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General Pathology > Chapter 1 > Flashcards

Chapter 1 Flashcards

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
Q

Granuloma is defined as…

A

walled-off collection of macrophages

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26
Q

Fat necrosis

A

localized fat destruction

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27
Q

2 causes for fat necrosis

A

acute pancreatitis: leaked pancreatic enzymes which cause fat saponification

trauma to breast

28
Q

Fibrinoid Necrosis

A

Caused by autoimmune reactions in which immune complexes + fibrin are deposited into arterial walls
Requires histological evaluation

29
Q

Examples of conditions that cause Fibrinoid Necrosis

A

Polyarteritis Nodosa
Systemic Lupus Erythmatosus
Malignant Hypertension
Transplant Rejections

30
Q

Apoptosis

A

Programmed/regulated cell death
caused by enzymatic breakdown
intact membranes –> no inflammation

31
Q

Mitochondrial (Instrinsic) Pathway of Caspase Activation

A

Decrease GF, DNA damage, Misfolded proteins
Increased mitochondrial membrane permiability
Utilizes Caspase 9

32
Q

Death Receptor (Extrinsic) Pathway of Caspase Activation

A

Binding with surface molecules “death receptors”
eliminates self-reactive lymphocytes or virus infected cells
utilizes Caspase 8

33
Q

What is autophagy

A

Lysosomal digestion of a cell’s components

34
Q

Depletion of ATP as a mechanism of cellular injury

A

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
Q

Mitochondrial damage as a mechanism of cellular injury

A

Hypoxia, toxins, irradiation
disrupted membranes –> necrosis
increased ROS production –> Apoptosis

36
Q

influx of calcium as a mechanism of cellular injury

A

ischemia and toxins

activates enzymes –> apoptosis

37
Q

Oxidative stress as a mechanism of cellular injury

A

ischemia-reprofusion, toxins, irradiation, cellular aging (redox), inflammation (macrophages and neutrophils)
accumulation of ROS –> apoptosis

38
Q

Defects in membrane permiability as a mechanism of cellular injury

A

ischemia, toxins, physical trauma, complement activation
phospholipids: decrease production & increase breakdown
involves many important membranes (mitochondrial, planma, lysosome)
hallmark of tissue necrosis

39
Q

DNA and protein damage as a mechanism of cellular injury

A

severe oxidative stress, irradiation, abnormal protein folding
severe/irreparable damage
stimulates apoptosis

40
Q

Ischemia and hypoxic injury impacts aerobic and anaerobic metabolism

A

aerobic: mitochondrial damage (decrease ATP, Increase ROS
anaerobic: decrease glycolysis substrates, increase waste

41
Q

ischemia and hypoxic injuries are reversible, true or false?

A

True, if blood supply and oxygen are restored in a timely manner

42
Q

Persistent ischemia

A

irreversible injury
ruptured membranes
necrosis and minimal apoptosis

43
Q

Ischemia reprofusion injury

A

temporary ischemia where restoration of blood flow causes inflammation which increases ROS

44
Q

Direct chemical injury

A

combination with cellular organelles
cells that absorb, use, excrete or store a toxin
inhibits use of ATP or damages membranes

45
Q

Indirect chemical injury

A

biologic conversion produces a reactive metabolite

46
Q

Intracellular accumulations are caused by (4)

A

Abnormal metabolism (fatty liver disease)
Defective protein folding/transport (mutations)
Defective or absent enzymes
Ingestion of indigestible materials (silica, asbestos, coal dust)

47
Q

Fatty change (steatosis)

A

abnormal accumulation of lipids within tissue parenchyma
triglycerides are common intracellular inclusions
Alcoholic liver disease and non-alcoholic liver disease

48
Q

2 types of pathologic calcification

A

dystropic calcification

metastatic calcification

49
Q

dystropic calcification

A

accumulation of Ca within damaged tissue
traumatized cells and necrotic cells
normal Ca metabolism

50
Q

Fibrodysplasia ossificans progressiva

A 
dysfunctional soft tissue repair
any trauma --> heterotopic ossification
joint ankylosis (fusion) severe deformation and dysfunction
51
Q

Metastatic calcification

A

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
Q

Cellular aging

A

reduced functional capacity of cells caused by accumulation of cellular/molecular damage

53
Q

3 causes of cellular aging

A

DNA damage: accelerated by ROS
Replicative senescence: shortened telomeres –> no more mitosis
defective protein homeostasis: decreased synthesis, increased turnover, more misfolding

54
Q

Progeroid syndromes

A

accelerated aging

55
Q

progeroid syndrome in teens

A

Bloom Syndrome

56
Q

Progeroid syndrome in adults (40s)

A

Werner Syndrome

57
Q

Karyolysis

A

Nuclear fading - chromatin dissolution due to action of DNAases and RNAases

58
Q

Pyknosis

A

Nuclear shrinkage - DNA condenses into shrunken basophilic mass

59
Q

Karyorrhexis

A

Nuclear fragmentation - pyknotic nuclei membrane ruptures & nucleus undergoes fragmentation

60
Q

myocardium subjected to persistent increased load, as in hypertension or with narrowed (stenotic) valve, adapts by undergoing…

A

hypertrophy

61
Q

pathologic adaptations are…

A

responses to stress that allow cells to modulate their strucure and function and thus escape injury

62
Q

metaplasia is thought to arise by…

A

reprogramming of stem cells to differentiate along a new pathway rather than a phenotypic change

63
Q

hypoxia

A

oxygen deficiency

64
Q

ischemia

A

loss of blood supply

65
Q

lipfuscin

A

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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