Unit 1 Flashcards
Pathology
Study of disease and it’s changes to body tissues
Pathogenesis
Cellular development of diseases and other mechanisms
Clinical pathology
Pathology apply to clinical issues. Should take into account, activity, level, participation, level of support, and environment.
Incidence
Number of new cases
Prevalence
All cases including new
Health
Physical, mental, and social well-being
Illness
Deviation from health. Perception of the feeling.
Disease
Bio medical condition resulting in malfunction of structures. Can be measured with data.
Acute illness
Rapid or short duration of disease.
1. Stage one: physical symptoms
2. Stage two: cognitive awareness.
3. Stage three: emotional response (denial, fear, anxiety)
Chronic illness
Permanent impairment or disability, requiring long-term care
Executive functions
Occur in right hemisphere of brain. Making goals, plans, and maintaining behavior.
Behavior
Social behaviors affected by cognitive disability
Problem-solving
Handling new information and filtering it appropriately. Can be affected by cognitive disabilities.
Information processing
Speed. That information travels to the brain, can be affected by cognitive disability.
Memory
Failure to store, retrieve information, can be affected by cognitive disability
International classification of functioning disability in Health (ICF)
Body structures and functions, activities, participation, environment, personal factors, and health conditions
Theories of health and illness
- PsychoNuroimmunology: study of interactions between behavior, neural, endocrine, enteric, immune.
- Mitochondrial DNA disorders.
- Quantum model: cells communicate with energetics units and high energy can increase health
- Consciousness based healthcare: how you perceive your reality
Epigenetics
How biological and environmental signals can determine gene expression
Physical environment built
Surroundings supporting human activity
Physical environment, natural
Air, water, soil, sun
Internal environment
Attitudes, thoughts, feelings, believes that affect physiological function
External environment
Community, purpose in life, spiritual, beliefs, suits, etc.
Factors influencing health
Geographic, variations, socioeconomic status, health, disparities, social support, environmental barriers, cultural influences, gender, and age
Transnational competence
Teachers healthcare professionals, how to address health issues with all aspects of culture in mind
Cultural relativity
Cultural influences, and environment contribute to genetic traits an expression of diseases
Steroid hormones
Can make Changes throughout the lifespan
Endocrine, disrupting mechanisms
Can I have multigenerational effects
Senescence
Condition of growing old, cellular metabolism
Environmental damage theory
Free radicals can cause tissue damage
Programmed based theory
Presumes aging is genetically driven. Biological clock.
Telomerase theory of aging
Shortening of telomeres that maintain the integrity of chromosomes
Epigenetic clock
DNA methylation as a marker of age
Centenarians
Living to 100+
Supercentenarians
110+
Enteric nervous system
Collection of 200 to 600 mil neurons in gut. Acts as the second brain, that stores and produces neurotransmitters.
Pharmacology
The study of drugs
Pharmacotherapeutic
Do use a specific drugs to prevent treat or diagnose
Toxicology
Study of harmful effects of drugs
Pharmacokinetics
Study of how drugs are absorbed, distributed, and eliminated
Pharmacodynamics
Analysis of what drugs do to the body and how
Pharmacogenetics
Genetic basis for drug responses with variations
Drug approval stages
Pre-clinical studies: animal studies, that test, PharmaKinetics, thermodynamics and toxicity
Phase 1: small number of healthy people to test toxicity in humans
Phase 2: phone number of people with the specific disease for dosage effectiveness
Phase 3: large patient population can be 7 to 9 years
Phase 4: post, marketing, surveillance
Orphan drugs
Treat rare diseases in small populations
Off label drugs
Drugs used to treat conditions different from FDA approval, legal and used frequently
Controlled substances
Schedule one: highest abuse, potential and illegal (heroin).
Schedule two: approved for therapeutic purposes, with high potential for abuse (morphine)
Schedule three: mild dependence (steroids.)
Schedule 4: low abuse, potential (antianxiety drugs)
Schedule five: lowest abuse, potential (cough meds)
Does response curve
Compares dose range versus effectiveness shows peak response
Potency
Lower dose to produce the same effects. How easily does it work.
Efficacy
How well does it work
Median effective dose
Ed50
half were effective
Median toxic dose
TD50
Half adverse effect
Therapeutic index
TI=TD50/ED50
Indicator for drug safety
Lethal dose
LD50
Half lethal dose in animals
Routes of administration of drugs
Enteral admission: goes through G.I. tract
Parenteral Admission: non-G.I. tract, more direct
Transdermal
Enteral Admission
G.I. tract.
Oral, sublingual/Buccal, rectal
Parenteral Admission
Non-G.I. tract
Inhalation, injection, topical
Transdermal
Through the skin, must not be graded
First pass effect
Drug does it make it to the liver and our degraded before use
Different kinds of injections
IV, intra-arterial, subcutaneous, intrathecal (sheath), intramuscular
Topical
Through skin, but not much absorption unlike transdermal
Bioavailability
Extent to which a drug reaches circulation
Factors affecting distribution
Tissue permeability, blood flow, binding to plasma proteins, finding two subcellular components
Volume of distribution
The amount of the drug administered, divided by the concentration in the blood plasma
Drug storage sites
Adipose, bone, muscles, organs
Biotransformation
Chemically altering original compound to inactivated or by excretion. Drug metabolism.
Ways that enzymes can break down drugs
Oxidation, reduction, hydrolysis, conjugation
-Smooth er
Organ most responsible for biotransformation
Liver
Drug excretion Methods
Kidneys, sweat, saliva, breastmilk
Clearance
Ability to eliminate drug
CL = Q x (ci-co)/ci
Half life
Amount of time that it takes 50% of drugs to be eliminated within the body
Surface membrane receptors
Transmembrane proteins, ion pores (acetyl choline), links directly to enzymes (insulin), linked directly to regulatory proteins (G proteins)
Intracellular receptors
Alters,, DNA and protein transition
Factors of drug receptor interactions
Size and shape, electrostatic attraction, affinity, efficacy
Affinity
Amount of attraction with drug receptor, tendency to bond
Efficacy
Amount of change of produces, how well it works
Allosteric modulators
Find a specific sites to increase or decrease affinity, local, regulators, not agonist or antagonist
Agonist
Find an initiate change, have efficacy and affinity
Partial agonist
Don’t evoke strong response
Inverse agonists
Opposite effect
Antagonist
Fines to receptor, but presents no change, prevents agonist from binding, has affinity only
Competitive antagonist
Vies for the same receptor as agonist
Non-competitive antagonist
Strong permanent bond, “no competition if I only win”
Mixed agonist antagonist
Stimulate some while blocking others
Desensitization
Prolonged exposure will decrease receptor function
Receptor down regulation
Decreases the number of receptors
Beta blockers
-olol
Antihypertensive, antianginal, antiarrhythmic, congestive heart failure
Calcium channel blockers
-ipine
Antihypertensive, antianginal
HMG CoA. Reductase inhibitors
-statin
Hyper lipidemia
Ace inhibitor
-pril
Antihypertensive, congestive heart failure
Angiotensin II receptor blockers
-sartan
Antihypertensive, congestive heart failure
Glucocorticoids
-sone
-olone
Anti-inflammatory, immuno suppressant
Cyclooxygenase type two inhibitors
-coxib
Pain, inflammation
Ischemia
Insufficient blood flow to maintain cell metabolism. Leads to hypoxia or anoxia, dropping waste removal, dropping ATP.
Cause of 2/3 of mortality in industrialized nations
Bacteria
Release, exotoxins and endotoxins causing cell inflammation
Viruses
- Kill from within by disrupting cellular processes.
- Code proteins to alter permeability of cell membrane.
- DNA viruses integrate themselves into cellular genome and produce foreign proteins to destroy immune system.
Chemical factors of cell injury
- Toxic substances, injure cells directly.(Heavy metals.)
- Toxic substances that require metabolic transformation to become toxic(CO2)
Free radicals
Create reactive, oxygen species, where free 02, binds to hydrogen ions for stabilization and causes damaging effects that lead to 90% of lifestyle diseases
Antioxidants
Neutralize free radicals in slow age related, macular degeneration
Endogenous agents : enzymatic, non-enzymatic defense mechanisms
Exogenous agents : vitamin C, vitamin E, and beta carotene
Nitric oxide
Free radicals with high reactivity that causes more oxidative stress when bio availability is decreased
Helps with neural connections , and wound healing
Genetic factors of cell injury
Alterations and structures or numbers of chromosomes, single mutations of genes, multiple gene mutations that the environment turns into disorders
Mechanical factors of cell injury
-Happen internally
- physical stress theory: physical stress, causes, adaptive responses, less stress tolerance, becomes atrophy linear stress, becomes hypertrophy, high stress, becomes tissue failure
Nutritional factors of cell injury
Kwashiorkor: protein deficiency
Marasmus: general nutritional deficiency
Physical factors of cell injury
Blunt trauma, physical agents (electricity, temperature, radiation)
Cellular aging
Ability of a cell to recover from injury. Mitochondria changes with age and cannot keep up with energy demands.
Lipofuscin
Anti-aging pigment found in the lysosomes of old cells
4 theories of aging
-Where in tear theory: cells that cannot regenerate in cause organ decline
-Free radical theory: DNA damage and oxidative stress cause cells to become damaged and age
-Telomere aging clock theory: molecular clock, sensing cell senescence
-Epigenetic clock theory: DNA affected by gene expression
Methylation of DNA
Winds DNA into hisstones, acetylation is the act of unwinding DNA
Steps of reversible sell injury
- Injury occurs in homeostasis is impaired, leading to an influx of sodium in calcium in the cell.
- The cell begins to swell.
- Mitochondria are impaired, increasing lactic acid, metabolism, and decreasing the pH.
- Decreased proteins synthesis due to decrease of ribosomes from rough ER.
Pure Hypertrophy
Occurs in the heart and striated tissues
Hyperplasia
Increase in number of cells. Due to hormonal stimulation or chronic and excessive simulation of some kind.
Metaplasia
Change in the cell and function
Dysplasia
Increase in cells with altered morphology
Apoptosis
Programmed cell death that is genetically mediated, structures remain intact, cell shrinks
Necrosis
Degradation of dead cells, in response to irreversible cell injury, structures are disrupted and inflamed
Nucleus breakdown during cellular death
Pyknosis: clumping
Karyorrhexis: fragment (apoptosis)
Karyolysis: disillusion
Inflammation
Getting rid of the cause of energy and the consequences of the energy. Redness, heat, Adema, pain.
Chronic inflammation
Extensive necrosis, underlying issue, not addressed, accumulation of macrophages lymphocytes and plasma cells. Granulation tissue.
Granulation
Endothelial cells seen in chronic inflammation. Highly vascularized, reddish scar.
Effusion
Escape of fluid, can be exudate or transudate
Exudation
Escape of fluid and protein from vasculature. High in protein.
Transudate
Escape a fluid with low protein or cell components. Ultra filtrated blood from osmotic balance.
Five types of exudation
- Hemorrhagic sanguinous: bright, red from trauma
- Serosanguineous: blood tinged, or pink. 2 to 3 days after injury.
- Serous: thin and yellowish. Contains proteins.
- Purulent: viscous in cloudy with pus.
- Catarrhal: thin and clear mucus. Occurs and mucous membranes.
Steps of inflammatory response
- Vasodilation
- Increased capillary permeability
- Loss of fluid.
- Blood clotting.
- Migration of leukocytes.
Vasodilation
Slowing or stopping of blood flow. Margination of white blood cells to accumulate and adhere to walls white blood cells bind to adhesion molecules that act as receptors.
Loss of fluid
Due to increased capillary, permeability, and increase blood viscosity
Migration of leukocytes
Diapedesis: oozing of white blood cells through vascular walls. Attracted to chemotactic agents after bacteria. Growth has decreased neutrophils, dominate. At the end macrophages, lymphocytes, eosinophils linger to finish
Histamines
Released from mast cells, basophils, platelets. Form a endothelial contraction to stop bleeding and vasodilation to increase gaps in increase capillary permeability.
Serotonin
Released from platelets and causes vasoconstriction that is typically overridden by histamines
Platelet activating factor
Stimulated from white blood cells in cell membranes. First step of platelet activation, and aggregation of white blood cells.
Prostaglandins
Changes, vasomotor tone and is essential to the formation of a fever
Prostacyclin
Platelet inhibitor and vasodilator
Leukotrienes
Produce allergic reactions and smooth muscle vasoconstriction
Archidonic acid derivatives
Produced by cell membranes and are controlled by cortical steroid shots
Cytokines
Produced by white blood cells, are proteins that can affect themselves or adjacent cells. Induces a fever.
IL: Fever inducer
Regulates release of growth factors
Blood coagulation
Activated by cell foreign materials to make clots. Hageman factor: clotting factor number 12
Fibronectin
Form scaffolding for tissue healing and glues other cells together. Binds protein and debris, attracts chemotaxis.
Proteoglycans
Carbohydrate chains. Secreted by fibroblasts to stabilize tissue and bind to fibronectin and collagen.
Elastin
Cross-linked to formed fibrils that create elasticity
Collagen
Structural support in tensile strength. Most abundant. Four types of collagen.
Type I Collagen
Most Common bundles that make strong tissues, in mature scars. 80 to 85% of the dermis.
Type II collagen
Thin, cartilaginous tissue, that forms growth plates and nucleus pulposus
Type III collagen
Thin but strong, filaments present in skin and blood vessels. Found in newborns. Secreted by fibroblasts. First response and wound healing. 15 to 20% of dermis.
Type IV collagen
Basement membranes and acts as a filter
Growth factors
Cells induced in tissue repair release growth factors to regulate cell growth, cell differentiation, and cell migration. Determines gene expression: tissue healing or cancer.
Platelet derived growth factor
Activates fibroblast, and macrophages to speed up healing process, and form cloths
Fibroblast growth factor
Stimulates endothelial cells to prepare for wound healing
Four phases of healing
- Hemostasis and generation.
- Inflammation.
- Proliferation and migration.
- remodeling and maturation
Hemostasis and degeneration
-Takes place over the course of hours
-Stops bleeding through coagulation and growth factors to summon anti-inflammatory cells
-Brings fluid to the area to dilute substances and bring white blood cells
-Formation of a hematoma, necrosis of dead cells, beginning of inflammatory phase
Inflammation phase
-Takes place over the course of days
-Goal is to inactivate injuries, agent, breakdown, dead cells, and promote healing
-Vasodilation, capillary, permeability, and increased white blood cells
-Key components are: blood vessels, blood cells, connective, tissue, chemical, mediators, collagen, basement membrane
Proliferation and migration
-takes place over the course of weeks
-Neovascularization starts making new vascular networks
-Angiogenesis forms, new capillaries
-Granulation tissue forms
-Tissue gaps are filled by proliferation
Remodeling and maturation
-Scar tissue, reduced in remodeled to increase strength and density
1. Tissue contraction.
2. Tissue regeneration.
3. Tissue repair.
Types of cells
Permanent: cannot regenerate or divide
Labile: divide continuously
Stable: can divide with appropriate stimulus
Myofibroblasts
Fiber baths within healing tissue, that gain functional characteristics of smooth muscle cells
Regeneration
Replacement of dead parenchymal cells to restore tissue, structure and function
Repair
Cell regeneration in replacement of connective tissue
Primary intention wounds
Small scar with sutures
Secondary intention wounds
Surgical intervention not used in granulation tissue forms a large scar
Tertiary intention
Contaminated wound
Hypertrophic scar
- keloid
Too much collagen forms during healing
Glial scar
Open cyst left in areas were parenchymal cells are not present (brain)
Lung tissue repair
Basement membrane must be intact for regeneration
Digestive tract tissue repair
Cells sloff off every five days, complete turnover occurs every 3 to 4 weeks
Peripheral nerve tissue repair
Wallerian degeneration: nerve demyelination and axonal fragmentation
Can regenerate in 24 hours
Skeletal muscle tissue repair
Can regenerate new fibers or stumps of new growth
Bone tissue repair
- Inflammatory phase (two weeks), hematoma forms, and initiates Fibrin
- Repairative phase(6 to 12 weeks): granulation tissue in fibrocartilage forms a soft Calus
- Endochondral ossification (months to years): soft calluses, replaced by bony callus.
Tendon healing
- Proliferation of tenoblasts
from cut ends - Vascular in growth and proliferation of fibroblasts.
- Inflammation begins 3 to 5 days after injury and proliferative phase last 2 to 3 weeks.
-Collagen orients into thick bundles and at three weeks type three collagen is replaced by type one
Tendinopathy
Clinical conditions of pain and morphology changes
Tendinitis
Inflammation
Tendinosis
Degenerative process from chronic overload
Ligament tissue healing
Extra-articular ligaments (MCL), similar to tendons
Intra-articular ligaments (ACL) have poor healing responses
Cartilage tissue healing
Without intervention, fiberous scar tissue, fails to heal in leads to arthritis
Meniscus tissue healing
- made up of 90% type one collagen
-At birth meniscus are fully vascular, at nine months inner 1/3 is avascular, add adulthood outer 10 to 30% vascularity remains
Synovial membrane tissue healing
Intimal layer is next to joint space
Sub, intimal, layer or supportive layer is fibrous and has adipose tissue
Disc degeneration
-Blood supply restricted to outer annulus, disc pain comes from annulus
-nucleus pulposus, lacks nerve supply, more senescent cells in nucleus, lose his ability to absorb water, become stick and fibrous, fissures form, overall decreased load capacity
