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patho > exam 1 > Flashcards

exam 1 Flashcards

1
Q

healthy people 2030 social determinates of health

A

economic stability
education access and quality
healthcare access and quality
neighborhood and built environment
social and community context

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2
Q

pathophysiology

A

study of the bodys response to dysfunction or disease

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3
Q

disease

A

an interruption, cessation, or disorder of a body system or organ structure

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4
Q

aspects of disease process

A

etiology, pathogenesis, morphologic changes, clinical manifestations, diagnosis, clinical course

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5
Q

etiologic factors

A

causes of disease/risk factors
biological agents (bacteria viruses)
physical forces (trauma, burns)
chemical agents (poison, alcohol)
nutritional excesses or deficits

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6
Q

etiolgic risk factors

A

congenital conditions- genetics, environmental(maternal drug use)
acquired defects- infection, injury, hypoxia, inappropriate immune responses

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7
Q

Pathogenesis

A

sequences of cellular and tissue events that take place from time of intial contact with etiologic agent until expression of disease

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8
Q

morphology

A

fundamental stucture or form of cells or tissues

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9
Q

histology

A

study if cells of body tissues
lesion: pathologic or traumatic discontinuity of a body organ or tissue

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10
Q

clinical manifestations

A

signs (objective) and symptoms (subjective)

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11
Q

syndrome

A

compilations of signs and symptoms

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12
Q

sequalae

A

lesions or impairments that follow or are caused by disease

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13
Q

complications

A

adverse extensions of disease or outcomes of treatment

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14
Q

diagnosis

A

designation as to the cause of the health problem… interpretation of diagnostic test results (CT, x-ray, labs, biopsy)

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15
Q

specificity

A

the proportion of people without the disease who are negative (true negative)

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16
Q

sensitivity

A

people with disease who are postive (true postive)

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17
Q

reliability

A

the extent to which an observation, when repeated, gives the same result

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18
Q

validity

A

the extent to which a measurement tool measure what it is intended to measure

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19
Q

predictive value

A

the extent to whic an observation or test result is able to predict the presence of a given disease or condition

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20
Q

clinical course

A

evolution of a disease

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21
Q

acute

A

severe, self limiting

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22
Q

sub acute

A

intermediate or between acute and chronic- not as prolonged

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23
Q

chronic

A

continuous long term

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24
Q

subclinical

A

not clinically apparent

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25
Q

epidemiolgogy

A

the study of disease occurence in human populations.
how it is spread, how to control, prevent, and eliminate

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26
Q

disease case

A

either existing case or the number of new episodes of an illness

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27
Q

incidence

A

the number of new cases arising in a population during a specific time

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28
Q

prevalence

A

measure of existing disease in a given population at a given point in time

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29
Q

morbitity

A

the effects an illness has on a persons life. related to incidence, presistance, and long term

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30
Q

mortality

A

causes of death in a given population

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31
Q

cross sectional study

A

compare prevalence of disease in those exposed vs unexposed

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32
Q

case control

A

compares people with outcome of interest and those know not to have the outcome of interest

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33
Q

cohort

A

group of people who were born around the same time or share characterisitcs

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34
Q

primary prevetion

A

removing risk factors

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35
Q

secondary prevention

A

detecting disease early before symptoms

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36
Q

tertiary prevention

A

clinical interventions that prevent further deterioration or reducing complications of disease

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37
Q

cell changes related to nursing

A

stroke alert- cells dying need to act quick before they die because its irreversible

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38
Q

atrophy

A

cells decrease in size in response to decreased work load or adverse environmental conditions
-cell cannot support its metabolic requirements
-cells smaller size is more efficeint

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39
Q

causes of atrophy

A

disuse (cast), denervation, loss of endrocine stimulation, inadequate nutrition, ischemia or decreased blood flow

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40
Q

hypertrophy

A

increase in cell size leading to an increase in the amount of functioning tissue mass
-cardiac and skeletal muscle tissues
-increase in functional components of the cells to achieve equilibrium

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41
Q

physiologic hypertrophy!

A

normal stimuli ex: increase muscle mass from exercise

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42
Q

pathologic hypertrophy!

A

result of disease conditions
-adaptive or compensatory

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43
Q

hyperplasia

A

increase in number of cells, only occurring in tissues/organs that are capable of mitotic division (epithelium and glandular)

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44
Q

physiologic hyperplasia

A

normal.Hormonal or compensatory (liver regeneration)

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45
Q

non physiologic

A

benign prostatic hyperplasia

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46
Q

metaplasia

A

replacement of one cell type by another cell type- genetic reprogramming in response to chronic inflammation or irritation -substitution of cells that are better able to survive under circumstances in which a fragile cell type wouldnt

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47
Q

dysplasia

A

cells varying in size shape and organization- deranged cellular growth in a tissue- ex. cervical dysplasia

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48
Q

intracellular accumulations

A

buildup of substances that cells canot immediately use or eliminate ex jaundice

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49
Q

Tay-sachs disease

A

lysosomal storage disease (intracellular accumulation)

50
Q

causes of cell injury and death

A

physical agents, radiation, chemicals, biologic, nutritional

51
Q

free radicals

A

highly reactive chemical species that establish chain reactions that generate free radicals- damanges cell memabranes, tissues, and DNA

52
Q

reactive oxygen species

A

oxygen containing molecules produced endongenously by normal metabolic processes (UV/radiation)

53
Q

oxidative stress

A

occurs when generation of ROS exceeds the ability of the body to neutralize and eliminate ROS (cancer, CVD)

54
Q

hypoxic cell injury!

A

deprives the cell of oxygen
-interrupts generation of ATP causing failure in the cell
-blood cannot deliver enough oxygen to cells
-brain cells die within 4-6 min without oxygen

55
Q

ischemia(decreased blood flow)

A

impaired oxygen delivery and impaired removal of metabolic products such as lactic acid

56
Q

reversible cell injury ?

A

mechanism of cell injury produce sublethal and reversible damange

57
Q

apoptosis (form of cell death)

A

removal of injured or worn out cells
-genetically programmed degeneraative change that results in cell death
-parkinsons and alzheimers

58
Q

necrosis (form of cell death)

A

cell death in an organ or tissue
-causes loss of cell membrane integrity and triggers inflammatory response
-interferes with cell replacement and tissue degeneration

59
Q

extrinsic pathway

A

pathway of apotosis
activation of tumor necrosis factor receptors leading to the formation of death initiating complexes

60
Q

intrinsic pathway

A

pathway of apoptosis
activated by DNA damage, ROS, hypoxia, decreased ATP, activation of p53 protein

61
Q

liquefaction necrosis

A

cells begin to liquefy

62
Q

coagulation necrosis

A

transforms to gray firm mass

63
Q

caseous necrosis

A

cheesy material by infiltration of fatlike subtances (center of TB granulomas)

64
Q

gangrene

A

when a larger mass of tissue dies
-dry: shrinks, brown, line of demarcation
wet: cold, pulseless, moist, black, line of demarcation

65
Q

gas gangrene

A

results from infection (Clostridium bacteria)
usually occurs in open wounds with debris
bubbles of hydrogen sulfide gas in muscle

66
Q

stress response

A

interactions require that homeostasis be maintained during changes that occur in the internal and external environments
requires feedback controls systems that reulates cellular function by mediating the physical, emotional, and behavioral reactions to stressors

67
Q

feedback systems

A

negative- most common, functions like thermostat
postive- interject instability rather than stability

68
Q

control systems: sensor

A

detects the change

69
Q

control systems: integrator

A

sums all incoming data and compares with normal

70
Q

control systems: effectors

A

attempts to reverse the damage

71
Q

Hans Selye: Alarm Stage

A

stimulation of the SNS and HPA axis
catecholamines and cortisol released (flight or flight)

72
Q

resistance stage

A

body selects the most effective channel of defense
cortisol levels drop

73
Q

exhaustion stage

A

resources are depleted
wear and tear
systemic damage

74
Q

Selyes stress response theory

A

describes the positive and negative stressors
coping mechanisms are the emotional and behavioral responses to manage threats to physiological and psychological homeostasis— due to conditioning internal and external factors

75
Q

neuroendocrine response: catecholamines

A

norepinephrine, epinephrine
-increase HR, cardiac contactility, relaxatio of bronchial smooth muscle
-decreased insulin release (so there is more glucose for energy)

76
Q

neuroendocrine response: corticotropin-releasing factor

A

stimulates ACTH release from the anterior pituitary
cortisol- attempts to inhibit the stress response, maintains blood glucose level

77
Q

adrenocorticotropic hormone (ACTH)

A

stimulates the synthesis and release of cortisol

78
Q

neuroendocrine response: Minrealcorticoid

A

aldosterone
increases sodium absorption by the kidney

79
Q

neuroendocrin response: antidiuretic hormone

A

vasoperssin, ADH
increases water absorption, produces vasoconstriction

80
Q

neuroendocrine response: Angiotensin 2

A

stimulates sympathetic nervous system
activates RAAS- renal retention of water and sodium

81
Q

SNS manifestation of stress

A

flight of fight response
increased HR and RR
decreased peripheral circulation, cold and clammy
pupils DILATE
dry mouth
decreased blood flow to GI and GU systems

82
Q

allostasis

A

cumulative effects of chronic stress on health
prolonged stress and release of hormones like cortisol lead to negative effects on immune, CV, and metabolic processses
-inflammation, hypertension, hyperglycemia
-!!! increases allostati load contributes to health disparities in marginalized communities

83
Q

physiologic reserve

A

the ability of the body systems to incresae their function given the need to adapt

84
Q

anatomic reserve

A

paired organs that are not needed to ensure the continued existence and maintenance of the internal environment

85
Q

Time affecting ability to adapt

A

adaptation is most efficient when changes occur gradually rather than suddenly (rapid changes can lead to shock)

86
Q

genetics affecting ability to adapt

A

genes that cause disease may have adaptive properties (ex: sex- differences in CV and respiratory function)

87
Q

health status affecting ability to adapt

A

physicla and mental health plays role in physiologic and psychologic reserves

88
Q

circadian rhythm

A

sleep is restorative- shift work disorder

89
Q

effects of acute stress

A

alertness, vigilance, cognition, focused attention, appropriate aggression
-life threatening trauma- diverts blood from less essential organs to more

90
Q

stress induced health problems

A

obesity, immune disorders, diabetes, eating/sleeping disorders, anxiety, depression, ptsd, atherosclerosis, hypertension

91
Q

PTSD

A

chronic activation of the stress repsonse as a result of experiencing a potential life treatening event

92
Q

characteristics of ptsd: intrusion

A

occurrence of flashbacks

93
Q

characteristics of ptsd: avoidance

A

emotional numbing that accompanies this disorder and disrupts important personal traits

94
Q

characteristics of ptsd: alteration in cognition and mood

A

encompasses negative thoughts and feelings, distorted beliefs about self and others

95
Q

characteristics of ptsd: alteration in arousal and reactivity

A

presence of increased irritability, difficulty concentration, an exaggerated startle reflez, and increase vigilanc and concern over safety

96
Q

studying physiologic manifestations of stress

A

ECG, blood pressure, physical exam

97
Q

inflammation (-itis)

A

a wide variety of physiologic and pathoglic responses intended to eliminate the initial cause of cell injury, remove damaged tissue, generate new tissue

98
Q

inflammatory response

A

reaction of vascularized tissues to injury (endothelial hyperpermeability(leaking of fluid))
-inflammation localized and eliminate microbes foreign particles and abnormal cells

99
Q

inflammatory mediators

A

tumor necrosis factor, vascular endothelial growth factors (VEGF) allows new growth, neutrophils, movement of fluid within cells or interstitial fluid

100
Q

cardinal signs of inflammation

A

rubor (redness), tumor (swelling), calor (heat), dolor (pain), functio laesa (loss of function)

101
Q

acute inflammation

A

characterized by exudation of fluid of fluid and plasma, emigration of leukocytes into tissues
-appears within minutes to hours
-occurs before adapative immunity is established

102
Q

causes of inflammation

A

infections, trauma, immune reactions, physical agents, chemical agents, tissue necrosis

103
Q

cells of inflammation: endothelial cells

A

barrier between circulating blood in vessels and surrounding tissues
-produce antiplatlet and antithrombotic agents
-maintain vessel patency
-vasodilators and vasoconstictors which regulate blood flow

104
Q

cells of inflammation:platelets

A

to stop bleeding (plug)
involved in hemostasis
releases potent inflammatory mediators increasing vascular permeability

105
Q

cells of inflammation: neutrophils, monocytes, macrophages

A

neutrophils arrive within 90 minutes
monocytes and macrophages produce potent vasoactive mediators- they get rid of microorganisms (pac man)

106
Q

cells of inflammation: eosinophils

A

parasitic infections, allergic reactions

107
Q

cells of inflammation: basophils

A

contain histamine- binding of IgE triggers release of histamine

108
Q

cells of inflammation: mast cells

A

degranulation releases histamine, TNF (hypotension, tachycardia, associated with sepsis), Il-16

109
Q

vascular phase

A

vasodilation induced by histamine and nitric oxide mediators
erythema, warmth, edema

110
Q

cellular stage

A

leukocyte accumulation to endothelium
chemotaxis: chemokines direct trafficking of leukocytes
phagocytosis

111
Q

inflammatory mediator: histamine

A

found in mast and basophil cells, involved IgE antibodies, causes dilation of vessels, sneezing, watery eyes, increases permeabiltiy

112
Q

inflammatory mediator: arachidonic acid metabolites

A

release of AA leads to production of prostaglandins, induce inflammation, potentiate effects histamine, promote platelet aggregation

113
Q

inflammatory mediator: platelet activating factor

A

induces platelet aggregation, causes bronchospasms, wheal and flare effect

114
Q

plasma proteins

A

clotting, complement and kinin systems

115
Q

cytokines

A

TNF, IL-1 released in response to bacterial toxins, endotoxins, dropBP

116
Q

nitric oxide and free radicals

A

no smooth muscle relaxation, hydrogen peroxide

117
Q

serous exudates

A

watery fluids, result from plasma entering the inflammatory site

118
Q

hemorrhagic exudates

A

severe tissue injury causes damages to blood vessels/significant leakage of red cells from capillaries

119
Q

membranous or pseudomembranous exudates

A

develop on mucous membrane surfaces

120
Q

purulent or suppurative exudates

A

contains pus- composed of degraded WBCs protiens and tissue debris

121
Q

fibrinous exudates

A

contain large amounts of fibrinogen and form a thick sticky meshwork

122
Q
A

patho (5 decks)

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