Unit 1 Flashcards
1
Q
Pathology
A
Study of disease and it’s changes to body tissues
2
Q
Pathogenesis
A
Cellular development of diseases and other mechanisms
3
Q
Clinical pathology
A
Pathology apply to clinical issues. Should take into account, activity, level, participation, level of support, and environment.
4
Q
Incidence
A
Number of new cases
5
Q
Prevalence
A
All cases including new
6
Q
Health
A
Physical, mental, and social well-being
7
Q
Illness
A
Deviation from health. Perception of the feeling.
8
Q
Disease
A
Bio medical condition resulting in malfunction of structures. Can be measured with data.
9
Q
Acute illness
A
Rapid or short duration of disease.
1. Stage one: physical symptoms
2. Stage two: cognitive awareness.
3. Stage three: emotional response (denial, fear, anxiety)
10
Q
Chronic illness
A
Permanent impairment or disability, requiring long-term care
11
Q
Executive functions
A
Occur in right hemisphere of brain. Making goals, plans, and maintaining behavior.
12
Q
Behavior
A
Social behaviors affected by cognitive disability
13
Q
Problem-solving
A
Handling new information and filtering it appropriately. Can be affected by cognitive disabilities.
14
Q
Information processing
A
Speed. That information travels to the brain, can be affected by cognitive disability.
15
Q
Memory
A
Failure to store, retrieve information, can be affected by cognitive disability
16
Q
International classification of functioning disability in Health (ICF)
A
Body structures and functions, activities, participation, environment, personal factors, and health conditions
17
Q
Theories of health and illness
A
- 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
18
Q
Epigenetics
A
How biological and environmental signals can determine gene expression
19
Q
Physical environment built
A
Surroundings supporting human activity
20
Q
Physical environment, natural
A
Air, water, soil, sun
21
Q
Internal environment
A
Attitudes, thoughts, feelings, believes that affect physiological function
22
Q
External environment
A
Community, purpose in life, spiritual, beliefs, suits, etc.
23
Q
Factors influencing health
A
Geographic, variations, socioeconomic status, health, disparities, social support, environmental barriers, cultural influences, gender, and age
24
Q
Transnational competence
A
Teachers healthcare professionals, how to address health issues with all aspects of culture in mind
25
Cultural relativity
Cultural influences, and environment contribute to genetic traits an expression of diseases
26
Steroid hormones
Can make Changes throughout the lifespan
27
Endocrine, disrupting mechanisms
Can I have multigenerational effects
28
Senescence
Condition of growing old, cellular metabolism
29
Environmental damage theory
Free radicals can cause tissue damage
30
Programmed based theory
Presumes aging is genetically driven. Biological clock.
31
Telomerase theory of aging
Shortening of telomeres that maintain the integrity of chromosomes
32
Epigenetic clock
DNA methylation as a marker of age
33
Centenarians
Living to 100+
34
Supercentenarians
110+
35
Enteric nervous system
Collection of 200 to 600 mil neurons in gut. Acts as the second brain, that stores and produces neurotransmitters.
36
Pharmacology
The study of drugs
37
Pharmacotherapeutic
Do use a specific drugs to prevent treat or diagnose
38
Toxicology
Study of harmful effects of drugs
39
Pharmacokinetics
Study of how drugs are absorbed, distributed, and eliminated
40
Pharmacodynamics
Analysis of what drugs do to the body and how
41
Pharmacogenetics
Genetic basis for drug responses with variations
42
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
43
Orphan drugs
Treat rare diseases in small populations
44
Off label drugs
Drugs used to treat conditions different from FDA approval, legal and used frequently
45
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)
46
Does response curve
Compares dose range versus effectiveness shows peak response
47
Potency
Lower dose to produce the same effects. How easily does it work.
48
Efficacy
How well does it work
49
Median effective dose
Ed50
half were effective
50
Median toxic dose
TD50
Half adverse effect
51
Therapeutic index
TI=TD50/ED50
Indicator for drug safety
52
Lethal dose
LD50
Half lethal dose in animals
53
Routes of administration of drugs
Enteral admission: goes through G.I. tract
Parenteral Admission: non-G.I. tract, more direct
Transdermal
54
Enteral Admission
G.I. tract.
Oral, sublingual/Buccal, rectal
55
Parenteral Admission
Non-G.I. tract
Inhalation, injection, topical
56
Transdermal
Through the skin, must not be graded
57
First pass effect
Drug does it make it to the liver and our degraded before use
58
Different kinds of injections
IV, intra-arterial, subcutaneous, intrathecal (sheath), intramuscular
59
Topical
Through skin, but not much absorption unlike transdermal
60
Bioavailability
Extent to which a drug reaches circulation
61
Factors affecting distribution
Tissue permeability, blood flow, binding to plasma proteins, finding two subcellular components
62
Volume of distribution
The amount of the drug administered, divided by the concentration in the blood plasma
63
Drug storage sites
Adipose, bone, muscles, organs
64
Biotransformation
Chemically altering original compound to inactivated or by excretion. Drug metabolism.
65
Ways that enzymes can break down drugs
Oxidation, reduction, hydrolysis, conjugation
-Smooth er
66
Organ most responsible for biotransformation
Liver
67
Drug excretion Methods
Kidneys, sweat, saliva, breastmilk
68
Clearance
Ability to eliminate drug
CL = Q x (ci-co)/ci
69
Half life
Amount of time that it takes 50% of drugs to be eliminated within the body
70
Surface membrane receptors
Transmembrane proteins, ion pores (acetyl choline), links directly to enzymes (insulin), linked directly to regulatory proteins (G proteins)
71
Intracellular receptors
Alters,, DNA and protein transition
72
Factors of drug receptor interactions
Size and shape, electrostatic attraction, affinity, efficacy
73
Affinity
Amount of attraction with drug receptor, tendency to bond
74
Efficacy
Amount of change of produces, how well it works
75
Allosteric modulators
Find a specific sites to increase or decrease affinity, local, regulators, not agonist or antagonist
76
Agonist
Find an initiate change, have efficacy and affinity
77
Partial agonist
Don’t evoke strong response
78
Inverse agonists
Opposite effect
79
Antagonist
Fines to receptor, but presents no change, prevents agonist from binding, has affinity only
80
Competitive antagonist
Vies for the same receptor as agonist
81
Non-competitive antagonist
Strong permanent bond, “no competition if I only win”
82
Mixed agonist antagonist
Stimulate some while blocking others
83
Desensitization
Prolonged exposure will decrease receptor function
84
Receptor down regulation
Decreases the number of receptors
85
Beta blockers
-olol
Antihypertensive, antianginal, antiarrhythmic, congestive heart failure
86
Calcium channel blockers
-ipine
Antihypertensive, antianginal
87
HMG CoA. Reductase inhibitors
-statin
Hyper lipidemia
88
Ace inhibitor
-pril
Antihypertensive, congestive heart failure
89
Angiotensin II receptor blockers
-sartan
Antihypertensive, congestive heart failure
90
Glucocorticoids
-sone
-olone
Anti-inflammatory, immuno suppressant
91
Cyclooxygenase type two inhibitors
-coxib
Pain, inflammation
92
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
93
Bacteria
Release, exotoxins and endotoxins causing cell inflammation
94
Viruses
1. Kill from within by disrupting cellular processes.
2. Code proteins to alter permeability of cell membrane.
3. DNA viruses integrate themselves into cellular genome and produce foreign proteins to destroy immune system.
95
Chemical factors of cell injury
1. Toxic substances, injure cells directly.(Heavy metals.)
2. Toxic substances that require metabolic transformation to become toxic(CO2)
96
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
97
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
98
Nitric oxide
Free radicals with high reactivity that causes more oxidative stress when bio availability is decreased
Helps with neural connections , and wound healing
99
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
100
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
101
Nutritional factors of cell injury
Kwashiorkor: protein deficiency
Marasmus: general nutritional deficiency
102
Physical factors of cell injury
Blunt trauma, physical agents (electricity, temperature, radiation)
103
Cellular aging
Ability of a cell to recover from injury. Mitochondria changes with age and cannot keep up with energy demands.
104
Lipofuscin
Anti-aging pigment found in the lysosomes of old cells
105
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
106
Methylation of DNA
Winds DNA into hisstones, acetylation is the act of unwinding DNA
107
Steps of reversible sell injury
1. Injury occurs in homeostasis is impaired, leading to an influx of sodium in calcium in the cell.
2. The cell begins to swell.
3. Mitochondria are impaired, increasing lactic acid, metabolism, and decreasing the pH.
4. Decreased proteins synthesis due to decrease of ribosomes from rough ER.
108
Pure Hypertrophy
Occurs in the heart and striated tissues
109
Hyperplasia
Increase in number of cells. Due to hormonal stimulation or chronic and excessive simulation of some kind.
110
Metaplasia
Change in the cell and function
111
Dysplasia
Increase in cells with altered morphology
112
Apoptosis
Programmed cell death that is genetically mediated, structures remain intact, cell shrinks
113
Necrosis
Degradation of dead cells, in response to irreversible cell injury, structures are disrupted and inflamed
114
Nucleus breakdown during cellular death
Pyknosis: clumping
Karyorrhexis: fragment (apoptosis)
Karyolysis: disillusion
115
Inflammation
Getting rid of the cause of energy and the consequences of the energy. Redness, heat, Adema, pain.
116
Chronic inflammation
Extensive necrosis, underlying issue, not addressed, accumulation of macrophages lymphocytes and plasma cells. Granulation tissue.
117
Granulation
Endothelial cells seen in chronic inflammation. Highly vascularized, reddish scar.
118
Effusion
Escape of fluid, can be exudate or transudate
119
Exudation
Escape of fluid and protein from vasculature. High in protein.
120
Transudate
Escape a fluid with low protein or cell components. Ultra filtrated blood from osmotic balance.
121
Five types of exudation
1. Hemorrhagic sanguinous: bright, red from trauma
2. Serosanguineous: blood tinged, or pink. 2 to 3 days after injury.
3. Serous: thin and yellowish. Contains proteins.
4. Purulent: viscous in cloudy with pus.
5. Catarrhal: thin and clear mucus. Occurs and mucous membranes.
122
Steps of inflammatory response
1. Vasodilation
2. Increased capillary permeability
3. Loss of fluid.
4. Blood clotting.
5. Migration of leukocytes.
123
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.
124
Loss of fluid
Due to increased capillary, permeability, and increase blood viscosity
125
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
126
Histamines
Released from mast cells, basophils, platelets. Form a endothelial contraction to stop bleeding and vasodilation to increase gaps in increase capillary permeability.
127
Serotonin
Released from platelets and causes vasoconstriction that is typically overridden by histamines
128
Platelet activating factor
Stimulated from white blood cells in cell membranes. First step of platelet activation, and aggregation of white blood cells.
129
Prostaglandins
Changes, vasomotor tone and is essential to the formation of a fever
130
Prostacyclin
Platelet inhibitor and vasodilator
131
Leukotrienes
Produce allergic reactions and smooth muscle vasoconstriction
132
Archidonic acid derivatives
Produced by cell membranes and are controlled by cortical steroid shots
133
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
134
Blood coagulation
Activated by cell foreign materials to make clots. Hageman factor: clotting factor number 12
135
Fibronectin
Form scaffolding for tissue healing and glues other cells together. Binds protein and debris, attracts chemotaxis.
136
Proteoglycans
Carbohydrate chains. Secreted by fibroblasts to stabilize tissue and bind to fibronectin and collagen.
137
Elastin
Cross-linked to formed fibrils that create elasticity
138
Collagen
Structural support in tensile strength. Most abundant. Four types of collagen.
139
Type I Collagen
Most Common bundles that make strong tissues, in mature scars. 80 to 85% of the dermis.
140
Type II collagen
Thin, cartilaginous tissue, that forms growth plates and nucleus pulposus
141
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.
142
Type IV collagen
Basement membranes and acts as a filter
143
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.
144
Platelet derived growth factor
Activates fibroblast, and macrophages to speed up healing process, and form cloths
145
Fibroblast growth factor
Stimulates endothelial cells to prepare for wound healing
146
Four phases of healing
1. Hemostasis and generation.
2. Inflammation.
3. Proliferation and migration.
4. remodeling and maturation
147
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
148
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
149
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
150
Remodeling and maturation
-Scar tissue, reduced in remodeled to increase strength and density
1. Tissue contraction.
2. Tissue regeneration.
3. Tissue repair.
151
Types of cells
Permanent: cannot regenerate or divide
Labile: divide continuously
Stable: can divide with appropriate stimulus
152
Myofibroblasts
Fiber baths within healing tissue, that gain functional characteristics of smooth muscle cells
153
Regeneration
Replacement of dead parenchymal cells to restore tissue, structure and function
154
Repair
Cell regeneration in replacement of connective tissue
155
Primary intention wounds
Small scar with sutures
156
Secondary intention wounds
Surgical intervention not used in granulation tissue forms a large scar
157
Tertiary intention
Contaminated wound
158
Hypertrophic scar
- keloid
Too much collagen forms during healing
159
Glial scar
Open cyst left in areas were parenchymal cells are not present (brain)
160
Lung tissue repair
Basement membrane must be intact for regeneration
161
Digestive tract tissue repair
Cells sloff off every five days, complete turnover occurs every 3 to 4 weeks
162
Peripheral nerve tissue repair
Wallerian degeneration: nerve demyelination and axonal fragmentation
Can regenerate in 24 hours
163
Skeletal muscle tissue repair
Can regenerate new fibers or stumps of new growth
164
Bone tissue repair
1. Inflammatory phase (two weeks), hematoma forms, and initiates Fibrin
2. Repairative phase(6 to 12 weeks): granulation tissue in fibrocartilage forms a soft Calus
3. Endochondral ossification (months to years): soft calluses, replaced by bony callus.
165
Tendon healing
1. Proliferation of tenoblasts
from cut ends
2. 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
166
Tendinopathy
Clinical conditions of pain and morphology changes
167
Tendinitis
Inflammation
168
Tendinosis
Degenerative process from chronic overload
169
Ligament tissue healing
Extra-articular ligaments (MCL), similar to tendons
Intra-articular ligaments (ACL) have poor healing responses
170
Cartilage tissue healing
Without intervention, fiberous scar tissue, fails to heal in leads to arthritis
171
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
172
Synovial membrane tissue healing
Intimal layer is next to joint space
Sub, intimal, layer or supportive layer is fibrous and has adipose tissue
173
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
