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NBS2, EXAM1 Biochem > NBS Exam 2 > Flashcards

NBS Exam 2 Flashcards

1
Q

Where does gas exchange first occur?

A

the respiratory bronchioles

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2
Q

the right and left bronchi have how many main stem bronchi?

A

Right has 3, Left has 2

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3
Q

constriction of bronchi is due to

A

PNS innervation / alpha adrenergic agonists

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4
Q

dilation of bronchi are due to

A

SNS inntervation/B2 adrenergic agonists

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5
Q

the diameter of bronchioles is dependent on what 2 main factors

A

lung volume and by local O2 and CO2 in the airways

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6
Q

local hypocapnia causes

A

local bronchiolar constriction to direct ventilation away from alveolar regions with poor perfusion

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7
Q

hypocapnia is

A

a state of reduced carbon dioxide in the blood

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8
Q

Local hypercapnia/hypoxia causes

A

local bronchiolar dillation, directing airflow to alveolar regions with better prefusion

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9
Q

pores of Kohn are important for

A

exchange of gasses btw alveoli via diffusion, and for the spread of Type II pneumocytes and macrophages btw alveoli

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10
Q

bronchiolar veins are an example of a

A

Right to Left shunt

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11
Q

what percent of the atmospheric air is O2

A

20.93

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12
Q

define O2 capacity

A

max amount of O2 combined w/ Hb at high PO2 = 1.39ml O2/gm Hb

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13
Q

define O2 saturation

A

the percent of capacity that is occupied by O2

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14
Q

define O2 content is (C o2)

A

(PO2s) + ([Hb]saturation*1.39)

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15
Q

what factors cause a right shift in the Hb binding curve

A

increasing Temp, 2,3BPG, CO2, and H+

Decreasing pH

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16
Q

right shift favors the ___ of O2

A

unloading of O2 (lower affinity)

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17
Q

left shift favors the ____ of o2

A

loading of O2 (higher affinity)

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18
Q

CO2 + H20 –>

A

H2CO3 –> H+ +HCO3-

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19
Q

most of the CO2 that the body transports is carried as

A

HCO3=

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20
Q

distral straight tubule is the same as the

A

Thick ascending limb

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21
Q

FF (filtration fraction)

A

GFR/RPF

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22
Q

Acetazolamide is

A

an carbonic anhydrase inhibitor leading to diuresis

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23
Q

Furosemide

A

inhibits the NKCC co transporter –> leading to diuresis. loop diuretic

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24
Q

chlorthiazide

A

inhibits the Na/Cl- cotransporter –> leading to diuresis. Type of diazide diuretic

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25
Q

Amiloride

A

sparing diuretic, inbitis the Na+ channel and inhibits K+ secretion

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26
Q

the macula densa senses

A

NaCl

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27
Q

calculate reabsoprtion

A

Filtration - excretion

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28
Q

clearance eqn

A

Clearance = [X}in urine * Urine flow rate / concentration C in arterial plasma

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29
Q

the Clearance of PAH is equal to

A

Renal plasma flow

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30
Q

what do you use to calculate the Renal plasma flow? why?

A

the clearance of PAH since PAH is completely cleared from the plasma in a single pass

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31
Q

normal GFR

A

120 ml/min

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32
Q

how do you calculate GFR?

A

Clearance of Inulin. You can also use creatinine.

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33
Q

what is filtration fraction

A

it is the fraction of the renal plasma flow that becomes glomerular filtrate

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34
Q

calculation of FF is

A

GFR / RPF = Cinulin/Cpah

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35
Q

normal plasma flow rate

A

600

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36
Q

RBF normal value?

A

1.2 L/min

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37
Q

when Na/Cl is high within the thick ascending limb, what transporter is responsible for the movement of Na/Cl into the macula densa?

A

NKCC (Na, K, 2Cl)

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38
Q

primary mechanism of tubuloglomerulae feedback : Na/cl control through the macula densa

A

increase in chloride from the macula densa –> increase in Ca+ movement into the macula densa –> increasein ATP and a decrease in NO. This leads ultimately to the constriction of the afferent arteriole and a decrease in GFR

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39
Q

secondary mechanism of tubuloglomerular feedback

A

Cl- in the macula densa communicates with the JG cells. The JG cells will stop secreting renin, leading to a decrease in aldosterone and angiotensin and thus a vasodillation. Vasodillation will increase GFR to restore

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40
Q

decreased NaCl leads to

A

vasodillation of the afferent arteriole to increase GFR

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41
Q

sympathetics lead to

A

AA constriction through NE release on alpha-1 adrenoreceptors. decrease in GFR and RBF

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42
Q

Angiotensin II at low physiologcal cocentrations

A

constriction of both afferent and efferent, but more of an effect on the efferent so increased GFR but decreased RBF

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43
Q

Angiotensin II at high concentrations

A

constriction of both afferent and efferent, leading to decreased GFR and RBF

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44
Q

Endothelin I

A

potent vasoconstricor that decreases GFR and RBF. comes from the mesangial cells

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45
Q

Adenosine

A

constriction of the afferent arteriole leading to a decrease in RBF and GFR

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46
Q

Prostaglandins

A

occur due to a result of some negavity. They are relased when sympathetic outflow is high

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47
Q

what causes the release of prostaglandins

A

when sympathetic outflow is high, dehydration, stress, ANGII

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48
Q

what is significant about prostaglandins

A

they are the escape from constrictor mechanisms

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49
Q

PGs do what

A

PG release PGI2, PGE2 and PGE1 which all help to prevent ischemic damage leading to an increase in RBF with no real change in GFR

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50
Q

nitric oxide and bradykinin

A

dillation of afferent and efferents leading to an increase in GFR and RBF

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51
Q

bradykinin stimules

A

release of NO and PG

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52
Q

ANP

A

from stretch receptors in the atrium which leads to dillation of the afferents and constriction of the efferents leading to an increase in GFR

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53
Q

renin

A

converts angiotensinogen and converts it to angiotensin I

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54
Q

calculate reabsoprtion

A

amount filtered - amount excreted

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55
Q

The net reabsorbed is

A

(GFR)(concentration in the plasma) - (Urine flow rate) (concentration in the urine)

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56
Q

if the ratio of Cx : C inulin is greater than one

A

then the substance is secreted

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57
Q

If the ratio of Cx:Cinulin is less than one then

A

the substance is reabsorbed

58
Q

what are the 4 transporters in the early proximal tubule that i should care about

A

1- the NHE3 on the apical side that exchanges H+ out for Na+ in.
2- the AE1 on the basolateral side that exchanges a HCO3- to the blood for a Cl-
3- the NBC1 ont he basolateral side that puts Na and HCO3- into the blood
4: the SGLT 2 ont he apical membrane that brings glucose in with a high capacity but a low affinity

59
Q

how does most of the Na/Cl come into the cells

A

through a transcelluar route (2/3!)

60
Q

What is the important exchanger in the 2nd half of the PCT

A

The anion chloride exchanger which sits on the apical side of the cell and pumps anions out and Cl- in. This is how we excrete a lot of the drugs we take.

61
Q

the high number of Na/K ATPases in the PCT function to

A

pump alot of sodium into the blood thus taking H20 with it through squaporin channels

62
Q

Test Q* define glomerulotubular balance

A

as GFR increases, the oncotic forces increase in the efferent arteriole which then asserts a high oncotic force to bring H20 back in

63
Q

is the thick ascending limb permeable to water?

A

NO!

64
Q

the thick ascending limb has what notable transporters

A

NKCC Na in, 2Cl- in, K in.

65
Q

where do you find the NKCC

A

the NKCC can be found in the Thick ascending limb and is responsible for the uptake of Na and Cl in the macula densa

66
Q

the diluting segment of the nephon is

A

the thick ascending limb since it is taking ions in but leaving the water in the tubule

67
Q

what important transporter is found in the early DCT?

A

The Na+/Cl- transporter which brings Na and Cl into the cell.

68
Q

what drug blocks the NKCC

A

Furosimide

69
Q

what kind of drugs will block the Na/Cl co transporter in the early DCT?

A

thiazide

70
Q

what are the main cell types that are found in the late DCT, collecting tubule and collecting duct?

A

Principal cells, alpha intercalated cells and beta intercalated cells

71
Q

AQP2 is found

A

on the apical side of principal cells of the late DCT and Collecting duct

72
Q

AQP3 and AQP4 are found

A

on the basolateral side of principal cells in the late DCT and the collecting duct

73
Q

alpha intercalated cells have what types of channels

A

secrete acid using an ATPase which exchanges H+ for K+, pumping H+ into the urine. They also have an ATP H+ pump to pump H+ into the urine. On the basolateral side they have an AE2 pump that pumps HCO3- into the blood in exchange for a cl-

74
Q

Beta intercalated cells have what types of channels

A

Pendrin (Cl/HCO3), which pumps HCO3- into the urine in exchange for a cl

75
Q

what is pendrin channel

A

in a b intercalated cell, it is responsble for pumping HCO3- into theurine in exchange for a cl-

76
Q

what is the glucose maximum that can be reabsorbed

A

375 mg/min

77
Q

angiotensin II

A

acts directly on PCT to increase Na+ and H20

78
Q

Aldosterone

A

acts on the TAL, CT and DCT on the principal cells where it stimulates reabsoprtion of Na and loss of K+

79
Q

Acute v chronic phase of aldosterone

A

acute phase (hours –> day): increase in the activity of the Na/K ATPase which decreases Na in the cell and drives the reabsoprtion of Na from the urine and secretion of K+. (saving Na and loss of K+)

Chronic: Na/K ATPase activity and # increase leading to high K+ in the cell and low Na+ putside. New K+ channels also get inserted on the apical side to pump it out and make the ATPase more efficient

80
Q

Angiotensin acts on the

A

PCT

81
Q

Aldosterone acts on the

A

DCT

82
Q

ADH acts on the

A

DCT and mainly in the collecting duct

83
Q

ADH is realeased from the

A

posterior pituitary

84
Q

ADh binds to the

A

V2 receptor

85
Q

V2 receptor increases

A

cAMP

86
Q

increase in PKA (in relation to ADH) as a result of ADH causes

A

the insertion of aquaporin channels on the apical membrane leading to the absorption of H20 and the insertion of urrea channels which also helps bring H20 in

87
Q

summary of ADH

A

vasoconstriction, insertion of AQP2 channels to increase H20 reabsoprtion, increase of urea uptake, stimulation of thirst, increase activity of the NKCC in the TAL

88
Q

low BP causes the JG cells to

A

release renin with cleaves angiotensinogen into ANT I which then goes to the liver to become ANT II which is a vasoconstrictor leading to an increase in BP. Angtiotesin II also causes secretion of aldosterone which increases blood volume

89
Q

PTH

A

inhibits Na+ and H20 reabsoption in the PT –> dumping volume. Inhibits phosphate reabsorption. It also increases bone resorption leading to an increase in Ca2+ resorption in the TAL &

90
Q

prostaglandins

A

dilates renal blood vessels to maintain nutritive aspects

91
Q

Natriuretic hormone

A

inhibits Na+ reabsoprtion –> dumping of fluid

92
Q

Urodilatin

A

inhibits the reabsprtion of Na in the collecting duct

93
Q

aldosterone

A

increases Na reabsoprtion in the loop of Henle, distal tubules and colelcting duct via Na/K ATPase

94
Q

Carbonic anhydrase inhibitor

A

acetozolamide

95
Q

diuretics that apply to the proximal and collecting duct often lead to

A

acidosis

96
Q

diuretics that act in the collecting duct often lead to

A

alkylosis

97
Q

Furosimide

A

diuretic that acts in the thick ascending limb to block the NKCC

98
Q

chlorothiazide

A

blocks the apical Na/Cl transporter in the DCT

99
Q

Amiloride

A

diuretic that acts int he collecting duct to inhibit the Na channel collecting duct

100
Q

Spironolactones

A

block aldosterone leading to an increase in Na+

101
Q

Hypoxic Hypoxemia

A

low Po2 stimulates breathing

102
Q

anemic hypoxia. Cause?

A

low hb int he blood, but normal PO2

-Can be from CO poisoning –> get no ventialtory response to CO2

103
Q

stagnant hypoxia cause and response

A

low blood flow –> ventialtory response from the CB

104
Q

Histotoxic hypoxia cause and response

A

low ATP production due to cyanide which will block the ETC

105
Q

fixed acids are

A

sulfuric and phsophoric acids which result from metabolism of sulfur or phosphate containig AA

106
Q

organic acids are

A

production of Lactic, pyruvic acid

107
Q

amount of fixed acid

A

50-100 mm/day

108
Q

alkylosis can lead to

A

hyperexcitablility

109
Q

most powerful and important bufferig systems are

A

proteins

110
Q

The 4 major physiochemical buffers are

A

bicarbonate, phosphate, ammonia and proteins

111
Q

Step 1 in the 6 step mechanism: shortcut for converting pH to H+ ion

A 
[H] =  80 -pH*XX 
[H] = 24 *(PaCO2/HCO3-)
112
Q

Buffering power pertains to what 2 things?

A
  1. concetration of the buffer

2. the zone of pH has to be +/- 1 to the proteins Pk

113
Q

if the pk of a buffer is at 6.1, what pHs is it good at buffering?

A

5.1 –> 7.1

114
Q

why is HCO3 considered to be an important buffer?

A

it cannot be saturated or pushed to one extreme ot the other since it is an open buffering system

115
Q

is phosphate a powerful buffer?

A

No! While its pk is appropriate, there is no enough Pi in the ECF/plasma to be powerful.

116
Q

the kidneys filter how much HCO3-/day

A

180 L/day * 24 mEq/L = 4320 mEq/Day

117
Q

What is a system that generates NEW bicarbonate?

A

the phosphate buffer system and the Nh4/NH3 system

118
Q

PTH does what to phosphate

A

PTH blocks the reabsoprtion of H2PO4 into the cell thus driving the excretion of phosphate and H+

119
Q

does ammonium or ammonia predominate at acific pH

A

Nh4+ (which cannot move across the lipid bilayer)

120
Q

what activates glutaminase

A

hydrogen

121
Q

what does glutaminase do

A

it breaks down glutamine to Nh4+ and HCO3-

122
Q

Where is NH4+ reabsorbed the most?

A

In the Thick ascending limb `

123
Q

most prevalent species of ammonia in urine is

A

NH4+ since urine is acidic

124
Q

calculate bicarbonate excretion

A

urine flow rate*urinary HCO3-

125
Q

an increase in H+ in the intracellular fluid results in

A

an increase in activity of the Na/H exchanger, an increased afinity of the exchanger, increase in H+ ATPase and a stimulation of glutaminase to make ammonia, an increase in the Na+ absorption (Na+ in, H+ out)

126
Q

describe the mechanism of volume based contraction alkylosis

A

When low blood volume –> angiotensinII is realsed to incresae Na+ absoprtion in the PCT (to bring H20 in with it). The increase in Na+ absorption causes the cell the excrete H+ –> alkylosis

127
Q

being hypokalemic leads to

A

alkylosis

128
Q

being hyperkalemic leads to

A

acidosis

129
Q

part of the tubule that drives the steepest excretion of H+

A

CD and Late Distil Tubule

130
Q

salicylic acid and treatment of overdose

A

salicilate causes the respiratory centers to increase ventilation which leads to an initial ventilation. This creates an alkilosis. The physicians then treat the alkalosis with acid, however the drug itself is an acid so this makes them much worse.

131
Q

diarrhea leads to

A

an increase in HCO3- loss and thus acidosis. Also leads to an increase in Cl

132
Q

carbonic anhydrase inhibitors

A

cant take the HCO3- back into the blood while you are conutously makng acid –> acidosis

133
Q

ethylene glycol is metabolized to

A

OXALIC ACID

134
Q

type I renal tubule acidosis

A

inability of the distal nephron to pump acid into the tubule and acidify the urine (further accentuating theproblem by reducing the ammonia trapping mechanism)

135
Q

Type II renal tubule acidosis

A

inability of the proximal to reabsorb HCO3- in the proximal region

136
Q

How do you differentiate Type I RTA

A

when NH4Cl challenge, you cannot excrete that excess acid that was given. A normalperson will have a urine pH below 5.5, but a person with Type I RTA will not have a urine pH below 5.5

137
Q

How to you diagnose Type II RTA

A

No problem in acidifying the urine.. the urine will have a ph below 5.5

138
Q

Type IV RTA

A

reduction in both K+ and H+ secretion by the collecting duct

139
Q

Type 4 RTA will present with

A

urine ph below 5.5 since there is decreased ammonia in the urine to buffer he secreted H+

140
Q

how does aldosterone affect Na, K and H

A

aldosterone increases reabsoprtion of Na+ and increases excretion of H+ and K+

141
Q

effect of vomiting on blood ph

A

you are losing acid to you ca become alkylotic

NBS2, EXAM1 Biochem (12 decks)

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