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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:
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myogenic, tubuloglomerulo-feedback, glomerulotubular balance
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does myogenic mech control GFR?
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partly
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how does myogenic work?
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-Smooth muscles in vessels contract changing pressure and resistance.
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-If P inc's arteriole muscle will contract and vessels constrict.
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-Vessel constriction prevents inc's P from causing inc'd blood flow
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equation: P=
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Flow x Vascular resistance
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Which mech regulates GFR against momentary changes in BP?
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Tubuloglomerlu feedback
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what structure carries out tubuloglom feedback
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Juxtaglomerular Aparatus (JGA)
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components of the JGA=
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macula densa, granular cells, extraglomerular mesangial cells, and sympathetic nerves
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where is macula densa located
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btw. the efferent and afferent arteries
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what does macula densa do
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detects even a slight inc in GFR due to increase in flow to distal tubule and increase in NaCl concentration
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what happens when mac densa detect inc in flow rate?
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sends signal to granular cells wich cause afferent arteriole to constrict causing GFR to decrease
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what do extraglomerular mesangial cells do?
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secrete chemical junk and respond to inflammation
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what does the glomerulotubular balance mechanism do?
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keeps amount of filtered solute (NaCl) constant; prevents increase in Na+ loss while GFR is temporariy inc'd (due to inc'd BP)
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how?
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it maintains a constant fraction of the filtrate reabsorbed by the tubule leading to a constant rate of Na+ reabsorption and excretion
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what are cause of acute changes in BP
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posture changes (sitting/laying), or brief exercise
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does kidney have parasympathetic innervation
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no, sympathetic only
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where do sympathetic fibers to the kidneys go?
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to the smooth muscle cells in all arteries and arterioles
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effect on arterioles?
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vasoconstriction
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branches of symp nerve fibers also innervate---
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granular cells
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activation of granular cells leads to what?
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gran cells secrete renin, leading to angio II which is a powerful vaso constrictor
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which two adrenergic receptors are involved in symp nerve stimulation
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alpha 1 and beta 1
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fx and location of alpa 1 receptors:
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located mostly on renal arterioles; : Sympathetic fibers innervating renal arteries release norepinephrine and cause vasoconstriction of the arteries/arterioles via alpha receptors
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what does this do to the renal blood flow (RBF) and GFR?
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decreases both of them
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where are beta 1 receptors located
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in granular cells of JGA
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beta 1 receptor fx:
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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.
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what is end result of norep release
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increase in Na+ reaborption to keep fluid volume up
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4 functions of Sympathetic NS activity in kids:
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1. regulate blood flow to kids
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2. regulate GFR
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3. regulate renin secretion
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4. regulate salt/H2O reabsorption
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does plamsa NLy get filtered into tubular fluid?
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on each pass through the glomeruli, some of the plasma gets filtered into the tubular fluid
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tubular cells active secretory/transport mechanism of tubular cells does what to drugs/toxins
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"sucks" them out of the peritubular capillaries & interstitium and secrete them into the tubular fluid (early urine)
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why are many toxins not readily filtered into the tubular fluid by the glomeruli
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b/c they bind to albumin
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what do lungs do in acid-base disturbances
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they increase or decrease ventilation (i.e blowing off or retaining CO2
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what do the kids do in acid base disturbances
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adjust the secretion and reabsorption of H+ and HCO3-ions
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How much is biologically available to get the job done
The fraction of drug absorbed into the systemic cirulation after extravascular administration |
bioavailability
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drug molecules must be released from the dosage form
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dissolution
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go across biologic membranes to reach systemic circulation
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absorbtion
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extravascular
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anything thats not IV
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IV has what bioavailability
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F=1 or 100% because it goes straight into the circulation
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1st Past Effect
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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 |
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IV drug filtered
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IV drugs still get to the liver because they will eventually in the hepatocytes
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Serum half life
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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 |
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Steady state
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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
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How many half lives does it take to reach steady state
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It takes 5 half lives to reach steady state
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