Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
198 Cards in this Set
- Front
- Back
|
pathophysiology
|
physiology of abnormal states (specifically functional changes that accompany)
|
|
|
pathology
|
structure, changes in tissue itself, anatomic and physiological deviations from normal
|
|
|
disease
|
state where sufficient departure from signs or symptoms
|
|
|
signs
|
measureable
|
|
|
symptoms
|
subjective
|
|
|
syndrome
|
group of signs and symptoms
|
|
|
etiology
|
cause of disease,
|
|
|
idiopathic
|
disease where cause is unknown
|
|
|
3 categories of diseases
|
genetic, congenital, acquired
|
|
|
pathogenesis
|
origination and development of disease
|
|
|
sequela
|
condition resulting from disease
|
|
|
lesion
|
abnormal change in structure of organ or part due to injury/disease
|
|
|
pharmacodynamics
|
impact of drugs on body,studies effects of drug and how it effects
|
|
|
pharmacology
|
biological effects of chemicals
--science of drugs: orign, composition, pharmacokinetics therapeutic use, toxicology -study of drugs and interactions with living systems |
|
|
mitigation
|
alleviate symptoms of disease
|
|
|
pharmacokinetics
|
absortion, distribution, biotransformation (metabolism), excretion
|
|
|
clinical pharmacology
|
effects on humans
|
|
|
toxicology
|
what are adverse effects
|
|
|
therapeutics
|
use of drugs to diagnose, prevent, or treat disease or to prevent pregnancy (medical use of drugs)
|
|
|
3 most important characteristics of a drug are
|
effectiveness (most important), safety, and selectivity
|
|
|
other important characteristics of a drug
|
reversible action, predictability, ease of administration, freedom from drug interactions, low cost, chemical stability, possession of a simple generic name
|
|
|
major pharmacokinetic processes
|
1. drug absorption 2. drug distribution 3. drug metabolism 4. drug excretion
|
|
|
What do cells to in response to stress?
|
adapt to maintain function--change in size, shape, number etc. (functional and structural changes) (affects homeostasis)
|
|
|
if cells fail to maintain function what happens?
|
injury
|
|
|
can normal stimuli lead to normal cell change?
|
Yes--exercise-- cells build (muscle cells increase in size)
|
|
|
Hydropic swelling
|
water moving into cells
|
|
|
what happens in hydropic swelling?
|
atp decreases--ionic disequilibrium: sodium-potassium pumps need ATP, water goes where sodium goes
|
|
|
intracellular accumulations
|
can mean--
-normal things building up(lipids, protein, carbs) -abnormal proteins(faulty metab or synthesis) -pigments(lipofusion in neurons, bilirubin) -inorganic particles (coat, lead, iron, silica) |
|
|
bilirubin
|
breakdown of RBC's heme molecule; can cause jaundice (is orange, buildup, sign of liver damage)
|
|
|
adaptation
|
alows tissue to survive/maintain function
-atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia |
|
|
atrophy
|
decrease in size--decrease work load (functional capacity), decrease O2 consumption, decrease in organelles
|
|
|
cause(etiology) of atrophy
|
disuse, denervation, ischemia (decrease O2, decrease blood flow), inadequate nutrition, loss endocrine, persistant injury, aging
|
|
|
HR (heart rate) x SV (stroke volume)=
|
output
|
|
|
hypertrophy
|
increase size, increase function
|
|
|
adaptive hypertrophy
|
cardiac muscle, heart struggling--tries to makeup thus muscles get bigger (to keep cardiac output up)
|
|
|
compensatory hypertrophy
|
lose one kidney, other gets larger to pic up slack (liver capable of coming back but other will makeup)
|
|
|
hyperplasia
|
increase function due to increase number of cells
ex.--epithelial cells form calluses, intestinal and glands too, import in wound healing to close gap |
|
|
physiological hyperplasia
|
hormonal: uterine wall--thicken wall for implant
compensating: liver coming back |
|
|
pathologic hyperplasia
|
excessive hormone product: goider
growth factor effects: warts (skin cells proliferate) |
|
|
metaplasia
|
(reversible) one recognizable cell type changes to another
|
|
|
why metaplasia occurs
|
in response to chronic irritation and inflammation
smokers--pseudostrat columnar epith changes to squamous strat (which protects); when stop smoking changes back, cilia and goblet cells come back too |
|
|
dysplasia
|
known cell becomes an unknown, deranged cell; comes from chronic irritation and inflammation: adaptive effort gone astray (precursor to cancer)
is reversible |
|
|
pathologic calcifications
|
when cells die, calcium leaks out, binds with phosphate, and builds up elsewhere
|
|
|
dystrophic calcification
|
occurs in dead/dying tissue (eyes common), calcium phosphate crystals form
|
|
|
metastatic calcification
|
occurs in normal tissues due to increased calcium levels
|
|
|
hypercalcemica
|
renal failure--dumps excess Calcium elsewhere doesn't go in urine, vit D intoxication
|
|
|
Etiology
|
stress damages cells by: direct damage to proteins, membranes, DNA and ATP depletion, free radical formation, increased intracellular calcium
|
|
|
how does hypoxia cause ATP depletion (powerfailure)?
|
aerobic metab stops--less ATP produced--Na+/K+ ATPase cant run fast enough--cells swell with water
anaerobic metab used--lactic acid produced--acid damages membranes, intracell structures, and DNA |
|
|
what are free radicals
|
molecules with unpaired electrons, unstable and reactive, damages normal cells turning them into free radicals--steal electrons, unstable and reactive, damages normal cells turning them into free radicals
|
|
|
what deals with free radicals
|
antioxidants
|
|
|
apoptosis
|
programmed cell death: normal process, "pruning", removes worn out and unwanted cells
|
|
|
necrotic cell death
|
unregulated, caused by injury to cells, cells swell and rupture, inflammation, dead tissue surrounded by living tissue
|
|
|
process of apoptosis
|
turn on own enzymes (especially caspases), chew up cellular compontents (protein and dna, destroyed by WBC)
|
|
|
extrinsic pathway of apoptosis
|
fast, TNF receptor--blebs--breakup--phagocytes eat
|
|
|
intrinsic pathway of apoptosis
|
growth factor stopped, mitochondria stops and breaks down
|
|
|
example of apoptosis in embryo's
|
hands and feet are webbed but tissue in between has apoptosis (gremlin protein in charge of this
|
|
|
pathogenic example of apoptosis
|
apoptosis used on wrong genes/cell made---neurodegenerative disorders= alzheimers(corticle cells etc apoptosis), parkinsons(dopamine lost)
|
|
|
necrosis
|
cell death and degradation of nucleus
|
|
|
liquefaction(type of necrotic tissue)
|
sluf cell into soup, liquid tissue (CNS, abcesses)
|
|
|
coagulation (type of necrotic tissue)
|
tissue dies but not all enzymes active--incomplete degradation
|
|
|
fat necrosis (type of necrotic tissue)
|
accumulation of fatty tissue replacing, lipases chew up free fatty acids, complexes with Ca+= soupy complex
|
|
|
caseous necrosis
|
"cheese-like curd", cardiac cell death (after heart attack)
|
|
|
Outcomes of necrosis (sequelan)
|
1. liquefaction
2. encapsulation (fiberblasts:try to keep from spreading) 3. sloughing (desquamation) 4. scar formation 5. gangrene-can feed on you, when exposed to O2 and saprophytic bacteria 6.atrophy of organ 7. regenertation |
|
|
necrotic means tissue is
|
dead and can't be reversed
|
|
|
aging cells
|
telomeres protect ends of DNA during replication, shorten with age--DNA damaged, more free radicals, lose ability to repair telomeres
|
|
|
telomeres
|
end of chromosome
|
|
|
nurses responsibility pertaining to drugs
|
administer, assess, intervene to make tolerable, provide education, monitor and prevent med err
|
|
|
common sources of drugs
|
plants(usually synthetic now)
animal products-used to replace human chemicals genetic engineering(insulin from pigs) inorganic compounds (salts, minerals) synthetic sources: alter bacteria (tech advances tweek OG formula to improve in specific areas) |
|
|
Drug evaluation and average cost to go through drug
|
pre clinical and 4 trials, 1 billion for each drug
|
|
|
preclinical drug eval
|
tested on lab animals
|
|
|
phase 1 drug eval
|
human volunteers
|
|
|
phase 2 drug eval
|
patients with disease
|
|
|
phase 3 drug eval
|
clinical market, physicans prescribe
|
|
|
phase 4 drug
|
used with continual eval of drug
|
|
|
orphan drugs
|
have promise but too much work to develop
|
|
|
FDA approved drugs
|
approved given brand (trade) name (phase 4), generic used in approval process (p1-p3), chem names reflect chem structure
|
|
|
legal regulation of drugs
|
1938- FDA has power to enforce standards for safey, toxicty, recall, labeling
1962- FDA can test and evaluate for efficacy and safety 1970- established categories of abuse potential and determined abuse potential -DEA enforces federal laws |
|
|
controlled substances
|
prescription, distribution, storage, and use of drugs closely monitored
|
|
|
schedule 1 controlled substances
|
high abuse potential and no therapeutic use
|
|
|
schedule 2 controlled substances
|
high potential for dependence but helpful in limited amounts
|
|
|
schedule 3 controlled substances
|
less but reason to be concerned
|
|
|
Scheduel 4 and 5 controlled substances
|
4- less
5- limited abuse potential |
|
|
Generic drugs
|
company only manufacturing from formula does not research
-must have bioequivilence, within margin of error effectiveness to brand name |
|
|
over the counter
|
self treatment, must remember that OTC can mask disease, taking with prescriptions could cause harmful interactions
|
|
|
Drug label
|
specific info by FDA
|
|
|
package insert
|
prepared by manufacturer
|
|
|
other sources of info
|
reference books (annually updated), journals, internet (sketchy)
|
|
|
what can be found on drug label?
|
generic name, yr of 1st FDA approval, list of approved indications, dosage details, less severe warnings, most freq side effects, drug interations
|
|
|
4 primary mechanisms of Action
|
1. replace or act as substitute ex. insulin
2. increase or stimulate cellular activities ex. stim/slow gland 3. depress or slow cellular activities 4. interfere with the functioning of foreign cells(ex tumor cells |
|
|
drugs act through what?
|
receptors
|
|
|
what affects receptors?
|
ligands
|
|
|
receptor site
|
reacts to certain chemicals
agonist- acts like natural ligand, binds and activites antagonist- can bind and block activation |
|
|
affinity
|
better fit, better desirable reaction
|
|
|
diamox
|
diuretic, block carbonic anhydrase enzyme (alters H+ and water exchange system in kidney and eye) -more water passed out--drives equation back to acid if--losing CO2-losing hydrogen ions-blood pH alkalatic
|
|
|
absorption
|
how get in?
rate effected by route of administration, oral drugs--goes to liver (absorbed through stomach) is metabolized |
|
|
distribution
|
where it go?
movement into tissue, lipids must be moved with carrier proteins (hydrophobic, wouldn't go through blood w/o) pKa--needs to be right pH, perfusion -must be careful of drugs that will cross placenta/breast milk |
|
|
metabolism (biotransformation
|
how long stay?
liver most important site |
|
|
excretion
|
how get rid of?
kidneys play most important role (excreted in urine) --other routes: skin, saliva, lungs, bile, feces |
|
|
which drugs will cross the blood brain barrier?
|
only lipid solvable drugs
|
|
|
phase 1 of metabolism
|
oxidation reaction/hydrolysis of drugs
-inactivated drug or may form active metabolite (codeine-> morphine) |
|
|
phase 2 of metabolism
|
conjugation reaction
verty little of active drug may actually reach the reactive sites |
|
|
half-life
|
time takes for amountof drug to drop by half
|
|
|
which route of drug as more prolonged effect?
|
Oral- takes more time to help but helps longer
Iv-comes in right away but decreases faster |
|
|
therapeutic range
|
concentration of blood where drug will do its thing
|
|
|
factors influencing drugs effect
|
wt., age, gender, physiological and pathological factors, genetics, drug tolerance, etc.
|
|
|
drug-to-drug (and food) interactions
|
can occur at any point
-drugs used to depress or slow cellular activites |
|
|
adverse drug reaction
|
any undesired effect of a drug
-can have other effects, patient sensitive, etc. |
|
|
types of reactions
|
-primary pharmacologic action (overdose)
-secondary pharmacologic action (side effects) -toxicity: drug-induced tissue and organ damage -over reactions (NOT hypersensitivity): excessive response |
|
|
type 1 drug allergy (hypersensitivities)
|
anaphylactic (IgE mediated)
|
|
|
type 2 drug allergy
|
cytotoxic reaction, (IgG and IgM) (mast cells degrade and result in histamine; antibodies bind to blood cells and kill them)
|
|
|
type 3 drug allergy
|
serum sickness
-immune complex sees foreign ID, drug complexes and wedged into capillaries (rash type thing) |
|
|
type 4 drug allergy
|
delayed allergic reaction
-cell-mediated (poison ivy-bind to skin, topical drug-sees foreign--blistering of skin--NOT antibody mediated |
|
|
most common drug reaction
|
reaction in skin
|
|
|
stomatitis
|
inflammation of mucous membranes (of mouth
-often happens to chemotherapy patients (kill rapidly dividing cells which also include epithelial cells) |
|
|
"magic mouthwash"
|
used with chemotherapy patients iwth stomatitis:
--anti-inflammatory, anesthetic, coating antacid, anti-fungal, antibiotics |
|
|
superinfections
|
destruction of body's normal flora
-assessment: fever, diarrhea, vaginal discharge -interventions: supportive care (mouth, skin care), antifungal meds, may stop drug resp for infection (like c. diff) |
|
|
blood dyscrasia
|
bone marrow suppression
-assessment: fever, chills, weakness -interventions: monitor blood counts, protective isolation |
|
|
toxicity
|
affects of drug too great to ignore
-liver (hepatic): jaundice, elevated liver enzymes, etc -kidney(renal): changes in urine output, elevated BUN and creatine, blood urea nitrogen |
|
|
poisoning
|
chem substances that injure, impair, or kill organism
-occurs when overdose damages multiple body systems |
|
|
hypoglycemia
|
low serum blood glucose level--restore glucose
|
|
|
hyperglycemia
|
high serum blood glucose--insulin
|
|
|
hypokalemia
|
decreased--replace serum potassium, monitor
|
|
|
hyperkalemia
|
increased--monitor heart rhythm, decrease potass concentrate
|
|
|
what do potassium and sodium levels change?
|
action potential of cells
|
|
|
ocular toxicity
|
visual changes--monitor
|
|
|
auditory damage
|
damage to 8th cranial nerve or hair cells in cocula--tinnitus (ringing), hearing loss
|
|
|
neurological effects
|
anything that changes brain function--drowsiness, make loopy (altered level of consciousness)
|
|
|
atropine-like (anticholinergic) effects from drugs
|
dry mouth, urinary retention, drowsy, blurred vision
|
|
|
parkinson-like syndrome from drugs
|
muscle tremors, changes in gait
|
|
|
neuroleptic malignant syndrome from drugs
|
extrapyramidal symptoms
|
|
|
teratogenicity
|
any drug that causes harm to developing fetus or embryo
|
|
|
2 lines of body defenses
|
-physical and chem barriers (skin, membranes)
-immune defences (innate and adaptive) |
|
|
innate defenses
|
phagocytic cells, inflammatory response
quick |
|
|
adaptive (acquired) immunity defenses
|
B and T lymphocytes
has memory cells |
|
|
lymphoid tissues
|
primary: thymus (t cells), bone marrow (b cells, all others)
secondary: encapsulated and patches |
|
|
leukocytes and inflammatory cells
|
granulocytes (neutrophils, eosinophils, basophils)
monocytes (turn into macrophages) lymphocytes (natural killer, T, B) mast cell (from basophils, relase histimine) |
|
|
granulocytes
|
neutrophils, eosinophils, basophils
|
|
|
monocytes
|
turn into macrophages
|
|
|
lymphocytes
|
natural killer, T cells, B cells
|
|
|
mast cell
|
releases histamine, comes from basophils
|
|
|
complement cascade
|
proteins that enhance inflammation, provide chemotasis, opsonization and cell lysis (membrane attack complex)
|
|
|
C3a
|
pro-inflammatory
|
|
|
C3b
|
opsonization
|
|
|
C5a
|
chemotaxis
|
|
|
which complement proteins are key players in inflammation?
|
C3a and C5a
|
|
|
chemical mediators
|
cytokines
bradykinin |
|
|
cytokines
|
protein messengers of cell that affect growth/activity of another cell (interleukin, interferons, TNF)
|
|
|
bradykinin
|
product of kinin cascade, associated with clotting system (pain, inflammation, vasodilation (swelling)
|
|
|
inflammation purpose
|
protective response
-eliminate the initial cause of cell injury -remove damaged tissue -prepare damage tissue for repair |
|
|
how does inflammation accomplish its effects?
|
diluting destroying and neutralizing harmful agents
|
|
|
5 signs of inflammation
|
1. redness (erythema)
2. swelling 3. heat 4. pain 5. loss of function |
|
|
inflammatory mediators
|
1. Those that affect diameter of blood vessels (vasoactive and smooth muscle constricting properties)
2. plasma proteases-initially trigger complement cascase, coagulation, kinin 3. chemotactic factors-follow signals 4. reactive molecules and cytokines released by PMN's (neutrophils) |
|
|
histamine
|
released by mast cells and basophils (IgE), binds to receptors (red, swell) on endothelial cells- dilates capillaries, increased blood flow and increased permeability
|
|
|
arachidonic acid metabolites
|
found in cell membranes, released by phospholipase and produces eicosanoid
|
|
|
2 cycloxygenase (arachidonic acid metab)
|
cox-1 and cox-2, increased BP usually means inflammation
|
|
|
2-lipoxygenase (arachidonic acid metab)
|
tissue damage calls chemotaxis, primarily engaged in lungs
|
|
|
Inflammatory events
|
1. increased vascular permeability
2. margination and emigration (extravastion of luekocytes) movement into blood, WBC's come 3. leukocyte activation and phagocytosis:WBC's phagocytosis |
|
|
selectins
|
produced by endothelial cells
|
|
|
integrins
|
allow neutrophils to stop and then extravate capillaries for damaged area
follow chemical trail and then destroy |
|
|
acute inflammation
|
short, min-days; exudation, emigration of leukocytes
|
|
|
chronic inflammation
|
macrophages accumulate; fibroblasts proliferate, scar tissue forms (nonspecific, chronic inflammation), granulomatous inflammation
|
|
|
anti-inflammatory
|
block/alter the chemical reactions associated with inflammatory response
|
|
|
antipyretic
|
fever reducing
|
|
|
analgesic
|
pain reducing
|
|
|
anti-inflam agents
|
corticosteroids(glucocorticoids)
salicylates-oldest, willow tree NSAIDS- w/o side effects antihistamines-block effect of histamine at receptor acetaminophen-(tylenol) (actually NOT an anti-inflam) |
|
|
what do corticosteroids affect?
|
cortext of adrenal gland (adrenal cortext)
|
|
|
Glucocorticoids actions
|
bind to cytoplasmic receptors in target cells (alter proteins being made in cell, change transcription and translation DNA)
-suppress imune system, have mineral corticoid activity |
|
|
what do you have to keep in mind when using glucocorticoids especially with diabetics?
|
-increase glucose blood levels for energy
-increase rate of muscle break down (to generate glucose) -stimulate fat production mobilization (liver convert to glucose) |
|
|
indication
|
when are they appropriate to use?
|
|
|
glucocorticoid indications
|
-short term treatment of inflam disorders
-relieve discomfort and pain - lock phospholipase, blocks membrane-lipid mediators |
|
|
pharmacokinetics of glucocorticoids
|
well absorbed from many sites, metab in liver mostly and excreted in urine (kidneys)
|
|
|
contraindications of glucocorticoids
|
known allergy, acute infection, lactation
|
|
|
cautions of glucocorticoids
|
diabetes (raises glucose), acute peptic ulcer (start eroding lining: dissolve prostaglandin), immunosuppression: infection
|
|
|
adverse reactions of glucocorticoids
|
related to route admin (oral is digested), systemic use-endocrine when withdraw must do in increments, otherwise adrenal gland won't be ready to produce all at once
|
|
|
drug-to-drug interactions
|
therapeutic and toxic effects INCREASE with erythromycin, ketoconazole, or troleandomycin
--salizyates(aspirin), barbiturate (sedative), pherytoin (anti-epileptic), rifamin (antibiotic) will DECREASE |
|
|
salicylates
|
antipyretic, analgesic, casprin, balsalazide, mesalamine (ulcerative colitis, last 2)
|
|
|
salicylates actions
|
-block prostagladin synthesis (cyclooxygenase inhibits)
-block synthesis of TXA (thromboxane AZ) (inhibits, platelet aggregation at low doses, "blood thinning") |
|
|
pharmacokinetics of salicylates
|
absorbed PO directly in stomach (5-30 min/ T 1/2=15 mi- 12 hrs, metabolized-liver, excreted-urine)
|
|
|
side effects of salicylates
|
GI irritation (goes through walls and blocks COX 1&2 which stomach needs); clotting system; reye's syndrom (children given-aspirin damages liver-can't process ammonia-levels increase-encephalopathy-child passes out, seizure, die) overdose- ringing ears, acidosis, nausea, vomiting, diarrhea, mental confusion
|
|
|
contraindiction of salicylates
|
known allergy, bleeding abnorm
|
|
|
NSAIDS
|
strong anti-inflam, analgesic effects; types are based on chemical structure
|
|
|
types of NSAIDS
|
propionic acids, acetic acids, fenamates, cyclooxygenase-2 inhibitors
|
|
|
indications of NSAIDS
|
relief of signs and symptoms of rheumatoid and osteoarthritis relief of mild-moderate pain, treatment of primary dysmennorhea
|
|
|
contraindication of NSAIDS
|
allergy, hypertension, peptic ulcer, preg and lat, renal/hepatic dysfunction
|
|
|
Antihistamines
|
block membrane bound receptor, anticholinergic and antipruitic( itchyness) effects
|
|
|
indications of Antihistamines
|
seasonal and perennial allergic rhinitis, allergic conjuctivity uncomplicated urticana (hives) and angioedema (blood vessels dilate and leaky)
|
|
|
pharmacokinetics of Antihistamines
|
well absorbed orally, metab liver, excreted urine and feces (some not fully aborbed)
|
|
|
contraindications of Antihistamines
|
preg and lactations
|
|
|
cautions of Antihistamines
|
renal and hepatic impairment, history of arrhythmia (sympathetic input)
|
|
|
adverse effects of Antihistamines
|
drowsiness and sedation; anticholinergic effects
|
|
|
1st gen (sedating) Antihistamines
|
cross blood-brain barrier (benedryl, ny-quil, vistaril, chlortimeton)
|
|
|
2nd gen (non-sedating) Antihistamines
|
claritin, zyrtec, clarininex
|
|
|
Acetaminiphen
|
not anti-inflam but lowers body temp
|
|
|
actions/indicators of Acetaminiphen
|
thermoregulatory, works in nervous system (mechanism not sure), treatment pain and fever
|
|
|
pharmacokinetics of Acetaminiphen
|
absorbed from GI tract, peaks in .5-2 hrs, metab liver, excrete urine, T 1/2 2 hrs
|
|
|
contraindications of Acetaminiphen
|
known allergy, caution with preg and lactation
|
|
|
adverse reactions of Acetaminiphen
|
headache, hemolytic anemia, renal dysfunction, skin rash, fever, hepatotoxicity
|
|
|
drug reactions of Acetaminiphen
|
oral anticoagulants increase bleeding
|
