Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathophysiology Spring 16 > Cellular Pathophysiology > Flashcards

Cellular Pathophysiology Flashcards

1
Q

stimulus that upsets normal homeostasis

A

insult/stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

bodies attempt to maintain homeostasis under stress + example

A

compensation, shivering in the cold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

cell injury is the result of

an example

A

stimulus in EXCESS of the cells immediate compensation response

hypothermia causing frostbite

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

an injury that dost kill the cell

A

reversible cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

example of reversible cell injury

A

muscles get bigger from working out

whatever doesn’t kill it makes it stronger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

injury that results in cell death

A

irreversible cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

clean/controlled cell death

A

apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

messy uncontrolled cell death

A

necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

hypertrophy

A

cells get larger but don’t change in number ex muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

atrophy

A

cells get smaller but don’t change in number

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cells that can undergo hypertrophy but not hyperplasia

A

anything that does not multiply: fat cells (adipocytes, skeletal muscle, cardiac cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

three reasons for cardiac hypertrophy

A

HTN, valvular stenosis, power athletes (cyclists, rowers, always pumping against high pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

____________ happens as a result of reprogramming cells in reaction to a stressor

A

metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

change from one cell type to another in reaction to a stressor, examples

A

metaplasia, smokers and GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Explain metaplasia in GERD

A

stratified squamous turn into columnar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

cells that are not a legitimate cell type in body, not necessarily cancerous, could progress to cancer

A

Dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Low grade dysplasia

A

less progressed towards cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

High Grade dysplasia

A

more progresses towards cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cancer cells will almost always be ____________

A

dysplastic and neoplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

New growth, tumor

A

Neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

example of neoplasia that is not cancer

A

warts, which are also dysphagic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Not all _______ is cancer; but all cancer results in _________.

A

neoplasia, neoplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

An example of a stressor that doesn’t kill a cell but makes it stronger

A

Heart attack. Cells that don’t die prepare for future MI, Cardiomyocytes NOT replaced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the four common themes in cell injury?

A
  1. ATP depletion,
  2. Free radical and reactive oxygen species (ROS)
  3. Increase in intracellular CA++
  4. Defects in plasma membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Explain the how ATP depletion causes cellular swelling in ischemia and hypoxia

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

causes the oxidation of membranes and other structures in hypes and ischemia

A

free radicals and ROS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Free radicals and ROS are particularly problematic for ___________.

A

reprofusion. Think hydrogen peroxide bleaches,burns and bubbles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name three ways Ca++ is increased intercellularly in cell injury

A
  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)
  3. The Ca++ cannot release from the mitochondria and ER r/t concentration gradient.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Two disadvantages to having high intercellular calcium

A
  1. Calcium activates MANY enzymes

2. High intercellular Ca++ signals APOPTOSIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

defects in plasma membrane cause ______ and _____ to flood into cell

A

Ca++, Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

loss of the sodium gradient r/t defects in plasma membrane will activate ____________

A

Proteases and phosphalipases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

the cell swells r/t _________ gradient and makes the ______________________. the plasma membrane swells then ruptures.

A

Na+

Plasma membrane permeable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

clinical findings with reversible cell injury

A

decreased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

clinical findings with irreversible cell injury

A

decreased pH and the release of intracellular enzymes

CPK, LH, Troponin ALT, AST, myoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do cells become acidotic with ischemic tissue injury

A
  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+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is lactate?

A

Lactate is pyruvate with an H+ added.

Lactate buffers H+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Autophagy

A

lysosomes swell and begin to rupture, digestive enzymes begin to break down the cells.

small amount in reversible cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What happens intercellularly when a tissue is acidotic?

A
  1. Nucleus clumping- reversible but no access to DNA = no protein being made
  2. lysosomes swell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

decreased ATP production causes an ___________ in extracellular _______, while it causes an ________ in intracellular ______

A

increase, potassium, increase calcium and sodium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Sodium is the driver for all _____________, if we lose the sodium gradient, we lose __________.

A

secondary active transport, Na/Ca exchanger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

In cellular damage, what causes the inability to maintain the cytoskeleton?

A

The rough ER is dilated and there is a DETACHMENT OF RIBOSOMES which will cause a decrease in protein synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

when does the cellular damage become irriversiible?

A

when the cell loses the ability to maintain the cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is also related to the inability to maintain the cytoplasm?

A

membrane damage

lipid deposition and breakdown

loss of phospholipids

Activation of inflammation

increased free radical

loss of phospholipids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

three things that are turned on with the activation of inflammation

A

complement

cytokines

leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

REVERSIBLE or IRREVERSIBLE

clumping of DNA nuclear chromatin

A

REVERSIBLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

REVERSIBLE or IRREVERSIBLE

Karyolysis

A

IRREVERSIBLE

Karyolysis = chopping up nucleus = DNA destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

REVERSIBLE or IRREVERSIBLE

Swelling and blebs on cell membrane

A

REVERSIBLE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

REVERSIBLE or IRREVERSIBLE

Defects in cell membrane

A

IRREVERSIBLE

lose Na gradient and Ca+ rushes in

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

REVERSIBLE or IRREVERSIBLE

Small densities

A

REVERSIBLE

small densities = clumping and swelling of mitochondria- change pH it will unclip

52
Q

REVERSIBLE or IRREVERSIBLE

Lysosome appearance

A

REVERSIBLE

Small amount of autophagy, lysosomes eat mitochondria that are in bad shape

53
Q

REVERSIBLE or IRREVERSIBLE

Lysis of ER

A

IRREVERSIBLE

54
Q

REVERSIBLE or IRREVERSIBLE

Lysis of Lysosomes

A

IRREVERSIBLE

AKA: Autophagy

55
Q

REVERSIBLE or IRREVERSIBLE

Large densities in mitochondria

A

IRREVERSIBLE

56
Q

REVERSIBLE or IRREVERSIBLE

Lysis of DNA in nucleus

A

IRREVERSIBLE

57
Q

How do we know cells have necrosed?

A

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
Q

hypoxia, hypoxemia, ischemia

A

Causes of oxygen deprivation Cell injury

59
Q

trauma, heat, cold, pressure, radiation

A

physical agents causing cellular injury

60
Q

poisons and drugs

A

chemical agents causing cell injury

61
Q

immunologic responses

A

infectious agents causing cellular injury

62
Q

x,y

A

genetic mutations causing cellular injury

63
Q

low tissue oxygen level, caused by hypoxemia or hemoglobin problems

A

hypoxia

64
Q

Anemia will not cause _________ but will cause ________ because the oxygen saturation’s still 100%

A

hypoxemia, hypoxia

65
Q

very low tissue oxygen

A

anoxia, extreme form of hypoxia

66
Q

low blood oxygen tension or pressure

A

hypoxemia

67
Q

caused by poor air exchange, difficulty breathing, suffocation and heart failure

A

hypoxemia

68
Q

caused by hypoxemia

A

decreased oxygen saturation

69
Q

insufficient blood supply to tissue or organ that is reversible

A

Ischemia

70
Q

Ischemia with necrosis

A

Infarction - if it doesn’t die it isn’t an infarct

71
Q

restoration of blood supply that had been cut off

A

reprofusion

72
Q

Oxygen returning to damaged tissues causes additional problems

A

reprofusion injury

73
Q

when blood flow is restored tissues are damaged with free radicals

A

Thrombus- with all theee ROS

74
Q

when blood flow is restored tissues are damaged with ROS

A

Embolism only suparaoxide and supraoxidedismutase NOT hydrogen peroxide

75
Q

fixed obstruction blood flow, must rid body of it

A

Thrombus

76
Q

Moving, breaks off and gets stuck somewhere THEN the blood supply is cut

A

Embolism

77
Q

molecule with unpaired electron written with a little dot

A

free radical

78
Q

highly reactive molecule that contains oxygen

A

Reactive oxygen species (ROS)

79
Q

superoxide dismutase

A

convers superoxide (02.) ion to hydrogen peroxide

80
Q

NOT a free radical, but a reactive oxygen species

A

Hydrogen peroxide

81
Q

produced by peroxisome

A

hydrogen peroxide

82
Q

catalase

A

converts hydrogen peroxide to water

83
Q

produced in miscellaneous metabolism

A

hydroxyl radical (OH-)

84
Q

glutathione peroxidase

A

gets rid of hydroxyl radical by converting it to hydrogen peroxide —- then caltalase can reduce it to H2O

85
Q

both superoxide and hydroxyl radicals are converted to______________, then converted into H20 by ____________,

A

hydrogen peroxide, catalase

86
Q

reprofusion injury

A
  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

  1. also get an influx of Ca+ which also causes harm
87
Q

NECROSIS or APOPTOSIS

enlarged size/swelling

A

NECROSIS

88
Q

NECROSIS or APOPTOSIS

reduced size/shrinkage

A

APOPTOSIS

89
Q

NECROSIS or APOPTOSIS

Chromosome clumping

A

NECROSIS

90
Q

NECROSIS or APOPTOSIS

nuclear chomatin condensation and fragmentation

A

APOPTOSIS

91
Q

NECROSIS or APOPTOSIS

plasma membrane disruption

A

NECROSIS

92
Q

NECROSIS or APOPTOSIS

membrane entact with altered structures/lipids

A

APOPTOSIS

93
Q

NECROSIS or APOPTOSIS

cellular contents leak out of cell

A

NECROSIS

94
Q

NECROSIS or APOPTOSIS

Pathologic- inflammation

A

NECROSIS

95
Q

NECROSIS or APOPTOSIS

Physiologic- Phagocytosis

A

APOPTOSIS

96
Q

NECROSIS or APOPTOSIS

apoptotic bodies have a membrane around them keeping cellular contents enclosed

A

APOPTOSIS

97
Q

Type of necrosis:

anywhere there is an infarction besides the brain

A

Coagualative Necrosis

98
Q

Type of necrosis:

Structures stand but tissue dead

A

Coagualative Necrosis, like an egg white-

Seen in kidney where tissue maintains architecture after cell deaths a result of infarction

99
Q

Type of necrosis:

Inflammatory cells completely destroy architecture of the area

A

Liquifactive Necrosis

100
Q

Type of necrosis:

Happens with infarctions in the brain

A

Liquifactive Necrosis

brain will have holes and tissue replaced with fluid

101
Q

Type of necrosis:

abcess filled with fluid

A

Liquifactive necrosis

102
Q

Type of necrosis:

Neutrophils -digestive enzymes

A

Liquifactive necrosis

103
Q

Type of necrosis:

yellow white and cheesy

A

Caseous necrosis

104
Q

Type of necrosis:

Happens specifically with TB

A

Caseous necrosis

105
Q

Type of necrosis:

waxy deposits

A

Caseous necrosis

106
Q

Type of necrosis:

typically seen in pancreas

A

Fat necrosis

107
Q

Type of necrosis:

lipase break down triglycerides - Free fatty acids released

A

Fat Necrosis

108
Q

Type of necrosis:

FFA combine with Ca++ to create soap (saponification)

A

Fat necrosis

this is why we see a decrease in calcium with pancreatitis

109
Q

Type of necrosis:

if pancreatic enzymes release, they digest fat in that area and calcium reacts and we get fatty calcium deposits

A

Fat necrosis

110
Q

Type of necrosis:

calcium deposits in breasts that show up on mammogram

A

Fat necrosis

111
Q

Type of necrosis:

occurs in dry tissue; involves infections exposed to air

A

Dry Gangrene

112
Q

Type of necrosis:

moist tissue, internal organs and bedsores; numerous bacteria involved

A

Wet gangrene

113
Q

Type of necrosis:

Clostridium

A

Dry gangrene

114
Q

Type of necrosis:

C perftingens

A

Wet Gangrene

115
Q

Type of necrosis:

similar to wet gangrene with the addition of gas production

A

Gas Gangrene

116
Q

Type of necrosis:

medical emergency can lead to sepsis and death

A

Gas Gangrene

117
Q

dosent code for anything

A

telomeres

118
Q

DNA cap ant end of chromosomes

A

telomeres

119
Q

when we have lost enough telomeres the cell doesn’t replicate anymore

A

replicative senescence

120
Q

have enzyme on to maintain telomere indefinitely

A

germ cells

121
Q

telomerase partially on

A

stem cells

122
Q

Telomerase activitvation turns off the “telomeric clock”

A

cancer cells

123
Q

the older a man, the longer his telomerase cap

A

on his spermatagonia

124
Q

Type of necrosis:

result of liquefactive necrosis, skin dry and shrinks

A

dry gangrene

125
Q

Type of necrosis:

neutrophils invade site, liquifactive

A

Wet gangrene

126
Q

Three factors needed for gangrene

A
  1. Infectious agent
  2. Poor circulation - can’t fight infection
  3. Neuropathies, cannot feel

Pathophysiology Spring 16 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions