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Exam 3 Physiology > Post Review Focus > Flashcards

Post Review Focus Flashcards

1
Q

three layers of filtration barrier

A

endothelium
basement membrane
podocytes

restricts based on charge and size

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2
Q

endothelium of filtration barrier

A

have fenestrae (slight pores) and negative charges

leaky

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3
Q

basement membrane of filtration barrier

A

has collagen and proteoglycan and negative charges

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4
Q

podocytes of filtration barrier

A

negative charges

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5
Q

what happens if there are problems in this filtration barrier?

A

we often find that the filtration barrier deformities lead to blood in the urine

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6
Q

what would happen if the negative charges of the filtration barrier were lost?

A

minimal change neuropathy

results in proteinuria

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7
Q

what is GFR determined by?

A

balance of hydrostatic and colloid osmotic forces acting across the membrane and the capillary filtration coefficient (Kf)

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8
Q

starling forces that impact GFR

A

glomerular hydrostatic pressure (Pg)
Bowman;s capsule hydrostatic pressure (Pb)
glomerular osmotic pressure (πg)
bowman’s osmotic pressure (πg)

inward forces: bowman’s hydrostatic and colloid osmotic pressure of bowman’s capsule

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9
Q

K1

A

capillary coefficient, product of permeability and surface area of capillaries

increase in K1 increases GFR and vice versa

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10
Q

GFR of normal, adult male

A

180 L/day

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11
Q

factors that influence glomerular capillary colloid osmotic pressure

A

arterial plasma colloid osmotic pressure and filtration fraction

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12
Q

factors that increase glomerular colloid osmotic pressure

A

increasing filtration fraction

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13
Q

variables that determine glomerular hydrostatic pressure

A

arterial pressure
affarent arteriolar resistance
efferent arteriolar resistance

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14
Q

increasing arterial pressure (increases/decreases) GFR?

A

increases

more blood to filter through

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15
Q

increasing afferent arteriolar resistance ((increases/decreases) GFR?

A

decreases

less blood getting there

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16
Q

increasing efferent arteriolar resistance (increases/decreases) GFR?

A

increases

more blood prevented from leaving = more to go through

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17
Q

sympathetic activity and GFR

A

strong activation of sympathetic response constricts renal arteries and decreases blood flowing to them, causing a decrease in GFR

moderate activation has little effect

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18
Q

hormones that autoregulate

A

norepinephrine, endothelin, angiotensin II, NO, prostaglandins and bradykinin

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19
Q

endothelin

source, effect

A

released by damaged vascular endothelial cells of kidneys and other tissues

renal vasoconstriction, decreasing GFR

increase during chronic uremia, acute renal failure, toxemia of pregnancy

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20
Q

angiotensin II

kidney auto regulation

source, effect

A

formed in situations associated with decreased arterial pressure or volume depletion

preferentially constricts efferent arterioles, increases GFR

afferent arterioles seemed to be protected against angiotensin II

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21
Q

nitric oxide

source and GFR effectt

A

derived from endothelial cells

basic levels help maintain renal vasodilation

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22
Q

autoregulation of kidneys

A

acts to prevent large changes to GFR that would normally occur with even small blood pressure changes

maintain constant GFR and allow precise control of renal water excretion and solutes

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23
Q

prostaglandins and bradykinins

A

vasodilators

offset effects of sympathetic and angiotensin II vasoconstrictor effects on afferent arterioles

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24
Q

normal daily fluid excretion

A

1.5 L/day

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25
Q

norepinephrine and epinephrine

A

parallel sympathetic nervous system effect on GFR

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26
Q

two components of tubuloglomerular feed back mechanism for auto regulation

A

afferent arteriolar feedback mechanism

efferent arteriolar feedback mechanism

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27
Q

juxtaglomerular complex and auto regulation

A

acts to control dilation of afferent and efferent arterioles

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28
Q

reabsorption of NaCl in the ascending limb has what effect on juxtaglomerular complex?

A

it is caused by decreased GFR and slow rate in loop of henle, decreases macula densa [NaCl]

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29
Q

decrease macula densa [NaCl] (juxtaglomerular complex)

A

causes dilation of afferent arterioles and a release of renin cells,therefore increasing angiotensin II and efferent arteriolar resistance

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30
Q

what part of the kidney reabsorbs glucose? what mechanism?

A

proximal convoluted tubule

secondary active transport, Na/glucose co transport

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31
Q

Na+/glucose transporters in proximal tubules

A

SGLUT 2 is in early, 90% reabsorbed

SGLUT 3 is in late, 10% reabsorbed

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32
Q

define transport maximum and the limiting factor and explain how this relates to glucose reabsorption

A

transport max: limit to the rate at which a solute can be transported

limiting factor: saturation of that system

glucose transport max: 375 mg/min

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33
Q

what makes proximal tubule so great for absorption?

A

highly metabolic with mitochondria (for ATP) and extensive membrane surfaces for rapid transport

reabsorbs 65% of filtered Na, Cl, bicarbonate, and K and all filtered glucose and AA

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34
Q

early proximal tubule

A

mostly reabsorbs glucose, AA, and bicarbonate and Na

Na prefers absorbing these, leaves the Cl for later

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35
Q

later proximal tubule

A

chloride defuses out with reabsorption of NA

has large concentration gradient, so goes from lumen through junctions

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36
Q

where in the kidney are most of the filtered electrolytes reabsorbed?

A

prox tubule

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37
Q

proximal tubule transport characteristics

A

high permeable to water

active NaCl transport

permeable to Urea

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38
Q

thin descending loop transport characteristics

A

moderately permeable to urea, sodium

high water permeability

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39
Q

the PCT cells are responsible for the (secretion/reabsorption) of acids, bases, H+ ions

A

secretion (antitransport)

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40
Q

thin ascending loop of Henle

water permeability

A

impermeable to water

allows for establishment of counter current system and concentration of urine

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41
Q

thick ascending loop of henle

A

water impermeable

secretion of H+, contain apical Na/2Cl/K channel (est. gradient)

paracellular transport

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42
Q

what mechanism is responsible for the reabsorption of Mg, Ca from lumen

A

paracellular transport

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43
Q

late distal tubule

A

impermeable to urea

diluting segment

water reabsorption is dependent on ADH

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44
Q

principal cells

location, action (and mechanism)

A

found in late distal collecting corvine

reabsorbs sodium and water form lumen, secretes k

via active transport of Na/K ATPase

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45
Q

intercalated cells

location, action (and mechanism)

A

found in late distal/collecting cortical membrane

reabsorb K+ from tubular lumen and secrete H+ into lumen via H/K transporter

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46
Q

aldosterone

  1. source
  2. function
  3. site of action
  4. stimulus for secretion
A
  1. adrenal cortex
  2. increase Na reabsorption and stimulates Na/K pump
  3. principal cells
  4. increase extracellular K, angiotensin II
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47
Q

absence of aldosterone causes

A

addison disease

results in marked loos of sodium and accumulation of potassium

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48
Q

hyper secretion of aldosterone causes

A

conn’s syndrome

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49
Q

angiotensin II

  1. function
  2. effect
A
  1. increase sodium, water reabsorption, returns BP and extracellular volume to normal
  2. stimulates aldosterone secretion and constricts arterioles, directly stimulates Na+ reabsorption in PCT, loos of Henle, distal Tube, collecting ducts
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50
Q

ADH

  1. source
  2. function
  3. effect
A
  1. posterior pituitary

binds to V2 receptors in late distal tubules, collecting tubules, collecting ducts

  1. increase water reabsorption
  2. increases cAMP formation
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51
Q

ANP

  1. source
  2. function
  3. effect
A
  1. cardiac atrial cells in response to distension

2. inhibits water and sodium reabsorption

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52
Q

how much water can be excreted by kidneys per day?

A

20 L/day

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53
Q

maximum urine concentration kidneys can produce

A

1200-1400 mosm/L

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54
Q

why is there an obligatory volume of excreted? what is it?

A

we must get rid of at least 600 oSm each day (products of metabolism produce this much)

600 per day/1200 = 0.5L

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55
Q

where are osmosreceptor cells

A

hypothalamus

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56
Q

describe the osmoreceptor ADH feed back mechanism

A

controls extracellular fluid [Na] and osmolarity

increase in ECF osmolarity causes a shrinking of osmorece. cells in hypothalamus, fires AP, releases ADH in the distal nephron to increase water permeability

osmoreceptor cells tell ADH

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57
Q

where is ADH produced? secreted?

A

supraoptic uncle and paraventricular nuclei (hypothalamus)

secreted in the posterior pituitary

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58
Q

osmoreceptor cells are (sensitive/very sensitive/not at all sensitive) to hydration of individual

A

very sensitive

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59
Q

clinical significance of elevated extracellular potassium

A

cardiac arrest, arrhythmia

extreme cases can cause fibrillation and death

this is if it is over 140 mEq/L

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60
Q

effect of aldosterone secretion o K excretion

A

increase in extracellular potassium [ ] stimulates incase in aldosterone system

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61
Q

what part of renal tube is responsible for K reabsorption

A

proximal tubule

ascending limb on henle

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62
Q

what part of renal tube is responsible for K secretion

A

late tubule

collecting duct

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63
Q

mechanism of principal cells

A

Na into cell via ENac pump

causes passive secretion of K from cell to lumen (secondary anti port) due to gradient created previously

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64
Q

what stimulates principal cells to secrete potassium?

A

[K] and aldosterone

increase in uptake of K, increase in place, stimulates aldosterone

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65
Q

relationship between tubular flow rate and potassium secretion

A

tubular flow increases K+ secretion bbq continuously flushing it out of fluid (low [K] causes more to secrete)

it also activated high conductance BK channels, which rapidly increase K levels

66
Q

why does high Na uptake have little effect on K excretion

A

high Na+ decrease aldosterone secretion and increases tubular flow rate

causing no net change

67
Q

metabolic acidosis and ECF [K]

A

increases [k] by increasing [h] and therefore decreasing na/k pump and movement of k in opposite direction

68
Q

metabolic alkalosis and ECF [K]

A

decreases ECF [k]

69
Q

intercalated cells and controlling potassium

A

reabsorb k+ during depletion

70
Q

major buffer systems of body

A

bicarbonate buffer system
protein buffers
phosphate buffer system

71
Q

define buffer

A

substance that can reversibly bind to H+

consists of a weak acid and its conjugate base

72
Q

which buffer system is most important extracellular buffer system

A

bicarbonate buffer system

73
Q

bicarbonate buffer system is regulated mainly by

A

kidney

74
Q

metabolic acid base disorders

A

caused by primary change in [bicarbonate] in ECF

m. acidosis: decrease in bicarb
m. alkalosis: increase

75
Q

respiratory acid base disorders

A

result from primary change in pCO2

r. acidosis: increase in pCO2
r. alkalosis: decrease in pCO2

76
Q

when lungs are in respiratory acidosis, what comes to its rescue? (compensates for this)

A

kidneys.

they release bicarbonate to compensate for the decrease in pH and restore it to normal

77
Q

major buffer of renal tubular fluid and intracellular fluid?

A

phosphate buffer system

78
Q

why is phosphate buffer system so effective on renal tubular fluid

A

it functions maximally at its proper pKa, which is coincidentally the pH of tubular fluid

79
Q

how does the excretion of excess hydrogen ions lead to the formation of new bicarbonate ions?

A

hydrogen ions combine with other buffers in the tubular lumen, (i.e. phosphate) allowing the leaves bicarbonate to be returned to blood

80
Q

carbonic anhydrase

A

forms carbonic acid from co2 to h20 in bicarbonate reabsorption

81
Q

describe the renal handling of excess base

A

alkalosis, kidneys reabsorb all filtered bicarbonate ion to return pH of ECF to normal

82
Q

lungs cause alkalosis from hyperventilation… what will the body do?

A

compensate by decreasing plasma bicarbonate via excretion of bicarbonate ion

remove bicarbonate

83
Q

capacity is a sum of volumes, true or false?

A

true

84
Q

tidal volume

normal value and definition

A

volume of air inspired or expired with ea. breath at rest

500 mL

85
Q

inspiratory reserve v.

normal value and definition

A

v. of air inspired that can be expired by forceful inspiration in addition to tidal volume

3000mL

86
Q

expiratory reserve v.

normal value and definition

A

additional volume of air that can be expired in forceful expiration

1100 mL

87
Q

residual volume

normal value and definition

A

volume of air remaining in lungs after forceful expiration

1200 mL

88
Q

vital capacity

normal value and definition

A

sum of all volumes that can be expired or exhaled

inspiration to the max extent plus expiration to the max extent

4600 mL

89
Q

total lung capacity

normal value and definition

A

sum of all the volumes

5800 mL

90
Q

inspiratory capacity

normal value and definition

A

3500 mL

sum of volumes above resting capacity = tidal volume + inspiratory reserve

91
Q

function residual capacity

A

2300 mL

sum of volumes below resting = expiratory reserve volume + residual

92
Q

minute ventilation

A

total v. of gases moved nour out of lungs per minute

= breaths per minute x tidal volume

93
Q

alveolar ventilation

A

total v of gasses that enter spaces participating in gas exchange per minute

= breaths per min x (tidal v - dead space)

94
Q

anatomical dead space

A

areas of no gas exchange

trachea, bronchi, bronchioles

95
Q

physiological dead spcae

A

anatomical + ventilated alveoli with poor or absent profusion

96
Q

which is greater, alveolar or minute ventilation

A

minute

for normal, minute - .5 x breath rate

alveolar = .35 x breath rate

97
Q

equation for calculating dead space

A

= V total (PaCO2- PeCO2)/PaCO2

pa is arterial co2
pe is expired co2

98
Q

pleural pressure

A

pressure of fluid between parietal pleura and visceral pleura

I: -.5 to -.75
e: -.75 to -.5

99
Q

alveolar pressure

A

pressure of air inside alveoli

i: 0- -1
e: 0 - 1

100
Q

transpulmonary pressure

A

difference between alveolar pressure and pleural pressure

101
Q

compliance

A

volume change in relationship to a change in pressure

EXTENT TO WHICH LUNGS WILL EXPAND FOR EA. UNIT INCREASE IN TRANSPUL. PRESSURE

102
Q

equation for compliance

A

increase in v./ increase in p

distensibily x Vo = Vinc/Pinc

103
Q

compliance is the ___ of elastance

A

reciprocal

104
Q

two circulations of the lungs

A

high pressure low flow

low pressure high flow

105
Q

describe low pressure high floqw

A

Pulmonary artery/branches –> alveoli

106
Q

describe high pressure low flow

A

thoracic aorta –> bronchial arterials –> bronchial tree, trachea, adventitia, CT

107
Q

pulmonary has a (greater/lesser) compliance than aorta

A

greater

1/3 wall thickness, so can store more blood

108
Q

agents that constrict pulmonary arterioles

A

norepinephrine
epinephrine
angiotensin II
prostaglandind

109
Q

agents that dilate pulmonary arterioles

A

isoprotenternol

acetylcholine

110
Q

effect of heavy exercise

A

blood flow through lungs increases 4x to 7x

increase in # of capillaries
capillaries are distended
increase in flow rate 2x

this causes there to be little change in atrial pressur

111
Q

describe the 3 zones

A

zone 1: no blood flow, local alveolar capillary pressure is nerve higher than alveolar air pressure (not normal)

zone 2: intermittent blood flow (systole) found in apices/top

zone 3: continuous blood flow, lower

112
Q

effect of exercise on zones of lungs

A

converts zone 2 regions to zone 3

113
Q

forces that move fluid out of capillary (value)

A 
hydrostatic p (-7)
interstitial fluid osmotic p (-14)
intersistal fluid hydrostatic p (-8)

total out: -29

114
Q

forces that move fluid into capillary

A

capillary osmotic pressure (28)

115
Q

mean filatriaon pressure of capillary

A

1 mm Hg

116
Q

left sided heart failure

A

causes damming of blood, increasing left atrial pressure from 1-5 normally to 40-50

above 8 mm Hg, pulmonary atrial pressure increases

above 25, causes pulmonary edema

117
Q

hypoxia

A

reduction of partial pressure O2

increases pressure in pulmonary artery

constrict blood vessels supplying poorly ventilated alveoli, declining the pH – causing vasodilation in other tissues (bronchial obstruction)

lowers alveolar PCO2, resulting in a constriction of bronchi supplying that part of lung

118
Q

what element makes up most of air?

A

N

79%

119
Q

daltons law

A

total pressure of mixture of gasses = sum of partial pressure of gasses

120
Q

boyles law

A

at a fixed temp and amount, p and v are inversely proportional

121
Q

henry’s law

A

@ constant t, amount of has dissolving in a type and volume of liquid is directly proportional to partial pressure of that das in equilibrium

122
Q

partial pressure is determined by

A

its concentration and solubility coefficient of gas

henry’s law in action

PP = [dissolved gas]/sol coefficient

123
Q

solubility of O2? CO2?

A

o2=0.024

co2 = 0.57

124
Q

CO2 is more soluble than water so it will

A

exert a PP that is less than 1/20th that of O2

125
Q

what effect would breathing in dry air to the lungs have on partial pressure in alveioli

A

lungs humidify the air, so adding more gas to a gassy area

therefore lowering partial pressure because water vapor is added to the liz

126
Q

why can’t we exceed PO2 past 149 mmHg in alveolar ventilation?

A

the maximum PO2 humidified in the atmosphere is 149 mmHg, therefore it can’t get above that in the capillary

127
Q

layers of the respiratory membrane

A

similar to filtration barrier

  1. fluid containing surfactant that reduces SA
  2. alveolar epithelium
  3. epithelial basement membrane
  4. intersistal space between alveolar epithelium and capillary membrane
  5. capillary basement membrane
  6. capillary endothelial membrane
128
Q

what does Va stand for?

A

ventilation

air flow

129
Q

what does q stand for?

A

blood flow

perfusion

130
Q

Va/Q

A

perfusion ratio

normal value is 0.8

131
Q

what happens when there is a complete obstruction of air flow

A

Va= 0

Va/Q = 0

blood/gas composition is unchanged

132
Q

what happens during vascular obstruction

A

Q= infinity

Va/Q= infinity

alveolar gas remains unchanged – no blood contact

133
Q

ADH source, function, effect

A

posterior pituitary

water retention, Aqp 2, LDCT, CT

AQP2 added to membrane, increases blood pressure and concentrates urine

134
Q

ANP source, function, effect

A

atrial cells, heart
stop reabsorption of water, Na
decreases Bp

135
Q

PTH source, function, effect

A

parathyroid gland
reabsorb Ca2+ from bone
increase calcium in blood

136
Q

shunted blood

A

Whenever PO2 is below normal, there is inadequate ventilation to provide the O 2 needed to fully oxygenate the blood flowing through the alveolar capillaries. Therefore, a certain fraction of the venous blood passing through the pulmonary capillaries does not become oxygenated. This fraction is called shunted blood

137
Q

oxygen utilization coefficient

A

percentage of blood that gives up its oxygen

138
Q

oxygen hemoglobin dissociato curve

A

used to determine oxygen uptake in the lungs and delivery to the tissues

in venous blood, 75%
in arterial blood, 97%

139
Q

when PO2 is high

A

oxygen binds with gemoglobin

140
Q

when PO2 is low

A

oxygen is released form hemoglobin

141
Q

what causes Hb curve to shift to right

A
  1. increase hydrogen ions
  2. increased CO2
  3. increased temperature
  4. increased BPG

normal BPG keeps curve slightly shifted to right at all time

142
Q

increase in PCO2 causes

A

decrease in pH, forcing O2 from hemoglobin

143
Q

Bohr effect and increase in blood [CO2] ions

A

shifts curve to right

enhances release of O2 from tissue and oxygenation in lungs

144
Q

Bohr effect and decrease in blood [CO2] ions

A

shifts O2 Hb curve to left

145
Q

haladiane effect

A

binding of O2 with Hb displaces CO2 from blood

binding of O2 causes Hb to become a stronger acid (more acidic is less likely to bind with CO2

increased acidic of Hb causes it to release H+ ions, shifting to right

146
Q

3 ways CO2 is transported in blood

A
  1. dissolved in blood (7%)
  2. transported as carbonic acid (carbonic anhydrase)
  3. carbamino Hb
147
Q

compare haldane and bohr

A

essentially opposite.

binding of O2 with Hb displaces O2

148
Q

what respiratory center est. ramp signal?

A

dorsal respiratory group

sets basic rhythm for respiration

149
Q

ramp signal

A

nervous signal transmitted to inspiratory muscles during normal respiration

150
Q

method for controlling respiration rate

A

ceasing the ramp… earlier better

Prg stops
Drg starts

151
Q

PRG CENTER– pneumonotaxic center

A

SWITCHES OFF INSPIRATORY RAMP

without additional input from vagus nerves (instead replies on depth of breathing)

152
Q

apneusis

A

failure to turn off inspiration

153
Q

ventral respiratory group

A

inactive during quite respiration

don’t do normal
spill over signals from DRG start, increases the respiratory drive.

154
Q

botzinger complex

A

associated with coordinating VRG output, rostral part

155
Q

intermediate VRG

A

associated with dilation of upper airway during inspiration

156
Q

where are APN and PNE centers found?

A

PONS

157
Q

Pre-BotC

A

complex that acts on rostral PRG

generates timing of respiratory rhythm

inspiratory neurons

158
Q

Mechanoreceptors

slow adapting pulmonary stretch receptors

A

located with airways of lungs

slow adapting

terminate inspiration and prolong expiration

travel in vagus nerve

controlling respiratorio (tidal volume) in infants and adults during exercise

159
Q

mechanoreceptors

rapidly adapting

A

located within airways

sensitive to irrigation, foreign bodies, stretch

travel vagus to brian

elicit cough

override normal control mechanism

160
Q

J receptors

A

sensory endings in alveolar wall in juxtaposition to pulmonary capillaries

sensitive to pulmonary edema
signals travel via vagus nerve

elicits cough, tachypnea

override normal

Exam 3 Physiology (11 decks)

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