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
2
Q
medical school subject that deals with general reactions of cells and tissues to injury (necrosis, inflammation, neoplasm, hemorrhage, etc)
A
General pathology
3
Q
_____ examines how these underlying mechanisms actually work out in the various organ systems
A
systemic pathology
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
5
Q
medical specialty focusing on other aspects of the lab:
hematology, clinical chemistry, blood banking, urinalysis, serology, and molecular pathology
A
clinical pathology
6
Q
disease
A
stuff on or under the skin that interferes with a person’s ability to work, plan, and/or love others
7
Q
Etiology
A
cause of the disease.
8
Q
etiology lies in
A
inherited genetic mutations (intrinsic etiology) and/or cell injury (extrinsic etiology). Most dz has both
9
Q
pathogenesis of a disease
A
how it develops
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
11
Q
set of anatomic changes that one sees in many dz’s
A
morphology.
this illustrates and informs your understanding of disease
12
Q
Dz that may not have a known morphologic correlate
A
functional disease.
migraine, schizophrenia, and even many cases of low back pain
13
Q
Becker’s nevus
A
skin on the trunk that is extra sensitive to testosterone
14
Q
Number of new cases per unit time
A
incidence
15
Q
number sick at any one time
A
prevalance
16
Q
prevalence=
A
incidence x average duration
17
Q
how much your unusual situation increases your chance of getting the disease
A
risk
18
Q
the name we give the dz
A
diagnosis
19
Q
the expected outcome for a particular dz
A
prognosis
20
Q
Congenital dz/birth defect
A
symptoms/signs at birth
21
Q
a disease process
A
is a mechanism common to many diseases - there are only a few (inflammation is one)
22
Q
biopsy
A
getting tissue from LIVING for diagnosis
23
Q
Closed biopsy
A
tissue was obtained for diagnosis without making a real surgical incision
24
Q
open biopsy
A
getting the tissue required access by surgery
25
incisional biopsy
a piece of tissue was taken for diagnosis from a larger structure that is diseased
26
excisional biopsy
the entire mass/organ was taken for diagnosis (and maybe cure)
27
autopsy/necropsy
the opposite of biopsy - person is dead
28
symptoms
what the patient tells you
29
signs
what you find on physical exam and other studies
30
Syndrome
a group of symptoms and/or signs with a common underlying pathophysiology, but many different possible underlying diseases
31
hearing loss, dizziness (vertigo) and tinnitus always results from disease in the inner ear, though which dz varies among patients
meniere's syndrome
32
pathognomonic
a particular abnormality is found in only one disease/condition
33
a mild variant of a longstanding typically much more severe disease
form fruste
34
pathogen
the microbe that causes a disease
35
agenesis/aplasia
complete failure of an organ to form
36
primordial embryologic organ didn't form
aplasia
37
no organ, but embryologic organ did form at one point
agenesis
38
atresia
a lumen completely failed to form
39
stenosis
the lumen is too narrow - congenital or acquired
40
occlusion
once open, now closed
41
spasm
inappopriate contraction of muscle
42
Failure of an organ to grow to normal size along with the rest of the body
hypoplasia
43
local gigantism
an organ is disproportionately large
44
malformation
shaped wrong from the beginning
45
syn- and holo -
both mean things didn't separate
46
supernumerary
an extra something
47
harmartoma
the right stuff in the right place, but the wrong arrangement/ mix
48
cysts
abnormal
fluid filled
epithelially lined
closed
49
mucocele
mucous cyst
50
choristomas
good stuff in the wrong place
| ie sebaceous glands in the mouth, cartilage, fat and gland on the eyeball
51
fistula
abnormal, epithelially lined communication between two surfaces.
52
law of epithelial cells
epithelial cell does not tolerate not having a neighbor . looks around and says, hey, there's nothing around me, starts to divide
53
pathological sinus
like a fistula, only one end is in a pathological sac, or leads to nowhere.
most familiar is the pilonidal sinus/pilonidal cyst
54
True diverticulum
includes the muscles
55
pseudodiverticulum
THROUGH the muscle but doesn't include it
56
atrophy
an organ becomes smaller
organ shrinks because the cells shrink. (reversible)
organ shrinks due to cell loss (irreversible)
57
Cachexia
wasting of the body as a result of cytokine activity/cancer
| selectively destroys muscle over fat
58
hypertrophy
increase in the sixes of cells, and hence in the size of the organ
sometimes helpful; sometimes not
59
individual cells become larger
hypertrophy
60
pregnant uterus adaptations
sm. m fiber undergo hypertropy and hyperplasia
61
myocardial hypertropy
many more than the normal 92 chromosomes
62
hyperplasia
the organ gets bigger because it now has more cells
| like in bone marrow, psychological stress in the adrenal cortex
63
prayer mark
hyperplasia of the epidermis
64
most goiters result from
hyperplasia of thyroid epithelium
65
hyperplasia of the sebaceous glands of the nose
rhinophyma/rosacia
66
Hyperplasia of the leydig cells of an older guy's testis
individual leydig cells lose some ability to make testosterone, and the pituitary asks for more, making them proliferate.
leydig cell hyperplasia in XXY
67
marrow hyperplasia in a patient who died of sepsis:
losts and lots of WBC precursors being cranked out
68
mononucleosis
lymphnode hyperplasia
69
hyperplasias are driven by
genetic mutations or other mysterious reasons
70
metaplasia
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
71
anaplasia
cells that are bizarre, unlike any normal cells
72
dysplasia
anaplasia confined (for now) to an epithelium.
this change precedes the development of many cancers.
73
irreversible injury
cells die, just like people die
74
certain cells die off physiologically, in health by
apoptosis
75
necrosis
death of cells due to injury, riot to the death of the organism and its visible and or microscopic evidence
76
Reversible cell injury
may or may not lead to necrosis. can often detect it on routine lab work (heavy drinkers, fitness buffs)
77
Ways in which cell death might occur (5)
```
pathological apoptosis
coagulation necrosis
liquefaction necrosis
caseation/caseous necrosis
enzymatic fat necrosis
```
78
apoptosis due to illness
pathological apoptosis
79
hypoxia/denaturation
coagulation necrosis
80
hydrolysis of proteins
liquefaction necrosis
81
mass apoptosis
caseation/caseous necrosis
82
saponified
enzymatic fat necrosis
83
The ____ tell you whether cells have died
nuclei
84
how busy a cell is
the amount of euchromatin
85
lose euchromatin=
dead
86
pyknosis
condensation of nucleus, very dark
87
karyorrhexis
nuclear dust
88
Karyolysis
nuclei disappear
89
The _____tells you HOW cells have died
cytoplasm
90
coagulation necrosis
cell was denatured by hypoxia and free radicals
(unless CNS, which would be liquefaction necrosis)
structure of cells is still intact
91
liquefaction necrosis
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
caseous necrosis
cell death by mass apoptosis by tuberculosis, some fungi
cells look crumbly
93
enzymatic fat necrosis
cell was saponified by lipase
enzymatic fat necrosis. calcium loving
94
lack of oxygen
hypoxia
95
hypoxia due to local ischemia
loss of arterial blood flow
| i.e. acute arterial stroke, testicular torsion, arterial gangrene
96
Lak of blood flow will permanently damage adult brain after
a few seconds
97
neurons die after______, but supporting cells can ______ unless deprived of blood for _____.
a few minutes
remain intact
hours
98
heart myocytes usually die after ______
30 minutes
99
other organs can last for ___ with lack of oxygen
hours
100
hypoxia due to systemic (total body) ischemia
the heart can not pump enough blood "shock"
| Total body ischemic hypoxia
101
hypoxemia
due to too little oxygen in the blood
| hypoxic hypoxia
102
anemia
hypoxia due to too little oxygen carrying capacity
| anemic hypoxia
103
histotoxic hypoxia
cytochrome failure
104
when a cell is deprived of oxygen
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
Calcified mitochondria in hypoxic injury
magnesium phosphate is soluble, but Ca phosphate is famously insoluble in water
106
myelin figures
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
mass apoptosis (as in ___) is more likely to be white than yellow as
TB
| membranes mummify instead of melting and separating into tlayers
108
necrotic myocardim. necrosis tends to be
yellow, because, as in fat, free lipid takes yellow pgments
109
Free radicals
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
free radical injury is commonplace
ionizing radiation
tylenol poisoning
sunburn
111
free radical injury tends to produce
apoptosis or coagulation necrosis depending on severity
112
H2O + radiation
H2 +OH' ("hydroxyl radical)
113
H2O2 + anything
OH' + OH'
114
O2'
superoxide
115
CCl3-'
carbon tetrachloride radical
116
NO'
(nitric oxide - a signal molecule in health) and its kin
117
proteases
like snake venom--> liquefactive necrosis
| acid burn
118
pus
tissue liquefied by enzymes produced by your own neutrophils
| collateral damage in the never ending war on bacteria
119
apoptosis
programmed cell death. if most of the cells in an area are spared, we do NOT even refer to it as 'necrosis'
120
little blebs coming off the edge of a cell
apoptosis
121
most poisons/free radical generators cause
apoptosis, which can ruin an organ. so do some of the viruses
122
if stroma is destroyed as well in an organ, the whole region becomes a fine powder, not quite solid not quite liquid
Caseous necrosis, (cheese)
123
TB is the best known cause of
caseous necrosis
124
KC dwellers usu have a bit of caseous necrosis in their
histoplasmosis scars
125
Death angel toadstool and its american kindred kill by
scrambling ribosomes
some things don't fit neatly into the previous categories
126
cloudy swelling in skin lupus
cells aren't dead, just injured (reversible injury)
127
fatty change
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
inclusion bodies
cytopathic viruses can cause cells to look abnormal. the masses of virus in nucleus an or cytoplasm are called inclusion bodies
129
cytolytic viruses
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
The _____ tell you whether cells have died
nuclei
pyknosis
karyorrhexis
karyolysis
131
ichthyosis
severe variant. apoptotic cells ar not shed from the skin
132
contraction bands in the heart
ions pouring in clamp sarcomeres in groups
133
simplistic to think damage brain liquefies because
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
tissue liquefied by bodes own neutrophils
pus
135
pus in a confined space
abscess
136
pancreatits -->
enzymatic fat necrosis near the pancreas
137
necrotic fat with blue haze
blue haze is Ca in the Ca/fatty acid precipitate
138
TB causes what type of necrosis
caseous
TB= full of little potatoes
TB cavities - caseous debris was coughed up
139
gangrene
visible necrosis
140
dry gangrene
tissue dried out before the clostridia got there
141
wet gangrene
the clostridia got there before it dried out
142
trench mouth
ulcerative/necrotizing gingivitis
143
Noma
necrosis of the mouth in malnutrition
144
fournier's gangrene
gangrene in the scrotum
145
fibrinoid necrosis
when the wall of a muscular artery dies for whatever reasons, it becomes rich in plasma proteins
146
syphilitic gummas can progress to
necrosis/gangrene
147
HOst of molecular mechanisms known in both apoptosis (and its variants) and pathological cell death/necrosis (4 big categories)
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
Lack of oxygen/BF generally kills tissues by the effects of lack of
oxydative phosphorylation
as the pH drops and little ATP is available to keep ions where they belong, the cell machinery is ruined
149
Signals for apoptosis are mediated through
mitochondria
150
influx of Ca into injured cells gets discussed a lot, especially as a cause of _____ injury
reperfusion
151
injured mitochondria generate
free radicals. (so do a lot of other things)
152
pathways leading to apoptosis (3)
Fas/FasL
TNF receptors
BCL family genes
153
___ is a big topic, especially in neurodegenerative dz
accumulation of misfolded proteins
154
proteins involved in autophagocytosis seem, when mutated, to have something to do with
Crohn's/ulcerative colitis
155
neither necroptosis or pyroptosis produce
apoptotic bodies, the morphology is more like common necrosis
156
necroptosis
triggered by TNFR1 may have been developed to fight viral infections
157
pyroptosis
triggered by caspase 1, which yields interleukin 1-b. probably developed to remove bacterially infected cells
158
necrosis
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
rigor mortis
body remains stiff after death
160
livor mortis
post mortem livididty. bedding pattern.
161
cadaveric spasm
happens
162
putrefaction
the familiar series of events during the days to months following death
163
fatty change
accumulation of neutral fat in cells
164
fatty liver
alcohol abuse
165
fatty heart
diptheria (prevents heart from burning up the lipids)
166
atherosclerosis
cholesterol accumulation. spiky spindles
167
Xanthoma
a mass of macrophages
| cholesterol can accumulate in a xanthoma
168
strawberry gallbaladder
cholesterol accumulation in the wall of a gallbladder
169
Storage disease
ie. Niemann pick
| with the accumulation of storage product throughout the body
170
Antitrypsin can build up in the ____ in a patient who cannot transport it into the _____
liver
| bloodstream
171
Hyaline
generic term for masses of a single protein, regardless of which protein, staining homogeneously pink
172
cytoskeletal proteins can
cause disease when they accumulate due to improper handling
173
Tau protein= accumulation in neurofibrillary tangles of
Alzheimers
174
protein that accumulates in a variety of local and systemic illnesses
amyloid Beta pleated protein
175
accumulates in myocardial fibers in Pompe's disease
glycogen (in pompe's glycogen storage disease)
176
lipofuscin
breakdown product of long-gone membranes. stored in lysosomes.
stuff you just can't break down
brownish
177
Melanin
seen in cancer. alerts clinician and pathologies that this is a malignant melanoma. black-brown
178
hemosiderin
compact storage form of iron, seen at sites of repeated small bleeds. causes damage by generating free radicals. yellow-brown
179
Dystrophic calcification
accumulation at sites of disease. may or may not be after necrosis
180
metastatic calcification
precipitation of CaPO4. due to elevated blood Ca, elevated blood PO4, or both
181
Clonal senescence (hayflick phenomenon) and aging
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
methotrexate kills
epithelial cells
183
90 degree hyphee
bread mold. seen in lungs when poor immune system
