Cellular Pathophysiology Flashcards
1
Q
stimulus that upsets normal homeostasis
A
insult/stress
2
Q
bodies attempt to maintain homeostasis under stress + example
A
compensation, shivering in the cold
3
Q
cell injury is the result of
an example
A
stimulus in EXCESS of the cells immediate compensation response
hypothermia causing frostbite
4
Q
an injury that dost kill the cell
A
reversible cell injury
5
Q
example of reversible cell injury
A
muscles get bigger from working out
whatever doesn’t kill it makes it stronger
6
Q
injury that results in cell death
A
irreversible cell injury
7
Q
clean/controlled cell death
A
apoptosis
8
Q
messy uncontrolled cell death
A
necrosis
9
Q
hypertrophy
A
cells get larger but don’t change in number ex muscles
10
Q
atrophy
A
cells get smaller but don’t change in number
11
Q
cells that can undergo hypertrophy but not hyperplasia
A
anything that does not multiply: fat cells (adipocytes, skeletal muscle, cardiac cells
12
Q
three reasons for cardiac hypertrophy
A
HTN, valvular stenosis, power athletes (cyclists, rowers, always pumping against high pressure)
13
Q
____________ happens as a result of reprogramming cells in reaction to a stressor
A
metaplasia
14
Q
change from one cell type to another in reaction to a stressor, examples
A
metaplasia, smokers and GERD
15
Q
Explain metaplasia in smokers
A
normal ciliated columnar epithelial cells change to stratified squamous which are thicker and stronger
stratified squamous do not have cilia or secrete mucous + LOSS OF PROTECTIVE MECHANISM
16
Q
Explain dysplasia in smokers
A
if smokers already have undergone metaplasia and continue smoking, or too much damage has been done cells change into a type NOT found in the body
pre cancerous
17
Q
Explain metaplasia in GERD
A
stratified squamous turn into columnar
18
Q
cells that are not a legitimate cell type in body, not necessarily cancerous, could progress to cancer
A
Dysplasia
19
Q
Low grade dysplasia
A
less progressed towards cancer
20
Q
High Grade dysplasia
A
more progresses towards cancer
21
Q
cancer cells will almost always be ____________
A
dysplastic and neoplastic
22
Q
New growth, tumor
A
Neoplasia
23
Q
example of neoplasia that is not cancer
A
warts, which are also dysphagic
24
Q
Not all _______ is cancer; but all cancer results in _________.
A
neoplasia, neoplasia
25
An example of a stressor that doesn't kill a cell but makes it stronger
Heart attack. Cells that don't die prepare for future MI, Cardiomyocytes NOT replaced
26
What are the four common themes in cell injury?
1. ATP depletion,
2. Free radical and reactive oxygen species (ROS)
3. Increase in intracellular CA++
4. Defects in plasma membrane
27
Explain the how ATP depletion causes cellular swelling in ischemia and hypoxia
1. As blood flow decreases, oxygen to tissue decreases
2. Decreased 02 = decreased ATP production
3. No ATP = Na/K ATPase pump cannot work
4. Sodium flow into the cell and and the Na gradient is lost
5. H20 follow Na+ and cell swells
28
causes the oxidation of membranes and other structures in hypes and ischemia
free radicals and ROS
29
Free radicals and ROS are particularly problematic for ___________.
reprofusion. Think hydrogen peroxide bleaches,burns and bubbles
30
Name three ways Ca++ is increased intercellularly in cell injury
1. Low ATP causes and increase in Na+ which then prevents the removal of CA++ via the Ca++/Na+ Exchanger which uses the sodium gradient to remove calcium
2. Likewise the low ATP does not allow the Ca++ ATPase pump to work (pump on plasma membrane and Sarcoplasmic reticulum)
2. The Ca++ cannot release from the mitochondria and ER r/t concentration gradient.
31
Two disadvantages to having high intercellular calcium
1. Calcium activates MANY enzymes
| 2. High intercellular Ca++ signals APOPTOSIS
32
defects in plasma membrane cause ______ and _____ to flood into cell
Ca++, Na+
33
loss of the sodium gradient r/t defects in plasma membrane will activate ____________
Proteases and phosphalipases
34
the cell swells r/t _________ gradient and makes the ______________________. the plasma membrane swells then ruptures.
Na+
Plasma membrane permeable
35
clinical findings with reversible cell injury
decreased pH
36
clinical findings with irreversible cell injury
decreased pH and the release of intracellular enzymes
CPK, LH, Troponin ALT, AST, myoglobin
37
How do cells become acidotic with ischemic tissue injury
1. Decreased O2 to tissues = decreased ATP production
2. Glycolysis increases to generate AS MUCH ATP as possible
3. BUT by increasing hydrolysis this INCREASES +
4. Cells become Acidotic
5. lactate buffers H+
38
What is lactate?
Lactate is pyruvate with an H+ added.
Lactate buffers H+
39
Autophagy
lysosomes swell and begin to rupture, digestive enzymes begin to break down the cells.
small amount in reversible cell injury
40
What happens intercellularly when a tissue is acidotic?
1. Nucleus clumping- reversible but no access to DNA = no protein being made
2. lysosomes swell
41
decreased ATP production causes an ___________ in extracellular _______, while it causes an ________ in intracellular ______
increase, potassium, increase calcium and sodium.
42
Sodium is the driver for all _____________, if we lose the sodium gradient, we lose __________.
secondary active transport, Na/Ca exchanger
43
In cellular damage, what causes the inability to maintain the cytoskeleton?
The rough ER is dilated and there is a DETACHMENT OF RIBOSOMES which will cause a decrease in protein synthesis
44
when does the cellular damage become irriversiible?
when the cell loses the ability to maintain the cytoplasm
45
What is also related to the inability to maintain the cytoplasm?
membrane damage
lipid deposition and breakdown
loss of phospholipids
Activation of inflammation
increased free radical
loss of phospholipids
46
three things that are turned on with the activation of inflammation
complement
cytokines
leukocytes
47
REVERSIBLE or IRREVERSIBLE
clumping of DNA nuclear chromatin
REVERSIBLE
48
REVERSIBLE or IRREVERSIBLE
Karyolysis
IRREVERSIBLE
Karyolysis = chopping up nucleus = DNA destruction
49
REVERSIBLE or IRREVERSIBLE
Swelling and blebs on cell membrane
REVERSIBLE
50
REVERSIBLE or IRREVERSIBLE
Defects in cell membrane
IRREVERSIBLE
lose Na gradient and Ca+ rushes in
51
REVERSIBLE or IRREVERSIBLE
Small densities
REVERSIBLE
small densities = clumping and swelling of mitochondria- change pH it will unclip
52
REVERSIBLE or IRREVERSIBLE
Lysosome appearance
REVERSIBLE
Small amount of autophagy, lysosomes eat mitochondria that are in bad shape
53
REVERSIBLE or IRREVERSIBLE
Lysis of ER
IRREVERSIBLE
54
REVERSIBLE or IRREVERSIBLE
Lysis of Lysosomes
IRREVERSIBLE
AKA: Autophagy
55
REVERSIBLE or IRREVERSIBLE
Large densities in mitochondria
IRREVERSIBLE
56
REVERSIBLE or IRREVERSIBLE
Lysis of DNA in nucleus
IRREVERSIBLE
57
How do we know cells have necrosed?
in necrosis, cellular enzymes leak out of the cell
these inflammation markers are present in the blood stream
LDH, CK, AST, ALT, Troponin, Myoglobin
58
hypoxia, hypoxemia, ischemia
Causes of oxygen deprivation Cell injury
59
trauma, heat, cold, pressure, radiation
physical agents causing cellular injury
60
poisons and drugs
chemical agents causing cell injury
61
immunologic responses
infectious agents causing cellular injury
62
x,y
genetic mutations causing cellular injury
63
low tissue oxygen level, caused by hypoxemia or hemoglobin problems
hypoxia
64
Anemia will not cause _________ but will cause ________ because the oxygen saturation's still 100%
hypoxemia, hypoxia
65
very low tissue oxygen
anoxia, extreme form of hypoxia
66
low blood oxygen tension or pressure
hypoxemia
67
caused by poor air exchange, difficulty breathing, suffocation and heart failure
hypoxemia
68
caused by hypoxemia
decreased oxygen saturation
69
insufficient blood supply to tissue or organ that is reversible
Ischemia
70
Ischemia with necrosis
Infarction - if it doesn't die it isn't an infarct
71
restoration of blood supply that had been cut off
reprofusion
72
Oxygen returning to damaged tissues causes additional problems
reprofusion injury
73
when blood flow is restored tissues are damaged with free radicals
Thrombus- with all theee ROS
74
when blood flow is restored tissues are damaged with ROS
Embolism only suparaoxide and supraoxidedismutase NOT hydrogen peroxide
75
fixed obstruction blood flow, must rid body of it
Thrombus
76
Moving, breaks off and gets stuck somewhere THEN the blood supply is cut
Embolism
77
molecule with unpaired electron written with a little dot
free radical
78
highly reactive molecule that contains oxygen
Reactive oxygen species (ROS)
79
superoxide dismutase
convers superoxide (02.) ion to hydrogen peroxide
80
NOT a free radical, but a reactive oxygen species
Hydrogen peroxide
81
produced by peroxisome
hydrogen peroxide
82
catalase
converts hydrogen peroxide to water
83
produced in miscellaneous metabolism
hydroxyl radical (OH-)
84
glutathione peroxidase
gets rid of hydroxyl radical by converting it to hydrogen peroxide ---- then caltalase can reduce it to H2O
85
both superoxide and hydroxyl radicals are converted to______________, then converted into H20 by ____________,
hydrogen peroxide, catalase
86
reprofusion injury
1. restore blood, new O2 causes an increase in free radical species and ROS species - further damages cells
problem when restoring blood during heart attack
2. also get an influx of Ca+ which also causes harm
87
NECROSIS or APOPTOSIS
enlarged size/swelling
NECROSIS
88
NECROSIS or APOPTOSIS
reduced size/shrinkage
APOPTOSIS
89
NECROSIS or APOPTOSIS
Chromosome clumping
NECROSIS
90
NECROSIS or APOPTOSIS
nuclear chomatin condensation and fragmentation
APOPTOSIS
91
NECROSIS or APOPTOSIS
plasma membrane disruption
NECROSIS
92
NECROSIS or APOPTOSIS
membrane entact with altered structures/lipids
APOPTOSIS
93
NECROSIS or APOPTOSIS
cellular contents leak out of cell
NECROSIS
94
NECROSIS or APOPTOSIS
Pathologic- inflammation
NECROSIS
95
NECROSIS or APOPTOSIS
Physiologic- Phagocytosis
APOPTOSIS
96
NECROSIS or APOPTOSIS
apoptotic bodies have a membrane around them keeping cellular contents enclosed
APOPTOSIS
97
Type of necrosis:
anywhere there is an infarction besides the brain
Coagualative Necrosis
98
Type of necrosis:
Structures stand but tissue dead
Coagualative Necrosis, like an egg white-
Seen in kidney where tissue maintains architecture after cell deaths a result of infarction
99
Type of necrosis:
Inflammatory cells completely destroy architecture of the area
Liquifactive Necrosis
100
Type of necrosis:
Happens with infarctions in the brain
Liquifactive Necrosis
brain will have holes and tissue replaced with fluid
101
Type of necrosis:
abcess filled with fluid
Liquifactive necrosis
102
Type of necrosis:
Neutrophils -digestive enzymes
Liquifactive necrosis
103
Type of necrosis:
yellow white and cheesy
Caseous necrosis
104
Type of necrosis:
Happens specifically with TB
Caseous necrosis
105
Type of necrosis:
waxy deposits
Caseous necrosis
106
Type of necrosis:
typically seen in pancreas
Fat necrosis
107
Type of necrosis:
lipase break down triglycerides - Free fatty acids released
Fat Necrosis
108
Type of necrosis:
FFA combine with Ca++ to create soap (saponification)
Fat necrosis
this is why we see a decrease in calcium with pancreatitis
109
Type of necrosis:
if pancreatic enzymes release, they digest fat in that area and calcium reacts and we get fatty calcium deposits
Fat necrosis
110
Type of necrosis:
calcium deposits in breasts that show up on mammogram
Fat necrosis
111
Type of necrosis:
occurs in dry tissue; involves infections exposed to air
Dry Gangrene
112
Type of necrosis:
moist tissue, internal organs and bedsores; numerous bacteria involved
Wet gangrene
113
Type of necrosis:
Clostridium
Dry gangrene
114
Type of necrosis:
C perftingens
Wet Gangrene
115
Type of necrosis:
similar to wet gangrene with the addition of gas production
Gas Gangrene
116
Type of necrosis:
medical emergency can lead to sepsis and death
Gas Gangrene
117
dosent code for anything
telomeres
118
DNA cap ant end of chromosomes
telomeres
119
when we have lost enough telomeres the cell doesn't replicate anymore
replicative senescence
120
have enzyme on to maintain telomere indefinitely
germ cells
121
telomerase partially on
stem cells
122
Telomerase activitvation turns off the "telomeric clock"
cancer cells
123
the older a man, the longer his telomerase cap
on his spermatagonia
124
Type of necrosis:
result of liquefactive necrosis, skin dry and shrinks
dry gangrene
125
Type of necrosis:
neutrophils invade site, liquifactive
Wet gangrene
126
Three factors needed for gangrene
1. Infectious agent
2. Poor circulation - can't fight infection
3. Neuropathies, cannot feel
