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
What is more commonly used to view coronal section of anterior axilla: MR or CT
CT (unless pt is allergic to contrast) because its a much sharper image and easier to create reconstructions
26
Which xray view is needed to see oblique fissure of the lung
Lateral view
27
Which X-ray angle is needed to see horizontal fissure
Lateral view or PA view
28
Where. Does the axis. Of the heart project
45 degrees anteriorly, 45 degrees left
29
When using echocardiography + doppler to image the heart, how do we know the direction of blood flow
Red is flow toward the transducer (anterior chest wall) and blue is away from the transducer. Yellow is turbulence
30
What causes a meniscus sign (seen on lung X-ray)
Pleural effusion (surface tension of fluid on pleura causes concavity near diaphragm dome)
31
Term describing: Pleural effusion confined to one or more pockets in pleural space seen in X-ray
Loculated
32
How do you identify interstitial pulmonary edema on X-ray
Kelley b lines
33
The tip of an enteric feeding tube should extend where
To upper left quadrant of abdomen (stomach)
34
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?
Silhouette sign
35
what condition causes destruction of alveoli creating large air spaces and loss of capillaries in the lungs
COPD/ emphysema
36
The body attempts to normalize mismatched V/Q ratios (like those created by emphysema) how?
1. hypoxic vasoconstriction (to correct low V/Q) | 2. bronchoconstriction (to correct high V/Q)
37
Who (capillaries or alveoli) is better at fixing a high V/Q ratio?
alveoli (they will bronchoconstrict)
38
Who (capillaries or alveoli) is better at fixing a low V/Q ratio?
capillaries (they will vasoconstrict)
39
inadequate oxygen available for use by tissues
hypoxia
40
inadequate oxygen in the blood
hypoxemia
41
total absence of oxygen delivered to tissue
anoxia
42
form of hypoxia where PaO2 is below normal because alveolar oxygen is reduced (altitude) OR because blood can't equilibrate with air (emphysema)
hypoxic hypoxia
43
form of hypoxia where lungs work but blood can't carry oxygen as well (like with CO binding or low RBC count)
anemic hypoxia
44
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)
circulatory hypoxia
45
name a disease which can cause two different forms of hypoxia
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
46
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
histotoxic hypoxia
47
what is the direct stimulus for the central chemoreceptors
H+ ions in the CSF
48
what blood gas do the central chemoreceptors tell the rest of the brain about
CO2
49
excess CO2 in the blood
hypercapnia
50
what do peripheral chemoreceptors detect
oxygen
51
who makes CSF
choroid plexus
52
what makes composition of CSF different than ECF or plasma
less protein and no cholesterol
53
how do our central chemoreceptors adjust to hypocapnia?
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)
54
what happens with H+ produced by the choroid plexus when it is adjusting CSF contents during hypercapnia
it gets deposited in the blood and taken care of by kidneys
55
what decreases as altitude increases
barometric pressure (and thus alveolar O2 pressure)
56
whats the first response to hypoxia?
peripheral chemoreceptors detect it and increase ventilation in response
57
when we increase ventilation it increases PaO2 and does what else?
decreases PaCO2
58
what does hypoxia do to the kidney
causes erythropoietin release (to increase RBC production and thus O2 carrying capacity of blood increases)
59
for every ___ m below water surface you go on a dive, the barometric pressure increases by ___ atm
10 m, 1 atm
60
what is the barometric pressure at 40 m below sea level
[40 m * (1 atm/10m)] due to water + [1 atm] due to air= 5 atm
61
why is too much oxygen bad
formation of superoxide anion and peroxide which are toxic to cells
62
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
air embolus enters blood stream
63
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
nitrogen narcosis
64
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
the bends / decompression sickness (pain, parasthesias, itching, paralysis)
65
how do we treat decompression sickness
hyperbaric chamber forces gas back into solution then we control rate of decompression to allow the N gas to be exhaled
66
site that generates core timing (frequency) of respiratory rhythm
pre-botzinger complex
67
transition from inspiration to expiration helps determine frequency. what controls this by turning off inspiration?
pontine pneumotaxic center
68
absence of breathing
apnea
69
being stuck in inspiration (due to lesion in pontine pneumotaxic center)
apneusis
70
Where does phrenic. Nerve get 95% of its premotor innervation
Dorsal respiratory group
71
What are the two function of ventral respiratory group
Rostral part- inspiratory muscles | Caudal part- expiratory muscles
72
Who controls depth of breathing
DRG, VRG
73
Pontine damage would lead to increased CO2, decreased. O2 and eventually death because of what condition
Apneusis
74
Medullary or spinal damage would lead to increased CO2, decreased. O2 and eventually death because of what condition
Apnea
75
Chemoreceptors increase their firing under what conditions
Increased CO2 or H+ | Decreased O2
76
Where do we find peripheral chemoreceptors
Carotid and aorta
77
Central chemoreceptors respond to what stimuli
H+ created in CSF after CO2 enters the brain
78
Which kind of chemoreceptors are faster at responding
Peripheral
79
How do. We keep. Track of our lung volume
Slowly adapting Pulmonary stretch receptors in the airways send signal to brain via vagus n (terminate. Inspiration)
80
When in life are slow-adapting pulmonary stretch receptors important for controlling respiration
Infancy, adults during exercise
81
Where do you. Find rapidly. Adapting pulmonary. Stretch receptors
Airways
82
What causes a response in rapidly adapting pulmonary stretch receptors of the airways
Irritation, foreign bodies, stretch
83
After the vagus nerve carries rapid adapting pulmonary stretch receptor signal to brain, what does brain tell body to do?
Cough
84
Who can detect pulmonary edema
J receptors
85
Where do you find j receptors
Near blood vessels of alveoli
86
What is the effect of J receptors after vagus takes their message to the brain
Cough and tachypnea
87
Protective reflexes that override the normal respiratory control system
J receptors and Rapidly adapting pulmonary stretch receptors
88
What brain. Structure can. Bypass medullary center completely and send input directly to muscles of respiration
Cortex
89
A. Measure of stretchability of the lungs (due to elastic fibers)
Compliance
90
When is compliance of the lung at its highest (stretchable lung that is easily inflated)
In normal breathing range
91
Why is there hysteresis between inspiration and expiration (hysteresis) in terms of their volume and pressure changes
Surfactant is not evenly distributed (randomly positioned moving apart during. Inspiration and. Back together. A. Different way during expiration)
92
How do. You calculate compliance
Change in volume/ change in pressure
93
What two structures combine their volume and pressure forces to make up the respiratory mechanics curve
Lungs (wanna shrink) and rib cage (wanna expand)
94
The elastic recoil of the lungs and that of the rib cage exactly balance each other out at what value
Functional residual capacity
95
why is the balance point (on a volume versus airway pressure graph) for the rib cage so much higher than for the lungs
because of expanding forces of joints and muscle attached to rib cage
96
in a normal person what is the FEV1/FVC ratio? (the air exhaled forcefully in the first second versus the vital capacity)
80%
97
who would have a reduced FEV1/FVC ratio (below 70%)
obstructive disorder (emphysema or asthma)
98
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)
restrictive disease (fibrosis)
99
explain alveolar interdependence
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
why must the lungs "do work"
to overcome elastic recoil, overcome resistance to airflow
101
Whats teh most common rib fracture
Middle ribs fracture just anterior to costal angle
102
What type of joint is manubriosternal
Symphysis
103
What type. Of joint is xiphisternal
Synchondrosis
104
What type of joint is sternocostal junction for rib 1? Ribs 2-7?
1: synchondrosis | 2-7: synovial planar
105
Rib dislocation occurs at what joint
Sternocostal
106
Rib separation occurs at what joint
Costochondral
107
Insert hypodermic needle through intercostal space to obtain fluid sample or drain fluid from pleural cavity
Thoracentesis
108
Insertion of tube to remove large amounts of air/ fluid/ blood from pleural cavity (5th or 6th space)
Chest tube insertion
109
Insert horoscope into pleural cavity through small incision for visualizing/ biopsying pleural cavity contents
Thoroscopy
110
Nerves that can be involved in lung cancer
Phrenic, vagus, recurrent laryngeal
111
Removal of lung
Pneumonectomy
112
Procedure used to remove a specific bronchopulmonary segment (segmentectomy)
Lung resection
113
Widespread narrowing of airways produced by contraction of smooth muscle,, edema of mucosa and. Mucus in lumen of bronchi
Bronchial asthma
114
What separates superior form inferior mediastinum
Sternal angle
115
What specific cavity does the heart lie in
Middle inferior mediastinum
116
Lack of blood flow to myocardium as a result of coronary artery blockage
MI
117
Buildup of lipids on internal walls of coronary arteries decreasing lumen size increasing likelihood of embolus or plug blocking vessel
Coronary atherosclerosis
118
Pain originating in the heart producing strangling pain of chest: usually result of narrow or obstructed coronary arteries that produces ischemia of myocardium
Angina pectoris
119
The fetus ductus arteriosus shunted blood in which direction
From pulmonary trunk to aorta to bypass nonfunctional lung (right to left)
120
Where do we insert catheter for cardiac visualization of R heart and pulmonary arteries
Femoral v
121
Atrial contraction
Diastole
122
Ventricles contract
Systole
123
Irregular twitching of atrial cardiac muscle fibers causing ventricles to respond at irregular intervals (circulatory usually remains fine)
Atrial fibrillation
124
Rapid irregular ventricle twitch which renders heart unable to pump blood: requires defibrillation
Ventricular fibrillation
125
Cardiac referred pain occurs where due to sharing spinal ganglion with other sensory fibers
Upper limb and superior lateral chest wall
126
Space that allows surgeons to access area posterior to aorta and pulmonary trunk to clamp or insert tubes of bypass machine
Transverse pericardial sinus
127
Pericarditis of pericardium can can lead to pericardial friction rub and what happens when left untreated
Pericardium can calcify
128
Accumulation of fluid or pus in periardial sac that can compresses heart
Pericardial fusion
129
Heart compression
Cardiac tamponade
130
Cardiac tamponade can be received by what procedure
Pericardiocentesis
131
When a small balloon is. Inserted to increase lumen size of coronary artery
Coronary angioplasty
132
When blood clot, fat globule, or air bubble obstructs pulmonary artery
Pulmonary embolism
133
How does the sympathetic nervous system indirectly decrease secretion through non-sweat glands
Vasoconstriction
134
lung buds begin to develop when in development
week 4
135
lungs derive from which germ layer
endoderm (they out pouch from foregut)
136
appearing on the floor of the caudal end of the anterior foregut is a median outgrowth called the __ to start lung development
laryngeotracheal groove
137
the laryngeotracheal groove at the end of week 4 protrudes to form a pouch called what
lung bud (laryngeotracheal diverticulum)
138
fusion of folds coming from laryngeotracheal diverticulum occurs in week 5 to create what
tracheoesophageal septum
139
ventral to the tracheoesophageal septum we find what structures
laryngeotracheal tube
140
dorsal to the tracheoesophageal septum we find what
pharynx and esophagus
141
the epithelium and glands of the trachea are derived from what embryonic tissue
endoderm
142
the pulmonary epithelium of trachea is derived from what embryonic tissue
endoderm
143
smooth muscle, connective tissue, and cartilage of the trachea are derived from what embryonic tissue
splanchnic mesenchyme
144
lung buds split into ____ during week 5
primary bronchial buds
145
primary bronchial buds branch into __ during week 6
lobar (secondary) bronchi
146
lobar bronchi branch into ___ during week 7
tertiary bronchi
147
how many tertiary bronchi form in the left lung? right lung?
left: 9 right: 10
148
who (demographically) has the best chance of surviving premature birth based on lung development
african american females
149
what stage of lung development occurs wk 5-17? can premature birth be viable in this stage?
``` pseudoglandular no survival (no alveolar-capillary membrane has formed) ```
150
what stage of lung development occurs wk 16-25? can premature birth be viable in this stage?
canalicular | some can survive after minimum 21 weeks (vascularization has occurred)
151
what stage of lung development occurs wk 24- birth? can premature birth be viable in this stage?
terminal sac | YES they will survive (they have I and II pneumocytes now)
152
what are Type I pneumocytes
squamous epithelium where gas exchange occurs
153
what are Type II Pneumocytes
secretory epithelium that create surfactant
154
when do I and II pneumocytes show up in lung development
during terminal sac stage (wk 24- birth)
155
when do alveoli fully mature (develop functional alveolocapillary membrane)
alveolar stage (from 32 wk- 8 years)
156
what happens in utero to cause aspiration of amniotic fluid (to help lung development)
fetal breathing movements (FBM)
157
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
on the fetal thorax during vaginal delivery
158
why is oligohydramnios bad for lung development
not enough fluid to help lungs expand/ develop = pulmonary hypoplasia
159
baby born with low lung volumes, tachypnea, nasal flaring, suprasternal retractions, cyanosis, with ground glass appearance on CXR probably has what
respiratory distress syndrome (hyaline membrane disease) | --lack of surfactant
160
which stage of lung development went wrong in a kid born with respiratory distress syndrome
they lack surfactant- terminal sac stage
161
polyhydramnios coupled with baby secretions (drool, choke, cough, gag, inability to feed) indicates what
esophageal atresia
162
whats the most common defect of the tracheoesophageal septum
tracheoesophageal fistula (esophagus ends in blind pouch superiorly and a lower segment originates above bifurcation of trachea)
163
what might provide a honeycomb appearance on X-ray of a newborn child
congenital lung cyst (fluid or air filled)
164
diffusing capacity of the lung can be reduced by anemia: true or false
true
165
measuring TLC is needed to confirm restrictive disease: true or fasle
true
166
air trapping leads to increase in RV: true or false
true
167
decreased FEV1/FVC ratio is consistent with what kind of problem
obstructive
168
what condition minimizes ability of blood to accept gas diffusing across alveolar memrbane
anemia
169
what condition minimizes the diffusion of gas into blood because of decreased surface area of alveolar-capillary membrane
emphysema, pulmonary embolism
170
what condition alter membrane permeability (or increase thickness) causing diffusion of gas to decrease
pulmonary fibrosis
171
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
obstructive AND restrictive disease
172
if FEV1/FVC is lower than normal and FVC itself is high or normal what is the problem
pure obstruction
173
TLC is decreased in what kind of lung dysfunction
restrictive pattern
174
bronchodilators help with what kind of lung issue
obstructive (like asthma, COPD)
175
what are extra-parenchymal causes of restriction
obesity, neuromuscular disease, chest wall deformity, pleural effusion
176
BP (and thus perfusion) is highest in what area of the lungs
zone 3, inferior
177
ventilation is highest in what area of the lungs
zone I, superior
178
what is intrapleural pressure distribution in the lungs?
its most negative at the apex (-10) and less negative at the base (-2).... thats why alveoli are bigger at the apex!
179
average V/Q ratio over the whole lung
4/5= 0.8
180
where do we have a high V/Q
apex of lung
181
where do we have low V/Q
base of lung
182
the V/Q ratio is 0 under what conditions
no ventilation: airway is blocked by something (foreign object)
183
when in V/Q ratio infinity?
when theres no blood flow to that alveoli
184
what pressure must the right ventricle reach before the pulmonary semilunar valve opens
15 (diastolic pressure)
185
what pressure must the left ventricle reach before the aortic semilunar valve opens
70 (diastolic)
186
mitral valve stenosis leads to what
pulmonary edema (remember: pulmonary veins got NO VALVES)
187
tricuspid valve stenosis leads to what
peripheral edema
188
whats the job of a papillary m
to hold AV valve closed during ventricular contraction
189
why do we get pulmonary hypertension in COPD patients
BP= CO*R loss of capillaries increases resistance in the others so BP goes up too
190
what eventually happens to the heart of patients with pulmonary hypertension
R heart pressure increases and it must work harder causing it to hypertrophy
191
major storage form of FA
TAGs
192
where do we process TAGs
intestine
193
de novo synthesis of TAGs happens where
adipocytes, hepatocytes
194
whats the backbone for TAG synthesis in the intestine
2-monoacylglycerol
195
whats the net result of TAG formation in intestine
form chylomicrons
196
whats the backbone for TAG synthesis in the liver
glycerol 3 phosphate
197
whats the net result of TAG formation in liver
form VLDL
198
whats the net result of TAG formation in adipocyte
storage of TAG in adipocyte
199
whats the backbone for TAG synthesis in the adipocyte
glycerol 3 phosphate
200
glycerol-3-phosphate is required to form TAG in adipocyte but we must make that from glucose. how does glucose get here?
via glut4 transport (in presence of insulin)
201
what controls insertion of glut 4 into membrane of adipocyte
insulin
202
where does breakdown of TAG into fatty acids occur
adipocyte
203
how do long chain fatty acids travel in blood
attached to albumin
204
where does breakdown of FA's occur
liver (beta oxidation)
205
key lipolytic enzyme in adipocytes
HSL: hormone sensitive lipase
206
why are mice with HSL knockout not obese
there are other hormone sensitive lipolytic enzymes (however they do accumulate DAGs)
207
HSL is rate limiting for breakdown of what
DAGs (its why they accumulate in HSL- mice)
208
what is the newly reported TAG lipase that is activated by phosphorylation via PKA
adipose triglyceride lipase ATGL
209
whats the active form of HSL
phosphorylated (by PKA after glucagon or epinephrine binds)
210
what inactivates HSL
desphosphorylation by PP1 (insulin)
211
what hormone promotes lipolysis in adipocytes (by opening perilipin and activating HSL and ATGL)
glucagon, epinephrine
212
what hormone inhibit lipolysis in adipocytes
insulin
213
proteins that coat lipid droplets in adipocytes and muscle cells (controlling physical access to HSL)
perilipin
214
over expression of perilipin 1 has what effect
inhibit lipolysis (obesity treatment target)
215
synthetic fat not absorbed by small intestine, excreted in stool (sometimes involuntarily), no calories
olestra
216
olestra causes depletion of what vitamins
hydrophobics: ADEK
217
what is the transport vehicle for cholesterol
lipoproteins (chilomicrons, VLDL)
218
what enzyme do we need to turn cholesterol into cholesterol ester (more hydrophobic and stored in lipid droplets)
ACAT: acyl coa acyl transferase
219
chylomicrons are large and least dense with lots of ___ and what surface proteins?
TAGs | ApoB, ApoC, ApoE
220
IDLs have what surface proteins
ApoE, ApoB
221
LDLs have what surface proteins
ApoB only
222
smallest, densest lipid transporter with lots of protein and phospholipid
HDL
223
surface proteins of HDL
ApoA, ApoC, ApoE
224
how do chylomicrons and HDLs activate LPL
they have ApoC which is a cofactor for the enzyme
225
type I familial hyperchylomicronemia causes creamy blood and high TAGs because why
deficient apoC or defective LPL
226
type II familial hyperchylomicronemia causes high cholesterol, TAG, LDL, and VLDL bc why
LDL receptor defective (can't uptake LDLs so they remain in plasma)
227
if type I familial hyperchylomicronemia is discovered in infancy what most likely is the cause of the problem
LPL deficiency
228
if type I familial hyperchylomicronemia manifests post adolescence what most likely is the cause
apoC deficiency
229
type II familial hyperchylomicronemia causes atherosclerosis (and CAD) why
LDL buildup in plasma because we can't do RME because the receptor is broken
230
how do you treat homozygous type II familial hyperchylomicronemia
LDL apheresis, liver transplant
231
how do you treat heterozygous type II familial hyperchylomicronemia
diet, statins, bile acid binding resin
232
how do statins lower cholesterol
mimic HMG coA and mevalonate to INHIBIT HMG CoA reductase (reduce cholesterol synthesis and increase uptake of LDL)
233
whats the rate limiting step in cholesterol biosynthesis
hmg coa reductase
234
people on statins get muscle fatigue why
cholesterol is precursor for coenzyme Q (ubiquinone) in ETC