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Pharmacology Exam 1

Terms in this set (97)

Electrolytes
Potassium (K+): 3.5 - 5.0 mEq/L

Calcium (Ca2+): 8.5 - 10.5 mEq/L

Phosphate (PO4): 3 - 4.5 mg/dL

Magnesium (Mg): 1.4 - 2.1 mEq/L

Sodium (Na+): 135 - 145 mEq/L

Chloride (Cl-): 96 - 109 mEq/L

BUN: 8-20 mg/dL
Creatinine:0.6-1.2 mg/dL
Urine
1. pH: 4.5-8

2. Creatinine clearance: 105-110 mL/min, 11.73 m
Normal Serum osmolarity
280-294 mOsm/kg
ABGs
PH: 7.35-7.45

PCo2: 35-45 mmHg

Po2: 80-100 mmHg

HCO3: 22-26 mEq/L

O2 Sat: 95-100%
what is meant when it is stated that a drug is described as easy to administer
Ease of administration refers to simplicity; the route of administration should be convenient, and the number of doses per day should be low.


This can enhance patient adherence and can decrease risk.
Desired Outcomes of Med Admin Include:
Effectiveness - MOST IMPORTANT PROPERTY A DRUG CAN HAVE. If the drug isn't effective, there is no justification for giving it

Safety: a safe drug is one that can't produce harmful effects, even if administered in very high doses for a very long time (in an ideal drug world)

Selectivity: a drug that elicits only the response for which it is administered

Reversible Action: want drugs to subside within an appropriate amount of time (also safer)

Predictability: knowing how a given pt will respond

Freedom from Drug Interactions: when a patient is taking 2 or more drugs (few medications are devoid of significant interactions)

Low Cost: easy to afford, expense becomes a key factor when a med must be taken chronically

Chemical Stability: wouldn't lose efficacy from chemical instability in storage or preparation for infusion or mixing into a solution

Possession of a Simple Generic Name: makes it easier to remember and pronounce
generic name
name given by U.S. Adopted Name Council and the last syllable represents its pharmaceutical class (also called nonproprietary name)
Ex. acetaminophen
**Patient should be given the GENERIC name**
brand name
name given by a marketing company, drugs can have many different brand names
ex. Advil vs ibuprofen (also called proprietary/ trade name)
Each brand name can have different active ingredients based on if it is a cream, oral med, spray
Once brand name patent has expired, other companies can market it as generic
brand vs generic name
Brand names and generic names have the same concentration of drug, but inactive ingredients could be different!

All products have to have the same dose of the drug but generic formulations may have different rates or extents of absorption
In few cases generic brands have caused increased absorption that led to toxicity
Metabolism
the chemical alteration of drug structure (aka biotransformation)

*Most often takes place within cells in the LIVER*

Some via the kidneys
Even fewer via the GI tract or skin

Liver metabolism performed by the hepatic microsomal enzyme system (P450 system)

P450 is a system made up of 12 dif. Enzyme families


**ONLY 3 P450 enzyme families metabolize drugs, CYP1, CYP2, CYP3.*

The other 9 metabolize endogenous compounds (steroids, fatty acids)
Metabolism by route:
1. IV: typically a lower dosage sufficient to produce desired effects
** IV drugs administered in the peripheral vein travel much of the body prior to being metabolized in the liver
A drug with a high first-pass effect: most of the drug made into an inactive metabolite by the liver, therefore the route needs to be IV

2. Oral meds
ORAL MEDS
travel from INTESTINE→ LIVER

Meds taken by mouth need to be metabolized through a longer process than IV, typically slower onset

Higher drug dosage typically needed than IV
Excretion:
The MOST IMPORTANT consequence of drug metabolism is promotion of renal drug excretion.

the removal of drugs from the body.

MOST IMPORTANT ORGAN for drug excretion is the KIDNEY

Kidneys are unable to excrete drugs that are highly lipid soluble.

Route: can exit the body via urine, bile, sweat, saliva, breast milk, and expired air.

by converting lipid-soluble drugs into more hydrophilic (water-soluble) forms, metabolic conversion can accelerate renal excretion of many agents.
first pass effect
The initial metabolism in the liver of a drug absorbed from the gastrointestinal tract before the drug reaches systemic circulation through the bloodstream.

inactivation of oral drugs
Drug Inactivation
Drug metabolism can convert pharmacologically active compounds to inactive forms.
Increased
Therapeutic Action
Metabolism can increase the effectiveness of some drugs
Activation of Prodrugs
A prodrug is a compound that is pharmacologically inactive as administered and then undergoes conversion to its active form via metabolism.
Increased or Decreased Toxicity
By converting drugs into inactive forms, metabolism can decrease toxicity.

**Conversely, metabolism can increase the potential for harm by converting relatively safe compounds into forms that are toxic.
Enterohepatic Recirculation:
A repeating cycle- drug is being filtered through the liver multiple times
LIVER ---via bile/bile duct----> DUODENUM to be reabsorbed ---- via hepatic portal vein----> LIVER ---> repeat!
Only happens for drugs that have undergone glucuronidation
why some patients are at a greater risk for an adverse drug reaction than other patients
- adverse drug reaction
- gender
- race
- diet
- genetic anomalies(idiosyncratic effects)
- body and weight composition
- body surface area
- Age
- severity of illness, presence of comorbidities, treatment with multiple drugs
- increased risk of drug-drug interactions
- pathological considerations
nursing process
ADPIE
Assessment
Diagnosis
Planning
Implementation
Evaluation
Assessment
Methods of data collection include interviewing the pt and family, observing the pt, performing physical examination, lab tests, pts medical and drug history.
Collection of baseline data to evaluate therapeutic effects
Collection of baseline data to evaluate adverse effects
Identification of high-risk patients
Patient's capacity for self-care
Diagnosis
Judge the appropriateness of the prescribed regimen

Identify potential health problems that the drug might cause

Determine the pts capacity for self-care
planning
Defining goals - formulate an achievable goal
Setting Priorities - requires knowledge of drugs and patients. High priority is given to life
threatening conditions
interventions
Implementation
4 Major Components:
Drug administration
Patient education
Interventions to promote therapeutic effects (ex: yoga, nutrition)
Interventions to minimize adverse effects (ex: taking drugs with food to minimize GI upset)
Evaluation
Therapeutic responses - evaluated by comparing pts current status with baseline data. Must know the reason the drug was given, criteria to evaluate, expected time course.

Adverse drug reactions and interactions - must know which adverse effects are likely to occur, how the manifest, and probable time course.
Adherence to the prescribed regimen - measurement of plasma drug levels, interviewing
the pt, and counting pills. Determines pts understanding about when to take meds, what dose, and technique of administration.
Satisfaction with treatment - dissatisfaction includes unacceptable side effects,
inconvenient dosing schedule, difficulty of administration, and high cost.
drugs binding to receptors, what happens in this process
Drug + Receptor ← → Drug-Receptor complex → Result; the first part of the equation is reversible
When a drug binds to a receptor it either increases or decreases the activity of the receptor
Receptors are:
"all functional macromolecules" in a cell to which a drug (a chemical) binds to produce its effects
normal points of physiologic process
Four types of receptors:
Cell membrane embedded enzymes: an agonist drug binds endogenously to the cell receptor that activates the enzyme on the inside catalytic site. Ex. Insulin

Ligand-gated ion channel: agonist drug binds to the channel on the cell which opens and allows an influx or outflux of ions. This is determined by the concentration gradient. Ex. Neurotransmitters like GABA

G protein - coupled receptors: drugs bind a receptor that activates a G protein that activates the effector. EXAMPLE:
Histamin


Transcription factors: Ligands must pass cell membrane to get inside the cell, attaches to DNA to regulate protein synthesis.
what occurs at the receptor site of the cell after continual exposure to the drug which may make the patient immune to the effects of the drug.
In response to continuous activation or continuous inhibition, the number of receptors on the cell surface can change, as can their sensitivity to agonist molecules.
When the receptors of a cell are continually exposed to an agonist, the cell usually becomes less responsive.
When this occurs, the cell is said to be desensitized or refractory, or to have undergone down-regulation.
Mechanism is destruction of receptors by the cell and modification of receptors such that they respond less fully.

Continuous exposure to antagonists has the opposite effect causing the cell to become hypersensitive or super sensitive. Mechanism is synthesis of more receptors.
atrophy
Decrease in cellular size
Occurs in a number of organ's cells, the entire organ shrinks or becomes atrophic
See most in sketetal muscles, heart, secondary sex organs and the brain

Can be physiologic or pathologic either way same end result
Physiologic occurs with early development

Pathologic occurs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal and nervous system simulation

Atrophy in muscle cells contains less endoplasmic reticulum, and fewer mitochondria and myofilaments (part of the muscle fiber that controls contraction) than found in normal cell
adaptation
Cells adapt to their environment to escape and protect themselves from injury.

An adapted cell is neither normal nor injured - it's a condition somewhere in-between
They are reversible also have limits and additional stress can lead to injury

They can be common and central part of many disease states

In the early stages of successful adaptive response, cells may have enhanced function making it harder to distinguish a pathologic response from an extreme adaptation to an excessive functional demand
calcification
Minerals are deposited and then crystallize
Minerals bind tightly to collagen fibers, producing tensile and compressional strength in bone and allowing it to withstand pressure and weight bearing
Sites of cellular death can cause accumulations of calcium resulting in pathologic calcification
apoptosis
Type 2 cell death apoptosis from the Greek means "dropping off"

This is normal cell death or programmed cell death
Our cells only live for so long

Things that can trigger the programmed death are hormonal cues, antigen stimulation, viral infection

With programmed death there is no cell swelling or inflammation

WBCs (white blood cells) move into the area and remove dead and worn out cells

Depends on a tightly regulated cellular program for its initiation and execution
This death program involves enzymes that divide other proteins—proteases, which are activated by proteolytic activity in response to signals that induce apoptosis
These proteases are called caspases
The activated suicide caspases cleave and, thereby, activate other members of the family, resulting in an amplifying "suicide" cascade
The activated caspases then cleave other key proteins in the cell, killing the cell quickly and neatly
The two different pathways that converge on caspase activation are called the mitochondrial (intrinsic) pathway and the death receptor (extrinsic) pathway

Cells that die by apoptosis release chemical factors that recruit phagocytes that quickly engulf the remains of the dead cell, thus reducing chances of inflammation
necrosis vacuoles
Type 1 cell death, necrosis, develops due to cell injury
This injury can be due to infection or hypoxia, loss of membrane integrity

That cell will swell, Na (sodium) rushes into the cell and fills with water and ruptures

This sets up an inflammatory response
With necrosis, cell death is not tidy because cells that die as a result of acute injury swell, burst, and spill their contents all over their neighbors, causing a likely damaging inflammatory response

Sites of necrotic cellular death can cause accumulations of calcium resulting in pathologic calcification. Whenever this happens, an accumulation of calcium, it means the area is hardened
four major forms of necrosis
coagulative, liquefactive, caseous, and fatty
Coagulative necrosis
result of protein denaturation, which causes the protein albumin to change from a gelatinous, transparent state to a firm, opaque state (think of an egg-white coagulating in a hot pan)
occurs primarily in the kidneys, heart, and adrenal glands
commonly results from hypoxia caused by severe ischemia or chemical injury
Site of transformation from gelatinous to a firm, opaque state is called an INFARCT (ex. Myocardial infarction)
Liquefactive necrosis
cells are digested by hydrolytic enzymes in cellular lysosomes
brain tissue is readily affected by liquefactive necrosis because
brain cells are rich in digestive hydrolytic enzymes and lipids and the brain contains little connective tissue

commonly results from ischemic injury to neurons and glial cells in the brain

can be caused by bacterial infection, especially Staphylococci, Streptococci, and Escherichia coli.

dead cells are digested, so the tissue becomes soft, liquefies, and segregates from healthy tissue, forming cysts.
Caseous necrosis
a combination of coagulative and liquefactive necrosis
commonly tuberculous pulmonary infection, especially by Mycobacterium tuberculosis
Fatty necrosis
cellular breakdown of adipose cells by lipases

commonly in the breast, pancreas, and other abdominal structures

lipases break down triglycerides, releasing free fatty acids that then combine with extracellular electrolytes (Ca, Mg, Na ions), creating soaps (saponification)

the necrotic tissue appears opaque and chalk white
hypoxic injury
lack of oxygen
can be reversible if oxygen returns in time
can cause cellular necrosis

most commonly an ischemia (stroke, MI), but can be caused by free radicals, poisons: carbon monoxide, cyanide, lead, alcohol, mercury
Also in: drowning, strangulation, suffocation
anaplasia
loss of mature or specialized features of a cell or tissue
as in malignant tumors, a reversal in differentiation, loss of structure and functional differentiation of normal cells,


more advanced stage than dysplasia, not reversible, characteristic of cancerous tumors
hyperplasia
a normal increase in the number of cells
from an increased cell rate division, can be in response to a severe injury that caused cell death - not pathological
metaplasia
reversible, replacement of one cell type with another


seen in reprogramming from stem cells, sometimes replaced with less mature cells, change in cell type
Dysplasia
pathological hyperplasia (not a true adaptive process)


deranged cell growth, changes in size, shape organization, seen in cervix, respiratory tract, neoplastic (abnormal) growth that may progress to cancer, classified as mild, moderate, severe or low/high grade, can be reversible
properties of an "ideal drug"
Effectiveness - most important quality. drug elicits the responses for which it was given.
Safety - a drug is safe when it cannot produce harmful effects even if given in high doses for a long time.
Risks can never be eliminated completely but can be decreased by proper drug selection and dosing.
Ex: anti-cancer drugs, opioid analgesics, aspirin.
Selectivity - a drug that elicits only the response for which it is given.
No such thing as a wholly selective drug because all drugs cause side effects.
Ex: drowsiness from antihistamines, edema from calcium channel blockers, and sexual dysfunction from antidepressants.
fluid and electrolyte balance, what happens when a person becomes dehydrated?
Fluid balance: cells live in fluid environment with electrolytes and acid base concentration, disturbances can be life-threatening
Fluid fluctuations affect blood volume and cell function


Dehydration will be loss of extracellular fluid and sodium caused by vomiting, diarrhea, bleeding(hemorrhage) burns (as you lose fluid with burns), and other causes.
signs and symptoms: weight loss, poor turgor, dry mucous membranes, rapid pulse, decrease in B/P, decrease in specific gravity, decrease in peripheral circulation

can cause fluid shifts if there is a severe enough fluid loss. With dehydration, we can either keep the Na where it is or it can increase or decrease depending on the fluid shifts in the body.

Nurse should anticipate the doctor will order IV fluid of 0.9 normal saline.

Patient can go into hypovolemic shock if they have too great a deficit of fluid balance
can cause death

Electrolyte balance: in ECF and ICF affects maintenance of electroneutrality between intracellular and extracellular compartments

ECF: Na, Cl, bicarb; small amounts of K, Ca
ICF: K, Mg, PO4
diuretics
Bumetanide [Bumex]
Furosemide [Lasix]
Spironolactone [Aldactone]
Hydrochlorothiazide [HydroDIURIL]
Bumetanide [Bumex]
loop diuretic; antihypertensive
- check k levels, give slowly(monitor vitals)
- makes them urinate, loss of fluids

effects:
Furosemide [Lasix]
loop diuretic
Indications: Pulmonary edema, edema, Hypertension (acute conditions requiring rapid intervention)

adverse effects: decrease vascular fluid volume, cardiac output and Blood Pressure, decrease electrolytes (EVERYTHING HYPO), dehydrated, increase uric acid levels

Administration: Give slowly, monitor vital signs, blood pressure, and fluid loss, give during day
Spironolactone [Aldactone]
potassium sparing diuregtic,

Mechanism of action: blocks the aldosterone in the distal nephron, prevents reabsorption of water and Na in the distal nephron - it is a weak diuretic

uses: hypertension, edema, heart failure

adverse effects: tumors, hyperkalemia
**DONT USE WITH KIDNEY/HEPATIC DISEASE, elevated k levels
avoid foods high in potassium*
Hydrochlorothiazide [HydroDIURIL]
Class: Thiazide diuretic
most commonly prescribed for essential hypertension

uses: hypertension, edema

adverse effectsL everything HYPO, HYPER, dehydration
Electrolyte Do's:
treat abnormalities through diet first

Start low, go slow

Get baseline labs

Avoid overcorrection: repeat labs frequently

Give oral supplements with plenty of food and water

IV solutions are diluted and administered with a pump over an hour
Electrolyte Don'ts:
You NEVER push electrolytes
Electrolytes are administered diluted in water
Potassium:
major intracellular cation/electrolyte, found inside cells, regulates acid-base balance, maintains membrane potential, nerve conduction, electrical conductivity, needed for cardiac contraction, major causes of dysrhythmias
Mild hypokalemia: increase K through dietary intake


Severe hypokalemia: Parenteral
Never give potassium IV push- must be diluted, give slow
Peripheral line: 10 meq over 1 hour
Central line: 10-20 meq over 1 hour
Ex. Can have 4 bags of 10 MEQ, 1 bag per hour, or 2 bags of 20 MEQ, 1 bag per hour
No more than 40 meq at during a replacement
Oral
Do not crush extended release tabs
Give with food and plenty of fluid
Therapeutic Objective
to provide maximum benefit with minimal harm. Because no drug is ideal we must exercise skill and care if treatment is to result in more good than harm.
Pharmacogenomics
study of how genes affect a person's response to drugs
Pharmacodynamics
the study of the biochemical and physiologic effects of drugs on the body and the molecular mechanisms by which those effects are produced.

Dose-response relationships
Drug-receptor interactions
Drug responses that do not involve receptors
Interpatient variability in drug responses
The therapeutic index
Pharmacokinetics
study of drug movement throughout the body. Includes what happens to the drug as it moves through the body.

4 phases:
1. Absorption - movement of a drug from its site of administration into the body
2. Distribution - drug mvmnt from blood to interstitial space of tissues and then into cells.
3. Metabolism - (biotransformation) enzymatically mediated alteration of drug structure
4. Excretion - movement of drugs and their metabolites out of the body.
Pharmacotherapeutics
use of drugs to diagnose, prevent or treat disease or to prevent pregnancy; rationale for drug dose, route and schedule of admin
Enteric-coated drugs
covered in a fatty acid, wax, or shellac that is designed to dissolve in the small intestines but not the acidic environment of the stomach

Advantage to using enteric coating is that it protects drugs from acid and pepsin in the stomach, as well as protecting the stomach from drugs that can cause gastric discomfort

Disadvantage is that the absorption of enteric coated drugs can be even more variable than with standard tablets
pain rating scale, i.e 0 to 10, with 0 no pain and 10 extreme pain. What would you do if after giving a pain medication to your patient, they tell you their pain level is a 9?
- Tolerance is a decreased responsiveness to a drug as a result of repeated drug administration.

- Patients who become tolerant to a drug require higher doses to produce effects equivalent to those that could be achieved with lower doses before the tolerance developed.

Inform the doctor - the patient may need a higher dose to achieve therapeutic effects
the electrolytes in the body primarily responsible for plasma oncotic pressure
Sodium
Potassium
Albumin

Sodium - this is the electrolyte that has the most effect outside the cell

Note that Osmotic/Oncotic pressure pulls water into the capillary primarily by albumin

Water, sodium and glucose readily move across the membrane
Plasma proteins do NOT move through the capillary effectively; their presence in the capillary increases oncotic pressure, drawing water into the capillary

Oncotic pressure: a type of osmotic pressure (colloidal osmotic pressure) that attracts water from the interstitial spaces BACK into the capillaries due to proteins in the bloodstream (mainly albumin)
what drug interactions can occur if a patient consumes certain foods
usually decreases rate and extent of absorption
Milk with tetracycline reduces absorption
Fiber with digoxin reduces absorption

Can also increase absorption too and increase peak effects
high calorie meal and squinavit (drug for HIV)

can increase drug toxicity: if on MAO inhibitors must avoid tyramine-rich food, need strict diet

Grapefruit juice inhibits Cytochrome p450 34A (responsible for metabolizing meds, if inhibited there is too much drug in the system and can be toxic)
if start drinking it or stop usual drinking then must tell doctor
Interacts with benzodiazepines (excessive sedation) and high cholesterol meds (risk of rhabdomyolysis (breakdown of tissue in body)

can decrease metabolism of drugs and increase drug blood levels (huge effects)


Many drugs cause stomach upset with food
Need to monitor when you give drugs and meal timing
w/food: shortly after meal
empty stomach: 1 hour before meal or two hours after


Decreased Absorption
Food can decrease rate of absorption. Delays onset of effects but doesn't decrease peak effects.

Food can decrease the extent of absorption which reduces intensity of peak effects.
Ex: Ca-containing foods and tetracycline antibiotics reduces absorption + antibacterial effects.
Ex: High-fiber foods reduce absorption of digoxin which can cause therapeutic failure.

Increases Absorption
Food can increase the extent of absorption which heightens peak effects.
Ex: high-calorie meals more than double the absorption of saquinavir, an HIV drug.
The Grapefruit Juice Effectd55
The Grapefruit Juice Effect
Inhibits metabolism of certain drugs

Raises drug levels by inhibiting CYP3A4 metabolism which decreases intestinal metabolism. Causes more intense peak effects b/c more drug is available for absorption.

Has no effect on IV drugs.

Inhibition of CYP3A4 is dose dependent and can persist up to 3 days after last glass.
creation of unique effects
It is very rare that two drugs used in combination produce effects that are unique and not seen when either of the drugs is used individually.

When it does occur, the effects are usually negative
increased therapeutic effects
...
inhibitory effects
Interaction of two or more drugs in which the effects of the drugs are reduced.
Can be beneficial or negative

1. Reduced Therapeutic Effect
Any inhibitory that decreased therapeutic effect is negative and undesirable

2. Reduced Adverse Effect
Usually prevents or decreases a drugs toxicity
EX: Naloxone has an inhibitory effect on morphine, reducing it's toxicity
Potentiative effects (SYNERGISTIC)
Interaction of two or more drugs in which one drug causes the effect of another drug to intensify.

Can have increased therapeutic effects or increased adverse effects.
Lead exposure
seizures, delirium, paralysis, anemia, kidney failure

- interferes with neurotransmitters & hemoglobin synthesis
Carbon monoxide
usually involves a family in scenario
- headache, agitation, tinnitus, nausea, weakeness

- binds w. hemoglobin and blocks oxygen from doing so
Ethanol exposure
alcoholism, CNS depression, disorientation, fatty liver
- depression of fatty acids oxidation in mitochondria with necrosis of hepatic cells
Mercury poisoning
headache, paresthesias, hearing loss, weakness, tremors, visual changes, gait and speech difficulty.

CNS interefers w/ cellular enzyme function
livor mortis
blood and fluids drain from face so features look sharp, blood settles in lowest tissues and they look purple
gangrene
from severe hypoxic injury- commonly arterioscerlosis (blockage of arteries often in legs and feet- vessels blocked and ischemia occurs, then hypoxia then bacteria invade), foul order, death can occur


3 types:
1. Dry gangrene
- Usually from coagulative necrosis
- Skin turns dark black/brown, shrinks, wrinkles
2. Wet gangrene
- Neutrophils invade site and cause liquefactive necrosis
- Often internal organs become cold, swollen, black
3.Gas gangrene
- Type of wet gangrene
- Infection of injured tissue by Clostridium which destroys connective tissue and produces gas bubbles in muscle cells
If enzymes lyse RBCs, patients can go into shock and die
algor mortis
body temperature falls gradually then rapidly, after 24 hours body is temperature of environment
rigor mortis
after 6 hours acid accumulates in muscles cases stiffness, small muscles like jaw affected first, in 12-14 hours entire body affected, after 36-62 hours it diminishes and the body becomes flaccid
guidelines in regard to medication use during breast feeding
Drugs can be excreted in breast milk
Take drugs immediately after feeding, avoid drugs with long half-life, choose drugs excluded from milk, avoid drugs know to be hazardous
Drug Therapy in Pediatric Patients
More sensitive, greater individual variation, increased risk for adverse reactions due to organ system immaturity, drug responses increased and is prolonged until organs mature

Immaturity of Organs:
-Determines the intensity of the duration of response:
-Elevated drug levels = more intense response
-Delayed elimination = prolonged response

Immature state of pharmacokinetic factors:
-Absorption in GI tract
-Protein binding of drugs
-Blood-brain barrier(BBB) - not fully developed
-Hepatic metabolism- low in newborns, sensitive to drugs, when reach 1 liver is matured, metabolizes faster
-Renal drug excretion- reduced at birth, drug-excreting capacity of infants is limited
o Infants need reduced dosing or longer dosing intervals
o Reach adult level by 1 year

**meds with CNS effects should be given in reduced doses

*more vulnerable to adverse effects*

**Young infants require larger doses of water-soluble medications because of increased water content
therapeutic range
that concentration of drug in the blood serum that produces the desired effect without causing toxicity

Plasma drug levels fall between the minimum effective concentration and the toxic concentration.
Narrow therapeutic range
drugs need to be monitored with lab test.

- difficult to administer safely
metabolic acidosis
low pH, low HCO3, normal PaCO2
metabolic alkalosis
elevation of HCO3- usually caused by an excessive loss of metabolic acids

high pH, high HCO3

causes: vomitting,
respiratory acidosis
low pH, high PaCO2, normal HCO3

Acid accumulates in the body because breathing is too slow... CO2 isn't getting released

Hypoventilation,
respiratory alkalosis
high pH, low PaCO2, normal HCO3

Acid is leaving the body at a rapid rate because breathing is too fast... CO2 is getting released quickly, body becomes more basic

hyperventilation
Intracellular fluid (ICF)
fluid inside the cells. 2/3 of total body water
Extracellular fluid (ECF)
fluid outside cells, 1/3 of total body water
Interstitial fluid
fluid in the spaces between cells, outside of the blood vessels
Intravascular fluid
blood plasma, fluid in capillaries
water movement between the intercellular fluid (ICF) and extracellular fluid (ECF)
hydrostatic pressure
oncotic pressure
Oncotic pressure (colloid osmotic pressure)
osmotically attracts water from interstitial space back into capillary (albumin and sodium responsible)

- reabsorption
COP exceeds CHP
hydrostatic pressure
outward movement of water from capillary to interstitial space

- filtration (HP exceeds COP)
types of dehydration
isotonic, hypotonic, hypertonic
Isotonic(isonatremia) dehydration
WATER LOSS = ELECTROLYTE LOSS aka Hypovolemia

Results: decreased circulating blood volume and inadequate tissue perfusion

MOST COMMON TYPE of dehydration!

Causes: prolonged diarrhea, and vomiting
Hypotonic(hyponatremic) dehydration
ELECTROLYTE LOSS> water loss

Results: fluid shifts between compartments causing a decrease in plasma volume and the cells to SWELL.


Causes: misuse of diuretics, prolonged vomiting, diarrhea, burns, and renal disease; in the hospital with too much IV fluids and no electrolytes (electrolyte dilution)
Hypertonic(hypernatremic) dehydration
WATER LOSS>electrolyte loss;

alteration in the concentration of specific plasma electrolytes

Results: fluid moved from the intracellular compartment into the plasma and interstitial fluid spaces causing cellular dehydration and SHRINKAGE
IV fluids
hypotonic, isotonic, hypertonic
Digoxin (Lanoxin)
cardiac stimulant and diuretic

Digoxin therapeutic index = 0.5-2 ng/mL

reduced significantly by wheat bran, rolled oats, and sunflower seeds

has a narrow therapeutic range, reduced absorption can result in therapeutic failure.

most serious toxicity of digoxin is production of potentially fatal dysrhythmias.
Low potassium = increased risk of digoxin-caused dysrhythmias
Monitor serum potassium
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