas diffusing across alveolar memrbane

A

anemia

169
Q

what condition minimizes the diffusion of gas into blood because of decreased surface area of alveolar-capillary membrane

A

emphysema, pulmonary embolism

170
Q

what condition alter membrane permeability (or increase thickness) causing diffusion of gas to decrease

A

pulmonary fibrosis

171
Q

if FEV1/FVC is lower than normal and FVC itself is lower than normal and the TLC is lower than normal what is the problem

A

obstructive AND restrictive disease

172
Q

if FEV1/FVC is lower than normal and FVC itself is high or normal what is the problem

A

pure obstruction

173
Q

TLC is decreased in what kind of lung dysfunction

A

restrictive pattern

174
Q

bronchodilators help with what kind of lung issue

A

obstructive (like asthma, COPD)

175
Q

what are extra-parenchymal causes of restriction

A

obesity, neuromuscular disease, chest wall deformity, pleural effusion

176
Q

BP (and thus perfusion) is highest in what area of the lungs

A

zone 3, inferior

177
Q

ventilation is highest in what area of the lungs

A

zone I, superior

178
Q

what is intrapleural pressure distribution in the lungs?

A

its most negative at the apex (-10) and less negative at the base (-2)…. thats why alveoli are bigger at the apex!

179
Q

average V/Q ratio over the whole lung

A

4/5= 0.8

180
Q

where do we have a high V/Q

A

apex of lung

181
Q

where do we have low V/Q

A

base of lung

182
Q

the V/Q ratio is 0 under what conditions

A

no ventilation: airway is blocked by something (foreign object)

183
Q

when in V/Q ratio infinity?

A

when theres no blood flow to that alveoli

184
Q

what pressure must the right ventricle reach before the pulmonary semilunar valve opens

A

15 (diastolic pressure)

185
Q

what pressure must the left ventricle reach before the aortic semilunar valve opens

A

70 (diastolic)

186
Q

mitral valve stenosis leads to what

A

pulmonary edema (remember: pulmonary veins got NO VALVES)

187
Q

tricuspid valve stenosis leads to what

A

peripheral edema

188
Q

whats the job of a papillary m

A

to hold AV valve closed during ventricular contraction

189
Q

why do we get pulmonary hypertension in COPD patients

A

BP= CO*R

loss of capillaries increases resistance in the others so BP goes up too

190
Q

what eventually happens to the heart of patients with pulmonary hypertension

A

R heart pressure increases and it must work harder causing it to hypertrophy

191
Q

major storage form of FA

A

TAGs

192
Q

where do we process TAGs

A

intestine

193
Q

de novo synthesis of TAGs happens where

A

adipocytes, hepatocytes

194
Q

whats the backbone for TAG synthesis in the intestine

A

2-monoacylglycerol

195
Q

whats the net result of TAG formation in intestine

A

form chylomicrons

196
Q

whats the backbone for TAG synthesis in the liver

A

glycerol 3 phosphate

197
Q

whats the net result of TAG formation in liver

A

form VLDL

198
Q

whats the net result of TAG formation in adipocyte

A

storage of TAG in adipocyte

199
Q

whats the backbone for TAG synthesis in the adipocyte

A

glycerol 3 phosphate

200
Q

glycerol-3-phosphate is required to form TAG in adipocyte but we must make that from glucose. how does glucose get here?

A

via glut4 transport (in presence of insulin)

201
Q

what controls insertion of glut 4 into membrane of adipocyte

A

insulin

202
Q

where does breakdown of TAG into fatty acids occur

A

adipocyte

203
Q

how do long chain fatty acids travel in blood

A

attached to albumin

204
Q

where does breakdown of FA’s occur

A

liver (beta oxidation)

205
Q

key lipolytic enzyme in adipocytes

A

HSL: hormone sensitive lipase

206
Q

why are mice with HSL knockout not obese

A

there are other hormone sensitive lipolytic enzymes (however they do accumulate DAGs)

207
Q

HSL is rate limiting for breakdown of what

A

DAGs (its why they accumulate in HSL- mice)

208
Q

what is the newly reported TAG lipase that is activated by phosphorylation via PKA

A

adipose triglyceride lipase ATGL

209
Q

whats the active form of HSL

A

phosphorylated (by PKA after glucagon or epinephrine binds)

210
Q

what inactivates HSL

A

desphosphorylation by PP1 (insulin)

211
Q

what hormone promotes lipolysis in adipocytes (by opening perilipin and activating HSL and ATGL)

A

glucagon, epinephrine

212
Q

what hormone inhibit lipolysis in adipocytes

A

insulin

213
Q

proteins that coat lipid droplets in adipocytes and muscle cells (controlling physical access to HSL)

A

perilipin

214
Q

over expression of perilipin 1 has what effect

A

inhibit lipolysis (obesity treatment target)

215
Q

synthetic fat not absorbed by small intestine, excreted in stool (sometimes involuntarily), no calories

A

olestra

216
Q

olestra causes depletion of what vitamins

A

hydrophobics: ADEK

217
Q

what is the transport vehicle for cholesterol

A

lipoproteins (chilomicrons, VLDL)

218
Q

what enzyme do we need to turn cholesterol into cholesterol ester (more hydrophobic and stored in lipid droplets)

A

ACAT: acyl coa acyl transferase

219
Q

chylomicrons are large and least dense with lots of ___ and what surface proteins?

A

TAGs

ApoB, ApoC, ApoE

220
Q

IDLs have what surface proteins

A

ApoE, ApoB

221
Q

LDLs have what surface proteins

A

ApoB only

222
Q

smallest, densest lipid transporter with lots of protein and phospholipid

A

HDL

223
Q

surface proteins of HDL

A

ApoA, ApoC, ApoE

224
Q

how do chylomicrons and HDLs activate LPL

A

they have ApoC which is a cofactor for the enzyme

225
Q

type I familial hyperchylomicronemia causes creamy blood and high TAGs because why

A

deficient apoC or defective LPL

226
Q

type II familial hyperchylomicronemia causes high cholesterol, TAG, LDL, and VLDL bc why

A

LDL receptor defective (can’t uptake LDLs so they remain in plasma)

227
Q

if type I familial hyperchylomicronemia is discovered in infancy what most likely is the cause of the problem

A

LPL deficiency

228
Q

if type I familial hyperchylomicronemia manifests post adolescence what most likely is the cause

A

apoC deficiency

229
Q

type II familial hyperchylomicronemia causes atherosclerosis (and CAD) why

A

LDL buildup in plasma because we can’t do RME because the receptor is broken

230
Q

how do you treat homozygous type II familial hyperchylomicronemia

A

LDL apheresis, liver transplant

231
Q

how do you treat heterozygous type II familial hyperchylomicronemia

A

diet, statins, bile acid binding resin

232
Q

how do statins lower cholesterol

A

mimic HMG coA and mevalonate to INHIBIT HMG CoA reductase (reduce cholesterol synthesis and increase uptake of LDL)

233
Q

whats the rate limiting step in cholesterol biosynthesis

A

hmg coa reductase

234
Q

people on statins get muscle fatigue why

A

cholesterol is precursor for coenzyme Q (ubiquinone) in ETC

CardioPulm (6 decks)

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