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Pathology > Cell Adaptation, Injury and Death > Flashcards

Cell Adaptation, Injury and Death Flashcards

1
Q

medical specialty that deals with laboratory diagnosis, and a sciene that bridges basic science and clinical medicine

A

pathology

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2
Q

medical school subject that deals with general reactions of cells and tissues to injury (necrosis, inflammation, neoplasm, hemorrhage, etc)

A

General pathology

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3
Q

_____ examines how these underlying mechanisms actually work out in the various organ systems

A

systemic pathology

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4
Q

medical specialty focusing on diagnosing disease by its morphology, as seen in the labe

A

anatomic pathology

autopsy/ forensic pathology, surgical/biopsy pathology and cytopahtology are the classic areas of focus

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5
Q

medical specialty focusing on other aspects of the lab:

hematology, clinical chemistry, blood banking, urinalysis, serology, and molecular pathology

A

clinical pathology

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6
Q

disease

A

stuff on or under the skin that interferes with a person’s ability to work, plan, and/or love others

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7
Q

Etiology

A

cause of the disease.

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8
Q

etiology lies in

A

inherited genetic mutations (intrinsic etiology) and/or cell injury (extrinsic etiology). Most dz has both

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9
Q

pathogenesis of a disease

A

how it develops

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10
Q

pathology looks at disease simultaneously at the levels of

A

molecules, cells, tissues, organ systems, the whole person, and even problems with society

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11
Q

set of anatomic changes that one sees in many dz’s

A

morphology.

this illustrates and informs your understanding of disease

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12
Q

Dz that may not have a known morphologic correlate

A

functional disease.

migraine, schizophrenia, and even many cases of low back pain

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13
Q

Becker’s nevus

A

skin on the trunk that is extra sensitive to testosterone

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14
Q

Number of new cases per unit time

A

incidence

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15
Q

number sick at any one time

A

prevalance

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16
Q

prevalence=

A

incidence x average duration

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17
Q

how much your unusual situation increases your chance of getting the disease

A

risk

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18
Q

the name we give the dz

A

diagnosis

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19
Q

the expected outcome for a particular dz

A

prognosis

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20
Q

Congenital dz/birth defect

A

symptoms/signs at birth

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21
Q

a disease process

A

is a mechanism common to many diseases - there are only a few (inflammation is one)

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22
Q

biopsy

A

getting tissue from LIVING for diagnosis

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23
Q

Closed biopsy

A

tissue was obtained for diagnosis without making a real surgical incision

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24
Q

open biopsy

A

getting the tissue required access by surgery

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25
Q

incisional biopsy

A

a piece of tissue was taken for diagnosis from a larger structure that is diseased

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26
Q

excisional biopsy

A

the entire mass/organ was taken for diagnosis (and maybe cure)

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27
Q

autopsy/necropsy

A

the opposite of biopsy - person is dead

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28
Q

symptoms

A

what the patient tells you

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29
Q

signs

A

what you find on physical exam and other studies

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30
Q

Syndrome

A

a group of symptoms and/or signs with a common underlying pathophysiology, but many different possible underlying diseases

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31
Q

hearing loss, dizziness (vertigo) and tinnitus always results from disease in the inner ear, though which dz varies among patients

A

meniere’s syndrome

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32
Q

pathognomonic

A

a particular abnormality is found in only one disease/condition

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33
Q

a mild variant of a longstanding typically much more severe disease

A

form fruste

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34
Q

pathogen

A

the microbe that causes a disease

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35
Q

agenesis/aplasia

A

complete failure of an organ to form

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36
Q

primordial embryologic organ didn’t form

A

aplasia

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37
Q

no organ, but embryologic organ did form at one point

A

agenesis

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38
Q

atresia

A

a lumen completely failed to form

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39
Q

stenosis

A

the lumen is too narrow - congenital or acquired

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40
Q

occlusion

A

once open, now closed

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41
Q

spasm

A

inappopriate contraction of muscle

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42
Q

Failure of an organ to grow to normal size along with the rest of the body

A

hypoplasia

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43
Q

local gigantism

A

an organ is disproportionately large

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44
Q

malformation

A

shaped wrong from the beginning

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45
Q

syn- and holo -

A

both mean things didn’t separate

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46
Q

supernumerary

A

an extra something

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47
Q

harmartoma

A

the right stuff in the right place, but the wrong arrangement/ mix

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48
Q

cysts

A

abnormal
fluid filled
epithelially lined
closed

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49
Q

mucocele

A

mucous cyst

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50
Q

choristomas

A

good stuff in the wrong place

ie sebaceous glands in the mouth, cartilage, fat and gland on the eyeball

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51
Q

fistula

A

abnormal, epithelially lined communication between two surfaces.

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52
Q

law of epithelial cells

A

epithelial cell does not tolerate not having a neighbor . looks around and says, hey, there’s nothing around me, starts to divide

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53
Q

pathological sinus

A

like a fistula, only one end is in a pathological sac, or leads to nowhere.
most familiar is the pilonidal sinus/pilonidal cyst

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54
Q

True diverticulum

A

includes the muscles

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55
Q

pseudodiverticulum

A

THROUGH the muscle but doesn’t include it

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56
Q

atrophy

A

an organ becomes smaller
organ shrinks because the cells shrink. (reversible)
organ shrinks due to cell loss (irreversible)

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57
Q

Cachexia

A

wasting of the body as a result of cytokine activity/cancer

selectively destroys muscle over fat

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58
Q

hypertrophy

A

increase in the sixes of cells, and hence in the size of the organ
sometimes helpful; sometimes not

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59
Q

individual cells become larger

A

hypertrophy

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60
Q

pregnant uterus adaptations

A

sm. m fiber undergo hypertropy and hyperplasia

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61
Q

myocardial hypertropy

A

many more than the normal 92 chromosomes

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62
Q

hyperplasia

A

the organ gets bigger because it now has more cells

like in bone marrow, psychological stress in the adrenal cortex

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63
Q

prayer mark

A

hyperplasia of the epidermis

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64
Q

most goiters result from

A

hyperplasia of thyroid epithelium

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65
Q

hyperplasia of the sebaceous glands of the nose

A

rhinophyma/rosacia

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66
Q

Hyperplasia of the leydig cells of an older guy’s testis

A

individual leydig cells lose some ability to make testosterone, and the pituitary asks for more, making them proliferate.
leydig cell hyperplasia in XXY

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67
Q

marrow hyperplasia in a patient who died of sepsis:

A

losts and lots of WBC precursors being cranked out

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68
Q

mononucleosis

A

lymphnode hyperplasia

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69
Q

hyperplasias are driven by

A

genetic mutations or other mysterious reasons

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70
Q

metaplasia

A

one adult type tissue component replaces another
(stem cells replace the usual type with a new type)

ie. columnar epithelium of uterine endocervix being replaced by stratified squamous epithelium
ie. pseudostratified epithelium of big airways being replaced by a more protective stratified squamous epithelium

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71
Q

anaplasia

A

cells that are bizarre, unlike any normal cells

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72
Q

dysplasia

A

anaplasia confined (for now) to an epithelium.

this change precedes the development of many cancers.

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73
Q

irreversible injury

A

cells die, just like people die

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74
Q

certain cells die off physiologically, in health by

A

apoptosis

75
Q

necrosis

A

death of cells due to injury, riot to the death of the organism and its visible and or microscopic evidence

76
Q

Reversible cell injury

A

may or may not lead to necrosis. can often detect it on routine lab work (heavy drinkers, fitness buffs)

77
Q

Ways in which cell death might occur (5)

A 
pathological apoptosis
coagulation necrosis
liquefaction necrosis
caseation/caseous necrosis
enzymatic fat necrosis
78
Q

apoptosis due to illness

A

pathological apoptosis

79
Q

hypoxia/denaturation

A

coagulation necrosis

80
Q

hydrolysis of proteins

A

liquefaction necrosis

81
Q

mass apoptosis

A

caseation/caseous necrosis

82
Q

saponified

A

enzymatic fat necrosis

83
Q

The ____ tell you whether cells have died

A

nuclei

84
Q

how busy a cell is

A

the amount of euchromatin

85
Q

lose euchromatin=

A

dead

86
Q

pyknosis

A

condensation of nucleus, very dark

87
Q

karyorrhexis

A

nuclear dust

88
Q

Karyolysis

A

nuclei disappear

89
Q

The _____tells you HOW cells have died

A

cytoplasm

90
Q

coagulation necrosis

A

cell was denatured by hypoxia and free radicals
(unless CNS, which would be liquefaction necrosis)

structure of cells is still intact

91
Q

liquefaction necrosis

A

cell was hydrolyzed by strong acids/alkalies, clostridia, snake venom, neutrophils (pus)
(unless CNS death by hypoxia or free radicals)

nothing left of cells

92
Q

caseous necrosis

A

cell death by mass apoptosis by tuberculosis, some fungi

cells look crumbly

93
Q

enzymatic fat necrosis

A

cell was saponified by lipase

enzymatic fat necrosis. calcium loving

94
Q

lack of oxygen

A

hypoxia

95
Q

hypoxia due to local ischemia

A

loss of arterial blood flow

i.e. acute arterial stroke, testicular torsion, arterial gangrene

96
Q

Lak of blood flow will permanently damage adult brain after

A

a few seconds

97
Q

neurons die after______, but supporting cells can ______ unless deprived of blood for _____.

A

a few minutes
remain intact
hours

98
Q

heart myocytes usually die after ______

A

30 minutes

99
Q

other organs can last for ___ with lack of oxygen

A

hours

100
Q

hypoxia due to systemic (total body) ischemia

A

the heart can not pump enough blood “shock”

Total body ischemic hypoxia

101
Q

hypoxemia

A

due to too little oxygen in the blood

hypoxic hypoxia

102
Q

anemia

A

hypoxia due to too little oxygen carrying capacity

anemic hypoxia

103
Q

histotoxic hypoxia

A

cytochrome failure

104
Q

when a cell is deprived of oxygen

A

anaerobic glycolysis kicks in and pH goes down–> change in tertiary structure of protein molecules

cell membrane becomes too permeable to Na–> hypoxic cells swell up with water, and causes most of the electrical chaos when the heart is deprived of Oxygen

Next, K starts to leak out

Last, Ca starts to leak in and intracellular Ca is displaced by H+ions from proteins. THIS IS DEADLY

105
Q

Calcified mitochondria in hypoxic injury

A

magnesium phosphate is soluble, but Ca phosphate is famously insoluble in water

106
Q

myelin figures

A

seen in electron microscopy.
lipid and aqueaous phases separate in dying tissue
lipid and water alternating tissue tends to turn yellow in necrosis as it separates

107
Q

mass apoptosis (as in ___) is more likely to be white than yellow as

A

TB

membranes mummify instead of melting and separating into tlayers

108
Q

necrotic myocardim. necrosis tends to be

A

yellow, because, as in fat, free lipid takes yellow pgments

109
Q

Free radicals

A

species with an unpaired electron -

the electron gets passed from molecule to molecule, producing a cascade of damage
(famously to C=C bonds in lipid, S-S bonds in proteins, and to DNA

the cascade ends only with one of the free radical squelching molecules. still not well understood.

110
Q

free radical injury is commonplace

A

ionizing radiation
tylenol poisoning
sunburn

111
Q

free radical injury tends to produce

A

apoptosis or coagulation necrosis depending on severity

112
Q

H2O + radiation

A

H2 +OH’ (“hydroxyl radical)

113
Q

H2O2 + anything

A

OH’ + OH’

114
Q

O2’

A

superoxide

115
Q

CCl3-‘

A

carbon tetrachloride radical

116
Q

NO’

A

(nitric oxide - a signal molecule in health) and its kin

117
Q

proteases

A

like snake venom–> liquefactive necrosis

acid burn

118
Q

pus

A

tissue liquefied by enzymes produced by your own neutrophils

collateral damage in the never ending war on bacteria

119
Q

apoptosis

A

programmed cell death. if most of the cells in an area are spared, we do NOT even refer to it as ‘necrosis’

120
Q

little blebs coming off the edge of a cell

A

apoptosis

121
Q

most poisons/free radical generators cause

A

apoptosis, which can ruin an organ. so do some of the viruses

122
Q

if stroma is destroyed as well in an organ, the whole region becomes a fine powder, not quite solid not quite liquid

A

Caseous necrosis, (cheese)

123
Q

TB is the best known cause of

A

caseous necrosis

124
Q

KC dwellers usu have a bit of caseous necrosis in their

A

histoplasmosis scars

125
Q

Death angel toadstool and its american kindred kill by

A

scrambling ribosomes

some things don’t fit neatly into the previous categories

126
Q

cloudy swelling in skin lupus

A

cells aren’t dead, just injured (reversible injury)

127
Q

fatty change

A

ever been drunk for a few days straight, you’ve done this to your liver. not dead, just injured, and very reversible, provided you sober up

128
Q

inclusion bodies

A

cytopathic viruses can cause cells to look abnormal. the masses of virus in nucleus an or cytoplasm are called inclusion bodies

129
Q

cytolytic viruses

A

viruses may simply lyse the cells in which the grow or not change the morphology. Other viral infected cells are killed by your own immunity. Sorting out which viruses are which is still underway

viruses can kill your cells or make them more numerous

130
Q

The _____ tell you whether cells have died

A

nuclei
pyknosis
karyorrhexis
karyolysis

131
Q

ichthyosis

A

severe variant. apoptotic cells ar not shed from the skin

132
Q

contraction bands in the heart

A

ions pouring in clamp sarcomeres in groups

133
Q

simplistic to think damage brain liquefies because

A

early in an infarct, brain swells and softens. ALL the major cell types must die, and even then it takes about a week to liquefy

134
Q

tissue liquefied by bodes own neutrophils

A

pus

135
Q

pus in a confined space

A

abscess

136
Q

pancreatits –>

A

enzymatic fat necrosis near the pancreas

137
Q

necrotic fat with blue haze

A

blue haze is Ca in the Ca/fatty acid precipitate

138
Q

TB causes what type of necrosis

A

caseous
TB= full of little potatoes
TB cavities - caseous debris was coughed up

139
Q

gangrene

A

visible necrosis

140
Q

dry gangrene

A

tissue dried out before the clostridia got there

141
Q

wet gangrene

A

the clostridia got there before it dried out

142
Q

trench mouth

A

ulcerative/necrotizing gingivitis

143
Q

Noma

A

necrosis of the mouth in malnutrition

144
Q

fournier’s gangrene

A

gangrene in the scrotum

145
Q

fibrinoid necrosis

A

when the wall of a muscular artery dies for whatever reasons, it becomes rich in plasma proteins

146
Q

syphilitic gummas can progress to

A

necrosis/gangrene

147
Q

HOst of molecular mechanisms known in both apoptosis (and its variants) and pathological cell death/necrosis (4 big categories)

A

Mitochondrial damage

  • decreased ATP
  • increased ROS

entry of Ca

  • increased mitochondrial permeability
  • activation of multiple cellular enzymes

membrane damage

  • plasma membrane–> loss of cellular components
  • lysosomal membrane–> enzymatic digestion of cellular components

protein misfolding, DNA damage
-activation of proapoptotic proteins

148
Q

Lack of oxygen/BF generally kills tissues by the effects of lack of

A

oxydative phosphorylation

as the pH drops and little ATP is available to keep ions where they belong, the cell machinery is ruined

149
Q

Signals for apoptosis are mediated through

A

mitochondria

150
Q

influx of Ca into injured cells gets discussed a lot, especially as a cause of _____ injury

A

reperfusion

151
Q

injured mitochondria generate

A

free radicals. (so do a lot of other things)

152
Q

pathways leading to apoptosis (3)

A

Fas/FasL
TNF receptors
BCL family genes

153
Q

___ is a big topic, especially in neurodegenerative dz

A

accumulation of misfolded proteins

154
Q

proteins involved in autophagocytosis seem, when mutated, to have something to do with

A

Crohn’s/ulcerative colitis

155
Q

neither necroptosis or pyroptosis produce

A

apoptotic bodies, the morphology is more like common necrosis

156
Q

necroptosis

A

triggered by TNFR1 may have been developed to fight viral infections

157
Q

pyroptosis

A

triggered by caspase 1, which yields interleukin 1-b. probably developed to remove bacterially infected cells

158
Q

necrosis

A

the signs we see that some tissue has died during the person’s life.
if death is sudden, we see NO necrosis anywhere in the body

159
Q

rigor mortis

A

body remains stiff after death

160
Q

livor mortis

A

post mortem livididty. bedding pattern.

161
Q

cadaveric spasm

A

happens

162
Q

putrefaction

A

the familiar series of events during the days to months following death

163
Q

fatty change

A

accumulation of neutral fat in cells

164
Q

fatty liver

A

alcohol abuse

165
Q

fatty heart

A

diptheria (prevents heart from burning up the lipids)

166
Q

atherosclerosis

A

cholesterol accumulation. spiky spindles

167
Q

Xanthoma

A

a mass of macrophages

cholesterol can accumulate in a xanthoma

168
Q

strawberry gallbaladder

A

cholesterol accumulation in the wall of a gallbladder

169
Q

Storage disease

A

ie. Niemann pick

with the accumulation of storage product throughout the body

170
Q

Antitrypsin can build up in the ____ in a patient who cannot transport it into the _____

A

liver

bloodstream

171
Q

Hyaline

A

generic term for masses of a single protein, regardless of which protein, staining homogeneously pink

172
Q

cytoskeletal proteins can

A

cause disease when they accumulate due to improper handling

173
Q

Tau protein= accumulation in neurofibrillary tangles of

A

Alzheimers

174
Q

protein that accumulates in a variety of local and systemic illnesses

A

amyloid Beta pleated protein

175
Q

accumulates in myocardial fibers in Pompe’s disease

A

glycogen (in pompe’s glycogen storage disease)

176
Q

lipofuscin

A

breakdown product of long-gone membranes. stored in lysosomes.
stuff you just can’t break down
brownish

177
Q

Melanin

A

seen in cancer. alerts clinician and pathologies that this is a malignant melanoma. black-brown

178
Q

hemosiderin

A

compact storage form of iron, seen at sites of repeated small bleeds. causes damage by generating free radicals. yellow-brown

179
Q

Dystrophic calcification

A

accumulation at sites of disease. may or may not be after necrosis

180
Q

metastatic calcification

A

precipitation of CaPO4. due to elevated blood Ca, elevated blood PO4, or both

181
Q

Clonal senescence (hayflick phenomenon) and aging

A

shortening of telomeres in many, not all, replicating cell lines in your body. reproductive life cycle of cell ends, won’t divide any further
cells that take it worst in aging are those that are already post mitotic, like neurons

182
Q

methotrexate kills

A

epithelial cells

183
Q

90 degree hyphee

A

bread mold. seen in lungs when poor immune system

Pathology (15 decks)

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