EXAM 1 final

congental

present at birth

acquired

events after birth

iatrogenic

disease related to tx/medical intervention

idiopathic

disease cause unknown

Nosocomial

disease from hospital

pathogenesis

development of disease

subjective

pt tell you

objective

provider finds

complication

adverse even during course of disease or tx (HTN causes stroke)

Sequelae

result/consequence of previous disease, tx, or injury (dysphagia dt stroke)

why does the cell adapt?

maintain function and permit survival

atrophy

decrease workload, decrease size, more efficient functioning

hypertrophy

increase workload, larger size, increase functioning tissue mass

cell communication

contact, remote, gap junctions

cell adaptation

hyperplasia, hypertrophy, metaplasia

hyperplasia

increase in number of cells

metaplasia

one cell replaced by another, reversible

dysplasia

deranged cell growth

necrosis

induced by injury, surrounding inflammatory response, large areas of contiguous cell involvement

apoptosis

genetically triggered, no inflammation, few scattered cells, normal cellular relation

reversible cellular injury

remove stressor

irreversible cellular injury

apoptosis (normal), necrosis (autolysis)

pregnancy X

evidence of fetal abnormalities

pregnancy D

risk

pregnancy B

animal studies show no risk

PK

how body affects drug

PD

how drug affects body

absorption

small intestine

distribution

circulatory system, capillaries

metabolism

liver

excretion

kidney, lungs

components of PK

ADME

enteral routes of administration

oral, sublingual, buccal, and rectal

parental routes of administration

transdermal, subcutaneous, intramuscular, intravenous, topical

bioavailability

extent to which drug reaches circulations

factors that vary absorption

pH of drug/stomach, lipid solubility, GI motility, presence/absence of food, SA, blood flow

what can cross the BBB?

lipid soluble molecules

most abundant and important protein

albumin

active drug

free/unbound

drug-protein complex maintained by

weak bond

biotransformation

converts to active or inactive forms

3 types of metabolism

-active to active

-active to inactive

-inactive to active (prodrug)

inhibition of CYP450

Decreased metabolism of drugs, so buildup of substrate

Induction of CYP450

Increased metabolism of drugs, so not enough of drug (not getting effect)

how are drugs excreted?

kidneys via urine

metabolism in neonates

-Decreased metabolizing enzyme activity

-Poorly developed BBB

-Immature execretion of drugs

metabolism in geriatrics

-Decreased enzyme activity

-Decreased renal function

half life

after 5 half lives drug should be excreted

serum creatinine

measures creatinine levels in serum (waste product)

creatinine clearance

high means good renal excretion

affinity

ability of drug to bind complex; potency

intrinsic activity

ability to initiate an effect; efficacy

agonist

drugs that occupy receptors and activate them

antagonist

drugs that occupy receptors, but do NOT activate them

adenoma

benign tumor from glands

lipoma

benign tumor from fat

hemangioma

benign tumor from BV

neuroma

benign tumor from nerve tissue

polyp

benign tumor in bowel lining

fibroid

benign tumor in uterus

carcinoma

epithelial cells

glands

adenocarcinoma

ducts

ductal carcinoma

squamous cells

SCC

sarcomas

mesenchymal cells

lymphomas

lymphocytes

leukemias

bone marrow cells

TP53

tumor suppressor gene, guardian of genome, regulates DNA repair/cell division

transcription factor hypoxia inducible factor 1- alpha

triggered by hypoxic conditions to increase VEGF to promote angiogenesis

HIF-1 alpha in cancer cells

upregulated dt mutations in TP53 leading to unchecked angiogenesis

obesity and cancer

-insulin like growth factor effects

-adipocyte derived cytokines

-sex hormone production

adsorption

two molecules in gut interacting with each there (makes complex)

challenges of prescribing older adults

multiple medical conditions, polypharmacy, multiple prescribers

absorption in geriatrics

altered by antacids or iron, lack of intrinsix factor, delayed gastric empting, increase gastric pH

distribution in geriatrics

less water, more fat, low albumin

elimination in geriatrics

decreased size/hepatic blood flow may flow clearance of drugs, renal clearance reduces, drugs may accumulate

ADR anticholinergics

confusion, drowsiness, blurred vision, difficulty urinating, dry mouth, constapation

ADR benzos

falls, fractures, cognitive impairment, delirium

alpha agents have a high risk of

orthostatic hypotension, CNS effects

high risk of hyperkalemia

spironolactone

avoid NSAIDs if

GI bleed, peptic ulcer

meperidine causes

neurotoxicity

ADR antipsychotics

increased risk of death dt cardiovascular events and infections, QTc prolongation, abnormal movements

eukaryote division

mitosis

prokaryote division

binary fission

gram negative

pink

gram positive

purple

gram stain

bacteria, fungi

acid fast stain

mycobacterium

calcofluor white stain

fungi

gomori methenamine silver

fungi

viruses

capsid, envelope, DNA or RNA, spikes, need host

viral replication

host, replication, spread, innate/adaptive immune system response

stages of viral infection

incubation (asymptomatic), prodromal (symptoms), specific illness (characteristic symptoms), recovery (illness wanes --> good health)

effects of viral infection

death, fusion of cells to form multinucleated cells, malignant, transformation, no apparent morphologic/functional change

fungi cell wall

chitin, beta glucan

fungi cell membrane

ergosterol

forms of parasites

bacterial cell wall

peptidoglycan

gram negative bacteria

thin peptidoglycan layer, outer membrane