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Physiology 1 > Renal (4) > Flashcards

Renal (4) Flashcards

1
Q

How does Kidney affect RBC

A

Produces Erythropoietin for RBC production in hypoxia

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2
Q

Types of Nephrons

A
  • Juxtamedullary Nephron
  • Cortical Nephron (90%)
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3
Q

Renal Circulation Arteries

A

Renal A, Segmental A, Interlobar A, Arcuate A, Intralobular A, Afferent a, Glomerular cap, Efferent A, Peritubular cap, Vasa recta

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4
Q

Renal Circulation Veins

A

Venules, Intralobular v, Arcuate v, Interlobar v, Renal V

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5
Q

Renal Blood Flow

A

1200 - 1300 ml/min
(20 - 25% of CO)

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6
Q

Renal Plasma Flow

A

600 - 700 ml/min

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7
Q

Natriuresis

A

When body excretes excess Na+ in Urine

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8
Q

What determines Renal vascular resistance

A

Afferent & Efferent Arterioles

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9
Q

Why do we need to regulate BP to kidney

A

To protect Glomerular Capillaries from Overfiltration

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10
Q

2 Autoregulatory Mechanisms to regulate RBF and GFR

A
  • Myogenic Mechanism (Bayliss)
  • Tubulo-glomerular Mechanism
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11
Q

Myogenic Autoregulatory mechanism (Bayliss)

A

Tendency of smooth muscle to contract when stretched (AFFERENT ARTERIOLE ONLY)
(90 - 180 mmHg)

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12
Q

Tubulo-glomerular Autoregulatory Mechanism

A

Feedback loop where change in GFR leads to alteration in conc. of NaCl in tubular fluid, sensed by macula densa sending signals to affect the Afferent arteriolar resistance

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13
Q

Adenosine A1 receptor

A
  • Gi
  • Less cAMP
  • Vasoconstriction in Afferent arteriole
    (inh. of granular cells)
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14
Q

Adenosine A2 receptor

A
  • Gs
  • More cAMP
  • Cardiac/Skeletal m
  • Vasodilator
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15
Q

Granular cells

A

Synthesize, store, and release Renin into bloodstream

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16
Q

Renin Production vs GFR

A
  • High GFR: Inh. Renin production
  • Low GFR: Renin angiotensin cascade leads to Efferent art. vasoconstriction
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17
Q

What happens when ECFV drops

A

Sympathetic nerves release NE and dopamine and E by adrenal Medulla
- NE/E act on a1-AR (Gq) = VC in Afferent art.
- NE/E act on B1-AR on granular cells (Gs)
- Renin-Ang cascade activated, ANGII, VC in Efferent art.

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18
Q

Angiotensin II

A

Constricts Afferent and Efferent arterioles
(Efferent more sensitive)

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19
Q

ANP

A
  • VD in Afferent art.
  • VC in Efferent art.
  • Increased GFR and same RBF (since VC and VD act together)
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20
Q

Glomerular Filtration Rate (GFR)

A

120 ml/min
(180 L/day)

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21
Q

Filtration Fraction (FF)

A

20%
Ratio of plasma filtered to total plasma flowing through glomerulus
FF = GFR / RPF = 120/600

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22
Q

Glomerular capillary Pressure vs normal capillaries

A

Twice as much Pressure in Glomerular

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23
Q

Filtration Barrier

A

1) Fenestrated Endothelium
2) Basement Membrane
3) Podocytes
(repel negative charges)

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24
Q

General Filtration Rule

A

The larger and more negative a molecule is, the less likely it will pass the filtration barrier

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25
Q

Renal Clearance

A

Volume of plasma / time
From which all given substances pass through the filtrate and are excreted in the urine (ml/min)

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26
Q

How to determine Amount excreted in Urine?

A

Filtered - Reabsorbed + Secreted

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27
Q

Albumin fate

A

Not filtered

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28
Q

Fate of different substances in Kidney

A
  • Not filtered (albumin)
  • Filtered & Completely reabsorbed (glucose)
  • Filtrated and Completely secreted (PAH)
  • Filtrated and not Reabsorbed, Secreted, or metabolized by Kidney. (creatine)
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29
Q

What can give us an Idea of GFR

A

Blood creatine levels since it is filtrated and not reabsorbed or secreted, all goes into urine.
So higher creatine means lower GFR

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30
Q

Proximal Tubule structure

A
  • Brush border
  • Highly invaginated BL membrane with mitochondria for active T
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31
Q

Cells in Collecting Duct

A
  • Principal cells
  • Intercalated cells
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32
Q

Principal Cells (collecting duct)

A
  • Moderately invaginated BL membrane with few mitochondria
  • Important for reabsorption of NaCl and K+
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33
Q

Intercalated Cells (collecting duct)

A
  • High mitochondria density
  • Important for Acid-Base balance
  • Some secrete H+ (a) and some HCO3- (B)
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34
Q

Formation of Urine 3 Processes

A

1) Ultrafiltration
2) Reabsorption
3) Secretion

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35
Q

What drives Ultrafiltration

A

Starling forces
(Hydrostatic & Oncotic pressures of Capillaries and Interstitial fluid)

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36
Q

Hydrostatic vs Oncotic Pressures

A
  • Hydrostatic drives fluid/substance OUT
  • Oncotic pressure KEEPS fluid
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37
Q

Hydrostatic Pressure in Capillaries

A
  • Afferent: + 53 mmHg
  • Efferent: + 51 mmHg
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38
Q

Oncotic Pressure in Capillaries

A
  • Afferent: - 26 mmHg
  • Efferent: - 33 mmHg
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39
Q

Hydrostatic Pressure in Bowman’s

A
  • Afferent: - 12 mmHg
  • Efferent: - 12 mmHg
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40
Q

Oncotic Pressure in Bowman’s

A
  • Afferent: 0 mmHg
  • Efferent: 0 mmHg
41
Q

NET ultrafiltration Pressure

A
  • Afferent: 15 mmHg
  • Efferent: 6 mmHg
42
Q

Proximal Tubule functions

A
  • 60-70% of Na reabsorption
  • Any protein/albumin filtered reabsorbed
  • Any osmotically active substances reabsorbed are followed by water to prevent a gradient
43
Q

First half of Proximal Tubule

A
  • Na is primarily reabsorbed with HCO3 (a.a, gluc, Pi)
  • Only 20% of Na reabsorbed
44
Q

Second half of Proximal Tubule

A
  • High Cl- conc due to first half taking other substances
  • other 40% of Na absorbed here
45
Q

Ways to reduce Na and Water reabsorption in Proximal Tubule

A
  • Acetazolamide: Inhibits carbonic anhydrase (no Na/HCO3)
  • Hg-containing compounds: Aquaporin inh.
  • Non-reabsorbing osmolarities: excessive gluc, ketone, cause water drawn back to tubules
46
Q

Loop of Henle

A
  • 20-25% NaCl absorption
  • Only passive transport in thin ascending/descending limbs
  • TAL has active transport
47
Q

Thin Descending limb (LOH)

A
  • Passive transport of Water via Aquaporin 1, poorly to NaCl
  • Water reabsorption without solutes leaves tube hyperosmotic
  • At the end of the TDL osm. goes from 300mosm to 1200 mosm.
48
Q

Thin Ascending Limb (LOH)

A
  • Passive Transport
  • Impermeable to water (no aq1)
  • Permeable to NaCl and Urea leaving tube hyposmotic
49
Q

Thick Ascending Limb TAL (LOH)

A
  • Active transport and reabsorption of osmolytes NKCC
  • No water reabsorption (no aq1)
50
Q

What inhibits the NKCC transporter in TAL

A

Furosemide

51
Q

Distal Convoluted tubule

A
  • 5-7% of NaCl reabsorption
  • Na/Cl Cotransporter
  • No water reabsorption
52
Q

What inhibits Na/Cl transporter in Distal convoluted tubule

53
Q

Collecting ducts

A
  • eNaCs drive Na into cells
  • Negative luminal potential created
  • Drives Cl absorption paracellularly
  • Luminal K+ channels to balance charge
54
Q

What affects eNaCs

A
  • Aldosterone: Increases expression/activity to raise BP
  • ANP: Inhibits eNaC causing Natriuresis (lower BP)
  • Amiloride: inhibits eNaC, no effect on K+
55
Q

Water reabsorption overview

A
  • Water absorbed from PT to end of TDL
  • Water IMPERMEABLE from thin descending limb to distal convoluted tubule
  • Water reabsorption from collecting duct to medullary collecting duct in presence of ADH
56
Q

Vasopressin (ADH) action

A

1) Binds basolateral Gs coupled V2-R
2) cAMP to PKA
3) Vesicle release of AQ2 on luminal side
4) More water reabsorption

57
Q

Where is Urea reabsorbed?

A

Inner medullary collecting ducts

58
Q

Overall K+ transport

A
  • PT: Paracellular K+ reabsorption
  • TAL: K+ reabsorption via NKCC
  • CD: K+ Secretion and Na reabsorption Na/K atpase and ROMK
59
Q

Overall Ca2+ transport

A
  • PT: Paracellular reab. with Na+
  • TAL: Paracellular reab. with Na+
  • DCT: Active transcellular reabsorp. (PTH stim.)
60
Q

What helps recover/reabsorb filtered proteins

A

Megalin & Cubulin
(endocytosis)

61
Q

Countercurrent Multiplication

A

Active Process to generate an osmotic gradient to enable water reabsorption from filtrate & to concentrate urine

62
Q

Countercurrent Exchange

A
  • Happens between Vasa recta and interstitium
  • Passive process
  • Maintains a gradient, doesnt create it
63
Q

Urea recycling

A
  • When water absorption is increased by ADH/Vasopressin
  • More water & Urea reabsorbed
  • Water in Outer medullary duct
  • Urea in Inner medullary duct only to form gradient for countercurrent multiplication
64
Q

Effective Arterial Blood Volume (EABV)

A

Portion of the ECF contained in the arteries and perfusing the tissues that is sensed by the Kidneys and is regulated by changes in Na+ excretion

65
Q

4 Mechanisms that affect Na+ excretion due to EABV

A
  • Sympathetic inn.
  • ANP
  • Peritubular capillary starling forces
  • Renin-ANG-Aldosterone system
66
Q

K+ overall movement

A
  • Proximal tubule reabsorption (2/3)
  • TAL by NKCC (20%)
  • DCT principal secrete under high K+
  • DCT a-intercallated cells reabsorb K using K/H atpase
67
Q

Aldosterone effect on K+

A

Increase K+ secretion in DT and CD
- Increased eNaC expression
- Increased Na/K atpase quantity
- Increase of luminal ROMK

68
Q

How do diuretics mostly affect K+

A

Increase K+ to drive secretion

69
Q

How to ensure Aldosterone specificity in Kidney

A

11B-OHSDH to convert gluco and mineralocorticoids to inactive form to allow Aldosterone to only bind MC-R

70
Q

What happens when Hyperosmotic activity is detected

A

Thirst is triggered by Osmoreceptor cells in Hypothalamus and Baroreceptors

71
Q

How do we prevent Overhydration after thirst?

A

Peripheral osmoreceptors in GI and stomach and mouth stop thirst

72
Q

Osmoreceptor responce in high Plasma effective osmolarity

A
  • Signal to Supraoptic & Paraventricular nuclei
  • Vasopressin secretion
73
Q

Amount of Non-volatile acid produced per day

A
  • 30 mmol/day Dietary
  • 40 mmol/day Metabolism
    = 70 mmol/day total which can not be exhaled
74
Q

How does the Kidney combat non-volatile acids

A
  • Produces 70mmol of HCO3- to buffer
  • 30 mmol buffered to H2CO3 then CO2 and exhaled
  • 40 mmol is trapped by NH3 to NH4+ and excreted in Urine
75
Q

pH

A

7.35 - 7.45

76
Q

paCO2

A

38 - 40 mmHg

77
Q

Standard HCO3-

A

23 - 25 mmol/L
(= to actual in normal acid-base balance)

78
Q

Base Buffer (BB)
and its use

A

44 - 49 mEq/L
- Indicates buffering capacity: How many proton molecules can be buffered in the blood

79
Q

Base Excess (BE)
and its use

A

+/- 2.5 mEq/L
- Shows difference/deviation from the normal value

80
Q

Volatile acids

A

Acids that can be converted into gaseous form and thus be eliminated by the Lungs
(mainly CO2)

81
Q

Nonvolatile (fixed) acids

A

Acid produced from sources other than CO2 and not excreted by the Lungs

82
Q

How are nonvolatile acids formed?

A
  • Amino acids with Sulfur (sulfuric acid)
  • Phospholipids (phosphoric acid)
83
Q

Buffers

A

A solution which resists change in pH when a small amount of acid/base is added
(weak a/b with its conjugate a/b)

84
Q

Open system

A

System where buffers can quickly be altered
(CO2 buffer - HCO3/H2CO3)

85
Q

Role of Proteins as Buffers

A

They can be Protonated/Deprotonated
- Usually bound to Ca2+ but in acidic conditions H+ can bind instead

86
Q

What is most important buffer in body

87
Q

Why does CSF only use 1 type of buffer

A

No proteins in CSF so only HCO3 buffer can be used

88
Q

Respiratory Acidosis

A
  • High pCO2
  • No change in BB / BE
  • Unchanged Standard HCO3-
  • Increased Actual HCO3-
89
Q

Respiratory Alkalosis

A
  • Low pCO2
  • No change in BB / BE
  • Unchanged Standard HCO3-
  • Lower HCO3-
90
Q

Metabolic Acidosis

A
  • No change in pCO2
  • Lower BB / BE
  • Lower Standard HCO3-
  • Lower Actual HCO3-
91
Q

Metabolic Alkalosis

A
  • No change in pCO2
  • Higher BB / BE
  • Higher Standard HCO3-
  • Higher Actual HCO3-
92
Q

Mixed Type Acidosis

A
  • High pCO2
  • Low BB / BE
  • Lower Standard HCO3-
  • complex Actual HCO3-
93
Q

Anion gap

A
  • The difference between measured Cations and measured Anions in the plasma
  • Used to diagnose metabolic acidosis
    = 8 - 16 mEq/L (normal)
    Na - (Cl + HCO3)
94
Q

High anion gap

A
  • Lower HCO3
  • Means there is unmeasured anions / new acid appearance
95
Q

Calcium Levels in High/Low pH

A
  • Low: More free Ca
  • High: Less free Ca (Albumin loses H+ and binds more Ca)
96
Q

Potassium Levels in High/Low pH

A
  • Low: High (ROMK inh. so less excreted)
  • High: Low
97
Q

How to calculate NAE

A

Titratable acidity (H bound to urinary buffers like phosphate) + NH4 excretion - HCO3 excreted

98
Q

Renal Buffers capacities

A
  • Phosphate buffer: 18 mmol
  • Criatinine buffer: 5.5 mmol
    = Total 23.5 mmol out of 70 mmol
99
Q

How does Kidney make NEW HCO3-

A
  • From Glutamine via Glutaminase
  • yields NH4+ and HCO3-
  • NH4+ broken to NH3 + H+
  • NH3 diffuses into tubule
  • H+ taken out by Na/H exchanger

Physiology 1 (12 decks)

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