Physio Test 2 Combined - Memorize

Front 1

Laplaces Law equation? interpretation?

Back 1

2T/r

As you increase radius you dilute surfactant so that T and r increase together. This keeps pressure in the airways equal and prevents collapse of small --> large

Front 2

Deep breathing stimulates its production. Surfactant is comprised primarily of

Back 2

dipalmitoyl phosphatidyl choline (DPPC)

Front 3

surfactant causes?

Back 3

-decreased surface tension
-decreased fluid drawn out of capilaries = decreased pulm edema
-INcreased lung compliance

Front 4

What CANT be measured by spirometry?

Back 4

RV
TLC
FRC

Front 5

Minute ventilation equation?

Back 5

VE = f*Vd + f*Va

Front 6

During expiration the first volume passing out of the lungs is the _______ volume with the composition of _________ gas; this is followed by the ______ gas enriched in ____ and depleted of ____. The gas remaining in the dead space at the end of the cycle has the composition of _______

Back 6

During expiration the first volume passing out of the lungs is the dead space volume with the composition of inspired gas; this is followed by the alveolar gas enriched in CO2 and depleted of O2. The gas remaining in the dead space at the end of the cycle has the composition of alveolar gas.

Front 7

PECO2?

PACO2

Back 7

PECO2 = mixed expired air = measured at the mouth

PACO2 = arterial CO2

Front 8

Fraction of tital volume that is physiological deadspace

Back 8

VD/VT = PACO2 - PECO2/PACO2

Front 9

Henry's Law

Back 9

Cx = Px*Sx

Front 10

Alveolar ventilation equation?

Back 10

VA = VCO2 [(PB-47)/PACO2]

Front 11

Respiratory quotient?

Back 11

VCO2/VO2

normally 0.8

Front 12

Situations where R=1

Back 12

breathing 100% O2

pure carb diets

Front 13

PAO2 equation?

Back 13

PAO2 = PIO2 - [PACO2/R]

Front 14

% saturation of hgB?

Back 14

O2bound /O2 capacity

O2 capacity hgb = 15g/dL * 1.34mL O2/gm

Front 15

% saturation?

Back 15

total O2 content - dissolved O2/O2capacity

Front 16

concentration of disolved O2?

Back 16

0.3 mL O2/dL

Front 17

oxygenated hgb is a stronger acid or base

Back 17

stronger acid

Front 18

FEV1/FVC

Back 18

normally 80%

low values suggest obstruction or lack of driving pressure

Front 19

Changes in Fibrosis or scoliosis:

FVC
FEV1
FEV1/FVC

Back 19

FVC = <80%
FEV1 = reduced
FEV1/FVC = normal

Front 20

Changes in obstruction:

FVC
FEV1
FEV1/FVC

Back 20

FVC = normal or reduced
FEV1 = reduced <80%
FEV1/FVC = reduced <70%

Front 21

Helium dilution problem method?

FRC via helium =?
RV via helium = ?

Back 21

P1V1=P2V2 then solve for V2 and subtract V2-V1

FRC = above result If the patient just completed a quiet repiration

RV = above result if maximal expiration

Front 22

How to convert PAO2 to [O2] dissolved?

Back 22

[O2] = PA02 · 0.003

Front 23

Order of respiratory groups from superior to inferior?
Each is associated with?

Back 23

PRG > VRG > DRG

DRG = inspiration
VRG = inspiration and expiration
PRG = stops inspiration/early cutoff

Front 24

Transect above PRG/NPBL =?

transcet + cut vagal?

Back 24

transect = almost normal respiratory pattern

transcet + cut vagal = slow deep respirations

Front 25

Transect between PRG and VRG?
transcet + cut vagal?

Back 25

Removal of PRG input:

transect = slower deeper breaths

transect + cut vagal = apneustic breathing

Front 26

____ bodies are more important than ____ bodies as respiratory regulatory organs

Back 26

carotid bodies are more important than aortic bodies as respiratory regulatory organs

Front 27

______ in the carotid and aortic bodies synapse with the afferent endings of the sensory nerves innervating the chemoreceptors.

Back 27

Type I glomus cells

Front 28

How do type 1 glomus cells work?

Back 28

closing of O2 sensitive K-channel causes depolarization and Ca2+ influx = NT release:

responds to increased PCO2, decresed PO2, and Increased H+

Front 29

_______ located in conducting airways and alveoli also respond to chemical and mechanical stimulation. Afferents travel in the vagus nerve in slowly conducting, unmyelinated, C-fibers. Activation results in rapid, shallow breathing, bronchoconstriction and mucus secretion. These receptors may play a role in dyspnea (difficulty breathing) associated with left heart failure.

Back 29

J Receptors (juxtacapillary receptors)

Front 30

Isohydric principle?

Back 30

when you add acid to a system every buffer soaks up the protons according to it's pKa

not just one

Front 31

Bicarb buffer equation?

Back 31

pH = 6.1 + log [HCO3- ] / 0.03 PCO2

0.03 is in mMoles/L/mmHg

HCO3 is in mMoles

Front 32

[H+] for the following pH values:

7.35 =
7.40 =
7.45 =

Back 32

7.35 = 45nM
7.40 = 40nM
7.45 = 35nM

For every increase in pH by 0.01 there is a 1nM decrease in [H+]

Front 33

Flow (Q) at the top of the lung?

Back 33

Apex = less distended = decreased radius = increased resistance = decreased flow

Front 34

Things that cause the apex/zone 1 of the lung to become unventilated?

Back 34

PPV and severe hemorrhage

Front 35

Flow and ventilation at the top and bottom of the lung

Back 35

The top of the lung is relatively poorly perfused (V is higher than Q)

The bottom of the lung is relatively poorly ventilated (Q is higher than V)

Q has a steeper slope

Front 36

1 unit of blood = ?

Back 36

450mL

Front 37

affect of decreased ATP on RBC?

Back 37

crenation

Front 38

echinocyte?

Back 38

calcium deposits on cells = sea urchants

Front 39

deficiency of spectrin?

Back 39

spherocyte

Front 40

Almost all of the red cell's metabolic energy is derived from ?

Back 40

anaerobic glycolysis (the conversion of glucose to lactic acid).

Front 41

Rapoport-Leubering shunt

Back 41

An offshoot of glycolysis, the Rapoport-Leubering shunt produces 2,3 DPG (or BPG) from 1,3 DPG via diphosphoglyceromutase which influences the affinity of hemoglobin for oxygen

Front 42

NADH levels in the RBC are maintianed by ______ and NADPH levels are maintained by the __________

Back 42

NADH levels in the RBC are maintianed by glycolysis and NADPH levels are maintained by the hexose monophosphate shunt

Front 43

Main function of NADH in RBC?

Back 43

to reduce ferric iron to ferrous iron

Front 44

How is NADH generated in the RBC?

Back 44

the methemoglobin reductace pathway:

G3P is converted to 1,3GP producing NADH
NADH is then used as a cofactor for Diphorase/methemoglobin reductase to reduce Fe3+

Front 45

denatured methemoglobin forms aggregates called

Back 45

heinz bodies

Front 46

__________ converts NADP to NADPH in the RBC

Back 46

glucose 6P dehydrogenase

Front 47

Function of NADPH in RBC

Back 47

used as a cofactor for glutithione reductase to reduce glutathione (GSSG) to to GSH

GSH protects the cell membrane and HGB from oxidants/hydrogen peroxide

Front 48

α and β-globin are synthesized ___________ of the normoblast. The porphyrin group of heme is synthesized ____________

Back 48

α and β-globin are synthesized on ribosomes in the cytosol of the normoblast. The porphyrin group of heme is synthesized in the mitochondria of this cell

Front 49

sources of iron for hgb synthesis in order of importance

Back 49

iron salvaged from RBC
iron from body stores
dietary iron

Front 50

Iron is carried in the blood as part of a complex with the protein _____

Back 50

transferrin

2Fe per 1 transferin

Front 51

The storage form of iron consists of the metal bound to one of two other structurally related proteins _____ or ___

Back 51

ferritin or hemosiderin.

Front 52

Hemoglobin liberated after lysis of red cells in free circulation dissociates into dimers which bind to the serum protein

Back 52

haptoglobin

Front 53

What happens to haptoglobin in anemia?

Back 53

it gets used up and decreases to trace levels cause iron to be excreted in urine = hemoglobinuria

Front 54

breakdown of porphyrin leads to what products

Back 54

CO (can be measured in expired air)

bilirubin (conjugated with glucuronic acid = urobilinogen)

Front 55

pernicious anemia?

Back 55

B12 deficiency

Front 56

________ can precipitate hemolytic crisis in G6PD patients?

Back 56

sulfa drugs

Front 57

CO2 narcosis?

Back 57

-Pt who is hypercapnic and hypoxemic is given 100% O2.
-The O2 relieves the hypoxic drive to breathe.
-The central CO2 receptors are desensitized because of increased HCO3 from compensation.
-Pt doesn't breathe and high CO2 causes vasodilation

Front 58

Factors released during the humoral response to an injury that participate in the vasoconstriction stage

Back 58

serotonin, thromboxane A2, prostaglandins/PGFs

Front 59

Platelet adhesion = ? mediated by ?

Back 59

Adhesion = platelets bind to subendothelial collagen

mediated by Von Willebrand Factor (VWF)

Front 60

Release reaction? Triggered by?

Back 60

changes in shape and the release of storage granules

triggered by binding of VWF/collagen or by thrombin binding to platelet membrane receptors

Front 61

substances extruded from platelets during release reaction:

Back 61

⁃calcium
⁃serotonin
⁃adenosine diphosphate (ADP)
⁃proteolytic enzymes, growth factors and other proteins.

Front 62

Platelet aggregation = ?

Back 62

binding of platelet to platelet

Front 63

At low levels of _____ with surface bound ______ platelets swell and begin to clump. Then what?

Back 63

At low levels of ADP with surface bound fibrinogen platelets swell and begin to clump.

Then if the ADP rises by a factor of 10 the platelets release ADP and more aggregation occurs

Front 64

Thromboxane A2 = ?

Back 64

potent aggregating agent that is derived from platelet membrane phospholipid

Front 65

ASA acetylates and inactivates the enzyme _________ that is required for ___________ formation —> ?

Back 65

ASA acetylates and inactivates the enzyme cyclo-oxygenase that is required for thromboxane A2 formation —> the function of a given platelet is irreversibly depressed following exposure to aspirin

Front 66

First step in the intrinsic pathway

Back 66

contact activation via binding of factor XII followed by the binding of
⁃prekallikrein
⁃high molecular weight kininogen
⁃factor XI

Front 67

Next Step in intrinsic pathway = Factors bind to ______ on surface of aggregated platelets —> only aggregated platelets express the factors necessary for clotting —> this allows clotting factors to bind and orient to activate ___ —> _____

Back 67

Next Step = Factors bind to phospholipid on surface of aggregated platelets —> only aggregated platelets express the factors necessary for clotting —> this allows clotting factors to bind and orient to activate X —> Xa

Front 68

________ bound to platelet phospholipid + _____ produce thrombin

Thrombin cleaves ___ to ______

Back 68

Prothrobin bound to platelet phospholipid + Xa produce thrombin

Thrombin cleaves Fibrinogen to Fibrin

Front 69

First step in extrinsic pathway = following an injury in which blood extravascates, ____________ binds to and activates the blood borne factor ________ to ___

Back 69

First step in extrinsic pathway = following an injury in which blood extravascates, tissue factor binds to and activates the blood borne factor VII to VIIa

Front 70

Factor VIIa can then ?

Back 70

Factor VIIa can then activate X to Xa and proceed from that point in the intrinsic pathway

Front 71

Why doesn’t platelet aggregation spread beyond injury site?

Back 71

endothelial cells of the normal surrounding vessels produce a powerful inhibitor of aggregation, prostacyclin (PGI2)

Front 72

Extrinsic pathway has a built in limiting effect in that prolonged digestion by __ ultimately inactivates factor _____

Back 72

Extrinsic pathway has a built in limiting effect in that prolonged digestion by Xa ultimately inactivates factor VII.

Front 73

Critical for the calcium binding clotting factors is the presence of a number of _________ residues in the amino acid sequences of these proteins. _________ is required for this carboxylation.

Back 73

Critical for the calcium binding clotting factors is the presence of a number of gamma-carboxyglutamic acid residues in the amino acid sequences of these proteins. Vitamin K is required for this carboxylation.

Front 74

The most important antithrombin component is a circulating plasma protein ________

activity is enhanced over 1000X by _____

Back 74

The most important antithrombin component is a circulating plasma protein, the alpha-2- globulin antithrombin III.

activity is enhanced over 1000X by heparin

Front 75

______________ binds thrombin and changes specificity to make thrombin activate ________ and not clot

Back 75

Thrombomodulin binds thrombin and changes specificity to make thrombin activate protein C and not clot

Front 76

Thrombomodulin binds ___________ and changes specificity to make it activate protein C.

Back 76

Thrombomodulin binds thrombin and changes specificity to make thrombin activate protein C and not clot

Front 77

Protein S + Protein C ?

Back 77

inactivate Factors VIII and V

Front 78

Tissue Factor Pathway Inhibitor:
produced by?
binds?
ultimate fxn?

Back 78

Tissue Factor Pathway Inhibitor:
-produced mostly by endothelial cells
-binds to and inactivates the VIIa:tissue thromboplastin
-inhibits extrinsic pathway.

Front 79

Plasmin fxn?

Back 79

Plasmin breaks down clots —> can break down both fibrin and fibrinogen

Front 80

What converts plasminogen to plasmin?

Back 80

tPA and Factor XIIa

Front 81

PT = ?

PTT = ?

IVY bleeding time = ?

Back 81

PT = Prothrombin time = assessment of extrinsic pathway —> normally 10-14s

PTT = Partial Thromboplastin Time = assessment of intrinsic pathway —> normally 30-50s

IVY bleeding time = assessment of primary hemostasis —> normal = 1-9min

Front 82

Hemophilia

Back 82

Hemophilia = deficiency of Factor VIII

Front 83

stuff that is filtered by the kidney

Back 83

small molecules
cationic molecules
small amounts of albumin

Front 84

Kidney is rich in _____ innervation and has no______ innervation

Back 84

lots of sympathetic

no parasympathetic

Front 85

Normal values:
RBF = ?

RPF = ?

GFR = ?

Back 85

RBF = 1 L blood/min

RPF = 0.6RBF = 600ml/min

GFR = 0.2 RPF = 125 ml/min

Front 86

Glomular filtrate contains?

Back 86

nearly all the substances present in plasma except proteins at the same concentration

Front 87

Does reabsorbtion occur along glomuler capilaries

Back 87

no

Front 88

Ex =? (2 equations; general and physiological)

Back 88

Ex = Fx + Sx - Rx

Ex = Ux * V

Front 89

Fx =?

Back 89

Px * GFR

Front 90

A-V O2 difference in the kidney?

Back 90

very low

Front 91

Cx = ?

Cx of inulin?

Cx of PAH?

Back 91

Cx = (Ux * V)/Px

Cx of inulin = GFR b/c all inulin is filtered and excreted with no secretion or reabsorbtion

Cx of PAH = RPF

Front 92

increased RBF = ____ GFR

decreased RBF = ____ GFR

Back 92

GFR increases only moderately with increasing RBF,

decreases greatly with declining RBF.

Front 93

myogenic response of the afferent arteriolar?

myogenic response of efferent?

Back 93

smooth muscle contracts when stretched and relaxes on lowering the distending pressure = mediated by stretch sensitive cation channels

no such response in efferents

Front 94

Low RBF effect on oncotic pressure?

Back 94

Low RBF = high oncotic pressure

Front 95

TGF?

Back 95

changes in GFR that can be induced by changes in the flow rate of the fluid perfusing the macula densa cells

Front 96

Mechanism of TGF?

Back 96

increased GFR = increased NaCl to macula densa = increased NKCC2 work = increased Ca2+ = increased adenosine/ATP = increased afferent constriction via A1 receptor

Front 97

volume contraction and expansion effect on TGF?

Back 97

contraction = increased sensitivity

expansion = decreased sensitivity

Front 98

sympathetic/norepinephrine release stimulated by? effects on kidney?

Back 98

stimulated by low perfusion pressure and decreased stretch of afferent arterioles

alpha-1 = contriction on afferent arterioles

beta-1 = afferent arterioles to release renin = AII production = efferent constriction

Front 99

effect of sympathetic stimulation on RBF and GFR?

Back 99

RBF = decreased

GFR = variable changes

Front 100

NE and AII effect on prostaglandin production?

Back 100

both stimulate it = prevents ischemia

NSAIDS can cause ischemia

Front 101

Endothelin?

Back 101

produced by endothelial and mesangial cells = afferent and efferent constriction

Front 102

neurohormal regulation by NO

Back 102

ECF expansion, ATP, bradykinin, histamine stimulate NO release = vasodilation

Front 103

neurohormal regulation by dopamine and ANP?

Back 103

levels of dopamine, synthesized by proximal tubule cells from circulating L-dopa, and atrial natriuretic peptide (ANP) are also increased with volume expansion. These substances are renal vasodilators that lead to increases in RBF and GFR

Front 104

Location and sensitive to?

NKCC2 = ?
NCC = ?
ENaC = ? ENaC is also upregulated by?

Back 104

NKCC2 = TAL = loop diuretics

NCC = early distal tubule = thiazides

ENaC = late distal tubule and collecting duct = amiloride and upregulated by aldosterone

Front 105

SGLT2, located in the _______________, is a ______- affinity/_______-capacity transporter with stoichiometry _____.

Back 105

SGLT2, located in the early proximal tubule, is a low- affinity/high-capacity transporter with stoichiometry 1:1.

Front 106

SGLT1, located in the __________, is a ___-affinity/____ capacity transporter, with a stoichiometry of ____

Back 106

SGLT1, located in the late proximal tubule, is a high-affinity/low capacity transporter, with a stoichiometry of 2Na+: 1glucose

Front 107

Glucose exits the cell at the basolateral membrane by ?

early segment? late segment?

Back 107

facilitated diffusion through two Na+-INdependent transporters

GLUT2 in the early segment; GLUT1 in the late segment

Front 108

The permeability to water of the _________ and __________ is regulated by the antidiuretic hormone (ADH).

Back 108

The permeability to water of the late distal tubule and collecting ducts is regulated by the antidiuretic hormone (ADH).

High ADH = increased permeability to water

Front 109

AQP1
AQP2
AQP3
AQP4

Back 109

AQP1 = luminal AND basolateral membrane of promixal tubule and decending limb

AQP2 = inserted into distal tubule and collecting duct via ADH

AQP3 + AQP4 = basolateral membrane of distal tubular segments NOT regulated by ADH

Front 110

GT-Balance via starling forces?

Back 110

A high GFR pushes more fluid out of blood and increases the CONCENTRATION of proteins which increases oncotic pressure and leads to MORE reabsorbtion of water and Na from interstitial fluid

Front 111

GT balance via other solutes?

Back 111

increased GFR means all other solute delivery is increased = increased reabsorbtion of Na because of cotransport = increased H2O reabsorbtion

Front 112

calculate RBF using HCT

Back 112

RBF = RPF * (1/1-Hct)

Front 113

FF =?

Back 113

GFR/RPF

Front 114

Rate of reabsorbtion?

Back 114

reabsorbed = filtered - excreted

Rx = (Px * GFR) - (Ux * V)

Front 115

Percentage of a filtered solute reabsorbed?

Back 115

= rate of reabsorbtion/rate of filtration

(Px * GFR) - (Ux * V)/(Px*GFR)

Front 116

relationship between plasma creatnine and GFR?

Back 116

if Pcreat increases GFR is decreased

If Pcreat decreases GFR is increased

Front 117

Effect of renal failure on using creatnine as a measure of GFR?

Back 117

decreased filtration in renal failure means the actual GFR will be LOWER than the estimated value

Front 118

%H20 reabsorbed using Ux and Px?

Back 118

%H2O = 1 - 1/(U/P)

Front 119

Positive balance?

Negative balance

Back 119

positive = ingestion of salt exceeds exretion

negative = excretion exceeds ingestion

Front 120

the monitoring of the body Na+ content is achieved by the ____________

The pressure of the blood perfusing these receptors, or the degree of filling in the arterial system is called the _______

Back 120

the monitoring of the body Na+ content is achieved by the baroreceptors that sense changes in pressure (or stretch) in the arterial system.

The pressure of the blood perfusing the baroreceptors, or the degree of filling in the arterial system is called the effective circulating volume (ECV)

Front 121

The major baroreceptors involved in the sensing of the Na+ content are?

Back 121

-carotid sinus, aortic arch -> increased stretch = decreased sympathetics

-cardiac atria respond to increased stretch by releasing atrial natriuretic peptide (ANP).

-afferent arterioles in the kidney -> decreased stretch = increased renin

Front 122

Reabsorbtion of Sodium along the nephron

Back 122

PCT and Thick ASCENDING limb = large capacity to reabsorb

distal convoluted tubule and collecting duct = limited reabsorbtion

Front 123

Increases in Na+ tend to ______ GFR, while loss of Na+/ECF volume tends to ______ GFR and the filtered load of Na+.

Back 123

Increases in Na+ tend to increase GFR, while loss of Na+/ECF volume tends to reduce GFR and the filtered load of Na+.

Front 124

Sympathetic control of GFR

Back 124

Innervate afferent arterioles:

decreased ECF volume = increased sympathetic tone = constriction of afferent arteriole = decreased GFR

Front 125

ANP effect on GFR

Back 125

dilates afferent and constricts efferent = INCREASED GFR

Front 126

_____________ in the Na+ content and ECF volume tend to reduce the fraction of filtered Na+ reabsorbed proximally, while _____________ in Na+ content and ECF volume have the opposite effect.

Back 126

Increases in the Na+ content and ECF volume tend to reduce the fraction of filtered Na+ reabsorbed proximally, while decreases in Na+ content and ECF volume have the opposite effect.

Front 127

Sympathetic nerves innervate the proximal tubule. ___________ sympathetic stimulation in response to ECF volume decreases _____________ proximal Na+ reabsorption.

Back 127

Sympathetic nerves innervate the proximal tubule. Increased sympathetic stimulation in response to ECF volume decreases stimulates proximal Na+ reabsorption.

via Na/H exchanger

Front 128

A-II effect on proximal Na reabsorbtion?

Back 128

increases Na reabsorption

via Na/H exchanger

Front 129

Starling Forces effect on Proximal Tubule Na reabsorption?

Back 129

Increased Na + H2O in ECF = increased GFR and increased RPF = DEcreased FF = decreased [protein] = decreased oncotic pressure =

DECREASED Na and Water reabsorption

Front 130

volume expansion effect on Proximal Tubule Na reabsorption?

Back 130

increases NO = DEcreased Na reabsorbtion

Front 131

Load Dependent Na reabsorbtion?

Back 131

The thick ascending limb (TAL) responds to increases or decreases in delivery of tubular fluid Na+ by immediate changes in Na+ reabsorption in the corresponding direction (“load dependent”).

Front 132

What stimulates reabsorption of Na at the TAL?

Back 132

ADH

Front 133

What stimulates ADH release?

Back 133

-small increases of plasma osmolality

-large (≥10%) reductions in ECF volume.

Front 134

What decreases reabsorption of Na at the TAL? when are they released?

Back 134

Prostanoids and NO

released when ECF/Na/volume INCREASES

Front 135

Under euvolemic conditions, with small changes in Na+ intake, _____________ is the primary regulator of Na+ reabsorption by its effects on distal segments of the nephron

Back 135

Under euvolemic conditions, with small changes in Na+ intake, aldosterone is the primary regulator of Na+ reabsorption by its effects on distal segments of the nephron

Front 136

Angiotensin II has several important physiologic functions ( 4)

Back 136

-stimulation of aldosterone secretion by the adrenal cortex
-arteriolar vasoconstriction
-stimulation of Na+ reabsorption by the proximal tubules
-stimulation of ADH secretion and thirst.

Front 137

Aldosterone acts on the ___________ of the distal nephron by binding to a ________ receptor ___________ that upon activation translocates to the nucleus and regulates gene transcription.

Back 137

Aldosterone acts on the principal cells of the distal nephron by binding to a cytoplasmic receptor (mineralocorticoid receptor, MR) that upon activation translocates to the nucleus and regulates gene transcription.

Front 138

Early effects (after 30 min latency) of aldosterone involve ?

Back 138

the recruitment of the apical Na+ channel (ENaC) and the basolateral Na+-K+ ATPase.

Front 139

Aldosterone secretion is also stimulated by

Back 139

a rise in plasma potassium concentration, and it enhances the secretion of K+ by the distal segments of the nephron

Front 140

What inhibits renin secretion

Back 140

increased intracellular Ca

Front 141

juxtaglomerular cells that increase renin secretion in response to ?

Back 141

juxtaglomerular cells that increase renin secretion in response to ECF Na+/volume depletion:

Front 142

three distinct inputs to the juxtaglomerular cells that increase renin secretion?

Back 142

1. renal sympathetics to juxtaglomerular cells

2. afferent arterioles have intrarenal barroreceptors

3. delivery of NaCl to macula densa

Front 143

renal sympathetics to juxtaglomerular cells effect on renin secretion?

Back 143

NE release binds beta 1 receptor and increases adenylate cyclase activity = increased renin release

Front 144

intrarenal barroreceptors effect on renin secretion

Back 144

increased BP in the afferent arteriole = increased intracellular Ca2+ = inhibit AC and the release of renin.

On the other hand when the perfusing pressure decreases, renin secretion is stimulated.

Front 145

delivery of NaCl to macula densa effect on renin secretion

Back 145

decrease in [Na] or [Cl] in ascending loop = increased renin

Front 146

The actions of ANP antagonize those of the renin- angiotensin-aldosterone system (5)

Back 146

o Increases GFR and Na+ filtered load
o Inhibits renin secretion by juxtaglomerular cells
o Inhibits aldosterone secretion by the adrenal cortex
o Inhibits (directly) Na+ reabsorption by the collecting duct o Inhibits ADH secretion by the posterior pituitary

Front 147

Urodilantin effect on Na reabsorbtion? secreted by?

Back 147

secreted by distal tubules and collecting ducts.

Acts locally and inhibits Na+ reabsorption by these segments.

Front 148

Local factors effect on Na reabsorbtion

Back 148

Local factors = NO, prostanoids and kinins are produced in the kidney and inhibit Na+ reabsorption.

Front 149

aldosteron escape?

Back 149

subjects given aldosterone, or patients with an aldosterone-secreting adrenal tumor, retain fluid for only a few days and then undergo a spontaneous diuresis that returns the volume (and arterial pressure) toward normal.

Front 150

whats the point of aldosterone escape

Back 150

renal artery pressure is the major factor determining natriuresis.

The kidney will "ignore" aldosterone if it makes renal art. pressure too high

Front 151

most abundant cation in the body?

Back 151

potassium

Front 152

Location of most intracellular K?

Back 152

muscle cells

Front 153

hyperkalemia effect on Vm

Back 153

increased K = increased Vm = excitability

Front 154

hypokalemia effect on Vm

Back 154

decreased K = decreased Vm = paralysis

Front 155

Responses to acute K changes?

Back 155

uptake of increased K by cells by activation of Na-K ATPase

Front 156

What stimulates the Na/K ATPase in K uptake?

Most important hormone promoting K uptake after a meal?

Back 156

increased plasma K
epinephrine
insulin

most important post meal = insulin

Front 157

Small elevations in plasma K+ (as little as 0.2- 0.3 mEq/L) do cause prompt increases in adrenal aldosterone secretion, which enhances

Back 157

colonic and renal K+ excretion

Front 158

a drop of ______ pH unit will result in an average increase of _______ mEq/L in plasma K

Back 158

a drop of 0.1 pH unit will result in an average increase of 0.6 mEq/L in plasma K

Front 159

effect of the following on K balance:
-metabolic acidosis or alkalosis associated with mineral acids or bases (e.g. HCl, NaHCO3, etc.) ?
-organic acids or bases (e.g. lactic acid, ketone acids)?
-respiratory acid-base disturbances?

Back 159

-mineral acids or bases (e.g. HCl, NaHCO3, etc.) = shifts in K+

organic acids or bases (e.g. lactic acid, ketone acids) = no shifts in K r

-respiratory acid-base disturbances = little shift of K+

Front 160

hyperosmolality effect on potassium?

Back 160

K enters the cell

cell swells

hyperkalemia

Front 161

hyperosmolality effect on potassium?

Back 161

K leaves the cell

cell shrinks

hypokalemia

Front 162

Most of the filtered K+ is reabsorbed at

Back 162

the proximal tubules and thick ascending loop of Henle.

Front 163

At the proximal tubule K+ is reabsorbed by

Back 163

diffusion through the intercellular pathway (tight junctions and intercellular spaces) as a result of the reabsorption of water and consequent elevation of the tubular K+ concentration

Front 164

At the late proximal tubule, ________________ also favors paracellular K+ reabsorption. The result is an overall reabsorption by the proximal tubule of near __% of the filtered K+

Back 164

At the late proximal tubule, the lumen positive transepithelial potential also favors paracellular K+ reabsorption. The result is an overall reabsorption by the proximal tubule of near 80% of the filtered K+

So the lumen is positive an K+ is "pushed away" from it toward the vasa recta

Front 165

Is the transcellular pathway involved in K reabsorption?

Back 165

no

Front 166

Reabsorption at the thick ascending limb (TAL) involves mainly cotransport of _____________ at the lumenal cell membrane and __________________ at the basolateral membrane.

Back 166

Reabsorption at the thick ascending limb (TAL) involves mainly cotransport of Na+- K+-2Cl- (NKCC2, inhibited by loop diuretics) at the lumenal cell membrane and K+-Cl- cotransport and K+ channels at the basolateral membrane.

Front 167

Some of the K+ entering the cell leaks back into the lumen through apical channels. Overall, the net reabsorption of K+ at the TAL accounts for % of the filtered load.

Back 167

10% of the filtered load.

Front 168

In contrast to the TAL which is capable of only reabsorbing K+, the distal segments

Back 168

have the capacity to either reabsorb or secrete K+

Front 169

changes in the excretion rate of K+ reflects the handling of K+ by

Back 169

the distal nephron.

Front 170

principal cell?

Back 170

Basolateral K+in and Na+ out --> K+ then diffuses into lumen via ROMK/BK

K secretion and Na reabsorbtion

Front 171

Intercalated cell

Back 171

alpha type:
Secrete H+ and reabsorb K+ (ATPase)

K+ enters blood/interstitium via basolateral K channels

Front 172

Can the MCD absorb K+ passively?

Back 172

The medullary collecting duct is also able to reabsorb K+ passively, through the highly K+ permeable tight-junctions, when the luminal K+ concentration is elevated, as happens with high K+ intake or with high distal reabsorption of water (elevated plasma ADH).

Front 173

Aldosterone secretion is stimulated by

Back 173

elevation of plasma Angiotensin II and [K+].

Front 174

main cellular effect of aldosterone

Back 174

increase the synthesis of transport proteins (Na+-K+ ATPases, Na+ channels, K+ channels) in the principal cells of the distal nephron, thus enhancing Na+ reabsorption and K+ secretion.

Front 175

Aldosterone secretion is inhibited by

Back 175

hypokalemia and atrial natriuretic peptide (ANP).

Front 176

A high flow rate is thought to promote K+ secretion by

Back 176

deforming the mechano-sensitive central cilium of the principal cell that protrudes into the lumen.

Front 177

deforming the mechano-sensitive central cilium of the principal cell that protrudes into the lumen causes

Back 177

intracellular release of Ca2+ that leads to opening of Ca2+-sensitive K+ channels (BK channels).

Front 178

A high tubular flow rate also favors a high chemical gradient for K+ secretion across the lumenal membrane by

Back 178

diluting and washing away the secreted K+

Front 179

If increased flow also increases Na delivery to the distal nephron what happens to K?

Back 179

enhanced Na+ reabsorption provokes more secretion of K+, since the entry of Na+ not only stimulates the basolateral Na+-K+ ATPase, but it also depolarizes the lumenal membrane, an effect that favors the secretion of K+, as mentioned earlier.

Front 180

single effect?

Back 180

At each level the descending limb and the interstitium are equal in osmolality and the ascending limp is 200 mOsm/kg less

Front 181

as the fluid moves through the descending limb water moves into the hyperosmotic interstitium. The solute concentration in the tubule lumen (mainly salt) increases until its osmolality balances that of the interstitium, which is due to salt ions and urea. The result is a luminal fluid with _________ osmolality but a _______ salt concentration than that in the medullary interstitium.

Back 181

The result is a luminal fluid with the same osmolality but a higher salt concentration than that in the medullary interstitium.

Front 182

Urea recycling?

Back 182

-Urea is absorbed the medullary portion of the collecting duct into the intersitium
-Urea then moves into the lumen of the thin ascending limb
-travels in the lumen until it reaches the collecting duct again and starts over

Front 183

Effect of ADH on urea

Back 183

enhances it's permability at the IMCD

this sends urea into the interstitium = high osmolality

Front 184

Effect of ADH on thick ascending limb?

Back 184

-stimulates salt transport
-depresses vasa recta blood flow
-enhances IMCD urea transport

Front 185

Things that inhibit the adenylate cyclase that ultimately produces APQ2

Back 185

prostaglandins
calcium
protein kinase C

Front 186

review figure 7

Back 186

page 36-7

Front 187

ADH is secreted by certain

ADH secretion is stimulated by

Back 187

hypothalamic neurons whose axons terminate in the posterior pituitary; nearby neurons act as osmoreceptors

increased osmolality = increased firing = increased ADH

Front 188

Can barroreceptors override the ADH osmoreceptors?

Back 188

Yes if volume drops by >10% if will override and release ADH even with a normal osmolarity = can lead to low osmolarity

Front 189

Free water clearance equations

Back 189

CH20 = V - Cosm

CH2O = V[1-U/P]

Front 190

Positive CH2O?

Negative CH2O?

Back 190

Positive = water is excreted

Negative = water is reabsorbed

Front 191

H+ secretion:
transporter in the Proximar tubule?

collecting duct?

Back 191

proximal tubule = Na+-H+ and Na+-NH4+ exchange via the NHE3 transporter

collecting duct = H+ ATPase

Front 192

Normally the titratable acidity accounts for about _______ of the acid excretion in the urine. The increase in T.A. excretion in acidosis is _______________

Back 192

Normally the titratable acidity accounts for about ONE THIRD of the acid excretion in the urine. The increase in T.A. excretion in acidosis is MINIMAL, except in disease states in which endogenous production of filterable buffer is increased greatly, as in diabetes with production of ketoacids.

Front 193

Hormones that increase expression of NHE-3 and NBCe1?

Back 193

Endothelin-1 and cortisol

Front 194

PTH response to acidosis?

Back 194

secretion stimulated by acidosis

inhibits phosphate reabsorption by the proximal tubule leaving more of it available to be used as T.A.

Front 195

principal or granular cell effect on acid-base regulation?

Back 195

no direct role

Front 196

Itercalated cell types and what they secrete?

Back 196

alpha = secretes H+

beta = secretes HCO3-

Front 197

Acid base equation

pH = ?

Back 197

pH = 6.1 + log [HCO3]/0.03pCO2
pH = 6.1 + log [HCO3- ] / 0.03 PCO2

0.03 is in mMoles/L/mmHg

HCO3 is in mMoles

Front 198

How is an acute acid load handled?

Back 198

50% is buffered in ECF HCO3-

50% is buffered in exchange for Na, K, or Cl

Front 199

NAE = ?

Back 199

Net Acid Excretion

NAE = Utitration + UNH4+ - UHCO3

Front 200

Initial detection of hemorrhage is by?

Initial response to hemorrhage is by?

Back 200

detection = cardiopulmonary receptors (reduced firing)

response = increased heart rate

Front 201

Reasons for reduced urine output in shock?

Back 201

1. Decreased GFR
2. Increased Na and water reabsorbtion
3. Increased ADH
-(increased Na reabsorbtion at thick ascending, decreased vasa recta flow, increased water permiability of collecting duct)

Front 202

Why can necessary potassium secretion be maintained with decreased GFR/tubular flow in the volume depleted individual?

Back 202

Because of increased aldosterone secretion

Front 203

contraction alkalosis?

Back 203

diuretics cause loss of body stores of NaCl which leave behind higher concentrations of HCO3

Front 204

anion gap

Back 204

anion gap = [Na] - ([Cl] + [HCO3])

normal = 5-11

Front 205

Acids that increase anion gap?

Back 205

lactic acid or ketoacid

Front 206

Effect of volume depletion on BUN?

Back 206

increases BUM greater than the increase in creatinie d/t increased ADH = reabsorbtion at collecting duct