Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharm 825 > Exam 1 > Flashcards

Exam 1 Flashcards

(179 cards)

Start Studying
1
Q

Dosing body weight DBW

A

IBW + 0.4 ( wt-IBW)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Nutritional Body Weight NBW

A

IBW + 0.25 ( wt- IBW)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

sensible fluid losses

A

urination
defecation
wounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

insensible fluid loss

A

skin/ sweat

lungs/respiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ADH does what to fluids

A

reduces diuresis and inc water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

RAAS does to fluids

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

ANP does to fluids

A

DEC ADH release

conuteracts RAAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

electrolytes found in urine

A

Na and K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

electrolytes found in NG output

A

Na/ Cl

small trace K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

electrolytes found in GI fluid

A

NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

electrolytes found in pancreas

A

Na/Cl/ Hco3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

electrolytes found in sweat

A

na/cl

faint trace K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

electrolytes found in diarrhea

A

na/cl/k/hco3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

isontonic tonicity

A

275 to 290 mosm/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hypotonic tonicity value

A

<275 mosm/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what do we experience w/ hypo tonicity

A
  • less concentrated fluid than extracellular fluid

- fluid will move into cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what do we experience w/ hyper tonicity

A
  • more concentrated than extracellular fluid

- fluid pulled from the cells into the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

this is the measure of solute concentration

A

osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

eqn of total osmolarity

A

Osmolarity of IV sln + Osmolarity of added electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

clinical estimation of adult daily fluid requirement

A

30-40 ml/Kg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ideal fluid has most importantly?

A

cost-effective
predictable effects
sustained INC in intravascular volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

normal sodium range

A

135-145

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Normal saline Vs balanced salts

A

balanced salts = way to go

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Are used to INC plasma oncotic pressure and

moves fluid from interstitual-> intravascular

A

colloid solutions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
These solutions maintain perfusion to organs
colloids
26
albumin indications
``` edema/ volume expansion shock burn ARDS cardiopulm bypass intraop fluid repletion *supportive / symptomatic tx ```
27
adverse effects of albumin
hypervolemia | azoemia ( renal failure)
28
colloids are good for patients low on _____
protein
29
two factors that determine synthetic colloid type
substitution ratio | molecular weight
30
higher SR ( sub ration) the more?
prolonged intravascular expansion
31
safety concerns for synthetic colloids
( black box) sepsis/ renal failure | use with caution
32
1 unit RBC's = ? mLs
230-350mL | -will INC Hb by 1g/dL
33
normL Hb range
12 | -low <7-8
34
indications for blood
- acute blood loss - inadeuate resusictaion from fluids alone - preop - low Hb
35
tachycardia, hypotension, weak pulses,dec urine output and BUN/SCr ratio<20 are signs of
dehydration
36
Goals of Fluid Resuscitation: ANCAR
achieve: stability/normal volume/perfussion normalize: cell metabolism/acid-base compensate: for fluid shifts avoid: inflam cascade/reperfusion injury reduce: vasopressors/edema
37
as acidosis resides we expect lactate levels to?
dec
38
goal of shock fluid resucitation
perfusion throughout patient w/ fluids and vassopressor support
39
shock fluid resucitation goals: CVP- MAP- UOP-
CVP: 8-12 MAP: 65 UOP: 0.5
40
Osm calculation
(2 X Na) + (BUN/2.8) + ( Glucose/18)
41
When does OG exist and what does it say
if the difference between measured and calculated osmolality > 15 -it identifies the presence of additional particles
42
elevated lipids and proteins increased plasma volume--> dilution experience OG
psuedohyponatremia
43
This sodium state is most likely seen with an increase of blood glucose
hypertonic hyponatremia
44
For every INC of BG over 100mg/dl... what happens to sodium serum levels
drop 1.6meq/L for ea 100mg/dL
45
Corrected sodium eqn
Na serum +1.6[( BG-100)/100]
46
Causes of hypovol, hypoton,hyponatremia
``` Renal (urine Na> 20meq) -diuretics -adrenal insufficiency -salt losing nephtopathy, cerebral salt wasting Non renal (urine Na< 20meq) -bloodloss/hemorrhage -skin losses -GI losses ```
47
Causes of isovol, hypoton, hyponatremia
- adrenal insufficency ( glucocorticoid def) - hypothyroidism - pscychogenic polydipsia - SIADH (most common cause)
48
signs of SIADH
urine Osm > 100mOsm/kg Urine Na generally > 20-30mEq/L -restric free water 1st line
49
causes SIADH
``` tumors, CNS disorders DRUGS -Antineoplastics -Antipschotics -Carbamzepine -SSRIs -Nicotine -NSAIDs -Oxycontin -TCa's ```
50
Clinical settings that hypervol, hypoton, hyponatremia can be seen
- cirrhosis - heart failure - kidney failure - nephrotic syndrome
51
This range of sodium is typical to asymptomatic hyponatremia
>125mEq/L
52
Most common goal is to avoid a rise in serum Na that is greater than??
0.5mEq/L/Hr or 8-12mEq/L/Day
53
hypovolemic tx
symptomatic: Hypertonic 3% NaCl asymptomatic: isotonic NaCl
54
isovolemic tx
symptomatic: Furosemide and 3%NaCl asymptomatic: water restriction and isotonic NaCl
55
hypervolemic tx
symptomatic: Furosemide and judiciously 3%NaCl asymptomatic: fureosemide
56
Rapid infusions of 3% NaCl @ 1-2 ml/kg/hr over 2-3 hrs only in what pt population?
pts with coma or sz
57
How do you IN sodium in a pt w/ acute symptomatic hyponatremia
``` 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 ```
58
What do Arginine Vasopressin V2/V1A receptor antagonists do?
promote excretion of free water - no loss electrolytes - INC urine output - DEC urine osmolarity - normalize Na+ levels
59
Arginine Vasopressin V2/V1A receptor antagonists are Vaptans and come in 2 what most common forms?
Conivaptan- IV | Tolvaptan- PO
60
Conivaptan treats what?
severe euvolemic and hypervolemic symptomatic hyponatremia
61
Tolvaptan treats what?
Asymptomatic euvolemic and hypervolemic hyponatremia
62
Vaptan contraindications
hypovolemic hyponat no sense of thirst anuria CYP3A4 inhibitors
63
monitoring measures for pts w/ sypmtomatic hyponatremia
- 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
64
hypernatremia is always associated w/ what tonicity
hyper | -loss of water thirst response
65
hypervol hypernatremia is assoc w/ ?
hypertonic fluid use
66
Steps to correcting hypovolemic hypernat
1) restore hemodynamic w/ NS | 2) Calculate free water deficit
67
Parameters for replacing free water
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
68
goal of Na decrease in hypernatremia
0.5ml mEq/L/hr decrease in Na serum
69
hyperntremia monitoring parameters
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
70
What kind of sodium balance does diabetes insipidus create
isovolemic hypernatremia
71
tx of isovolemic hypernatremia
Desmopressin | Vasopressin
72
Normal range of K
3.5-5mEq/L
73
factors affecting Potassium lvls
``` Na/K pump -insulin -glucagon -catecholamines -aldosterone kidneys arterial pH/ acid base status ```
74
Hypokalemia causes
- diuretic loss - beta agonist meds - NG drainage--> metabolic alkalosis - Diarrhea - Mag depletion
75
Hypokalemia presentation
- nonspecific/ highly variable - weakness or muscle wkness - N/V - Change in cardiac fxn or rythym ( higher risk pt) - cramping
76
hypokalemia tx
``` 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
Correction of K in hypokalemia
for every 10meQ of K given, you INC the Serum Na by 0.1mEq/L
78
serum lvls of severe hypokalemia and symptoms that warrant an IV
<2.5 or 3 meq | ECG or muscle spasms, unable to tolerate PO
79
severe hyperkalemia
>7
80
hyperkalemia is what serum lvl
> 5.5
81
clinical presentation of hyperkalemia
peaked T wave/ flattened T wave cardiac arrthymias VF or asystole > 9mEq/L
82
Severe Hyperkalemia goals of therapy
antagonize memb actions DEC extra cell K remove K from the body
83
what two medications used to treat Hyperkalemia must go hand in hand and why
D5W and insulin because insulin draws back the K into the cell
84
Normal level of magnesium
1.5-2.5 mg/dL
85
Lvls are regulated by the kidneys and related to Ca 2+ and K+ metabolism
Mg2+
86
Usually associated w/ disorders of GI tract or kidneys Diarrhea/ Dec intestinal absorp malnutrition drugs or alcohol cause
hypormagnesemia
87
Common drugs that cause hypomagnesemia
amphotericin aminoglycosides diuretics cyclosporine
88
clinical presentaions of hypomagnesemia
- assoc w/ hypocalcemia and hypokalemia - cardio arrthymias, tetany - neuromusc: ataxia/ sz - CNS: lethargy, confusion
89
causes of hypermagnesmia
- rare - renal failure - excessive laxatives
90
Clinical presentations of hypermagnesemia
- mg2+ >4 - neuromuscular: deep tendon reflex loss, somnolence, resp muscle paresis - Cardio: hypoTN, arrthymias, heart block
91
hypermagnesemia tx
CaCl or furosemide or supportive care -for renal dysfxn: diuresis or hemodialysis
92
Normal lvls Calcium
8.5-10.5 mg/dL
93
low calcium causes
``` large blood V products mag deficiency post-op hypoparathyroid Vit D deficiency meds ```
94
Parasthesis, muscle cramps, tetany, depression, anxiety, sz, hairloss, eczema, brittle nails, hypotension, bradycardia, arrthymias are all clinical presentations of what?
Hypocalcemia
95
usual admin rate of calcium is??
1gm of calcium/ hr
96
Important for hypocalcemia tx
gluconate preferred for PIV do not add Ca to bicarb or phosphate give Vitamin D supplementation
97
Three main mech of hypercalcemia
INC bone reabsorp INC GI absorp DEC elimination via kidneys
98
Hypercalcemia clinical presentation
``` typically asymptomatic ( esp <13mg/dL anorexia, constipation, polyuria or dipsia, nocturia, coma arrthymias, metastic calcification, nephrolithiasis ```
99
Tx for hypercalcemia
volume expansion/ loop diuretics calcitonin bisphosphonates glucocorticoids
100
Normal levels of Phosphorous
2.5-4.5mg/dL
101
clinical hypophosp presentations
sz, coma, paresthesias, hemolysis, myalgia, dysphagia, osteopenia, cardiomyopathy, dec contract, acute resp, resp muscle fatigue
102
hyperphos causes
renal failure/ insufficiency hypoparathyroid excessive intake
103
clinical presentation of hyperphos
soft tissue calc
104
hyperphos tx
IV calcium for severe
105
normal physiological pH range
7.35-7.45
106
most carbonic acid in the plasma is in the form of?
carbon dioxide
107
normal paCO2 range
35-45 mmHg (think 40)
108
normal HCO3 range
22-26 mEq (think 24)
109
Normal PaO2 range
95-100 mmHg
110
normal SaO2 range
>95%
111
Dec CO, INC PVR and arrthymias and imparement of contractility are signs of
acidemia cardiac consequences
112
insulin resistance, inhibition of anaerobic glycolysis and hyperkalemia are signs of?
metabolic consequences of acidosis
113
other acidosis consequences
coma, alt mental status, dec resp muscle strength, hypervent, dyspnea
114
cardio consequences of alkalemia
dec coronary flow arteriolar constriction dec anginal threshold arrthymias
115
``` DEC K+, Ca, and mag Over stimulation of anerobic glycolysis Dec cerebral blood flow sz DEC respirations ```
consequence of alkalosis
116
acid- base first line of defense
extra/ intracell buffering system
117
common buffers include
bicarb/carbonic acid phosphate and proteins
118
acidity can be controlled extracellularly by?
HCO3 or pCO2
119
two main fxns of the kidneys
- reabsorb filtered HCO3 | - excrete H+ ions released from nonvolatile acids
120
4000-45000 mEq of HCO3 re filtered daily through?
loop of Henry
121
where does bicarb reabsorption take place
proximal tubule
122
where can we find carbonic anhydrase
RBC, brush borders of renal tubular cells, and other tissues
123
in case of carbonic anhydrase inhibitors
- result in urinary bicarb losses due to DEC entry of H2O and CO2 - metabolic acidosis occurs w/ increase bicarb loss
124
H+ excretion takes place primarily in the ?
distal tubule
125
50 % of net acid excretion comes from this route
distal tubular H secretion
126
H+ is transported back to tubular lumen by?
ATPase
127
Lungs are very important in ventilatroy regulation because?
rapid onset and Large capacity
128
When chemoreceptors detect an INC in PaCO2 what happens
INC in rate and depth of ventilation
129
Peripheral chemoreceptors are activated by?
arterial acidosis, hypercapnia, hypoxia
130
Central chemoreceptors in medulla are activated by?
CSF acidosis
131
Hepatic regulation of acid base
- 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
Meta Acid primary change
DEC HCO3
133
Meta Alka primary change
INC HCO3
134
Resp Acid primary change
INC PaCO2
135
Resp Alka primary change
DEC PaCO2
136
Meta Acid compensation
DEC PaCO2
137
Meta Alkalosis compensation
INC PaCO2
138
Resp Acid compensation
INC HCO3
139
Resp Alka compensation
DEC HCO3
140
PCO2 should fall by 1-1.5 times the fall in plasma HCO3
metabolic acidosis
141
PCO2 should INC by 0.4-0.6 times the rise in plasma HCO3
metabolic alkalosis
142
plasma HCO3 should rise by 0.4 times the INC in PCO2 + or - 4
chronic resp acidosis
143
plasma HCO3 should rise by 0.1 times the increase in PCO2 + or - 3
acute resp acidosis
144
Plasma HCO3 should fall 0.1-0.3 times the decrease in PCO2 but not usually less than 18mEq/L
acute resp alkalosis
145
Plasma HCO3 should fall by 0.2- 0.5 times the dec in PCO2 but not usually less than 14 mEq/L
chronic resp alkalosis
146
these provide water and or sodium maintain osmotic gradient between intravascular and extravascular "workhorses"
crystalloids
147
used for intravascular fluid replacement - resucitation, hypotension, septic shock Sodium/ or chloride replacement
Normal saline
148
maintenance fluid
0.5 NS
149
used for replacement of blood loss approximates human plasma used for recsusitaion
Lactated ringers
150
used for free water replacement NOT a resuscitative fluid not a maintenance fluid by itself
dextrose
151
normal anion gap values
3-11 mEq
152
a loss of plasma bicarb is rplaced with CL
non-anion gap acidosis
153
delta gap
differences between patients anion gap and the normal anion gap
154
causes of non anion gap acidosis
``` gastrobicarb loss renal bicarb losses reduced renal H+ excretion - Type I RTA -Type IV RTA -Chronic renal failure Acid and chloride admin ```
155
``` shock drugs/ toxins seizures leukemia hapatic/ renal failure diabetes mellitus malnutrition rhabdomyloysis are all potential cases of ```
lactic acidosis
156
sx of lactic acidosis
``` kussmaul respiratios periph vasodialationcausing tachycardia hyperkalemia lethargy coma N/V bone demineralization ```
157
lactic acidosis acute tx
underlying cause bicarb therapy -use if pH < 7.10-7.15
158
Bicarb dosing eqn - need to know | - use for lactic acidosis
[ 0.5L/Kg (IBW) ] X ( desired HCO3- actual HCO3)
159
Bicarb therapy parameters
- use 12 as desired - give 1/3 or 1/2 the calculated dose - Cardiac arrest : 1mEq/Kg - Supplement K if needed
160
hazrds of bicarb therapy
``` over alkanization -left shift in oxgen-Hb saturation curve hypernatremia/ hyperosmolality CSF acidosis electrolyte shift ```
161
flow of potassium in acid base disorders
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
chronic bicarb therapy for chronics metabolic acidosis
avg dose 1-3 mEq/kg/day
163
how does tromethamine work
combines with H from H2CO3 to form bicarb
164
adverse affects of tromethanmine
hyperkalemia, hypoglycemia, hypocalemia, impaired coagulation
165
three main mechanisma in which a rise of Bicarb would occur
loss of acid from GI tract admin of too much bicarb/ precursor contraction alkalosis -loss of Cl rich and HCO3 poor fluid
166
volume and chloride depletion may contribute to alkalosis due to?
- Dec in arterial blood volume - Dec ability of kidneys to excrete bicarb - w/ volume depletion, capacity of proximal tubule to reabsorb HCO3 increases
167
main cause of metabolic alkalosis is
saline responsive alkalosis
168
with aldosterone INC we see?
Na reabsorption inc H secretion----> HCO3 reabsorption inc K secretion
169
Diuretic therapy's causes of saline responsive alkalosis
- 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
Three main causes of saline responsive alkalosis
Vominting/ NG Diuretics exogenous HCO3 admin/ blood transfusion
171
Why there is a maintenance of an alkaline environment in saline responsive alkalosis
- reduced GFR - enhanced proximal tubular HCO reabsorp - effects of hypokalemia
172
in terms of hypokalemia; when less K, H is scereted while Na is_______
reabsorbed
173
difference between saline responsive and resistant alkalosis
no chloride depletion or an inability to absorb CL in resistant
174
causes of saline resistant alkalosis
INC mineralcorticoid activity hypokalemia renal tubular chloirde wasting
175
INC ammoniagenesis can be causes by a low level of
potassium | due to an INC in H secretion
176
muscle cramps, weakness, dizziness, myocardial supression, mental confusion, CV collapses are symptoms of
saline resistant alkalosis
177
When would you use carbonic annhydrase inhibitors
pts that are fluid restricted or cant have excess sodium
178
carbonic annh inhibitor dosing
250-375 mg once/ twice daily
179
Therapies for persistent metabolic alkalosis
HCl ammonium chloride arginine monohyrdrochloride

Pharm 825 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions