Block Vii, Week Via

Front 1

on average, what is the amount of our total body water?

Back 1

42L

Front 2

on average, what is the amount of our extracellular fluid (ECV)?

Back 2

14L

Front 3

on average, what is the amount of our intracellular fluid?

Back 3

28L

Front 4

two compartments within the extracellular?

Back 4

1. Interstitial fluid (11L)
2. Plasma (3L)

Front 5

ratio of TBW: ICV: ECV

Back 5

60:40:20

Front 6

what would alter the percentage of our body weight that is water?

Back 6

fat content (increase fat, decrease water)

Front 7

which compartment do RBCs fall into?

Back 7

intracellular

Front 8

which electrolyte is found in highest concentration in the intracellular compartment?

Back 8

K+

Front 9

which electrolytes are found in highest concentration in the extracellular compartment? (3)

Back 9

Na+
Cl-
HCO3-

Front 10

if you hydrate a patient with IV saline, in which compartment does the fluid distribute?

Back 10

extracellular

Front 11

what are some clinical s/s that indicate an expanded ECF volume? (5)

Back 11

1. HTN
2. elevated JVP
3. hepatic congestion
4. hepatojugular reflex
5. edema, rales

Front 12

what are some clinical s/s that indicate a diminished ECF volume? (7)

Back 12

1. orthostatic hypotension
2. decreased JVP
3. hypotension
4. shock
5. dry mouth and membranes
6. diminished skin turgor
7. diminished intraocular pressure

Front 13

3 lab values that would indicate a diminished ECFV?

Back 13

1. BUN/Cr > 20
2. FENA <1%
3. Urine osmolality >600mOSM/L

Front 14

what is the formula for calculating FENA?

Back 14

FENA = U[Na+] / P[Na+] x P[Cr] / U[Cr] x 100

Front 15

treatment for an ECFV loss?

Back 15

infuse isotonic saline (4:1)

Front 16

what is the site of action of thiazide diuretics?

Back 16

distal tubule

Front 17

which ion do thiazides excrete in urine?

Back 17

NaCl
K+

Front 18

which type of diuretic is used to treat glaucoma?

Back 18

carbonic anhydrase inhibitor
(acetazolamide)

Front 19

site of action of carbonic anhydrase inhibitors?

Back 19

proximal tubule

Front 20

ions excreted in urine when using a carbonic anhydrase inhibitor?

Back 20

NaHCO3
(great for use in volume overload or alkalotic patient - gets rid of bicarb)

Front 21

where do K+ sparing diuretics work?

Back 21

distal and cortical collecting tubule

Front 22

name three K+ sparing diuretics

Back 22

1. triamterene
2. amiloride
3. spironolactone

Front 23

site of action of loop diuretics?

Back 23

Loop of Henle - Duh!
:)

Front 24

MOA of loop diuretics?

Back 24

inhibit Na/K/Cl pumps, therefore ions aren't pumped out of the lumen

Front 25

what could make a loop diuretic not work?

Back 25

they must be secreted into the proximal tubule, so if there is no secretion they won't work.

Front 26

where in the nephron are Na+ channels found on the apical membrane?

Back 26

in the DT and CD

Front 27

where in the nephron is NaCl symport found?

Back 27

DT

Front 28

on which side of the tubular epithelial cell is the Na/K/ATPase found?

Back 28

basolateral membrane (interstitial side)

Front 29

which hormone regulates Na+ transport in the distal tubule and collecting duct?

Back 29

Aldosterone

Front 30

what effect does increased fluid flow in the tubular lumen have on K+ excretion?

Back 30

increase flow -> increase K+ excretion
(diffusion only, remember?)

Front 31

if you can't concentrate your urine, what three types of problems could you have?

Back 31

1. Loop Problem
2. No ADH production or release
3. No receptors for ADH in CD

Front 32

how does ADH regulate urine concentration?

Back 32

adds water channels (aquaporins) to the collecting duct: water diffuses out as needed

Front 33

if ADH regulates water retention, what does Aldosterone regulate?

Back 33

Na+ retention

Front 34

what are the two receptors for ADH?

Back 34

V1 - vascular smooth muscle
V2 - distal tubule and collecting duct

Front 35

which receptors can trigger ADH release?

Back 35

1. osmoreceptors in hypothalamus (sense plasma osmolality and [Na+])
2. low volume receptors (atria)
3. arterial baroreceptors

Front 36

which receptor is the most sensitive?

Back 36

osmoreceptors

Front 37

what happens to [Na+] during ECFV depletion?

Back 37

hyponatremia

Front 38

at what plasma [Na+] do we start to have serious neurological concerns?

Back 38

Plasma [Na+] <120 mMol/L

Front 39

what is the formula to calculate plasma osmolarity?

Back 39

Posm = 2 x [PNa+] + [glucose] / 18 + BUN/2.8

Front 40

what [PNa+] counts as hyponatremia?

Back 40

[PNa+] < 130 mEq/L

Front 41

using the Posm formula: how would we know if we had pseudohyponatremia?

Back 41

if the measured Posm >10 mOsm greater than calculated Posm. (This means there is an extra osmolyte producing hyponatremia via osmoreceptor stimulated ADH release)

Front 42

what is the most common euvolemic cause of hyponatremia?

Back 42

SIADH (syndrome of innapropriate ADH secretion)

Front 43

what is the therapy for hypovolemic hyponatremia?

Back 43

isotonic saline infusion

Front 44

what is the therapy for euvolemic hyponatremia?

Back 44

fluid restriction

Front 45

therapy for hypervolemic hyponatremia?

Back 45

fluid restriction

Front 46

clinically, which is more dangerous: hypernatremia or hyponatremia?

Back 46

hyponatremia

Front 47

what [PNa+] couts as hypernatremia?

Back 47

[PNa+] > 145 mEq/L

Front 48

in a hypernatremic state which fluid compartment is depleted?

Back 48

intracellular fluid compartment

Front 49

what are the three main classes of causes of hypernatremia?

Back 49

1. pure water loss
2. more water loss than Na+ loss
3. Sodium gain in excess of water

Front 50

examples of pure water loss resulting in hypernatremia?

Back 50

1. respiratory
2. burns
3. DI (ADH deficiency)
4. nephrogenic DI (no AHD receptors)

Front 51

two ways there could be more water loss than Na+ loss?

Back 51

1. GI losses
2. Diuretics

Front 52

therapy for hypernatremia?

Back 52

add water
remove salt from diet

Front 53

what are some ways to differentiate DI (nephrogenic or central)?

Back 53

1. measure AHD blood levels
(increased in nephrogenic DI, decreased in central DI)
2. water deprivation test
(complete DI will respond to exogenous ADH, NDI will not)

Front 54

what is the MC outpatient cause of acute renal failure?

Back 54

NSAIDs

Front 55

clinical recognition of drug-induced renal disease?

Back 55

1. increased BUN, SCr
2. decreased urine output

Front 56

what symptoms are associated with uremia?

Back 56

malaise
anorexia
vomiting

Front 57

clinically, how can you tell if the proximal tubule vs. the distal tubule is damaged?

Back 57

proximal tubule: glycosuria, hypophosphatemia, hypouricemia
distal tubule: polyuria, hyperkalemia

Front 58

which drug classes are MC associated with drug-induced renal disease? (6)

Back 58

1. aminoglycosides
2. amphotericin B
3. NSAIDs
4. ACEIs and ARBs
5. Radiocontrast dyes
6. chemotherapeutic agents (cisplatin)

Front 59

what is pseudo-renal failure?

Back 59

a rise in BUN and/or SCr despite a normal GFR

Front 60

what could cause pseudo-renal failure? (3)

Back 60

1. steroids
2. tetracyclines
3. patients of TPN (due to high aa content)

Front 61

what is the pathogenesis behind renal damage caused by ACEIs and ARBs?

Back 61

decreased glomerular capillary hydrostatic pressure
(pressure at glomerulus is reduced, therefore GFR is reduced)

Front 62

which 2 vasoactive substances act on the afferent arteriole?

Back 62

1. PGE2
2. angiotensin II

Front 63

which vasoactive substance acts on the efferent arteriole?

Back 63

angiotensin II

Front 64

what are two risk factors for renal disease caused by ACEIs/ARBs?

Back 64

1. Renal Artery Stenosis
2. decresed effective arterial renal blood flow for any reason

Front 65

how can renal disease caused by ACEIs/ARBs be prevented?

Back 65

when starting the medication:
use a short acting med (captopril), start with low doses, and titrate slowly. if all is well convert to long term med.
*monitor renal function and K+ during initiation of therapy*

Front 66

how can we manage acute hyperkalemia if it is seen with renal disease caused by ACEIs/ARBs?

Back 66

sodium polystyrene sulfate (kaexalate - K+ binding agent).

Front 67

which NSAID has been associated with ARF after just one dose?

Back 67

ketorolac
(parenteral NSAID)

Front 68

pathogenesis of ARF caused by NSAIDs?

Back 68

* COX inhibitor decreases prostaglandin synthesis
* no more vasodilatory prostaglandins to dilate afferent arteriole. get unopposed vasoconstriction -> reduced blood flow -> decreased GFR

Front 69

other analgesics that have less prostaglandin inhibition (therefore we would recommend them for anyone at risk for ARF)? (3)

Back 69

acetaminophen
sulindac
nonacetylated salicylates

Front 70

what is unique about the clinical presentation of ARF caused by aminoglycosides?

Back 70

decreased urine volume is uncommon.
(ARF caused by other drugs typically presents with decreased urine output).

Front 71

pathogenesis of aminoglycoside induced nephrotoxicity? (big picture)

Back 71

* proximal tubul epithelial cell damage leads to obstruction of tubular lumen and backleak of glomerular filtrate across damaged epithelium.

Front 72

how does nephrotoxicity vary among different aminoglycosides?

Back 72

nephrotoxicity is related to the # of cationic charges the drug has (facilitates binding to epithelial cell)
* neomycin has highest nephrotoxicity (most + groups)
* gentamycin - intermediate
* amikacin - least

Front 73

what happens once the aminoglycosides are bound to the epithelial cell?

Back 73

they are taken up into the cells and concentrated in the lysosomes
*cellular dysfunction and death is due to release of lysosomal enzymes

Front 74

risk factors (related to dosing)that lead to aminoglycoside nephrotoxicity? (4)

Back 74

1. large total accumulated dose
2. prolonged therapy
3. high trough concentrations
4. recent previous aminoglycoside therapy

Front 75

four drugs that synergistically can be nephrotoxic alongside aminoglycosides?

Back 75

1. cyclosporine
2. amphotericin B
3. vancomycin
4. diuretics

Front 76

prevention of aminoglycoside toxicity?

Back 76

* adequate hydration
* avoid concomitant nephrotoxic drugs
* higher doses less frequently (once daily)

Front 77

what is an alternative antibiotic that is "kidney friendly" if a switch from aminoglycosides is desired?

Back 77

Ciprofloxacin

Front 78

when a patient is on aminoglycosides - how often should SCr be monitored?

Back 78

every 2-4 days

Front 79

what is the pathogenesis of radiographic contrast media induced nephrotoxicity?

Back 79

direct tubular toxicity and renal ischemia
-ischemia is due to dehydration (contrast dye is a very osmolar compound, acts as a diuretic)

Front 80

#1 prevention tactic for radiographic contrast media nephrotoxicity?

Back 80

HYDRATION
(isotonic saline IV)

Front 81

what is mucormyst (n-acetylcysteine)?

Back 81

antioxidant, free radical scavenger - thought to lower chances of radiographic contrast media induced nephrotoxicity?

Front 82

what is the pathogenesis of cisplatin induced nephrotoxicity?

Back 82

proximal, distal and collecting duct tubular necrosis

Front 83

4 risk factors for cisplatin induced nephrotoxicity?

Back 83

1. increased age
2. dehydration
3. renal irradiation
4. ETOH abuse

Front 84

what can be administered if a patient has cisplatin induced nephrotoxicity?

Back 84

amifostine
(Chelates cisplatin)

Front 85

pathogenesis of Amphotericin B induced nephrotoxicity?

Back 85

proximal and distal tubule damage
(direct toxicity with increased tubular permeability and necrosis)
- results in arterial vasoconstriction

Front 86

Cockraft-Gault formula for estimating creatinine clearance (CrCl)?

Back 86

CrCl = (140-age)LBW / 72(SCr)

Front 87

what is the CrCl "cutoff" for renal dosing?

Back 87

when CrCl is below 30 - dose adjustment required