Respiratpry Flashcards Preview

BMS > Respiratpry > Flashcards

Flashcards in Respiratpry Deck (186):
1

What is responsible for sigmoidal curve of Hb?

cooperative binding:
Increase slope due to cooperative binding
decrease slope due to saturation

2

in anemia:and in CO, cooperativity is maintained or lost?

CO: lost
Anemia: maintain

3

High temp shift the curve to the (L/R)? What does it mean?

to the right
Low temp, low metabolism, hang on to O2

4

3 forms that CO2 is transported?

Dissolved CO2 (5%)
Bicarbonate (HCO3) (90%)
Carbamino compound
Total contain CO2 include 3 forms

5

Ez that catalyzes Co2 hydration

carbonic anhydrase

6

What is carbamino compound?

CO2 bind to terminal amine group, especially of Hb
RXN is facilitated in low O2 tissue

7

Haldane effect

at any PCO2, decreasing PO2 will increase CO2 content

8

Role of lipid

mmb, energy, hormone

9

Muscle in respiratory and their innervation

Diaphragm - phrenic nerve
Intercostal muscle: intercostal nerve
Upper airway muscle: vagus

10

Lung mechanoR
> Upper airway
> Lower airway an lungs

Upper airway: nose, larynx, pharynx, trachea: cough, sneeze
Lower airway and lungs:
> Pulmonary stretch R
> Pulmonary irritant receptors
> J (juxtacapillary) receptors

11

Pulmonary stretch R (location, stim, afferent pathway, response, note)

Location: smooth muscle of large and small airways
Stimulus: lung distention, discharge during inflation
Afferent path: vagus nerve
Response: inhibit respiration, terminate inspiration, allow expiration, decrease HR
Note: Hering-Breuer Reflex

12

Pulmonary irritant R (location, stim, afferent pathway, response, note)

Location: epithelium of large airways
Stim: irritant, smoke, dust, histamine
Afferent airways: Vagus X
Response: cough, bronchoconstriction (reflex)
Note; asthma (histamine)

13

J (Juxtacapillary) R (location, stim, afferent pathway, response, note)

location: near walls of pulmonary capillaries
Stim: pulmonary edema
Afferent pathway: vagus
Response: rapid, shadow breathing

14

common afferent pathway of lung mechanoR - lower airway and lung?

Vagus Nerve X

15

Peripheral chemoreceptor of the respiratory system? (2) each stimulated by what?

which one is more effective

Carotid bodies: decrease PaO2, increase PaCO2, decrease pH

Aortic bodies : stim by decrease PaO2, increase PaCO2
Carotid is more effective

16

Carotid body chemoR: pH and CO2, which one has higher effect? MOA of both?

Effect of pH is smaller than that of CO2
both act via inhibition K channel

17

central chemoreceptors: location, afferent to where? response to what stim?

on the ventrolateral surface of the medulla
afferent to medullary respiratory center
- response to H+ and (PCO2) of local interstitial fluid and cerebral spinal fluid (CSF), not affected by PO2

18

Ventilation response to hypoxia

Hypercapnia (too much CO2) increase ventilation rate
- Effect of hypoxia is minimal until PO2 <60 mmHg

19

Ventilation response to Hypercapnia.

Hypoxia potentiates the effect of PCO2 on ventilation rate.

20

asthma

a chronic inflammatory disorder of the airways characterized by episodes of wheezing, shortness of breathm chest tightness, and cough

21

causes of asthma

Airway narrowing
bronchial hyper-reactivity
irreversible airflow obstruction

22

Constricted airway

smooth muscle consttraction
mucus
reversible

23

obstructed airway

thick mucus plug
not reversible by bronchodilators

24

Asthma treatment: 2 approaches

Managing symptoms: bronchodilators:
> beta 2 agonist
> muscarinic antagonist
> methylxanthines

Managing disease: anti- inflammatory agents
> corticoids
> mast cell antagonist
> Anti IgE Ab
Inhibitor of LT synth and LT Receptor antagonist

25

Beta Agonist in asthma
>List
> toxicity

(Epi)
Albuterol
Metaproterenol
Terbutaline
Salmeterol (long acting 12h)

Toxicity: Tachyphylaxis is common with overuse( rapid loss of effect)
skeletal muscle tremor
Tachycardia and arrythmia (rare)

26

Muscarinic R Antagonist
> MOA
> Listed

relax smooth muscle by antagonizing Ach released at post -ganglionic nerve ending

Ipratropium (Atrovent): short term (4-6h)
Titropium (Spirive) long term 24h
block M R, relax smooth muscle and decrease glandular secretion

Adjunctive to Beta agonist in severe cases
Atropine life side effects (minor)

27

Effect of leukotrienes in Asthma.

Mucin secretion (submucosal gland)
chemotactic (esinophil and neutrophil)
Vasoactive (blood vessel)
Bronchioconstriction (smooth muscle)

28

Leukotriene Antagonists (think lukast)
how many types? list nams of each, use, toxicity

- LT4 Receptor blockers:
> Zafirlukast, montelukast used orally
> Toxic:GI distress, increase liver transaminases

5-lipoxygenase inhibitor: Zileuton inhibits enzyme that form intermediates in synthesis of LT
> Toxicity: as above, monitor liver ez

29

Corticosteroids (MOA, net effect) asthma

bind to intracellular glucocorticoid R
> direct activiation of gene expression (upregulate anti inflam gene)
>interference with transcription factors (down regulating of pro-inflam genes)

Net effect:
>inhibition of production of cytokines
> reduce activity of mast cell and eosinophils
> stabilize microvascular permeability
> increase expression of beta receptor

30

Corticosteroid list of drugs
> systemic
> topical

Systemic: prednisone, methhylprednisone
> acute severe asthma
> chronic asthma
> toxicity: severe for long term use: weght gain , cataract, osteoporosis, glucose intolerance, growth inhibition

Topical: Beclomethazone, triamcinolone. budesonide, fluticasone
> persistent asthma
> minimal toxicity at low -moderate dose

31

Corticosteroid toxicity

Local:
>Oropharyngeal candidiasis (thrush)
>Hoarseness

Systemic:
> ostesporosis
>cataracts
>inhibition of growth

32

methylxanthines
MOA
Use and eliminate
tocxicity

MOA: inhibit phosphodiesterase (PDE)( increase cAMP) and increase adenosine bronchioconstriction

Oral absorption, eliminate via hepatic P450

Toxic: narrow theurapeutic window, GI distress, tremor and insomnia are common, hypotension, arrythmias, seisure

33

Cromolyn and Nedocromil (MOA)

Mast cell stabilizer: block histamine and LT from mast cells

not bronchodilator:
Use: mild, persistent asthma, throat irritation and cough, hay fever, food allergy

34

Immuno-moduatory Therapy (MOA), ex

Anti IgE block mast cell binding
Omalizumab (sub Q)

35

Patient with asthma: what kind of dental problem?

xerostomia, halitogis, gingivitis, cavities,
Oral infection from steroid

36

two types of nephron?

cortical (85%)
Juxtamedulallary (15%) deep into medulla: water balance

37

What affects the filtration of substance in kidney?

1. Size: macromolecules >70kDa dont pass
2. Charge basement mmb and coast of the podocytes are negatively charged

38

Three functions of the kidney:

Filtration
homeostasis
endocrine (production and secretion of hormone)

39

metabolic wastes in urine

urea (from protein metabolism)
uric acid ( from Nucleic acid )
creatinine ( from muscle creatine)
bilirubin ( from Hb)

40

Drug Filtration in kidney
- are all drugs metabolized in liver before excreted ?
- how do they gte in the tubule?
- does reabsorption happen?
- what does affect the excretion of drug

- most drugs are metabolized in the liver before being excreted, but not all
- many drugs do not traverse the filtration barrier. but enter the kidnet tubule by secretion
- some drugs may be reabsorbed
- excretion of drugs is affected by urine pH

41

endocrine function of the kidney: what hormones?

Renin and erythropoietin

42

Renin
- released by ...
- is it a hormone or ez?
- what does it do

released by granular cells od kidney
- an ez with hormone -like actions
- convert angiotensinogen >> angiotensin I
- required for the generation of the powerful vasoconstrictor angiotenosin II

43

Erythropoetin:
- what kind of hormmone?
required for what ?
- source
what stimulate

- glycoprotein
- required for erythropoiesis
- 80% comes from a group of cell in the interstitium of the renal cortex and outer medulla of the kidney
- hypoxia and several hormones (prostagglandin) stim secretion

44

renal corpuscle: mesangial cells
location, what they do?

locate between and within capillary loops
Support glomerular capillary
phagocytes: keep filtration barrier clean
contraction: contain myofibrils
> contraction cause decrease in filtration area
> contraction is regulated sympathetic activity and angiotensin II

45

Proximal tubule: how many sections? structure, number of mitochondria, role ?

what is special about apical and basolateral mmb?

Proximal convoluted tubule
proximal straight tubule

Very prominent brush border > large SA
Large number of mitochondria provide energy for active transport
Important site of secretion

Both apical and basolateral mmb are extensively amplified (connect to each other via tight junction

46

Two route of reabsoption and secretion

Paracellular Route : diffuse across tight junctions down an electrochemical gradient between the lumen ans blood

Transcellular route: pass across the cell by active or passive processes

47

3 forms of acwtive transport

1. primary active transport: directly ATP hydrolysis (Na-K ATPase)
2. secondary active transport: indirect involves ATP hydrolysis (glucose - Naa symport)
3. endocytosis: mmb invaginate and pinches off a vesicle

48

in micropuncture experiment in the proximal tubule to measure reabsoption and secretion: [inulin] is increased 3X, but [Na] unchanged. Why? what does it mean?

inulin is neither secreted or reabsorbed

Na reabsorbed to maintain the conc.

This is that 2/3 of filtered water has been reabsorbed , 2/3 filtered Na must also have been reabsorbed.

49

Changes in tubular fluid to plasma ratio (TF/P): >3 or <3, what does it mean

TF/P >3: net secretion (PAH, penicillin)
TF/P < 3: net reabsoprtion (Cl, NA, Glu, amino acids , HCO3)

50

what is the TF/P of bownman's space

1

51

By the end of the proximal tubule: what is the osmolarity and Na conc compared to arterial blood?
- Cl, Na, glu, aminoacid ?
Transepithlial voltage?

- most filtered Na reabsorbed
- Most filtered Glu, La, amino acid, HCO3 follow Na to reabsorbed
- Transepithelial voltage is positive

52

T/F : the secretion of H in linked to the reabsorption of HCO3-

what is the enzyme involved ?

True

carbonic anhydase

53

If TF/P for H increase, how is TF/P for HCO3

decrease

54

what drives Na reabsorption via extracellular (paracellular route?

TF Cl > PCl
> concentration gradient
Cl reabsorbed via paracellulaar route
lumen turns positive
drive Na reabsorption

55

the main driving force of H2O reabsorption ?

Na reabsorption

56

reabsorption of Kreb's cycle intermediates and glucose?

sencondary active co-transport with Na

57

driving force of K reabsorption?

H20 reabsorption

58

2 ways reabosption of protein and peptide

Protein: by endocytosis, degraded in lysosomes to aa, then enters the peritubular capillary

peptide: are degraded by ez in brush border to aa, which then are reabsorbed

59

Passice reabsorption of weak organic acids and bases

the conc of weak acid and base in TF increases as H2) reabsorbed . only unionized form will pass the epithelium.
theh extent to which an organic acid or base is ionized in the TF depends on the pH of the TF ( and the pKA of the substance)

many drugs are weak acids or bases

60

if TF becomes alkaline, what happens to reabsorption of weak acids ?

more inonized, reabsorption is diminished
(treat aspirin overdose)

61

Diuretics

drugs that ncrease renal excretion of salt and water

62

Na handling in the kidney

Proximal: 60% - NAHCO3 form
Thick ascending loop: 20-40% - Na -
Distal tubule: 10-12% - NaCl - Thiazide
Collecting duct: 2-4% Nacl - Aldosterone antagonist

63

Loop of henle: The Na/K/2Cl transporter

transport Na, K and 2 Cl from the lumen into the cell. Na/K pump pump

64

bronchiole attaches to what?

alveolar wall

65

Pulmonary infections:
> definition
> what population of patients?

inflammation of the lungs: pneumonitis or pneumonia
occurs in 1/3 of immuno compresses patients

66

lobar pneumonia: location, consequence

in 1 lobe, Strep Pneumonia
red hepatization (neutrophill)> gray hepatization (break down of PMN)> resolution

67

Bronchopneumonia

Staph, Strep
inflammatory consolidation around small bronchi and bronchiole
everywhere in the airway to lung

68

TB

communicable disease resulting in necrotizign granulomatous inflammatory reactions

69

MIliary TB

granulomas
caseous necrosis

70

Fungal Pneumonia

a visceral or deep mycosis leading to pneumonitis
oppottunitstic infection

71

What types of fungal pneumonia found in Immunocompromised induviduals?

candidiasus
Apergillosis

72

Viral pneumonia: population

infants, elderly, immunocompromised individuals

73

diffuse infiltrative lung disease

activate MO>recruit others

74

Pulmonary Interstitial fibrosis:


honeycombs
thickening: collagen and scar tissue

75

Cor Pulmonale

right heart is bigger than left: work hard

76

Origins of Pulmonary Emboli

most frequently from deep leg venous thrombi
air, amniotic fluid, right sided infective endocarditis

77

Etiology of primary Pulmonary hypertension

unknown

78

Causes of secondary pulmonary hypertension

chronic pulmonary emboli
congenital heart disease
AIDS, PIF

79

Morphology of pulmonary hypertension

pulmonary arteries: atheromas, thickening/ fibrosis/hypertrophy

80

Obstructive lung disease
def
4 types

a decreased abilit to expired
exL emphysema
chronic bronchitis
asthma
bronchiectasis

81

Emphysema
> def
> classification

Def: abnormal enlargement of air spaces distal to the terminal bronchioles
> classification: centriacinar, panacinar, paraseptal

82

chronic bronchitis

chronic excessive mucus production in the airways

83

bornchiectasis

chronic necrotizing infection of the bronchi and bronchioles leading to dilation

84

centrianinar emphysema:
> def
> common in ?
> major cause

dilation of the proximal portions of the acini and distal portions of the acini are spared
> upper lobes
> smoking

85

panacinar Emphysema
> def
> location
> associated with ?

uniform dilation of the acini at the level of respiratory bronchioles to the terminal alveoli.
- lesions are more frequent in the lower zones of the lungs
- associated with alpha- l-antitrypsin deficiency

86

chronic bronchitis
> def
> common in?
> pathogenesis

> def: productive cough for 3 consecutive months for 2 or more years
> skoker or dwellers living in smog
> inhale substances lead to activation of neurohormonal pathways that stimulate airway secretory cells to release chemical mediators
> attract inflammatory cells and stimulate airway mucous secretion

87

asthma
> def
> classification

- reversible bronchocontriction in response to varied stimuli
- classification:
> extrincsic (immunologic or allergic)
> intrinsic (non-immunologic or idiosyncratic)

88

bronchiectasis
> def
causesGFR

obstruction of airways impaired mucocillary clearance and persistent infection due to dilated airways
> most common cause is inflection

89

major types of lung cancer

adenocarcinoma
squamous cell carcinoma
small cell carcinoma

90

common disorders in lipid metabolism

obesity
atherosclerosis
fatty liver

91

2 ways of naming FA

C system COO = C1
omega system, start at the other end, only define the first double bond of the system

92

C system C X:Y; A,B....what does it mean

X : length
Y # double bonds
A, B position of double bonds (between n , n+1)

93

Essential FA
> why essential
precursor of ?
deficiency causes?

in human, double bonds cannot be inserted beyond C9-10
>precursors of Eicosanoids (regulatory molecule)
> deficiency: skin leison, kidney damage, weight loss

94

What is the major storage and transport form of FA?

Triglyceride

95

amphipathic

one end is hydrophobic, one is hydrophilic

96

cholesterol
> define
> accumulation will cause?
> transport formr?

structural component of mmb (stiffener)
precursor for steroid hormone
abnormal accuulation: atherosclerosis
> cholesterol ester

97

digestion of dietary lipids

in intestine, bile acid - glycocholate

cholecystokinin (CCK) secreted by upper part of small intestine triigers gall bladder to release bile salt, emulsifies TG, CE

CCk also triggers pancreas to elease lipases and cholesterol esterase: emulsified TG/CE >>> 2-monoglycerides FA cholesterol which then transferred to intestinal cell. Here there are 2 options:
1. transport to portal vein directly (serum albumin)
2. chylomicron assembly (CE and TG)

98

how is lipid soluble in blood ?

use carrier.
Serum albumin: which has FA binding sites
or
form A lipoprotein particle: with hydrophobic core and hydrophilic shell

99

Cystic Fibrosis
> def
> consequence
> treatment

- inherited disorder in electrolyte transfer across mmb
- consequence:
> lung infection/congestion
> cannot secrets digestive ez
> malabsoption of lipids, proteins. and lipud soluble vitamins
> visual impairment
- Treatent:
> dieat rich n short and medium FA
oral pacreatic ez and vitamin supplement

100

Alli (MOA)

MOA: block lipases and cholesterol esterase
> fat droplets excreted

101

Olestra

a succrose polyester
not a substrate for pancreatic lipase but mough fell as TG,
used as fat substitution in some tooth
>>> anal leakage

102

The 4 types of lipoprotein particle
which form(s) have both TG and CE?

ranking good, bad

chylomycron
VLDL
LDL
HDL
> hylomicron and VLDL have both TG and CE
> LDL and HDL have CE only

> from chylomicron to HDL: increasing density (decreasing % lipid), increasing % protein
>> HDL good

103

Why LDl bad, HDL good?

LDL: longer half life, more damage and accumulation in the arteries
HDL: involve in removal of cholesterol from tissue.

104

What are the sources of chylomicron, VLDL, LDL, HDL?

Chylomicron: intestinal cells
VLDL: liver cell
LDL: VLDL derived
HDL: liver cells chylomicron- derived

105

What is required for assembling and secretion chylomicron?

B48
(AI: function is not well unsterstood )

106

role of HDL in assembling chylomicron

donate apoE and apoCII required gor chylomicron function

107

release of chylomicron cargo for storage

ApoCII activate LPL (lipoproten Lipase found in cells lining cappilaries)
>dipose tissue reak chylomicron to FA + remnant , FA stored in api

108

roles of apolipoprotein: ApoB48, Apo CII, Apo E

Apo B48: assembly and structure
ApoCII trnasfer of lipid from chylomicron to tissue
Apo E: removal old chylomicron by liver

109

What stimulate lipoprotein lipase? (2)

Insulin and ApoCII
Insulin deficientcy : ineffecient storage

110

Hyperlipidemias from elevated chylomicron: type I a, And Ib?

Ia: LpL
Ib: Apoprotein CII

111

Fate of chylomicron remnant

Apo CII block uptake by liver, ApoCII and Apo E transferred to HDL when TG content decreases.
Then ApoE bind to LRP and LDL in liver (LDL receptor-like protein - more dominant than LDL R in liver)
>endocytosis in liver> break down to FA +C+ amino acid in lysosome

112

Assembly of VLDL

new secreted VLDl from liver has B100 and AI
HDL comes in donate A and ApoCII
Delivery of FA via LPL
2 fates of VLDL:
1. uptake by liver again via endocytosis, E +LRP like chylomicron
2. Hepatic lipase: FA + LDL+Apo E, free FA take up by liver cell

113

LDLhow many apoprotein, how to get access to the cargo?

only Apo protein B100
B100 adotp new conformation to bind LDL R

114

two pathway for LDL removal from plasma

1. 75%: LDL receptor to cell. to produce free cholesterol, FA and aa. Free cholesteroll inhibits this
2. 25% scavenger R of MO: scavenger: low affinity for LDL, high affinity for oxidized and glycosylated LDl (correlated with high glucose level). Rceptor is not regulated bu intracellular cholesteroll

115

Foam cell?

uncontrolled accunmulation of cholesterol in cell
contribute to atherogenesis

116

Reverse cholesterol transport

HDL & peripheral cell
- Apo AI mediates binding cell surface
- Free cholesterol from cell diffuse to HDL
- Apo AI stimulated LCAT
- LCAT esterifies transferred free cholesterol

117

LCAT

Lecithin-cholesterol acyl transferase,
-makes cholesterol >> CE

118

transfer of CE from HDL to liver (2 ways )

1. Transfer CE to chylomicron and VLDL remnant, couple to removal of TG , uptake by liver
2. Transfer of CE to liver via SR-B1 receptor allows CE transfer to lover cells without endocytosis

119

Fates of Excess cholesterol ester in liver,(2), which one has feed back inhibition

1. bile acids (feedback, too many bile will inhibits)
2. new VLDL

120

Synthesis cholesterol
1. starting compound
2. step products
2. which one is rate-limiting step

1. Acetyl coA
2. HMG CoA> Mevalonate> Squalene > lanosterol> cholesterol
3. HMG CoA reductase

121

What are 3 FB of free cholesterol

inhibits HMG CoA reductase
stim ACAT turn to droplet for storage
inhibit synth of new LDL receptor

122

What ACAT?

cholesterol acyltransferase
convert free cholesterol to CE to store in small intracellular droplet

123

how cholesterol regulate gene transcription?
via what receptor

LDL R and HMG CoA reductase genes
> high Free cholesterol> low gene expression (via SRE binding)
High cholesterol: SREBP, SCAP, Insig in ER
Low: INSIG release SCAP, SREBP, these 2 travel to golgi, travvel to nucleus, activate SRE

124

2 strategies to reduce LDL

- increase removal of LDL from bloodstream by LDL receptor-mediated endocytosis
- decrease synth of LDL

125

pharmacological agents that reduce cholesterol levels

1. Bile-acid biding resins
2. Statins
3. Ezetimibe
4. Niacin

126

how does cholestyramine work?

what natural product works the same?

Reduce intracellular cholesterol by inhibiting reapsoption in small intestine >> excretion in large amount

fiber (oatmeal) bind to bile acids prevent reabsoption

more bile acids excretion > less free cholesterol > More LDL R? reduce LDL level in blood

127

What does Statins do?
would statin work for homozygoud defect in LDl receptor

inhibit HMG CoA reductase> inhibit cholesterol synth
ExL lovastatin
> decrease cholesterol synth > less free cholesterol> More LDL R to uptake > reduce LDL in blood
No, will not work

128

How does Ezetimibe work?

inhibit absorption of dietary cholesterol into intestinal cells (to assemble chylomicron)

less cholesterol from chylomicron remnant > less free cholesterol? more LDL R

129

Niacin ?

inhibits VLDL synth > less VLDL, less LDL, mechanism unclear

130

effect of insulin in FA metabolism

Insulin: glucose> stored as triglyceride > VLDL > FA

131

effect of glucagone in FA metabolism

triglyceride > FA + glycerol > FA

132

Oxidation of FA:

FA >beta oxidation> Acetyl coA> TCA> oxidative phosphorylation

133

Beta oxidation: location in the body, locaation in cells

in heart, muscle, kidney and liver
happened in mitochrondrion

134

How FA cross the inner mitochondrial mmb

step of the shuttle

Carnitin Shuttle :
FA> FA acyl coA synthetase
carnitine + FA coA > acyl carnitine
carnitine transporter
carnitine release for the next shuttle

135

beta oxidation
Starting product
enzyme (2)
end product

Acyl CoA >>Acyl coA dehydrogenase (FAD to FADH2) > double bond > add H2O> oxidation (NAD to NADH) > ez Thiolase (SH-CoA) >
Acetyl Co A + new FA is 2 C shorter than before

136

What happens when FA has odd number of carbon? pathway after that ?

the last 3C FA rleased as propionyl -CoA
Propionnyl CoA caarboxylase (biotin )
Methylmalonyl CoA racemase
Methyylmalonyl CoA Mutase (metabolite of Vitamin B12)
>> Succinyl CoA : fees into TCA cycle

137

FA Synthesis
1. location
2. primary product
3. building block

1. cytoplasm, liver
palmitic acid (16C)
Acetyl CoA and malonyl CoA

138

how does Acetyl co A from inside mitochondria trnafer to cytoplasm for FA synthesis?

Citrate shuttle
Acetyl coA > Citrate synthase> Citrate > outside > citrate lyase> acetyl coA

139

Multi ez complex in FA synthesis
what are the 2 groups attached on it

FA synthase
cystein and phosphopantethine (Vit B5)
>> it is a acyl carrier protein

140

5 Steps in FA synthesis

1. priming (attachment of Acetyl coA and malonyl co A in FAS)
2. condensation: connect the 2, release Co2
3. reduction if beta ketone group
4. dehydration of the reduced intermediate
5. reduction of double bonds
transfer the new product to

141

FA product release when reach 16 C

palmitoyl thioesterase> palmitic acid

142

regulation of FA synthesis by substrate and product:
what is the rate limiting step in FA synth?

AcetylcoA > MalonylCoA (AcetylCoA carboxylase)
Citrate activates this ez
palmitoyl coA inactivate

143

how insulin ans glucagon regulate FA synth?

Glucagon> cAMP> PKA> acetyl CoA carboxylase active > inactive
insulin > protein phosphatase> inactive> active

144

Hormone sensitive lipase: role, process
what +/- it?

convert TG into DG/MG/Glycerol + FA(s)
- serum albumin prefer short FA to transport
- insulin: inhibit it > reduce mobility
- glucagon, NE, ACTH> activate it > increase
mobility

145

regulation of FA synthesis and oxidation in liver

1. direct regulatory controls
2. prevent crosstalk between the 2 pathway

146

Most statin are metabolized by CYP except

Pravastatin
(rosuvastatin 10% metabolized by CYP)

147

Teratogenic (Pregnant Cat. X) of Statin

cannnot prescribe HMG CoA reductase inhibitor to prego

148

MOA of resin ( treating hyperlipidemics)

bile acid binding, prevent the reabsoprtion of bile acids
Ex: cholestyramine, colestipol
- works best with patient with LDL R
increase VLDL ( >> no use with pt with hyper TG )

149

MOA of Ezetimibe

prevent take up of cholesterol into small intestinal cell

150

MOA of Niacin , side effect

reduction of VLDL secretion

hot flush , GI distress, hepatotoxicity, hyperuricemia

151

Fibrates

enhance oxidation of FA:rduce VLDl secretion from liver, increase VLDL uptake in muscle

side effect: myopathy, hepatotoxicity, gallstones
Ex: Gemfibrozil (renal elim)
Fenofibrate (glucuronide)

152

Omega 3 acid ethyl esters
MOA , side effects

only for patient with side TG> 500 mg/dL
reduce synthesis of TG and enhance TG removal
side effect: burping, upset stomach, allergy , bleeding

153

Macula densa: location, roles

in juxtaglomerular apparatus:
thicckened portion of the distal convoluted tubule: sense the composition of the tubular fluid

154

Granular cell

in juxtaglomerular apparatus: specialized smooth muscle cells in the wll of the afferent arteiol, secretes the ez renin

155

Renal blood flow

= 20-25% X Q ml/min

156

Renal plasma flow

= 55% Renal blood flow (RBF)

157

Glomerular filtratio rate

= 20% renal plasma flow

158

Net filration pressure (NFP)

NFP = Force favoring - force opposing filtration
= PGlomerular cap - P Bowman's - Pi Glomerular Cap

159

Force of filtration does not change along the glomerular length (T/F)

F
Afferent > efferent

160

Permeability of filtration coefficient Kf
GFR in terms of Kf

Kf = hydraulic permeability * SA
GFR = NFP * Kf

161

How hypoalbuminemia affect GFR?

decrease Glomerular cap oncotic pressure
increase GFR

162

What is autoregulation of kidney ?
how does it work

the ability to regulate on its own blood flow without involvement of extrinsic factor

1. Myogenic FB: - increase perfusion pressure> increase stretch smooth muscle > open stretch-activated, non-selective cation channels > depolarizing, influx of Ca> contraction > increase R

2. Tubuloglomerular feedback : a transient increase in pressure in the glomerular cappilaries increase GFR> more NaCl to macula densa> vasocontriction in adjacent afferent aterioles

163

actions of angiotensin II

stim aldosterone secretion
increase thirst
Stim Na reabsorption
Stim ADH secretion

164

Prostaglandin

vasodilator
synth by kidney,
protective role: provide a buffer against excessive vasoconstriction

165

GFR formula using innulin

GFR = U.V/P = (conc inulin. flow rate )conc plasma

166

Renal: the entry of Na across the apical mmb is (down/up hill)
the Na across the lasolateral is (down/up hill)

apical: down
basolateral: up

167

renal: for a weak acid, renal clearance is low at an (acidic/alkalike) pH?

high at an (acidic/alkaline) pH ?

acidic: low pH = low clearance of weak acid

alkaline: high pH = high clearance of weak acid

(aspirin)

168

what affects the pH of Urine?

diiet
exercise (lactic acid)
dsease condition (ketoacidosis in type I diabetes)
drugs
hydration state: prolong vomiting deplete water volume, stim acid secretion

169

Probenecid
combine with peniciline?

competitive inhibitor of secretory mechanism
slow down the clearance of peniciline

170

cimetidine

block creatinien secretion

171

Inulin clearnace is independent of inulin plasma conc ( T/F)

T

172

why mannitol cause osmotic diuresis ?

mannitol is freely filtered but not reabsorbed in proximal tubule
> increase osmotic pressure
> water retention > Na diffuse into the lumen
> excess Water and Na
> diuresis

173

Polyuria and poly dipsia in Type I diabetes

Tm for glucose and ketone increase
> osmotic diuresis

174

how is a hyperosmotic medulla generated?

countercurrent multiplication

175

Peritubular capillaries vs Vasa Recta ?

Peritubular Cap: reabsobed material quickly removed
Vasarecta: not immediatedly removes, enabling maintenace of gradient

176

Furosemide

diuretics
Adverse: hypokalemia, sulfa- allergy- ototoxicity, NSAID decrease efficacy of loop agents: NSAID inhibit protaglandin (vasodiator)

177

Thiazides

diuretics
indication: hypertension, mild edema, chronic hypercalciuria, stone formers

178

Spirolactone , eplerenon

aldosterone antagonist: inhibit Na reabsorption iin cortical collecting duct > prevent K excretion
K sparing diuretics

Adverse: HyperK, antiandrogen effect: gynecoastia, impotence

179

amiloride, triamterene

physiologic antagonist of aldosterone: block Na channel in cortical colecting tubules

K sparing diuretics

Adverse: HyperK

180

Osmoreceptor
cell swell
cell shrink ?

Cell swells: decrease in solute concentration in interstitial fluid > OsmoR gains water > need to stop diuretic> ADH promoted

cell shrink: increase in conc of interstitial fluid , water comes out, need to promote diuretics > prevent ADH relelased

181

baroR compared to osmoR in controlling ADh

less sensitive but incudes a greater ADh release

182

what happens to Diabetes insipidus?

ADH is either not produces or is incapbable acting
> Massive urine flow, low osmolarity

183

Aldosterone
> secretion from where?
stimulated by?

from zona glomerulosa
stim by:
- Small increase in plasma K
- Decrease in plasma Na
- Angiotensin II (most important)

184

Atrial Ntruretic Peptide (ANP)

secreted from cells in atria
Blood increase atria stretch > ANP secretion
> increase NA excretion in 3 ways
1. increasing GFR
2. inhibit Na reabsorption in the medullary collecting duct
3. inhibiting renin , aldosterone and ADH

ANP also a vasodilator

185

High Extracellular K stim which hormones? (3)
mechanism

insulin: K goes to muscle and liver
Epinephrine : K goes to muscel
aldosterone: stim K secretion in CCD

stimulate Na-k ATPase pumps K into the cell to low ECF K

186

Digitalis and ECF K ?

severe HyperK
inhibit NaK ATPase pump