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Pathology > Chapter 1 > Flashcards

Chapter 1 Flashcards

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1
Q

What is pathology?

A

study of disease

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2
Q

What are observable changes?

A

signs and symptoms

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3
Q

What is Etiology?

A

origin of disease. “why”

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4
Q

What is Pathogenesis?

A

the steps in development (how etiologic factors induce cellular change): the “how”

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5
Q

What does Homeostasis require?

A

adaptions to stress

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6
Q

What is homeostasis

A

the attempt of a cell to preserve viability and function

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7
Q

What are the cellular adaptions?

A
  1. hypertrophy
  2. hyperplasia
  3. atrophy
  4. metaplasia
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8
Q

When does cellular injury occur?

A

when the ability to adapt is exceeded

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9
Q

What kind of cellular injuries are there?

A
  1. reversible cell injury

2. irreversible cell injury (cell death)

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10
Q

What is hypertrophy?

A

increase in size of cells/organ without new cells.

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11
Q

How is hypertrophy caused?

A
  1. overloading

2. increasing growth factors (GF’s)

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12
Q

What is hyperplasia?

A

increase in number of cells

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13
Q

What must a cell be able to undergo in order to go through hyperplasia?

A

Cells must be able to replicate

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14
Q

How does hyperplasia occur?

A
  1. Hormonal factors

2. Compensatory factors

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15
Q

Name an example of pathologic hyperplasia

A

HPV

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16
Q

How is hyperplasia controlled?

A

Hyperplasia responds to a decrease in GF

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17
Q

What is atrophy?

A

reduction in cell size/organ and decrease in function but it is not dead

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18
Q

what causes a cell to reduce in size when undergoing atrophy?

A

decrease protein synthesis and increase in protein breakdown

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19
Q

What are the causes of atrophy?

A
  1. disuse
  2. Denervation
  3. Ischemia
  4. Endocrine disruption
  5. Aging
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20
Q

What is metaplasia?

A

reversible replacement of 1 mature cell type by another

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21
Q

What are the consequences of metaplasia?

A

altered structure = decrease function and risk for malignant transformation

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22
Q

What causes Metaplasia?

A

adaption to prolonged stressors such as smoking.

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23
Q

What is steatosis?

A

fatty accumulation which causes cellular swelling

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24
Q

What type of cellular injury causes damage to mitochondria cellular membranes?

A

Irreversible injury

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25
When does Reversible injury heal?
healing occurs if the stressor is removed
26
What irreversible cell injury is always pathological?
Necrosis
27
What irreversible cell injury can be pathological or physiological?
apoptosis
28
Inflammation is always present in what type of cell injury?
necrosis
29
What necrosis preserves structure?
coagulative necrosis
30
What causes coagulative necrosis?
vascular occlusion (ischemia) causes tissue death
31
What is gangrene necrosis?
coagulative necrosis in an extremity
32
What are the varieties of gangrene?
dry, wet and gas
33
In liquifactive necrosis what happens to dead cells?
they are completely digested
34
WBC produce a liquid viscous mass in what type of necrosis?
liquefactive
35
What are the causes of liquefactive necrosis?
1. Infections- bacterial is most common | 2. CNS ischemia/hypoxia
36
what happens to the liquid viscous mass in liquefactive necrosis?
eventually goes through phagocytosis
37
What is the appearance of caseous necrosis?
it has a "cheese-like" appearance: friable, yellow/white
38
What is a granuloma?
a walled-off area of macrophages
39
what necrosis is enclosed within a distinctive boarder?
Caseous necrosis
40
What is a typical cause of Caseuous necrosis?
tuberculosis
41
What is fat necrosis?
localized fat destruction
42
In fibrinoid necrosis weakened vessel walls can lead to a risk of what?
aneurysm
43
what is fibrinoid necrosis?
autoimmune reactions
44
What is apoptosis?
programmed/regulated cell death by enzymatic breakdown
45
what cells go through apoptosis?
cells that unneeded or irreparable
46
What are apoptotic bodies?
bodies that fall off the cell that go to a phagocyte
47
When caspases are activated what happens?
apoptosis starts
48
What pathway is caspase-9 associated with?
Mitochondrial (intrinsic) pathway
49
What pathway is caspase-8 associated with?
Death receptor (extrinsic) pathway
50
What happens in the Mitochondrial pathway for apoptosis?
decrease in GF, DNA damage, misfolded proteins, increase in mitochondrial membrane permeability
51
what marks a cell to go through the death receptor pathway of apoptosis?
binding with surface molecules coined "death receptors"
52
What does the death receptor apoptosis pathway eliminate?
self-reactive lymphocytes or virus infected cells
53
what protein is not correctly working in alzheimer's disease?
Beta-amyloid proteins (excess of them)
54
what is our survival mechanism during nutrient deprivation?
Autophagy (self-eating)
55
what is autophagy?
self-eating: lysosomal digestion of a cell's components
56
What are the mechanisms in cellular injury?
1. depletion of ATP 2. Mitochondrial damage 3. Influx of calcium 4. oxidative stress 5. defects in membrane permeability 6. DNA and protein dmg
57
What causes depletion of ATP?
hypoxia, nutritional defiency, mitochondrial damage, toxins
58
What causes Mitochondrial damage?
hypoxia, irradation, toxins (HIT)
59
What causes an influx of calcium?
ischemia and toxins
60
what does an influx of calcium do?
activates enzymes that lead to cell death
61
what occurs when membranes are disrupted?
necrosis
62
what happens when we have an increase of ROS? (Mitochondrial damage)
apoptosis
63
what is oxidative stress?
accumulation of ROS
64
What causes oxidative stress?
ischemia-reperfusion, toxins, irradiation, cellular aging (redox), inflammation
65
what causes membrane permeability
ischemia, toxins, physical trauma, complement activation
66
what is the hallmark of tissue necrosis?
defects in membrane permeability
67
When we have defects in membrane permeability, what happens to phospholipids?
decrease in production and increase in breakdown
68
what causes DNA and protein damage?
severe oxidative stress, irradiation, abnormal protein folding
69
what is ischemia?
decrease in blood flow
70
what does ischemia produce?
acute cellular injury
71
what kind of metabolism does ischemia impact?
both types (aerobic and anaerobic)
72
when is ischemia reversible?
when there is a restoration of blood supply (and oxygen) without persistent ischemia
73
When does ischemia produce irreversible injury?
when it's persistent ischemia
74
what are the products of persistent ischemia?
ruptured membranes, necrosis and minimal apoptosis
75
What is ischemia-reperfusion?
a temporary ischemia that cause injury when blood flow is restored
76
what's an example of ischemia-reperfusion?
Myocardial infarction (MI) and strokes
77
What is direct chemical injury?
when toxins combine with cellular organelles
78
What is indirect chemical injury
the biological conversion produces a reactive metabolite
79
What are examples of indirect toxic injury?
Cytochrome p-450 and Acetominophen
80
in what cells can direct chemical injury occur?
in cells that absorb, use, excrete, or store a toxin?
81
what does chemical injury inhibit?
use of ATP or it damages membranes
82
what are examples of intracellular accumulations?
1. abnormal metabolism 2. defective protein folding/transport 3. defective or absent enzymes 4. ingestion of indigestible materials
83
what are some examples of indigestible materials?
silica, coal dust and asbestos
84
What is dystrophic calcification?
accumulation of Ca++ within damaged tissue with Normal Ca++ metabolism
85
what is joint ankylosis?
heterotopic ossification (fusion of bones)
86
when is theonset for fibrodysplasia ossificans progressiva ?
infancy
87
What is fibrodysplasia ossificans progressiva?
dysfunctional soft tissue repair of chromosome 4
88
What is metastic calcification?
accumulation of Ca++ within normal tissue with Abnormal Ca++ homeostasis
89
What is hypercalcemia?
an increased serum Ca++
90
What are the common sites for metastatic calcification
vessels, kidneys, lungs, G.I. tract

Pathology (3 decks)

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