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Internal Medicine > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

Pathology

A

Study of disease and it’s changes to body tissues

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2
Q

Pathogenesis

A

Cellular development of diseases and other mechanisms

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3
Q

Clinical pathology

A

Pathology apply to clinical issues. Should take into account, activity, level, participation, level of support, and environment.

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4
Q

Incidence

A

Number of new cases

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5
Q

Prevalence

A

All cases including new

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6
Q

Health

A

Physical, mental, and social well-being

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7
Q

Illness

A

Deviation from health. Perception of the feeling.

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8
Q

Disease

A

Bio medical condition resulting in malfunction of structures. Can be measured with data.

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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)

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10
Q

Chronic illness

A

Permanent impairment or disability, requiring long-term care

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11
Q

Executive functions

A

Occur in right hemisphere of brain. Making goals, plans, and maintaining behavior.

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12
Q

Behavior

A

Social behaviors affected by cognitive disability

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13
Q

Problem-solving

A

Handling new information and filtering it appropriately. Can be affected by cognitive disabilities.

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14
Q

Information processing

A

Speed. That information travels to the brain, can be affected by cognitive disability.

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15
Q

Memory

A

Failure to store, retrieve information, can be affected by cognitive disability

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16
Q

International classification of functioning disability in Health (ICF)

A

Body structures and functions, activities, participation, environment, personal factors, and health conditions

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17
Q

Theories of health and illness

A
  1. PsychoNuroimmunology: study of interactions between behavior, neural, endocrine, enteric, immune.
  2. Mitochondrial DNA disorders.
  3. Quantum model: cells communicate with energetics units and high energy can increase health
  4. Consciousness based healthcare: how you perceive your reality
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18
Q

Epigenetics

A

How biological and environmental signals can determine gene expression

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19
Q

Physical environment built

A

Surroundings supporting human activity

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20
Q

Physical environment, natural

A

Air, water, soil, sun

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21
Q

Internal environment

A

Attitudes, thoughts, feelings, believes that affect physiological function

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22
Q

External environment

A

Community, purpose in life, spiritual, beliefs, suits, etc.

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23
Q

Factors influencing health

A

Geographic, variations, socioeconomic status, health, disparities, social support, environmental barriers, cultural influences, gender, and age

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24
Q

Transnational competence

A

Teachers healthcare professionals, how to address health issues with all aspects of culture in mind

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25
Q

Cultural relativity

A

Cultural influences, and environment contribute to genetic traits an expression of diseases

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26
Q

Steroid hormones

A

Can make Changes throughout the lifespan

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27
Q

Endocrine, disrupting mechanisms

A

Can I have multigenerational effects

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28
Q

Senescence

A

Condition of growing old, cellular metabolism

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29
Q

Environmental damage theory

A

Free radicals can cause tissue damage

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30
Q

Programmed based theory

A

Presumes aging is genetically driven. Biological clock.

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31
Q

Telomerase theory of aging

A

Shortening of telomeres that maintain the integrity of chromosomes

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32
Q

Epigenetic clock

A

DNA methylation as a marker of age

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33
Q

Centenarians

A

Living to 100+

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34
Q

Supercentenarians

A

110+

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35
Q

Enteric nervous system

A

Collection of 200 to 600 mil neurons in gut. Acts as the second brain, that stores and produces neurotransmitters.

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36
Q

Pharmacology

A

The study of drugs

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37
Q

Pharmacotherapeutic

A

Do use a specific drugs to prevent treat or diagnose

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38
Q

Toxicology

A

Study of harmful effects of drugs

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39
Q

Pharmacokinetics

A

Study of how drugs are absorbed, distributed, and eliminated

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40
Q

Pharmacodynamics

A

Analysis of what drugs do to the body and how

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41
Q

Pharmacogenetics

A

Genetic basis for drug responses with variations

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42
Q

Drug approval stages

A

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

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43
Q

Orphan drugs

A

Treat rare diseases in small populations

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44
Q

Off label drugs

A

Drugs used to treat conditions different from FDA approval, legal and used frequently

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45
Q

Controlled substances

A

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)

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46
Q

Does response curve

A

Compares dose range versus effectiveness shows peak response

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47
Q

Potency

A

Lower dose to produce the same effects. How easily does it work.

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48
Q

Efficacy

A

How well does it work

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49
Q

Median effective dose

A

Ed50
half were effective

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50
Q

Median toxic dose

A

TD50
Half adverse effect

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51
Q

Therapeutic index

A

TI=TD50/ED50
Indicator for drug safety

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52
Q

Lethal dose

A

LD50
Half lethal dose in animals

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53
Q

Routes of administration of drugs

A

Enteral admission: goes through G.I. tract
Parenteral Admission: non-G.I. tract, more direct
Transdermal

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54
Q

Enteral Admission

A

G.I. tract.
Oral, sublingual/Buccal, rectal

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55
Q

Parenteral Admission

A

Non-G.I. tract
Inhalation, injection, topical

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56
Q

Transdermal

A

Through the skin, must not be graded

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57
Q

First pass effect

A

Drug does it make it to the liver and our degraded before use

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58
Q

Different kinds of injections

A

IV, intra-arterial, subcutaneous, intrathecal (sheath), intramuscular

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59
Q

Topical

A

Through skin, but not much absorption unlike transdermal

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60
Q

Bioavailability

A

Extent to which a drug reaches circulation

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61
Q

Factors affecting distribution

A

Tissue permeability, blood flow, binding to plasma proteins, finding two subcellular components

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62
Q

Volume of distribution

A

The amount of the drug administered, divided by the concentration in the blood plasma

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63
Q

Drug storage sites

A

Adipose, bone, muscles, organs

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64
Q

Biotransformation

A

Chemically altering original compound to inactivated or by excretion. Drug metabolism.

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65
Q

Ways that enzymes can break down drugs

A

Oxidation, reduction, hydrolysis, conjugation
-Smooth er

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66
Q

Organ most responsible for biotransformation

A

Liver

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67
Q

Drug excretion Methods

A

Kidneys, sweat, saliva, breastmilk

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68
Q

Clearance

A

Ability to eliminate drug
CL = Q x (ci-co)/ci

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69
Q

Half life

A

Amount of time that it takes 50% of drugs to be eliminated within the body

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70
Q

Surface membrane receptors

A

Transmembrane proteins, ion pores (acetyl choline), links directly to enzymes (insulin), linked directly to regulatory proteins (G proteins)

71
Q

Intracellular receptors

A

Alters,, DNA and protein transition

72
Q

Factors of drug receptor interactions

A

Size and shape, electrostatic attraction, affinity, efficacy

73
Q

Affinity

A

Amount of attraction with drug receptor, tendency to bond

74
Q

Efficacy

A

Amount of change of produces, how well it works

75
Q

Allosteric modulators

A

Find a specific sites to increase or decrease affinity, local, regulators, not agonist or antagonist

76
Q

Agonist

A

Find an initiate change, have efficacy and affinity

77
Q

Partial agonist

A

Don’t evoke strong response

78
Q

Inverse agonists

A

Opposite effect

79
Q

Antagonist

A

Fines to receptor, but presents no change, prevents agonist from binding, has affinity only

80
Q

Competitive antagonist

A

Vies for the same receptor as agonist

81
Q

Non-competitive antagonist

A

Strong permanent bond, “no competition if I only win”

82
Q

Mixed agonist antagonist

A

Stimulate some while blocking others

83
Q

Desensitization

A

Prolonged exposure will decrease receptor function

84
Q

Receptor down regulation

A

Decreases the number of receptors

85
Q

Beta blockers

A

-olol
Antihypertensive, antianginal, antiarrhythmic, congestive heart failure

86
Q

Calcium channel blockers

A

-ipine
Antihypertensive, antianginal

87
Q

HMG CoA. Reductase inhibitors

A

-statin
Hyper lipidemia

88
Q

Ace inhibitor

A

-pril
Antihypertensive, congestive heart failure

89
Q

Angiotensin II receptor blockers

A

-sartan
Antihypertensive, congestive heart failure

90
Q

Glucocorticoids

A

-sone
-olone
Anti-inflammatory, immuno suppressant

91
Q

Cyclooxygenase type two inhibitors

A

-coxib
Pain, inflammation

92
Q

Ischemia

A

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
Q

Bacteria

A

Release, exotoxins and endotoxins causing cell inflammation

94
Q

Viruses

A
  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
Q

Chemical factors of cell injury

A
  1. Toxic substances, injure cells directly.(Heavy metals.)
  2. Toxic substances that require metabolic transformation to become toxic(CO2)
96
Q

Free radicals

A

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
Q

Antioxidants

A

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
Q

Nitric oxide

A

Free radicals with high reactivity that causes more oxidative stress when bio availability is decreased
Helps with neural connections , and wound healing

99
Q

Genetic factors of cell injury

A

Alterations and structures or numbers of chromosomes, single mutations of genes, multiple gene mutations that the environment turns into disorders

100
Q

Mechanical factors of cell injury

A

-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
Q

Nutritional factors of cell injury

A

Kwashiorkor: protein deficiency
Marasmus: general nutritional deficiency

102
Q

Physical factors of cell injury

A

Blunt trauma, physical agents (electricity, temperature, radiation)

103
Q

Cellular aging

A

Ability of a cell to recover from injury. Mitochondria changes with age and cannot keep up with energy demands.

104
Q

Lipofuscin

A

Anti-aging pigment found in the lysosomes of old cells

105
Q

4 theories of aging

A

-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
Q

Methylation of DNA

A

Winds DNA into hisstones, acetylation is the act of unwinding DNA

107
Q

Steps of reversible sell injury

A
  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
Q

Pure Hypertrophy

A

Occurs in the heart and striated tissues

109
Q

Hyperplasia

A

Increase in number of cells. Due to hormonal stimulation or chronic and excessive simulation of some kind.

110
Q

Metaplasia

A

Change in the cell and function

111
Q

Dysplasia

A

Increase in cells with altered morphology

112
Q

Apoptosis

A

Programmed cell death that is genetically mediated, structures remain intact, cell shrinks

113
Q

Necrosis

A

Degradation of dead cells, in response to irreversible cell injury, structures are disrupted and inflamed

114
Q

Nucleus breakdown during cellular death

A

Pyknosis: clumping
Karyorrhexis: fragment (apoptosis)
Karyolysis: disillusion

115
Q

Inflammation

A

Getting rid of the cause of energy and the consequences of the energy. Redness, heat, Adema, pain.

116
Q

Chronic inflammation

A

Extensive necrosis, underlying issue, not addressed, accumulation of macrophages lymphocytes and plasma cells. Granulation tissue.

117
Q

Granulation

A

Endothelial cells seen in chronic inflammation. Highly vascularized, reddish scar.

118
Q

Effusion

A

Escape of fluid, can be exudate or transudate

119
Q

Exudation

A

Escape of fluid and protein from vasculature. High in protein.

120
Q

Transudate

A

Escape a fluid with low protein or cell components. Ultra filtrated blood from osmotic balance.

121
Q

Five types of exudation

A
  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
Q

Steps of inflammatory response

A
  1. Vasodilation
  2. Increased capillary permeability
  3. Loss of fluid.
  4. Blood clotting.
  5. Migration of leukocytes.
123
Q

Vasodilation

A

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
Q

Loss of fluid

A

Due to increased capillary, permeability, and increase blood viscosity

125
Q

Migration of leukocytes

A

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
Q

Histamines

A

Released from mast cells, basophils, platelets. Form a endothelial contraction to stop bleeding and vasodilation to increase gaps in increase capillary permeability.

127
Q

Serotonin

A

Released from platelets and causes vasoconstriction that is typically overridden by histamines

128
Q

Platelet activating factor

A

Stimulated from white blood cells in cell membranes. First step of platelet activation, and aggregation of white blood cells.

129
Q

Prostaglandins

A

Changes, vasomotor tone and is essential to the formation of a fever

130
Q

Prostacyclin

A

Platelet inhibitor and vasodilator

131
Q

Leukotrienes

A

Produce allergic reactions and smooth muscle vasoconstriction

132
Q

Archidonic acid derivatives

A

Produced by cell membranes and are controlled by cortical steroid shots

133
Q

Cytokines

A

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
Q

Blood coagulation

A

Activated by cell foreign materials to make clots. Hageman factor: clotting factor number 12

135
Q

Fibronectin

A

Form scaffolding for tissue healing and glues other cells together. Binds protein and debris, attracts chemotaxis.

136
Q

Proteoglycans

A

Carbohydrate chains. Secreted by fibroblasts to stabilize tissue and bind to fibronectin and collagen.

137
Q

Elastin

A

Cross-linked to formed fibrils that create elasticity

138
Q

Collagen

A

Structural support in tensile strength. Most abundant. Four types of collagen.

139
Q

Type I Collagen

A

Most Common bundles that make strong tissues, in mature scars. 80 to 85% of the dermis.

140
Q

Type II collagen

A

Thin, cartilaginous tissue, that forms growth plates and nucleus pulposus

141
Q

Type III collagen

A

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
Q

Type IV collagen

A

Basement membranes and acts as a filter

143
Q

Growth factors

A

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
Q

Platelet derived growth factor

A

Activates fibroblast, and macrophages to speed up healing process, and form cloths

145
Q

Fibroblast growth factor

A

Stimulates endothelial cells to prepare for wound healing

146
Q

Four phases of healing

A
  1. Hemostasis and generation.
  2. Inflammation.
  3. Proliferation and migration.
  4. remodeling and maturation
147
Q

Hemostasis and degeneration

A

-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
Q

Inflammation phase

A

-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
Q

Proliferation and migration

A

-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
Q

Remodeling and maturation

A

-Scar tissue, reduced in remodeled to increase strength and density
1. Tissue contraction.
2. Tissue regeneration.
3. Tissue repair.

151
Q

Types of cells

A

Permanent: cannot regenerate or divide
Labile: divide continuously
Stable: can divide with appropriate stimulus

152
Q

Myofibroblasts

A

Fiber baths within healing tissue, that gain functional characteristics of smooth muscle cells

153
Q

Regeneration

A

Replacement of dead parenchymal cells to restore tissue, structure and function

154
Q

Repair

A

Cell regeneration in replacement of connective tissue

155
Q

Primary intention wounds

A

Small scar with sutures

156
Q

Secondary intention wounds

A

Surgical intervention not used in granulation tissue forms a large scar

157
Q

Tertiary intention

A

Contaminated wound

158
Q

Hypertrophic scar

A
  • keloid
    Too much collagen forms during healing
159
Q

Glial scar

A

Open cyst left in areas were parenchymal cells are not present (brain)

160
Q

Lung tissue repair

A

Basement membrane must be intact for regeneration

161
Q

Digestive tract tissue repair

A

Cells sloff off every five days, complete turnover occurs every 3 to 4 weeks

162
Q

Peripheral nerve tissue repair

A

Wallerian degeneration: nerve demyelination and axonal fragmentation
Can regenerate in 24 hours

163
Q

Skeletal muscle tissue repair

A

Can regenerate new fibers or stumps of new growth

164
Q

Bone tissue repair

A
  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
Q

Tendon healing

A
  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
Q

Tendinopathy

A

Clinical conditions of pain and morphology changes

167
Q

Tendinitis

A

Inflammation

168
Q

Tendinosis

A

Degenerative process from chronic overload

169
Q

Ligament tissue healing

A

Extra-articular ligaments (MCL), similar to tendons
Intra-articular ligaments (ACL) have poor healing responses

170
Q

Cartilage tissue healing

A

Without intervention, fiberous scar tissue, fails to heal in leads to arthritis

171
Q

Meniscus tissue healing

A
  • 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
Q

Synovial membrane tissue healing

A

Intimal layer is next to joint space
Sub, intimal, layer or supportive layer is fibrous and has adipose tissue

173
Q

Disc degeneration

A

-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

Internal Medicine (4 decks)

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