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311 Cards in this Set

  • Front
  • Back
ac
before meals
ad
right ear
as
left ear
am
before noon, morning
Amp
ampule
aq
water
ATC
around the clock
au
each ear
bid
twice a day
bm
bowel movement
BSA
body surface area
c
with
caps
capsules
cc
cubic centimeter
= milliliter
Dil
dilute
DC, disc
an order to stop medication
DW
distilled water
D5W
dextrose 5% in water
g, gm, Gm
gram
gr
grain
gtt
drop
h or hr.
hour
ha or h/a
headache
hs or HS
at bedtime
ID
intradermal
IM
intramuscular
Inj
injection
IV
intravenous
IVP
intravenous push
Liq
solution
mcg or ug
microgram
MEq
milliequivalent
mg
milligram
mg/kg
milligram per kilogram of body weight
mg/m2
mg of drug per sq. meter of body surface
ml or mL
milliliter
NPO
nothing by mouth
NS or NSS
normal saline or normal saline solution
N&V
nausea and vomiting
od
right eye
os
left eye
ou
each eye
pc
after meals
pm
afternoon/evening
po
by mouth
prn
as necessary
Q or q
each, every
Qd, qd
every day
Qh, or qh
every hour
qid
four times a day
qs
as much as sufficient
rect or R
use rectally
repet
let it be repeted
s
without
Sig
you write
sl
sublingual
ss
one half
state
immediately
subc or subq or sc or sq
subcutaneously
supp
suppository
susp
suspension
Syr
syrup
tab
tablet
Tbsp
tablespoon
tid
three times a week
tiw
three times a week
tsp
teaspoon
U or u
unit
ud
as directed
ut dict
as directed
L
fifty
C
one hundred
D
five hundred
M
one thousand
Solution
20 drops per mL
-clear and doesnt need to be shaken
Suspension
12-15 drops per mL
-needs to be shaken to be mixed
Pharmacology
broad description of a drug or medication; includes mechanism of action, pharmacokinetic/dynamic parameters, drug interactions, adverse effects, toxic effects
Pharmacotherapeutics
pharmacology + disease state + patient; takes into consideration the pharmacology of a medication and broadens the concept by looking at how to use the medication in patients with various disease states
Polypharmacy
basically, too many medications are taken by a patient; very common in the elderly; very common in patients seeing multiple practitioners
Pharmacokinetics
what the body does to the drug; absorption, distribution, metabolism, elimination
Pharmacogenetics
considers genetic factors (in patients) that may have an effect on a drug’s responsiveness
Receptor
specific target where a medication will “do its job” or exert its effect; receptors may be a membrane protein, an enzyme, or a nucleic acid; the “lock and key hypothesis”—the drug and receptor must be structurally complementary to recognize each other and exert an effect
Agonists
meds that bind to a receptor and activate it
Antagonists
meds that bind to a receptor, but that do not have the exact structural features needed to activate it
Beneficial or Therapeutics Effects
what the drug is supposed to do via its mechanism of action (MOA); what is the drug’s job?
Toxic Effects vs. Side effects
what the drug is supposed to do via its mechanism of action (MOA); what is the drug’s job?
Chemical Name
the name given to the chemical compound
-often long and burdensome and hard to recognize or pronounce
Generic name
Internationally recognized name
-only one generic name for every drug or medication; nonproprietary
Brand Name
Patented property name from the pharmaceutical company that discovered or made the medication; drugs/medications may have more than one brand/proprietary name
Factors to Consider in Choosing Drug Therapy
1.Accurate Diagnosis
2. Pathophysiology of the disease
3.Patient Care Setting (Hospital vs. Ambulatory care)
4.Non-Pharmacologic Therapy
5.Pharmacologic Therapy
6. Predictable adverse drug reactions or side effects
7. Hypersensitivity reactions
8. Cost
Patient Specific Factors that Influence Pharmacotherapy decisions
•Age
•Weight
•Gender
•Race
•Genetics
•Drug allergies or adverse drug reactions
•Medical history (Renal/Hepatic function)
•Health status
•Pregnancy or lactation
•Education
•Psychological variables
•Social/Economic factors
•Effectiveness of Past Therapy
Therapeutic Goals or Outcomes
1.Cure: infection

2.Control or relieve symptoms: Asthma, Diabetes

3.Prevent acute complications: HTN (stroke), DM (hyper/hypoglycemia)

4.Prevent long term morbidity & mortality: HTN (CHF), DM (neuropathy, dialysis)

5.Avoid adverse drug reactions or drug interactions - chronic medical conditions

6.Improve compliance/adherence: chronic medication (HTN - diuretics)

7.Improve quality of life: HIV, CHF, palliative treatment

8.Decrease health care costs
Why do steroids get tapered?
because exogenous steroids compete with endogenous steroids and may throw off balance
If the refil spot is left blank on a perscription...
there are no refils
Non-controlled substance refills
Anything without addiction potention
12 months
Non-controlled substance
Anything without addiction potention
Controlled Substance
Anything with addiction potential
C1
High abuse potential & no accepted medical use in the US

ex. Opiates, opium derivatives (heroin, dihydromorphine)
Hallucinogens (LSD, marijuana)
C2
High abuse potential, but do have a currently accepted medical use in treatment in the US and with severe dependence liability

ex: Opiates & opium derivatives (morphine, codeine, methadone, oxycodone (Oxycontin, Percocet) Demerol)
CNS stimulants (Dexedrine, Ritalin
C3
Less abuse potential than schedule II drugs and moderate dependence liability

ex: Narcotic/non-narcotic combinations (Tylenol No. 3, Vicodin)
Nonbarbiturate sedatives
prnp
as needed for pain
C4
Less abuse potential than schedule III drugs and limited dependence liability

ex: Long-acting barbiturates (phenobarbital)
sleep aids (Ambien®, Sonata®, Lunesta®)
Anti-anxiety agents (benzodiazepines)
C5
Limited abuse potential. Drugs that have the lowest potential for abuse

ex: Small amounts codeine (Robitussin AC)
Some may be sold OTC, depending on state law
CIII-V Refils
6 months
can be phoned or faxed in
CII Refils
No refils
cannot be phoned or faxed except in emergency
Must have hard copy
CII Narcotics Perscriptions
Will only go through a 30 day supply on insurance
1 ounce
30 gm
1/2 ounce
15 gm
2 ounces
60 gm
1 kg
2.2 lbs
1 pint
473 ml
1 fluid ounce
30 ml
1 tablespoon
15 mL
1 teaspoon
5 mL
1/2 teaspoon
2.5 mL
2 tablespoonfulls
1 fluid ounce or 30 mL
Pregnancy Categories
is a drug safe for pregnant women??

THESE DO NOT REFER TO BREAST FEEDING!
Pregnancy Category A
Adequate studies in pregnant women have not demonstrated a risk to the fetus in the first trimester of pregnancy and there is no evidence of risk in later trimesters.

ex: Nystatin
Pregnancy Category B
Animal studies have not demonstrated a risk to the fetus but there are no adequate studies in pregnant women or Animal studies have shown an adverse effect, but adequate studies in pregnant women have not demonstrated a risk to the fetus during the first trimester of pregnancy and there is no evidence of risk in later trimesters.

ex: Penicillins, cephalosporins, diphenhydramine, chlorpheniramine
Pregnancy Category C
Animal studies have shown an adverse effect on the fetus but there are no adequate studies in humans; the benefits from use of the drug in pregnant women may be acceptable despite its potential risks… or … There are no animal reproduction studies and no adequate studies in humans.

ex: Calcium channel blockers
Do pregnancy categories pertain to breastfeeding?
NO!
Which pregnancy category is used most often?
C
Pregnancy Category D
There is evidence of human fetal risk, but the potential benefits from the use of the drug in pregnant women may be acceptable despite its potential risks.

ex: Asprin, ACE inhibitors, benzodiazepines, chemotherapeutic agents
Pregnancy Category X
Studies in animals or human demonstrate fetal abnormalities or adverse reaction reports indicate evidence of fetal risk. The risk of use in a pregnant women clearly outweighs any possible benefit.

ex: Oral contraceptives, Cytotec, Comadin, Accutane
Phases of Drug Development
•Preclinical Testing
•Clinical Testing
•NDA Review
•Postmarketing Surveillance
Early research and Pre-Clinical Testing
•studies in vitro
•laboratory and animal testing
•assess safety and biologic activity
•determine ED50 and LD50
•1 - 5 years
•average is 2.6 years
•success rate: 5000 compounds evaluated
•Once completed, INDA is drafted and submitted to the FDA for review and approval prior to human experimentation
ED 50
effective dose in 50% of subjects
LD 50
Lethal dose in 50% of subjects
Phase I- Clinical Testing
•test a new drug or treatment
•20 - 80 healthy volunteers (usually healthy young males)
•determine safety and dosage
•determine mechanism of action in humans
•evaluate pharmacokinetic profile of the drug
•not powered to detect most adverse effects
•takes approximately 1.5 years
•success rate: 5 compounds enter clinical trials
Phase I- Clinical Testing
starting to test on a very small group of humans
Phase II – Clinical Testing
•study drug or treatment in patients with disease or condition
•100 - 300 selected patients
•evaluate effectiveness and look for short-term side effects
•performed by clinical pharmacologists and investigators
•takes approximately 2 years
Phase II – Clinical Testing
Small number of people with the condition
Starting to look at effectiveness
Phase III – Clinical Testing
•study drug or treatment is given to large groups of people
•1000 - 3000 volunteer patients
•confirm effectiveness, monitor adverse reactions, from long term use
•powered to detect differences in efficacy
•Approximately 1/3 of investigational new drugs make it to this stage
•takes approximately 3.5 years
•once Phase III is complete, NDA is submitted to the FDA
Phase III – Clinical Testing
Study drug given to large groups of people

takes about 3.5 years to get here
Phase IV Post-Marketing Surveillance
•verify the effectiveness of the drug/treatment after marketing
•Focus on special populations that may not have been included in clinical trials
•monitor for adverse reactions, patterns of drug utilization, additional indications
•identify rare but serious adverse effects
Phase IV Post-Marketing Surveillance
After the drug goes on the market. Really examines the long term effectiveness
Fast-Tracked Drugs
Drugs that meet unmet medical needs

ex: HIV drugs, chemotherapy agents
How long does it take from discovery of a drug to patent expiration?
around 17 years
what are the 4 main functions of the kidney/nephron?
1. reabsorb filtered nutrients 2. tubular secretion 3. eliminate/conserve H20 4. adjust plasma pH
Where does reabsorption take place?
proximal tubule
What are things that get reabsorbed?
Vitamins, glucose, minerals, amino acids
Where does secretion take place
in the renal tubular cells
what gets secreted
drugs/toxins
How does secretion take place?
via secretory/transport mechanisms in the tubular cells
how do the mechanisms work
tubular cells grab the substance from the peritubular capillaries and actively secrete them into the tubular fluid
Do drugs get filtered into the urine on their own
no- usually bind to plasma proteins like albumin
How is urine osmolality adjusted?
by eliminating or conserving H20
When the body is H20 deprived, what happens to osmolality?
increases: very concentrated urine (1200 milliosmoles/liter)
When there's too much water what happens?
decreases osmolality: urine contains more water
How is plasma pH adjusted?
by secreting H+ ions and making and conserving
bicarbonate ions
What's the normal [H+] in the plasma?
10-7.4
whats the NL [Na+] in plasma?
0.14
What causes many problems with the acid/base balance?
sulfuric acid breakdown
When problems arise, what do the kidneys do?
adjust the H+/HCO3- ions
When problems arise, what do the lungs do?
adjust by ventilating more or less
What hormone does the kidney secrete and what does it do?
erythropoetin; RBC production
What is another hormone the kidney produces?
renin
What does renin do?
renin stimulates production of Angio II which is a powerful vasoconstrictor. Angio II stims the adrenal cortex to produce aldosterone
What does aldosterone do?
inc's Na+ reabsorption in renal tubules and increases K and H+ secretion into tubular fluid.
What does the kidney have to do with Vitamin D?
it converts 25-OH Vitamin D to 1.25 (OH)2 Vitamin D (the active form)
What is the significance of this conversion?
1. increases Ca2+ absorption in the gut 2. assimilates dietary stuff into blood
What effect does parathyroid hormone have on the kidney?
causes increased Ca2+ reabsorption from tubular fluid; causes osteoclastic activity
When is it secreted?
decreased Ca2+ in plasma
What secretes ADH (vasopressin)?
posterior pituitary
What affect does ADH have on kidneys
when osmolality is too high (you get dehydrated) it causes kidney to increase H2O reabsorption in collecting ducts
What is the proportion of plasma to cells in blood flowing into the kidney?
55% plasma, 45% cells
trace the bloodflow thru the kidneys
afferent artery -> glomerular capillaries -> efferent artery -> peritubular capillaries
What is the structure of glomerular capillaries?
single fenestrated layer of endothelial cells on top of a basement membrane and foot processes of visceral podocytes
What features easily allow movement in and out
single layered and fenestrations
contractile, phagocytic cells that respond to complement cascade by secreting chemical junk; also secrete a matrix
mesangial cells
describe glomerular filtration barrier
triple layer of glomerulus with a negative charge
significance of neg charge?
keeps neg charged particles out of urine like albumin
definition of GFR
the amount of plasma filtered out of the capillaries into bowman's space
quantify the rate at which plasma is filtered
amt excreted = amt. filtered + amt. secreted - amt. reabsorbed
What was the basis for the inulin experiment?
inulin is neither secreted nor reabsorbed and is freely filtered; therefore the amt filtered = the amt excreted
What was the avg GFR determined to be?
125 mL of plasma/minute
does all plasma go thru glomeruli?
no
What is the ERPF?
effective renal plasma flow= the total amount of plasma going to the kidneys and thru the glomeruli
difference btw EFRP and GFR
GFR is only a fraction of total plasma flow, it represents only one glomerulus; ERPF represents the collective glomeruli
What substance was used to determine ERPF?
para-aminohippuric acid (PAH)
What was ERPF determined to be?
585 mL/min
How much of this goes out the efferent arteriole (not being filtered)?
585 - 125 = 460 mL/min
%age of renal blood flow that goes to glomeruli?
90%
what is the total renal plasma flow-TRPF (amt delivered to whole kidney)?
585/0.9 = 650 mL/min
What is hematocrit (hct)
the fraction of blood composed of RBCs, usually 45%
approx amt of RBF total
1200 mL/min
what %age of total blood volume is filtered each time around
20%
What is the macula densa?
the part of the tubule that passes thru the branches of the afferent/efferent arterioles
What detects a BP decrease
nearby granular cells with stretch receptors in teh afferent arteriole
renal flow thru kidneys
thru afferent arteriole which branches into glomerular capillaries. from the glom caps, blood exits thru efferent arterioles which branch into peritubular caps. also, glom caps release fluid called the glomerular filtrate with enters the bowmans capsule. then goes to PCT, the descending loop, the loop of Henle, the DCT, and then to the collecting duct.
where is H2O reabsorbed
interstitial tubule
how?
passively, thru osmosis: the counter current multiplier of henle's loop creates 1200 Osm fluid. NaCl circulates btw tubular fluid and interstitium
action of Na+ and Cl- in ascending limb
Cl- is pumped out and Na+ is pumped in
What part of the nephron does ADH act on
the collecting duct
What does it do to the duct?
causes holes to be inserted to increase H2O reabsorption
how fast your kidney secretes a substance/drug is called
clearance
what organs are involved in clearance
kidneys and liver
why is it called virtual clearance
b/c it doesn't measure how much substance is actually in the urine but rather how many individual mL of blood are cleared of the solute they're carrying.
clearance equation
Cx = (Ux x V)/P
clearance
the volume of plasma cleared of X
why is creatinine used
b/c its not reabsorbed and it's freely excreted
where is creatinine normally found
striated skeletal muscles
easiest to measure: plasma creatine or urine creatinine
plasma
high conc of Cre plasma =
poor renal function
low conc of Cre plasma =
person is sick
does creatinine clearance measure GFR exactly
no- overestimates GFR slightly b/c it's slightly secreted
why is that important
b/c it can miss early renal failure
GFR decreases in a vast amount of this
ARF
What does decreased GFR do physiologically
dec.'d urine production (anuria or oliguria), creatinine clearance, and urea clearance
dec'd creatinine clearance =
inc'd plasma creatinine
dec'd urea clearance =
inc'd BUN
azotemia
inc'd plasma cre and inc'd BUN =
azotemia is indicitave of ---
ARF
NL urine output =
750-2000 mL/day
oliguria =
= <500 mL/day
anuria =
= <100 mL/day
polyuria =
= >2500 mL/day
What is the most important determinant of body fluid volume
sodium
how measured?
Fraction Excretion of Na+
Fractional Excretion of Na+ tells what
quantifies the percentage of filtered sodium that is actually excreted in the urine.
FE Na+ =
= (UNa x PCre)/(PNa x UCre) x 100
FE Na+ when excess Na+ intake =
up to 5%
FE Na+ when too little Na+ intake =
low as 0.1%
sodium in the body fluid volume is a collective measure of...
Na+ in extracellular space, including the plasma
if little Na+ intake, filterted Na+ is ....
conserved (reabsorbed).
if too much Na+ intake....
it's excreted
Inc'd FE Na+ is usually a good indicator of ....
the presence of a physiologic stimulus for the retention of sodium by the kidneys
what are some physiolgical stimuli for Na+ retention?
dehydration, x-treme blood loss, heart failure
circulating fluid volume measures what?
blood perfusion
poor perfusion (an inc'd FEna) leads to
dec'd GFR, dec'd urine output and azotemia (in'd BUN and Cre plasma)
pre-renal failure or pre-renal azotemia
the kidneys are not getting enough blood flow to do their job of filtering the plasma
are the kidneys ill in pre-renal azotemia?
no- the kidneys themselves are still OK, but the stuff being delivered to the kidneys, the circulation, is inadequate.
what do kids do if they detect pre-renal azotemia?
start conserving sodium in order to pump up the circulating fluid volume, so FE Na goes down
FE Na in pre-renal azotemia =
< 1%
Intrinsic Renal Failure (Structural renal failure)
kidneys themselves are sick, but blood flow is adequate
post-renal failure (obstructive renal failure)
both the kidneys themselves and the circulation to them are both OK, but there is an obstruction to urine output
FE Na in renal azotemia
> 1%
if renal azotemia is intrinsic what happens to UNa and Uosm?
Una in's and Uosm dec's
What is ARF?
abrupt decline in renal fx: dec’d GFR and therefore dec’d excretion of nitrogenous waste, dec’d urine output
are most forms of ARF reversible
yes
What is uremia?
azotemia w/ Sx
what are the sx of uremia? 11
-N/V and anorexia
-pruritis
-yellow pigmentation
-weakness
-myalgia/twitching
-peripheral neuropathies (stocking, feet, and glove sensation loss; and loss of proprioception)
-dysrhythmias
-pericarditis
-anemia
-anion gap acidosis
-lethargy, confusion, seizures, coma
What causes pre-renal ARF
hypotension or edematous states
what would cause hypotension
sepsis, volume depletion (blood loss, dehydration, hemorrhaging, untreated burns, diarrhea)
what causes edematous states?
CHF (loss of fluid volume into tissue), cirrhosis of the liver (hydrostatic pressure builds up, fluid leaves filling abdom cavity), nephrotic syndrome (xs protein in urine c/b leaky glomeruli; water leaves too and changes osmotic pressure)
What is affected in intrinsic renal failure
renal parenchyma
The types of intrinsic:
acute tubular necrosis, glomerulonephritis, interstitial nephritis, Infectious interstitial nephritis , and vasculitis (SLE)
causes of acute tubular necrosis
ischemia to kidney parenchyma, or nephrotoxic drugs
what are nephrotoxic drugs?
aminoglycosides (streptomycin and gentamicin) or radiocontrast drugs (no CT Scans!)
What is the major Sx of glomerulonephritis?
proteinuria
most common cause of post-renal failure:
uric acid stones
what causes uric acid stones?
hyperuricemia (i.e. from chemo)
other causes of post-renal failure:
nephrolithiasis or urolithiasis, tumors, BPH
The 3 mechanisms kids use to regulate blood flow:
myogenic, tubuloglomerulo-feedback, glomerulotubular balance
does myogenic mech control GFR?
partly
how does myogenic work?
-Smooth muscles in vessels contract changing pressure and resistance.
-If P inc's arteriole muscle will contract and vessels constrict.
-Vessel constriction prevents inc's P from causing inc'd blood flow
equation: P=
Flow x Vascular resistance
Which mech regulates GFR against momentary changes in BP?
Tubuloglomerlu feedback
what structure carries out tubuloglom feedback
Juxtaglomerular Aparatus (JGA)
components of the JGA=
macula densa, granular cells, extraglomerular mesangial cells, and sympathetic nerves
where is macula densa located
btw. the efferent and afferent arteries
what does macula densa do
detects even a slight inc in GFR due to increase in flow to distal tubule and increase in NaCl concentration
what happens when mac densa detect inc in flow rate?
sends signal to granular cells wich cause afferent arteriole to constrict causing GFR to decrease
what do extraglomerular mesangial cells do?
secrete chemical junk and respond to inflammation
what does the glomerulotubular balance mechanism do?
keeps amount of filtered solute (NaCl) constant; prevents increase in Na+ loss while GFR is temporariy inc'd (due to inc'd BP)
how?
it maintains a constant fraction of the filtrate reabsorbed by the tubule leading to a constant rate of Na+ reabsorption and excretion
what are cause of acute changes in BP
posture changes (sitting/laying), or brief exercise
does kidney have parasympathetic innervation
no, sympathetic only
where do sympathetic fibers to the kidneys go?
to the smooth muscle cells in all arteries and arterioles
effect on arterioles?
vasoconstriction
branches of symp nerve fibers also innervate---
granular cells
activation of granular cells leads to what?
gran cells secrete renin, leading to angio II which is a powerful vaso constrictor
which two adrenergic receptors are involved in symp nerve stimulation
alpha 1 and beta 1
fx and location of alpa 1 receptors:
located mostly on renal arterioles; : Sympathetic fibers innervating renal arteries release norepinephrine and cause vasoconstriction of the arteries/arterioles via alpha receptors
what does this do to the renal blood flow (RBF) and GFR?
decreases both of them
where are beta 1 receptors located
in granular cells of JGA
beta 1 receptor fx:
norepinephrine is relased from symp nerve branches and binds to beta-1 receptors. The agonism of the B-1 receptor causes renin release from the granular cells.
what is end result of norep release
increase in Na+ reaborption to keep fluid volume up
4 functions of Sympathetic NS activity in kids:
1. regulate blood flow to kids
2. regulate GFR
3. regulate renin secretion
4. regulate salt/H2O reabsorption
does plamsa NLy get filtered into tubular fluid?
on each pass through the glomeruli, some of the plasma gets filtered into the tubular fluid
tubular cells active secretory/transport mechanism of tubular cells does what to drugs/toxins
"sucks" them out of the peritubular capillaries & interstitium and secrete them into the tubular fluid (early urine)
why are many toxins not readily filtered into the tubular fluid by the glomeruli
b/c they bind to albumin
what do lungs do in acid-base disturbances
they increase or decrease ventilation (i.e blowing off or retaining CO2
what do the kids do in acid base disturbances
adjust the secretion and reabsorption of H+ and HCO3-ions
How much is biologically available to get the job done

The fraction of drug absorbed into the systemic cirulation after extravascular administration
bioavailability
drug molecules must be released from the dosage form
dissolution
go across biologic membranes to reach systemic circulation
absorbtion
extravascular
anything thats not IV
IV has what bioavailability
F=1 or 100% because it goes straight into the circulation
1st Past Effect
By mouth--> gut --> to liver via portal circulation

only one that avoids the 1st pass effect is IV meds

liver is a sponge for toxins pulls out medications
IV drug filtered
IV drugs still get to the liver because they will eventually in the hepatocytes
Serum half life
the time is takes for the serum concentration of the drug to increase or decrease by one half

determines how long between taking the medication
Steady state
point where the amount of drug going into the body is the same as the amt being eliminated in the body in one half life
How many half lives does it take to reach steady state
It takes 5 half lives to reach steady state