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Pathophysiology > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

What is meant by altered cellular tissue

A

not normal or abnormal but changed

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2
Q

Disease

A

Anything outside of normal (the failure to maintain homeostatic conditions)

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3
Q

What is meant by idea conditions?

A

An average of the normal range

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4
Q

Homeostasis

A

maintenance of a relatively constant range of environment within the body

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5
Q

If homeostatic mechanisms cannot cope with a particular stress what happens?

A

physiologic values will drift outside the normal range

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6
Q

Stress

A

non-specific response of the body to any demand placed on it

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7
Q

Stressor

A

agent responsible for producing stress

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8
Q

Distress

A

harmful or unpleasant stress

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9
Q

Eustress

A

positive events that stimulate growth

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10
Q

Stress forms

A

may come in small, chronic doses; single, sudden large doses; or somewhere in between

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11
Q

Responses to stress

A
  • specific homeostatic adjustments

- General Adaptation Syndrome

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12
Q

General Adaptation Syndrome

A
  • Alarm phase
  • Resistance phase
  • Exhaustion phase
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13
Q

Alarm phase

A
  • immediate response
  • directed by SNS
  • energy reserves are mobilized
  • “fight or flight” responses
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14
Q

Dominant hormone in alarm phase

A

epinephrine (o adrenaline)

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15
Q

Supporting hormones in alarm phase

A

renin & ADH, glucocorticoids (control glucose in the brain levels)

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16
Q

Resistance phase

A
  • either from emergency or build up of things in life
  • occurs when stress lasts longer than a few hours
  • mobilize lipid and protein reserves to conserve glucose for neural tissues
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17
Q

Resistance phase dominant hormone

A

glucocorticoids

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18
Q

Supporting hormones in resistance phase

A

Thyroid, ADH, renin, GH, epinephrine (supporting hormones control metabolism, retain H2O, and synthesize proteins (GH))

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19
Q

Goals of resistance phase

A
  • mobilize lipid and protein reserves
  • conservation of glucose for neural tissues
  • elevation of blood glucose concentrations
  • conservation of salts and water
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20
Q

Problems with resistance phase

A
  • glucocorticoids: anti-inflammatory; suppresses healing & immune system
  • conservation of fluid: -> high BP -> stress for L heart, gain of Na+ leads to loss of K+
  • depletion of lipid reserves: tear down structural proteins
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21
Q

Exhaustion Phase

A
  • collapse of vital systems
  • causes: exhaust of lipid reserves, inability to produce glucocorticoids, failure of electrolyte balance, cumulative structural or functional damage to vital organs
  • unless corrective actions are taken almost immediately, the failure of one or more systems will prove fatal
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22
Q

Stress related disorders

A
  • Hypertension (renin/ADH)
  • Ulcers (prostaglandins)
  • skin disorders
  • cardiovascular disease
  • migrane headaches
  • eating disorders
  • anxiety
  • arrhythmias
  • asthma
  • cancer (immunosurveillance)
  • alcoholism
  • drug abuse
  • endocrine disorders
  • GI disorders
  • muscular tension
  • sleep difficulty
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23
Q

Etiology

A

the initial cause of disease (what started everything)

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24
Q

Pathogenesis

A

Sequence of events in the development of disease (the story)

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25
Q

Pathophysiology

A

Study of functional and structural changes caused by disease

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26
Q

Types of etiologies

A
  • inherited
  • congenital
  • acquired
  • multifactorial
  • idiopathic
  • iatrogenic
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27
Q

Inherited

A

Due to a genetic defect

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28
Q

Congenital

A

present at birth

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29
Q

acquired

A

developed during lifetime

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30
Q

multifactorial

A

more than one factor

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31
Q

idiopathic

A

no understood cause

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32
Q

iatrogenic

A

treatment-induced

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33
Q

Intrinsic Etiologies

A

From within the body itself

  • degenerative
  • immunologic
  • metabolic
  • nutritional
  • psychogenic
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34
Q

degenerative

A

progressive loss of normal structure and function

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35
Q

immunologic

A

abnormal immune response (allergies)

36
Q

metabolic

A

abnormal body chemistry

37
Q

nutritional

A

abnormal dietary intake or nutrient use (something inside of the body differs from one person to another)

38
Q

psychogenic

A

related to psychological state

39
Q

Extrinsic Etiologies

A

From the environment

  • Infectious
  • trauma
  • hypoxia
  • chemicals, drugs, toxins
  • environmental agents
40
Q

Infectious

A

due to a microorganism (bacterial, viral, fungal) or parasite (internal-tapeworm or external-lice, ticks)

41
Q

hypoxia

A

insufficient oxygen

42
Q

environmental agents

A
  • temperature or atmospheric pressure
  • radiation
  • electrical
43
Q

Cellular Adaptations

A
  • adapted cells are neither normal or abnormal, they are stressed
  • reversibile is stressor is removed
  • often only temporarily successful
  • may lead to cell injury or death
44
Q

Cellular injury

A
  • reversible (may recover)
  • irreversible (will die)
  • the cell is unable to maintain homeostasis above or below normal range
  • macromolecules, enzymes, and organelles within the cell are closely interdependent
  • difficult to distinguish between the primary target of injury from any secondary or ripple effect
  • the precise cut-off point between reversible and irreversible is often difficult to determine.
45
Q

Dysplasia

A
  • is not an adaptation it is ALWAYS abnormal = pre-cancerous
  • an abnormal change in the size shape, and arrangement of mature cells in response to a stimulus
  • often called atypical hyperplasia
  • dysplasia may be reversible if the stimulus is discontinued
  • if the stimulus persists, it may progress to neoplasia (benign or malignant growth)
  • examples: cervix, breast
46
Q

Atrophy

A

shrinkage in cell size by loss of cell substance

-these cells have diminished function

47
Q

Causes of cell atrophy:

A
  • decreased workload
  • loss of innervation
  • diminished blood supply
  • inadequate nutrition
  • loss of endocrine stimulation
  • aging
  • brain can atrophy
48
Q

Hypertrophy

A

Increase in the size of individual cells

  • no new cells, just larger ones
  • not swollen by fluid, but by increased synthesis of structural proteins and organelles
  • these cells have improved function
  • a limit is reached beyond which more enlargement is no longer helpful
49
Q

Hypertrophy caused by?

A
  • increased functional demand

- specific hormonal stimulation

50
Q

Hypertrophy examples

A

-skeletal muscle and cardiac muscle

51
Q

Hyperplasia

A

An increase in the number of individual cells in an organ or tissue
-process remains controlled

52
Q

3 cell types that are unable to undergo hyperplasia

A

neural, skeletal m., and cardiac m.

53
Q

Types of hyperplasia

A
  • compensatory hyperplasia: one kidney example
  • hormonal hyperplasia: breasts enlarge with hormones
  • pathogenic hyperplasia: problem
54
Q

Metaplasia

A

the reversible replacement of one cell type by another in response to a particular stress or stimuli

  • an orderly arrangement of the new cell type is found
  • example: cigarette smokers
  • if stressor continues, may progress to dysplasia
55
Q

cellular response to injury depends on?

A
  • type of injury
  • duration of the injury (makes a difference)
  • severity of the injury
56
Q

Consequences of injury depend on?

A
  • type of cell injured (different cells have different abilities to heal)
  • the cell’s current health status
  • the cell’s adaptability (regenerative ability)
57
Q

Descriptions of disease for how bad it is

A
  • peracute (super-fast onset)
  • acute (today)
  • subacute (a little longer)
  • chronic (over a longer time period)
58
Q

Descriptions of disease for where it is

A
  • focal or localized (one area)
  • multifocal (several areas)
  • systemic or generalized (over whole body or in entire system)
59
Q

General mechanisms of cell injury

A
  • hypoxia injury ( cells don’t have enough O2)
  • Free radicals and reactive oxygen species
  • chemical injury
  • tissue trauma
60
Q

Reperfusion injury

A

oxygen restored to ischemic tissue -> generation of free radicals

61
Q

Free radicals

A
  • unstable unpaired electrons: “activated oxygen species”
  • they come from UV light, X-rays, oxidative rxns, normal metabolism
  • they cause injury by lipid peroxidation, fragmentation of polypeptide chains and alteration of DNA
  • we can decrease damage of this by using antioxidants (vitamin C, E)
62
Q

Chemical injury

A
  • toxic chemical agents can injure cell membranes and cell structures, clock enzymic pathways, coagulate cell proteins, and disrupt osmotic and ionic balance
  • carbon tetrachloride (can cause liver damage)
  • carbon monoxide (it loves hemoglobin, no O2 carried)
  • alcohol (ethanol -> aldehydes cause damage)
63
Q

Traumatic tissue injury

A
  • blunt force
  • contusion (bruise)
  • hematoma (blood clot)
  • abrasion (scrape)
  • laceration (cut)
  • stab wound - deeper than it is long
  • incision- longer than it is deep
  • Avulsion (degloving inj.)
  • gunshot wound (speed)
  • Asphyxiation (air not going to lungs)
  • suffocation (nose and mouth)
  • strangulation (trachea)
  • drowning (lungs fill with H2O)
64
Q

Anoxia

A

a complete lack of oxygen

65
Q

Hypoxia

A

a lack of sufficient oxygen supply to the tissues

66
Q

ischemia

A

inadequate blood flow in the tissues

67
Q

Hypoxia can result from

A
  • decreased amount of oxygen in air
  • diseases of lungs or heart
  • lack of RBCs/anemia (decreased production of RBCs or increased loss of RBCs)
  • inadequate or dysfunctional hemoglobin
  • ischemia
68
Q

Effects of hypoxia

A
  • decreased ATP production
  • mitochondria needs O2 to make ATP
  • lactic acid and is less efficient
69
Q

ATP depletion leads to

A
  • increased anaerobic glycolysis: problem is that it’s much less efficient (36 ATP vs. 2 ATP), lactic acid -> acidosis
  • leads to myocardial infarction
  • failure of the potassium pump: sodium accumulates in the cell, potassium diffuses out of the cell, and the net gain in sodium results in an osmotic gain of H2O
  • acute cellular swelling results (not the same as hypertrophy)
70
Q

Acute cellular swelling

A
  • cellular swelling causes:
  • dilation of the endoplasmic reticulum (ribosomes pop off/detach)
  • lysosomal swelling leads to leakage of lysosomal enzymes
  • if severe, can cause mitochondria to swell. Can’t do Kreb’s cycle
71
Q

Reversible cell inury

A
  • if injury is mild or short-lived
  • ATP production must be restored to reestablish O2
  • cell recovers by pumping out the water
  • cell reverts from state of acute cellular swelling to the original steady state
  • must take place before mitochondrial and membrane damage occurs
72
Q

Mechanisms of irreversible injury

A
  • inability to reverse mitochondrial dysfunction
  • cell membrane damage: increased permeability of membrane, loss of volume regulation, massive calcium influx (activated proteases, phospholipases, ATPases, Ca++ goes to mitochondria), and loss of proteins, essential coenzymes, and ribonucleic acids
  • clinical: liver cells die and liver enzymes get into blood and same with any enzyme not normally found in the blood
73
Q

Necrosis

A

changes that follow cell death in living tissue (often due to hypoxia)

74
Q

Apoptosis

A

programmed cell death that occurs normally in developing and adult tissues

75
Q

Autolysis

A

postmortem dissolution and disintegration of cells or tissues by the enzymes present in those tissues

76
Q

Types of necrosis

A
  • coagulative
  • liquefactive
  • caseous
  • fat
77
Q

coagulative necrosis

A
  • protein denaturation (coagulation)
  • kidneys, heart
  • often due to hypoxia
78
Q

Liquefactive necrosis

A
  • solid tissue is dissolved into fluid by hydrolyses
  • brain: neural and glial cells
  • often due to hypoxia
79
Q

caseous necrosis

A
  • combination of coagulative and liquefactive

- dead cells disintegrate, but the debris is not complete digested (tuberculosis)

80
Q

fat necrosis

A
  • lipases degrade triglycerides

- free fatty acids combine with calcium ions to form soaps (pancreas, and breast tissue)

81
Q

Gangrene

A

necrosis + bacterial infection

  • wet gangrene
  • dry gangrene
  • gas gangrene
82
Q

wet gangrene

A

-neutrophils invade necrotic site causing secondary liquefaction

83
Q

dry gangrene

A

area of coagulative necrosis becomes dried out, wrinkled, and dark black (likely diabetics since they have poor circulation)

84
Q

gas gangrene

A

infection of necrotic tissue by clostridium species

85
Q

pathologic calcification

A
  • dystrophic calcification

- metastatic calcification

86
Q

dystrophic calcification

A
  • deposition of calcium in dead or dying tissues
  • advanced arteriosclerosis
  • evidence of previous cell injury
  • often a cause of organ dysfunction
  • for example: damaged heart valves
  • normal blood levers but high number of injured cells
87
Q

metastatic calcification

A
  • occurs in normal tissues whenever there is hypercalcemia

- high blood levers and normal cells

Pathophysiology (11 decks)

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