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The BIG Test > Renal > Flashcards

Renal Flashcards

1
Q

When talking about regulating osmolality, we are talking about regulating ______ concentration.

A

Sodium

*Sodium salts represent 90% of total osmolality

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2
Q

What is normal osmolality?

A

300 mOsm/kg

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3
Q

Why is the patient with chronic renal disease hypocalcemic?

A

Kidney converts Vit D to its active form

Calcium absorption from the intestines is impaired when there is a Vit D deficiency

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4
Q

What % of CO flows to the kidneys?

A

25%

1.25 L/min

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5
Q

What are the 2 types of nephrons?

A
  1. Cortical - short loops of Henle, glomeruli located near the surface
  2. Juxtamedullary - long loops of Henle, glomeruli located deep
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6
Q

What is the name of the peritubular capillaries of the loops of Henle of the juxtamdullary nephrons?

A

Vasa recta — constitutes a countercurrent exchange system

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7
Q

What 2 structures are found in the medulla?

A
  1. Loops of Henle

2. Collecting ducts

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8
Q

What part of the nephron is most vulnerable to ischemia?

A

Inner stripe of the outer medulla

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9
Q

From tubule to capillary…
From capillary to tubule…
From glomerulus to Bowman’s capsule…

A

Reabsorption
Secretion
Filtration

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10
Q

Function of the PCT

A

Reabsorption! 67%

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11
Q

Function of the LOH

A

Establishes and maintains an osmotic gradient in the medulla
Descending - permeable to water
Ascending - impermeable to water
*Countercurrent multiplier

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12
Q

Function of DCT and CD

A

Final adjustments

ADH (water) and Aldosterone (Na and K)

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13
Q

Osmolality in the medulla increases from 300 mOsm (croticomedullary junction) to ______ mOsm deep in the medulla.

A

1200-1500

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14
Q

ALL of the filtered glucose is normally completely reabsorbed from the _______ by active transport mechanisms.

A

PCT

*The amount of filtered glucose normally does NOT exceed the transfer max.

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15
Q

What happens with the renal tubular handling of glucose in DM?

A

Amount of glucose filtered exceeds the transfer max
Glucose that escapes reabsorption from the PCT is excreted - ALL segments of the renal tubule beyond the PCT are impermeable to glucose

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16
Q

Why does urine flow increase in the untreated patient with DM?

A

Unreabsorbed glucose causes an osmotic diuresis

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17
Q

The rate of ADH release is directly related to what?

A

Osmolality of the extracellular fluid

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18
Q

Extracellular fluid osmolality (sodium concentration) is regulated by…

A

ADH

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19
Q

Where is ADH synthesized?

Where is ADH stored?

A

Synthesized in paraventricular and supraoptic nuclei of the hypothalamus
Stored in posterior pituitary (neurohypophysis)

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20
Q

Which is more potent: angiotensin II or ADH?

A

ADH

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21
Q

What is the most sensitive to changes in extracellular fluid osmolality?

A

Paraventricular and supraoptic nuclei

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22
Q

What is the most powerful stimulus triggering release of ADH?

A

Increase in extracellular fluid osmolality

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23
Q

In the absence of ADH, the DCT and CD are _________ to water.

A

Impermeable

A large volume of dilute urine is formed

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24
Q

What are other triggers for ADH release?

A 
Hypotension
Decrease in plasma volume 
Stress
Pain 
Vomiting 
CPAP
PEEP
Volatile agents 
Morphine 
Nicotine
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25
Q

What % of the filtered water is reabsorbed in the…
PCT
Descending LOH
Ascending LOH

A

PCT - 67%
Descending LOH - 13%
Ascending LOH - impermeable to water (NaCl is reabsorbed here!)

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26
Q

Responses Following a Decrease in Body Fluid Osmolality

A 
Hypothalamic nuclei swell 
Decrease in nerve impulse frequency 
Decrease in ADH release 
DCT and CD become impermeable to water 
Large volumes of dilute urine
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27
Q

A __% increase in osmolality is sufficient to stimulate the release of large quantities of ADH.

A

2%

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28
Q

Are sodium intake and excretion important in regulating extracellular fluid osmolality?

A

NO b/c significant changes in body sodium content take a long time to be achieved
*The control of water is involved in the control of body fluid osmolality (and sodium concentration)

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29
Q

+ ADH
Urine osmolality
Urine volume

A

+ ADH
Urine osmolality: 1200-1500
Urine volume: 0.5 mL/kg/hr

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30
Q
  • ADH
    Urine osmolality
    Urine volume
A
  • ADH
    Urine osmolality: 50-100
    Urine volume: 2-25 mL/kg/hr
31
Q

What are causes of DI?

A

Failure of ADH synthesis
Failure of ADH release (most common)
Insensitivity of the DCT and CD (nephrogenic)

32
Q

What are causes of SIADH?

A 
Surgery
Intracranial tumors
Hypothyroidism 
Porphyria
Small (Oat's) cell carcinoma of the lung
33
Q

What is the diagnosis?
Inappropriately increased urine sodium concentration and urine osmolality in the presence of hyponatremia and decreased plasma osmolality

34
Q

What is the major determinant of extracellular fluid volume?

A

Amount of sodium

35
Q

What is the most important hormone for regulating extracellular fluid volume?

A

Aldosterone

36
Q

Does sodium excretion increase or decrease when glomerular filtration rate increases?

37
Q

List 3 determinants of sodium excretion.

A
  1. GFR - direct
  2. ANP - direct
  3. Aldosterone - indirect
38
Q

Where is aldosterone produced?
Where does aldosterone act?
What are the actions of aldosterone?

A

Zona glomerulosa of the adrenal cortex
Acts on the late DCT and CD*
Increases Na reabsorption + Increases K excretion

39
Q 
What % of the sodium is reabsorbed in the...
PCT
Descending LOH 
Ascending LOH
DCT + CD
A

PCT - 67%
Descending LOH - impermeable to Na (water is reabsorbed here!)
Ascending LOH - 25%
DCT + CD - 7% in the presence of aldosterone
*Na reabsorption is an active process

40
Q

With aldosterone present, < ___% of the filtered sodium load may be excreted.

41
Q

Result of High Sodium Intake

A 
Body fluids become concentrated
ADH output increases 
Thirst mechanism activated
Expanded fluid volume 
Hypervolemia + HTN
Corrected by increasing the renal excretion of sodium: increase GFR, decrease renin, increase ANP
42
Q

Where does aldosterone work?

A

Late DCT and CD

Primarily on the principal cells of the CD

43
Q

What % of the potassium is reabsorbed in the…
PCT
Descending LOH
Ascending LOH

A

PCT - 67%
Descending LOH - passive K secretion
Ascending LOH - 25%
*About 92% of the filtered K is reabsorbed prior to DCT and CD

44
Q

List 3 determinants of K excretion.

A
  1. Aldosterone - direct
  2. DCT flow rate - direct (how diuretics deplete K)
  3. Bicarb concentration in DCT - direct (why Bicarb administration works in the setting of hyperkalemia)
45
Q 
Loop Diuretics
Furosemide
Bumetanide
Ethacrynic acid
Torsemide
A

Ascending LOH
Inhibit the Na-K-2Cl symporter (reabsorption is blocked)
Destroys the super salty medulla
Water excretion increases
SE: damage to CN 8, hypokalemic metabolic alkalosis

46
Q

Why does Furosemide cause BP to drop?

A

Triggers the release of prostaglandins

Venodilation

47
Q

Thiazides
-thiazide
Chlorthalidone
Metolazone

A

Early DCT

Inhibit Na reabsorption

48
Q

Potassium-Sparing
*Spironolactone
Triamterene
Amiloride

A

Late DCT and CD*
*Competitively inhibits aldosterone
Inhibit Na reabsorption and K excretion
SE: hyperkalemia

49
Q

Carbonic Anhydrase Inhibitor

Acetazolamide

A

PCT
Inhibits carbonic anhydrase
Inhibits Bicarb + Na reabsorption
SE: hyperchloremic metabolic acidosis

50
Q

How does acetazolamide decrease intraocular pressure?

A

Inhibition of carbonic anhydrase decreases the rate of formation of aqueous humor

51
Q

Osmotic Diuretic

Mannitol

A

Freely filtered in Bowman’s capsule - BUT then remains trapped in the renal tubule (polar molecule)
Exerts an osmotic force preventing the reabsorption of water
SE: pulmonary edema, CHF
*Does NOT depend on rental tubular concentrating mechanisms to produce diuresis - benefit

52
Q

Explain the SE of hypokalemia as a result of Mannitol administration.

A

K secretion is increased secondary to increase flow through the DCT

53
Q

How does the fractional excretion of filtered sodium (FEna) compare in prerenal vs. renal failure?
*In acute renal failure, the renal tubule reabsorbs sodium poorly, so sodium appears in the urine.

A

Prerenal < 0.01 (1%)
*Flow through tubule is slow - considerable time for Na reabsorption

Renal failure > 0.03 (3%)
*This test is 90% specific and sensitive

54
Q

What is the normal GFR?
Decreased renal reserve?
Renal insufficiency - S/S appear? Lab issues?
Uremia?

A

Normal - 125 mL/min
Decreased renal reserve - 80 mL/min
Renal insufficiency - 50 mL/min *
Uremia - < 12 mL/min

55
Q

What is the best test of renal reserve?

A

Creatinine clearance

*This measures GFR

56
Q

Chronic Renal Failure
Anemia
Why? Tx?

A

Decreased production or erythropoietin

Administer recombinant erythropoietin - SE: HTN

57
Q

Chronic Renal Failure
Pruritus
Tx?

A

Administer erythropoietin - this lowers the plasma concentration of histamine - decreases itching

58
Q 
Chronic Renal Failure 
Coagulopathies 
What is normal? 
What is abnormal? 
What is the most frequent site of bleeding?
Tx?
A 
Normal PT, PTT, plt 
Abnormal bleeding time (plt dysfunction!)
Release of defective vWF
Most frequent uremic bleed - GI tract 
Tx - dialysis, DDAVP, cryoprecipitate
59
Q

Chronic Renal Failure
Electrolyte Disturbances
What goes up? Down?

A

HYPER: K, Mag, Phos
HYPO: Ca - secondary hyperparathyroidism (triggers bone resorption of Ca - vulnerable to fractures)
*Metabolic acidosis (retention of acids)

60
Q

What % of ESRD patients have HTN?

61
Q

What is the most serious electrolyte abnormality in chronic renal failure?

A

HYPERkalemia

*AVOID LR (4 mEq/L K)

62
Q

Nervous System abnormalities in chronic renal failure include peripheral motor and sensory polyneuropathies. What 2 nerves are most often involved?

A
  1. Median

2. Common peroneal

63
Q

What is the most common cause of death in patients with renal failure?

64
Q

Are kidneys autoregulated? What structure is responsible?

A

Yes - 80-180 mmHg
Myogenic response - afferent arteriole
Tubuloglomerular feedback - juxtaglomerular apparatus - afferent arteriole

65
Q

Name the 3 major renal functions. Do they require energy?

A
  1. Filtration
  2. Reabsorption - active
  3. Secretion - active
66
Q

What is an example of a countercurrent multiplier? Exchanger?

A

Multiplier - LOH
Exchanger - vasa recta
*Allows for adjustments in the osmolality of the urine

67
Q

State 2 actions of ADH.

A
  1. Increase water reabsorption in CD

2. Vasoconstrictor - increases BP

68
Q

List 3 stimuli for renin release.

A
  1. Decreased renal perfusion pressure*
  2. Hyponatremia
  3. SNS stimulation of beta-1 receptors of the juxtaglomerular cells
69
Q

Which electrolyte promotes renin release from the juxtaglomerular apparatus?

A

Changes in Cl ion flow past the macula densa

70
Q

Does angiotensin II have a greater constrictor effect on afferent or efferent arterioles?

A

Efferent arterioles

This is good b/c GFR is not decreased

71
Q

What % of nephron mass loss correlates with s/s of renal dysfunction?

72
Q

What are hallmarks of nephrotic syndrome?

A 
Bloody, protein urine 
HYPOalbuminemia 
HTN, Na retention, edema, hypovolemia
HLD
Thromboembolism
73
Q

Creatinine Clearance
Mild
Mod
Severe

A

Mild 60 mL/min
Mod 40 mL/min
Severe < 25 mL/min

74
Q

Describe the MOA of most diuretics simply.

A

Inhibit Na reabsoprtion
Water follows
*Plasma volume decreases, while plasma osmolality does NOT change

The BIG Test (21 decks)

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