Post Review Focus Flashcards
(160 cards)
1
Q
three layers of filtration barrier
A
endothelium
basement membrane
podocytes
restricts based on charge and size
2
Q
endothelium of filtration barrier
A
have fenestrae (slight pores) and negative charges
leaky
3
Q
basement membrane of filtration barrier
A
has collagen and proteoglycan and negative charges
4
Q
podocytes of filtration barrier
A
negative charges
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
6
Q
what would happen if the negative charges of the filtration barrier were lost?
A
minimal change neuropathy
results in proteinuria
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)
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
9
Q
K1
A
capillary coefficient, product of permeability and surface area of capillaries
increase in K1 increases GFR and vice versa
10
Q
GFR of normal, adult male
A
180 L/day
11
Q
factors that influence glomerular capillary colloid osmotic pressure
A
arterial plasma colloid osmotic pressure and filtration fraction
12
Q
factors that increase glomerular colloid osmotic pressure
A
increasing filtration fraction
13
Q
variables that determine glomerular hydrostatic pressure
A
arterial pressure
affarent arteriolar resistance
efferent arteriolar resistance
14
Q
increasing arterial pressure (increases/decreases) GFR?
A
increases
more blood to filter through
15
Q
increasing afferent arteriolar resistance ((increases/decreases) GFR?
A
decreases
less blood getting there
16
Q
increasing efferent arteriolar resistance (increases/decreases) GFR?
A
increases
more blood prevented from leaving = more to go through
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
18
Q
hormones that autoregulate
A
norepinephrine, endothelin, angiotensin II, NO, prostaglandins and bradykinin
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
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
21
Q
nitric oxide
source and GFR effectt
A
derived from endothelial cells
basic levels help maintain renal vasodilation
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
23
Q
prostaglandins and bradykinins
A
vasodilators
offset effects of sympathetic and angiotensin II vasoconstrictor effects on afferent arterioles
24
Q
normal daily fluid excretion
A
1.5 L/day
25
norepinephrine and epinephrine
parallel sympathetic nervous system effect on GFR
26
two components of tubuloglomerular feed back mechanism for auto regulation
afferent arteriolar feedback mechanism
| efferent arteriolar feedback mechanism
27
juxtaglomerular complex and auto regulation
acts to control dilation of afferent and efferent arterioles
28
reabsorption of NaCl in the ascending limb has what effect on juxtaglomerular complex?
it is caused by decreased GFR and slow rate in loop of henle, decreases macula densa [NaCl]
29
decrease macula densa [NaCl] (juxtaglomerular complex)
causes dilation of afferent arterioles and a release of renin cells,therefore increasing angiotensin II and efferent arteriolar resistance
30
what part of the kidney reabsorbs glucose? what mechanism?
proximal convoluted tubule
secondary active transport, Na/glucose co transport
31
Na+/glucose transporters in proximal tubules
SGLUT 2 is in early, 90% reabsorbed
SGLUT 3 is in late, 10% reabsorbed
32
define transport maximum and the limiting factor and explain how this relates to glucose reabsorption
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
33
what makes proximal tubule so great for absorption?
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
34
early proximal tubule
mostly reabsorbs glucose, AA, and bicarbonate and Na
Na prefers absorbing these, leaves the Cl for later
35
later proximal tubule
chloride defuses out with reabsorption of NA
has large concentration gradient, so goes from lumen through junctions
36
where in the kidney are most of the filtered electrolytes reabsorbed?
prox tubule
37
proximal tubule transport characteristics
high permeable to water
active NaCl transport
permeable to Urea
38
thin descending loop transport characteristics
moderately permeable to urea, sodium
high water permeability
39
the PCT cells are responsible for the (secretion/reabsorption) of acids, bases, H+ ions
secretion (antitransport)
40
thin ascending loop of Henle
water permeability
impermeable to water
allows for establishment of counter current system and concentration of urine
41
thick ascending loop of henle
water impermeable
secretion of H+, contain apical Na/2Cl/K channel (est. gradient)
paracellular transport
42
what mechanism is responsible for the reabsorption of Mg, Ca from lumen
paracellular transport
43
late distal tubule
impermeable to urea
diluting segment
water reabsorption is dependent on ADH
44
principal cells
location, action (and mechanism)
found in late distal collecting corvine
reabsorbs sodium and water form lumen, secretes k
via active transport of Na/K ATPase
45
intercalated cells
location, action (and mechanism)
found in late distal/collecting cortical membrane
reabsorb K+ from tubular lumen and secrete H+ into lumen via H/K transporter
46
aldosterone
1. source
2. function
3. site of action
4. stimulus for secretion
1. adrenal cortex
2. increase Na reabsorption and stimulates Na/K pump
3. principal cells
4. increase extracellular K, angiotensin II
47
absence of aldosterone causes
addison disease
results in marked loos of sodium and accumulation of potassium
48
hyper secretion of aldosterone causes
conn's syndrome
49
angiotensin II
1. function
2. effect
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
50
ADH
1. source
2. function
3. effect
1. posterior pituitary
binds to V2 receptors in late distal tubules, collecting tubules, collecting ducts
2. increase water reabsorption
3. increases cAMP formation
51
ANP
1. source
2. function
3. effect
1. cardiac atrial cells in response to distension
| 2. inhibits water and sodium reabsorption
52
how much water can be excreted by kidneys per day?
20 L/day
53
maximum urine concentration kidneys can produce
1200-1400 mosm/L
54
why is there an obligatory volume of excreted? what is it?
we must get rid of at least 600 oSm each day (products of metabolism produce this much)
600 per day/1200 = 0.5L
55
where are osmosreceptor cells
hypothalamus
56
describe the osmoreceptor ADH feed back mechanism
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
57
where is ADH produced? secreted?
supraoptic uncle and paraventricular nuclei (hypothalamus)
secreted in the posterior pituitary
58
osmoreceptor cells are (sensitive/very sensitive/not at all sensitive) to hydration of individual
very sensitive
59
clinical significance of elevated extracellular potassium
cardiac arrest, arrhythmia
extreme cases can cause fibrillation and death
this is if it is over 140 mEq/L
60
effect of aldosterone secretion o K excretion
increase in extracellular potassium [ ] stimulates incase in aldosterone system
61
what part of renal tube is responsible for K reabsorption
proximal tubule
| ascending limb on henle
62
what part of renal tube is responsible for K secretion
late tubule
| collecting duct
63
mechanism of principal cells
Na into cell via ENac pump
causes passive secretion of K from cell to lumen (secondary anti port) due to gradient created previously
64
what stimulates principal cells to secrete potassium?
[K] and aldosterone
increase in uptake of K, increase in place, stimulates aldosterone
65
relationship between tubular flow rate and potassium secretion
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
why does high Na uptake have little effect on K excretion
high Na+ decrease aldosterone secretion and increases tubular flow rate
causing no net change
67
metabolic acidosis and ECF [K]
increases [k] by increasing [h] and therefore decreasing na/k pump and movement of k in opposite direction
68
metabolic alkalosis and ECF [K]
decreases ECF [k]
69
intercalated cells and controlling potassium
reabsorb k+ during depletion
70
major buffer systems of body
bicarbonate buffer system
protein buffers
phosphate buffer system
71
define buffer
substance that can reversibly bind to H+
consists of a weak acid and its conjugate base
72
which buffer system is most important extracellular buffer system
bicarbonate buffer system
73
bicarbonate buffer system is regulated mainly by
kidney
74
metabolic acid base disorders
caused by primary change in [bicarbonate] in ECF
m. acidosis: decrease in bicarb
m. alkalosis: increase
75
respiratory acid base disorders
result from primary change in pCO2
r. acidosis: increase in pCO2
r. alkalosis: decrease in pCO2
76
when lungs are in respiratory acidosis, what comes to its rescue? (compensates for this)
kidneys.
they release bicarbonate to compensate for the decrease in pH and restore it to normal
77
major buffer of renal tubular fluid and intracellular fluid?
phosphate buffer system
78
why is phosphate buffer system so effective on renal tubular fluid
it functions maximally at its proper pKa, which is coincidentally the pH of tubular fluid
79
how does the excretion of excess hydrogen ions lead to the formation of new bicarbonate ions?
hydrogen ions combine with other buffers in the tubular lumen, (i.e. phosphate) allowing the leaves bicarbonate to be returned to blood
80
carbonic anhydrase
forms carbonic acid from co2 to h20 in bicarbonate reabsorption
81
describe the renal handling of excess base
alkalosis, kidneys reabsorb all filtered bicarbonate ion to return pH of ECF to normal
82
lungs cause alkalosis from hyperventilation... what will the body do?
compensate by decreasing plasma bicarbonate via excretion of bicarbonate ion
remove bicarbonate
83
capacity is a sum of volumes, true or false?
true
84
tidal volume
normal value and definition
volume of air inspired or expired with ea. breath at rest
500 mL
85
inspiratory reserve v.
normal value and definition
v. of air inspired that can be expired by forceful inspiration in addition to tidal volume
3000mL
86
expiratory reserve v.
normal value and definition
additional volume of air that can be expired in forceful expiration
1100 mL
87
residual volume
normal value and definition
volume of air remaining in lungs after forceful expiration
1200 mL
88
vital capacity
normal value and definition
sum of all volumes that can be expired or exhaled
inspiration to the max extent plus expiration to the max extent
4600 mL
89
total lung capacity
normal value and definition
sum of all the volumes
5800 mL
90
inspiratory capacity
normal value and definition
3500 mL
sum of volumes above resting capacity = tidal volume + inspiratory reserve
91
function residual capacity
2300 mL
sum of volumes below resting = expiratory reserve volume + residual
92
minute ventilation
total v. of gases moved nour out of lungs per minute
= breaths per minute x tidal volume
93
alveolar ventilation
total v of gasses that enter spaces participating in gas exchange per minute
= breaths per min x (tidal v - dead space)
94
anatomical dead space
areas of no gas exchange
trachea, bronchi, bronchioles
95
physiological dead spcae
anatomical + ventilated alveoli with poor or absent profusion
96
which is greater, alveolar or minute ventilation
minute
for normal, minute - .5 x breath rate
alveolar = .35 x breath rate
97
equation for calculating dead space
= V total (PaCO2- PeCO2)/PaCO2
pa is arterial co2
pe is expired co2
98
pleural pressure
pressure of fluid between parietal pleura and visceral pleura
I: -.5 to -.75
e: -.75 to -.5
99
alveolar pressure
pressure of air inside alveoli
i: 0- -1
e: 0 - 1
100
transpulmonary pressure
difference between alveolar pressure and pleural pressure
101
compliance
volume change in relationship to a change in pressure
EXTENT TO WHICH LUNGS WILL EXPAND FOR EA. UNIT INCREASE IN TRANSPUL. PRESSURE
102
equation for compliance
increase in v./ increase in p
distensibily x Vo = Vinc/Pinc
103
compliance is the ___ of elastance
reciprocal
104
two circulations of the lungs
high pressure low flow
| low pressure high flow
105
describe low pressure high floqw
Pulmonary artery/branches --> alveoli
106
describe high pressure low flow
thoracic aorta --> bronchial arterials --> bronchial tree, trachea, adventitia, CT
107
pulmonary has a (greater/lesser) compliance than aorta
greater
1/3 wall thickness, so can store more blood
108
agents that constrict pulmonary arterioles
norepinephrine
epinephrine
angiotensin II
prostaglandind
109
agents that dilate pulmonary arterioles
isoprotenternol
| acetylcholine
110
effect of heavy exercise
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
describe the 3 zones
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
effect of exercise on zones of lungs
converts zone 2 regions to zone 3
113
forces that move fluid out of capillary (value)
```
hydrostatic p (-7)
interstitial fluid osmotic p (-14)
intersistal fluid hydrostatic p (-8)
```
total out: -29
114
forces that move fluid into capillary
capillary osmotic pressure (28)
115
mean filatriaon pressure of capillary
1 mm Hg
116
left sided heart failure
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
hypoxia
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
what element makes up most of air?
N
79%
119
daltons law
total pressure of mixture of gasses = sum of partial pressure of gasses
120
boyles law
at a fixed temp and amount, p and v are inversely proportional
121
henry's law
@ 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
partial pressure is determined by
its concentration and solubility coefficient of gas
henry's law in action
PP = [dissolved gas]/sol coefficient
123
solubility of O2? CO2?
o2=0.024
| co2 = 0.57
124
CO2 is more soluble than water so it will
exert a PP that is less than 1/20th that of O2
125
what effect would breathing in dry air to the lungs have on partial pressure in alveioli
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
why can't we exceed PO2 past 149 mmHg in alveolar ventilation?
the maximum PO2 humidified in the atmosphere is 149 mmHg, therefore it can't get above that in the capillary
127
layers of the respiratory membrane
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
what does Va stand for?
ventilation
air flow
129
what does q stand for?
blood flow
| perfusion
130
Va/Q
perfusion ratio
normal value is 0.8
131
what happens when there is a complete obstruction of air flow
Va= 0
Va/Q = 0
blood/gas composition is unchanged
132
what happens during vascular obstruction
Q= infinity
Va/Q= infinity
alveolar gas remains unchanged -- no blood contact
133
ADH source, function, effect
posterior pituitary
water retention, Aqp 2, LDCT, CT
AQP2 added to membrane, increases blood pressure and concentrates urine
134
ANP source, function, effect
atrial cells, heart
stop reabsorption of water, Na
decreases Bp
135
PTH source, function, effect
parathyroid gland
reabsorb Ca2+ from bone
increase calcium in blood
136
shunted blood
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
oxygen utilization coefficient
percentage of blood that gives up its oxygen
138
oxygen hemoglobin dissociato curve
used to determine oxygen uptake in the lungs and delivery to the tissues
in venous blood, 75%
in arterial blood, 97%
139
when PO2 is high
oxygen binds with gemoglobin
140
when PO2 is low
oxygen is released form hemoglobin
141
what causes Hb curve to shift to right
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
increase in PCO2 causes
decrease in pH, forcing O2 from hemoglobin
143
Bohr effect and increase in blood [CO2] ions
shifts curve to right
| enhances release of O2 from tissue and oxygenation in lungs
144
Bohr effect and decrease in blood [CO2] ions
shifts O2 Hb curve to left
145
haladiane effect
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
3 ways CO2 is transported in blood
1. dissolved in blood (7%)
2. transported as carbonic acid (carbonic anhydrase)
3. carbamino Hb
147
compare haldane and bohr
essentially opposite.
binding of O2 with Hb displaces O2
148
what respiratory center est. ramp signal?
dorsal respiratory group
sets basic rhythm for respiration
149
ramp signal
nervous signal transmitted to inspiratory muscles during normal respiration
150
method for controlling respiration rate
ceasing the ramp... earlier better
Prg stops
Drg starts
151
PRG CENTER-- pneumonotaxic center
SWITCHES OFF INSPIRATORY RAMP
without additional input from vagus nerves (instead replies on depth of breathing)
152
apneusis
failure to turn off inspiration
153
ventral respiratory group
inactive during quite respiration
don't do normal
spill over signals from DRG start, increases the respiratory drive.
154
botzinger complex
associated with coordinating VRG output, rostral part
155
intermediate VRG
associated with dilation of upper airway during inspiration
156
where are APN and PNE centers found?
PONS
157
Pre-BotC
complex that acts on rostral PRG
generates timing of respiratory rhythm
inspiratory neurons
158
Mechanoreceptors
slow adapting pulmonary stretch receptors
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
mechanoreceptors
rapidly adapting
located within airways
sensitive to irrigation, foreign bodies, stretch
travel vagus to brian
elicit cough
override normal control mechanism
160
J receptors
sensory endings in alveolar wall in juxtaposition to pulmonary capillaries
sensitive to pulmonary edema
signals travel via vagus nerve
elicits cough, tachypnea
override normal
