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Pharm 825 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Dosing body weight DBW

A

IBW + 0.4 ( wt-IBW)

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2
Q

Nutritional Body Weight NBW

A

IBW + 0.25 ( wt- IBW)

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3
Q

sensible fluid losses

A

urination
defecation
wounds

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4
Q

insensible fluid loss

A

skin/ sweat

lungs/respiration

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5
Q

ADH does what to fluids

A

reduces diuresis and inc water retention

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6
Q

RAAS does to fluids

A

renin secretion
Na/h20 regukation
active transport sodium
INC water retention

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7
Q

ANP does to fluids

A

DEC ADH release

conuteracts RAAS

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8
Q

electrolytes found in urine

A

Na and K

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9
Q

electrolytes found in NG output

A

Na/ Cl

small trace K

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10
Q

electrolytes found in GI fluid

A

NA

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11
Q

electrolytes found in pancreas

A

Na/Cl/ Hco3

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12
Q

electrolytes found in sweat

A

na/cl

faint trace K

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13
Q

electrolytes found in diarrhea

A

na/cl/k/hco3

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14
Q

isontonic tonicity

A

275 to 290 mosm/L

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15
Q

hypotonic tonicity value

A

<275 mosm/L

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16
Q

what do we experience w/ hypo tonicity

A
  • less concentrated fluid than extracellular fluid

- fluid will move into cell

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17
Q

what do we experience w/ hyper tonicity

A
  • more concentrated than extracellular fluid

- fluid pulled from the cells into the bloodstream

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18
Q

this is the measure of solute concentration

A

osmolarity

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19
Q

eqn of total osmolarity

A

Osmolarity of IV sln + Osmolarity of added electrolytes

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20
Q

clinical estimation of adult daily fluid requirement

A

30-40 ml/Kg/day

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21
Q

Ideal fluid has most importantly?

A

cost-effective
predictable effects
sustained INC in intravascular volume

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22
Q

normal sodium range

A

135-145

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23
Q

Normal saline Vs balanced salts

A

balanced salts = way to go

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24
Q

Are used to INC plasma oncotic pressure and

moves fluid from interstitual-> intravascular

A

colloid solutions

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25
Q

These solutions maintain perfusion to organs

A

colloids

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26
Q

albumin indications

A 
edema/ volume expansion
shock
burn
ARDS
cardiopulm bypass
intraop fluid repletion
*supportive / symptomatic tx
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27
Q

adverse effects of albumin

A

hypervolemia

azoemia ( renal failure)

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28
Q

colloids are good for patients low on _____

A

protein

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29
Q

two factors that determine synthetic colloid type

A

substitution ratio

molecular weight

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30
Q

higher SR ( sub ration) the more?

A

prolonged intravascular expansion

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31
Q

safety concerns for synthetic colloids

A

( black box) sepsis/ renal failure

use with caution

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32
Q

1 unit RBC’s = ? mLs

A

230-350mL

-will INC Hb by 1g/dL

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33
Q

normL Hb range

A

12

-low <7-8

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34
Q

indications for blood

A
  • acute blood loss
  • inadeuate resusictaion from fluids alone
  • preop
  • low Hb
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35
Q

tachycardia, hypotension, weak pulses,dec urine output and BUN/SCr ratio<20 are signs of

A

dehydration

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36
Q

Goals of Fluid Resuscitation: ANCAR

A

achieve: stability/normal volume/perfussion
normalize: cell metabolism/acid-base
compensate: for fluid shifts
avoid: inflam cascade/reperfusion injury
reduce: vasopressors/edema

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37
Q

as acidosis resides we expect lactate levels to?

A

dec

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38
Q

goal of shock fluid resucitation

A

perfusion throughout patient w/ fluids and vassopressor support

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39
Q

shock fluid resucitation goals:
CVP-
MAP-
UOP-

A

CVP: 8-12
MAP: 65
UOP: 0.5

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40
Q

Osm calculation

A

(2 X Na) + (BUN/2.8) + ( Glucose/18)

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41
Q

When does OG exist and what does it say

A

if the difference between measured and calculated osmolality > 15
-it identifies the presence of additional particles

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42
Q

elevated lipids and proteins
increased plasma volume–> dilution
experience OG

A

psuedohyponatremia

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43
Q

This sodium state is most likely seen with an increase of blood glucose

A

hypertonic hyponatremia

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44
Q

For every INC of BG over 100mg/dl… what happens to sodium serum levels

A

drop 1.6meq/L for ea 100mg/dL

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45
Q

Corrected sodium eqn

A

Na serum +1.6[( BG-100)/100]

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46
Q

Causes of hypovol, hypoton,hyponatremia

A 
Renal (urine Na> 20meq)
-diuretics
-adrenal insufficiency
-salt losing nephtopathy, cerebral salt wasting
Non renal (urine Na< 20meq)
-bloodloss/hemorrhage
-skin losses
-GI losses
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47
Q

Causes of isovol, hypoton, hyponatremia

A
  • adrenal insufficency ( glucocorticoid def)
  • hypothyroidism
  • pscychogenic polydipsia
  • SIADH (most common cause)
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48
Q

signs of SIADH

A

urine Osm > 100mOsm/kg
Urine Na generally > 20-30mEq/L
-restric free water 1st line

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49
Q

causes SIADH

A 
tumors, CNS disorders
 DRUGS
-Antineoplastics
-Antipschotics
-Carbamzepine
-SSRIs
-Nicotine
-NSAIDs
-Oxycontin
-TCa's
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50
Q

Clinical settings that hypervol, hypoton, hyponatremia can be seen

A
  • cirrhosis
  • heart failure
  • kidney failure
  • nephrotic syndrome
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51
Q

This range of sodium is typical to asymptomatic hyponatremia

A

> 125mEq/L

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52
Q

Most common goal is to avoid a rise in serum Na that is greater than??

A

0.5mEq/L/Hr
or
8-12mEq/L/Day

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53
Q

hypovolemic tx

A

symptomatic: Hypertonic 3% NaCl
asymptomatic: isotonic NaCl

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54
Q

isovolemic tx

A

symptomatic: Furosemide and 3%NaCl
asymptomatic: water restriction and isotonic NaCl

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55
Q

hypervolemic tx

A

symptomatic: Furosemide and judiciously 3%NaCl
asymptomatic: fureosemide

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56
Q

Rapid infusions of 3% NaCl @ 1-2 ml/kg/hr over 2-3 hrs only in what pt population?

A

pts with coma or sz

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57
Q

How do you IN sodium in a pt w/ acute symptomatic hyponatremia

A 
MAX: 8-12 mEq/L/ first 24hrs
or
1-2mEq/L/hr
good short term goal is 120meq/L
use 3% Hypertonic NaCl: 1/2 in first 24hrs, then rest 24-72 hours
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58
Q

What do Arginine Vasopressin V2/V1A receptor antagonists do?

A

promote excretion of free water

  • no loss electrolytes
  • INC urine output
  • DEC urine osmolarity
  • normalize Na+ levels
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59
Q

Arginine Vasopressin V2/V1A receptor antagonists are Vaptans and come in 2 what most common forms?

A

Conivaptan- IV

Tolvaptan- PO

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60
Q

Conivaptan treats what?

A

severe euvolemic and hypervolemic symptomatic hyponatremia

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61
Q

Tolvaptan treats what?

A

Asymptomatic euvolemic and hypervolemic hyponatremia

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62
Q

Vaptan contraindications

A

hypovolemic hyponat
no sense of thirst
anuria
CYP3A4 inhibitors

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63
Q

monitoring measures for pts w/ sypmtomatic hyponatremia

A
  • monitored in ICU or highly monitored unit
  • serial exams of heart, lungs, neuro status several times over first 12 hours
  • serum Na q2-4 hours until asymptomatic
  • serial Na q4-8 hours until WNL
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64
Q

hypernatremia is always associated w/ what tonicity

A

hyper

-loss of water thirst response

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65
Q

hypervol hypernatremia is assoc w/ ?

A

hypertonic fluid use

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66
Q

Steps to correcting hypovolemic hypernat

A

1) restore hemodynamic w/ NS

2) Calculate free water deficit

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67
Q

Parameters for replacing free water

A

D5W continuously or enteral feeding tube
match ins and outs
dont correct too quickly
give 1/2 deficit over 24 hours and rest over next 48

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68
Q

goal of Na decrease in hypernatremia

A

0.5ml mEq/L/hr decrease in Na serum

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69
Q

hyperntremia monitoring parameters

A

Serum Na and fluid status
-check every 3-6 hrs until symptoms resolve ( then q 6-12 hours)
I/O q 8-12 hours
overall fluid balance

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70
Q

What kind of sodium balance does diabetes insipidus create

A

isovolemic hypernatremia

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71
Q

tx of isovolemic hypernatremia

A

Desmopressin

Vasopressin

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72
Q

Normal range of K

A

3.5-5mEq/L

73
Q

factors affecting Potassium lvls

A 
Na/K pump
-insulin
-glucagon
-catecholamines
-aldosterone
kidneys
arterial pH/ acid base status
74
Q

Hypokalemia causes

A
  • diuretic loss
  • beta agonist meds
  • NG drainage–> metabolic alkalosis
  • Diarrhea
  • Mag depletion
75
Q

Hypokalemia presentation

A
  • nonspecific/ highly variable
  • weakness or muscle wkness
  • N/V
  • Change in cardiac fxn or rythym ( higher risk pt)
  • cramping
76
Q

hypokalemia tx

A 
serum lvl  3-3.4 
-tx debatable, give PO K for cardiac risk pt
serum lvl <3mEq/L
-ALWAYS TX
-PO if asymptomatic or IV for sx
-also correct Mg deficit if present
77
Q

Correction of K in hypokalemia

A

for every 10meQ of K given, you INC the Serum Na by 0.1mEq/L

78
Q

serum lvls of severe hypokalemia and symptoms that warrant an IV

A

<2.5 or 3 meq

ECG or muscle spasms, unable to tolerate PO

79
Q

severe hyperkalemia

A

> 7

80
Q

hyperkalemia is what serum lvl

A

> 5.5

81
Q

clinical presentation of hyperkalemia

A

peaked T wave/ flattened T wave
cardiac arrthymias
VF or asystole > 9mEq/L

82
Q

Severe Hyperkalemia goals of therapy

A

antagonize memb actions
DEC extra cell K
remove K from the body

83
Q

what two medications used to treat Hyperkalemia must go hand in hand and why

A

D5W and insulin because insulin draws back the K into the cell

84
Q

Normal level of magnesium

A

1.5-2.5 mg/dL

85
Q

Lvls are regulated by the kidneys and related to Ca 2+ and K+ metabolism

A

Mg2+

86
Q

Usually associated w/ disorders of GI tract or kidneys
Diarrhea/ Dec intestinal absorp
malnutrition
drugs or alcohol cause

A

hypormagnesemia

87
Q

Common drugs that cause hypomagnesemia

A

amphotericin
aminoglycosides
diuretics
cyclosporine

88
Q

clinical presentaions of hypomagnesemia

A
  • assoc w/ hypocalcemia and hypokalemia
  • cardio arrthymias, tetany
  • neuromusc: ataxia/ sz
  • CNS: lethargy, confusion
89
Q

causes of hypermagnesmia

A
  • rare
  • renal failure
  • excessive laxatives
90
Q

Clinical presentations of hypermagnesemia

A
  • mg2+ >4
  • neuromuscular: deep tendon reflex loss, somnolence, resp muscle paresis
  • Cardio: hypoTN, arrthymias, heart block
91
Q

hypermagnesemia tx

A

CaCl or furosemide
or supportive care
-for renal dysfxn: diuresis or hemodialysis

92
Q

Normal lvls Calcium

A

8.5-10.5 mg/dL

93
Q

low calcium causes

A 
large blood V products
mag deficiency
post-op hypoparathyroid
Vit D deficiency
meds
94
Q

Parasthesis, muscle cramps, tetany, depression, anxiety, sz, hairloss, eczema, brittle nails, hypotension, bradycardia, arrthymias are all clinical presentations of what?

A

Hypocalcemia

95
Q

usual admin rate of calcium is??

A

1gm of calcium/ hr

96
Q

Important for hypocalcemia tx

A

gluconate preferred for PIV
do not add Ca to bicarb or phosphate
give Vitamin D supplementation

97
Q

Three main mech of hypercalcemia

A

INC bone reabsorp
INC GI absorp
DEC elimination via kidneys

98
Q

Hypercalcemia clinical presentation

A 
typically asymptomatic ( esp <13mg/dL
anorexia, constipation, polyuria or dipsia, nocturia, coma arrthymias, metastic calcification, nephrolithiasis
99
Q

Tx for hypercalcemia

A

volume expansion/ loop diuretics
calcitonin
bisphosphonates
glucocorticoids

100
Q

Normal levels of Phosphorous

A

2.5-4.5mg/dL

101
Q

clinical hypophosp presentations

A

sz, coma, paresthesias, hemolysis, myalgia, dysphagia, osteopenia, cardiomyopathy, dec contract, acute resp, resp muscle fatigue

102
Q

hyperphos causes

A

renal failure/ insufficiency
hypoparathyroid
excessive intake

103
Q

clinical presentation of hyperphos

A

soft tissue calc

104
Q

hyperphos tx

A

IV calcium for severe

105
Q

normal physiological pH range

A

7.35-7.45

106
Q

most carbonic acid in the plasma is in the form of?

A

carbon dioxide

107
Q

normal paCO2 range

A

35-45 mmHg (think 40)

108
Q

normal HCO3 range

A

22-26 mEq (think 24)

109
Q

Normal PaO2 range

A

95-100 mmHg

110
Q

normal SaO2 range

A

> 95%

111
Q

Dec CO, INC PVR and arrthymias and imparement of contractility are signs of

A

acidemia cardiac consequences

112
Q

insulin resistance, inhibition of anaerobic glycolysis and hyperkalemia are signs of?

A

metabolic consequences of acidosis

113
Q

other acidosis consequences

A

coma, alt mental status, dec resp muscle strength, hypervent, dyspnea

114
Q

cardio consequences of alkalemia

A

dec coronary flow
arteriolar constriction
dec anginal threshold
arrthymias

115
Q 
DEC K+, Ca, and mag
Over stimulation of anerobic glycolysis
Dec cerebral blood flow
sz
DEC respirations
A

consequence of alkalosis

116
Q

acid- base first line of defense

A

extra/ intracell buffering system

117
Q

common buffers include

A

bicarb/carbonic acid phosphate and proteins

118
Q

acidity can be controlled extracellularly by?

A

HCO3 or pCO2

119
Q

two main fxns of the kidneys

A
  • reabsorb filtered HCO3

- excrete H+ ions released from nonvolatile acids

120
Q

4000-45000 mEq of HCO3 re filtered daily through?

A

loop of Henry

121
Q

where does bicarb reabsorption take place

A

proximal tubule

122
Q

where can we find carbonic anhydrase

A

RBC, brush borders of renal tubular cells, and other tissues

123
Q

in case of carbonic anhydrase inhibitors

A
  • result in urinary bicarb losses due to DEC entry of H2O and CO2
  • metabolic acidosis occurs w/ increase bicarb loss
124
Q

H+ excretion takes place primarily in the ?

A

distal tubule

125
Q

50 % of net acid excretion comes from this route

A

distal tubular H secretion

126
Q

H+ is transported back to tubular lumen by?

A

ATPase

127
Q

Lungs are very important in ventilatroy regulation because?

A

rapid onset and Large capacity

128
Q

When chemoreceptors detect an INC in PaCO2 what happens

A

INC in rate and depth of ventilation

129
Q

Peripheral chemoreceptors are activated by?

A

arterial acidosis, hypercapnia, hypoxia

130
Q

Central chemoreceptors in medulla are activated by?

A

CSF acidosis

131
Q

Hepatic regulation of acid base

A
  • new mech learning more about
  • ox of proteins= HCO3 and NH4
  • diminished hepatic urea synthesis can cause metabolic alkalosis
  • a change in the urea cycle will affect HCO3 pool
132
Q

Meta Acid primary change

A

DEC HCO3

133
Q

Meta Alka primary change

A

INC HCO3

134
Q

Resp Acid primary change

A

INC PaCO2

135
Q

Resp Alka primary change

A

DEC PaCO2

136
Q

Meta Acid compensation

A

DEC PaCO2

137
Q

Meta Alkalosis compensation

A

INC PaCO2

138
Q

Resp Acid compensation

A

INC HCO3

139
Q

Resp Alka compensation

A

DEC HCO3

140
Q

PCO2 should fall by 1-1.5 times the fall in plasma HCO3

A

metabolic acidosis

141
Q

PCO2 should INC by 0.4-0.6 times the rise in plasma HCO3

A

metabolic alkalosis

142
Q

plasma HCO3 should rise by 0.4 times the INC in PCO2 + or - 4

A

chronic resp acidosis

143
Q

plasma HCO3 should rise by 0.1 times the increase in PCO2 + or - 3

A

acute resp acidosis

144
Q

Plasma HCO3 should fall 0.1-0.3 times the decrease in PCO2 but not usually less than 18mEq/L

A

acute resp alkalosis

145
Q

Plasma HCO3 should fall by 0.2- 0.5 times the dec in PCO2 but not usually less than 14 mEq/L

A

chronic resp alkalosis

146
Q

these provide water and or sodium
maintain osmotic gradient between intravascular and extravascular
“workhorses”

A

crystalloids

147
Q

used for intravascular fluid replacement
- resucitation, hypotension, septic shock
Sodium/ or chloride replacement

A

Normal saline

148
Q

maintenance fluid

A

0.5 NS

149
Q

used for replacement of blood loss
approximates human plasma
used for recsusitaion

A

Lactated ringers

150
Q

used for free water replacement
NOT a resuscitative fluid
not a maintenance fluid by itself

A

dextrose

151
Q

normal anion gap values

A

3-11 mEq

152
Q

a loss of plasma bicarb is rplaced with CL

A

non-anion gap acidosis

153
Q

delta gap

A

differences between patients anion gap and the normal anion gap

154
Q

causes of non anion gap acidosis

A 
gastrobicarb loss
renal bicarb losses
reduced renal H+ excretion
- Type I RTA
-Type IV RTA
-Chronic renal failure
Acid and chloride admin
155
Q 
shock
drugs/ toxins
seizures
leukemia
hapatic/ renal failure
diabetes mellitus
malnutrition
rhabdomyloysis are all potential cases of
A

lactic acidosis

156
Q

sx of lactic acidosis

A 
kussmaul respiratios
periph vasodialationcausing tachycardia
hyperkalemia
lethargy coma
N/V
bone demineralization
157
Q

lactic acidosis acute tx

A

underlying cause
bicarb therapy
-use if pH < 7.10-7.15

158
Q

Bicarb dosing eqn - need to know

- use for lactic acidosis

A

[ 0.5L/Kg (IBW) ] X ( desired HCO3- actual HCO3)

159
Q

Bicarb therapy parameters

A
  • use 12 as desired
  • give 1/3 or 1/2 the calculated dose
  • Cardiac arrest : 1mEq/Kg
  • Supplement K if needed
160
Q

hazrds of bicarb therapy

A 
over alkanization
-left shift in oxgen-Hb saturation curve
hypernatremia/ hyperosmolality
CSF acidosis
electrolyte shift
161
Q

flow of potassium in acid base disorders

A

in acidosis K moves extracellularly and is excreted. When bicarb therapy is used to treat acidosis, K will move back intracellularly ( more severe hypokalemia

162
Q

chronic bicarb therapy for chronics metabolic acidosis

A

avg dose 1-3 mEq/kg/day

163
Q

how does tromethamine work

A

combines with H from H2CO3 to form bicarb

164
Q

adverse affects of tromethanmine

A

hyperkalemia, hypoglycemia, hypocalemia, impaired coagulation

165
Q

three main mechanisma in which a rise of Bicarb would occur

A

loss of acid from GI tract
admin of too much bicarb/ precursor
contraction alkalosis
-loss of Cl rich and HCO3 poor fluid

166
Q

volume and chloride depletion may contribute to alkalosis due to?

A
  • Dec in arterial blood volume
  • Dec ability of kidneys to excrete bicarb
  • w/ volume depletion, capacity of proximal tubule to reabsorb HCO3 increases
167
Q

main cause of metabolic alkalosis is

A

saline responsive alkalosis

168
Q

with aldosterone INC we see?

A

Na reabsorption
inc H secretion—-> HCO3 reabsorption
inc K secretion

169
Q

Diuretic therapy’s causes of saline responsive alkalosis

A
  • extracellular volume expansion ( due to Nacl/ water secretion)
  • INC distal tubule Na reabsorp/ H and K secretion ( aldosterone
  • intracellular movement of H ( response to hypokalemia)
  • Hypochloremic state
170
Q

Three main causes of saline responsive alkalosis

A

Vominting/ NG
Diuretics
exogenous HCO3 admin/ blood transfusion

171
Q

Why there is a maintenance of an alkaline environment in saline responsive alkalosis

A
  • reduced GFR
  • enhanced proximal tubular HCO reabsorp
  • effects of hypokalemia
172
Q

in terms of hypokalemia; when less K, H is scereted while Na is_______

A

reabsorbed

173
Q

difference between saline responsive and resistant alkalosis

A

no chloride depletion or an inability to absorb CL in resistant

174
Q

causes of saline resistant alkalosis

A

INC mineralcorticoid activity
hypokalemia
renal tubular chloirde wasting

175
Q

INC ammoniagenesis can be causes by a low level of

A

potassium

due to an INC in H secretion

176
Q

muscle cramps, weakness, dizziness, myocardial supression, mental confusion, CV collapses are symptoms of

A

saline resistant alkalosis

177
Q

When would you use carbonic annhydrase inhibitors

A

pts that are fluid restricted or cant have excess sodium

178
Q

carbonic annh inhibitor dosing

A

250-375 mg once/ twice daily

179
Q

Therapies for persistent metabolic alkalosis

A

HCl
ammonium chloride
arginine monohyrdrochloride

Pharm 825 (5 decks)

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