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Veterinary Physiology > Renal Physiology (Test 1 - Winter) > Flashcards

Renal Physiology (Test 1 - Winter) Flashcards

1
Q

Functions of the kidney

A

Excretion of metabolic waste products including endogenous organic compounds and exogenous compounds.

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2
Q

Name some endogenous organic compounds

A

Urea, creatinine, bilirubin, hormones, enzymes, vitamins, phenols, amines etc.

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3
Q

Name some exogenous compounds

A

Regulation of:
- Water, electrolytes, extracellular fluid volume
- Blood pressure
- Acid-base balance
- Plasma osmolality
- RBC production
- Vitamin D production

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4
Q

Uremia

A

Urine in the blood

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5
Q

Why is urea toxic?

A

Urea spontaneously dissociates to form cyanate, which reacts irreversibly with proteins and free amino groups in a reaction known as carbamylation

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6
Q

Common symptoms associated with renal dysfunction

A
  • Uremia
  • Azotemia
  • Hyperkalemia
  • Metabolic Acidosis
  • Hypocalcemia
  • Bradycardia
    Etc.
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7
Q

Path of blood into the kidney

A
  1. Renal artery
  2. Segmental artery
  3. Interlobar artery
  4. Arcuate artery
  5. Cortical radiate artery
  6. Interlobular aa.
  7. Afferent arteriole
  8. Glomerulus
  9. Efferent arteriole
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8
Q

Path of blood out of kidney

A
  1. Efferent arteriole
  2. Peritubular capillaries
  3. Venue
  4. Cortical radiate vein
  5. Arcuate vein
  6. Interlobar vein
  7. Renal vein
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9
Q

What is the functional unit of the kidney?

A

The nephron: glomerulus and tumulus system

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10
Q

How does the kidney help remove a substance from the body?

A

Excretion:
1. Filtration
2. Secretion
3. Reabsorption

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11
Q

Where does filtration take place?

A

Glomerulus
- Allows efficient and selective filtration

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12
Q

Pathway of filtration

A
  1. Afferent arteriole carries blood to the glomerulus
  2. Water and solutes cross the glomerular capillary wall into Bowman’s space—forming glomerular filtrate
  3. Filtered blood leaves the glomerulus via efferent arteriole
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13
Q

What is glomerular filtration rate (GFR)?

A

The volume of plasma filtered into Bowman’s space per unit time

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14
Q

3 variable determine the amount filtered:

A

A. Mean net filtration pressure
B. Area available for filtration
C. Permeability of the filtration barrier

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15
Q

Two forces favoring filtration:

A
  1. Hydrostatic pressure of the glomerular capillary (drives filtration)
  2. Oncotic pressure of filtrate in Bowman’s space (should be close to zero)
  • Proteins are NOT supposed to be in urine
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16
Q

Forces opposing filtration:

A
  1. Hydrostatic pressure of Bowman’s space
  2. Oncotic pressure of the blood
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17
Q

Vasoconstriction of afferent arteriole _____ filtration

A

Opposes

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18
Q

Increase in renal blood flow ______ filtration

A

Favors

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19
Q

Increase in hydrostatic pressure in Bowman’s capsule ______ filtration

A

Opposes

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20
Q

A urethral obstruction _____ filtration

A

Opposes

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21
Q

Large diameter of afferent arteriole _____ amount of filtrate

A

Increases

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22
Q

Small diameter of efferent arteriole _____ amount of filtrate

A

Increases

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23
Q

How is surface area increased for better filtration?

A

Mesangial cells contract and relax which affects capillary surface area and flow

Regulated by vasoactive substance

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24
Q

What makes up the filtration barrier?

A
  • Capillary endothelium
  • Basement membrane
  • Podocytes (visceral epithelium)
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25
Q

What forms the filtration barrier?

A

Bowman’s capsule
- Barrier is selectively permeable for molecules of a certain charge and size

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26
Q

How does molecule size affect filtration?

A

The bigger the molecule, the less it’s able to fit through the membrane and thus less likely to be filtered.

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27
Q

How does charge of a molecule affect filtration?

A

The more positive the charge, the more likely it is to be filtered/pass the membrane.

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28
Q

Why does the selective permeable glomerular capillary wall favor filtration of positively charge molecules?

A

Laminitis and fibronectin (glycoproteins) and peptidoglycans are part of the barrier and have a negative charge, which favors filtration of positively charged molecules

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29
Q

Glomerulus wall is permeable for molecules smaller than ____.

A

4 nm

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30
Q

What does freely filtered mean?

A

It means a molecule passes freely through the membrane. It does not get altered by filtration. Water and the substance are filtered in the same proportion.

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31
Q

What 2 molecules are freely filtered at equal concentrations?

A

Sodium and glucose concentrations are equal before and after filtration

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32
Q

Where and how much of water and solutes are reabsorbed?

A

85% is reabsorbed by proximal tubule and loop of henle?

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33
Q

How are filtered solutes and water reabsorbed?

A
  • Passive/Active
  • Primary active (ATP dependent)
  • Secondary active (dependent on gradient)
  • Antiporter/Exchanger (two solutes go in opposite directions)
  • Symporter/Co-transporter go in same direction)
  • Channels (aquaporins)
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34
Q

What is clearance?

A

The volume of plasma from which all of the substance (x) was removed and excreted in a given time

  • Sometimes, some substances are reabsorbed from the primary filtrate, some are neither reabsorbed or secreted, some are secreted into filtrate.
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35
Q

What does it mean if clearance = 0?

A

Substance will not appear in the urine (i.e. glucose)

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36
Q

What does it mean if clearance is at max?

A

Substance is removed on a single passage through the kidney.
- Examples: organic acids/bases like morphine

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37
Q

What does it mean if clearance is > 0 but < than max?

A

The volume cleared of X in a given time is less than total renal perfusion flow. Solute is not cleared on a single passage (the renal venous plasma still contains some X

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38
Q

How much blood reaches the kidneys at rest?

A

20% of cardiac output

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39
Q

What gets delivered to the cells of the nephron?

A

Oxygen, nutrients, and hormones

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40
Q

What is returned to general circulation after the nephron?

A

CO2 and reabsorbed fluid and solutes

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41
Q

What modifies the rate of solute and water reabsorption?

A

The proximal tubule

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42
Q

Are there differences in blood supply between cortex and medulla?

A

Yes, O2 rich blood arrives 1st to cortex.
Cortex has high level of O2 saturation.
Medulla is predisposed for O2 deficiency

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43
Q

What is renal failure (in general)?

A

A decrease in GFR.
- Most renal functions are compromised when GFR decreases

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44
Q

Examples of compromised renal functions:

A
  • Excretion of metabolic waste products
  • Regulation of water, electrolytes, and extracellular fluid volume
  • Regulation of blood pressure
    And more…
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45
Q

What determines glomerular filtration rate (GFR)?

A

Renal blood flow

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46
Q

How does K affect GFR?

A

K increases GFR when glomerular surface area increases as glomerular mesangial cells relax

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47
Q

How does Pgc (osmotic pressure of glomerular capillaries) affect GFR?

A

GFR increases when renal arterial pressure increases and arteriole dilates

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48
Q

How does Pbs (osmotic pressure in Bowman’s space) affect GFR?

A

GFR decreases when intratubular pressure increases (e.g. an obstruction)

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49
Q

How does (Pi)gc (oncotic pressure in glomerular capillaries) affect GFR?

A

GFR decreases when systemic plasma oncotic pressure is increased

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50
Q

What causes a drop in plasma oncotic pressure?

A

Anything that leads to a drop in plasma proteins
Ex: liver disease/hypalbuminemia

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51
Q

Relationship between oncotic pressure and GFR

A

Decrease in arterial plasma protein concentrations decreases arterial oncotic pressure which increases GFR

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52
Q

Hydrostatic pressure in the glomerular capillary

A
  • Changes little.
  • Small resistance to blood flow
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53
Q

Oncotic pressure in the glomerular capillary

A
  • Opposes filtration and increases as fluid is removed from capillaries while large proteins remain behind
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54
Q

True or False: Protein concentration decreases from afferent end to efferent end of glomerular capillary.

A

False: it increases as water is removed and proteins are left behind in capillary

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55
Q

What is the most important factor for favoring filtration?

A

Plasma concentration in the GC.
- Renal arterial pressure increases and afferent arteriole dilates

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56
Q

Factors that affect contraction of a/efferent arteriolar resistance

A

Sympathetic nerves
Angiotensin II

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57
Q

Factors that affect relaxation of a/efferent arteriolar resistance

A

PGE2
PGI1

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58
Q

True or False: MAP fluctuates with physiological conditions and disease majorly affecting GFR

A

False: GFR is tightly controlled and maintained within limited ranges

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59
Q

What happens if GFR becomes too low?

A

The excretion of waste products will be insufficient

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60
Q

What happens if GFR becomes to high?

A
  • Tubules might be overwhelmed with salt/water reabsorption.
  • High vascular pressure could cause hypertensive damage (atrophy)
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61
Q

What does dilation of the afferent arterioles do?

A

Raises hydrostatic pressure in glomerular capillaries and GFR

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62
Q

What does constriction of the afferent arteriole do?

A

Decreases hydrostatic pressure in glomerular capillaries and GFR

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63
Q

What does dilation of the efferent arteriole do?

A

Lowers hydrostatic pressure in glomerular capillaries and GFR

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64
Q

What if afferent and efferent arteriolar resistance change in the same direction?

A

Exert opposite effects on hydrostatic pressure in glomerular capillaries and GFR

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65
Q

Autoregulatory mechanisms to keep RBF & GFR within a limited range?

A

Myogenic response
Tubulo-glomerular feedback

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66
Q

Other mechanisms to keep RBF & GFR in a limited range?

A

Prostaglandins
Hormones (Angiotensin II, ANP, Dopamine)
Sympathetic Innervation

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67
Q

What is the point of the autoregulatory/other mechanisms?

A

Prevent large changes in GFR in the face of changes in arterial pressure. They preserve GFR a healthy GFR and prevent hypertensive damage.

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68
Q

What is the myogenic response?

A

Contraction/relaxation of arteriolar smooth muscle in response to changes in vascular pressure

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69
Q

True or False: Myogenic response downregulates RBF and thereby returns GFR to normal levels.

A

True :)

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70
Q

True or False: The myogenic response is slow process.

A

False: From 0 to constricted in under 10 seconds

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71
Q

True or False: While the myogenic response accounts for about 50% of the total regulatory capacity of renal vessels, tubuloglomerular feedback accounts for the other 50%.

A

True!!

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72
Q

What is the juxtaglomerular apparatus?

A

Specialized structure formed by distal convoluted tube and glomerular afferent arteriole.

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73
Q

Macula densa in the juxtaglomerular apparatus

A

The cells sense delivered salt load in the tubular lumen

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74
Q

What component of tubular fluid is sensed in TGF?

A

Na and Cl

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75
Q

What vasoactive substances are secreted in TGF?

A

Adenosine: via a paracrine mechanism affect smooth muscles of arteriole and granular cells
- Afferent tone increases for as long as mediator is present
- Renin production/secretion is decreased

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76
Q

True or False: TGF is a positive feedback mechanism.

A

False: Negative feedback.
- Net effect: increased salt delivery to the nephron results in decreased glomerular blood flow, which decreases salt delivery

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77
Q

What would happen if autoregulation fails?

A

Afferent arteriole does not constrict –> Renin increase –> tubule damage

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78
Q

What two prostaglandins vasodilate the afferent arterioles primarily?

A

PGE2 & PGI2

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79
Q

Where are prostaglandins produced?

A

Within the kidney

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80
Q

How are prostaglandins stimulated?

A

Synthesis and release stimulated by increased renal sympathetic nerve nerve activity AND increased levels of angiotensin II.
*thought to modulate effects of vasoconstrictors to reduce possibility of ischemic damage

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81
Q

If a patient is on NSAIDs too long, what is the affect?

A

Medullary hypoxic injury

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82
Q

Are hormones (angtiotensin II, ANP, dopamine) vasodilators or vasoconstrictors?

A

Vasoconstrictors of efferent arteriole.

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83
Q

What 3 renal structures are innervated by autonomics?

A
  1. Afferent arteriole
  2. Collecting duct
  3. Juxtaglomerular apparatus
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84
Q

Autonomic innervation affects on afferent arteriole

A

1.Norepinephrine causes vasoconstriction
2. Increased afferent sympathetic nerve activity decreases RBF and GFR

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85
Q

Autonomic innervation affects on collecting duct

A
  1. Norepinephrine increases sodium and potassium exchange
  2. Increases Na reabsorption and water retention
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86
Q

Autonomic innervation affects on juxtaglomerular apparatus

A
  1. Norepinephrine stimulates renin release
  2. activates RAAS
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87
Q

True or False: Sympathetic stimulation of the kidneys is important to maintain GFR during emergencies.

A

True: Like during hypovolemic shock

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88
Q

What is GFR?

A

The volume of plasma filtered into Bowman’s space in a given time (ml/min)

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89
Q

What is clearance?

A

The volume of plasma from which all of the substance is removed and excreted in a given time.

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90
Q

If a substance is reabsorbed, it goes where?

A

From the tubules to the vasculature.

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91
Q

True or False: If a substance is secreted, it goes from the vasculature to the tubules and out the urine.

A

True!!

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92
Q

True or False: Some substances are freely filtered but not reabsorbed/secreted, thus they can be used to calculate GFR.

A

True: example-inulin

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93
Q

What substance is freely filtered, secreted but mostly (99%) reabsorbed?

A

Sodium!!

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94
Q

What is creatinine?

A

Waste product formed in muscle from creatine phosphate.
Creatine synthesized by liver, kidney, pancreas, and used in brain and muscle.

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95
Q

True/False: Creatinine is synthesized at a constant rate and is produced 2x greater than muscle mass.

A

False: It is produced proportional to muscle mass.

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96
Q

What percentage of creatinine is filtered at the glomerulus?

A

About 15-20%.
*Similar to GFR

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97
Q

Why does creatinine excretion increase if plasma creatinine concentration increases?

A

(Creatinine increases with diet, exercise etc.)
GFR remains constant thus creatinine excretion increased because more creatinine is filtered

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98
Q

Why does creatinine clearance remain the same as plasma concentration goes up?

A

B/c GFR remains constant so clearance doesn’t change.

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99
Q

True/False: Creatinine clearance changes when GFR changes.

A

True!

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100
Q

Creatinine clearance tends to be an ____ estimation of GFR because _____.

A

Over; it is secreted to a small extent in the proximal tubule

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101
Q

What substance is a GFR marker used in vetmed?

A

Iohexol.
Test:
1. 12 hours fasting
2. 300mg/kg administered IV
3. Blood samples @ 2, 3, 4 hours later
4. Measurement of iohexol concentrations
5. GFR calculated using tables

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102
Q

What is BUN?

A

Blood urea nitrogen.
- The amount of nitrogen derived from urea

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103
Q

True or False: Urea constitutes about 75% of usual solute content of urine.

A

False: About half.

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104
Q

How does urea plasma concentration change with GFR changes?

A

As GFR decreases, plasma concentration increases

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105
Q

How does the kidney handle urea?

A

Freely filtered by glomerulus. Reabsorbed in tubular system. About 1/2 filtered load is excreted.

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106
Q

When do BUN and creatinine begin to rise in plasma?

A

When kidneys have lost OVER HALF of their original filtering

107
Q

What is a more sensitive marker for kidney distress than BUN/creatinine?

A

SDMA

108
Q

True/False: SDMA is less impacted by extrarenal factors (body condition, advanced age, disease state, etc.)

A

True: Its specific for kidney function

109
Q

Primary source of SDMA?

A

Nucleolar proteins

110
Q

Where is SDMA mainly excreted?

A

Urine!

111
Q

True or False: Reabsorption and secretion of filtered substances is the same amongst all the segments of the renal tubule.

A

False: They are different amongst the different segments because there are differences in permeability and in profiles of transporters/channels.

112
Q

Apical channels in proximal tubule

A
  • SGLT-1/2: transports glucose with Na
113
Q

Basolateral channels in proximal tubule

A
  • Na/K ATPase: transports Na/K
  • Glut 1/2: Glucose channel (passive)
114
Q

How much water is reabsorbed in the proximal tubule and descending limb-LOH?

A

80% of water
- Reabsorbed through paracellular pathway and via aquaporins

115
Q

Where is about 30% of the NaCl filtered by the glomerulus reabsorbed?

A

Ascending limb of LoH via NKCC-2

116
Q

True or False: Thick ascending limb is water impermeable.

A

True

117
Q

How does the NKCC-2 transporter work?

A

Na, K, Cl cotransporter via secondary active. Na gradient is the driving force on the apical membrane

118
Q

How is NaCl reabsorbed in the distal convoluted tubule?

A
  • NCC co transporter for Na, Cl - secondary active
  • Na/K ATPase pump removes Na
119
Q

Why is the collecting duct important?

A

It plays an important role in adjusting final urine composition.

120
Q

Aquaporins in the collecting duct

A

Reabsorb water
Hormone dependent

121
Q

ROMK in the collecting duct

A

Secrete K
Principle cells
Linked to reabsorption of Na

122
Q

ENaC in the collecting duct

A

Na channel reabsorbs Na
Principle cells
Linked to secretion of K

123
Q

K/H-ATPase in collecting duct

A

Exchange of K and H
Intercalated cells

124
Q

Pendrin in the collecting duct

A

Exchange of Cl and HCO3
Intercalated cells

125
Q

Freely filtered plasma constituents

A

Glucose, Water, Sodium, Creatinine

126
Q

Where does glucose/amino acid reabsorption take place?

A
  • Proximal tubule
  • Apical membrane: sodium dependent transporters SGLT1/2
  • Basolateral membrane: passive diffusion and facilitated diffusion
127
Q

Na-Glc co-transport on apical membrane

A

Glucose reabsorbed from lumen of nephron back into cells of PT by secondary active, linked to sodium ions

128
Q

Facilitated diffusion of glucose on the basolateral membrane

A

Glucose diffuses from inside PT cells into interstitial space through proteins located in basolateral membrane

129
Q

Diffusion of glucose into capillary driven by oncotic pressure

A

Glucose pulled into porous peritubular capillaries by solvent drag driven by protein oncotic pressure

130
Q

What is the tubular maximum (TM)?

A

Maximum rate of reabsorption that is reached when all membrane transport proteins are saturated.
- Mainly found in proximal tubule

131
Q

What happens below TM?

A

Filtered load is reabsorbed

132
Q

What happens above TM?

A

Filtered load is excreted

133
Q

Flux of mediated transport is determined by?

A
  1. # of binding sites (total number of protein carriers and their binding sites is limited)
  2. # of transport molecules
  3. Rate of transport
134
Q

True or False: Bicarbonate moves across the membrane easily.

A

False: it is broken down to move across and then resynthesized back into bicarb

135
Q

Reabsorption of bicarbonate in the kidney?

A
  • Proximal tubule
  • Apical membrane: Sodium dependent transporters removes proteins (NHE3)
  • Na/H exchange depends on activity of carbonic anhydrase
  • CO2 can move into epithelial cells via transmembrane diffusion or AQP1
136
Q

Reabsorption of Na in PT

A

Sodium dependent solute transporter
- glucose, AA, citrate, phosphate, sulfate
- Na/H exchanger

137
Q

Reabsorption of Na in LoH

A

NKCC-2 co transporter in apical membrane
*not associated with water!! Causes dilution

138
Q

Reabsorption of Na in DCT

A

NCC co transporter
*not associated with water!! Causes dilution

139
Q

Reabsorption of Na in CD

A

ENaC promotes sodium uptake

140
Q

True or False: Na/K ATPase is present in basolateral membrane in epithelial cells of all segments

A

True!!

141
Q

Potassium in the kidney

A

The body stores K in every cell so potassium levels in kidney aren’t as important. More used for transporting.
- To some extent low K diet or K loss can trigger its reabsorption

142
Q

Potassium secretion in CD (principle cells)

A

Apical K-channel (ROMK) facilitate secretion

143
Q

Potassium secretion in DCT and CD (intercalated cells)

A

K can be reabsorbed in exchanged for H by an ATP-dependent pump

144
Q

Reabsorption of chloride

A

Occurs in all segments of the nephron!
- Paracellular (through tight junction) pathway
- Transcellular mechanisms

145
Q

What occurs during paracellular pathway

A

1.Water is taken up w/ glucose, AA, Na, HCO3
2. Increases chloride concentration –> creates chemical gradient for Cl
3. Cl moves from tubule lumen toward basolateral space

146
Q

What are Cl transcellular mechanisms?

A

Cl coupled transporters and Cl channels
Ex: pendrin, NCC, NKCC-2

147
Q

Factors that upregulate phosphate transporter expression

A

Dietary phosphate deficiency, TH, IGF

148
Q

Factors that downregulate phosphate tranporter expression

A
  • PTH: secreted by parathyroid; secreted in response to low blood serum calcium levels
  • Dietary potassium deficiency, metabolic acidosis, high phosphate diet, estrogen, glucocorticoids
149
Q

Reabsorption of Urea

A
  • In PT and LoH by simple diffusion
  • in CD: approx. 50% by urea transporter
  • urea accumulates in inner medulla (to establish high concentration)
150
Q

Reabsorption of water

A

50-80% in PT and LoH
- follows the solute concentration gradient
- CD paracellular uptake and aquaporin
- LoH TAL & DCT are water impermeable

151
Q

Secretion of Organic Anions

A

2 main transport mechanisms in PT:
- 1 for organic cations
- 1 for organic anions

152
Q

Organic compounds secreted

A
  • metabolites, waste products, foreign chemicals (“tagged” by liver), penicillin, morphine
153
Q

Carbonic anhydrase inhibitor diuretics

A

Na/H exchange blocked
- Blocks Na reabsorption in PT

154
Q

Loop diuretic

A

Main target: NKCC2 in TAL of LoH
- 30% of the filtered sodium chloride is reabsorbed

155
Q

Thiazide diuretics

A

Inhibit NCC in DT

156
Q

Potassium-sparing diuretics

A

Blocking ENaC in CD reduces sodium uptake and potassium secretion

157
Q

What is the purpose of diuretics?

A

Prevents the sodium absorption therefore reducing water reabsorption

158
Q

Osmotic diureses

A

Loss of water and electrolytes in urine
- Urine production increases as a result of the osmotic diuretic effect of glucose (appearing in urine)

159
Q

Factors causing fluid deficiency

A
  1. Volume depletion (hypovolemia)
  2. Dehydration
  3. Most serious effects (circulatory shock, neurological dysfunction)
160
Q

Factors causing fluid excess

A
  1. Volume excess
  2. Hypotonic hydration
  3. Most serious effects (pulmonary and cerebral edema
161
Q

What is volume depletion?

A

Total water reduced, osmolarity normal
- Hemorrhage, severe burns, chronic vomiting/diarrhea

162
Q

What is dehydration?

A

Total body water decreases, osmolarity rises
- Lack of drinking water, diabetes, profuse sweating, diuretics
- Affects all fluid compartments

163
Q

True/False: Species with high metabolic rate are less vulnerable to dehydration.

A

False: More vulnerable b/c high metabolic rate demands high excretion rate of urea waste

164
Q

What happens with volume excess?

A

Both Na and water retained
ECF isotonic
Aldosterone hypersecretion

165
Q

What happens with hypotonic hydration?

A

More water than Na retained or ingested
ECF hypotonic
Can cause cellular swelling

166
Q

Renal response to fluid deficiency

A

Kidneys excrete concentrated urine

167
Q

Renal response to fluid excess

A

Kidneys excrete diluted urine

168
Q

Water balance intake vs losses

A

Intake: food/drink & metabolic water
Losses: skin, lungs, GI, kidneys, milk

169
Q

True/False: A hypertonic medullary interstitial space is needed to form concentrated urine.

A

True

170
Q

2 mechanisms to draw water out of descending limb and maintain medullary hypertonicity

A
  1. Urea accumulation in inner medulla & NaCl accumulation in outer medulla
  2. Variable water and salt permeability in LoH: Descending limb reabsorbs water; AL water impermeable but NaCl is reabsorbed
171
Q

Urea recycling steps

A
  1. Medullary osmotic gradient in inner medulla is mostly urea
    - Filtered urea is reabsorbed in the CD via transporters (UT-A1, UT-A3)
    - Also a recycling process: returns from vasa recta to tubule lumen into thin limbs
  2. Hypertonic interstitium allows water to be reabsorbed from the thin DL LoH and CD
172
Q

NaCl reabsorption by ascending limb LoH

A
  • Outer medulla = mostly NaCl (creates medullary osmotic gradient)
  • Water impermeable but not to Na
  • Sodium drawn into interstitium due to Na concentration gradient and by secondary active
  • Equilibrium occurs by diffusion of NaCl from tubule fluid into interstitium
  • NKCC transporter
173
Q

True/False: Active sodium reabsorption by the TAL is critical for the osmotic gradient

A

True

174
Q

How does osmolarity change through the LoH?

A
  1. Isosomotic from PT into DL LoH
  2. Flows from low osmolality to high = water is drawn into hypertonic medullary interstitial space in DL LoH
  3. Tubule fluid in LoH equilibrates with hypertonic interstitial fluid and becomes more concentrated
  4. In TAL, tubule osmolarity decreases because NaCl leaves via NKCC
  5. Tubule fluid becomes less concentrated
175
Q

If water is reabsorbed in TDL-LoH, shouldn’t that produce a more dilute medullary interstitial space?

A

No, b/c water is quickly reabsorbed in the vasa recta.
- There is an increase in oncotic pressure so increase in water uptake

176
Q

Effects of countercurrent exchange mechanisms in the vasa recta to maintain hypertonicity in the medullary interstitial space

A
  1. Prevents dissipation of the medullary concentration gradient
  2. Net removal of water due to low hydrostatic pressure but high oncotic pressure in vasa recta
177
Q

Water permeability of the CD is determined by?

A

Antidiuretic hormone (ADH) aka vasopressin
- Level of available ADH determines the osmolality of excreted urine

178
Q

Water overload = ADH is ____

A

Absent; urine is dilute

179
Q

Dehydration = _____ levels of ADH

A

Raised; urine is concentrated

180
Q

How much can urine be concentrated?

A

Depends on the tonicity of the renal medulla and on the waste load
*Max urinary concentration is species specific

181
Q

What happens to urine concentration if GFR increases more than normal?

A

GFR increases –> ultrafiltrate increases = limited uptake of solutes (pressure diuresis)

182
Q

What happens if medullary hypertonicity is disturbed?

A

Less water reabsorption b/c Na stays in ultrafiltrate = lower tonicity of inner medulla
*same effect of diuretics

183
Q

What is ADH?

A
  • Peptide hormone produced by neurons of the supraoptic nucleus in hypothalamus and released by posterior pituitary
184
Q

Release stimuli and inhibition of ADH

A

RS: hypertonicity monitored by hypothalamus; pressure monitored by atrial and pulmonary receptors
I: ethanol, ANP, cortisol

185
Q

Function of ADH

A
  1. Stimulate kidneys to reabsorb solute-free water from the tubules of the nephron and return it to circulation (normal tonicity)
  2. Vasoconstriction (raise BP)
  3. Effects in brain affecting behavior (thirst)
186
Q

What is RAAS?

A

Renin Angiotensin Aldosterone System
- Activated in response to a decrease in circulating blood volume causing reduced RBF

187
Q

What does renin catalyze?

A

Angiotensin I in the liver & AII in the lungs

188
Q

Angiotensin II has direct intrarenal effects

A
  1. vasoconstriction of efferent arteriole
  2. increased Na absorption in PT, TAL, DCT, CD; stimulates NHE, NCC, ENaC
189
Q

Angiotensin II had extrarenal effects

A
  1. Stimulates release of aldosterone from adrenal gland
  2. Cardiac output, vasoconstriction –> increase BP
    Etc.
190
Q

Aldosterone effects in kidney

A

Stimulates Na reabsorption in DCT and CD; more sodium reabsorption = more water retention

191
Q

Sympathetic nervous system on kidney

A

Adrenoreceptors on renal vasculature, nephrons, and PTs contribute to vasoconstriction, sodium reabsorption, glycogenesis, production of prostaglandins

192
Q

Homeostatic mechanisms of the body monitor and maintain ___ & ____

A

tonicity & volume

193
Q

What is the main goal of regulating sodium and water?

A

Support requirements of the cardiovascular system:
1. keep osmolality of ECF at levels consistent with cell health
2. maintain ECF volume to fill vascular space

194
Q

What monitors changes in tonicity?

A

Osmoreceptors located in the hypothalamus.
- Increased activity of osmosreceptors stimulates ADH synthesis and release

195
Q

Where is ADH produced?

A

Supraoptic nucleus neurons in hypothalamus and released by posterior pituitary

196
Q

What happens to osmoreceptors when there is a increased solute concentration of interstitial fluid?

A

They lose water and shrink in size.
- Consequence is a change in firing rate causing ADH neurons to release ADH

197
Q

ADH levels increase with?

A

Plasma sodium concentration causing urine osmolality to increase up to a urine concentration max

198
Q

What happens to water intake after the urine is maximally concentrated?

A

Water intake is mediated by thirst

199
Q

How does ADH stimulate water reabsorption in CDT, CD?

A
  • ADH binds to V2 receptor stimulating movement of AQP to apical membrane.
  • Water moves into blood
200
Q

What monitors a change in blood volume?

A

Baroreceptors located in the carotid sinus and aortic arch

201
Q

How do baroreceptors release ADH?

A

They must be suppressed, which comes after a fall in blood pressure

202
Q

True or False: A fall in mean arterial pressure causes ADH to be produced.

A

True

203
Q

How does the RAAS defend agains ECF volume loss?

A

Aldosterone stimulates Na reabsorption in DCT and CD in principle cells by inducing EnaC and Na/K ATPase
*More Na –> More water retained –> increased BP

204
Q

Hyposthenuria

A

USG is reduced (urine is diluted more than plasma)

205
Q

Isothenuria

A

Same as protein-free plasma; neither concentrated nor diluted; ability of kidneys to concentrate urine is compromised

206
Q

Hypersthenuria

A

USG is increased; water deprivation, ADH needed

207
Q

Primary hyperaldosteronism

A

Adrenal disorder characterized by excessive, independent, non-suppressible secretion of aldosterone

208
Q

Secondary hyperaldosteronism

A

Low blood circulating volume or low BP
Ex: cardiac failure; obstructed renal artery

209
Q

What is atrial natriuretic peptide (ANP)?

A

A polypeptide produced by muscle cell in the atria
- Released when sodium levels increase
- Inhibited by low sodium levels

210
Q

What is the function of ANP?

A

Stimulate kidneys to increase Na excretion
1. Vasodilation of afferent arterioles/relaxation of mesangial cells
2. increased capillary permeability
3. renin secretion inhibition

211
Q

What is erythropoietin?

A

A glycoprotein produced by interstitial cells in the cortex peritubular capillary bed.
Released: hypoxia
Inhibited: normal oxygen saturation
Function: increases number of Epo-sensitive stem cells in the bone marrow that are converted to RBC precursors

212
Q

True or False: Potassium from the ECF is a good measure of total body K.

A

False: Most of K is stored in cells so a patient can be hyperkalemic and still be depleted of total body K

213
Q

T/F: Small shifts of K in or out of cell can lead to large change in ECF concentration

A

True

214
Q

How does a K-rich meal affect ECF [K]?

A

If not moved to ICF, K is taken up by cells during meals affecting muscle tissue, insulin, and epinephrine

215
Q

How do kidneys handle potassium?

A
  • Freely filtered in glomerulus
  • 90% absorbed in PT & TAL
  • Paracellular diffusion driven by electrical gradient
  • Active transport coupled to other ions (Na)
216
Q

Why is uncontrolled, sustained high blood pressure is a strong risk factor for chronic kidney disease?

A

Causes hypertensive damage:
a. Loss of individual nephrons (pressure atrophy)
b. sclerosis and enlarged arterioles in the glomerulus (modifies tissues)

217
Q

Hypertensive damage to vessels

A

They become thick, stiff, and unable to dilate/constrict

218
Q

Hypertensive damage to the nephrons

A

Kideny tissue in medulla begins to “starve” for oxygen and nutrients causing nephrons to shrink and harden –> fibrosis

219
Q

A high K diet suppresses NCC activity meaning:

A
  • More Na is delivered to the collecting duct
  • Natriuresis
  • Kaliuresis
  • reduced BP
220
Q

Potassium vs. Sodium deficiency

A
  • Volume depletion = NaCl retention is stimulated w/ minimal K secretion
  • Hyperkalemia = K secretion is maximized without Na retention
221
Q

Thiazide effect on K

A

decreases NaCl cotransport in DCT causing hypokalemia

222
Q

Loop diuretics effect on K

A

Blocks NKCC in LoH causing hypokalemia

223
Q

Potassium sparing effect on K

A

Blocks ENaC in CD causing hyperkalemia

224
Q

Why should a starving animal be refed slowly?

A

A fatal shift in fluids in electrolytes can occur due to insulin increasing Na/K ATPase activity.
- Uptake of K into muscle cells decreases membrane potential which can lead to irregular heartbeat

225
Q

Phosphate in the kidney

A
  • Reabsorbed in PT regulated by PTH which determines abundance of Na-dependent phosphate transporters
  • High PTH = fewer Na-dependent transporter
  • PTH controlled by free Ca in blood (low Ca stimulates PTH release)
226
Q

Calcium in the kidney

A
  • Reabsorption 65% in PT (passive)
  • 20% TAL (passive)
  • 10% DCT (active: Ca-ATPase)
  • Low PTH increases –> stimulates Ca channel
  • VitD vital for transcellular transfer of Ca
227
Q

pH equation

A

-log10[H] = log10(1/[H])

228
Q

Relationship between [H] and pH is _____ and _____.

A

Inverse and nonlinear

229
Q

Alkalemia

A

arterial blood pH > 7.45

230
Q

Alkalosis

A

excess removal of H

231
Q

Acidemia

A

arterial blood pH < 7.35

232
Q

Acidosis

A

excess addition of H

233
Q

Metabolism of carbohydrates and fats are considered ________ acids.

A

Volatile

234
Q

What are non-volatile (fixed) acids?

A

Metabolism of protein and phospholipid
- have to be dissolved in water
- removed by other means

235
Q

What is the purpose of a buffer?

A

Resists a change in pH; can accept or donate hydrogen ions and minimize change in pH
- Weak acids/bases act as buffers

236
Q

Bicarbonate as a buffer

A

*most important
- pK is low (6.1)
- effective due to its concentration and b/c both acid (CO2) and base (HCO3-) are regulated

237
Q

Hemoglobin as a buffer

A

Imidazole groups on histidine and AA groups are primary buffer sites on all proteins

238
Q

Minor extracellular/blood buffers

A
  1. Proteins: physiological pKs (6.4-7.9) but concentrations are low
  2. Phosphate: not important in blood due to low concentration; very important in urine
239
Q

Intracellular buffers

A
  1. inorganic/organic phosphate, proteins
  2. bone
240
Q

Relative importance of a given buffer depends on:

A
  1. its concentration
  2. its pK
  3. the prevailing [H]
241
Q

True or False: Buffers help to minimize the pH change and returns pH to normal

A

False: buffers do not return pH to normal

242
Q

Respiratory disturbances to pH

A

Changes in CO2 levels are respiratory disturbances and must be compensated for by kidney if lungs can’t

243
Q

Metabolic disturbances to pH

A

Changes in bicarb. Loss or gain can be compensated for by both kidneys and the lungs

244
Q

What receptors monitor CO2 and pH?

A

Brainstem receptors

245
Q

What are peripheral receptors?

A

Carotid and aortic bodies monitor O2, CO2, and pH

246
Q

When do glomus cells depolarize?

A

When oxygen tension and/or pH decreases; or CO2 increases

247
Q

How do central chemoreceptors monitor CO2/pH?

A

CO2 diffuses across BBB, exerts its main effects on breathing via increasing [H] in brain interstitial fluid activating chemoreceptors

248
Q

Bicarbonate reabsorption

A
  • Freely filtered, shows up in filtrate
  • H secretion in PT
  • Net absorption of filtered bicarb
  • Dependent on activity of CA in the cell
249
Q

How do kidneys excrete an acid load?

A
  1. Bicarbonate reabsorption
  2. Titratable acidity
  3. Ammoniagenesis and NH4 excretion
  4. Bicarb secretion if available in excess
250
Q

Ammoniagenesis and NH4 excretion summary

A
  1. The kidney metabolizes glutamine
  2. NH4 is either excreted or returned to blood
  3. HCO3 is returned to the blood
251
Q

How do kidneys excrete a base load?

A

Bicarbonate secretion if available in excess

252
Q

Purpose of blood gas analysis

A

Gas analyzer reports pH and Pco2
- Helps evaluate underlying disease

253
Q

Steps to interpret the arterial blood gas

A
  1. Look at pH
  2. Look at pCO2 and [HCO3-]
    a. distinguish the initial change from compensatory response
    b. identify the specific disorder
  3. Acute or chronic?
  4. Anion gap
  5. Compensation adequate?
254
Q

Response to fixed acid load

A
  1. W/in min: H ions titrate bicarb ion in ECF, then intracellular buffers
  2. Min-hrs: alveolar ventilation is stim, Pco2 decreases ratio of [HCO3-] and Pco2 normalized
  3. Hrs-days: kidneys regenerate titrated [HCO3-], excrete TA and NH4
255
Q

Response to volatile acid load

A
  1. w/in min: H+ titrate intracellular buffers
  2. Hrs-days: increased renal [HCO3-] reabsorption and net acid excretion
256
Q

What is law of mass action?

A

When Pco2 changes, it causes a small change in [HCO3-] due to mass action

257
Q

What is the anion gap?

A

Difference between commonly measured plasma cations (Na, K) and anions (Cl, HCO3)
- (Na + K) - (Cl + HCO3)
*Useful information in differential diagnosis of metabolic acidosis

258
Q

Hyperchloremic metabolic acidosis w/ normal anion gap

A

Cl increases to meet the drop in HCO3 and therefore maintains balance

259
Q

Normochloremic metabolic acidosis w/ increased anion gap

A

Gap increases in acidosis where there is an excess of unmeasured acids

260
Q

True or False: Fixed acids liberate H which is buffered by HCO3 w/o changing Cl levels

A

True: increases the anion gap

261
Q

Uncompensated disturbance

A
  • Defect in [HCO3] OR Pco2
  • no change in other parameter
262
Q

Simple disturbances with compensation

A
  • defect in [HCO3] OR Pco2
  • other parameter is compensating (moving in same direction)
263
Q

Mixed states of compensation

A
  • Both [HCO3] and Pco2 are contributing to the acid/base disturbance
  • [HCO3] and Pco2 move in opposite directions

Veterinary Physiology (8 decks)

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