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T1 - Integrated (Full Review) > Physiology - Pulmonary / Renal Block (II) > Flashcards

Physiology - Pulmonary / Renal Block (II) Flashcards

1
Q

A 20-year-old, unresponsive woman is brought to the ED with respiratory distress after ingesting ‘ecstasy’ and subsequently drinking large amounts of fluid.

Her lab results are shown below. Explain why she has these results.

Electrolytes:

  • Na+ — 117 mmol/L*
  • Cl- — 87 mmol/L*
  • HCO3- — 15 mmol/L*

Serum osmolarity: 245 mOsm/kg

Urine specific gravity: 1.015

A

Her large intake of fluid has (due to dehydration and extreme thirst caused by ecstasy) has diluted out her electrolytes, so all are low, and her fluids are extremely dilute

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2
Q

In a healthy adult, what percentage of the body is typically made up by adipose?

What is the rest classified as?

A

20% (men: 10 - 20; women: 18 - 25);

lean body mass (80%)

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3
Q

How many liters of water are found in the average healthy 70 kg individual?

How much of this is intracellular? Extracellular? Plasma?

A

40 L;

25 L

15 L (11.5 L interstitial; 3.5 L plasma)

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4
Q

What is the 60-40-20 rule of thumb for fluids?

A

60% of body weight

40% intracellular

20% extracellular

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5
Q

What is the state of the water in the interstitium?

A

It is gel-like (combined with ground substance and other extracellular materials)

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6
Q

What term describes excess fluid in the interstitial space?

A

Edema

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7
Q

What proportion of lean body mass is water?

What percentage of a healthy individual is made up by lean body mass (non-adipose tissues, including water)?

A

73%;

80%

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8
Q

Body fat = Total weight - ____________________.

Lean body mass = total body water / _____.

A

Lean body mass;

0.73

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9
Q

Calculate the lean body mass and adipose fraction for the following patient.

5’4 woman

91 kg weight

40 L water

A

40 L / 0.73 = 54.8 L lean body mass

91 - 54.8 = 36.2 kg fat

36.2/91 = 40% adipose

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10
Q

Obesity can be defined by an individual’s adipose content (as a fraction of weight).

What percentage defines obesity in a man?

What percentage defines obesity in a woman?

A

≥ 25%

≥ 32%

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11
Q

What proportion of body water is intracellular?

What proportion is extracellular?

Of the extracellular, what proportion is plasma?

A

~2/3

~1/3

~1/4

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12
Q

The quantity of a substance in fluid is equal to the volume of fluid multiplied by:

A

The concentration of the substance

(Quantity = volume * concentration)

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13
Q

Evans blue dye is a substance that binds plasma proteins.

You administer 10 mg into an 80 kg patient’s bloodstream and remove a sample 10 min later. The evans blue dye concentration of the sample is 0.4 mg / 100 mL.

What is the plasma volume of the individual?

What is the blood volume of the individual?

A

Quantity administered = volume * concentration

10 mg = V * 0.4 mg / 100 mL

10 mg / 0.4 mg / 100 mL = V = 2500 mL

Plasma volume / fraction of plasma in the blood = blood volume

2500 mL / 0.55 = 4546 mL

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14
Q

What body fluid compartment volumes can be directly measured?

Which can only be indirectly measured?

A

Total body water,

ECF, plasma, blood volume;

ICF,

interstitial fluid

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15
Q

What substance can be used to measure total body water?

What substance can be used to measure ECF?

What substance can be used to measure blood volume?

What substance can be used to measure plasma volume?

A

D2O

Inulin

Radiolabeled iron

Radiolabeled albumin

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16
Q

How is the anion gap measured?

A

Cations - anions

(Na+ + K+) - (Cl- + HCO3-)

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17
Q

Calculate the anion gap for the following electrolytes.

Na+ — 117 mmol/L

Cl- — 87 mmol/L

HCO3- — 15 mmol/L

K+ — 4 mmol/L

A

(117 + 4) - (87 + 15) = 19

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18
Q

Besides electrolyte abnormalities, what might cause a change in the anion gap?

A

A change in organic anion concentrations (e.g. protein, ketones, etc.)

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19
Q

A 20-year-old, unresponsive woman is brought to the ED with respiratory distress after ingesting ‘ecstasy’ and subsequently drinking large amounts of fluid.

Her lab results are shown below. What is your diagnosis?

Electrolytes:

  • Na+ — 117 mmol/L*
  • Cl- — 87 mmol/L*
  • HCO3- — 15 mmol/L*

Serum osmolarity: 245 mOsm/kg

Urine specific gravity: 1.015

A

Hyponatremia;

cerebral and pulmonary edema

(hypoosmolar syndrome)

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20
Q

What is the normal serum osmolality?

True/False. It is not a colligative property.

A

290 mOsm/kg;

false

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21
Q

What is a severe consequence of body hypoosmolality?

A

Cerebral edema (and eventual death)

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22
Q

Describe how each of the following will impact the ECF:

  1. An infusion of hypotonic fluid
  2. An infusion of isotonic fluid
  3. An infusion of hypertonic fluid
A
  1. Expands by less than the volume infused
  2. Expands by the volume infused
  3. Expands by more than the volume infused
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23
Q

How is the renal fraction calculated?

What is it normally?

A

Renal blood flow / cardiac output

20%

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24
Q

True/False.

The kidneys use up virtually 100% of the oxygen they receive.

A

False.

The kidneys actually use very little of the oxygen coming in and there is some shunting of oxygen through the arteriovenous system

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25
Q

True/False.

The renal arterial system is non-anastomotic, and it is easy for small segments to be infarcted.

A

True.

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26
Q

True/False.

Albumin’s size is the main reason it doesn’t leave the glomerulus through the filtration slits.

A

False.

Its charge is the main reason it doesn’t pass through

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27
Q

Protein loss in the urine will happen either because of loss of the _____________ or a widening of the ____________.

A

Charge barrier;

filtration slits

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28
Q

Renal resistance happens in which vessels?

A

The arteries, afferent arteriole, and efferent arteriole

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29
Q

The glomerular filtration rate is maintained at a high pressure to overcome what pressure that would keep fluid in the glomerulus?

A

The colloid osmotic pressure

(hydrostatic pressure - osmotic pressure)

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30
Q

What is the average GFR?

What is the average renal blood flow?

A

125 mL / min (180 L / day);

1200 mL / min

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31
Q

What are the three intrinsic mechanisms of renal blood flow control?

A

Autoregulation (myogenic)

Tubuloglomerular feedback (tubular pressures increase –> glomerular pressure increases in response)

Paracrine factors

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32
Q

What are the main extrinsic mechanisms of renal blood flow control?

A

Sympathetic nerves

Hormones (including ANP)

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33
Q

Which are the vasoconstricting hormones affecting renal blood flow?

A

Epinephrine

Angiotensin II

Endothelin

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34
Q

Which are the vasodilating hormones affecting renal blood flow?

A

Prostaglandins

Bradykinin

Atrial natriuretic peptide

Nitric oxide

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35
Q

Does angiotensin II affect glomerular filtration or systemic arteriolar constriction?

A

Both

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36
Q

In what electrolyte circumstance is an NSAID more likely to decrease GFR?

A

Sodium-depleted circumstances

(increased vasoconstriction effect)

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37
Q

Atrial natriuretic peptide causes a decrease in the release of what two other hormones?

What effect does ANP have on the vasculature?

A

Renin,

aldosterone;

renal vasodilation

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38
Q

What effect do tubuloglomerular feedback and autoregulation have on renal blood flow?

What effect do they have on GFR?

A

Both maintained during fluctuations in arterial pressure

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39
Q

What effect does the renin-angiotensin system have on renal blood flow?

What effect do they have on GFR?

A

Reduces both

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40
Q

What substance partially counteracts the effects of angiotensin II?

A

Prostaglandins

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41
Q

Via what clearance equation is GFR calculated?

A

Clearancex = Urine flow * Urinex / Plasmax

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42
Q

True/False.

In order for a substance to be useful in calculating GFR via the clearance equation, it must be:

freely filtered at the glomerulus,

not reabsorbed or secreted,

not metabolized or degraded,

easily measured.

A

True.

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43
Q

What are some endogenous substances that can be used for measuring GFR?

A

Inulin;

mannitol;

radiolabeled compounds

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44
Q

Calculate the GFR for the following patient using the results of this 24-hour urine collection:

1.6 L urine

Urine creatinine 105 mg / dL

Plasma creatinine 0.9 mg / dL

A

130 ml/min

((1600 mL / 24 hours / 60 min) * 105 mg / dL) / 0.9 mg / dL

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45
Q

The plasma concentration of what substance is a good indicator of their GFR?

What is a normal value for this substance?

A

Creatinine;

1 mg/dL

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46
Q

If the plasma creatinine level is 1, what does this indicate about the glomerular filtration rate?

If it increases to 2, what does this indicate?

If it increases to 3, what does this indicate?

If it increases to 4, what does this indicate?

A

Normal GFR (~120 mL/min) (i.e. 100%/1)

GFR down to 50% (~60 mL/min) (i.e. 100%/2)

GFR down to 33% (~40 mL/min) (i.e. 100%/3)

GFR down to 25% (~30 mL/min) (i.e. 100%/4)

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47
Q

What would a plasma creatinine concentration of 5 roughly indicate about GFR?

A

A GFR of 24 mL/min (normal: 120 mL/min)

(100% function / 5)

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48
Q

Calculate the GFR for the following patient using the results of this 24-hour urine collection:

Urine flow: 3 mL/min

Urine inulin 9.5 mg / mL

Plasma inulin 0.26 mg / mL

A

110 mL/min

(UF * Ux)/Px

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49
Q

If calculating GFR via renal plasma flow, what equation would be used?

A

Renal plasma flow = (Urine flow * Urinex) / (Pa(x) - Pv(x))

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50
Q

What is a useful substance for calculating GFR via renal plasma flow?

Why?

A

Para-aminohippurate;

it is fully secreted

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51
Q

True/False.

Measuring GFR via clearance necessitates a substance that is fully filtered.

AND

Measuring GFR via renal plasma flow necessitates a substance that is neither secreted nor reabsorbed.

A

False.

  • Measuring GFR via renal plasma flow necessitates a substance that is fully filtered (e.g. para-aminohippurate).*
  • AND*
  • Measuring GFR via clearance necessitates a substance that is neither secreted nor reabsorbed (e.g. inulin).*
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52
Q

If a substance’s clearance is less than the GFR, what does this indicate?

A

There is net reabsorption

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53
Q

If a substance’s clearance is greater than the GFR, what does this indicate?

A

There is net secretion of the substance

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54
Q

If a substance’s clearance is less than the GFR, what does this indicate?

If a substance’s clearance is greater than the GFR, what does this indicate?

A

Net reabsorption;

net secretion

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55
Q

Where does the majority (67%) of filtered sodium and water get reabsorbed in the nephron?

Where does the next 25% get reabsorbed?

And the final 7 - 8%?

A

The proximal convoluted tubule;

the loop of Henle;

the DCT/collecting duct

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56
Q

True/False.

< 1% of filtered water and sodium actually gets excreted in the urine.

A

True.

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57
Q

Describe the relative amounts of sodium and water reabsorbed in each part of the nephron.

A
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58
Q

Which portion of the nephron is known as the ‘bulk reasborber?’

A

The proximal convoluted tubule

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59
Q

Basolateral Na+/K+ ATPases maintain a low sodium concentration in the proximal tubular cells.

What process does this facilitate and of what substances?

A

Apical reabsorption via sodium-linked cotransport;

glucose, amino acids, lactate, citrate, succinate, etc.

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60
Q

Via what mechanism is sodium maintained at a very low concentration in proximal tubule cells so that a gradient exists for sodium-linked cotransport of a variety of organic anions and other substances?

A

Basolateral Na+/K+ ATPases

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61
Q

What type of inhibition exists between solutes vying for position with the sodium-solute cotransporters in the PCT lumen?

A

Competitive inhibition

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62
Q

What will happen to PCT reabsorption during ATP-depletion?

A

It decreases due to decreased Na+/K+ activity

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63
Q

Normal plasma glucose is about:

Normal urine glucose concentrations are about:

Glucose is reabsorbed until what concentration?

A

100 mg/dL

0 mg/dL

375 mg/dL

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64
Q

Is most organic anion reabsorbtion in the PCT by passive or active transport?

What is the main form of transport used?

A

Active;

sodium-linked cotransport (secondary active transport)

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65
Q

Is sodium-linked cotransport active or passive transport?

A

Active (secondary)

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66
Q

Is urea actively or passively reabsorbed in the nephron?

An increase in what will increase urea excretion (i.e. what will decrease reabsorption)?

A

Passively;

urine flow rate

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67
Q

How is phosphate reabsorbed in the PCT?

A

Actively

(sodium cotransport)

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68
Q

What sodium exchanger is present at the PCT basolateral surface?

What cotransport is present at the PCT apical surface?

What sodium exchanger is present at the PCT apical surface?

A

Na+/K+ ATPase

Sodium-linked cotransport

Na+/H+ ATPase

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69
Q

Where does most Cl- reabsorption happen in the nephron?

How?

A

The late PCT;

the Cl- level builds up and then passively flows down its gradient (between the cells)

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70
Q

True/False.

Na+/H+ exchangers in the nephron alkalize the tubular lumen and increase bicarbonate reabsorption by making the lumen more positive.

A

False.

Na+/H+ exchangers in the nephron acidify the tubular lumen and increase bicarbonate reabsorption by making the lumen more negative.

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71
Q

What effect does passive Cl- reabsorption in the late proximal tubule have on Na+ reabsorption?

A

The tubular lumen becomes more positive, driving Na+ out passively

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72
Q

Sodium reabsorption in the early PCT is:

Sodium reabsorption in the late PCT is:

A

Secondary active (sodium-linked cotransport)

Passive (following Cl- loss)

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73
Q

Chloride in the PCT can be exchanged (1:1 exchange) into the tubular cells for any of what three bases?

A

OH-

HCO3-

Formate

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74
Q

In the PCT, chloride ions can be exchanged for bases (formate, OH-, HCO3-). What happens to these bases once they are in the tubule lumen?

A

They bind hydrogen ions and diffuse back into the cells

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75
Q

Bases (OH-, formate, HCO3-) can be exchanged for Cl- reabsorption in the PCT.

H+ can be exchanged for Na+ reabsorption in the PCT.

Are all of these bases and H+ then excreted?

A

No;

they combine (neutralizing charge) and diffuse back into the cells

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76
Q

Which image depicts NaCl reabsorption in the early PCT?

Which image depicts NaCl reabsorption in the late PCT?

A

2;

1

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77
Q

Describe how HCO3- is reabsorbed in the PCT at the apical membrane.

A

Na+/H+ exchangers pump hydrogen into the tubular lumen.

The H+ and HCO3- form H2CO3.

Tubular carbonic anhydrase forms CO2 and H2O, which then diffuse into the cells.

Cellular carbonic anhydrase then recreates HCO3-.

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78
Q

In the PCT lumen, after HCO3- is turned first into H2CO3 and then CO2 / water, what happens next?

A

The CO2 and H2O diffuse into the cell and carbonic anhydrase recreates H2CO3.

HCO3- is then cotransported with Na+ and also exchanged for Cl- at the basolateral cell membrane.

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79
Q
A

A.

B.

C.

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80
Q

True/False.

The PCT is not very soluble to water.

A

False.

It is very soluble to water (via apical and basolateral aquaporins).

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81
Q

Why does solute not concentrate in the tubular cells and interstitium as solute is reabsorbed in the PCT?

A

The capillary movement continuously whisks the solute and fluid away

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82
Q
A

B.

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83
Q

You administer 1 L of isotonic saline to a patient. What effect does this have on their blood osmolality?

A

It decreases

(diluted plasma proteins)

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84
Q

Describe the Starling mechanism of the nephron.

A

If a patient’s blood osmolality is low, less fluid will be drawn from the renal interstitium to the capillaries.

Fluid builds up in the interstitium, weakening tight junctions and allowing H2O/Na+/Cl-/HCO3- to reenter the PCT lumen for excretion

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85
Q
A

B.

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86
Q

What are the two types of nephron (based on anatomical location)?

What is the distinction?

A

Cortical, juxtmedullary (7:1 ratio);

the length of their loops of Henle

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87
Q

What are the three portions of the loop of Henle?

A

Thin descending

Thin ascending

Thick ascending

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88
Q

Describe the thin descending loop of Henle.

A

Highly permeable to H2O, urea, NaCl, etc.

No active NaCl transport

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89
Q

Describe the thin ascending loop of Henle.

A

NO PERMEABILITY TO H2O

Highly permeable to urea, NaCl, etc.

No active NaCl transport

90
Q

Describe the thick ascending loop of Henle.

A

Active NaCl transport

No permeability to H2O

91
Q

Which portion of the loop of Henle is the concentrating portion?

A

The descending limb (thin)

92
Q

Which portion of the loop of Henle is the diluting portion?

A

The ascending limb (thin and thick)

93
Q

Where in the loop of Henle can NaCl/urea/solutes be passively reabsorbed?

Where in the loop of Henle can H2O be reabsorbed?

Where in the loop of Henle can NaCl be actively reabsorbed?

A

The entire loop;

the descending limb;

the thick ascending limb

94
Q

True/False.

The concentration of the urine is largely decided by activity in the loop of Henle.

A

True.

95
Q
A

A.

B.

96
Q
A

A.

B.

C.

D.

97
Q

(Select all that apply)

A

B.

D.

98
Q
A

A.

B.

C.

99
Q

Describe active reabsorption in the ascending loop of Henle.

A

Basolateral membrane: Na+/K+ ATPases maintain low Na+ in the cell.

Apical membrane: The Na+/Cl-/K+ cotransporter brings in 1 Na+, 1 K+, and 2 Cl- all at the same time.

100
Q

What does furosemide do in the nephron?

Where?

A

Blocks Na-K-Cl cotransport in the ascending loop of Henle

101
Q

What form of passive Na+ reabsorption occurs in the thick ascending limb of the loop of Henle?

A

K+ is brought into the cell by Na-K-Cl cotransport.

The K+ diffuses back out into the lumen via leak channels.

The lumen becomes +10 mV.

This charge drives Na+ out of the lumen via passive, transcellular pathways.

102
Q

(In the nephron)

A

A.

B.

103
Q
A

A.

104
Q

True/False.

The renal cortex and medulla have similar intersitial tonicities.

A

False.

The medulla is hypertonic when compared with the cortex

105
Q

Why does H2O passively leave the loop of Henle in the thin descending limb?

A

It follows the corticomedullary osmolality gradient

106
Q

ADH acts on which portions of the nephron?

A

The late DCT and the collecting duct

107
Q
A

A.

B.

C.

D.

108
Q

What is the ‘single effect’ in the countercurrent multiplier system?

What is the single effect osmolality change?

A

The thick ascending limb pumps Na+ out into the intersitium, diluting the fluid sent to the DCT

(in the image, loop of Henle 1 is basically being turned into loop of Henle 2);

this is a ~200 mOsm/kg difference.

109
Q
A

A.

C.

D.

110
Q
A

A.

B.

C.

111
Q

At its deepest point, what is the osmolality of the lumen of the loop of Henle?

At its deepest point, what is the osmolality of the vasa recta?

A

1200 mOsm/kg

1200 mOsm/kg

112
Q
A

C.

D.

113
Q

What three solutes play the biggest role in urine concentration?

A

Na+, Cl-, and urea

114
Q

Where are the only locations in the nephron where urea reabsorption occurs?

A

The PCT (50%);

the collecting duct of the inner medulla

115
Q

Is urea reabsorbed in the outer medullary portion or the inner medullary portion of the collecting duct?

A

Inner medullary portion

116
Q

True/False.

Some urea that is reabsorbed in the collecting duct (in the inner medullary portion) will be secreted into the loop of Henle to affect countercurrent multiplication.

A

True.

117
Q

True/False.

Urea is responsible for 40% of medullary interstitial osmolality, meaning that the higher NaCl concentration in the loop of Henle provide a chemical gradient to drive NaCl out into the interstitium, even though the intersititum’s total osmolality is higher.

A

True.

118
Q
A

A.

B.

C.

119
Q

Where is the macula densa located?

A

At the junction of the (1) thick ascending limb of the loop of Henle and (2) the DCT

120
Q

What are the two halves of the distal tubule of the nephron?

A

The early D.T. (DCT) and the late D.T. (connecting tubule)

121
Q

What is the main purpose of the early distal tubule of the nephron?

What is the main purpose of the late distal tubule of the nephron?

A

NaCl reabsorption;

NaCl and H2O reabsorption

122
Q

What type(s) of cell line(s) the early distal tubule of the nephron? What are the functions?

What type(s) of cell line(s) the late distal tubule of the nephron? What are the functions?

A

Distal tubule cells (NaCl reabsorption);

connecting tubule cells (NaCl + H2O reabsorption),

intercalated cells (H+ secretion)

123
Q
  1. What type of cell in the distal tubule is responsible for NaCl and H2O reabsorption? Early or late distal tubule?
  2. What type of cell in the distal tubule is responsible for only H+ secretion? Early or late distal tubule?
  3. What type of cell in the distal tubule is responsible for only NaCl reabsorption? Early or late distal tubule?
A

Collecting tubule cells (late, 75% of late);

intercalated cells (late, 25% of late);

distal convoluted cells (early, 100% of early)

124
Q

What are the three sections of the collecting duct in the nephron?

A

Cortical,

outer medullary,

inner medullary

125
Q

What are the two main cell types in the collecting duct?

Describe the changes in cell type concentrations found in the cortical CD vs. the outer medullary CD vs. the inner medullary CD.

A

Principal cells;

intercalated cells

  • (CCD - 75:25*
  • OMCD - 80:20*
  • IMCD - 99:1)*
126
Q

What is the function of collecting duct principal cells?

What is the function of collecting duct intercalated cells?

A

NaCl and H2O reabsorption, K+ secretion;

H+ secretion

127
Q

Via what mechanism do distal convoluted cells absorb NaCl?

A

Apical Na+/Cl- cotransport;

basolateral Na+/K+ ATPases

128
Q

What type of transmembrane protein structure is abundant on the basolateral membranes of cells of the nephron?

It maintains intracellular Na+ concentrations at a very ____ level.

A

Na+/K+ ATPases;

low

129
Q

How do thiazide diuretics (e.g. hydrochlorothiazide) affect the kidney?

A

They block Na+/Cl- cotransport in the early distal convoluted tubule

130
Q
A

C.

(remember, these are separate from the connecting tubule cells and intercalated cells of the late distal tubule)

131
Q

Describe the electrolyte transport of *collecting tubule cells (late distal tubule) and *principal cells (of the collecting duct).

*Note: these can be considered virtually identical for our purposes.

A

(Note: chloride is reabsorbed through the transcellular space)

132
Q

Where does potassium secretion occur in the nephron?

Via what type(s) of cell?

In exchange for what ion?

A

The late distal tubule and collecting duct;

collecting tubule cells, principal cells;

Na+

133
Q

Describe the ion transport of intercalated cells in the nephron.

A
134
Q

True/False.

Chloride reabsorption in the nephron often follows sodium reabsorption because the loss of sodium leaves a slightly positive charge in the tubules.

A

False.

Cl- reabsorption in the nephron often follows Na+ reabsorption because the loss of Na+ leaves a slightly negative charge in the tubules.

135
Q
A

B.

136
Q

ADH causes water reabsorption in what tubules?

A

The collecting tubule (late distal tubule) and the collecting duct

137
Q

Why does urea leave the collecting duct to the inner medulla?

A

ADH concentrates the fluid so there is a high [Urea] the time it reaches the inner medulla portion

138
Q

In the late distal tubule and the collecting duct

A

A.

B.

139
Q

What are the three mechanisms regulating late distal tubule and collecting duct Na+ reabsorption?

A
  1. Tubular flow
  2. Plasma [K+]
  3. Aldosterone
140
Q

Why can drugs like furosemide cause hypokalemia?

A

Furosemide increases loop of Henle tubular Na+, thus increasing K+ secretion in the late distal tubule and collecting duct

(see principal cells in image)

141
Q

Describe the tubular flow mechanism regulating late distal tubule and collecting duct Na+ reabsorption.

A

Since this portion utilizes Na+ and K+ leak channels, increased Na+ delivery (increased tubular flow) causes increased Na+ reabsorption and K+ secretion

142
Q

Describe the plasma [K+] mechanism regulating late distal tubule and collecting duct Na+ reabsorption.

A

Increased plasma [K+] causes increased basolateral Na+/K+ ATPase activity and increased Na+ reabsorption and K+ secretion

143
Q

Describe the aldosterone mechanism regulating late distal tubule and collecting duct Na+ reabsorption.

A

(1) Increased insertion of Na+ channels into the apical membrane;
(2) increased insertion of Na+/K+ ATPases into the basolateral membrane

144
Q

How does aldosterone get into the renal cells?

Its effects are then on ________ receptors.

A

Simple diffusion (its a steroid hormone);

nuclear (affecting transcription)

145
Q
A

A.

B.

C.

146
Q
A

D.

147
Q
A

A.

D.

148
Q

What makes ADH and oxytocin so similar that they are both synthesized in the hypothalamus (paraventricular and supraoptic nuclei)?

A

Their structures are very similar.

149
Q

What receptor does ADH bind on the basolateral surface of nephron cells?

What is the effect?

A

V2;

protein phosphorylation and aquaporin2 insertion into the apical membrane

150
Q

Which aquaporin is inserted into the apical membrane of the collecting tubule and collecting duct when ADH is present?

Which aquaporins are present on the basolateral membrane regardless of ADH presence?

A

Aquaporin2;

aquaporin3, aquaporin4

151
Q
A

A.

C.

D.

152
Q

What are the main two factors regulating ADH release?

A
  1. Plasma osmolality (hypothalamic osmoreceptors)
  2. Blood volume (atrial stretch receptors)
153
Q
A

C.

154
Q
A

A.

E.

155
Q

What is the major mediator of the effects of the renin-angiotensin system?

A

Angiotensin II

156
Q

Besides the pulmonary circulation, where is another location where ACE is located?

A

The basolateral surface of renal cells

157
Q

True/False.

Most angiotensinogen is produced by the PCT, but some is also produced in the liver.

A

False.

Most angiotensinogen is produced by the liver, but some is also produced in the PCT.

158
Q

Angiotensin II primarily acts on ___ receptors.

AT2 receptors are primarily involved in:

A

AT1;

renal development

159
Q

True/False.

A fraction of bodily angiotensin II can be produced completely within the kidney without any hepatic or pulmonary or circulatory involvement.

A

True.

Some angiotensinogen is produced in the renal interstitium, and ACE can be found on the basolateral epithelial surface.

160
Q

What cell type produces renin?

A

Juxtaglomerular cells

161
Q

What is the rate-limiting factor of the renin-angiotensin system?

A

Renin production

162
Q
A

A.

B.

C.

163
Q

Name the four major activating mechanisms for renin secretion.

A

(First row)

164
Q

Name the three mechanisms for increasing renin secretion.

A

(Second row)

165
Q

What happens in the juxtaglomerular cells for renin to be secreted?

A

(Third row)

166
Q
A

A.

B.

C.

D.

167
Q
A

C.

168
Q
A

C.

169
Q

True/False.

Angiotensin II has many diverse actions.

A

True.

173
Q
A

A.

B.

C.

179
Q

What renal mechanism senses increased renal arteriolar stretch?

What is the result?

A

Baroreceptors in juxtaglomerulus (calcium channels opened);

inhibition of renin release

180
Q
A

A.

181
Q
A

C.

182
Q
A

A.

B.

C.

D.

E.

183
Q

What effect does increased sympathetic tone have on juxtaglomerular cells?

A

β1 activation –> cAMP –> increased renin secretion

184
Q

What effect does an increase in NaCl delivery to the macula densa have on the juxtaglomerular cells?

Why?

A

Decreased renin secretion;

the JG cells interpret this as increased ECF

(maybe mediated via PGE2)

186
Q

What effect does a decrease in NaCl delivery to the macula densa have on the juxtaglomerular cells?

Why?

A

Increased renin secretion;

the JG cells interpret this as decreased ECF

(maybe mediated via PGE2)

187
Q

Name the major functions of angiotensin II in the following systems: renal, adrenal, blood vessels, heart, intestines, CNS, PNS.

A
  1. Renal: Reduce RBF, increase NaCl reabsorption
  2. Adrenal: Aldosterone release
  3. BV: Vasoconstriction
  4. Heart: Cardiac contractility
  5. Intestine: NaCl + H2O reabsorption
  6. CNS: Thirst, salt appetite, ADH release
  7. PNS: Sympathetic activity
188
Q

What effect (if any) does angiotensin II have on the renal arterioles?

What effect (if any) does angiotensin II have on the Kf?

A

Efferent arteriole constriction (with no change in GFR);

it decreases it (mesangial contraction)

189
Q

What parts of the nephron are stimulated to reabsorb NaCl by angiotensin II?

A

The PCT and DCT

190
Q

What overall effect does angiotensin II have on the GFR?

How?

A

It maintains it;

efferent arteriole constriction

191
Q

True/False.

Increases in Na+ retention via aldosterone will also result in an increase in K+ loss.

A

True.

195
Q

What are the major prostaglandins produced in the kidney?

A

PGE2

PGI2 (prostacyclin)

Thromboxane A2

196
Q

What are the major vasodilating prostaglandins produced by the kidney?

What do they dilate?

A

PGI2 (prostacyclin), PGE2;

both the afferent and efferent arterioles

197
Q

What effect do renal prostaglandins have on GFR?

Which arterioles do they affect? How?

How do they affect NaCl reabsorption?

A

Virtually no effect;

both afferent and efferent, dilation;

decreased

198
Q

When are renal prostaglandins produced?

Why?

A

When ECF and MAP are decreased;

to counteract angiotensin II, norepinephrine, ADH, etc.

199
Q

What hormone(s) promote(s) renal arteriolar dilation? Which arterioles?

What hormone(s) promote(s) renal arteriolar constriction? Which arterioles?

A

PGE2, PGI2, bradykinin,

afferent and efferent;

angiotensin II,

efferent

200
Q

Along with prostaglandin production, renal __________ helps counteract angiotensin II.

A

Bradykinin

201
Q

___________ digests high-molecular weight ____________ to produce bradykinin.

A

Kallikrein;

kininogen

202
Q

Where is renal kallikrein found?

A

The renal collecting tubule (late DCT)

203
Q

How does bradykinin exert an effect on the kidney?

A

By binding B2 receptors –> increase NO, PGE2, and PGI2 secretion

204
Q

Upon carbonic anhydrase creation of bicarbonate in the PCT cells, what happens to the bicarbonate next?

A

Basolateral co-transport of 3 HCO3- to every 1 Na+;

also, HCO3-/Cl- exchangers

205
Q

How does acetazolamide affect the kidneys?

A

Increased HCO3- excretion via blockage of lumen carbonic anhydrase

206
Q

What is a normal blood pressure?

What is an elevated blood pressure?

A

<120 / <80 mmHg

120 - 129 / <80 mmHg

207
Q

What is hypertension stage I?

What is hypertension stage II?

A

130-139 mmHg SBP OR 80-89 mmHg DBP

≥ 140 mmHg SBP OR ≥ 90 mmHg DBP

208
Q

What BP defines a hypertensive crisis?

A

≥ 180 mmHg SBP OR ≥ 120 mmHg DBP

209
Q

True/False.

Hypertension can cause (among other effects): stroke, heart attack, retinopathy, peripheral vascular disease, renal failure, left ventricular hypertrophy, congestive heart failure, etc.

A

True.

210
Q

What is malignant hypertension?

A

≥ 200 mmHg SBP and ≥ 100 mmHg DBP

211
Q

True/False.

Excess salt intake is often accompanied by little-to-no elevation in plasma sodium levels.

A

True.

212
Q

True/False.

Many monogenetic causes of hypertension have been identified in the kidneys.

A

True.

213
Q

True/False.

Sodium excretion has little to do with hypertension reduction in sodium-replete states.

A

False.

214
Q

True/False.

Loss of alkali can occur via the kidneys and GI tract.

A

True.

215
Q

Loss of ______ (pH) substances often occurs due to diarrhea.

Loss of ______ (pH) substances often occurs due to vomiting or nasogastric tube usage.

A

Alkaline;

acidic

216
Q

What is the principal mechanism for renal acid buffering?

A

Phosphate secretion

(Net acid excretion = titratable acid + NH4+ - HCO3-)

217
Q

True/False.

Daily renal pH excretion is typically about 70 mEqv of base.

A

False.

Daily renal pH excretion is typically about 70 mEqv of acid.

(And a resultant 70 mEqv of carbonic acid created to buffer/replace it)

220
Q

What effect do angiotensin II, glucocorticoids, and endothelin have on HCO3- renal reabsorption?

A

All increase reabsorption

221
Q

In the collecting tubule and duct, type A intercalated cells do what?

In the collecting tubule and duct, type B intercalated cells do what?

A

Secrete H+, reabsorb HCO3-;

secrete HCO3-

222
Q

True/False.

H+ secretion in the nephron can be through H+/K+ exchange, H+/Na+ exchange, and H+ ATPases.

A

True.

223
Q

What is the major acid of urine excretion?

What is the major buffer of urine excretion?

A

NH4+;

PO3-

224
Q

True/False.

Excretion of NH4+ corresponds exactly with creation of HCO3-.

A

True.

Both are made from glutamine.

225
Q

True/False.

Very small increases in plasma K+ can be deadly.

A

True.

226
Q

If a person ingests their daily quantity of potassium in just a few minutes (~100 mEq/day), are they at risk for cardiac complications?

A

No, this ingested K+ is quickly moved to the intracellular fluid

227
Q

What is the initial defense against hyperkalemia?

A

Uptake into cells

(often via insulin, osmolality, β-adrenergic effects)

228
Q

What cell type in the nephron is responsible for K+ secretion?

A

Collecting tubule cells / principal cells

229
Q

What are some easy methods by which you can check for ECF volume depletion in a patient?

A

Tachycardia;

hypotension (may be orthostatic);

skin turgor (variable);

dry mucus membranes (variable)

230
Q

Total body __ determines ECF volume.

A

Na+

231
Q

A patient that has been vomiting presents with a HCO3- of 35 and a K+ of 3.0.

What explains this finding? Why don’t they just urinate out the excess bicarbonate?

How do you treat them?

A

The ECF volume is depleted (regulatory mechanisms are reabsorbing all the Na+, H2O, and HCO3-; Na+ can be in exchange for K+ and H+);

IV saline (correct the ECF depletion and the alkalosis will resolve itself)

232
Q

What effect does Conn’s syndrome usually have on Na+ levels?

What effect does Conn’s syndrome usually have on pH levels?

What effect does Conn’s syndrome usually have on K+ levels?

A

Not much;

alkalemia;

decrease

233
Q

What happens when plasma Na+ levels rise?

A

ADH is released to increase H2O reabsorption

(diluting the Na+ and maintaining osmolality)

234
Q

How would an ADH-secreting small cell carcinoma of the lung present on laboratory findings?

A

Low osmolality;

normal BP;

lowered plasma Na+

235
Q

Do relatively small changes in blood volume affect ADH secretion?

A

No.

236
Q

What are the three ionic main effects of aldosterone?

A

Na+ reabsorption

K+ secretion

H+ secretion

T1 - Integrated (Full Review) (29 decks)

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