Renal Physiology pt 3 (Final Exam) Flashcards

1
Q

What stimulates the Vasopressin release system?

A
  • ↑ Serum osmolarity
  • Hypotension
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2
Q

What receptors sense osmolarity?
Where are these located?

A
  • Osmoreceptors
  • Hypothalamus
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3
Q

5/6 of ADH release is determined from this structure.
Where is this located?

A
  • Supraoptic Nuclei
  • Anterior near optic nerves.
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4
Q

1/6 of ADH release is determined from what structure?
Where is this located?

A
  • Paraventricular Nuclei
  • Posterior; close to 3rd ventricle.
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5
Q

What are the two lobes of the pituitary gland?
Which of the two secretes vasopressin?
What coordinates with osmoreceptors & baroreceptors to induce vasopressin release?

A
  • Adenohypophysis (anterior) & Neurohypophysis (posterior)
  • Neurohypophysis secretes vaso
  • Supraoptic & Paraventricular Nuclei.
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6
Q

What would occur with a cell if placed in a hypotonic solution?

A
  • Swelling of the cell
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7
Q

What would occur with a cell if placed in a hypertonic solution?

A
  • Cellular Shrinkage
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8
Q

What areas of the nephron are affected by ADH?

A
  • Everywhere except the Proximal Tubule.
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9
Q

What areas are more affected by ADH?

A
  • Descending thin limb
  • Medullary collecting duct
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10
Q

What would occur immediately after head injury in regards to ADH?
What would occur over a longer period in this same trauma scenario?

A
  • Short term: ADH release = SIADH
  • Long term: no ADH = DI
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11
Q

What is a pathology characterized by excessive ADH called?
What things can cause this condition?

A

SIADH:
- Short term head trauma
- NSAIDs & opioids
- Anti-depressants (with high dose)
- Lung Cancer (lots of junk made by this cancer)

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12
Q

What pathology is characterized by insufficient levels of ADH?
What things can cause this condition?

A

Diabetes Insipidus:
- Head Injury (Long-term)
- EtOH
- Nephrogenic DI

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13
Q

What mechanism causes DI with EtOH use?

A
  • EtOH inhibits release of ADH at the pituitary through Ca⁺⁺ current reduction.
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14
Q

What is nephrogenic DI?
What is an example of this condition?

A
  • Inability of kidney to respond to ADH.
  • Lithium - super high doses = 20L UO/day
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15
Q

What is the treatment for Central DI?
What type of drug is this?

A
  • Desmopressin (DDAVP) - V2 Receptor Agonist.
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16
Q

What would characterize Addison’s disease?
What electrolyte abnormalities would be seen?

A
  • Low Aldosterone
  • ↓ Na⁺ & ↑ K⁺
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17
Q

What would characterize Conn’s Syndrome?
What would cause this?
What electrolyte abnormalities would be seen?

A
  • High Aldosterone
  • Adrenal Tumor causing hyperactivity
  • ↓ K⁺ & ↑ Na⁺
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18
Q

What areas of the nephron are permeable to Urea?

A
  • Proximal Tubule
  • Thin descending limb
  • Thin ascending limb
  • Medullary Collecting Duct with ADH.
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19
Q

What areas of the nephron have NaCl permeability?

A
  • Proximal Tubule
  • Thin descending limb
  • Thin ascending limb
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20
Q

What areas of the nephron are permeable to water?

A
  • Proximal Tubule
  • Thin Descending Limb
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21
Q

What areas of the nephron become permeable to water with ADH?

A
  • Distal Tubule
  • Cortical & Medullary Collecting Ducts
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22
Q

What areas of the nephron utilize active NaCl Transport?

A
  • Proximal Tubule
  • Thick Ascending Limb
  • Distal Tubule
  • Cortical & Medullary Collecting Duct

Everywhere except the thin limbs

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23
Q

What prevents volatility in serum sodium levels?

A
  • ADH/Vasopressin System
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24
Q

Increased ADH & Angiotensin II will cause ________ thirst.

25
Decreased ADH & Angiotensin II will cause ______ thirst.
decreased
26
What makes us crave salt?
- Angiotensin II
27
What causes decreased sensation of thirst?
- ↓ Osmolarity - ↑ Blood volume - ↑ Blood pressure - ↓ Ang II - Gastric Distension
28
What causes an increased sensation of thirst?
- ↑ Osmolarity - ↓ Blood Volume - ↓ Blood pressure - ↑ Ang II - Mouth Dryness
29
What drugs (discussed in lecture) will decrease ADH?
- Alcohol - Clonidine - Haloperidol
30
What drugs, discussed in class, will increase ADH?
- Morphine - Nicotine - Cyclophosphamide
31
What two bodily conditions will increase ADH levels?
- Nausea - Hypoxia
32
What occurs with potassium homeostasis in renal failure? Why?
- K⁺ homeostasis fails - Aldosterone system fails due to low nephron count.
33
If a kidney is donated, how much can the other kidney compensate? How long would it take to develop this compensatory capability?
- 50% - 6-12 months
34
What is the pathophysiology of a left stenotic renal artery?
- Left kidney sees ↓ BP at nephrons due to the stenosis. - Renin is released, Angiotensin II is formed. - Angiotensin II affects healthy Right Kidney and BP increases.
35
What would the treatments of a stenotic renal artery be in order of least invasive to most invasive?
- ACE inhibitors or ARBS - Stenting - Nephrectomy
36
What demographics are affected by Na⁺-sensitive hypertension?
- African Americans - Asian Americans
37
What organ is not working correctly in essential hypertension? How much would salt intake affect someone with healthy kidneys?
- Kidneys - None
38
What endogenous molecule can mimic mannitol?
- Glucose
39
What natriuretic can cause acid/base problems? Why is this? What other condition can this drug treat?
- Acetazolamide; ↓ HCO₃⁻ reabsorption - Glaucoma
40
What drug is generally more effective; ACE inhibitors or ARBs?
- ARBs
41
Potassium sparing diuretics generally interfere with what?
- Aldosterone
42
NO donors & calcium channel blockers (CCBs) primarily affect what? What does this result in?
- Afferent Arteriole; results in ↑PCAP = ↑ Filtration.
43
What is the most common thiazide diuretic? What drug class & specific drug is this thiazide often combined with?
- Hydorchlorothiazide (HCTZ) - Triamterene (K⁺-sparing)
44
β agonism will result in what (in regards to the kidneys)?
- Water conservation
45
Does increased urine output postoperatively always mean that you have healthy kidneys? Why or why not?
- No; increased urine output could be from efferent arteriole constriction, meaning that their is still low perfusion downstream of the EA.
46
What would characterize Renal Insufficiency?
- 50-20% of normal GFR
47
What would characterize Renal Failure?
- 20-5% of normal GFR
48
What would characterize End-Stage Renal Disease (ESRD) ? If the patient had 2million nephrons originally, what is the most they could now have if diagnosed with this condition?
- <5% GFR - 100,000 nephrons left (1/20 original nephrons left)
49
At about what age would we start to see loss of nephrons?
- 40 years old
50
Vasa Recta are dependent on what to remain open? What drugs would then be detrimental to the medullary nephrons where these are found?
- Prostaglandins - NSAIDs (via COX2 inhibition specifically)
51
What would occur with the serum creatinine if GFR were cut in half? How about if we had a scenario of 75% nephron loss?
- Creatinine would double. - GFR 1/4 of normal = 4x serum creatinine.
52
Regarding osmolarity, intracellular fluid volume, and extracellular fluid volume what would occur if isotonic (0.9%) NaCl were given?
- Osmolarity would stay the same - ICF would stay the same - ECF would exand
53
Regarding osmolarity, intracellular fluid volume, and extracellular fluid volume what would occur if hypertonic (3%) NaCl were given?
- Osmolarity for ICF & ECF would increase - ICF volume would contract - ECF volume would expand
54
Regarding osmolarity, intracellular fluid volume, and extracellular fluid volume what would occur if hypotonic (0.45%) NaCl were given?
- Osmolarity for ICF & ECF would decrease - ICF volume would expand - ECF volume would expand
55
What drugs can make the body less tolerant of blood loss? Why is this?
- ACE inhibitors & ARBs - RAA-System is inhibited and BP can't be raised as easily.
56
How much is surface area increased by the brush border?
- 20x
57
Differentiate Type A and Type B intercalated cells?
- Type A get rid of H⁺ - Type B retain H⁺
58
Where are Intercalated cells located? What types are there? What are they responsive to?
- Late Distal Tubule, Cortical & Medullary Collecting Ducts. - Type A & B Intercalated Cells - ADH