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A&P I 2024 > Renal Physiology pt 3 (Final Exam) > Flashcards

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.

A

increased

25
Q

Decreased ADH & Angiotensin II will cause ______ thirst.

A

decreased

26
Q

What makes us crave salt?

A
  • Angiotensin II
27
Q

What causes decreased sensation of thirst?

A
  • ↓ Osmolarity
  • ↑ Blood volume
  • ↑ Blood pressure
  • ↓ Ang II
  • Gastric Distension
28
Q

What causes an increased sensation of thirst?

A
  • ↑ Osmolarity
  • ↓ Blood Volume
  • ↓ Blood pressure
  • ↑ Ang II
  • Mouth Dryness
29
Q

What drugs (discussed in lecture) will decrease ADH?

A
  • Alcohol
  • Clonidine
  • Haloperidol
30
Q

What drugs, discussed in class, will increase ADH?

A
  • Morphine
  • Nicotine
  • Cyclophosphamide
31
Q

What two bodily conditions will increase ADH levels?

A
  • Nausea
  • Hypoxia
32
Q

What occurs with potassium homeostasis in renal failure? Why?

A
  • K⁺ homeostasis fails
  • Aldosterone system fails due to low nephron count.
33
Q

If a kidney is donated, how much can the other kidney compensate?
How long would it take to develop this compensatory capability?

A
  • 50%
  • 6-12 months
34
Q

What is the pathophysiology of a left stenotic renal artery?

A
  • 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
Q

What would the treatments of a stenotic renal artery be in order of least invasive to most invasive?

A
  • ACE inhibitors or ARBS
  • Stenting
  • Nephrectomy
36
Q

What demographics are affected by Na⁺-sensitive hypertension?

A
  • African Americans
  • Asian Americans
37
Q

What organ is not working correctly in essential hypertension?
How much would salt intake affect someone with healthy kidneys?

A
  • Kidneys
  • None
38
Q

What endogenous molecule can mimic mannitol?

A
  • Glucose
39
Q

What natriuretic can cause acid/base problems? Why is this?
What other condition can this drug treat?

A
  • Acetazolamide; ↓ HCO₃⁻ reabsorption
  • Glaucoma
40
Q

What drug is generally more effective; ACE inhibitors or ARBs?

A
  • ARBs
41
Q

Potassium sparing diuretics generally interfere with what?

A
  • Aldosterone
42
Q

NO donors & calcium channel blockers (CCBs) primarily affect what? What does this result in?

A
  • Afferent Arteriole; results in ↑PCAP = ↑ Filtration.
43
Q

What is the most common thiazide diuretic?
What drug class & specific drug is this thiazide often combined with?

A
  • Hydorchlorothiazide (HCTZ)
  • Triamterene (K⁺-sparing)
44
Q

β agonism will result in what (in regards to the kidneys)?

A
  • Water conservation
45
Q

Does increased urine output postoperatively always mean that you have healthy kidneys? Why or why not?

A
  • No; increased urine output could be from efferent arteriole constriction, meaning that their is still low perfusion downstream of the EA.
46
Q

What would characterize Renal Insufficiency?

A
  • 50-20% of normal GFR
47
Q

What would characterize Renal Failure?

A
  • 20-5% of normal GFR
48
Q

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?

A
  • <5% GFR
  • 100,000 nephrons left (1/20 original nephrons left)
49
Q

At about what age would we start to see loss of nephrons?

A
  • 40 years old
50
Q

Vasa Recta are dependent on what to remain open?
What drugs would then be detrimental to the medullary nephrons where these are found?

A
  • Prostaglandins
  • NSAIDs (via COX2 inhibition specifically)
51
Q

What would occur with the serum creatinine if GFR were cut in half?
How about if we had a scenario of 75% nephron loss?

A
  • Creatinine would double.
  • GFR 1/4 of normal = 4x serum creatinine.
52
Q

Regarding osmolarity, intracellular fluid volume, and extracellular fluid volume what would occur if isotonic (0.9%) NaCl were given?

A
  • Osmolarity would stay the same
  • ICF would stay the same
  • ECF would exand
53
Q

Regarding osmolarity, intracellular fluid volume, and extracellular fluid volume what would occur if hypertonic (3%) NaCl were given?

A
  • Osmolarity for ICF & ECF would increase
  • ICF volume would contract
  • ECF volume would expand
54
Q

Regarding osmolarity, intracellular fluid volume, and extracellular fluid volume what would occur if hypotonic (0.45%) NaCl were given?

A
  • Osmolarity for ICF & ECF would decrease
  • ICF volume would expand
  • ECF volume would expand
55
Q

What drugs can make the body less tolerant of blood loss?
Why is this?

A
  • ACE inhibitors & ARBs
  • RAA-System is inhibited and BP can’t be raised as easily.
56
Q

How much is surface area increased by the brush border?

A
  • 20x
57
Q

Differentiate Type A and Type B intercalated cells?

A
  • Type A get rid of H⁺
  • Type B retain H⁺
58
Q

Where are Intercalated cells located?
What types are there?
What are they responsive to?

A
  • Late Distal Tubule, Cortical & Medullary Collecting Ducts.
  • Type A & B Intercalated Cells
  • ADH

A&P I 2024 (18 decks)

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