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NBS1 > Renal Physiology > Flashcards

Renal Physiology Flashcards

1
Q

Innervation

A

T10-L2 SNS
Hypo gastric Ganglion/Nerve–bladder relaxation, internal sphincter contraction

PNS (S2-S4)
Pelvic nerve
—bladder contraction
–internal sphincter relaxation

Voluntary–
Pudendal nerve
–external sphincter

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2
Q

Process of micturation

A

Bladder pressure stimulates afferent sensory nerves
Urethral sphincter relaxes

Pudendal nerve contraction to override parasympathetic micturation reflex

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3
Q

Filling of the bladder

A

Contraction of striated sphincter (somatic)
Contraction of smooth muscle (sympathetic)
Inhibition of destructor muscle (sympathetic

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4
Q

Emptying the bladder

A

Relaxation of striated spin her (somatic)
Relaxation of smooth muscle sphincter and opening of the bladder neck (sympathetic)
Detrusor muscle contraction (para)

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5
Q

Pressure

A

Stretch receptors–>SNS efferent–>pons–>SNS afferent–>NE–> B3
–>destrusor relaxation (inhibition of contraction)

NE–>alpha1–>contraction of internal urethral sphincter

SNS efferent and afferent so=hypo gastric

Pudendal–>ACh–>contract external urethral spinner

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6
Q

Pressure>10cmH20 (emptying phase)

A

> 10cmH2O–>pelvic PNS afferents–>pons–>pelvic PNS efferents–>ACh–>M3 receptors–>destrusor contraction

NO–>internal urethral sphincter relaxes

Pons–>pudendal–>ACh–>nicotinic–>contraction of external urethral sphincter until it is ready

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7
Q

Major functions of the Kidneys

A

Regulate body fluid osmolality and volumes, electrolyte balance, acid-base balance, excretion of metabolites and substances, production and secretion of hormones

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8
Q

Kidney Blood Flow

A

Renal artery, interlobar artery, arcuate artery, interlobular artery (comes second, longer name), afferent arteriole, glomerular capillaries, efferent arterioles, peritubular capillaries, interlobular vein, arcuate vein, interlobar vein, renal vein

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9
Q

Artery that enters the nephron

A

Afferent arteriole

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10
Q

Portion of the peritubular capillary that dives into the renal medulla

A

Vasa recta then back into an interlobular vein

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11
Q

Glomerulus vs peritubular capillary system

A

Glomerulus–high pressure, fluid out of capillaries

Peritubular–low pressure, filter fluid into capillaries

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12
Q

Two major divisions of peritublar capillary system

A

Cortical capillaries and deep medullary capillaries

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13
Q

3 layers of the barrier that any solute must pass from the glomerular capillary blood into bowman’s space

A 
Capillary epithelium (Fenestrations)
Combined basement membrane(most restrictive)
Podocytes (filtration slits,structural integrity)
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14
Q

What does the nephron clear from blood plasma

A

Unwanted substances:

Urea, creatinine, Uris acid, unrated, Na+, K+, Cl-, H+, Drugs, organics

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15
Q

Blood supply to glomerular capillaries

A

Afferent arteriole

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16
Q

Blood supply to peritubular capillaries

A

Efferent arteriole

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17
Q

GFR values

A

100-140 ml/min (120 ml/min)
180 L/day
99% reabsorbed, 179 liters/day

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18
Q

Always permeable to H20

A

Proximal convoluted
Thick descending limb
Thin descending limb
Half of loop

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19
Q

Never permeable to H2O

A

Half of loop
Thin ascending limb
Thick ascending limb (distal straight tubule)
Distal convoluted tubule (early)

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20
Q

ADH permeable to H2O

A

Late distal convoluted tubule, cortical and medullary collecting tubule

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21
Q

GFR

A

Glomerular capillary permeability/surface area product (Kf)
Times the net hydrostatic pressure (glomerular capillary minus bowman’s) minus the PCOP (colloid pressure of glomerular capillary blood)

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22
Q

Kf

A

Permeability times surface area
Permeability: Fenestrations, basement membrane, filtration slits

Surface area:capillary size and number

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23
Q

Major Determinants of GFR

A

1) hydrostatic or blood pressure
2) permeability/cell-cell junctions
3) plasma components

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24
Q

Pt normal value

A

Normally 0 due to the drainage by the PCT

Blocking of a structure beyond the glomerulus will cause problems

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25
Q

Actual GF

A

Kf X ((Pc-Pt)-PIc)

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26
Q

Efferent Arteriole protein concentration

A

Higher on oncotic pressure, increased protein concentration

Even point where filtration=reabsorption is right before the efferent arteriole, therefor you are ALWAYS FILTERING
The high osmotic pressure will draw H2O back into the peritubular capillary from the PCT, more water into extracellular space

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27
Q

Why does reabsorption back into the capillary on the venular end occur?

A

Colloid osmotic pressure is much greater than tissue colloid pressure
Water in via osmosis

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28
Q

Equal point of filtration in skeletal muscle vs glomerular capillaries

A

Due to the high hydrostatic pressure in glomerular capillaries, the colloid osmotic pressure doesn’t reach or surpass it until the efferent capillary

The equal point is when hydrostatic pressure=colloid osmotic pressure

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29
Q

WHat can/cannot pass through glomerular capillary wall?

A

Water, urea, glucose, inulin, creatinine–Can

Myoglobin, Hb, serum albumin cannot

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30
Q

Renal blood flow effect on Glomerular filtration

A

Increase flow, increases GFR
Increasing Glomerular pressure
Decreasing osmolality of blood passing through glomerulus since there is less time for blood to lose fluid and increase osmolality

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31
Q

Arterial pressure effect on GFR

A

Increase arterial pressure, increase GFR by increase glomerular pressure
But–auto regulation makes this a disproportional increase

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32
Q

Afferent arteriole diameter on GFR

A

Constriction decreases RBF, decrease blood to glomerulus, decreasing glomerulus pressure, decreasing GFR

Dilation–>increase RBF–>increase GP—>increase GFR

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33
Q

Efferent Diameter effect on GFR

A

Small construction will decrease outflow, increase pressure, increase GFR
Moderate degree of constriction will decrease GFR because blood stays longer in the Glomerulus–>plasma osmolality increases–>filtration decreases

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34
Q

Sympathetic stimulation effect on GFR

A

Afferent arterioles constrict preferentially to decrease GFR

Could decrease GFR to small perfect, and urinary output could decrease to 0

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35
Q

Kidney stone blocking ureter

A

Increase hydrostatic pressure in bowman’s space, decreasing GFR, no change in RBF

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36
Q

Reabsorption

A

Transfer of solute so from tubular fluid (pre-urine) to blood
Solute are subtracted from the filtered amount of pre-urine
Can be passive but often requires ATP

Glucose filtered-glucose excreted

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37
Q

Ureters

A

Visceral smooth muscle tubes
More urine via peristalsis waves
30 cm long
Connects posterior base of the bladder neck

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38
Q

Clearance

A

Result of filtration to the tubules or secretion back into the tubule.

Dimensions are crucial
VOLUME/TIME
INPUT=OUT
Only input=arterialx=venousx+urinex

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39
Q

Renal Clearance of a Solute verbal equation

A

Plasma concentration of a solute times the renal plasma flow of the solute in the artery is equal to (plasma venous concentration of solute times renal plasma flow in veins) plus (urine concentration of X times urine flow rate)

But venous content of X should be 0 (since all is excreted)

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40
Q

Cx

A

Virtual input volume
Or
RPFa

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41
Q

Classic Clearance Equation

A

Cx= (Ux times V)/Pax (arterial plasma concentration)

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42
Q

Formula for RPF

A

Clearance of PAH

Cpah=(Upah times V)/Ppah

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43
Q

RBF equation

A

RPF/(1-Hct)

(Upah X V)/Ppah all divided by 1-Hct

Cpah/(1-Hct)

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44
Q

Normal value of GFR

A

120 ml/min

Cannot be considered a clearance because there’s no volume component

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45
Q

GFR conditions

A

Amount filtered=amount excreted

NO REABSORPTION OR SECRETION CAN TAKE PLACE

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46
Q

Two substances that can be used to measure GFR

A

Inulin, creatinine

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47
Q

Normal values for Creatinine in urine and plasma

A

Urine–125
Creatinine-1-2

If Ccr isn’t equals to Ci or GFR, you have renal disease

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48
Q

Filtration Fraction

A

Fraction of renal plasma flow that becomes glomerular filtrate
FF= GFR/RPF
GFR=120
RPF=600
Normal FF=0.2
On average, a person gets about 20% of their plasma filtered per minute by the kidneys

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49
Q

Cpah equals GFR, RPF, or RBF?

A

RPF

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50
Q

Changes in afferent arteriolar resistance to GFR

A

Decrease resistance (increase radius) increases GFR more blood flow

Increase resistance (decrease radius) decreases GFR

51
Q

Changes in efferent arteriolar resistance to GFR

A

Decrease resistance (increase radius) decreases GFR

Increase resistance (decrease radius) increases GFR

52
Q

Myogenic mechanism of GFR

A

Increase pressure, brief increase in flow until compensation takes place, decrease diameter increase resistance, back to normal flow

Resulting diameter is smaller than original via meter

53
Q

Structures that make up the JGA

A

Macula densa cells of DCT at the transitions from the TAL

Extra glomerular mesangal cells
Renin producing JG cells

54
Q

What if macula densa sees too much NaCl in tubule?

A

Want to decrease GFR by constricting afferent and possibly dilating efferent

55
Q

Purpos of NKCC2 in TAL

A

Transport NaCl into MDC via apical NKCC2

56
Q

General mechanism of GFR tubuloglomerular feedback

A

in GFR, inc salt in tubular fluid of TAL, inc salt to MDC via NKCC1, inc Cl in intercellular, Cl transport across MDC basolateral membrane, activation of non-selective cation channel on basolateral membrane, inc Ca2+ in MDC, MDC secrete ATP increase, decrease PGE2 and JG release of renin, CONSTRICTION of afferent, decrease GFR

57
Q

What two dilator mechanisms are decreased when Calcium moves into the MDC

A

Decrease of PGE2 and NO (while increase ATP)

58
Q

What happens to the extracellular Cl- increase after MDC measures increase NaCl in tubular fluid?

A

Cl increases and inhibits the JG cell release of renin, decreasing circulating renin, decreasing AngII and aldosterone (entire systemic reduction in resistance, decrease of blood pressure, decreasing GFR

59
Q

Regulation by SNS of GFR

A

Dehydration, low blood pressure, strong emotions fear and/or pain

NE to alpha 1 adrenocrecptors
Afferent constriction
Decrease RBF, decrease GFR

60
Q

Low AGTII on GFR

A

Constricts both efferent and afferent, but preference for efferent due to the diameter of the afferent

Decrease RBF, increase GFR

NO released from afferent when AGTII stimulated (counteracting constrictor)
Decrease RBF, increase GFR due to the dissimilar affects on efferent and afferent

61
Q

High levels of AGTII

A

Decrease both RBF GFR

62
Q

ET1 on GFR

A

Similar to high AGTII
Renal blood vessels, mesagnium, distal tubule secretion
Or in response to ANGII, bradykinin, epi, or decreased shear stress

63
Q

Adenosine effect of GFR

A

Produced by kidneys
A1-adensonsine constriction of afferent
Decrease RBF and GFR

64
Q

Mechanisms that decrease both RBF and GFR

A

Adenosine, high concentrations of AGTII, ET1, sympathetically

65
Q

Substances that decrease RBF but increase GFR

A

Small concentration of AGTII

66
Q

Prostaglandins effect on GFR

A

Sympathetic escape to increase RBF to avoid ischemic damage. Dampens sympathetic constriction of the afferent arterioles and its consequences.

No real change in GFR

67
Q

Nitric oxide on GFR

A

Increase RBF, increase GFR
Vasodilates both afferent and efferents

Stimulated by ACh, Histamine, Bradykinin, ATP and increased shear stress

68
Q

Bradykinin effect on GFR

A

Increase RBF, increase GFR
Stimulates NO and PG release

Vasodilation

69
Q

ANP and BNP on GFR

A

No change in RBF, increase in GFR

Released by increased in extracellular volume (more Na in the body) so you’d want to increase GFR, dilation of Afferent Arterioles, constriction of efferent

Ultimate goal–decrease blood volume

70
Q

Histamine affect on GFR

A

Dilation of both afferent and efferent

Increase RBF and GFR

71
Q

Substances that increase both RBF and GFR

A

Histamine, bradykinin, NO

72
Q

Two outliers that only effect GFR OR RBF

A

Increase GFR only–Natriuretic peptide

Think, make up pee.

Increase RBF only–Prostaglandins (sympathetic escape)

73
Q

Net Reabsorptoin

A

Filtered-excreted

In mg/min

74
Q

Net secreted

A

Excreted-filtered

Reversal of net Reabsorptoin

75
Q

relative U/P ratios

A

Positive value>1, you are secreting something back into the urine because it is greater than something that is being filtered completely, so something must have happened to add more of it back into the urine

Positive value

76
Q

Relative U/P for something less than 1

A

Make sure to subtract the decimal you get from 1, so that you can calculate the amount that is reabsorbed. The decimal you get is the amount that is filtered

77
Q

Na+/H+ exchanger and Na/K+ATPase

A

Na from tubular fluid into tubule cell, H+ into tubular fluid

ATPase– promotes reabsorption gradient

78
Q

SGLT-2

A

Simport to bring Na+ and Glucose down their concentration gradient to promote reabsorption
Apical

High capacity but a low affinity for glucose because this is where the high concentration of glucose is. Can transport as much as possible. Will take in any glucose moiety
FIRST HALF

79
Q

GLUT-2

A

Basolateral transport of glucose into peritubular capillary network
1st half proximal tubule

80
Q

3 random transport proteins in first half proximal tubule

A

Na/Amino acids
Na/P
Na/Lactate

All symport
All can flow freely through into blood (reabsorbed)

81
Q

Anions that can be reabsorbed in the 2nd half of proximal tubule cell

A 
OH
Formate
Oxalate
Bicarb
Sulfate

This is an H+-anion exchanger that brings anions in, and then the H+ and anion leave to bring in Na and Cl.

Cl will exit the cell though K+/Cl- symport to be reabsorbed

82
Q

SGLT-1

A

Late proximal tubule cell
Na/Glucose symport
Higher affinity, low capacity for glucose
Catch anything SGLT2 missed,

83
Q

Influence of GFR on reabsorption

A

As GFR increase, reabsorption of solute and H2O increases

More H2O is filtered into the tubule, and that makes the peritubular capillary blood (from efferent) have a higher concentration of protein=higher oncotic pressure, as the peritubular capillary surround PT, the blood osmotic forces draws H2O and solute out of the tubule and into the capillary

84
Q

NaKCC location

A

Thick ascending limb (impermeable to H2O)
Furosemide blocks in loop of Henle, diuretic.
Ions come in, but water cannot follow

85
Q

Transport in early distal tubule

A

Water impermeable, NaCl symport

Thiazide blockage, diuretic, excess sodium stays in tubule nephron, decreasing BV

86
Q

Principle Cell

A

Late distal tubule or collecting duct
AQP2–apical
AQP 3 and 4, basolateral
Potassium flows into urine via concentration gradient. Sodium flows into blood

87
Q

Alpha intercalated cells

A

Secrete acid for K+ and take in Cl- from blood to conserve bicarbonate
Impermeable to H2O
Late distal tubule or collecting duct

88
Q

Beta intercalated cell

A

Late distal tubule or collecting duct
Secrete bicarb, save/reabsorb acid (to neutralize bicarb in blood)
CA
Impermeable to H2O

89
Q

Transport Maximum

A

Co-transporters limited by Maximum rate and maximum activity

The plasma glucose concentration at which glucose begins to appear in the urine

90
Q

Tm for glucose

A

375

91
Q

Splay

A

Not all nephrons are identical, smaller (shorter) nephrons will have thier SGLT and/or Na+/K+ ATPases saturated before bigger ones

92
Q

What does a low Tm show?

A

Failure of some nephron filter. Decrease in Tm represents dysfunction at the level of capillaries.

93
Q

Excreted-filtered?

A

Secreted

94
Q

Decrease of PAH Tm

A

The transporters for PAH are on the basolateral (peritubular side) of the proximal tubule eipthelium, meaning they are the ones not getting blood.

95
Q

Limits for Tm for PAH and Glucose

A

PAH–peritubular basolateral membrane

Glucose–luminal membrane

96
Q

ANGII

A

Released due to decrease blood volume

Effects proximal tubule to increase Na+ and H2O Reabsorptoin, to increase BV

97
Q

Aldosterone

A

TAL, distal tubule, collecting duct
Stimulates Na+ reabsorption
Stimulates K+ secretion

98
Q

Aldosterone effect on principle cells during acute phase

A

Increase activity of Na/K+-ATPase BLM

By stimulation of Mineralocorticoid Nuclear

99
Q

Aldosterone effects on principle cells during chronic phase

A

Increase number of Na/K+ ATPase on basolateral membrane
Increase the expression of Na+ and K+ in apical membrane
Release of more K+ from the cell into the urine due to addition of K+ transporters in apical membrane

100
Q

ADH

A

From posterior pituitary in response to low blood volume or decrease plasma osmolality

Add AQP2 to the apical membrane to increase blood volume
Antidiuretic

Vasoconstriction of systemic

Increases activity of NKCC in TAL
V2 transporter on basolateral membrane

101
Q

Mechanism of ADH

A

Binds V2 on basolateral membrane, increasing GS, increasing ardently Cyclase activity, increase cAMP, stimulating more PKA that inserts AQP2 in apical membrane

102
Q

ADH and urea in principal cell of medullary collecting duct

A

Draws urea into intersitial fluid of medulla, urea is osmotically active
Ureaporins (UTA1 and UTA3)
A1–apical
A3–basolateral

103
Q

Summary of ADH

A

Inserts AQP2 into apical membrane of distal nephron

Stimulates thirst

Increases activity of NKCC in the TAL

Increases inner medullary collecting duct permeability to urea, increasing the osmolality of the interstitium

Vasoconstriction to decrease the tank

104
Q

Juxtaglomerular regulation of blood pressure, volume, and GFR

A

Increase GFR, increase NaCL in PCT, if NaCl greater than Tm Macula densa senses increase NaCl in urine, decrease secretion of NO, afferent arteriolar constriction, decrease blood flow to glomerulus, decreas GFR`

105
Q

Two mechanisms of renin release

A

Stretch of Mechanoreceptors trigger JG cells to convert pro-renin to renin

Sympathetic stimulation to beta one adrenergic mechanism,

106
Q

Renin release in response to low blood pressure/ low blood volume

A

decrease BP, decrease glomerulus pressure, Afferent arteriole mechanoreceptors stimulate, JCG cells convert pro-renin to renin, ANGII, constriction of peripheral arterioles (increasing TPR), aldosterone secretion, late DCT and CT H2O and Na+ secretion of K+
Stimulates release of ADH aquaporins,

107
Q

PTH

A

Inhibits Na and H20 reabsorption in PCT secondary to phosphate reabsorption inhibition

108
Q

Urodilatin

A

Secreted by the DT and CD, paracrine effects to inhibit Na+ reabsorption in collecting duct
Water loss

109
Q

Countercurrent Exchange

A

Vasa recta capillaries lose water to the medullary intersitium due to the osmotic gradient created by the loop of henle’s counter current multiplier

110
Q

Calcium homeostasis in kidney depends on

A

Total amount of body Ca2+

Distribution of Ca2+ between bone and ECF/Plasma

111
Q

PCT and Calcium Homeostasis

A

70% (80 para, 20 trans via Ca2+-ATPase)

Keep proximal tubular Ca2+ small

112
Q

Hypocalcemia

A

Low blood Ca2+
PTH secretion, increasing bone resorption, increase Ca2+ reabsorption by TAL and DT
Stimulates release of calcitrol (vit d3 metabolite produced by proximal tubule)

113
Q

Calcitrol

A

Metabolite of Vit D3 produced by Proximal Tubule

114
Q

Hypercalcemia

A

Calcitonin from thyroid
Bone formation
Decrease plasma Ca

115
Q

PTH effects in Kidney Nephron

A
  1. Increased Ca Reabsorptoin in ascending loop and distal tuble
  2. Decrease PO4- reabsorption in proximal loop by decreasing Tm
  3. Activating renal 1-alpha hydroxylated in PT cells to activate vitd

Everything is proximal is normal
Ca-ATPase in basolateral is most effected in neprhon

116
Q

Active form of Vit D

A

1,25

Without PTH there is no activated 1-alpha-hydroxylated. The enzyme 24-hydroxylase will from inactive VIt D (24,25)

117
Q

2 actions of Vit D

A

Synthesis of calcium binding protein that is needed:
Kidney distal tubule epithelium to efficient reabsorb filtered calcium

In the intestinal epithelium to efficiently absorb calcium from the diet.—> increase calcium in the blood

118
Q

Where is the majority of phosphate absorbed in the proximal tubule?

A

85% of phosphate is absorbed in the proximal tubule, larger loss here
15 is lost in the urine due to the distal sections of the nephron not reabsorbing phosphate.

PTH causes phosphaturia

119
Q

Four main groups of diuretics

A
  1. Things that increase GFR (more across glomerulus)
  2. Substance that inhibit ADH cause increased urine output
  3. Excess osmotically active particles (exceeding Tm for most of them, you will urinate)
  4. Renal transport inhibiting substances (Furosemide)
120
Q

Inhibition of ADH as a diuretic

A

Pituitary disease
Diabetes insipidus (lack of ADH from pituitary)
Alcohol (inhibits ADH release)
Narcotics (depress CNS, inhibit ADH)

Lack of adequate ADH or lack of receptor

121
Q

Carbonic Anhydrase Inhbitors

A

PCT (Because there is not brush border in DCT)
Inhibits filtered bicarb from reabsorption (losing water with this), promoting H+ and bicarb secretion
Short term effect
Metabolic acidosis

122
Q

Loop Diuretics

A

Furosemide
Apical NaK2Cl cotranpsorter in TAL
K_ wasting diuretic

123
Q

Thiazide Diuretics

A

Cholorthiazide

Inhibit Na-Cl cotranpsorter in the DCT

124
Q

Amiloride and Triamterene

A

K+ sparing diuretic
Inhibit the apical Na+ channels in the Collecting Ducts

Spironolactones
Interfere with the actions of aldosterone
Increase Na+ and K+

NBS1 (9 decks)

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