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ACVIM Reading List > Fluid and Renal Physiology > Flashcards

Fluid and Renal Physiology Flashcards

1
Q

What are the 2 largest compartments of ECF?

A
  1. Interstitial Fluid

2. Plasma

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2
Q

What electrolytes are in ECF?

A

LOTS of Na and Chloride, small amount of Mg, K, P, Ca, organic acids

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3
Q

What electrolytes are in ICF?

A

Lots of K and phosphate, moderate amount of Mg, sulfate

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4
Q

What is osmolality?

A

Number of osmoles per kg of water

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5
Q

What is osmolarity?

A

Number of osmoles per liter of water

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6
Q

Causes of hyponatremia = hypoosmotic dehydration

A

Primary hyponatremia; Adrenal insufficiency - Addison’s dz; overuse of diuretics

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7
Q

Causes of hyponatremia = hypoosmotic overhydration

A

Excess water diluting Na; Excess ADH (Syndrome of inapporpirate ADH) = Kidney absorbs more water

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8
Q

Causes of hypernatremia = hyperosmotic dehydration

A

Due to loss of water; Dehydration (most common); Inability to secrete ADH (Diabetes insipidus)

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9
Q

Causes of hypernatremia = hyperosmotic overhydration

A

Due to gain of Na; Excessive secretion of Na retaining hormone = Aldosterone

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10
Q

What happens with hyponatremia?

A

Hyponatremia = Cell Swelling → Osmotic mediated demyelination of neurons

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11
Q

What happens with hypernatremia?

A

Hyponatremia = Cell Shrinking → Stimulating thirst mechanism in hypothalamus

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12
Q

What are the 4 major causes of Extracellular Edema?

A
  • Increased Capillary pressure (excessive kidney retention of salt and water, high venous pressure and venous constriction, decreased arteriole resistance)
  • Decreased plasma proteins (Loss of proteins in urine, loss of proteins from denuded skin (burns), failure to produce proteins (liver failure))
  • Increased capillary permeability (Immune rxn = histamine, toxins, bacterial infections, Vitamin def (esp Vit C), prolonged ischemia, burns)
  • Blockage of Lymph Return (cancer, infections, sx, congenital/lymphatic abnormality)
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13
Q

What is intracellular edema?

A

Swelling in the cell itself; caused by hyponatremia, decreased cellular metabolic activity or nutrient delivery

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14
Q

What are the 4 safety factors that normally prevent edema?

A

o Low interstitial compliance: normal interstitial pressure is subatmospheric = low compliance; when interstitial fluid is present, this increase in interstitial hydrostatic pressure deters capillary filtration; when pressure is zero or positive, increased compliance occurs = more fluid contributes less to hydrostatic pressure = allows more water accumulation
o Interstitial gel: most water in the interstitium is in the form of a gel (bound to proteoglycans) = provides the low compliance at negative pressures; as the pressure increases and the increased compliance allows for more water accumulation, it becomes free (not bound to proteoglycans) = “pitting edema”; in edema, excess fluid forms channels through proteoglycans = fluid can flow to gravity-dependent regions
o Increased lymph flow: can increase 10-50 X normal
o Washdown of the interstitial fluid protein: as the interstitial fluid pressure increases, the lymph flow also increases and removes proteins at a more rapid pace.

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15
Q

Name 7 functions of the kidenys in homeostasis.

A

o Regulation of water and electrolyte balance
o Excretion of metabolic waste products (urea, creatinine, uric acid, bilirubin)
o Regulation of arterial blood pressure (via renin)
o Regulation of acid-base balance
o Produces 1,25 cholecalciferol (active VitD, calcitriol - Ca deposition in bone, Ca reabsoprtion in GIT)
o Produces EPO from the peritubular endothelial cells
o Glucose synthesis (rivals liver in some situations)

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16
Q

Why is the renal circulation unique?

A

Two capillary beds separated by efferent arteriole; afferent arterioles →glomerular capillaries →efferent arteriole →peritubular capillaries →venous system

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17
Q

How do the 2 capillary beds in the kidney work?

A 
Glomerulus (high pressure) = Filtration
Peritubular caps (low pressure) = Reabsorption
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18
Q

How does the kideny regulate hydrostatic pressure?

A

By adjusting resistance in afferent and efferent arterioles - Kidney can regulate hydrostatic pressure in both capillary beds (glomerular and peritubular) to change the rate of glomerular filtration and tubular reabsorption, or both

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19
Q

Each nephron contains….

A
  1. Glomerulus

2. Long tubule

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20
Q

Name the order to tubular segments of the nephron.

A

Glomerular capillaries surrounded by Bowman’s capsule = proximal tubule = Loop of Henle (descending thin, ascending thin, ascending thick) = distal tubule = cortical collecting tubule = cortical collecting ducts

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21
Q

What is the macula densa?

A

At end of the thick ascending limb; Plaque of specialized epithelial cells (aids in controlling nephron function)

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22
Q

What are the regional differences in nephron structure?

A
  1. Cortical nephrons are located in the cortex and have short loops of Henle
    • Have peritubular capillaries
  2. Juxtamedullary nephrons are adjacent to the medulla and have long loops of Henle
    • Have vasa recta which originate as efferent arterioles that form an extensive capillary network around the Loop of Henle, return to the cortex and enter into cortical veins
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23
Q

What is the name of the reflex that results in urine in bladder being propelled backwards?

A

Vesicoureteral Reflex

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24
Q

Name the 3 major nerves involved in bladder innveration and their function.

A
  1. Pelvic nerve (PNS)
    • Sensory fibers detect the degree of stretch
    • Motor fibers facilitate detrusor contraction
  2. Pudendal nerve (skeletal): innervates the external urethral sphincter
  3. Hypogastric nerve (SNS, from L1-L4):
    • B-adrenergic = detrusor relaxation
    • A-adrenergic = internal urethral sphincter contraction
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25
Q

Describe the storage phase of micturition.

A

Storage phase: under SNS tone via hypogastric nerve
• b-adrenergic: detrusor relaxation
• α-adrenergic: contract IUS
• Somatic: contract external urethral sphincter

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26
Q

Describe the micturition reflex.

A

Micturition reflex = causes the transition from storage to voiding phase
• Afferent limb: stretch receptors in bladder wall → impulses via pelvic nerve → micturition center in brainstem → reach threshold for reflex
• Efferent limb: motor discharges to the sacral PNS nuclei initiate the voiding phase

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27
Q

Describe the voiding phase of micturition.

A

Voiding phase: under PNS tone via the pelvic nerve
• PNS stimulation → detrusor contraction
• Inhibition of SNS activity → relaxation of IUS
• Urine flow should be sustained until emptying is complete

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28
Q

Why is the glomerular capillary bed unique?

A

It has 3 membranes (instead of two)

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29
Q

What are the 3 layers of the glomerular capillary membrane?

A
  1. Capillary endothelium: contains fenestrations, large enough to allow protein passage
  2. Glomerular basement membrane: negatively charged proteoglycans that effectively prevent the passage of plasma proteins
  3. Epithelial cells (podocytes) surrounding the outer layer of the basement membrane = contain slit-pores with some filtration restriction
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30
Q

What is the main barrier to filtration of plasma proteins in glomerulus?

A

Basement membrane

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31
Q

What determines the filterability in the glomerulus?

A
  1. Solute size

2. Electrical Charge (negatively charged proteoglycans prevent passage of plasma proteins)

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32
Q

How can albumin not get through glomerulus?

A

Albumin is small enough to fit through the pores but the negative charge is what prevents its passage

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33
Q

What are the equation for GFR?

A

GFR = Kf x net filtration

Kf: capillary filtration coefficient = product of the permeability and surface area of the capillaries

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34
Q

What is the major factor for altering GFR?

A

Glomerular hydrostatic pressure

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35
Q

What are the 3 factors that an influence glomerular hydrostatic pressure?

A
  1. Increased arteriole pressure: increase GFR, but is regulated by autoregulatory systems
  2. Constriction of the afferent arteriole decreases hydrostatic pressure and decreases GFR
  3. Constriction of the efferent arteriole will increases resistance to outflow of the capillaries and raises the hydrostatic pressure → increases GFR
    • However, if the efferent arteriolar constriction is too much, it will decrease the renal blood flow and significantly increase the capillary COP = decreases GFR
    • Moderate efferent arteriolar constriction will increase GFR, severe constriction will decrease GFR
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36
Q

How does autoregulation work in the kidney?

A

Autoregulation will maintain renal blood flow within an arterial pressure range of 80-170 mm Hg, despite what systemic blood pressure is - needed to maintain relatively constant GRF and excretion of water and solutes

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37
Q

How does the SNS control GFR?

A

NE, epi, endothelin = decreases GFR and RBF (constricts afferent and efferent arterioles)

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38
Q

How does angiotensin II control GFR?

A

Constricts the efferent arterioles
Raises glomerular hydrostatic pressure while reducing RBF → increases GFR
The decreased RBF through the peritubular capillaries causes increased resorption of sodium and water

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39
Q

How does endothelial-dervied NO control GFR?

A

decreases renal vascular resistance and increases GFR

Functions to prevent excessive vasoconstriction of the renal vessels

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40
Q

How do renal vasodilators control GFR?

A

Prostaglandins: especially PGE2 and PGI2; function to maintain GFR and RBF during volume depletion

Bradykinin

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41
Q

What is glomerulotubular balance?

A

Adaptive mechanism in renal tubules that allow them to increase reaborption rate when GFR rises

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42
Q

What is tubuloglomerular feedback?

A

Feedback in autoregulation of GFR = to ensures constant delivery of NaCl to the distal tubule at macula densa

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43
Q

What are the 2 major components of the juxtaglomerular complex?

A
    1. Macula densa cells in the initial portion of the distal tubule (close contact with afferent and efferent arterioles) → detects NaCl levels
    1. Juxtaglomerular cells in the walls of the afferent and efferent arterioles
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44
Q

What happens when there is a decreased in BP in the glomerulus?

A

Decreased BP →decreased RBF → increased resorption of NaCl in the Loop of Henle →decreased delivery of NaCl to the macula densa

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45
Q

What are the 2 main effects of decreased macula densa [NaCl]?

A
  1. Dilation of afferent arterioles → raises glomerular hydrostatic pressure → increase GFR
  2. Increases renin release from the JG cells → AgII → constricts efferent arterioles
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46
Q

How do ACEi affect GFR?

A

ACEi block the action of Ang II = decreased GFR (inability to constrict efferent arteriole) = decreased renal perfusion in the face of systemic hypotension = can lead to ARF

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47
Q

How is Na reabsorbed in the proximal tubules?

A
  1. Na diffuses across luminal membrane (apical membrane) into cell down electrochemical gradient established by Na-K-ATPase pump (basolateral side of cell)
  2. Na transported across basolateral membrane AGAINST electrochemical gradient by Na-K ATPase
  3. Na, water, and others reabsorbed from interstitial fluid into peritubualr capillaries by ultrafiltration (passive process driven by hydrostatic and colloid osmotic pressure)
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48
Q

What are the 4 major transporters of glucose in the proximal tubules and where are they located?

A
  1. Sodium Glucose Co-Transporters (SGLT2 and SGLT1): Carry glucose
    • 90% filtered glucose is reabsorbed by SGLT2 in early part of proximal tubule (S1segment)
    • 10% transported by SGLT1 in later proximal tubular segments
  2. Glucose Transporters (GLUT2 and GLUT1): Glucose diffuse out of cells into interstitial space
    • GLUT2: S1 segment
    • GLUT1: S3 segment (later portion)
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49
Q

How is glucose reaborbed in the proximal tubules?

A

Secondary Active transport at apical membrane (via SGLT), passive facilitated diffusion at basolateral membrane (GLUT), and passive uptake by bulk flow at peritubular capillaries

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50
Q

How is water passively resorbed in tubules?

A
  1. Concentrations within renal interstitium HIGH = osmosis of water from tubular lumen into renal interstitium
    o Proximal tubule is HIGH permeability to water (also permeable to Na, Cl, K, Ca, Mg)
  2. Osmosis through tight junctions btwn cells and through cells
  3. As water moves through tight junctions (osmosis) it carries solutes = solvent drag
  4. Changes in Na reabsorption significantly influence water reabsorption (plus other solutes)
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51
Q

Describe the permeability of water in the tubular segments?

A
  1. Proximal tubule: HIGH water permeability
  2. Ascending Loop of Henle: LOW water permeability (despite large osmostic gradient)
  3. Distal tubules, collecting tubules, and collecting ducts: Can be HIGH or LOW (depends on ADH)
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52
Q

What organ makes aldosterone?

A

Zona glomerulosa cells (adrenal cortex)

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53
Q

Where is the site of action of aldosterone?

A

Principle cells of cortical collecting tubules = Stimulate Na-K ATPase pump (basolateral) and ↑ Na permeability on luminal side

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54
Q

What is the sitmulus for aldosterone secretion?

A

↑ Extracellular K and ↑ Angiotensin II (dt low Na or blood pressure)

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55
Q

What occurs with absent or excess aldosterone?

A

o Absence of Aldosterone (Addison’s): Marked loss of Na and accumulation of K
o Excess of Aldosterone (Conn’s): Na retention and ↓ K

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56
Q

What is the most powerful Na retainer?

A

Angiotensin II, caused by low BP, ECF volume (hemorrhage, vomiting, dehydration)

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57
Q

What are the 3 effects of angiotensin II?

A
  1. Stimulates aldosterone (↑ Na reabsoprtion)
  2. Constricts Efferent Arteriole: ↓ Peritubular capillary hydrostatic pressure (↑ net tubular reabsorption in PT) and ↓ renal blood flow = ↑ filtration fraction in glomerulus and ↑ concentration of proteins/colloid osmotic pressure in capillaries → ↑ Net reabsorptive force (more Na and water reabsorbed)

Helps to maintain excretion of waste products (urea and creatinine)
3. Directly stimulates Na reabsorption in PT, Loop of Henle, distal tubules and collecting tubules via Na-K ATPase (basolateral), Na-H exchanger (luminal, PT), and Na-bicarbonate co-transporter (basolateral)

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58
Q

What are the 3 sites of action of ADH?

A

Distal tubules, collecting tubules, collecting ducts (when no ADH = low peramebaility of water)

59
Q

How does ADH work?

A

o ADH binds to V2 receptors in the late distal tubules, collecting tubules, and collecting ducts → ↑ formation of cAMP (stimulatory G protein that activates adenylate cyclase) → stimulation of protein kinase A → Movement of intracellular proteins (aquaporin-2) to the luminal membrane
o Molecules of AQP-2 cluster together to fuse in cell membrane by exocytosis to form water channels = Rapid movement of water through cells
o When ADH low, AQP-2 shuttled back intracellularly = ↓ permeability of water

60
Q

What controls urine concentration?

A

ADH (Antidiuretic hormone)

61
Q

Where is ADH made?

A

Posterior pituitary gland

62
Q

When is ADH secreted?

A

o Osmolarity ↑ above normal → Posterior pituitary gland to release MORE ADH → ↑ permeability of distal tubules and collecting ducts to water (does NOT change the renal excretion of solutes)
o Excess water (↓ ECF osmolarity) → ↓ ADH secretion → permeability of water in distal tubules and collecting ducts = Large amount of DILUTE urine
o Thus rate of ADH secretion determines if dilute or concentrated urine

63
Q

How does urine appear concentrated with glucosuria?

A

↑ 0.001 USG for every 35-40mOsmol/L in urine osmolarity (can change with bigger molecules, like glucose = resulting in falsely concentrating urine with normal urine osmolatity)

64
Q

What are the 2 requirements for excreting concentrated urine?

A
  1. High Levels of ADH: ↑ permeability of distal tubules and collecting ducts to water (marked ↑ in water reabsorption)
  2. High Osmolarity of the renal medullary interstitium: Provides osmotic gradient for water reabsorption (with ADH present)
    o In collecting ducts, renal medullary interstitium is hyperosmotic → water moves into interstitium via osmosis → carried away by vasa recta into blood
    o Countercurrent Mechanism depends on special anatomical arrangement of the loops of Henle and vasa rectans that go deep into the medulla (25% in humans)
    o Juxtamedullary nephro
65
Q

What is the most important cause of solutes be trapped in renal medulla in the Loop of Henle?

A

Active transport of Na and co-transport of K, Cl, other ions out of thick ascending Loop of Henle into medulla; this selection is impermeable to water

66
Q

What is the countercurrent multiplier?

A

Countercurrent Multiplier = Repetitive reabsorption of NaCl by thick ascending Loop of Henle and continued inflow of new NaCl from the proximal tubule
o NaCl from ascending Loop of Henle keeps addings to newly arrived NaCl in medulla

67
Q

What are 3 disorders of urine concentrating ability?

A

o Inappropriate secretion of ADH
o Impairment of Countercurrent Mechanism: Regardless of ADH presence if degree of hyperosmolarity of medulla is low, can’t concentrate urine
o Inability of distal tubules, collecting tubules and ducts to respond to ADH

68
Q

What is central diabetes insipidus?

A

Failure to Produce ADH: “Central Diabetes Inspidius”
o No production or release of ADH from posterior pituitary = Large volumes of dilute urine
o Thirst mechanism activated to maintain body fluid, OK if water is not restricted, problem if so = dehydration
o Can give Desmopressin (synthetic analog of ADH) that selectively acts at V2 receptors in late distal and collecting tubules – can concentrate urine

69
Q

What is nephrogenic diabetes insipidus?

A

Inability of the Kidneys to Respond to ADH: “Nephrogenic Diabetes Inspidius”
o Renal tubular segments DO NOT respond to ADH OR failure of countercurrent mechanisms within medulla = Large volumes of dilute urine
o Ex renal diseases, loop diuretics, tetracyclines, etc
o When you give desmopressin = NO change

70
Q

What drives the thirst center?

A

Located in the third ventricle, preoptic nucleus = driven by changes in osmolarity of CSF and ECF
o If Na ↑ 2mEq/L above normal = thirst mechanism stimulated = Threshold of drinking

71
Q

What are the stimuli for thirst?

A

o ↑ ECF osmolarity – intracellular dehydration in thirst center = sensation of thirst
o ↓ ECF volume and ↓ arterial pressure (even if no change in plasma osmolarity): Neural input from arterial baroreceptor and cardiopulmonary reflexes
o Angiothensin II: Acts on subfornical organ and organum vasculosum of lamina terminalis (outside BBB)
o Dryness of mouth and mucous membranes of esophagus
o Gastrointestinal and pharyngeal stimuli influence thirst: Partial relief after drinking, GI distension (short-lived), helps to meter fluid intake to prevent overhydration

72
Q

What are the 2 mechanisms that regulate K+?

A
  1. Redistribution of intracellular/extracellular

2. Control of renal excretion

73
Q

What are factors that shift K+ into cells?

A

Decrease in Extracellular K+

  1. Insulin
  2. Aldosterone
  3. B-Adrenergic stimulation
  4. Alkalosis
74
Q

What are factors that shift K+ out of cells?

A

Increased in extracellular K+

  1. Insulin def (DM)
  2. Aldosterone def (Addison’s dz)
  3. B-adrenergic blockade
  4. Acidosis
  5. Cell Lysis
  6. Strenuous exercise
  7. Increase in extracellular fluid osmolarity
75
Q

What are the factors that affect renal K+ excretion?

A
  1. Rate of K+ filtration (based on GFR)
  2. Resorption of K+ by tubules
  3. K+ secretion by tubules
76
Q

How much of the filtered K+ is reabsorbed by the proximal tubule?

A

65%

Only 25% is resorbed in thick ascending LOH (with cotransport of Na/Cl)

77
Q

What is the main factor in daily variations in potassium excretion?

A

Secretion in late distal tubules and collecting ducts, NOT resorption in proximal tubule or LOH (these are constant)

78
Q

Which cells are responsible for K+ sercetion in the late distal tubules/collecting ducts?

A

Principal cells

79
Q

What are the 3 factors that regulate K+ secretion in the late distal tubules/collecting ducts?

A
  1. activity of Na/K ATPase
  2. K+ gradient
  3. permeability of luminal membrane for K+
80
Q

Which cells reaborb K+ when it is depleted?

A 
Intercalated cells (principal cells stop secreting K+)
K+/H+ ATPase (exchanger) = K+ reaborbed and H+ secreted
81
Q

What are the 2 major roles of aldosterone?

A
  1. Stimulates sercetion of K+ and resorption of Na+ in the principal cells (distal and collecting tubules) = via stimulation of N/K ATPase pump and increased permeability of the luminal membrane)
  2. Stimulates cellular uptake of K+
82
Q

What extracellular electrolyte stimulates aldosterone secretion?

A

Potassium

Small change in K+ can result in large increased in aldosterone

83
Q

How does insulin result in uptake of K+ by cells?

A

Insulin stimulates the Na/K ATPase on cells = Uptake of K+

Ensures that cells are taking up K+ when a person is eating

84
Q

What is the effect of alkalemia on K+?

A

Alkalemia = H+ leaves the cell and K+ enters the cell (H/K exchanger) = Hypokalemia

85
Q

What is the effect of acidemia on K+?

A

Acidemia = H+ enters the cell and K+ leaves the cell (H/K exchanger) = Hyperkalemia

86
Q

Why do acid-base disturbances NOT always cause K+ shifts?

A

Respiratory changes = Change in CO2 (not H+) and CO2 is lipid soluble and can diffusion across cell membrane within an exchange of K+
Metabolic acidosis = Organic acid (lactate) can enter cell with H+

87
Q

What is the major factor that determines K+ secretion in the kidney?

A

Size of the electrochemical gradient for K+ across luminal membrane
NOTE: Any factor that increases magnitude of gradient = Increases K+ secretion)

88
Q

How does aldosterone affect Na+ reabsorption?

A
  1. In principal cells induced sythesis of luminal Na+ channels and basolateral Na/K ATPase pumps
  2. As more Na is moved from lumen into cell there is more Na+ for the pumps to use and thus more K+ is pumped into cell
89
Q

On what cell type does aldosterone act in the kidney?

A

Principal cells!!

90
Q

How do loop diuretics and thiazide diuretics affect K+ levels?

A

These diuretics inhibits Na reaboprtion ““upstream”” of principal cells = Increased Na+ delivery to principal cells, which results in more Na+ resorbed and MORE K+ secreted
THUS K+ wasting!!! = Hypokalemia

91
Q

What is the mechanism of diuretic-induced hypokalemia?

A

Increased K+ excretion = Increased K+ secretion by the principal cells in the kidney
Increased flow rates = Which drive the luminal K+ gradient to favor K+ secretion
If loop diuretic: Inhibit N/K/.2Cl cotransporter in the thick ascending LOH = K+ NOT reaborbed here

92
Q

How do K+ sparing diuretics work?

A

Spironolactone

Inhibit ALL actions of aldosterone on principal cells = Inhibit K+ secretion = NO kaliuresis

93
Q

What are the 3 major why that PTH regulates calcium?

A
  1. Stimulates bone resoprtion of Ca
  2. Activates Vit D = Enhances intestinal Ca absorption
  3. Directly increases renal tubular Ca resorption in thick ascending loop and distal tubule
94
Q

What are the 2 main ways that Ca is excretion by the kidney?

A
  1. Filtered Ca
  2. Reabsorbed
    Ca is NOT secreted!!
95
Q

Where does resorption of Ca occur? How does it occur?

A 
65% = Proximal tubule
25%  = Thick ascending LOH
Rest = Distal tubule/collecting ducts
Majority = Paracellular (passive diffusion)
Some = Transcellular (Ca ATPase or Na/Ca countertransporter)
96
Q

PTH stimulates Ca reabsoprtion in which parts of the nephron?

A

Thick ascending LOH
Distal tubule/collecting ducts
NOT in the proximal tubule
Stimulated by low Ca+ and increased phosphorus

97
Q

What determines that rate of Ca reabsorption in the proximal tubule?

A

Parallels Na (PTH independent)

98
Q

Where in the nephron is Ca reabsoprtion not coupled to Na+?

A

Distal Tubule = Instead it is regulated by PTH (resulting in basolateral receptor that is regulated by cAMP)

99
Q

What is the major site of absorption of Mg in the nephron?

A

Thick ascending LOH (about 60%)

100
Q

How do loop diuretics affect Mg levels?

A

Since the major of Mg is reabsorbed in the thick ascending LOH, if a loop diuretic inhibits the Na/K/2Cl cotransporter = leads to no lumen + difference and thus Mg cannot be reaborbed = Increased Mg excretion = Hypomagnesemia

101
Q

What are the 2 mechanisms that PTH affects phosphorus homeostasis?

A

PTH increases bone resorption = More phosphate in plasma

  1. PTH decreased transport max for phosphorus = greater proportion lost in urine
  2. PTH causes INCREASED renal excretion of phosphorus
102
Q

What solutes contribute the the osmotic gradient in the medulla?

A
  1. Countercurrent multiplication (LOH - Deposits NaCl in deeper regions of kidney)
  2. Urea Recycling (inner medullary collecting ducts - deposit urea)
103
Q

What are the 2 steps in the countercurrent multilpication process?

A
  1. Single Effect: Function of thick ascending LOH, NaCl reabosrbed via Na/K/2Cl cotransporter, impermeable to water - diluting tubular fluid here. Na now in interstitial fluid (increased osmolarity), descending LOH permeable to water = Ascending limb decreased osmolarity, descending limb increased osmolarity. ADH increased acitvity of Na/K/2Cl co-transporter = Enhancing single effect! (good in dehyration)
  2. Flow of Tubular Fluid = fluid shifts from high osmolarity to low in the descending limb of LOH
104
Q

How does ADH level affect urea recycling?

A

Increased ADH (water deprivation) = increased inner medullary collecting ducts to water AND urea (contributing to corticopapillary osmotic gradient)

105
Q

What are the 3 major roles of ADH in the nephron?

A
  1. Increase water permeability of principal cells of late distal tubule and collecting ducts
  2. Increase activity of Na/K/2Cl co-transporter of thick ascending limb = enhancing countercurrent multiplication and osmotic gradient
  3. Increases urea permeability in inner medullary collectin ducts (not in others!) - enhancing urea recycling and osmotic gradient
106
Q

What type of urine is produced when ADH levels are high?

A

Hyperosmotic = concentrated urine

107
Q

What is an osmotic diuretic, and what is its MOA and tubular site of action?

A

Mannitol
MOA: Inhibits water and solute reabsoprtion by increasing osmolarity of tubular fluid
Site of Action: Mainly proximal tubules

108
Q

What is a Loop diuretic, and what is its MOA and tubular site of action?

A

Furosemide
MOA: Inhibits Na/K/2Cl co-transporter in luminal membrane
Site of Action: Thick ascending loop of Henle

109
Q

What is a thiazide diuretic, and what is its MOA and tubular site of action?

A

Hydrochlorothiazide
MOA: Inhibits Na/Cl co-transporter in luminal membrane
Site of Action: Early distal tubule

110
Q

What is a carbonic annydrase inhibitor, and what is its MOA and tubular site of action?

A

Acetazolamide
MOA: Inhibit H+ secretion and HCO3- reabsorption, which reduces Na+ reabsorption
Site of Action: Proximal tubules

111
Q

What is an K+ sparing diuretic, and what is its MOA and tubular site of action?

A

Spironolactone (aldosterone antagonists)
MOA: Inhibit action of aldosterone on tubular receptor = Decrease in Na+ reabsorption and decrease in K+ secretion
Site of Action: Collecting tubules

112
Q

What are the 3 primary lines of defense again pH change?

A
  1. Buffers: any substance that can reversibly bind H+ = prevent change in pH
  2. Respiration: removal of CO2 and carbonic acid (H2CO3) = seconds
  3. Kidneys: excrete alkaline or acidic urine (hours/days)
  4. Secretion of H+ (in all areas except thin limb of LOH)
  5. Reabsorption of filtered HCO3 (99% of filtered HCO3 is resorbed); for each HCO3- resorbed, a H+ must be secreted
     3. Production of new HCO3
113
Q

What are the kidneys 3 major roles in acid-base balance?

A

Kidneys: excrete alkaline or acidic urine (hours/days)
1. Secretion of H+ (in all areas except thin limb of LOH)

  1. Reabsorption of filtered HCO3 (99% of filtered HCO3 is resorbed); for each HCO3- resorbed, a H+ must be secreted
     3. Production of new HCO3
114
Q

What is the most important extracellular buffer system?

A

Bicarbonate buffer system

115
Q

What is the most important intracellular buffer system?

A

Phosphate buffer system

116
Q

How does respiratory system regulate acid-base balance?

A 
o Hyperventilation (increased alveolar ventilation) → increased expiration of CO2 → decreased pCO2, decreased [H+], increased pH (alkalosis)
o Hypoventilation → decreased expiration of CO2 → increased pCO2 → increased [H+], decreased pH (acidosis)
117
Q

What determines if urine is acidic or basic?

A

Balance btwn H+ secretion and HCO3- resorption

118
Q

What MUST HCO3 combine with in order to be resorbed? “”

A

H+

And H+ MUST be secreted in order for HCO3- to be resorbed!!

119
Q

What are the 3 processes of the kidney to regulate ECF [H+]?

A
  1. Secretion of H+
  2. Resorption of HCO3-
  3. Production of new HCO3-
120
Q

In what parts of the nephron do H+ secretion and HCO3- resorption NOT occur?

A

Descending limb and ascending thin LOH

121
Q

What parts of the nephron secrete H+ and resorbed HCO3-?

A

Proximal tubule (80-90%)
Thick ascending LOH (10%)
Distal tubule

122
Q

Where does active secretion of H+ occur in the nephron?

A

Intercalated Cells = Late distal tubule and collecting ducts

123
Q

How is “new” HCO3- produced in the kidney?

A

H+ combines with phosphate (NaHPO4- to yield sodium salt) and ammonia to generate “new” HCO3-

124
Q

What occurs in chronic acidosis with HCO3- production in the kidney?

A

Increase in ECG [H+] = Stimulates renal glutamine metabolism and increase in formation of HCO3- and NH4+ excretion

125
Q

How does the kidney try to correct for acidosis?

A

o Kidneys resorb ALL filtered HCO3- and contribute new HCO3- through formation of NH4+ and titratable acid
o Chronic acidosis: leads to increased production of NH4+ in tubules (from glutatmine metabolism)

126
Q

How does the kidney try to correct for alkalosis?

A

o Excess of HCO3- that cannot be resorbed from tubules →excreted into urine
o Loss of HCO3- is same as addition of H+ to ECF

127
Q

What are volatile acid and fxied acids in the body?

A

Volatile Acid = CO2
Fixed Acid = sulfuric acids (AA metabolism), phosphoric acid (phospholipid metbaolism), Beta-hydrozybutyric acid/acetoacetic acid (ketones), lactic acid, salicyclic acid (aspirin overdose), formic acid (methanol), glycolic/oxalic acid (eythlene glycol)

128
Q

In the proximal tubules what is Na+ reabsoprtion linked to?

A

Na+ reabsorption is linked directly to the reaboprtion of filtered HCO3-
The rest of Na+ linked to reabsoprtion of glucose, AA, Cl-, phosphate

129
Q

What is the net result of reabosption of HCO3- in proximal tubules?

A

HCO3- and Na+ reabsorption

NO NET secretion of H+

130
Q

What is contraction alkalosis?

A

When angiotensin II stimulates N/H exchange in proximal tubules, thus stimulating HCO3- reabsorption and increasing blood HCO3- concentrations
Metabolic alkalosis occurs secondary to ECF volume contraction that stimulates RAAS

131
Q

What is contraction alkalosis?

A

When angiotensin II stimulates N/H exchange in proximal tubules, thus stimulating HCO3- reabsorption and increasing blood HCO3- concentrations
Metabolic alkalosis occurs secondary to ECF volume contraction that stimulates RAAS

132
Q

What are the 3 segments of the nephron that participate in excretion of H+ as NH4+?

A

Proximal Tubules, thick ascending LOH, intercalated cells in collecting ducts

133
Q

How do plasma [K+] effect NH3 synthesis in the kidney?

A

Hyperkalemia INHIBITS NH3 synthesis and reduces ability to excrete H+ as NH4+ = Type 4 renal tubular acidosis (reults from K+ entering cell and thus H+ leaving cell = higher pH in cell inhits process)
Hypokalemia STIMULATES NH3 synthesis and increased ability to excrete H+ and NH4+

134
Q

With anion gap what are the measured cation and anions?

A

Cation: Na+
Anion: HCO3- and Cl-

135
Q

With anion gap what are the unmeasured anions?

A

Unmeasured anions: plasma proteins, phosphate, citrate, sulfate

136
Q

What is the equation for plasma anion gap?

A

Plasma anion gap = [Na+] - ([HCO3-] + [Cl-])

Plasma anion gap = unmeasured anions

137
Q

What is the equation for plasma osmolarity?

A

Plasma osmolarity = (2x Na+) + (glucose/18) + (BUN/2.8)

138
Q

What is the effect of Na+ on acid-base status?

A 
HypoNa+ = Acidifying
HyperNa+ = Alkalizing
139
Q

What is the effect of Cl- on acid-base status?

A 
HyperCl- = Acidifying
HypoCl- = Alkalizing
140
Q

What is the effect of proteins on acid-base status? What is the major protein?

A 
Hyperproteinemia = Acidifying
Hypoproteinemia = Alkalizing
Albumin = Negative charge
141
Q

What is the effect of phosphorus on acid-base status?

A 
Hyperphosphatemia- = Acidifying
Hypophosphatemia = Alkalizing
142
Q

Name 4 events that are considered to be alkalizing.

A
  1. Free water deficit (hyperNa+)
  2. Hypochloremia
  3. Hypoalbuminemia
  4. Increased unmeasured cations
143
Q

Name 6 events that are considered to be acidifying?

A
  1. Free water excess (hypoNa+)
  2. Hyperchloremia
  3. Hyperalbuminemia
  4. Hyperphosphatemia
  5. Hyperlactatemia
  6. Increased unmeasured anions

ACVIM Reading List (27 decks)

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