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Renal > Physio-Jackson > Flashcards

Physio-Jackson Flashcards

1
Q

List 8 functions of the kidney

A
  1. Excretion of endogenous and exogenous wastes
  2. Regulation of water and electrolyte balance
    (Na, K, Cl, Ca2+, Mg 2+, PO4 2-)
  3. Regulation of body fluid pH
  4. Regulation of arterial blood pressure
  5. Regulation of erythrocyte production
  6. Regulation of vitamin D activity
  7. Gluconeogenesis (not as much as liver)
  8. Plasma Hormone clearance
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2
Q

List 8 consequences of impaired renal function

A
  1. Metabolic Acidosis** (pH < 7.4)
  2. Hyperkalemia* (plasma K > 4.0 mEq/L)
  3. Uremic Toxicity (Azotemia: increased plasma creatinine and BUN)
  4. Na/Water imbalance
  5. Calcium/Phosphate imbalance (decr. Vit-D -> decr. plasma Calcium)
  6. Plasma protein imbalance (Edema: excess fluid deposition in the interstitial space)
  7. Anemia (decr. EPO)
  8. Depressed immune system
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3
Q

What is the action of angiotensin II

A

increase vasoconstriction

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4
Q

What is the action of aldosterone?

A

decrease urinary Na (incr. urinary K+ and H+)

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5
Q

What constitutes acidosis?

A

pH < 7.4

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6
Q

What constitutes Hyperkalemia?

A

plasma K+ > 4.0 mEq/L

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7
Q

Define Azotemia.

A

increase plasma creatinine and BUN

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8
Q

Define Edema.

A

excess fluid deposition in the interstitial space

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9
Q

What is renal function reserve capacity?

A

Body fluid homeostasis can be maintained until renal function decreases to ~ 20% normal.

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10
Q

What are the 3 types of Acute renal failure (ARF)?

A
  1. Pre-renal ARF - decr. renal blood flow -> decr. GFR
  2. Intra-renal ARF - acute tubular necrosis (ATN) - ischemia/toxin induced (ex. gentomycin)
  3. Post-renal ARF - urinary tract obstruction
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11
Q

What is Chronic renal failure (CRF) and what are the 3 main causes?

A 
irreversible, usually progressive renal injury
Causes:
1. Diabetes (34%)
2. HTN (29%)
3. Glomerulonephritis (14%)
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12
Q

How is End-stage renal disease (ESRD) defined?

A

GFR < 10%

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13
Q

What are the stages of renal disease?

A

Stages:

  1. Kidney damage GFR >= 90
  2. Mild decr. GFR 89-60
  3. Moderate. GFR 59-30
  4. Severe. GFR 29-15
  5. Kidney failure =< 15
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14
Q

What are some generalizations about water mass? ie. % body weight, ECF v ICF, etc.

A

60-40-20 rule:
60% total body mass is water
40% ICF
20% ECF

Of ECF
25% (5% total body weight) is plasma
75% (15% total body weight) is interstitial
5% is transcellular: CSF, aqueous humor, GI secretions, urine

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15
Q

What is normal Osmolarity?

A

290 mOsm/L

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16
Q

Is blood ICF or ECF?

A

Both plasma is ECF and Blood cells are ICF

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17
Q

How do solute contents of ECF and ICF compare? What about plasma?

A

Cations: ECF = Na+ ICF = K+ due to membrane Na/K ATPAse pumps (HIKIN = HIgh K INtracellular)

Anions: ECF = Cl-/HCO3- ICF = organic phosphates/proteins

Plasma: Same as ECF except plasma has more Ca2+/MG2+ (bound to protein)

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18
Q

How can plasma osmolarity be calculated (estimate)?

A

Posm = (2 x [Na] + ([glucose]/18) + ([BUN]/2.8)

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19
Q

What is the dilution principle? How does this apply to directly measuring body fluid volume?

A

Fluid Volume = Amount X/equilibrium [X]

Compartment Volume = [(Amount X given) - (Amount X lost)]/[X} at equilibrium

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20
Q

How can we calculate fluid volumes indirectly?

A
  1. Interstitial V = ECF volume - Plasma volume

2. ICF V = Total body water - ECF

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21
Q

Define Osmosis and Osmotic pressure. How else might we express osmotic pressure?

A

Osmosis: the movement of water across cell membranse
Osmotic Pressure: The driving force of movement of water across cell membranes

Osmolarity is another way to express osmotic pressure.
Osmolarity = [X] x # of dissociable particles
= mmol/L x # particles

At E, osmotic pressure = hydrostatic pressure

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22
Q

Describe Tonicity. What are the 3 types?

A

Tonicity is determined by the effect of the solution on the volume of exposed cells (normal 290 mOsm/L)

  1. Isotonic: no change in cell volume (no net H2O flux)
  2. Hypotonic: cells swells (osmotic H2O flux A -> B)
  3. Hypertonic: cells shrink (osmotic H2O flux B -> A)
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23
Q

List 4 ways normal ECF/ICF osmolality can be disrupted.

A
  1. Ingestion of water
  2. Dehydration
  3. IV infusions
  4. Fluid loss

At equilibrium, osmolarities of ECF and ICF must be =
Shifts results from water movement only.

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24
Q

Describe the regulation of erythrocyte production.

A

decrease in renal O2 -> incr. EPO synthesis -> erythrocyte production

Normal oxygenation: Hypoxia-inducible factor 1 (HIF1)a is degraded by propyl hydroxylase (PH)/ubiquitin protein degradation pathway (E3)

Low oxygenation: HIFa and b dimerize -> incr. EPO transcription/translation.

Site of syn: Peritubular fibroblasts, endothelial cells.

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25
Q

What is the site of EPO synthesis?

A

Peritubular fibroblasts, endothelial cells

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26
Q

What regulates 1a-hydroxylase?

A

+ low calcium, low phosphate, High PTH

- high calcium, high phosphate, High 1,25-Vit D3

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27
Q

What is the site of activation for Vit-D? ie where is 1a hydroxylase made?

A

Proximal tubule cells.

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28
Q

What are the four sub-segments of a nephron (in order)?

A

Proximal tubule -> loop of Henle -> distal tubule -> collecting tubule

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29
Q

Which segment of the nephron contains a luminal brush border?

A

Proximal convoluted tubule

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30
Q

what are the two types of nephrons and how are they different?

A

Cortical (superficial): glomerulus located close to the surface of the kidney, short-looped nephrons with no thin ascending limb

Juxtamedullary: glomerulus located close to the border between cortex and medulla, ‘long-looped’ nephrons, essential for urine concentration.

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31
Q

What is the kidney composition of the two types of nephrons?

A

80% cortical : 20% juxtamedullary

the ratio correlates with capacity to concentrate urine. with incr. JXM = incr ability to concentrate urine.

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32
Q

Describe renal blood flow

A

Renal a. -> segmental branches -> interlobar a. -> arcuate a. -> interlobular a. -> afferent arteriole -> glomerular capillaries -> efferent arteriole -> peritubular capillaries -> interlobular v. -> arcuate v. -> interlobar v. -> renal v.

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33
Q

What are vasa recta and what is their orientation and function?

A

Vasa recta are a subset of peritubular capillaries derived from efferent arterioles of juxtamedullary nephrons that are oriented parallel to the loops of Henle. They maintain the hypertonicity of the renal medulla.

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34
Q

Approximately what percent of cardiac output does the kidney receive?

A

~25% (1.2-1.5 L/min)

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35
Q

Describe the 3 Phase relationship between renal blood flow, renal O2 consumption, and renal a-v O2 difference.

A

Phase 1: as blood flow decr. .. O2 consumption decr. proportionally .. no change in a-v O2 difference

Phase 2: from 150-75 ml/100 g Kidney … a-v O2 difference incr. to maintain O2 consumption.

Phase 3: Below 75 ml/100g Kidney .. a-v O2 difference maximal .. renal ischemia.

During Phase 1: ^ RBF -> ^GFR -> ^ filtered Na -> O2 requirement for NaCl reabsorption.

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36
Q

Name 3 principle components of renal function

A
  1. Glomerular filtration
  2. Tubular Reabsorption
  3. Tubular Secretion
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37
Q

What is glomerular filtration? FF?

A

Glomerular filtration is plasma filtered from glomerular capillaries into Bowmen’s space. Only 20% of the plasma entering the glomerular capillaries is filtered “filtration fraction” (FF). FF = GFR/RPF (renal plasma flow rate)

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38
Q

What is tubular reabsorption?

A

Tubular reabsorption is movement of substance FROM lumen INTO the peritubular capillary. This is the principle mechanism for modifying the composition of the filtered fraction.

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39
Q

What is tubular secretion?

A

Tubular secretion is movement of substance FROM the peritubular capillary INTO the lumen. Secretion mostly restricted to solute that are poorly filtered due to size, charge or protein binding.

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40
Q

The presence of _, _, and _ in the urine are suggestive of impaired renal function.

A

Proteins, glucose, amino acids

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41
Q

Describe the micturition reflex

A

as the bladder fills with urine, bladder stretch ^ -> ^ parasympathtic activity -> ^ detrusor muscle contraction

decr. skeletal motor neuron input (pudendal nerve) -> relaxes (opens) external sphincter

Micturition reflex can be modulated (suppressed or potentiated) by the pons and cerebral cortex

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42
Q

Describe 2 abnormalities of micturition

A

Automatic bladder: spinal cord damage above the sacral region - loss of higher center control (partial suppresion) of the micturition reflex - periodic unintended bladder emptying.

Atonic bladder: loss of sensory nerve fibers - no micturition reflex therefore bladder overflows a few drops at a time - overflow incontinence

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43
Q

Automatic bladder

A

spinal cord damage above the sacral region - loss of higher center control (partial suppresion) of the micturition reflex - periodic unintended bladder emptying.

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44
Q

Atonic bladder

A

loss of sensory nerve fibers - no micturition reflex therefore bladder overflows a few drops at a time - overflow incontinence

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45
Q

Describe the filtration barrier

A
  1. Glomerular endothelium (fenestrated)
  2. Basement membrane (collagen, laminin, fibronectin)
  3. Podocytes (foot processes encircle outer surface of capillaries, connected by slit membranes)
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46
Q

What are the 3 major components of the filtration slit diaphram? Give examples of each.

A
  1. Connector proteins (Neph-1, Neph-2, Nephrin, FAT1, FAT2, p-cadherin)
  2. Linker proteins (catenins, zona occludens, CD2AP)
  3. Actin cytoskeleton complex
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47
Q

List 5 functions of Mesangial cells

A
  1. provide structural support for capillaries
  2. secrete extracellular matrix
  3. posses phagocytic activity
  4. secrete prostaglandins and cytokines
  5. possess contractile activity
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48
Q

What size molecules can be freely filtered by the glomerulus? what effect does that have of the concentration gradient?

A

Solutes < 5 kDa.

If they are freely filtered then the concentration of that solute must be equal in Bowmen’s space and the plasma

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49
Q

What 2 things dictate the filtration of solutes larger than 5 kDa?

A
  1. Size

2. Charge

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50
Q

What are 4 potential systemic consequences of protenuria?

A
  1. Arterial/venous thrombosis (loss of anticoags)
  2. Infection (loss of Igs)
  3. Hyperlipidemia (increased hepatic syn.)
  4. Edema (reduced ECV/Renal salt retention)
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51
Q

Describe renal handling of para-aminohippuric acid (PAH).

A

PAH is avidly secreted (amount excreted = amount entering the kidney in the renal artery)

Amount excreted = amount filtered (+ amount secreted) - amount reabsorbed.

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52
Q

Describe the renal handling of Na+, Cl- and H2O.

A

A percentage of the filtered Na+, Cl-, and H2O is reabsorbed (amount excreted < amount filtered).

Amount excreted = amount filtered (+ amount secreted) - amount reabsorbed.

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53
Q

Describe the renal handling of glucose and HCO3-.

A

All filtered glucose and HCO3- are reabsorbed (amount excreted = 0)

Amount excreted = amount filtered (+ amount secreted) - amount reabsorbed.

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54
Q

What are the 2 types of transport across the renal epithelial cells. Describe both.

A
  1. Transcellular: through the cell across TWO membranes (luminal and basolateral)
  2. Paracellular: between cells (across tight junctions) by simple diffusion.
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55
Q

Which type of transport is the more common route, paracellular or transcellular?

A

Transcellular

56
Q

List the 3 types of transcellular transport systems.

A
  1. Channel-mediated diffusion (“passive” require electrochemical gradient)
  2. Carrier-mediated diffusion (uniport, symport, antiport)
  3. Carrier-mediated “active transport” (needs energy to transport against electrochemical gradient)
57
Q

Describe Na reabsorption.

A

In the cortical collecting tubule, Na enters cell via luminal Na-selective channels. ie. [Na+]lumin > [Na+]ic.

It exits the cell via Na/K/ATPases located only on the basolateral membrane in order to maintain a low intracellular Na concentration. ie. [Na+]ic < [Na+]ec

Sodium concentrations:
Luminal > IC < EC

58
Q

What is the site of Na reabsorption?

A

The cortical collecting tubule

59
Q

Describe Na/glucose co-transporter. What is it’s site of action?

A

Na/glucose co-transporter:
Movement of Na down it’s concentration gradient across the luminal membrane facilitates the movement of glucose up it’s concentration gradient.

Glucose uniporter transports glucose out of the cell across the basolateral membrane.

Concentrations:
Glucose: Lumen < IC > EC
Sodium: Lumen > IC < EC

60
Q

What are the 2 luminal Na/glucose co-transporters?

A

SGLT-2: High capacity, Low affinity (early PCT)

SGLT-1: Low capacity, High affinity (late PCT)

61
Q

How can Na/glucose transporter modulators be used as a diabetic therapy? Which transporter is targeted?

A

SGLT-2 inhibitors can be used to shut down the high capacity reabsorption of glucose in the early PCT, thus increasing [glucose] excreted and decreasing plasma [glucose]

62
Q

Other than Na/glucose co-transporters, list 3 other classes of luminal membrane Na-coupled transporters

A
  1. Three amino-acid co-transporters
    Neutral, dibasic (cationic), and dicarboxylic (anion)
  2. Two phosphate co-transporters
  3. Na/H exchanger
63
Q

Describe protein transport in the PCT.

A
  1. Receptor-mediated endocytosis: Filtered proteins bind megalin (M) and cubulin (C) in the luminal membrane clathrin-coated pits.
  2. Endocytosed proteins degraded to amino acids and released basolaterally.
  3. Similar mechanism for uptake of 25-OH vitamin D prior to mitochondrial conversion to 1,25 diOH Vit D by 1a Hydroxylase
64
Q

Approximately how much of the glomerular filtrate is reabsorbed in the proximal tubule?

A

~67%

180 L H20/day -> 120 L reaborbed proximally/day
26,000 mEq of Na/day -> 17,000 mEq reabsorbed PCT/d

65
Q

List 3 solutes that are completely reaborbed proximally.

A

Glucose, amino acids, HCO3-

66
Q

Why is PCT reabsorption isosmotic fluid reabsorption?

A

Because 67% of filtered water and 67% of filtered solute is reabsorbed from the lumen of the proximal tubule. thus the fluid remains isotonic.

67
Q

If tubular fluid and intersitial fluid are both isotonic (~300 mOsm/kg), where is the required osmotic gradient for water reaborption? Explain with 2 steps.

A

Step 1: solute transport creates a small tranepithelial osmotic gradient (tubular fluid (TF) osmolality is slightly lower than that of the extracellular (EC) fluid)

Step 2: water moves from the lumen to interstitium down this concentration gradient.

68
Q

Explain how the isotonic fluid is completely reabsorbed from the lumen of the PCT into the peritubular capillaries.

A
  1. H20 goes from the lumen -> interstitium
  2. H20 goes from interstitium -> peritubular capillaries
    this phase is dependent of Starling forces
69
Q

Explain 2 factors influencing the peritubular capillary (PC) fluid uptake? (think starling forces)

A
  1. Low P(pc) (dowstream of afferent/efferent resistance points
  2. High pi(pc) (filtration creates high PC plasma protein concentration.
70
Q

What is the Glomerulotubular (GT) balance? what is it’s function?

A

the proximal tubule reabsorbs a constant PERCENTAGE (~67%) of the filtered load.

The GT balance helps to maintain a relatively constant delivery of fluid to the distal nephron.

71
Q

If GFR is 100ml/min, what is the flow rate into the loop of henle?

A

33 ml/min. ~67% of the filtered load is reabsorbed by the PCT ie. 67 ml/min.

72
Q

If GFR is 150 ml/min, what is the flow rate into the loop of henle?

A

50 ml/min. 67% of 150 is 100. 150 (filtered load ) -100 (reabsorbed) = 50 ml/min in LOH

73
Q

What are the effects of an increase in efferent arteriolar resistance (ie constriction)? from resistance to tubule. What is the effect on fluid reabsorption?

A

^ constriction of efferent arteriole -> ^resistance -> ^P(gc) (hydrostatic pressure of glomerulus) -> ^GFR but
TUBULAR reabsorption also increases due to:

  1. ^ resistance -> decr. P(pc)
  2. ^ resistance -> decr. renal blood flow (RBF) -> ^FF -> pi(pc) (oncotic pressure of peritubular capillary)

Bottomline: incr. Efferent resistance = incr. Net Fluid reabsorption

74
Q

Describe in vivo micropuncture as a way of analyzing renal tubular function.

A
  1. Pipette A samples tubular fluid at last accessible point of the PCT, the difference in composition of this fluid and plasma represents transport along proximal tubule.
  2. Difference in composition of of fluid sampled from pipettes A and B (initial DCT) represents composite effects of late proximal tubule (pars recta) and segments of the loop of Henle.
  3. Cannot assess collecting tubule function or juxtamedullary nephrons because neither are accessible from the surface of the kidney.
75
Q

Describe in vitro microperfusion as a way of analyzing renal tubular function.

A
  1. Transport capacity of essentially any sub-segment of the nephron can be assessed by microperfusion.
  2. Bathing fluid and perfusion fluid compostion can be modified.
  3. Potential transport modulators (hormones, drugs, etc.) can be selectively applied to either the basolateral or luminal membranes.
76
Q

What is the point of tubular transport maximum (Tm)?

A

The point at which all the carriers of a given substance are fully saturated.

77
Q

What is “splay?”

A

Slight variance in Tm between individual nephrons.

78
Q

What is “threshold?”

A

The plasma concentration at which Tm is exceeded.

79
Q

Describe glucosuria in DM. Is this compensatory?

A

Glucosuria is NOT a compensatory response to the elevated levels of plasma glucose in DM, rather it is the result of having surpassed the Tm of glucose. (GFR x P(gl)&raquo_space; Tm

Note: normal plasma glucose is well below threshold

80
Q

What is the primary site of secretion for organic cations and anions?

A

The proximal convoluted tubule. Must be secreted due to:

  1. Size or charge
  2. Plasma protein binding
81
Q

Describe the transport of organic anions (OAs).

A

Transport from the peritubular capillary into the epithelial cell requires 3 transporters:

  1. OAs are taken up across the basolateral membrane (BM) in exchange for a-ketoglutarate (aKG) via Organic Anion Transporters 1 and 3 (OAT 1, 3)
  2. effluxed aKG taken back into the cell via Na/dicarboxylate co-transporter (NaDC)
  3. Na flux back into the cell via NaDC possible because of [ ] gradient due to Na/K/ATPase

Transport of OAs across luminal membrane (LM) via

  1. OAT4 antiporter
  2. Multidrug resistance-associated protein 2 (MDRP-2)
82
Q

Describe the tubular secretion of organic cations (OCs).

A
  1. electrical gradient favors OC uptake across BM via OC transporters (OCT-1,2,3)
  2. Luminal membrane transport mediated by OC-H antiporters (OCTN) and MDR1 (p-glycoprotein)
83
Q

Are OATs selective? what clinical implications does this have?

A

No, they are relatively non-selective.

Thus, if something like penicillin was given with something like PAH, the plasma concentrations would be higher than penicillin alone.

84
Q

What are the primary requirements for a substance to be used as a marker of GFR?

A
  1. Not reabsorbed or secreted by nephron

2. Not metabolized or produced by kidneys

85
Q

What are 2 GFR markers?

A
  1. Inulin: polyfructose (must be infused)

2. Creatinine: endogenous metabolite

86
Q

Express GFR in terms of inulin.

A

amount filtered = amount excreted in the urine

GFR = V x U(in)/P(in) where
V = urine flow rate
U = urine conc. of inulin
P = plasma conc of inulin
87
Q

How does clearance of inulin related to GFR?

A

C(in) = V x U(in)/P(in) = GFR

because inulin is completely cleared by kidney. Creatinine also

88
Q

How can we determine how the kidney handles substance X?

A

Compare the clearance of X with the clearance of inulin or creatinine.

If C(x) < C(in) then X must undergo net reabsorption
If C(x) > C(in) then X must undergo net secretion
If C(x) = C(in) then X completely cleared by kidney
89
Q

How can we measure renal plasma flow (RPF)?

A

Xrenal artery = Xrenal vein + Xurine thus
RPF(a) x P(x) = [RPF(v) x P(x)] + [U(x) x V]

Use PAH (completely filtered or secreted) (RPF(v)=0)
RPF = U(pah) x V/P(pah)
U = urine [PAH]
V = urine flow rate
P = plasma [PAH]
90
Q

Express Renal Plasma Flow (RPF) in terms of blood

A

RBF = RPF/(1-HCT)

91
Q

What would happen to P(gc), GFR, RPF, and FF if the afferent arteriole was constricted?

A

P(gc) decrease
GFR decrease
RPF decrease

92
Q

What would happen to P(gc), GFR, RPF, and FF if the afferent arteriole was dilated?

A

P(gc) increase
GFR increase
RPF increase

93
Q

What would happen to P(gc), GFR, RPF, and FF if the efferent arteriole was dilated?

A

P(gc) decrease
GFR decrease
RPF increase

94
Q

What would happen to P(gc), GFR, RPF, and FF if the afferent arteriole was constricted?

A

P(gc) increase
GFR increase
RPF decrease

95
Q

What is the balance concept?

A

Multiple sources of water input/output into/out of the body. Water input = Water ouput

Only 1 output can be precisely controlled: Urine

96
Q

What are the major sources of water input and water output from the body?

A

Input: Fluid, Metabolism , Food
Output: Feces, Sweat, Urine, insensible losses

97
Q

What are the ranges for urine volume and osmolality during maximum diuresis?

A

Urine volume: 20-25 L/day

Urine osmolality: 50-75 mOsm/kg

98
Q

Why, in cases of extreme water deficit, can we not stop urine output completely to conserve water?

A

not sure, look it up

99
Q

What are the ranges for urine volume and osmolality during maximum antidiuresis?

A

Urine volume: 0.5 L/day

Urine osmolality: 1200-1400 mOms/kg

100
Q

Describe the regulation of ADH secretion.

A

ADH secretion is regulated primarily by hypothalamic osmoreceptors. But also volume receptors

^ in hydrostatic pressure -> ^ ADH -> ^H2O reabsorption -> decrease in hydrostatic pressure (Posm) (down towards normal)

101
Q

What is the function of ADH?

A

increase water reabsorption (antidiuresis)

102
Q

What class of hormone is ADH?

A

ADH is a peptide hormone. AKA arginine vasopressin (AVP). 1.1 kDa octapeptide.

103
Q

Where is ADH synthesized? stored? secreted?

A

ADH is synthesized in the supraoptic and paraventricular nucleii of the hypothalamus. It is stored in and released by the posterior pituitary (neurohypophesis)

104
Q

What are the 2 principal mechanisms that regulate ADH? Which mechanism is more sensitive? Do these 2 mechanisms interact?

A
  1. Hypothalamic osmoreceptors.

^ Posm -> ^ADH -> ^H2O reabsorption -> decr. Posm

  1. Volume receptors.
    decr. Pvol -> ^ADH -> ^H2O reabsorption -> ^Pvol

The sensitivity of the osmoreceptor system is much higher than the baroreceptor system.

Yes.

105
Q

What is the osmotic set point?

A

the plasma osmolality at which ADH secretion = 0

106
Q

Are large changes in plasma ADH required to elicit changes in urine volume and osmolality.

A

No, very small changes in ADH can elicit large changes in urine osmolality. ^ plasma osmolality = decr. urine volume

107
Q

In a state of water deficit, will an increase in ADH and thus increased water reabsorption alone restore normal fluid volume?

A

No, this will only minimize further losses of water, not restore fluid volume.

108
Q

Describe thirst. how is it controlled?

A

The body responses to increased osmolality (which it interprets as hypovolemia) by trying to increase fluids via thirst induction.

109
Q

Which is more sensitive, the baroreceptor system or the osmoreceptor system?

A

The sensitivity of the osmoreceptor system is much higher than the baroreceptor system. Small changes in plasma osmolality can elicit large changes in ADH secretion.

110
Q

Describe the interaction between the baroreceptor and osmoreceptor systems.

A

decr. volume -> decr. set point and ^ sensitivity to changes in osmolality

111
Q

What is ADH (AVP) MOA?

A

upregulates Aquaporin-2 expression in DCT and collecting duct basolateral membrane. Also peripheral vasoconstriction.

112
Q

What is SIADH?

A

Syndrome of Inappropriate ADH secretion which causes hyponatremia. Severe hyponatremia can cause encephalopathy leading to coma.

113
Q

What are 3 categories of causes of SIADH?

A
  1. Head truama, encephalitis, meningitis
  2. ADH secreting tumor (small cell carcinoma of lung, pancreas, etc.)
  3. Drug-induced (nicotine, morphine, chemo)
114
Q

What are physiologic effects of SIADH?

A
  1. ^ADH -> ^H2O reabsorption -> Hyponatremia

2. decr. serum Na -> decr. plasma osm -> influx of H2O (esp brain cells) -> coma

115
Q

What are the 2 principal forms of diabetes insipidus?

A
  1. Hypothalamic (central) DI: decr. production or release of ADH
  2. Nephrogenic DI: renal unresponsiveness to ADH.
116
Q

How DI treated? How is water balance maintained?

A

not sure

117
Q

What is Free Water Clearance?

A

the amount of distilled water that must be added to (during antidiuresis) or removed from (during diuresis) the urine to create an isotonic fluid.

118
Q

How can free water clearance provide an assessment of ascending limb function?

A

The ascending limb of the loop of henle is responsible for water reabsorption. Thus free water clearance is a non-invasive assessment of the diluting efficiency of the thick ascending loop

119
Q

What is the formula for free water clearance?

A

C(h2o) = V - C(osm) = V - (V x C(osm)/P(osm))

120
Q

When is free water clearance = 0?

A

When C(osm) = P(osm)

121
Q

What are 3 causes of nephrogenic DI?

A
  1. Mutation in ADH receptor:
    decr. AVP binding -> decr. cAMP -> decr. H2O channel insertion
  2. Impaired synthesis/translocation of aquoporins
  3. Drugs (litium, tetracyclines), hypokalemia
122
Q

Why is ECF directly related to total body sodium? (3 reasons)

A
  1. H2O shifts between intra - extracellular.
  2. Effects of ADH secretion, thus collecting duct H2O reabsorption.
  3. Effects of thirst.
123
Q

How do the kidneys contribute to the maintenance of ECF volume?

A

The kidneys adjust NaCl excretion to match NaCl intake. Typically 1% or less of the filtered load of sodium is excreted (<250 mEq/day)

124
Q

What is primarily controlling the regulation of sodium reabsorption/excretion?

A

The action of Aldosterone on the cortical collecting tubule.

decr. ECF Na -> ^Aldosterone -> ^Na reabsorption -> decr. Na excretion

125
Q

What is the site of action for aldosterone?

A

the cortical collecting tubule.

126
Q

What is the mechanism of action of aldosterone?

A

Aldosterone stimulates the principle cells of the cortical collecting duct to increase Na reabsorptiong and K secretion. It also cause the intercalated cells to secrete H.

127
Q

How much of the Na filtered load is controlled by aldosterone?

A

~5-7%

Keep in mind, retention of 0.56% of the filtered load (~ 140 mEq) would obligate a 1 L retention of water to maintain isotonicity.

128
Q

what is filtered load?

A

GFR x plasma [X]

129
Q

What 2 things happen in the cortical collecting tubule?

A
  1. Reabsorbs sodium

2. Secretes potassium

130
Q

How does Aldosterone control reabsorption of Na? (3 ways)

A
  1. ^number of luminal membrane Na channels
  2. ^ Na/K/ATPase (de novo synth.)
  3. ^ Krebs cycle enzyme synth. (more ATP)
131
Q

Will a change in total body Na content be reflected in a Na concentration change in the ECF?

A

No

132
Q

Does the infusion of isotonic saline or hemorrhage affect Na concentration change in the ECF?

A

No

133
Q

How are changes in total body Na sensed?

A

Changes in total body Na are sensed as changes in Effective Circulating Volume (ECV) which monitored by baroreceptors

134
Q

Where are baroreceptors located?

A 
Cardiac atria
Pulmonary vasculature
Carotid sinus
Aortic arch
Juxtaglomerular apparatus
135
Q

What is the rate-limiting step in aldosterone release from the adrenal cortex?

A

Renin release by the kidney.

Note: Renin is NOT a hormone, it’s an enzyme.

136
Q

Describe the Renin-Angiotensin-Aldosterone system

A
  1. Renin is released from the kidneys.
  2. Renin converts angiotensinogen into Angiotensin I
  3. Angiotensin I is converted to Angiotensin II by pulmonary ACE.
  4. Angiotensin II increases release of Aldosterone.

Renal (6 decks)

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