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Pathophysiology I > Cell Injury & Adaptive Response > Flashcards

Cell Injury & Adaptive Response Flashcards

1
Q

symptoms

A

patient’s subjective observations, usually not quantifiable

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2
Q

signs

A

abnormalities on physical exam, usually quantifiable

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3
Q

findings

A

x-rays or results

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4
Q

syndrome

A

cluster of related symptoms and or signs typically due to a single cause in an individual patient

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5
Q

etiology

A

the cause of a disease

overly simplistic to think of a disease having a single cause

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6
Q

pathogenesis

A

sequence of events by which the disease develops

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7
Q

pathognomonic

A

a particular abnormality is found only in one condition

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8
Q

forme fruste

A

very mild variant of a more serious disease

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9
Q

incidence

A

number of new cases per unit time (usually a year)

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10
Q

how is incidence expressed?

A

“new cases per 100,000 people per year”

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11
Q

prevalence

A

number of cases at any one time

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12
Q

how is prevalence expressed?

A

“cases per 100,000 people”

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13
Q

risk

A

how much your particular situation increases your chance of getting a disease compared with everyone else

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14
Q

diagnosis

A

name given to the particular disease once identified

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15
Q

prognosis

A

expected outcome for a particular case of a disease

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16
Q

what influences prognosis?

A

influenced by diagnosis, the age & general health of the patient, available treatments

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17
Q

what hurts cells?

A

hypoxia
poor nutrition-cells respond in different ways
infectious agents-several mechanisms depending on agent
immune injury-4-5 types, antibody or t-cell mediated
chemical agents-noxious stuff or too much good stuff
physical agents-trauma, radiation, etc.

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18
Q

what is the prototype for cell injury?

A

hypoxia

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19
Q

mechanisms of hypoxia

A
  1. ischemia
  2. hypoxemia
  3. failure of oxidative phosphorylation
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20
Q

ischemia

A

ischemic hypoxia
lack of arterial blood flow (arterial occlusion, venous occlusion)
pump failure

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21
Q

hypoxemia

A

hypoxic hypoxia
failure to ventilate or perfuse the lungs
failure of lungs to oxygenate blood
inadequate RBC mass
inability of hemoglobin to carry or release oxygen

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22
Q

failure of oxidative phosphorylation

A

histotoxic hypoxia

cyanide, carbon monoxide, dinitrophenol

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23
Q

how do different cells tolerate hypoxia?

A

differently

brain can last 3 minutes without oxygen while leg can last 6 hours

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24
Q

which types of hypoxia can be treated?

A

ischemia
hypoxemia
we can supply oxygen ut we cannot make cells use it

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25
Q

hypoxic injury

A
  1. lack of O2 stops oxidative phosphorylation/ETC
    - Na/K ATPase fails
  2. Na and H2O enter cell-acute cellular edema
    - early sign of cell injury
  3. anaerobic metabolism leads to lactic acid accumulation and pH drop
    - denatures proteins
  4. Ca ATPase fails
    - Ca enters cytoplasm from ECF and ER
    - Transition from reversible to irreversible injury
  5. Ca entry is key step leading to cell death
  6. rigor mortis due to Ca-induced sarcomere shortening
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26
Q

Ca entry steps leading to cell death

A

activates phospholipases that damage membranes
activates proteases that destroy proteins
activates endonucleases that destroy DNA
opens pores in outer mitochondrial membrane
-shuts down oxidative phosphorylation
-mitochondria release free radicals
-mitochondria release capsases that induce apoptosis

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27
Q

free radical injury mechanisms

A

common mechanism of cell injury

-radiation, poisons, normal metabolism

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28
Q

free radical injury cause

A

unpaired electron in outer (valence) orbital, typicall O2 derivatives
-superoxide (O2), hydroxyl (OH), hydrogen peroxide (H2O2)

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29
Q

free radical injury effects

A

damage cell membranes
cause DNA mutations
aging

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30
Q

how to combat limited ability to dispose of free radicals

A

superoxide dismutase and catalase

antioxidants-vitamin e, vitamin c

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31
Q

chemical injury mechanism

A

depends on nature of poison

  • acids/alkalis destroy membranes
  • formalehyde crosslinks proteins and DNA
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32
Q

other poison examples

A 
cyanide-blocks ETC
mushrooms (toadstools)-destroy ribosomes
chemotherapy-damages DNA
strychnine-motor neuron synapses
carbon monoxide-replaces O2 on hemoglobin, blocks ETC
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33
Q

cellular accumulations/deposits

A

can indicate cellular injury or systemic disease

  • triglycerides (fatty change, steatosis)
  • glycogen
  • complex lipids or carbohydrates
  • pigments
  • calcium
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34
Q

what organs do fatty changes involve?

A

liver

heart

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35
Q

what do fatty changes indicate?

A

not injurious to cells but marker for injury

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36
Q

what are fatty changes linked to?

A 
heavy drinking
obesity and metabolic syndrome
-non-alcoholic steatohepatitis (NASH)
malnutrition/hyperalimentation
outdated tetracycline
ileal bypass for weight reduction
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37
Q

hyperalimentation

A

feeding by vein

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38
Q

fatty change mechanisms

A

too much free fat coming to the liver
too much fatty acid synthesis by the liver
impaired fatty acid oxidation by liver
excess esterification of fatty acid to triglycerides by liver
too little apoprotein synthesis by liver
failure of lipoprotein secretion by liver

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39
Q

glycogen/other lipids or polysaccharides storage diseases

A

infusions of glucose (dextrose)
inborn errors of metabolism
cannot be broken down, builds back up

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40
Q

pigments-carbon

A

smoke and soot
engulfed by macrophages
lungs-anthracosis
inert, ugly

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41
Q

pigments-lipofuscin

A 
remnants of intracellular membranes damaged by free radicals
indicator of oxidative stress
wear and tear pigment
inert
seen in hard working organs-liver, heart
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42
Q

pigments-melanin

A

present in melanocytes and their tumors (melanomas)

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43
Q

eumelanin

A

protects from UV light

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44
Q

pheomelanin

A

generates free radicals on UV exposure

redheads

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45
Q

albinos

A

do not produce melanin

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46
Q

hyperpigmentation

A

increased ACTH-increased production of melanin

47
Q

hemochromatosis

A

do not break down melanin adequately

48
Q

pigments-bilirubin

A 
yellow-orange
product of hemoglobin breakdown
conjugated by live and excreted by bile
elevated levels produce jaundice-check nailbeds and sclera
multiple causes
49
Q

pigments-jaundice

A

too many red cells being broken down
-hemolytic processes (sickle cell, thalassemias, pernicious anemia)
liver can’t conjugate bilirubin fast enough

50
Q

example conditions that cause jaundice

A

liver cannot conjugate bilirubin fast enough:
liver disease
newborn “physiologic jaundice of the newborn”
breast feeding (first few weeks)
hereditary defects (Gilbert’s non-disease, Crigler-Najjar)
biliary obstruction:
gallstones, pancreatic cancer

51
Q

pigments-calcium

A

calcium phosphate, calcium hydroxide buildup

52
Q

dystrophic calcification

A

occurs with normal calcium metabolism

53
Q

examples of normal dystrophic calcification

A

pineal gland, airway cartilages, mitral valve annulus, aortic valve sinuses-can lead to aortic stenosis

54
Q

examples of abnormal dystrophic calcification

A

breast cancers, caseous necrosis of TB, surgical scars, pancreatic necrosis-intractable pain, retained abortions-“lithopedion”

55
Q

results of abnormal calcium metabolism

A

metastatic calcification

  • occurs with high calcium and/or phosphate levels
  • indicators of disease causing increased ca/phos
56
Q

calcium precipitation-pH gradients

A

sites of pH gradients make precipitation of ca and phos more likely to occur
small airway walls, gastric fundus epithelium, renal tubular walls

57
Q

necrosis

A

gross and microscopic changes that indicate cell death

58
Q

types of necrosis

A

coagulation
liquefactive
caseous
apoptosis

59
Q

coagulation necrosis

A

usually due to ischemic hypoxia or free radical injury

death of groups of cells

60
Q

gross characteristics of coagulation necrosis

A

soft, pale

61
Q

micro characteristics of coagulation necrosis

A

loss of nuclei but cytoplasm intact

62
Q

coagulation necrosis response

A

dead cells product acute inflammatory response

may be replaced by scar, destroyed, walled-off, infected, or even heal

63
Q

liquefaction necrosis

A

usually due to bacterial infections or poisons or ischemic hypoxia in CNS
death of groups of cells

64
Q

what causes liquefaction necrosis?

A

hydrolysis via lysosomal or WBC enzymes “pus”

65
Q

gross characteristics of liquefaction necrosis

A

gelatinous mass or nothing there

66
Q

caseous necrosis

A

aka saponification (soap formation)
usually due to immune injury in response to certain infections (TB, fungus)
deaths of groups of cells
midpoint between coagulation and liquefaction

67
Q

gross characteristics of caseous necrosis

A

crumbled, friable devris

pale, cheesy

68
Q

terms for apoptosis

A

programmed cell death
cell suicide
physiologic way for cell to die

69
Q

two triggers for apoptosis

A

mitochondrial damage-leak enzymes called caspases (Ca2 entry can cause this)
death receptor-Fas (CD95) or TNF receptors bind their ligands

70
Q

examples of apoptosis

A 
embryologic remodeling of hands
breast shrinkage after lactation period
cells in outer layers of epidermis
neurons that don't synapse
killing of virally-infected cells
71
Q

what causes apoptosis?

A

usually due to immune response or in response of cellular damage

72
Q

what happens with apoptosis?

A

death of single cell
cell membrane remains intact-no leakage of cell contents
no inflammatory response
remains phagocytized by microphages

73
Q

gangrene

A

advanced and grossly visible necrosis

74
Q

mostly coagulation gangrene

A

“dry” gangrene

usually no infection

75
Q

mostly liquefactive gangrene

A

“wet” gangrene
foul-smelling
infected

76
Q

types of bacterial gangrene

A

clostridial “gas” gangrene
trench mouth
fournier’s gangrene

77
Q

clostridial gangrene

A

flesh eating bacteria that produce cell membrane disrupting toxin

78
Q

trench mouth

A

bacterial gangrene caused by malnutrition

79
Q

fournier’s gangrene

A

scrotal necrosis

80
Q

living cell adaptations

A

changes in response to stress or injury or lack of normal stimulation

81
Q

what happens if cells are effective with adaptations?

A

mitigate injurious agent

82
Q

what happens if cells are ineffective with adaptations?

A

cell death

83
Q

what triggers cell adaptations?

A

reversible alterations in gene activity

84
Q

atrophy

A

decrease in cell size may result in decreased organ size
reversible, usually
fewer organelles and decreased function, some may die

85
Q

causes of atrophy

A 
loss of motor innervation
decreased blood supply
loss of hormonal stimulation
malnutrition
aging
86
Q

examples of atrophy

A

loss of breast tissue after menopause
loss of muscle mass inside a cast
shrinkage of kidney with arterial disease

87
Q

misnomers of atrophy

A

not cell loss, but decrease in cell size

88
Q

hypertrophy

A

increase in cell size, may result in increased organ size

cells have increased protein synthesis, increased organelles

89
Q

causes of hypertrophy

A

increased workload

increased hormonal stimulation

90
Q

examples of hypertrophy

A

skeletal muscle of strength athlete
heart of obese person
heart of hypertensive person
smooth muscle of uterus in pregnancy

91
Q

misnomers of hypertrophy

A

BPH

calluses

92
Q

heart hypertrophy can be _______or ______

A

physiologic

pathologic

93
Q

hyperplasia

A

increase in cell number, may result in increased organ size
generally reversible with stimulatory agent
genetic mutations will not reverse

94
Q

hyperplasia may be _________ or ________

A

physiologic

pathologic

95
Q

causes of hyperplasia

A

compensatory-“growing back”
hormonal stimulation
genetic mutations-risk for cancer

96
Q

examples of hyperplasia

A 
female breast at puberty
endometrium during menstrual cycle
lymph nodes close to infection
adrenal cortex under "stress"
bone marrow after blood donation
gingival tissue in people on phenytoin (Dilantin)
97
Q

metaplasia

A

adaptive substitution of one cell type for another
theoretically reversible
often involves epithelium in response to a stimulus
certain metaplasias due to gene mutations-they won’t reverse

98
Q

examples of metaplasia

A

columnar to stratified squamous epithelium in gallbladder with stones
columnar to stratified squamous epithelium in cervix of women with HPV
stratified squamous to columnar epithelium in esophagus of people with chronic reflux (Barrett’s)
is it really adaptive?

99
Q

dysplasia

A

bad growth, atypia, atypical hyperplasia
used in reference to epithelium
loss of cell uniformity and orientation

100
Q

is dysplasia cancer?

A

no, they resemble cancer cells but are not invasive

101
Q

what causes dysplasia?

A

genetic mutations that create a growth advantage

102
Q

anaplasia

A

nuclear changes

103
Q

what promotes dysplastic process?

A

ongoing epithelial injury promotes dysplastic process
bronchi of smokers
cervix of HPV-infected women
reflux of acid into esophagus

104
Q

what is really ugly anaplasia

A

carcinoma in situ

105
Q

what happens with bizarre cells obtain blood supply?

A

form a mass, neoplasia

106
Q

neoplasia

A

new growth

107
Q

what do anaplasia cells look like and what are they capable of?

A

ugly cells; can be:

  1. dysplasia-confined to an epithelium OR
  2. cancer-invading
108
Q

what is dysplasia in terms of types of cells?

A

precancerous anaplastic cells confined to an epithelium and not invading, not neoplasm

109
Q

what is neoplasm with anaplasia?

A

malignant (cancer)

will invade and spread

110
Q

what if neoplasm does not exhibit anaplasia?

A

it is benign, not cancer

may compress surrounding structures but will not invade or spread

111
Q

what mediates atrophy, hypertrophy, hyperplasia and metaplasia?

A

normal growth and differentiation genes

proto-oncogenes

112
Q

proto-oncogenes

A

normal gene

113
Q

what mediates dysplasia and cancer?

A

same growth and differentiation genes that now function abnormally
oncogenes

114
Q

oncogenes

A

loss of cell regulation

Pathophysiology I (10 decks)

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