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Therapeutics P2 > Exam 1 lecture 5 > Flashcards

Exam 1 lecture 5 Flashcards

1
Q

CrCl formula

A

(SCR x 72)

That is for males. Multiply by 0.85* for females

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2
Q

When to use CrCl? when not to use CRCL?

A

Use for patients that have stable kidney function, never for AKI patients

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3
Q

IBW formula

A

IBW men- 50+2.3(inches over 60)
IBW women- 45.5 + 2.3 (inches over 60)

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4
Q

When to use adjusted body weight? Formula?

A

AdjBW= IBW + 0.4 (ABW-IBW)
Use is patient is >130% of IBW

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5
Q

What are the 4 functions of kidney

A

excretes waste products of metabolism from the blood (urea/uric acid)

regulates bodys concentration of water and salt

Maintains acid balance of plasma (secretes H+ ions)

synthesizes calcitrol

secretes hormones (erythropoietin)

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6
Q

What is uremia

A

Build up of waste products in blood.

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7
Q

Uremia monitoring parameters

A

(Increased BUN, pruritis, confusion, nausea)

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8
Q

How does the kidney maintain PH of plasma

A

secretes H+ ions

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9
Q

What are the 5 complications that could result when the functions of the kidney are compromised

A
  1. metabolism & excretion- uremia
  2. fluid regulation- edema
  3. Acid balance of plasma- acidosis, electrolyte imbalances
  4. calcitrol synthesis- Mineral and bone disorder
    erythropoietin secretion- Anemia
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10
Q

What is uremia caused by

A

Accumulation of waste molecules in blood that are normally removed by kidney

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11
Q

What should we monitor in uremia pts

A

BUN

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12
Q

BUN normal range

A

Normal BUN< or = 15

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13
Q

effects of uremia on body

A

Encephalopathy
uremic factor (breath)
nausea
uremic frost on skin (itching)

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14
Q

how does kidney disease effect removal of fluid in body

A

Kidney disease leads to fluid retention. This will lead to edema and increased BP

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15
Q

How to treat patients with diuretic resistance

A

Use a loop diuretic with a thiazide

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16
Q

Where do loop diuretics exert effect

A

Loop of henle

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17
Q

Why is using thiazides and loop diuretics more effective than just using loop diuretics

A

loop diuretics block sodium in loop of henle.
eventually these sodium molecules pass loop and go to DCT.
Cells in DCT start uptaking Na and water goes with Na. Loop diuretics stop working. We can use thiazides to block DCT.

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18
Q

T/F if one loop diuretic stops working we can try using another loop diuretic

A

False, poor response to one means poor response to all.

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19
Q

Thiazides are ineffective when CRCL os

A

Less than 30
Loops work below 30

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20
Q

Loop diuretic that is not a sulfa type drug?

A

Ethacrynic acid
patients that have sulfa allergies can use this as loop diuretic

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21
Q

Loop diuretics examples that have sulfa

A

Furosemide, bumetadine, torsemide

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22
Q

Effect of kidney decline on electrolyte imbalance

A

patients hold on to sodium if their kidney declines.

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23
Q

What to do in patients that have electrolyte imbalances (K and Na)

A

There is no need to severely restrict sodium beyond a no salt added diet (<2 g sodium per day) or <5g NaCl)
Make outpatients aware of foods with high sodium (hotdogs, canned soup)

restrict K to <3gm/day
avoid high K foods (tomatoes, dried fruits, salt substitute)
We can use dialysis for hyperkalemia pts

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24
Q

How does progressive kidney disease affect phosphate excretion

A

PKD leads to impaired phosphate excretion. This leads to phosphate retention.

25
Q

How does progressive kidney disease lead to osteoporosis and bone disorder

A

-Impaired PO4 excretion
-leads phosphate retention
- leads to hypocalcemia (due to formation of calcium phosphate in blood)
- leads to an increase in PTH production
- leads to hyperparathyroidism
-parathyroid hormone pumps out Ca into blood, gets Ca from bones
-leads to osteoporosis

26
Q

How does phosphorous retention caused by progressive kidney disease cause hypocalcemia

A

Phosphate binds calcium in blood, forming calcium phosphate (soft tissue calcification), this leads to less free calcium. This calcium phosphate leads to formation of rocks that deposit in body.

27
Q

How does hypocalcemia affect PTH

A

low calcium leads to increased PTH secretion, causing Ca to be pumped out of bones, leading to osteoporosis

28
Q

Where is vit D activated

A

Kidney

29
Q

what effect does kidney deterioration have of vit D and the body

A

Usually, vit D is activated in kidney, when kidney deteriorates, it does not activate vit D

This leads to decreased intestinal absorption of phosphorous and calcium, leading to hypocalcemia.

This causes the parathyroid gland to produce PTH

PTH pumps Ca out of blood, leads to osteoporosis

30
Q

What are the 3 main factors that cause an increase of PTH leading to osteoporosis

A

increased PTH
Decreased Ca
decreased vit D

31
Q

T/F hyperphosphatemia is a problem for all ESRD patients

A

True

32
Q

What is a normal phosphorous range

A

2.5-4.5

33
Q

Can we pull phosphorous out of the blood once it is in?

A

No

34
Q

What is the only way to make phosphorous go down?

A

Being used in normal biologic activities

35
Q

Two ways to manage phosphorous inside body

A

diet
phosphate binders

36
Q

What are the two types of phosphate binders

A

Calcium containing phosphate binders
non-calcium containing phosphate binders

37
Q

Name the calcium containing phosphate binders

A

Tums (calcium carbonate)
calcium acetate (phosLo)

38
Q

mechanism behind calcium phosphate binders

A

Calcium binds phosphorous before it gets absorbed (may cause soft tissue calcification)

always give with food. absorbs phosphate from food

39
Q

calcium carbonate mechanism

A

give with food to prevent absorption of of po4

40
Q

What number must not be exceeded with tums (calcium carbonate)? why?

A

1500 mg/d of elemental calcium.
may get absorbed in blood and bind phosphate, soft tissue calcification.)

41
Q

What percent elemental calcium is tums

A

40%

42
Q

what percent elemental calcium is phosLo? What is the maximum amount to take per day?

A

25%
1500 mg/day

43
Q

side effects of phoslo and tums

A

Constipation
do not exceed 1500 mg /day for either

44
Q

What patients do we not use (calcium acetate) phoslo or tums in

A

Pts with high phosphate, could cause soft tissue calcification

45
Q

how many g of elemental calcium in a tums

A

300

46
Q

how many g of elemental calcium in phoslo

A

169

47
Q

what are some non-calcium containing phosphate binders

A

sevelamer carbonate(renvela)
lanthanum carbonate (fosenrol)
sucroferric oxyhydroxide (velphoro)
Auryxia (ferric acetate)

48
Q

which phosphate binder reduces LDL and uric acid

A

sevelamer carbonate

49
Q

Is sevelamer absorbed?

A

No

50
Q

dose of sevelamer

A

14gm/day x 8 days

51
Q

ADR for sevelamer

A

NONE
maybe a little stomach upset

52
Q

What is the unique thing about lanthanum

A

maintains efficacy over broad PH range

53
Q

how is lanthanum eliminated

A

feces, does not cross BBB.

54
Q

mechanism of sucroferric oxyhydroxide

A

Contains Iron, iron binds phosphate so strongly that it does not get absorbed into body.

55
Q

Does sucroferric oxyhydroxide get absorbed in the body?

A

No, iron levels do not change

56
Q

Which non calcium phosphate binder abxorbs iron in body (can be used for patients with low iron?

A

auryxia (ferric acetate)

57
Q

why should we not use amphojel (aluminum hydroxide?

A

can cause kidney toxicity (Al eliminated by kidney)

58
Q

dietary phosphorous intake should be restricted to

A

800-1000 mg/day

59
Q

what are some foods high in phosphorous

A

meat, nut dairy, dried beans, colas, beer

Therapeutics P2 (41 decks)

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