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Pharmacology & Drugs > Renal-Electolytes > Flashcards

Renal-Electolytes Flashcards

1
Q

What is the role and effect of increased TRPV5

A

TRPV5 increases the amount of calcium that is reabsorbed in the distal convoluted tubule

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2
Q

Where is calcium reabsorbed and what is the mechanism

A
  • 65 in the proximal tubule via paracellular manner
  • 20 in the thick ascending loop via positive voltage paracellular manner
  • 8 in distal tubule, but is active transport and very regulated
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3
Q

The Chvostek’s sign and Trousseau’s sign are seen in which conditions

A
  • Hypocalcemia (main one)

- hypomagnesemia and alkalosis (decreased ionized calcium)

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4
Q

What are the general causes of extracellular edema

A
  • Increased capillary hydrostatic pressure
  • loss of plasma proteins
  • Increased capillary permeability
  • Blockage of lymph return
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5
Q

What is the main location and the main mechanism of phosphate reabsorption in the kidneys

A

55-85% in the proximal convoluted tubule vie NaPi2

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6
Q

Where is the majority of calcium in the body stored

A

Bone

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7
Q

What is the mechanism that chronic renal disease cause bone demineralization (aka renal osteodystrophy)

A
  • Kidneys start to fail and unable to excrete the Needed phosphate, causing hyperphosphatemia
  • Hyperphosphatemia causes secondary hyperPTHism (causes bone demineralization)
  • Kidney is unable to activate Vitamin D to calcitriol, which results in inability to absorb Calcium from the diet
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8
Q

What is the treatment of hypermagnesemia in patients with reduced renal function

A

Add saline and diuretic

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9
Q

What is the treatment for hypocalcemia

A
  • Intravenous calcium (emergency situations0
  • Oral calcium, can be with vitamin D (chronic, mild hypocalcemia)
  • Calcium and Vitamin D (hypoPTH)
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10
Q

What are the main causes of hyperphosphatemia

A
  • Chronic kidney diseases stage 3-5

- Acute renal failure/injury

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11
Q

RBC cell lysis can cause which pseudosyndrome

A

Pseudohyperkalemia

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12
Q

Hypokalemia leads to changes in which metabolic serum level

A

Causes hyperglycemia because the glucose can not be brought into the cell since potassium is needed

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13
Q

What is the merchandise of fibroblast growth factor 23 (FGF) on phosphate levels

A

-Released by bones that promote phosphate excretion by the kidneys

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14
Q

What is usually the result of renal failure on phosphate levels

A

Because the kidneys are the main excretion route, a decreased GFR results in inability to clear the necessary 900mg/day

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15
Q

What is the treatment for level 1 hyponatremia

A

Very minimal symptoms, so fluid restrictions

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16
Q

What is the conductance of calcium across TRPV5 regulated by

A

PTH and locally synthesis of kallikrein

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17
Q

Which drugs will cause ECF potassium to be excreted

A

Aldosterone

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18
Q

What is the effect of aldosterone ad where is it working

A

Works in the principal cells in the collecting duct, and serves to increased the amount of sodium reabsorption, which causes potassium to leak out into the lumen and urine

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19
Q

What are the sites or calcium regulation

A

Kidney, bone, intestine

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20
Q

What is the treatment for hyperphosphatemia

A
  • Calcium and vitamin D supplementation
  • Restriction of phosphate in diet and phosphate binders
  • Hemodualysis and renal transplant
  • Cinacalcet (lowers PTH)
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21
Q

What is the correction amount for hypernatremia

A

Over 48 hours as

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22
Q

What is the effect of increased calcium levels on the threshold

A

Increases the threshold

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23
Q

What is the function of angiotensin 2 on maintaining GFR

A

Maintains the resistance in efferent arterioles, so as a result, the GFR is maintained

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24
Q

Plasma ADH levels are most sensitive to which plasma level content

A

The plasma osmolality is the largest determiner

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25
Q

How is the level of PTH controlled

A

-Serum calcium sensor receptors on parathyroid cells that is activated with low [Ca] levels

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26
Q

What are the most common causes of hypercalcemia

A
  • Bone resorption
  • Intestine absorption
  • Usually in conjunction with decreased renal calcium clearance
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27
Q

What are the causes of intracellular edema

A
  • Depression of the metabolic systems of tissues
  • Lack of adequate nutrition into the cell (Sodium potassium pump stops working, so sodium builds up in the cell, and water follows
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28
Q

What are the the clinical features of hypercalcemia

A
  • GI symptoms: anorexia, nausea, vomiting, and constipation
  • Neuro symptoms: weakness, fatigue, confusion
  • Vomiting causes a volume contraction, furthering the issue of hypercalcemia
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29
Q

What are the treatments for hyperphosphatemia

A
  • Saline diuresis (acute condition)

- Reduced dietary intake (end stage kidney disease)

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30
Q

With regards to serum phosphate levels, what is the result of increased PTH

A

Decreased due to increased renal excretion with increased calcium reabsorption

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31
Q

What is a common cause of hypophosphatemia and what is the mechanism

A 
Refeeding hypophophosphatemia (feeding a starving person)
*Because feeding a once starving person, the increased glucose causes phosphate to be pulled into the cell, lowering the ECF levels
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32
Q

What are the 3 ways that calcitonin lowers blood [Calcium]

A
  • Inhibits Calcium from the intestine
  • Inhibits osteoclast activity in bones
  • Inhibits renal tubular cell reabsorption of Calcium (increases calcium)
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33
Q

How is calcitriol created

A

Stimulated by PTH

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34
Q

With regards to serum phosphate levels, what is the result of increased vitamin D

A

Increased due to increased intestinal absorption

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35
Q

What are the symptoms of hypocalcemia seen in the CNS

A
  • Irritabilty, depression
  • coma
  • Tonic clonic seizures
  • papilledema
36
Q

What are the clinical signs of hypophosphatemia

A
  • only appears when there is total body phosphate depletion
  • Muscular abnormalities with respiratory failure and failing diaphragmatic function
  • Hemolysis and platelet dysfunction
  • Chronic hypophosphatemia leading to rickets and osteomalacia
37
Q

What are the general treatments for patients with hypophosphatemia

A

Administration of phosphates (whether oral or IV depending on the severity)

38
Q

What regulates the levels of phosphate reabsorption via NaPi2

A

PTH and FGF23

39
Q

What is the result of increased amounts of Klotho

A

An enzyme that breaks down complex carbs, and serves to stimulate and active the TRPV5 to increase calcium reabsorption

40
Q

What is the role of calcium levels in the activity of nerves, smooth, cardiac, and skeletal muscle

A

The threshold is determined by the level of free calcium

41
Q

What are the general targets of treatment for acute hypercalcemia

A
  • Increasing calcium excretion
  • decreasing resorption of calcium from bone
  • Decreasing absorption of intestinal calcium
42
Q

What is the method of regulation and reabsorption of calcium in the distal tubule

A
  • Active transport
  • Renal epithelial Ca channel (TRPV5)
  • Calbindin, regulated by calcitriol
43
Q

What is the treatment for acute hypercalcemia

A
  • ECF volume replacement with .9% saline
  • Furosemide
  • bisphosphonates if not responding to diuretics or is a malignancy
44
Q

Which conditions commonly are present in patients with hypophosphatemia

A

-Hypokalemic and hypomagnesemic

45
Q

What calcium values should be used if the albumin levels are abnormal in a patient

A

Should be based on the ionized calcium levels

46
Q

What is the result on GFR in the cause of using an ACE inhibator

A

Decreased angiotensin 2 release, resulting in the loss of resistance in the efferent arterioles, resulting in vasodilation and the decrease in GFR and increased creatinine levels

47
Q

What are the common patients seen to have hypomagnesium and what are the common causes

A

60% of ICU patients

  • Decreased nutrition
  • Diuretics
  • Decreased albumin
  • Aminoglucosides
  • Decreased reabsoprtion (due to PPI)
48
Q

Where is the majority of magnesium reabsorbed and its mechanism

A

Thick ascending limp via transepithelial gradient from the potassium/sodium/chloride transporter there
*This is nice that PCT is not the major site

49
Q

What are the clinical features of hyperphosphatemia

A
  • Usually seen as the result on concurrent hypocalcemia
  • Tissue ischemia or calciphylaxis (vascular calcification)
  • Chronic hyperphosphatemia cause lead to renal osteodystrophy
50
Q

What are the common things reabsorbed in the early proximal tubule

A
  • Sodium
  • Glucose
  • Amino Acids
51
Q

What is the effect of hypoalbuminemia on calcium levels

A

Decreases the total serum calcium levels, but does not affect the level of ionized calcium levels

52
Q

Which malignancy is classically a cause of SIADH

A

-Small cell lung cancer (OAT cell) that produces mass amounts of ADH

53
Q

Which drugs will cause ECF potassium to be places in tissue stores

A

Insulin
Epinephrine
Aldosterone

54
Q

What is the effect of changes to albumin with regards to calcium

A

Changes in albumin will result in a change in the total calcium, but not the ionized calcium levels

55
Q

Of the 49% of the magnesium in the ICF, what percentage is ionized and what is its main function

A

-10% is ionized and used as a cofactor in biochemical processes such as ATPases and ion channels

56
Q

What is the classical EKG finding with hyperkalemia

A

High T wave

57
Q

What is the result of carbohydrate of glucose infusion on the phosphate serum level

A

Decreases it

58
Q

What is the only hormone regulator of magnesium

A

EGF

59
Q

What are the symptoms of hypocalcemia seen in the dermatological and ocular system

A
  • Dry skin, course har, brittle nails

- Cataracts

60
Q

What is the effect of increased levels of calcitriol

A
  • Promotes absorption of calcium in GI tract
  • Increased renal tubular reabsorption (reuptake)
  • Stimulates release of calcium from bone
  • Overall, causes the increased [Ca] plasma
61
Q

What are the general factors that could cause hypercalcemia

A
  • Primary hyperPTH
  • Malignancy
  • immobilization Syndrome
  • Vitamin D intoxication
  • thiazides
62
Q

What is the effect of decreased calcium levels on the threshold

A

Decreases the threshold

63
Q

With regards to serum phosphate levels, what is the result of increased FGF-23

A

Decreased due to increased renal excretion

64
Q

What is the mechanism of GFR changes seen during increased sodium increase

A

Increased sodium leads to increased ECF resulting in:

  • Decreased sympathetics —> dilation of afferent arterioles and increased GFR
  • Increased ANP —> Increased GFR
  • Decreased renin —> Increased GFR
  • Decreased angiotensin and ADH—> increased excretion of Na and H2O
65
Q

With the production of PTH, what are the serum level values and their mechanisms

A
  • Increased plasma [Ca] (increased calcium reabsorption in the distal nephron
  • Decreased plasma [PO4] (inhibits PO4 reabsorption in the proximal tubule)
  • Increased ionized [Ca] (enhanced bone release of calcium)
66
Q

Of the 1% if the magnesium that is in the ECF, what percent is ionized

A

60%

67
Q

What is the treatment of hypermagnesemia in patients with end stage renal disease

A

Dialysis

68
Q

What are the symptoms of hypocalcemia seen in the Neuromuscular system

A
  • Tetany, carpopedal spasms
  • Chvostek’s sign
  • peresthesias, numbness
  • Muscle twitching or cramping
69
Q

What is the role of vitamins D in the kidneys with regards to calcium regulation in the distal convoluted tubule

A

Regulates the levels of calbindin-D28K and TRPV5 expression

70
Q

What is the treatment of hypermagnesemia in patients with normal renal function

A

Stop administering of Mg and let normal renal function do the job, or add a loop diuretic

71
Q

What are the effects of calcitonin on the levels of blood [Calcium]

A

Lowers the amount of blood [Calcium]

72
Q

What is the mechanism of reabsorption of magnesium in the PCT

A

Paracellular

73
Q

What are the effects of calcitriol and PTH on calcium levels

A

Increase the amount of blood [Calcium]

74
Q

What is the treatment for level 3 hyponatremia

A

Hypertonic NaCl and vaptans with Fluid Restriction

75
Q

What is the treatment for level 2 hyponatremia

A

Moderate symptoms, given a vaptan or hypertonic NaCl

76
Q

With regards to serum phosphate levels, what is the result of increased insulin

A

Decreased due to phosphate pulled into cells

77
Q

What is the classically EKG finding in hypokalemia

A

High U wave, low T wave

78
Q

What is the physiological responses to hypercalcemia

A
  • Decreased PTH —> decreased resorption (breakdown) from bone
  • Decreased vitamin D—> Increased calcium excretion, Decreased intestinal calcium absorption
79
Q

What are the symptoms of hypocalcemia seen in the CCV

A
  • lengthened QT
  • Hyoptension
  • CHF
  • Dysrhythmias
80
Q

How is the majority of excess phosphate excreted

A

In the urine (910 mg/day)

81
Q

When is hypermagnesia usually seen

A
  • very rarely
  • End stage renal disease
  • Large epsom salt intake
  • Magnesium infusion (usually in preeclampsia women)
82
Q

What is the mechanism of action in the kidneys when increased RBF and GFR are detected

A
  • Increased RBF and GFR
  • increased delivery to JG apparatus and macula densa
  • Increased resistance to the afferent arteriole
  • Leads to decrease in the RBF and GFR
83
Q

What portion of the calcium is regulated

A

Only the free, ionized calcium in the ECF is regulated

84
Q

What are the clinical signs of hypomagnesium

A

Usually follow the symptoms of hypocalcemia

*Because usually associated with hypocalcemia and hypokalemia

85
Q

Where are the locations of magnesium storage

A
  • 50 in the bone

- 49 in the cell (ICF)

Pharmacology & Drugs (43 decks)

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