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General Pathology > Chapter 1 > Flashcards

Chapter 1 Flashcards

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1
Q

Pathology is the study of ______

A

disease (suffering)

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2
Q

Etiology is defined as:

A

Origin of disease (why)

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3
Q

Pathogenesis is defined as:

A

Steps in development (how)

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4
Q

What are the 4 types of cellular adaptations to stress

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia

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5
Q

Define Hypertrophy

A

Increase size of cells/organ, with no new cells

cells are incapable of replication

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6
Q

Define Hyperplasia

A

increase number of cells

cells must be able to replicate

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7
Q

Defne Atrophy

A

Reduction in cell/organ size
decreased protein synthesis
increased protein breakdown
decreases overall function but not dead!

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8
Q

Denervation and ischemia to a muscle will cause _______

A

atrophy

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9
Q

Features of cerebral atrophy

A

narrowed gyri

widened sulci

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10
Q

Causes of cerebral atrophy

A

atherosclerosis (ischemia)
alzheimer disease
cerebral palsy
malnutrition

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11
Q

Define Metaplasia

A

reversible replacement of 1 mature (differentiated) cell type by another
more resilient cell type

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12
Q

What is a common cause of metaplasia

A

adaptation to prolonged stressors like chronic irritation from smoking or GERD

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13
Q

2 consequences of metaplasia

A

altered structure can decrease function

risk for malignant transformation

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14
Q

injury occurs once stressors…

A

exceed a cells ability to adapt

directly induce abnormalities

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15
Q

2 types of injury

A

reversible and irreversible

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16
Q

3 steps of necrosis

A

Karyolysis, pyknosis and karyorrhexis

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17
Q

5 general types of necrosis

A

coagulative, liquifactive, caseous, fat, and fibrinoid

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18
Q

Coagulative Necrosis is caused by…

A

ischemia (aka, ischemic necrosis)

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19
Q

Define solid organ infarction

A

phenomenon that occurs when coagulative necrosis occurs in a solid organ like a kidney.
tissue structure is preserved due to the denaturation of proteolytic enzymes, which lasts for a few days-weeks

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20
Q

Gangrenous necrosis

A

coagulative necrosis in an extremity
commonly caused by peripheral vascular disease (diabetes, atherosclerosis)
dry, wet, gas –> all equally gross

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21
Q

Liquifactive necrosis

A

dead cells get completely digested
WBC enzymes produce a liquid viscous mass
eventual phagocytosis

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22
Q

2 instances of liquifactive necrosis

A

infections (bacterial: pus and abscess; fungal)

CNS ischemia/Hypoxia

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23
Q

Caseous Necrosis

A

“cheese-like” appearance: friable

ENCLOSED WITHIN A DISTINCTIVE BORDER

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24
Q

Most common cause of Caseous Necrosis

A

Tuberculosis (TB)

“caseating granuloma”

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25
Granuloma is defined as...
walled-off collection of macrophages
26
Fat necrosis
localized fat destruction
27
2 causes for fat necrosis
acute pancreatitis: leaked pancreatic enzymes which cause fat saponification trauma to breast
28
Fibrinoid Necrosis
Caused by autoimmune reactions in which immune complexes + fibrin are deposited into arterial walls Requires histological evaluation
29
Examples of conditions that cause Fibrinoid Necrosis
Polyarteritis Nodosa Systemic Lupus Erythmatosus Malignant Hypertension Transplant Rejections
30
Apoptosis
Programmed/regulated cell death caused by enzymatic breakdown intact membranes --> no inflammation
31
Mitochondrial (Instrinsic) Pathway of Caspase Activation
Decrease GF, DNA damage, Misfolded proteins Increased mitochondrial membrane permiability Utilizes Caspase 9
32
Death Receptor (Extrinsic) Pathway of Caspase Activation
Binding with surface molecules "death receptors" eliminates self-reactive lymphocytes or virus infected cells utilizes Caspase 8
33
What is autophagy
Lysosomal digestion of a cell's components
34
Depletion of ATP as a mechanism of cellular injury
hypoxia, nutritional deficiency, mitochondrial damage, toxins decrease oxidative phosphorylation (glycolytic capacity in liver and brain) ATP-dependent pumps (increase Na and Ca) Glycolysis (decrease pH)
35
Mitochondrial damage as a mechanism of cellular injury
Hypoxia, toxins, irradiation disrupted membranes --> necrosis increased ROS production --> Apoptosis
36
influx of calcium as a mechanism of cellular injury
ischemia and toxins | activates enzymes --> apoptosis
37
Oxidative stress as a mechanism of cellular injury
ischemia-reprofusion, toxins, irradiation, cellular aging (redox), inflammation (macrophages and neutrophils) accumulation of ROS --> apoptosis
38
Defects in membrane permiability as a mechanism of cellular injury
ischemia, toxins, physical trauma, complement activation phospholipids: decrease production & increase breakdown involves many important membranes (mitochondrial, planma, lysosome) hallmark of tissue necrosis
39
DNA and protein damage as a mechanism of cellular injury
severe oxidative stress, irradiation, abnormal protein folding severe/irreparable damage stimulates apoptosis
40
Ischemia and hypoxic injury impacts aerobic and anaerobic metabolism
aerobic: mitochondrial damage (decrease ATP, Increase ROS anaerobic: decrease glycolysis substrates, increase waste
41
ischemia and hypoxic injuries are reversible, true or false?
True, if blood supply and oxygen are restored in a timely manner
42
Persistent ischemia
irreversible injury ruptured membranes necrosis and minimal apoptosis
43
Ischemia reprofusion injury
temporary ischemia where restoration of blood flow causes inflammation which increases ROS
44
Direct chemical injury
combination with cellular organelles cells that absorb, use, excrete or store a toxin inhibits use of ATP or damages membranes
45
Indirect chemical injury
biologic conversion produces a reactive metabolite
46
Intracellular accumulations are caused by (4)
Abnormal metabolism (fatty liver disease) Defective protein folding/transport (mutations) Defective or absent enzymes Ingestion of indigestible materials (silica, asbestos, coal dust)
47
Fatty change (steatosis)
abnormal accumulation of lipids within tissue parenchyma triglycerides are common intracellular inclusions Alcoholic liver disease and non-alcoholic liver disease
48
2 types of pathologic calcification
dystropic calcification | metastatic calcification
49
dystropic calcification
accumulation of Ca within damaged tissue traumatized cells and necrotic cells normal Ca metabolism
50
Fibrodysplasia ossificans progressiva
``` dysfunctional soft tissue repair any trauma --> heterotopic ossification joint ankylosis (fusion) severe deformation and dysfunction ```
51
Metastatic calcification
accumulation of Ca within normal tissues caused by abnormal Ca homeostasis (hypercalcemia) may deposit into any tissue most common are vessels, kidneys, lungs, GI tract
52
Cellular aging
reduced functional capacity of cells caused by accumulation of cellular/molecular damage
53
3 causes of cellular aging
DNA damage: accelerated by ROS Replicative senescence: shortened telomeres --> no more mitosis defective protein homeostasis: decreased synthesis, increased turnover, more misfolding
54
Progeroid syndromes
accelerated aging
55
progeroid syndrome in teens
Bloom Syndrome
56
Progeroid syndrome in adults (40s)
Werner Syndrome
57
Karyolysis
Nuclear fading - chromatin dissolution due to action of DNAases and RNAases
58
Pyknosis
Nuclear shrinkage - DNA condenses into shrunken basophilic mass
59
Karyorrhexis
Nuclear fragmentation - pyknotic nuclei membrane ruptures & nucleus undergoes fragmentation
60
myocardium subjected to persistent increased load, as in hypertension or with narrowed (stenotic) valve, adapts by undergoing...
hypertrophy
61
pathologic adaptations are...
responses to stress that allow cells to modulate their strucure and function and thus escape injury
62
metaplasia is thought to arise by...
reprogramming of stem cells to differentiate along a new pathway rather than a phenotypic change
63
hypoxia
oxygen deficiency
64
ischemia
loss of blood supply
65
lipfuscin
wear and tear pigment that can accumulate in a variety of tissue as a function of age or atrophy

General Pathology (6 decks)

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