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Pharmacology > Renal > Flashcards

Renal Flashcards

1
Q

Formula for clearance

A

C=(UxV)/P

Clearance
Using concentration
Urine flow rate
Plasma concentration

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2
Q

GFR

A

Clearance PAH

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3
Q

Filtration fraction

A

GFR/eRPF

Effective renal blood flow=effective plasma flow/fraction of blood that is plasma

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4
Q

Usually FF

A

.17-.21

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5
Q

Early stages of DM are associated with what

A

Glomerular hypertension/hyperfiltration. Give ACE inhibitors or angiotensin receptor blockers

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6
Q

What is the clearance of a solute

A

Ml/min plasma from which all of solute x has been removed

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7
Q

To calculate GFR we use 24 hour infusion of insulin. Why

A

Freely filtered
Not reabsorbed
Not secreted

Not endogenous molecule satisfies those conditions

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8
Q

How calculate true GFR

A

Insulin clearance

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9
Q

What must happen for clearance to exceed GFR

A

Tubular secretion

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10
Q

What endogenous chemical clearance equals the effective renal plasma flow

A

PAH (p-aminohippurate)

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11
Q

How calculate effective renal blood flow (RBF)

A

ERPF/fraction of blood that is plasma

?????
Fraction of blood that is plasma=1-hematocrit

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12
Q

Filtration fraction

A

True GFR(inulin clearance)/EPRF (PAH clearance)

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13
Q

T1/2

A

(.693 Vd)/clearance

Vd =apparent volume of distribution for the solute (I-iothalamate) freely filtered and not reabsorbed but has tubular secretion

Vd and T1/2 then allows the clearance rate to be calculated

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14
Q

Creatinine

A

Freely filtered, not reabsorbed but some secretion

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15
Q

Error in GFR from creatine

A

Creatinine clearance-inulin/inulin clearance ???

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16
Q

Why does error increase as GFR increases

A

As DFR falls the fraction of the total mass of creatinine ending in the urine decreases and more Plasma Cr

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17
Q

Creatine can be used to calculate GFR, but what’s thie issue with old people

A

Produce less creatine due to a decline in muscle mass—-so can remain normal despite significant decline in renal function

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18
Q

Cockcroft galt forma for creatine clearance (ml/min)

A 
((140-age)x(wt(kg))/
serum creatinine (mg/dL)x72) (x.85 for females)
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19
Q

MDRD formula for GFR

A

Takes into account race,surface area

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20
Q

Fraction of filtered solute that ends up in the urine

A

(VxU)/GFRxP

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21
Q

If inulin concentration in infusion is doubled. What happens to

Clearance
U V

FE

A

Idk

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22
Q

How does glucose clearance change

A

Doesn’t
Clearance is always 0

If above issue osmotic retention and polyuria and polydipsia

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23
Q

Clearance H20

A

V-Cosm

=-.88?????

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24
Q

Free water clearance 0

Free water clearance positive

Free water clearance negative

A

Plasma osmolality=urine osmolality

Urine dilute

Urine is concentrated

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25
Q

How calculate daily sodium intake

A

Daily input=output

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26
Q

TBW white male

A

23-(.03age)+(.5weight)-(.62xBMI)

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27
Q

TBW black male

A

-18.37-(.09age)+(.34weight)+(.25height)

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28
Q

TBW white female

A

-10.5-(.01age)+(.2weight)+(.18height)

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29
Q

TBW black female

A

-16.71-(.05age)+(.22weight)+.24height

Height cm and weight kg

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30
Q

Na requirement

A

TBWx(desired Na-serum Na)

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31
Q

Wish to raise the resum Na from 120 to 135 when TBW is 35.8. How many ml of 3% NaCl solution (513mmol/L0 would need to be infused to meet the Na requirement

A

1046.78

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32
Q

Fractional Excretion Na

A

Usually near 1%

Na excreted/Na filtered= UxV/PxGFR=Cna/Ccr

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33
Q

BUN:Cr normal

A

10-15:1

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34
Q

Low BUN:Cr

A

Acute tubular necrosis (damage to kidney parenchyma so urine is more of an extracelular fluid ooze-cant concentrate)specific granite <1.01

Low protein intake

Starvation

Severe liver disease

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35
Q

High BUN:Cr

A

Pre renal acute kidney injury (small amount of concentrated urine, specific gravity >1.02)

High protein intak e

After GI bleed

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36
Q

Post renal AKI

A

Small amount of normal uring
Imaging will show accumulation upstream from block

Relief of obstruction can lead to post obstructive diuresis, can be life threatening

Blood uring

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37
Q

24 hour protein excretion (mg/day)

A

UproxV

Uprox(24hrUcr/Ucr)

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38
Q

Calculate 24 hour creatine. Excretion

A

UcrxV

V=24 hr U Cr/UCr

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39
Q

Upro/Ucr

A

Grams/day of protein excreted

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40
Q

Microalbumin

A

Detect small amounts in urine (trace amounts)

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41
Q

Name thiazide diuretics (hypertension, edema)

A

Hydrochlorothiazide
Metolazone
Chlorthilidone

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42
Q

Name loop diuretics (edema, hypertension)

A

Furosemide
Torsemide
Bumetanide
Ethacrynic acid

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43
Q

K sparing diuretics

A

Na channel blocker

  • amigo ride
  • triamterene

Aldosterone antagonist

  • spironolactone
  • eplerenone
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44
Q

Aquaretics (hyponatremia

A

Conivaptan

Tolvaptan

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45
Q

Carbonic anhydrase inhibitor (urinary alkalinization, mountain sickness, glaucoma)

A

Acetazolamide

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46
Q

Osmotic diuretic (maintain uring flow, pull water from cells for excretion)

A

Mannitol

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47
Q

Natriuretic

A

Substance that promotes the renal excretion of sodium

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48
Q

Aquaretic

A

Substance that produces free water clearance

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49
Q

CH2O

A

V-Cosm

V-(UosmxV/Posm)

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50
Q

Damage to any vessel branch or renal arterial vessels is a HUGE problem. Why

A

No arterial anastomoses

Ischemia and death downstream

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51
Q

What diuretics work at the proximal tubule

A

Osmotic diuretics

Carbonic anhydrase inhibitors

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52
Q

What diuretics work on thin descending loop of Henley

A

Osmotic diuretics

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53
Q

What diuretics work on thick ascending limb of henle

A

Loop diuretics

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54
Q

What diuretics work on distal convoluted tube

A

Thiazide diuretics

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55
Q

What diuretics work on cortical collecting duct

A

Na channel blockers spironolactone

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56
Q

What diuretics work on collecting duct

A

Vaptans

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57
Q

Why give diuretics

A

Essential hypertension

Edema associatedwith

  • congestive heart failure
  • liver failure
  • kidney failure
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58
Q

What are K sparing diuretics and how do they work

A

Triamtrene, amiloride…Na channel blockers

Spironolactone-aldosterone antagonist

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59
Q

Name K losing diuretics and how they work

A

Thiazides-Na Cl cotransporter blockers

Loop diuretics-Na K 2Cl cotransporter blockers

Carbonic anhydrase inhibitors (seldom used)

Osmotic diuretics-non reabsorbable solutes

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60
Q

Where does mannitol work

A

PCT

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61
Q

Where does furosemide work

A

Thick segment

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62
Q

Where do thiazides work

A

EarlyDT

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63
Q

Where do K losing diuretics work

A

Early DT

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64
Q

Where do K sparing work

A

Late DT

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65
Q

Where do spironolactone and triamterene work

A

Late DCT

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66
Q

Effect of hypokalemia and hyperkalemia

A

Hypo-neurons don’t fire hyperpolarized

Hyper-depolarizes maybe lethal since Na channels cant reactivation

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67
Q

Why are K losing diuretics and digitalis often given together to patients with CHF

A

Hypokalemia increases the toxicity of the digitalis

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68
Q

Heart and hyperkalemia

A

Tall T wave
Prolonged PR interval
Wide QRS interval
Flattened P waves
Arrhythmias including bradycardia, ventricular tachycardia or fibrillation
Sinus arrest or nodal rhythm with possibl easystole

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69
Q

Hypokalemia heart

A

Flattened T waves

ST segment depression
Prolonged QT interval

Tall U waves*

Atrial arrhythmias
Ventricular tachycardia or ventricular fibrillation

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70
Q

What diuretics have greatest amount of diuresis

A

Loop

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71
Q

Where do loop diuretics act

A

TAL

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72
Q

MOA furosemide

A

Inhibits reabsorption of sodium and chloride in the thick ascending limb of the loop by blocking Na K 2Cl cotransporter

Inhibits paracellular reabsorption of Ca and Mg by the TAL due to loss of K backleak responsible for lumen+transepithelial potential

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73
Q

Effects furosemide

A

Causes increased excretion of water, sodium, K, Cl, Mg, and Ca

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74
Q

What use furosemide for

A

Edema, heart fail, hepatic disease, renal disease, acute pulmonary edema by decreasing preload (decrease EC vol, rapid dyspnea relief), HTN(works with low GFR)

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75
Q

SE furosemide

A

Hypokalemia, hyponatremia, hypocalcemia, hypomagnesia, hypochloremic metabolic alkalosis, hyperglycemia, hyperureicemia, hyperuricemia, ototoxicity (vertigo), hypersensitivity BC IT IS A SULFONAMIDE

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76
Q

Torsemide MOA

A

Similar to furosemide with longer T1/2 better oral absorption and some evidence that is works better in heart failure

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77
Q

Bumetadine

A

Sulfonamide similar to furosemide,but more predictable oral absorption ethacrynic acid: non sulfonamide loop diuretic reserved for those with sulfa allergy

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78
Q

Clinical effect of furosemide

A

Max doses_>profound diuresis! From dissatisfaction of the medullary interstitial gradient —irrespective of whether urine was dilute or concentrated, get large volume of isotonic urine

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79
Q

How give furosemide

A

PO, IV, IM

IV 5 min last 2 hours
PO 30-60 min lasts 8 hours

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80
Q

When prescribe furosemide

A

When rapid and massive fluid removal is needed (edema, cardiac, renal origin), acute pulmonary edema, HTN that is unresponsive to other diuretics (still works with RBF and GFR are low)

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81
Q

Furosemide and acute pulmonary edema

A

Rapid effects <5min that are though to be due to prostagladin mediated venodilaion that reduces preload

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82
Q

SE furosemide

A

HypoNa, hypoCl, hypoK, which lead to hypovolemia and hypotension

HypoMg

HypoCa

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83
Q

Furosemide as a K losing diuretic causing hypoCl metabolic acidosis

A

K H exchange at cells try to maintain plasma K

Also Na K exchange

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84
Q

Risk of hypoCa and furosemide

A

Kidney stones (OPPOSITE OF THIAZides

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85
Q

Ototoxicity of furosemide

A

Hyperglycemia
Hyperuricemia (gout)
Decrease HDL, increase LDL, increase TG (atherosclerosis

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86
Q

Preg and furosemide

A

NO

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87
Q

Digoxin and loop diuretics

A

Frequent interactions since both drugs are often used to treat heart failure and the risk of digoxin toxicity is increased by low K due to the diuretic

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88
Q

Ototoxicity drugs and loop diuretics

A

Increased chance of hearing loss if combined with drugs having similar toxicity

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89
Q

Potassium sparing diuretics and loop diuretics

A

Can counterbalance potassium wasting effects

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90
Q

Loop diuretics other drug interactions

A

Lithium toxicity, potentialte effects of other antihypertensive agents and have diuretic effects antagonized by NSAIDS

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91
Q

Bumetanide

A

More predictable absorption

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92
Q

Toresimide

A

Long T1/2 better for absorption, may work better in heart failure

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93
Q

Ethacrynic acid*

A

Among the few diuretics that can be used by people who are allergic to sulfa drugs

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94
Q

Loop diuretics cause the largest Na loss, are K losing, and cause similar __ loss than either loop of K sparing diuretics

A

HCO3

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95
Q

Thiazide diuretics most used

A

Hydrochlorothiazide-sulfa drug

12 others often ending in thiazide

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96
Q

Where do thiazides work

A

early DCT

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97
Q

MOA hydrochlorothiazide

A

Inhibitors Na reabsorption in the DT via blockade of NaCl cotransporter

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98
Q

Effects of hydrochlorothiazide

A

Increases urinary excretion of Na and H2O

Increases urinary excretion of K and Mg

K losing

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99
Q

Clinical use of hydrochlorothiazide

A

HTN (not effective in patients with low GFR)

Edema

Calcium nephorlithiasis

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100
Q

SE hydrochlorothiazide

A

Orthostatis hypotension

Hypo k, mg, na, cl, metabolic alkalosis

Hyper ca, hyperglycemia, hyperuricemia

Sulfa-hypersensitivity

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101
Q

Chlorothiazide

A

Similar to HCTZ but poor oral absorption

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102
Q

Chlorthaliodne

A

Similar to HCTZ but half life of f40-60 hrs..prolonged/stable response with proven benefits is reason it is preferred by some hypertension specialists

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103
Q

Metolazone

A

Another long acting thiazide diuretic, this’s is a favorite of cardiologists for use as an adjunct diuretic in the treatment of CHF

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104
Q

MOA thiazide

A

Block Na Cl cotransporter

More Ca reabsorption in PT bc of volume contraction

Mg only reabsorbed in TALH.distal nephron …loss greater with thiazides than loop diuretics

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105
Q

Location of thiazide diuretics means its diuresis _ with loop diuretics, _ downstream acting K sparing diuretics

A

<

>

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106
Q

THIAZides and low GFR and RBF

A

Don’t work

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107
Q

THIAZides cause the greater __ loss. Implications?

A

HCO3

Impairs distal nephron H secretion

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108
Q

Pharmacokinetics thiazide

A

Diuresis begins < 2 hours after oral ingestion with peak at 406 hours and effects lasting 12 hours.. in other works shouldn’t take this one at bedtime

Drug is exceed unchanged in uring

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109
Q

Uses of thiazide diuretics

A

primary HTN and edema
Nephrotoxicity diabetes insipidus
Decreases Ca excretion, day decraese risk of kidney stones (opposite of loop diuretics(

Can be added to loop diuretics to increase diuresis

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110
Q

Adverse effects thiazides

A

Hypovolemia

K losing (downstream Na K exchanger tried to salvage Na at hte expense of K)

Hypochloremic metabolic alkalosis

Hypomagnesia

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111
Q

Drug interactions thiazide

A

Combined with antiHTN meds

K loss can be offset by combining K sparing diuretics

Increase risk of digoxin and lithium toxicity

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112
Q

Chlorthalidone

A

1-2 x more potent
Different structure
Longer HL
Larger volume of distribution than HCTX, prescribed much less commonly in the US

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113
Q

Doses of thiazide 12.5-25

A

Reduce CVD mortality and morbidity

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114
Q

THIAZides are intermediate with _ loss, are _ losing, and cause larger _ lossdue to inhibtion of distal H secretion

A

Na K HCO3

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115
Q

Where does spironolactone act

A

Cortical collecting duct

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116
Q

K sparing diuretics

A

Triamterene, amiloride..Na channel block

Spironolactone..aldosterone antagonist

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117
Q

MOA amiloride

A

Blocks the luminal Na channels in CT

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118
Q

MOA spironolactone

A

Blocks aldosterone receptor in CD

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119
Q

Effects amiloride

A

Small increase in Na excretion

Blocks major pathway for K elimination so K is retained

H Mg Ca excretion also decreased

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120
Q

Clinical applications amiloride

A

Counteracts K loss induced by other diuretics in the treatment of HTN or heart failure

Ascites, pediatric HTN

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121
Q

SE amiloride

A 
Hyper K
Hypo Na
Hypo vol
HyperCl metabolic acidosis
Dizzy, fatigue, headache

Nauseas vom

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122
Q

Triamterene

A

Similar to amiloride for edema and off label HTN rapidly absorbed, duration of 6-9 hrs, eliminated as drug metabolites

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123
Q

Spironolactone MOA

A

Competitive antagonist of aldosterone receptors

Partial agonist at androgen receptors

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124
Q

Effects of spironolactone

A

K sparing

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125
Q

Clinical applications spironolactone

A

Counteracts K loss induced by other diuretics in the treat of HTN, heart failure, ascites

Hyperaldosteronism

Reduce fibrosis post MI

Hirsutism

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126
Q

SE spironolactone

A

HyperK

Amenorrhea, hirsutism, gynecomastia, impotence

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127
Q

Eplerenone

A

More selective aldosterone antagonist, approved for use in post MI heart failure and alone or in combination for HTN

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128
Q

Amiloride and triamterene _ urinary Na excretion and _ unitary K excretion

A

Increase
Decrease

If Na cant get into the cell, K cant get out of the cell into the tubular lumen

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129
Q

Pharmacokinetics amiloride triamterene

A

Channel is blocked directly, effects are seen more rapidly than with spironolactone but smaller and therefore harder to detects lasts 12-16 hours

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130
Q

Uses of triamtene

A

HTN, edema, often in combo with loop of thiazide diuretic

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131
Q

Adverse effects K sparing

A

Hyperkalemia

Nausea, vom, leg cramps, dizzy, bloody dyscrasias rare

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132
Q

MOA spironolactone

A

Blocks ability of aldosterone to bind to its receptor and increase Nareabsorption int he CCD

Leads to increased Na accretion

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133
Q

Pharmacokinetics spironolactone

A

Can take 48 hours to work

Steroid hormones produce effects with a slow onset

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134
Q

Uses spironolactone

A

HTN and edema, often in combination with a loop or thiazide diuretic

Primary hyperaldosteronism

Reduce mortality rate in patients with severe heart failure

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135
Q

SE spironolactone

A

HyperK, endocrine effects include gynecomastia, importance’s, menstrual irregularities, hirsutism and deepening voice

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136
Q

Drug interactions spironolactone

A

Often combined with thiazide and loop diuretics to counteract their K loss
Should NEVER be given with drugs that increase plasma potassium levels, but used cautiously with ACE inhibtiors

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137
Q

Amiloride/triamtere and spironolactone are _ sparing and cause the smallest _ loss while causing _ excretion to fall below normal. They also cause significant __ loss by interfering with distal H secretion

A

K Na HCO3

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138
Q

Where do vaptans work

A

CD

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139
Q

MOA vaptans

A

Block antidiuretic hormone receptor in the CD

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140
Q

MOA conivaptan

A

Non peptide arginine vasopressin receptor antagonist

V1A and V2

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141
Q

Effects conivaptan

A

Promotes excretion of free water

Decreasing Uosm
Increasing Posm

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142
Q

Clinical applications conivaptan

A

Euvolemic and hypervolemic hyponatremia in patients that are hospitalized, symptomatic, not responsive to fluid restriction

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143
Q

Why monitor plasma sodium and nuerological status in conivaptan

A

Too rapid serum sodium correction can lead to seizures, osmotic demyelination, coma, or death

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144
Q

SE conivaptan

A

Orthostatic hypotension, fatigue, thirst

Polyuria, bedwetting

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145
Q

Tolvaptan

A

Selective V2 receptor antagonist given ORALLY

Initiate and reinitiate tolvaptan in patients ONLY IN A HOSPITAL where plasma sodium can be closely monitored

Must use <30 days for hyponatremia, longer use can kill by hepatoxicity

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146
Q

MOA conivaptan and tolvaptan

A

Prevents ADH mediated insertion of the aquaporin water channels into luminal membrane of principle cells in collecting duct

Prevents the reabsorption of water, therefore increases water excretion

Decrease plasma volume and increase plasma osmolality primarily due to an increase in plasma sodium

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147
Q

Pharmacokinetics conivaptan and tolvaptan

A

Conivaptan-t1/2 5.3-8.1 hours

Tolvaptan effects increase to peak at 4 hrs, lasts 4-8hours

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148
Q

Uses of vaptans

A

Hypervolemic or euvolemic hyponatremia

AD polycystic kidney disease

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149
Q

SE vaptans

A

Orthostatic hypotension
Fatugue
Thirst
Polyuria, bedwetting

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150
Q

Drug interactions vaptans

A

Metabolized by CYP3A4, so inhibitors and inducers of this enzyme can alter its half life and potential for toxicity

Selective water loss means

  • possibility of hypovolemia
  • other electrolytes and drugs can become concentrated..hyperNa, K uricemia

Toxic levels

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151
Q

Where do carbonic anhydrase inhibitors act

A

PT

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152
Q

Where do osmotic diuretics act

A

Tin descending limb

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153
Q

Main carbonic anhydrase inhibitor

A

Acetazolamide-sulfa drug

Causes metabolic acidosis and alkaline urine

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154
Q

MOA carbonic anhydrase inhibitors

A

Na bicarbonate diuresis

Bicarbonate remains in early proximal tubule

H cyclone lose, inhibiting Na/H exchange

Hyperchloremic acidossi

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155
Q

Uses of carbonic anhydrase inhibtiors

A

Urinary alkalinization

Metabolic alkalosis

Glaucoma:acetazolamide, dorzalamide

Acut mountain sickness

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156
Q

Adverse effects carbonic anhydrase inhibitors

A

Hyperchloremic metabolic acidosis

Nephrolithiasis: renal stones

Potassium wasting

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157
Q

Main osmotic diuretic

A

Mannitol

Also use urea, glycerin and isosorbide

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158
Q

MOA mannitol

A

Non metabolized 6 carbon sugar, freely filtered with minimal reabsorption

The inability to reabsorbed. This keeps water water in the proximal tubular lumen; this water is delivered to the distal portions of the nephron where much of it is excreted

Pull water out of cells

Excrete TBW in excess of plasma electrolytes

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159
Q

Pharmacokinetics mannitol

A

Distributes in ECF, must give IV large amounts 50-2000 g

Effects are noticeable within 30-60 minutes and mannitol is eliminated unchanged in the urin over a period of 6-8 hours

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160
Q

SE mannitol

A

EC volume is acutely increased bc mannitol sucks water out of the cells which can exacerbate heart failure

Headache, nausea, vomiting and fluid electrolyte imbalances also occur

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161
Q

Uses of mannitol

A

Prophylaxis of renal failure

Reduction of intracranial pressure

Reduction of intraocular pressure

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162
Q

Carbonic anhydrase causes _ Na excretion _ K and _ Hco3

A

Some more MOST

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163
Q

Osmotic diuretics cause _ Na, _ K _ KCO3 excretion

A

More, smoke,some

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164
Q

Herbal diuretics

A

Many souls ith claims that they are effective

Some can

Probably OK by themselves BUT DO NOT MIC WITH CONVENTIONAL DIURETICS bc of potential for adverse effects

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165
Q

Licorice

A

Contains sweet glycyrrhizic acid , potentials aldosterone effects in kidney and dose-dependently increases systolic blood pressure

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166
Q

Treat renal insufficiency or nephrotic syndrome

A

Loop diuretic
Add thiazide according to ClCr

Add distal diuretic

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167
Q

Treat cirrhosis

A

Spironolactone

ClCr >50 add HCTZ

ClCr<50 do to loop diuretic and treat like renal insuff or nephrotic syndrome

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168
Q

Treat CHF

A

Treat like renal insufficiency or nephrotic syndrome if not mild

Mild and ClCr <50 treat like “”

Mild and ClCr>50 add HCTZ then treat like rest

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169
Q

Causes of diuretic resistance

A

Incorrect diagnosis (venous or lymphatic edema)

Inappropriate NaCl or fluid intake
)

Inadequate drug reaching tubule lumen in active form
-poor absorption (uncompensated HF)
-decreased RBF (HF, cirrhosis, old)
Decreased functional renal mass (AKI, CKD, old

Inadequate renal response
-low GFR (AKI, CKD)
, decreased effective arterial volume (edema)
-activation RAAS (edema
-nephron adaptation (prolonged diuretic therapy
-NSAIDS(indomethacin, asprin

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170
Q

How lower bp

A

Thiazide diuretics, furosemide, K sparring diuretics

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171
Q

Treat HTN

A

ACE I or ARB or CCB not black

Black thiazide

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172
Q

Diuretics for heart failure

A

Stage C-HF
Diuretics to relieve congestion

Aldosterone antagonists

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173
Q

Diabetes insipidus

A

Excesssice passing of urine , tasteless

Central-lack of ADH
Can treat with ADH agonist

Nephrogenic-unresonveness to ADH
Treat with thiazide diuretic

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174
Q

Treat diabetes insipidus

A

Desmopressin, a synthetic V2 agonist if central

If lack of ADH response frominterstitial fibrosis, Li, antagonism of ADH in principal cells

Thiazide diuretics

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175
Q

___ is the most common cause of nephrogenic DI

A

Appearance of DI symptoms in this case coincides with use of Li to treat bipolar disorder

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176
Q

Thiazide diuretics are contraindicated in ___

A

Li induced DI bc Li reabsorption-like Na reabsorption is increased in the proximal tubule and can cause Li toxicity

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177
Q

How treat Li induced diabetes insipidus

A

Amiloride..blocks influx of Li into CCD cells

Very dilute urine->urine of appropriate concentration to maintain water homeostasis bc amiloride blocks Li influx into principal cells, allowing ADH to work

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178
Q

THIAZides treat nephrogenic diabetes insipidus IF

A

It is NOT caused by lithium

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179
Q

If Li causes nephrogenic DI (from bipolar treatment), _____ is the treatment

A

Amiloride

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180
Q

Describe the distribution of calcium in the body

A

Plasma least, more intracellularly, most IN THE BONE

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181
Q

Why is it important to control Ca within a narrow range

A

Muscle contraction
Intracellular signaling
Bone formation
Neuronal excitation

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182
Q

Effects of hyper and hypocalcemia

A

Hyper-raise threshold

Hypo-lowers threshold

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183
Q

How does hypoalbuminia effect calcium. What are the implications

A

Decreases total serum calcium without affecting ionized.

If serum albumin is abnormal, clinical decisions should be based on ionized calcium levels

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184
Q

Corrected calcium

A

Measured total Ca (mg/dL)+.8 (4-serum albumin )

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185
Q

Hormones that control calcium

A

Calcitrion (1,25 OH vitamin D3)

PTH

Calcitonin

Sites of regulation—-kidney, bone, intestine

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186
Q

Effects of calcitonin

A

Lowers blood Ca levels in three ways:
-inhibits Ca absorption by the intestines
-inhibits osteoclast activity in bones
-inhibits renal tubular reabsorption of Ca (increase Ca excretion)
Like PTH it inhibits tubular phosphate reabsorption

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187
Q

Effects of PTH

A

Increase plasma Ca, decrease plasma PO4–>increased ionized plasma Ca

  • acts in distal nephron to increase Ca reabsorption
  • inhibits PO4 reabsorption int he proximal tubule
  • enhances bone release of Ca
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188
Q

What controls secretion of PTH

A

Serum Ca acting on calcium sensing receptors on Parathyroid cells in a negative feedback manner

Activated by low Ca

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189
Q

Calcitrion (1,25-OH D3)

A

Renal synthesis from 25-OH vitamin D3 is stimulated by PTH

Acts through calcitrion receptor

Increases blood Ca levels

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190
Q

How does calcitrion (VD3) increase Ca levels

A

Promotes absorption of dietary calcium from GI tract

Increases renal tubular reabsorption of filtered Ca

Stimulates release of Ca from bones…acts on osteoblasts to activate osteoclasts

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191
Q

__ of filtered calcium is reabsorbed in the PT. How

A

65

Paracellular, but some active transport

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192
Q

The thick ascending limb of loop henle has lumen positive voltage that drives ____ Ca reabsorption of __%

A

Paracellular

20

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193
Q

Distal tubule is site of _% of calcium reabsorption but major site of regulation. How

A

8
Active transport along electrical and chemical gradients
Renal epithelial Ca channel(TRPV5)-along with calbindin, regulated by calcitriol

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194
Q

Calcium reabsorption is _ in CD

A

5%

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195
Q

Klotho

A

Enzyme that can break down complex carbs, disruption leads to premature aging…has a direct stimulators effect on TRPV5

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196
Q

How is conductance of TRPV5 regulated

A

PTH and locally synthesized tissue kallikrein

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197
Q

Calbindin-D28K and TRPV5 expression is regulated by __

A

Vitamin D

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198
Q

What is the response to hypercalcemia

A

Decreased Ca absorption

Increased Caexcretion

Decrease bone resorption

NORMOCALCEMIA

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199
Q

Causes of hypercalcemia

A

*entry of calcium into ECF by bone resorption and intestinal absorption

Primary hyperparathyroidism, thiazide diuretics, milk alkali syndrome, familial hypocalciuric hypercalcemia, malignancy, immobilization syndrome, granulomatous disease, VD intoxication

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200
Q

Clinical features of hypercalcemia

A

Mild-asymptomatic

Severe-neurologic (weak, fatigue, confusion, stupor, coma) and GI (anorexia, nausea, vomiting and constipation)

NV cause hypovolemia —impaired calcium excretion—worsening

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201
Q

How manage acute hypercalcemia

A

Increasing calcium excretion

Decreasing resorption

Decreasing absorption

—-ECF volume replacement with .9% saline
——furosemide
—-calcitonin

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202
Q

What give if hypercalcemia not responding to saline diuresis, and espicially if secondary to malignancy

A

Bisphosponates

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203
Q

Causes of hypocalcemia

A

Decreased calcium absorption from GI or decreased resorption

Hypoparatyroidism, chronic kidney disease,familial hypocalcemia, rhabdomyolysis, septic shock, VD defiency, parathyroidectomy, acute pancreatitis (Ca soaps)

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204
Q

What is true hypocalcemia

A

When ionized calcium concentration is reduced

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205
Q

Hypocalcemia clinical feature

A

Neuromuscular irritability (fatigue, paresthesia, circumpolar, twitching, tetany, chvostek, trousseau, laryngeal and bronchial spasm)

Altered central nervous system function (emotional disturbances, depression, coma, seizures, papilledema, cerebral calcifications)

CVD (lengthen QT, dysrhythmias, hypotension, CHF)

Derm(dry skin, coarse hair, brittle nails, cataracts)

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206
Q

How manage hypocalcemia (seizures, tetany, hypotension or cardiac arrhythmias)

A

IV calcium

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207
Q

How manage chronic mild hypocalcemia

A

Oral calcium supplements +/- VD

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208
Q

How treat hypocalcemia with hypoparathyroidism

A

Calcium and VD supplements

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209
Q

Why need phosphorus

A

Bone formation, cellular energy metabolism, regulation of protein/enzyme function

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210
Q

Describe body distribution of phosphorus

A

85% bone rest in cells

1% ECF

2/3 organic phosphate
1/3 inorganic

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211
Q

What increases serum phosphate

A

Decrease by carbohydrate or glucose infusion

Increase by high phosphate meal

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212
Q

Effect of PTH on PO43

A

Decreases serum by increases renal excretion

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213
Q

FGF-23 effect on PO43

A

Decreases serum PO4 by increases renal excretion

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214
Q

1,25 (OH)2D3 effect on phosphorus

A

Increase serum PO4s..increases intestinal phosphate absorption

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215
Q

Insulin effect on phosphate

A

Decrease serum PO43..shirt phosphate into cells

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216
Q

What is FGF-23

A

Phosphatonin released by bone that promote PO43 excretion by the kidney…familial problems also can be secreted by tumor to cause phosphate wasting

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217
Q

The dietary intake is 900 mg/day

A

70kg man filters 200 molecules PO42 per day with 12.5 excreted int he urine

  • contrast with 1% of filtered Na excreted in urine
  • corresponds to 900 mg/day or 64% of dietary intake/day that needs to be laminated by kidneys

Becomes problematic when GFR falls

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218
Q

PhosphorusReabsorption..55-85% is reabsorbed in PCT

A

3 Na dependent PO43 transporters

NaPi2 is responsible for 85% transport, highly regulated

FGF-23 and PTH regulate

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219
Q

In the kidney phosphorus is regulated by what

A

PTH and FGF-23

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220
Q

Causes of hyperphosphatemia: decreases renal excretion of phosphorus

A

Chronic kidney disease stages 3-5

Acute renal failure/acute kidney injury

Hypoparathyroidism, pseudohypoparathyroidism

Acromegaly

Tumoral calcinosis

FGF-23 inactivating gene mutation

GALNT3 mutation with aberrant FGF-23 glycosylation

KLOTHO inactivating mutation with FGF-23 resistance

Bisphosphonatesc

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221
Q

Causes of hypophosphatemia:exogenous phosphorus administration

A

Ingestion of phosphate, phosphate-containing enemas

IV phosphate delivery

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222
Q

Redistribution of phosphorus : causes of hyperphosphatemia

A 
Respiratoy acidosis/metabolism acidosis
Tumor lysis syndrome
Rhabdomylosis
Hemolytic anemia
Catabolic state
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223
Q

Causes of hyperphosphatemia: pseudohperphosphatemia

A

Hyperglobulinemia, hyperlipidemia, hemolysis, hyperbilirubinemia

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224
Q

Clinical features of hyperphosphatemia

A

Deposition of Calvclium in soft tissues and resultant fall in ECF ionized calcium

Calciphylaxis

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225
Q

Chronic hyperphosphatemia causes what

A

Renal osteodystrophy

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226
Q

How manage hyperphosphatemia

A

Acute-saline diuresis

End stage kidney disease-reduce dietary intake/intestinal absorption (phosphate binder)

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227
Q

Describe secondary hyperparathyroidism in CKD

A

CKD causes decreased 1,25 (OH)2D3 and increased phosphorus causing decreased calcium and increased FGF-23…increases PTH

Both FGF-23 and PTH are phosphatic

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228
Q

Renal osteodystrophy

A

Bone demineralization due to chronic kidney disease

Can cause bonejoint pain, bone deformation or fracture

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229
Q

What causes renal osteodystrophy

A

Hyperparathyroidism secondary to hyperphosphatemia…kidney is unable to excrete phosphate

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230
Q

Renal osteodystrophy combined with hypocalcemia

A

Kidney unable to activate vitamin D to calcitrion needed for Ca absorption from diet

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231
Q

Treat renal osteodystrophy

A

Ca/VD supplement

Restriction of dietary phosphate, use of phosphate binders

Hemodialysis/renal transplantation

China cal et (calcium sensitized drug, lowers PTH)

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232
Q

What may cause hypophosphatemia

A

Redistribution of extracellular phosphate into the intracellular space

Decrease in intestinal absorption of phosphate

Decrease in renal reabsorption of phosphate

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233
Q

Re-feeding hypophosphatemia

A

Can be cause of death in starving people/anorexics as hexokinase phosphorylation glucose taken into cells

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234
Q

Alcohol related hypophosphatemia

A

Tend to be malnourished so re feeding syndrome partially responsible

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235
Q

Diabetes mellitus hypophosphatemia

A

When treated with large doses of insulin

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236
Q

Urinary loss causing hypophosphatemia

A

Faccini

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237
Q

Oncogene osteomalacia causing hypophosphatemia

A

Tumor makin FGF23

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238
Q

Clinical signs of hypophosphatemia (occur only if total body phosphate depletion is present)

A

Muscular abnormalities-weak, rhabdomyolysis, impaired diaphragmatic function, respiratory failure, heart failure

Neurologic abnosmalities-paresthesia, confusion, stupor, dysarthria, seizures, and coma

Hemolysis and platelet dysfunction

Chronic hypophosphatemia-rickets, in kids, stromal Asia in adults

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239
Q

Manage moderate hyphosphatemia

A

Asymptomatic and requires no therapy except treatment of the underlying cause

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240
Q

Manage persistent hypophosphatemia

A

Oral phosphate

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241
Q

Manage severe hypophosphatemia

A

IV phosphate therapy espicially when associated with serious clinical manifestations

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242
Q

Hypophosphatemia patients frequently are also hypo____ and hypo__ and these disorders must also be corrected

A

Kalemic

Magnesemic

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243
Q

Describe distribution of Mg

A

50% mineralized in bone
49% intracellularly
10% ionized but has crucial role as cofactors in many biological processes such as ATPases, regulation of ion channels and translational processes
1% extracellular with 60% of that ionized , 30% bound albumin, 10% complexed with phosphatase

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244
Q

15% of Mg is reabsorbed in the PCT> how

A

Paracellular and follows Na

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245
Q

70% of Mg is reabsorbed in the TAL. How

A

Driven by the transepithelial gradient generated by Na K 2Cl cotransporter

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246
Q

10% of Mg is reabsorbed in DCT. How

A

Via TRPM6 channels

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247
Q

Why is Mg absorption unique

A

PCT not major site of reabsorption

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248
Q

Describe Mg reabsorption in DCT

A

Mg concentration same inside and outside, so electrical potential is primary driver of cellular Mg influx, intracellular shuttling is not well understood

Hormonal regulation is uncertain and thought to be indirect, EGF is only hormone identified thus far

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249
Q

_% of ICU patients have hypomagnesemia

A

60

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250
Q

What causes hypomagnesia in ICU patients

A

Decreased nutrition, diuretics, decreased albumin, aminoglycosides, decreased reabsorption (PPI)

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251
Q

Common causes of Mg defiency

A

Alcoholism, malabsorption, parenteral nutrition, PPI, familial hypomagnesia with secondary hypocalcemia

Increased losses

Redistribution -hungry bone syndrome

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252
Q

Clinical signs of hypomagnesia

A

Neuromuscular manifestations(weak, tremor, seizures, tetany, positive chvostek and trousseau (but think Ca first), nystagmus

CVD-T wave changes, U waves, prolonged QT and QU, repolarized alternans, premature ventricular contractions, v fib, monomorphic ventricular tachycardia, enhanced digitalis toxicity)

Metabolic-hypoK and Ca

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253
Q

Treat hypomagnesia

A

Oral or IV Mg

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254
Q

When is hypermagnesia seen

A

End stage renal disease

Massive intake..epsom salt

Magnesium infusion..administration to limit neuromuscular excitability in pregnant women with pre-ecclampsia/ecclampsia

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255
Q

Clinical signs of hypermagnesemia

A

<3.6 asymptomatic

  1. 8-7.2-nauseas flushing headache
  2. 2 to 12 somnolence, hypoca, absent DTR, hypotension, bradycardia

> 12 -muscle paralysis-flaccid

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256
Q

Treat hypermagnesemia

A

Normal renal function-stop administration and wait and/or add loop or thiazide diuretic

Reduced renal function -stop administration and wait and/or add loop thiazide diuretic then ADD SALINE

End stage kidney disease-dialysis

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257
Q

With hypertension why do expel feel better when not taking meds

A

Side effects

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258
Q

Risk of HTN

A 
Family history
Age
Males
Black
Diabetes
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259
Q

Primary HTN

A

92%, no cause found, chronic and progressice, use drugs that lower BP but DONT treat underlying cause

Low renin

Normal renin

High renin

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260
Q

Secondary HTN

A

Primary cause identified, less, can be cured by treating cause

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261
Q

Causes of secondary HTN

A 
Chronic kidney disease
Renovascular
OC
Coarctation
Primary aldosteronism
Cushing
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262
Q

Calculate arterial pressure

A

COxperipheral resistance

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263
Q

Resistance formula

A

8nl/pir^4

N-viscosity
L length
R radius

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264
Q

Sympathetic baroreceptor reflex

A

Reflex circuit keeps arterial pressure at present level on a second by second basis

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265
Q

How does the sympathetic baroreceptor reflex “sense”

A

Stretch receptors located in the carotid sinus and aortic arch

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266
Q

What happens when sympathic baroreceptor reflex is opposed

A

Attempts to reduce arterial reassure with drugs

Innervated the heart and travel along the blood vessels, forming multiple synapses such that the nerves resemble a string of beads

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267
Q

A1 adrenergic receptor

A

On bc to cause vasoconstriction to maintain venous return with changes in posture

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268
Q

A2 adrenergic receptors

A

Act both in the brain and in the periphery in a presynaptic receptors act in both the brain and in their periphery in a presympathetic tone

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269
Q

B1 adrenergic receptors

A

Increase heart rate and contractility, and stimulate renin secretions by the kidneys

270
Q

B2 adrenergic receptors

A

Dilate skeletal muscle vasculature

-important during fight or flight response with concomitant a1 receptor vasoconstriction blood shunted to msucles

271
Q

What is the ultimate regulator of blood pressure

A

Renal blood volume, it is slow!

But keep in mine, high salt intake causes hormonal changes that shift the intrinsic renal relationship between arterial pressure and urinary output of Na to the left, low salt to the right

272
Q

In HTN, the blood pressure set point is resent to a higher level, but can be either salt resistant or salt sensitive

A

Salt resistant, not changes in slope but increases

Salt sensitive, bo up in dose response

273
Q

Drugs for lowering bp

A

Vascular smooth muscle

Vascular a1 receptors

Renal tubules (B1 juxtagloerular cells, angiotensin converting enzyme, angiotensin II receptors, aldosterone receptors)

Brainstem

Sympathetic ganglia

Adrenergic terminals

Cardiac B1 receptors

274
Q

Hypertension drugs

A

Thiazide diuretics, ACEI or ARB, and CCB

275
Q

Why are B blockersnow generally limited to other compelling indications

A

Do not prevent MI, heart failure, or death as well as other therapies

Associated with a significantly higher incidence of stroke than other therapies

276
Q

Describe RAAS

A

Angiotensin I cleaved from angiotensinogen by renin is cleaved by angiotensin converting enzyme to form angiotensin II.

277
Q

Effects and angiotensin II

A

Vasoconstrictor, increases total peripheral resistance

Acts to increase extracelllular fluid volume

  • stimulating thirst
  • stimulating aldosterone secretion
  • stimulating ADH secretion
278
Q

Why get increase in TPR in chronic hypertension

A

Follow an initial increase in cardiac output

In some cases TPR increase is initiating event

279
Q

Why is hypertensive vascular remodeling reduced by ACEI or ARB and CCB

A

Idk

280
Q

Lifestyle modifications for essential hypertension

A

Weight reduction

Na restriction

Alcohol restriction

Exercise

Smoking cessation

Maintence of K and Ca intake

Stress management

281
Q

What drugs affect the angiotensin II formation or action

A

Aliskirin

ARBS

ACEI

282
Q

How does RAAS inhibition effect kidney

A

Serum creatinine increases (preserves kidney function in hyperfiltering diabetics, can also alarm. Physicians)

Ang II tone helps maintain resistance in efferent arterioles

283
Q

MOA captopril

A

Competitive inhibitor of ACE

284
Q

Effects of captopril

A

Prevents conversion of angiotensin I to II

Lowers levels of angiotensin II
Increase renin and decrease aldosterone

Lowers bp

285
Q

Clinical application captopril

A

Hypertension, add thiazide or loop diuretic if additional lowering is needed at max recommended dose

Acute HTN

HF with reduced ejection fraction

LV dysfunction following MI

Diabetic nephropathy

286
Q

SE captopril

A

Cough
Angioedema
Hypotension
Headache

287
Q

Enalapril

A

Another early ACEI, a prodrug with active form available for IV

288
Q

Benzapril

A

ACE inhibitor, longer half life permitting 1 dose a day

289
Q

Lisonopril

A

Now widely used ACE inhibitor, longer half life permitting 1 dose a day

290
Q

What is the main reason to stop taking ACE inhibitor

A

Cough

291
Q

Deadly side effect of ACE inhibitor

A

Angioedema can be deadly

CHOKE AND SWALLOW ON OWN TONGUE

292
Q

Losartan MOA

A

Competitive nonpeptide angiotensin II receptor antagonist for AT1

293
Q

Effects of losartan

A

Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II

Induces a more complete inhibition of the renin angiotensin system than ACE inhibitors

Does not affect the response to bradykinin

294
Q

Clinical applications of losartan

A

Treatment of diabetic nephropathy with increased Scr and proteinuria in type 2 diabetes and HT

HT, Akon or in combination with other antihypertensives

Hypertension with left ventricular hypertrophy to reduce risk of stroke

CKD and HT regardless of race or diabetes status, to improve kidney outcomes

Heart failure if intolerant of ACE inhibtiors

Off label Marian

295
Q

SE losartan

A

More common in diabetic nephropathy

Hypotension, first dose hypotension, orthostatic hypotension

Fatigue, dizzy

Hypoglycemia, hyperkalemia

Diarrhea, gastritis, nausea, weight gain

Anemia

Weakness, back/knee

Cough

296
Q

Valsartan

A

T1/2 6-10 hrs, noteworthy in that not a prodrug requiring activation, excreted primarily in feces as unchanged drug

297
Q

Candesartal

A

T1/2 is 5-9 hrs, noteworthy for its relatively irreversible binding

298
Q

Aliskiren MOA

A

Direct renin inhibitor, resulting in black of the conversion of angiotensinogen to angiotensin I

299
Q

Effects aliskiren

A

Decreases the formation fo angiotensin II, a potent blood pressure elevating peptide elevating peptide viavasoconstriction, aldosterone release and Na retention

ACE inhibitor and ARB therapy can be offset by increases in plasma renin activity (PRA), which is blocked by direct renin inhibitors

300
Q

Clinical applications aliskiren

A

Treatment of HTN alone or in combination with other antihypertensive agents

301
Q

SE aliskiren

A

Few

Rash
Cough
Diarrhea

302
Q

Rout of aliskiren

A

2 weeks see effects

T1/2=24hrs

303
Q

What should new drug for HTN be based on

A

Age, race, Conor I’d conditions

304
Q

Asthwhen should you not use a drug like B blocker like propranolol

A

Asthma B2 agonists are used for bronchodilator

Diabetes..B2 receptor effects offset hypoglycemia and alert patient via palpitations

305
Q

When should you not use calcium channel blockers for HTN

A

Heart failure

306
Q

Blacks health problems

A

HTN at earlier age

Average bp higher

Worse disease severity

More stroke, heart disease, and stage KIDNEY disease, heart failure

307
Q

__, ___ and ___ are less effective as monotherapy than in whites but __ and ___ work well

A

B blockers, ACE inhibitors and ARBS

Diuretics , calcium channel blockers

308
Q

B blockers, ace inhibitors and ARBS work well when added with a

A

Diuretic

Should be used first line combinations herapy if SBP>15 and DBP>10

309
Q

Secondary HTN is more common in kids, what do

A

Identify cause and treat

310
Q

Do not give _ or _ to sexually active girls

A

ACE inhibitors

ARBS

311
Q

What can angII decrease cause

A

Efferent tone
Precipitate renal failure in patients with bilateral renal stenosis

Can help preserve renal function in diabetic patients

312
Q

ACEI contraindication

A

Pregnancy

All trimesters

313
Q

Manifestations of renal artery stenosis

A

Asymptomatic incidental RAS

Renovascular hypertension

Accelerated CV disease CHF, stroke, scndoary aldosteronism

Ischemic nephropathy

314
Q

Appearance of what suggests bilateral renovascular hypertension rather than primary hypertension

A

Flash pulmonary edema, progressive renal failure, refractory congestive cardiac failure

315
Q

Essential HTN vs renovascular HTN

A

Renovascular has more abdominal bruit, blood urea, potassium, duration, urinary casts and proteinuriia

316
Q

Effect of bilateral renal stenosis

A

Reduced renal perfusion

Increase RAAS, impaired

Na and water excretion ->volume exmpasion inhibitors RAAS

Overall-reduced arterial pressure only after volume depletion may lower GFR

Detect with renin plasma

317
Q

Unilateral renal artery stenosis block of RAS

A

Reduced arterial pressures
Enhanced lateralization of diagnostic tests
GFR fallelevated plasma renin

318
Q

Systemic effects of increased renin due to stenosis

A

Vasoconstriction, Na retention, aldosterone secretion, vascular, sympathetic nervous system, Myocardial effects

319
Q

How treat renal stenosis

A

Not surgery it fails to materially recover kidney function

Use drugs to block the RAAS and statin therapy

320
Q

Red urine

A

Hematuria

321
Q

Cloudy urine

A

Pyuria +/- bacteria

322
Q

Beeturia

A

Rhubarb and blueberries

323
Q

Green urine

A

Asparagus

324
Q

Blue urine

A

Methylene blue in viagara

325
Q

Yellow urine

A

Riboflavin (BIRGHT yellow)-can be used to turn it yellow if drinking a lot of water to pass a drug test

326
Q

Defiency branched chain alpha keto acid dehydrogenase (BCKDC)

A

AR maple syrup I urine disease
Buildup of branched chain aa (leucine, isoleucine, valine) and their toxicity by products (ketoacidosis) in the blood and the urine unless dietary intake is carefully managed

327
Q

Everyone has smelly pee after asparagus due to breakdown of sulfurous aa into volatile/odorous compounds

Only a fraction can smell

A

Woah

328
Q

Sweet smell and taste or urine or see if it attract ants

A

DM

329
Q

Smell of urine with UTI and/or kidney stones

A

Fishy

330
Q

Specific gravity low urine (normal 1.01-1.025)

What does 1.025 mean

A

DI
Glomerulonephritis
Pyelonephritis
Can’t concentrate urine

Highly concentrated

331
Q

Normal pH of urine

A

6 ——fixed acid is being excreted as ammonium

332
Q

What does a negative reading for urine dipstick leukocytes indicate

A

A high power field likely has 3-5 neutrophils

333
Q

Brown urine, dipstick positive for blood, no RBC visible by microscopy

A 
MYOGLOBINURIA
Intravascular hemolysis
Nephrotic syndrome
Urine contains a dye
Nephrotic syndrome
Analgesi nephropathy
334
Q

Positive nitrate urine test?

A

Gram negative organism?

335
Q

50 for urine ketones

A

Diabetic ketoacidosis

336
Q

Bilirubin in urine

A

Liver disease

337
Q

Urobilinogen in urine

A

Hemolytic disease

338
Q

Protein over 1000 in urine

A

Nephrotic

339
Q

Foamy urine suggesting protein but protein negative and sulfasalicylic acid test indicates presence of protein

A

Bcence Johnson protein in multiple myeloma

340
Q

Urine over 100 mg/dL glucose

A

Filtered load of glucose is greater than PCT reabsorption capacity

341
Q

Triple phosphate crystals (struvite) in either common form (coffin lid) or rapidly precipitated form, ammonium urate crystals

Calcium phosphate crystals

Amorphous phosphates

A

Urine infected with ammonia producing organisms

ALKALINE

342
Q

System needs, tyrosine, and leucine in urine

Cystine crystals (hexagon) tyrosine cryastals (fine delicate needles), calcium oxalate crystals (enveloped), uric acid footballs), sodium irate, sulfonamide crystals (antibiotics), amorphous-specs(urate)

A

Acidic urine

Metabolic origin

343
Q

Urine casts

A

Damage to the glomerular endothelial cells

Form when the tubule cells die and slough off
WBC casts form HTN there is tubulointerstitla nephritis

344
Q

Tamm horsfall protein

A

Encase/lubricate junk in the tubular lumen to facilitate elimination

Keep distal tubules from collapsing if GFR ceases

Sop up waste products secreted by the proximal tubule that bind to protein so that my protein transporters and channels continue to function properly

345
Q

The __ __ is the first fluid barrier found between the extracellular subcompartments with a one way lymphatic shunt returning interstitial fluid to the plasma

A

Capillary membrane

346
Q

The __ __ is the seconda barrier to fluids, separating intracellular from extracellular fluids

A

Cell membrane

347
Q

Fluid distribution between plasma, interstitial fluid and intracellular

A

IC>IS>plasma

348
Q

Extracellular Iona

A

Na Cl HCO3

349
Q

Intracellular ions

A

K, PO43 protein

350
Q

The kidneys maintain the extracellular __ ion concentrations from which the cells of the body extract their needs

A

Small

351
Q

Major sources of ions

A

Liver, lymphocytes

352
Q

Gibbs-donnan equilibrium

A

Maintains cell volume constant

With protein inside the cell and na outside

353
Q

Causes of extracellular edema:increased capillary hydrostatic pressure

A

Increased capillary hydrostatic pressure

Excess kidney retention of salt and water (acute or chronic kidney fail, mineralocorticoid excess)

High venous pressure (heart failure, venous obstruction , failure of venous pumps)

Decreased arteriolar resistance (excessive body heat, insuffiency of the sympathetic nervous system, vasodilator drugs)

354
Q

Causes of extracellular edema : decreased plasma proteins

A

Loss of protein (nephrotic syndrome)

Loss of protein from denuded skin areas (burns, wounds)

Failure to produce proteins (liver disease, severe protein or caloric malnutrition)

355
Q

Causes of extracellular edema : increased capillary permeability

A

Immune reactions that cause release of histamine, toxins, bacterial infections, vitamin defiency, espicially vitamin C, prolonged ischemia, burns

356
Q

Causes of extracellular edema: blockage of lymph return

A

Cancer, infections(filariasis, nematodes), surgery, congenital absence or abnormality of lymphatic vessels

357
Q

What prevents extracellular edema

A

Interstitial normally has low compliance

Lymph flow can increase 10-50 fold

Increased amounts of protein poor capillary fluid flow wash protein out from the interstitial space, decreasing net capillary filtration pressure

358
Q

What are the two main causes of intracellular edema

A

Depression of metabolic systems of tissues

Lack of adequate nutrition to the cells

*cells lack the resources to drive the NaKATPase pump, so Na accumulates in cells and they expand and water follows sodium into the cells

359
Q

Other causes of intracellular edema

A

Too little extracellular Na or too much water

360
Q

What does high extracellular edema cause

A

Brain cell swell

361
Q

Are water and Na regulated separately

A

Yup

Na content and concentration are not the same thing

362
Q

Na content

A

Sensed by effective vascular volume, stretch receptors

AngII Aldo SNS ANF

363
Q

H2O

A

Plasma osmolality
Osmoreceptors

ADH

364
Q

RBF and GFR are ______ but urinary output of Na and H2) increases as __ increases

A

Autoregulated

MAP

365
Q

Tubuloglomerular feedback of increased GFR and RBF

A

Increased delivery of solute to juxtaglomerular apparatus

Increased resistance of afferent arterioles

Decreased RBF and GFR

366
Q

What happens to creatinine when GFR falls due to ACEI

A

Creatinine increases

This presernves kidney function in hyperfiltering diabetics can also alarm physicians

367
Q

Glomerulotubular balance

A

Small increase in GFR dueto increased MAP, get increase Pc, ensuring that there is proportional reabsorption of filtrate. More is reabsorbed but more is also delivered to the thin limbs and more reaches the distal portions

With volume expansion, dilution of plasma proteins+ increased RBF leads to these changes in the peritubular capillary

368
Q

Countercurrent multiplier

A

Create gradient of 2 across the transported is multiplied along the length of the transporter array due to countercurrent flow

In TAL to provide solute for the hypertonic renal medullary interstitial while simultaneously diluting the tubular fluid

369
Q

Concentrated outflow

A

Generated hypertonic renal medullary interstitial

370
Q

Dilute outflow

A

Neededfor the possible excretion of excess water

371
Q

Vascular sensory for circulating volume

A

Vascular
Low pressure-cardiac atria, pulmonary vasculature

High pressure-carotid sinus, aortic arch, juxtaglomerular apparatus of kidneys

372
Q

Hormones that effect PT where 67% of reabsorption occurs through NaH exchange, Na cotransport and organic solute, NaH CL anion exchange

A

Angiotensin II
NE
E

373
Q

Hormones that regulate the late distal tubules and collecting duct which reabsorbed 3% of load with Na channels

A

Aldosterone

ANP

374
Q

Low Na intake, hormones

A

Ability to retain na will become maxed out and arterial pressure then falls to a level where intake=output on the curve

375
Q

High Na intakehoromones

A

Hormones minimal values and Na dumping hormones are a maximal values, and further increases in Na intake will cause arterial pressure to increase to a value where intake=output

376
Q

What happens with increased ECF volume from increased Na intake

A

Decreased sympathetic activity, increased ANP, decreased pi, decreased RAAS

All leading to increased excretion of Na

377
Q

What does decreased sympathic activity do

A

Dilation of afferent arterioles

Decreased Na reabsorption

378
Q

What does increased ANP do

A

Constriction of efferent arterioles

Decreased Na reabsorption

379
Q

What does decreased pi cause

A

Decreased Na reabsorption

380
Q

What does decreased RAAS cause

A

Decreased reabsorption

381
Q

Signs of hypovolemia

A 
Decreased skin tumor
Thirst
Dry mucous membranes
Sunken eyes
Oliguria
As worsens get tachycardia, hypotension, tachypnea, confusion
382
Q

Signs of hypervolemic

A

Edema, bounding pulse

383
Q

Relative hypovolemia

A

Decrease ECFV and increase in total body sodium

384
Q

Renal causes of relative hypovolemia

A

Severe nephrotic syndrome

385
Q

Renal causes of renal absolute hypovolemia

A

Diuretics, Na wasting tululopathies, genetic or acquired tubulointerstitila disease, Obstructive uropathy/postobstructive diuresis, hormone defiency, hypoaldosteronism, adrenal insuffiency

386
Q

Causes of volume excess

A

Oliguric acute renal failure, acute glomerulonephritis, severe chronic renal failure, nephrotic, nephrotic syndrome, primary hyperaldosteronism, Cushing, liver disease, conn, gordon, Liddell

387
Q

Hypernatremia levels

A

Plasma >145

388
Q

Hyponatremia values

A

<135

389
Q

Calculate plasma osmolality

A

2xNa in plasma

More accurate

2plasma Na+glucose in plasma/18+ BUN plasma/2,8

390
Q

Normal plasma osmolality

A

285-295

391
Q

Effect of vasopressin

A

Plasma osmolality up and blood pressure or volume decrease

392
Q

What increased ADH

A

Increase plasma osmolality
Decrease blood volume
Decrease blood pressure

Nausea, hypoxia

Morphine, nicotine, cyclophosphamide

393
Q

What Decreases ADH

A

Decreased plasma osmolality
Increased blood volume
Increased blood pressure

Alcohol, clonidine, haloperidol

394
Q

What increases thirst

A

Increased osmolality
Decreased blood volume
Decreased blood pressure
Increased angiotensin II

Dry mouth

395
Q

Decrease thirst

A

Decreased osmolality
Increased blood volume
Increased blood pressure
Decreased angiotensin II

Gastric distention

396
Q

Response to drinking water and decrease in plasma osmolality

A

Inhibits osmoreceptors in anterior hypothalamus—THIRST decreased

Decrease ADH

Decrease H2O permeability in late distal tubule and CD

Decrease H2O reabsorption

Decrease urine osmolarity and increase volume

Increase plasma osmolarity toward normal

397
Q

Response to water deprivation and increase in plasma osmolarity

A

Stimulates osmoreceptors in anterior hypo->increase thirst

Increase ADH from PP

Increase H2O permeability in late DT and CD

Increase H2O reabsorption

Increase urine osmolarity
Decrease urine vol

Decrease plasma osmolarity toward normal

398
Q

Volume compartment lose na and H2O

Diarrhea

A

Lose volume from ECF

399
Q

Body compartment: lost H2O

Water deprived

A

Lose volume os ICF and ECF

Increase osmolarity in ICF and ECF

400
Q

Body compartment
Lost Na

Adrenal insuffiency

A

Lose volume ECF gain volume ECF lost osmolarity in ICF and ECF

401
Q

Body comparemtn gain na and H2O

Infusion of isotonic NaCl

A

Gain volume in ECF

402
Q

Body compartment gain Na

High NaCl intake

A

Increase volume ECF lose volume ICF

Gain osmolarity in ICF and ECF

403
Q

Body compartment gain H20

SIADH

A

Gain volume ECF, ICF, lose osmolarity ICF and ECF

404
Q

What is the most common electrolyte abnormality encountered in clinical practice

A

Hyponatremia

<135 mEq/L

In 15-20% of hospitalized patients!!!

405
Q

What causes hyponatremia

A

CHF
Liver disease sepsis

Nephrotic syndrome
Prego

406
Q

Drugs for euvolemic

A

SIADH

407
Q

SALT LOSS hyponatremia symptoms

A 
Stupor/coma
Anorexia, nausea, vom
Tendon reflexes decreased
Limp muscles (weak
Orthostatic hypotension 
Seizures/headache
Stomach cramping
408
Q

Treat minimal hyponatremia

A

Fluid restriction

409
Q

Treat moderate symptoms of hyponatremia

A

Vaptans or hypertonic NaCl

410
Q

Treat severe hyponatremia

A

Hypertonic NaCl

411
Q

Normonatremia brain

A

NaKCli and H2O

412
Q

Acute hyponatremia brain

A

NaKCl and INCREASED H2O

413
Q

Chronic hyponatremia brain

A

NaKCL and H2O decrease

414
Q

Osmotic demyelination

A

Increase na and decrease H2O

415
Q

Calculate infusion rate for NaCl 3%

A

Ptweightxdesired correction rate

416
Q

Overly rapid correction of hyponatremiacan cause what

A

Osmotic demyelination syndrome

Can do 2.5 mEq/L/hr in acute

In chonic .5?

417
Q

Causes of SIADH

A

Desmopressin, oxytocin, NSAIDS, MDMA, tumors producing vasopressin , brain tumors, HIV, traumatic brain injury

418
Q

Hypernatremia common in hospitalized?

A

1% associated with high mortality and morbidity in the elderly

See in people that live alone and fall
Indicator of neglect in nursing home

Ppl in desert

419
Q

Causes of hypovolemia hypernatremia

A

Administration of hypertonic saline, hypertonic sodium bicarbonate

Hypertonic dialysis

Hypertonic feedings

Primary hyperaldosteronism

Cushing

420
Q

Causes of euvolemic hypernatremia

A

Diabetes insipidus

Hypodipsia

Insensible dermal and skin loses

421
Q

Causes if hypovolemia hypernatremia

A

Lack of access to water broken thirst MOA

422
Q

Mnemonic for hypernatremia symptoms

TRIP

A

Twitching tremors, hyperreflexia

Restlessness, irritable, confusion

I intense thirst, dry mouth, decreased urine output

Pulmonary and peripheral and peripheral edema

423
Q

Treat hypovolemia hypernatremia

A

Isotonic saline

424
Q

Treat hypernatremia

A

Hypotonic IV solutions

425
Q

Calculate water deficit

A

.6% body weightx (1-140/Na)

426
Q

Why correct hypernatremia slowly

A

Will cause brain edema

Correct over 48 hours at .5mEq/L/hr

427
Q

What keeps ion distribution between ICF and ECF

A

NaKATPase

428
Q

Define hyperkalemia

A

> 5.3

429
Q

Define hypokalemia

A

<3.7 mEq/L

430
Q

High K

A

Cells stay refractory since Na channels are not deactivated

High T wave, prolonged PR interval, v fib

431
Q

Low K effect

A

Hyperpolarized

Low T wave

High U wave low ST

432
Q

What is the normal K range

A

3.5-5

433
Q

Academia ICF and H and K

A

ICF takes in H

Low ECF pH<7,35
High H buffered by raising ECFK

434
Q

Alkalemia ICF K and H

A

ICF donates H so ECF has ph>7.45

Low H, bufferented by lowering ECF K

435
Q

How can too much K cause death

A

K into ECF could lead to fatal hyperkalemia if not for its rapid redistribution into the ICF; insulin is most important

436
Q

K into ICF hormones

Enhance cell uptake

A 
Insulin!!!!!
B2 agonist
Aldosterone defiency
A blockers
Alkalosis
Hypoosmolarity
437
Q

K into cell hormones

A 
A agonist (NE, EPI)
Insulin defiency
Aldosterone
B2 blockers
Acidosis
Hyperosmolarity
Exercise
Lysis
438
Q

Aldosterone does what

A

Increase Na in

K out at principal cells of collecting duct

439
Q

What enhances K secretion if normal or excess potassium

A 
Plasma K
Aldosterone
ADH
Acid base balance
Tubular fluid flow rate

DISTAL NEPHRONNNN

440
Q

Low levels of aldosterone

A

Limit Na permeability in distal nephron, and without Na influx, do not have K secretion/excretion

441
Q

Increased Na delivery and increased flow rate

A

Combine to promote increased K secretion/excretion

442
Q

Hypokalemia with what K levels

A

<3.5

443
Q

Acid base balance normal with hypokalemia

A

Due to redistribution or extrearenal k losses

444
Q

Acid base metabolic acidosis hypokalemia

A

With renal or extrarenal K loss

445
Q

Hypokalemia metabolic alkalosis

A

Love K excretion
High Cl excretion
-BP normal diuretics
-BP high hyperaldosteronism

446
Q

Hyperkalemia with what K level

A

> 5.5

447
Q

Pseudohyperkalemia with hyperkalemia

A

Due to RBC cell lysis

448
Q

Causes of hypokalemis

GRAPHIC IDEA

A

GI losses (vomit, diarrhea)

Renal tubular acidosis (types I and II)

Aldosterone

Paralysis

Hypothermia

Insulin excess

Cushing

Insufficient intake
Diuretics
Elevated beta adrenergic activity
Alkalosis

449
Q

Signs and symptoms of hypokalemia

A

CNS-drowsi

Neuromuscular-weak skeletal and weak smooth (ileus and constipation)

CV-ventricular arrhythmias, hypotension, cardiac arrest

Renal-impaired concentrating ability causes polyuria and nocturnal

Metabolic?

450
Q

Goals of treating hypokalemis

A

Prevent life threatening conditions

Replace K

Diagnose/correct underlying cause

451
Q

Hyperkalemia causes RED FETS

A

Renal disease: ARF, CKD, type iV RTA

Excessive intake: food, K+IV fluids, blood transfusion

Drugs: K sparing diuretics, K salts of penicillin

Fictitious: prolonged use of tourniquet, hemolysis

Endocrine: Addison’s

Tissue release: rhabdomysis, burns, hemolysis, cytotoxic therapy

Shift out of cell: acidosis, B antagonist, insulin defiency, tissue damage

452
Q

Cardiac signs of hyperkalemia

A

Abnormal heart rhythm, bradycardia, v fib, peaked T wave

453
Q

Neuromuscular signs of hyperkalemia signs and symptoms

A

Numbnesss, weakness

454
Q

Common causes of hyperkalemia: meds targeting RAAS

A

NSAIDS, COX2 inhibitors , aliskiren beta blockers

ACEI

ARBS

Spironolactone

Amiloride

455
Q

Treat hyperkalemia

A

Antagonize cardiac effects (IV Calcium)

Redistribute K into cells (give insulin and glucose, B2 agonist such as albuterol)

Facilitate K elimination (administer K losing diuretic consider mineralocorticoid (if have hypoaldosteronsm , cation exchange resin, dialysis)

456
Q

Pseudohyperkalemia

A

Hemolysis
Thrombocytopenia
Leukocytosis

457
Q

Redistribution hyperkalemia

A 
Acidosis. 
Decreased insulin
B block
Arginine infusion 
Digitalis overdose
Periodic paralysis
458
Q

Impaired renal K excretion

A

GFR<5 mL/mim oliganuria

> 20 impaired K secretion
-low or normal aldosterone

459
Q

Low aldosterone

A

Addison disease
Hyporeniinemic
Drugs

460
Q

High aldosterone

A

Primary tubular disorders

Drugs-spironolactone, amiloride, triamterene

461
Q

UTI can result in what

A 
Cystitis
Prostatis
Pyelonephritis
Renal damage in young children
Pre term birth
Complications from frequent antibiotic use
-antibiotic resistance, C diff
462
Q

Asymptomatic UTI

A

Asymptomatic bacteriuria

463
Q

UTI pathophysiology

A

Contamination of the periurethral area with a uropathogen from the gut

Colonization of the urethra and migration to the bladder

Colonization and invasion of the bladder, mediated by pili and adhesins
Neutrophil invasion

Bacterial multiplication and immune system subversion

Biofilm formation

Epithelial damage by bacterial toxins and proteases

Ascension to the kidneys

Colonization o the kidneys

Host tissue damage by bacterial toxins

Bacteraemia

464
Q

Uncomplicated UTI

A

Acute cystitis or pyelonephritis
-likely in nonpregnant outpatient women without an atomic abnormalities or instrumentation of the urinary tract

Cystitis

Pyelonephritis

465
Q

Complicated UTI

A

Compromised urinary tract or host defense

  • urinary obstruction
  • urinary retention caused by neurological disease
  • immunosuppression
  • renal failure
  • renal transplantation
  • pregnancy
  • foreign bodies (calculi, indwelling catheters)
466
Q

Inflammatory response in the bladder and __ accumulation int he catheter

A

Fibrinogen

467
Q

Most common uncomplicated and complicated uTI pathogens

A

EPUC

Uropathogenic E. coli

468
Q

UPEC

A

Biofilm like intracellular bacterial communities

Type 1 pili*, antigen 43, curli

469
Q

P. Mirabilis

A

Produce urease

Calcium crystals and magnesium ammonium phosphate precipitates

Crystalline biofilm

470
Q

P aeruginosa

A

Microcolony formation by changing hydrophobicity of P aeruginosa surface

Lectins, rhamnolipids

471
Q

E faecalis

A

Fibrinogen

472
Q

What are the types of UTI

A

Asymptomatic bacteriuria

Cystitis

Pyelonephritis

Complicated UTIprostatis

473
Q

Symptoms ASB

A

None

474
Q

Clinical presentation ASB

A

Urine screen unrelated to GU tract symptoms

Bacteriuria

475
Q

Treat ASB

A

None

476
Q

Cystitis symptoms

A

Dysuria, urinary frequency, urgency

Nocturia, hesitancy, suprapubic discomfort, gross hematuria

477
Q

Clinical presentation cystitis

A

Likely a young, non pregnant female with above symptoms

478
Q

Treat cystitis

A

Nitrofurantoin, TMP-SMX, fosfomycin

Oral beta lactam (amoxicillin, cefpodoxime, cefdinir, cefadroxil)

Fluoroquinolones (ciprofloxacin, levofloxacin, ofloxacin)

479
Q

First line cystitis for gram + and - bacteria (P aeruginosa and proteus)

A

Nitrofurnation

480
Q

MOA nitrofurnation

A

Not fully understood

Conversion of nitrofurantoin into highly reactive intermediates by bacterial reductase

Toxic intermediates react nonspecifically with many ribosomal proteins and disrupt synthesis of proteins, RNA, DNA, and metabolic processes

481
Q

Pharmacokinetics nitrofurantoin

A

Metabolized and excreted so quickly that no systemic antibacterial action is acheived

482
Q

Adverse reactions nitrofurnation

A

Anorexia, nausea, vomiting

Antagonizes nalidixic acid (synthetic quinolone antibiotic)

483
Q

Contraindications nitrofurnation

A

Glucose 6 phosphate DH defiency

Antagonizes nalidixic acid (synthetic quinolone antibiotic)

484
Q

Cystitis first line fosomycin for gram positive and negative bacteria MOA

A

CELl wall synthesis inhibitor

Inhibits the cytoplasmic enzyme enolpyruvate transferase by covalently binding to the cysteine residue of the active site and blocking the addition of phosphoenolpyruvate to UDP-N-acetylglucosamine

485
Q

Resistance for fosofomycin

A

Due to inadequate transport of drug into the cell

486
Q

Pharmacokinetics fosfomycin

A

Only oral form approved in USA, oral bioavailability is 40%

487
Q

AE fosfomycin

A

Limited (headache and diarrhea)

488
Q

CE fosfomycin

A

Safe in pregnancy!

489
Q

First line for cystitis

A

Nitrofurnation and fosfomycin

TMP-SMX

490
Q

Can you take nitrofurantoin and fosfomycin is suspect early pyelonephritis

A

No doesn’t achieve adequate renal tissue levels

491
Q

Why should TMP-SMX be avoided

A

If prevalence of resistance is known to exceed 20%

492
Q

Second line cystitis oral beta lactam

A

Amoxicillin-aminopenicillin

Cefpodoxime-3rd generation cephalosporin

Cefdinir-3rd generation ceph

Cefadroxil-1st gen cephalosporin

Less effective than fluoroquinolones (more side effects) and TMP-SMX

493
Q

Why are fluoroquinolones third line for cystitis

A

SE

494
Q

Name fluoroquinolones

A

Ciprofloxacin

Levofloxacin

Ofloxacin

Moxifloxacin is NOT RECOMMENDED bc attains lower urinary levels than other fluoroquinolones

495
Q

FDA warning fluoroquinolones

A

Disabling and potentially irreversible adverse effects of systemic fluoroquinolones outweighs their benefits in treating uncomplicated cystic

Tendinitis and tendon rupture

Peripheral neuropathy

CNS effects

496
Q

Why not use ampicillin and amoxicillin to empirically treat cystitis

A

Resistance

497
Q

Resistance to oral antibiotics is rare

A

Espicially among outpatients with uropathogenic E. coli

498
Q

How treat cystitis if resistance is identified

A

Ertapenem (a car ape EM)

499
Q

Ertapenem

A

As a class carbapenems have a wide spectrum with good activity against gram negatives (including p aeruginosa), gram positive, and anaerobes

Ertapenem specifically is insufficiently active against P aeruginosa

500
Q

Symptoms of pyelonephritis

A

Unilateral back or flank pain, fever

Mild-low grade fever with or without lower back pain or costovertebral angle pain

Severe-high fever, rigors, nausea, vomiting, and flank andor loin pain

Development of bacteremia

501
Q

Clinical presentation pyelonephritis

A

Fever (not present in cystitis), low back pain

May or may not have symptoms of cystitis

502
Q

Treat pyelonephritis

A

Fluoroquinolones (ciprofloxacin, levofloxacin)

TMP-SMX, oral beta lactam, aztreonam

503
Q

Fluoroquinolones for first line pyelonephritis

A

Ciprofloxacin or levofloxacin

Give for severe pyelonephritis or risk factors for resistance
-administered with parenteral broad spectrum antibiotic until susceptibility data is available

Aminoglycosides used are gentamicin and tobramycin

504
Q

What are aminoglycosides gentamicin and tobramycin active against

A

Gram negative and P aeruginosa

505
Q

MOA aminoglycosides gentamicin and tibramycin

A

Irreversible protein synthesis inhibitos, binds to 30s ribosomal subunit

Interference with the initiation complex of peptide formation

Misreading of mRNA leading to production of non functional proteins

506
Q

Pharmacokinetics amioglycosides gentamicin and tobramycin

A

Cleared by kidneys

507
Q

Adverse effects of aminoglycosides gentamicin and tibramycin

A

8th CN toxicity: vertigo, hearing loss

Renal toxicity

Neuromuscular blockade

508
Q

Second line for pyelonephritis

A

TMP SMX, oral beta lactams, aztreonam

509
Q

When use TMP SMX , oral beta lactams, or aztreonam for pyelonephritis

A

Fluoroquinolone patient hypersensitivity or fluoroquinolone resistance

510
Q

Name oral beta lactams

A

Amoxicillin cefpodoxime

Cefdinir

Cefadroxil

511
Q

What give to pyelonephritis if patient cant tolerate TMP SMX or oral beta lactams

A

Aztreonam

512
Q

Aztrenonam second line pyelonephritis

A

Monobactam, monocyclic beta lactam ring

513
Q

What does aztreonam work against

A

Activity against aerobic gram negatives (P aeruginosa)

514
Q

Why can aztreonam be used in patients with penicillin hypersensitivity

A

Little cross reactivity with bicycling beta lactams

515
Q

MOA aztreonam

A

Cell wall synthesis inhibitor, transpeptidase inhibitor

516
Q

Pharmacokinetics aztreonam

A

IV formulation, 1-2 hour half life, prolonged in renal failure

517
Q

Adverse effects aztreonam

A

Limited, neutropenia (children 3-11%) , pain at injection (children 12%)

518
Q

Complicated UTI symptoms

A

Similar to uncomplicated cystitis and pyelonephritis

Can by cystic, pyelonephritis or both

519
Q

Clinical presentation complicated UTI

A

Severe dysuria

70-80% of all complicated UTI are due to an indwelling catheter

520
Q

Treat complicated UTI

A

Organisms causing complicated UTIs are more likely to be resistant to commonly used oral agents recommended for empiric treatment of uncomplicated cystitis

521
Q

Cystitis

A

Ciprofloxacin or levofloxacin

522
Q

Pyelonephritis (mild)

A

Ceftriaxone, ciprofloxacin, levofloxacin or azteronam

523
Q

Pyelonephritis severe

A

Beta lactam and beta lactamase inhibitor or a carabapenem

524
Q

First line for complicated cystitis fluoroquinolones

A

Ciprofloxacin or levofloxacin

Covers p aeruginosa

MOXIFLOXACIN is not recommended
-attains lower urinary levels than other fluoroquinolones

525
Q

How treat complicated cystitis with presence of gram + cocci on gram stain suggests enterococci UTI (E faecalis, E faecium)

A

Mpicillin or amoxicillin

526
Q

Poor empiric choices due to high precenalnce of resistance

A

Nitrofurantoin

TMP SMX

Fosfomycin
Oral beta lactams (amoxicillin, cefpodoxime, cefdinir, cefadroxil)

Use these drugs only is uropathogenic is known to be susceptible

527
Q

Phenazopyridine

A

Urinary analgesic with unknown mechanism, can cause significant nausea

Colors urine orange/red

528
Q

First line for complicated (mild ) pyelonephritis

A

Ceftriaxone,

ciprofloxacin or levofloxacin

  • covers P aeruginosa
  • moxifloxacin is NOT recommended
  • attains lower urinary levels than other fluoroquinolones

Aztreonam

529
Q

Ascomplicated pyelonephritis first line severe

A

Cefepime

Piperacillin+ tazobactam
-if P aeruginosa suspected a higher dose can be used

Ceftolozane+tazobactam

Ceftazidime+avibactam

Meropenem
-if p aeruginosa suspected a higher dose can be used

Imipenem

Doripenem

530
Q

Tazobactam and avibactam

A

B lactamase inhibtiors

531
Q

How are b lactamase inhibitors given

A

Piperacillin+tazobactam

Ceftolozane+tazobactam

Ceftazidime+avibactam

532
Q

What determines tha antibacterial spectrum of b lactamase inhibtiors : tazobactam and avibactam

A

By companion beta lactam

533
Q

MOA tazobactam and avibactam

A

Resemble B lactam molecules, very weak antibacterial action

Protect hydrolysable B lactams from inactivation by these enzymes

Good inhibtors of amber class A B-lactamase
-these b lactamase are produced by staphylococci, H influenzae, N gonorrhea, salmonella, shigella, E. coli* and K pneumoniae*
Poor inhibtiors of class C b lactamase
-these B lactamase are produced by enterobacter app, citrobacter spp, S marcescens, and P aeruginosa
534
Q

Adverse effects tazobactam and avibactam

A

Limited (<10%), diarrhea, constipation, vomiting, skin rash

535
Q

Bacteria that can cause complicated UTI

A

E. coli, K pneumoniae, enterobacter, P aeruginosa

536
Q

Name carbapenems for complicated pyelonephritis first line

A

Imipenem, doripenem, meropenem, ertapenem (resistant cystitis)

537
Q

What are carbapenems good against

A

Wide spectrum with good activity against gram negatives (including p aeruginosa), gram positives, and anaerobes

  • doripenem and meropenem have greater activity against gram negatives and slightly less activity against gram positives
  • ertapenem insufficiently active against P aeruginosa
538
Q

Carbapenems are resistant to ___

A

B lactamases

539
Q

MOA carbapenems

A

Inhibit transpeptidase, similar to penicillins and cephalosporins

540
Q

Imipenem pharmacokinetics

A

Metabolized by dihydropeptiase in kidney

541
Q

Doripenem, meropenem, ertapenem

A

Not metabolized by dihydropeptidase

542
Q

of the carbapenems, ___has the longest half life ( 4 hours), administered with lidocaine to reduce irritation after intramuscular injection

A

Ertapenem

543
Q

Adverse effects imipenem (more common)

A

Nausea, vomiting, diarrhea, skin rashes, infusion site reactions, seizures

544
Q

Doripenem, meropenem, ertapenem AE

A

Less likely to cause seizures

545
Q

Complicated pyelonephritis (severe) first line b lactams

A

Piperacillin-anti-pseudomonas penicillin

Ceftazidime-3rd gen cephalosporincefepime-4th gen cephalosporin

Ceftolozane-5th gen ceph

546
Q

Which b lactams are given in combo with a b lactamase inhibtor to extend the spectrum

A

Piperacillin

Ceftazidime

Ceftolozane

547
Q

MOA b lactams

A

Cell wall synthesis inhibitors, bind and inhibit transpeptidase

548
Q

AE complicated pyelonephritis b lactams

A

B lactam hypersensitivity

549
Q

Prostatic pathogen

A

E. coli (most), proteus, P aeruginosa

Enterobacteriaceae including klebsiella, enterobacter, and seratia spp

550
Q

Symptoms prostatis

A

Fever, chills, malaise, myalgia, dysuria, lower urinary tract symptoms (frequency, urgency, urge incontinence), pelvic of perineal pain and cloudy urine

551
Q

Clinical presentation prostatis

A

Patient is acutely ill with spiking fever, possible complaint of pain

During the exam, a prostate will be warm, firm, edematous and tender

552
Q

Treat prostatis

A

TMP SMX
Ciprofloxacin
Levofloxacin

553
Q

Post streptococcal glomerulonephritis

A

Most common cause of acute nephritis in kids
-97% of cases occur in regions with poor ppl

Caused by prior infection with group A beta hemolytic strep(gram+)

554
Q

Clinical presentation post strep glomerulonephritis

A

Asymptomatic, microscopic hematuria

Acute nephritic syndrome (red/brown urine, proteinuria, edema, HTN, elevation in serum creatinine)

555
Q

Treat post strep glomerulonephritis

A

Management-loop diuretic, anti HTN agent, dialysis

Recurrent group A beta hemolytic strep infection
-antibiotics

556
Q

Treat recurrent strep

A

With agents greater B lactamase stability

Penicillin G
-IM injection if adherence to previous antibiotic uncertain

Cephalexin or cefadroxil
-1st gen cephalosporins

Cefpodoxime or cefdinir
-3rd gen cephalosporins

Amoxicillin or clindamycin

557
Q

What is clindamycin effective against

A

Streptococci, staphylococci, and pneumococci

  • enterococci and gram negative aerobes resistant
  • very effective against anaerobes
558
Q

MOA clindamycin

A

Protein synthesis inhibitor, binds 50S ribosomal subunit

559
Q

Pharmacokinetics clindamycin

A

Penetrates most tissue (not brain and CSF)

Metabolized in the liver and excreted int he urine

560
Q

AE clindamycin

A

Diarrhea, nausea, skin rashes

Risk factor for C diff induced diarrhea and colitis
-GI filled with anaerobes

561
Q

Case questions

A

Ok

562
Q

Benign prostatic hyperplasia causes bladder outlet ___

A

Obstruction

563
Q

Lower urinary tract symptoms

A

Interrupted stream, frequency, hesitation, fullness, dribbling, urgency, weak stream

564
Q

Moxafloxacin

A

Don’t pick it-doesn’t go into urine

565
Q

A1 adrenergic receptor antagonists for BPH

A

Terazosin, doxazosin, tamsulosin, silodosin, alfuzosin

566
Q

What do a1 adrenergic receptors do

A

Relax muscle tone

Rapid relief of symptoms

567
Q

A1>a1 for blood vessels vascular resistance

A

B

A

568
Q

What does prostate smooth muscle contraction

A

A1A

569
Q

Detruser receptor for instability

A

A1D>a1A

570
Q

Spinal cord

Control of urinary function

A

A1D

571
Q

Stimulation of __ receptors mediates lower urinary tract symptoms

A

A1

572
Q

A1 receptors +NE

A

Muscle contraction

Bladder outlet obstruction

573
Q

A1D receptors and NE

A

Detruser instability

574
Q

A1 antagonists compete with NE

A

Reduce spasm

Promote muscle relaxation

Improve urine flow

575
Q

Terazosin and doxasin specificity

A

A1»a2

Take 1 hours prior

576
Q

Terazosin and doxazosin uroselective

A

No

577
Q

AE terazosin and doxazosin

A

Postural hypotension, dizziness fatigue

578
Q

Terazosin and doxazosin drug interactions

A

PDE-5 inhibitors (sildenafil, vardenafil)

579
Q

Tamulosin and silodosin specificity

A

A1a=a1D>a1B

580
Q

Tamsulosin and silodosin uroselective

A

Yes

A1a-a1D

581
Q

AE tamsulosin and silodosin

A

Reduced ejactulation, IFIS

582
Q

Drug interactions tamulosin and silodosin

A

PDE inhibitors (sildenafil, vardenafil)

Increase concentration of CYP3A4

583
Q

Alfuzosin specificity

A

Non specific

A1 selective

584
Q

Alfuzosin uroselective

A

Yes (functional)

585
Q

AE alfuzosin AE

A

QT prolongation

586
Q

Drug interactions alfuzosin

A

PDE-5 inhibitors (sildenafil, vardenafil)

Increase concentration of CYP 3A4 substrates

587
Q

Clinical summary of a1 adrenergic receptor antagonists

A
  • best monotherapy for prompt relief of symptoms (days)
  • all have comparable clinicalefficacy
  • alfuzosin has functional uroselectivity
  • distributes into the prostate>serum
  • avoid in hepatic impairment
  • take immediately after the same meal every day

Tamsulosin-FDA approved as generic

588
Q

Steroid 5a reductase inhibitors

A

Finasteride, dutasteride

Prevents enlargement and shrinks prostate

Delayed action
-shrinkage takes 3-6 months

589
Q

Why does the prostate enlarge

A

Aging+dihydrotestosterone

590
Q

Steroid 5a reductase inhibitors blunt prostate enlargement

A

Ok

591
Q

What enables prostate epithelium survival and growth

A

Androgenic steroids, testosterone, and DHT

592
Q

__ is 10times more potent than its precursor

A

DHT

593
Q

_____ coverts serum T to DHT in cells

A

Steroid 5a reductase type 1 and type 2

594
Q

A hyperplastic prostate has excess ___

A

SAR-2

595
Q

DHT starvation causes what

A

Epithelial atrophy, shrinkage, and gradual relief of LUTS

596
Q

Direct effects of steroid 5a reductase inhibitors

A

T accumulation

DHT depletion

597
Q

Indirect effects of steroid 5a reductase inhibitors

A

Androgen receptor less occupied

No gene transcription

598
Q

Finasteride

A

Specific inhibitors SAR2

599
Q

Dunasteride

A

Dual inhibitorSAR1 and 2

600
Q

Finasteride

Selectivity, SAR in BPH, prostate DHT, PSA, serum T, serum DHT

A

SAR2
SAR2»1

90% decreased

PSA 50% decreased

15-20% increased

70% decreased

601
Q

Dutasteride

Selectivity, SAR in BPH, prostate DHT, PSA, serum T, serum DHT

A

SAR 1 and 2

SAR2»1
90% decreased

50% decreased

15-20% increased

90% decreased

602
Q

Clinical summary of finasteride and dutasteride

A

Take 3 months for measurable effect to be observed

Have similar efficacy

  • improved LUTS
  • reduced prostate volume and reduced serum PSA
  • reduced need for surgery

Have similar AE

  • erectile dysfunction
  • gynecomastia
  • depressed libido
  • ejaculation disturbance

No dosage adjustment necessary for:
Age, renal insuffiency

No established clinically significant drug interactions

Use caution with liver abnormalities
-metabolized by hepatic CYP3A

603
Q

Combination therapy:

A1 adrenergic antagonist+5a reductase inhibitor.

A

For severe symptoms of BPH, known to have large prostate, no response from monotherapy

Long term combination therapy significant improves patient symptoms versus either drug alone

604
Q

BPH treat

A

PDE-5 inhibtors tadalafil

-for patients with both BPH and ED

605
Q

ED

A

Consistent or recurrent inability to acquire or sustain an erection of sufficient regidity and duration for sexual intercourse

606
Q

Risk factors for ED

A

Obesity, smoking, stress, CVD, adverse drug effect (diuretics, antidepressants SSRI)

607
Q

Physiology of penile erection

A

Blood flows into corpora cavernous and corpus spongiosum (glans penis)

NO facilitates smooth msucle relaxation

  • maximize blood flow
  • penile engorgement

Relaxed smooth muscle leads to blood in sinusoids and a rigid organ

608
Q

What does NO lead to

A

Increase in cGMP, decreases in iCa, smooth muscle relaxation and erection

609
Q

What do PDE-5 inhibitors do

A

Competitive inhibitors of the PDE-5 enzyme

610
Q

Sildenafil onset, duration, stomach contents, t1/2, clearance

A

Take 1 hour prior, 4 hours, empty, 4, hepatic CYP3A4

611
Q

Vardenafil onset, duration, stomach contents, t1/2, clearance

A

Take 1 hour prior, 4-5 hours, empty, 4, hepatic CYP3A4

612
Q

Tadalafil onset, duration, stomach contents, t1/2, clearance

A

Take 1 hour prior, 36 hours(1 weekend), doesn’t matter, 18, hepatic CYP3A4

613
Q

Avanafil onset , duration, stomach contents, t1/2, clearance

A

Take 15 min prior (high dose)**
Take 30 min prior (normal dose)
4 hours, doesn’t matter, 4 hours, hepatic CYP3A4

614
Q

PDE-5 inhibtors have high specificity for the

A

PDE-5 enzymes

615
Q

Adverse effects of sildenafil, vardenafil, and avanafil

A

Blue vision and blurred vision

PDE-5 1 fold in corpus cavernosum

PDE-6 10 fold in retina

616
Q

PDE-1 80 fold

Vasculature, heart, brain

A

But little significance

617
Q

PDE-11 800 fold pituitary, testes, heart

A

Negligible

618
Q

Side effects PDE-5 inhibitors

A

Reasonably well tolerated

PDE-5

619
Q

SE PDE-5 inhibitors

A

Well tolerated

PDE-5 related
-headache, dyspepsia, nasal congestion

PDE-6 related (sildenafil, vardenafil, and avanafil)
-blurred blue vision

Specific to tadalafil
-back pain, myalgia, limb pain

620
Q

Contraindications PDE-5 inhibitors

A
  • organic nitrates
  • extreme and dangerous

Specific to vardenafil
-patient needs to be hemodynamically stable

Specific to tadalafil
-when used for BPH, concurrent a1 blockers not recommended

Specific to sildenafil
-concurrent a blockers initiated at lowest recommended dose

621
Q

Second line ED theapies

A

Vacuum erection devices
-try first, l,ess expensive and non invasive

Penile injections with alprostadil
-prostagladin E1

622
Q

MOA alprostadil

A

Leads to increase in cAMP, decreases in iCa, smooth muscle relaxation, and erection

623
Q

Adverse effects alprostadil

A

Prolonged erection (priapism)-medical emergency, need to evacuate clogged blood

  • can result in permanent corporal fibrosis and ED
  • 6% of men using intrapenile alprostadil injection (can also occur with PDE-5 inhibitors )
624
Q

Treat priapism from alprostadil

A

Sympathomimetic (phenylephrine)+aspiration

625
Q

Nephrin thick wall vs thin wall transport

A

Thick active

Thin passive

626
Q

Faconi

A

PCT

Filtered glucose, aa, uric acid, phosphate, and bicarbonate are passed into the urine instead of being absorbed

Not considered to be a defect in a specific channel, but a more general defect in the function of the proximal tubules

627
Q

Clinical features faconi

A 
Polyuria, polydipsia, hypovolemia
Hypophosphatemia rickets
Growth failure
Type 2 renal tubular acidosis
Hypokalemia
Hyperchloremia
Hypophosphatemia/phosphaturia
Glycosuria
-recall this also can be caused by the sodium glucose co transporter 2 SGlT2 inhibtors (the gliflozins such as canaglofloxin)
-proteinuria/aminoaciduria
-hyperuricosuria
628
Q

Treat faconi

A

Treat underlying causes

Replace substances water in the urine

  • HCO3 (can use citrate), phosphate+vitamin D to promote bone growth
  • if genetic causes, minimize intake of substance that is not handled properly (cysteine, tyrosine, galactose, copper)
629
Q

Inherited salt losing renal tubulopathies

A

Bartter syndrome type I

Bartter syndrome type II

Barter syndrome III

Bartter syndrome type IV

Bartter syndrome IVB

Bartter syndrome type V

Gitelman Syndrome

630
Q

Bartter

A

Concentrating capacity reduced and diluting capacity reduced

631
Q

Gitelman

A

Concentrating capacity normal.near normal and diluting capacity reduced

632
Q

Barter syndrome

A

Dysfunction inNKCC2 , ROMK, CLC-kB ,CLC-Ka

633
Q

Classic bartter type 3

A

CLCNKB gene

Defect in Cl channel

634
Q

Inheritance bartter

A

AR
Rare
Presents in childhood

635
Q

Neonatal bartter

A

Seen 24-30 weeksof gestation as polyhydramnios;polyuria/polydipsia with hypercalcuria after birth

636
Q

Classic bartter

A

No noticeable symptoms until school agi

  • polyuria/polydipsia
  • vomiting, growth retardation
637
Q

Symptoms of bartter are identical to those taking what

A

Loop diuretics

638
Q

Treat barrett

A

Life long increases in dietary Na and K and K sparing diuretics to limit K loss
-also PGE2 directly stimulates renin release from juxtaglomerular cells and contributes to the electrolyte abnormalities that are seen in bartter syndrome..NSAIDS can help correct this

639
Q

Symptoms of bartter (like loop diuretics)

A

Normal to low BP

Polyuria/polydipsia

Elevated plasma renin and aldosterone

Hypokalemia

Hyponatremia

Hypocalcemia

Hypomagnesia

Hypochloremic alkalosis

Hyperglycemia

Hyperuricemia

Increased cholesterol and triglycerides

ISOTONIC URINE

640
Q

Gitelman syndrome

A

Defect in. NaCl symporter-defective in gitelman syndrome

641
Q

Inheritance Gitelman

A

AR less rare than bartter

Mutations in the gene coding for the thiazide sensitive NaCl cotransporter in distal tube

642
Q

Presentation gitelman

A

Late childhood or adulthood, may be more severe in females

Mimics chronic use of thiazide diuretics

May get htn at later stage

643
Q

Symptoms gitelman

A 
Polyuria/polydipsia
Hypokalemia
Hyponatremia
Hypercalcemia
Hypomagnesemia
Hypochloremic metabolic alkalosis
Hyperglycemia
Hyperuricemia
Increased cholesterol and triglycerides

And can DILUTE OR CONCENTRATE URINE

644
Q

Treat gitelman syndrome

A

Life long

Cornerstone is taking NaCL to avoid sodium depletion (which would increase Aldo) and providing supplementation of K and Mg
-but supplementation->side effects

Aim for asymptomatic stable hypokalemia and borderline hypomagnesemia
-an aldosterone antagonist can stabilize the hypokalemia, but it competes with compensatory secondary hyperaldosteronism

NSAIDS are ineffective in gitelman syndrome (defect is downstream from macula densa)

645
Q

Gitelman is more __ than bartter

A

Benign

646
Q

Diagnosis bartter or gitelman

A

Exclusion

Made in someone who presented with unexplained hypokalemia and metabolic alkalosis with a moral or low bp

647
Q

Urine in bartter and gitelman

A

Gitelman-dilute

Bartter-isotonic

648
Q

Calcemia/calciuria in bartter and gitelman

A

Bartter-hypocalcemia/hypercalciuria, opposite of gitelman

649
Q

In bartter/gitelman urine __ concentration is typically greater than 25 mEq/L despite volume contraction

A

Chloride

Patients who secretively take diuretics have a variable urine chloride concentration correlations with or without diuretic effect..so a urine diuretic screen should be obtained

650
Q

Failure to respond to loop or thiazide diuretics appropriately can aid in diagnosis of _ and _, respectively

A

Bartter

Gitelman

651
Q

Liddle syndrome

A

ENaC channel doesn’t degrade properly

652
Q

Inheritance liddle (pseudoaldosteronism)

A

Rare AD

Mutation changes ENaC Chen also so that they are not degraded correctly by ubiquitin proteasome system->increased Na reabsorption with K loss
—early and often severe hypertension associated with
-low plasma renin activity, low aldosterone
-metabolic alkalosis
-hypokalemia

653
Q

Treat liddle

A

Low Na diet and K sparing diuretics

654
Q

Pseudohypoaldosteronism

A

Caused by a failure of response to aldosterone, leading to renal tubular acidosis and hyperkalemialevevls of aldosterone are actually elevated due to a lack of feedback inhibition

655
Q

Therapy pseudohypoaldosteronism

A

Large amounts of Na

656
Q

Renal tubular acidosis

A

Due to unmeasured anions (anion gap)

Normal 8-16 mEq/L

657
Q

Type 2 renal tubular acidosis

A

Renal loss of HCO3(cant reabsorbed)

Normal anion gap

Hyperchloremia

658
Q

Type 1 renal tubular acidosis

A

Decrease excretion of H as titratable acid and HN4

Decrease ability to acidity urine

Normal anion gap

659
Q

Type 4 renal tubular acidosis

A

Hypoaldosteronism

Decreased excretion of NH4

Hyperkalemia inhibits NH3 synthesis

Normal anion gap

660
Q

Renal tubular acidosis

A

Acidemia, normal anion gap, normal serum creatinine, no diarrhea

661
Q

Type 1 renal tubular acidosis

A

Distal

Impaired H secretion

<15 HCO3

Urine pH>5.5

Low K

Autoimmune disorder related

Severe

662
Q

Renal tubular acidosis 2

A

Proximal tubule

Impaired proximal HCO3 reabsorption

Plasma HCO3 12-20

Ph urine under 5.5, over 7 when give alkali therapy

Los plasma K

Related to faconi, multiple myeloma, drugs

663
Q

RTA3

A

Combo of 1 and 2, very rare genetic form (carbonic anhydrase II defiency)

664
Q

RTA4

A

ADRENAL
Hyperkalemia
Lack of Aldo or failure of kidney to respond to it

Plasma HCO3>17

Urine pH <5.5

High plasma K

Related to diabetic nephropathy, drugs (ACEI, ARB, heparin, NSAIDS)

Normal anion

665
Q

Renal tubular acidosis

A

Accumulation of acid in the body due to a failure if the kidneys to properly acidity the urine

666
Q

Type 1 RTA

A

H secretion by a intercalated cells is somehow impaired

Recall this is how new HCO3 is generated to maintain acid base homeostasis

Phosphate and ammonia buffer this H

667
Q

Treat renal tubular acidosis type 1 (major consequence is low blood K, leading to extreme weakness, irregular heartbeat, paralysis)

A

Untreated->growth retardation in kids, progressive kidney and bone disease in adults

Restore normal growth and preventing kidney stones are the major goals of therapy

  • sodium bicarbonate or sodium citrate to treat acidosis (1-2 mEq/kg/day)
  • > correction of low k, salt depletion and Ca leakage..without Ca leakage, also decrease kidney stone development
668
Q

Type 2 RTA

A

HCO3, the major buffer in the body, is among the good stuff normally reclaimed by the proximal tubules

669
Q

Treat renal tubular acidosis type 2 (PT HCO3 wasting, very rare, often part of faconi)

A

Identify the correcting the underlying causes of acquired forms of proximal RTA

Children with this disorder would likely receive large doses of potassium citrate, and oral alkali (10-15 mEq/kg/day)

  • correcting acidosis and low potassium levels restores normal growth patterns, allowing bone to mature while preventing further renal disease
  • vitamin D supplements may also be needed to help prevent bone problems
670
Q

Type 4 RTA

A

Low Aldo
High K
Low NH3 synthesis by pT

Recall how new HCO3 is generated by having NH3 accept H->NH4 to maintain acid base homeostasis

671
Q

Treat renal tubular acidosis

A

Type 4 (most common; hyperkalemia from no Aldo or failure to respond to it)

  • patients may require alkaline agents to correct acidosis, but therapy is aimed primarily at reducing serum K
  • low K diet and a loop diuretic
  • alter drug doses and/or change drugs (spironolactone, ACE inhibitors, angiotensin receptor blockers, NSAIDS)

Pharmacology (52 decks)

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