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Anaphy Lec > Unit 2 Part 2 > Flashcards

Unit 2 Part 2 Flashcards

1
Q

Study of disease

A

Pathology

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2
Q

infection, genetic etc. and often mutifactoral

A

Etiology of cause

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3
Q

Progression of disease

A

Pathogenesis

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4
Q

Signs and symptoms

A

Clinical manifestations

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5
Q

Pathology 4 studies

A

Etiology
Pathogenesis
Molecular and morphologic changes
Clinical manifestations

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6
Q

Structural and functional units of tissues and organs

A

Cells

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7
Q

Capable of adjusting their structure and functions in response to physiological and pathological conditions

A

Cell adaptation

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8
Q

New steady state
Preserving viability

A

Adaptation

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9
Q

Cell poliferation (3 variables)

A

Labile
Stable
Permanent

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10
Q

Continously dividing

A

Labile cells

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11
Q

Labile cells example

A

Epithelium
Bone marrow
Hematopoietic cells

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12
Q

Quiescent
In g0 stage

A

Stable cells

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13
Q

Stable cells example

A

Hepatocytes
Smooth muscle
Lmphocytes

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14
Q

Nondividing

A

Permanent cells

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15
Q

Permanent cells example

A

Neurons
Skeletal and cardiac muscle

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16
Q

Types of adaptations are conrolled by

A

Complex molecular mechanisms

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17
Q

Types of cellular adaptation

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Dysplasia*

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18
Q

normal stressor/stimuli; results in enhanced function

A

Phsyiologic adaptation

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19
Q

abnormal stressor/stimuli; results in dysfunction and mortality

A

Pathologic

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20
Q

adaptation to positively counteract reduction in function

A

Compensatory adaptation

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21
Q

Increase in size; organ enlargement
No new cells
Increase in mrna and proteins

A

Hypertrophy

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22
Q

in response to increased demands
seen in cells that cannot divide
changes usually revert to normal if cause is removed

A

Hypertrophy

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23
Q

Gym body

A

Physiologic hypertrophy

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24
Q

Heart of patient with long standing hypertension

A

Pathologic hypertrophy

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25
Q

Increased number of cells
Co-exist with hypertrophy
Takes place IF cell if capable of replication

A

Hyperplasia

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26
Q

Female breast in puberty and pregnancy

A

Physiologic hyperplasia

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27
Q

Excessive hormonal stimulation

A

Pathologic hyperplasia

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28
Q

Hypertrophy and hyperplasia example

A

Gravid uterus during pregnancy

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29
Q

Loss of substance-Shrinkage in the size of cell
Sufficient number of cells is involved
Entire tissue or organ diminishes in size
Not dead

A

Atrophy

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30
Q

Atrophy results from both

A

Decreased protein synthesis
Increased protein degradation

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31
Q

Lysosomes with hydrolytic enzymes
Ubiquitin-proteasome pathway

A

Increased protein degradation

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32
Q

Brain atrophy
Uterus atrophy

A

Physiologic atrophy

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33
Q

Inadequate nutrition (malnutrition)
Diminished blood supply

A

Pathologic atrophy

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34
Q

-Reversible change
-Adult cell type is replaced by another cell type for adverse envi
-occurs in response to stress or chronic irritation

A

Metaplasia

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35
Q

Mechanisms of metaplasia

A

Re-programming of stem cells
Induced by cytokines, growth factors, envi signals
Retinoic acid may play a role
Unknown exact mechanism

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36
Q

Metaplasia SOM

A

Squamous
Osseous
Myeloid

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37
Q

Cigarette smoking
Gastroesophageal reflux disease
Glandural epithelium

A

Squamous metaplasia

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38
Q

TRUE OF FALSE
Atrophy, hypertrophy, hyperplasia, and metaplasia are reversible changes

A

TRUE

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39
Q

TRUE OR FALSE
Hyperplasia and Metaplasia are not premalignant changes

A

TRUE

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40
Q

Fertile fields for dysplasia

A

Hyperplasia and metaplasia

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41
Q

Atypical proliferative changes
due to chronic irritation or inflammation
Cells vary in size and shape
Large nuclei
Increased rate of mitosis
Premalignant change

A

Dysplasia

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42
Q

Cells are undiferrentiated w nuclear and cell structures and mitotic figures
Cancer and tumor is the basis for grading its aggressiveness

A

Anaplasia

43
Q

New growth
Tumor

A

Neoplasia

44
Q

Less serious cancer cells
Do not spread and are not life threatening (except in the brain)

A

Benign

45
Q

Progressive cancer cells

A

Malignant

46
Q

Failure of cell production
During fetal development, it results to agenesis

A

Aplasia

47
Q

Absence of an organ due to failure of production

A

Agenesis

48
Q

Incomplete development of an organ
Decrease in cell production

A

Hypoplasia

49
Q

Examples of hypoplasia

A

Hypoplastic left ventricle
Hypoplastic kidney

50
Q

control the composition of their immediate environment and intracellular milieu within a narrow range of physiological parameters

A

homeostasis

51
Q

denotes pathologic changes that can be reversed when the stimulus is removed, or if the cause of injury is mild

A

Reversible cell injury

52
Q

denotes pathologic changes that are permanent and cause cell death

A

Irreversible injury

53
Q

oxygen deprivation

A

Hypoxic Cell injury

54
Q

loss of blood supply
more rapidly and severely injures

A

Ischemia

55
Q

cardiorespiratory failure

A

Inadequate oxygenation

56
Q

anemia, carbon monoxide poisoning

A

Loss of oxygen carrying capacity of blood

57
Q

Causes of Cellular Injury
Hypoxic Cell injury

A

a. Ischemia
b. Inadequate oxygenation
c. Loss of oxygen carrying capacity of blood

58
Q

High Susceptibility of Cells to Hypoxic Injury

A

Neurons (3-4 min)

59
Q

Intermediate Susceptibility of Cells to Hypoxic Injury

A

Myocardium, hepatocytes, renal epithelium (30 min-2hr)

60
Q

Low susceptibility of cells to hypoxic injury

A

Fibroblasts, epidermis, skeletal
muscle (many hours)

61
Q

ROS

A

Hydroxyl, Hydrogen, Superoxide

62
Q

-with a single unpaired electron in an outer orbital
-Chemically unstable=chemical damage
- Initiate autocatalytic reactions

A

Free Radical Injury

63
Q

If not adequately neutralized, free radicals
can damage cells by

A

Lipid peroxidation of membranes
DNA fragmentation
Protein cross-linking

64
Q

double bonds in polyunsaturated
membrane lipids are vulnerable

A

Lipid peroxidation of membranes

65
Q

react with thymine in nuclear and mitochondrial

A

DNA fragmentation

66
Q

promote sulfhydryl-mediated protein cross
linking

A

Protein cross-linking

67
Q

Neutralization of Free Radicals

A

SpoSuGCaEn

  1. Spontaneous decay
  2. Superoxide dismutase
  3. Glutathione (GSH)
  4. Catalase
  5. Endogenous and exogenous antioxidants
    (Vitamins E, A, C and β carotene)
68
Q

cellular injury trauma, heat, cold,
radiation, electric shock

A

physical agents

69
Q

-Therapeutic drugs - paracetamol
-Nontherapeutic agents – lead, alcohol
-Binding of mercuric chloride to sulfhydryl
groups of proteins
-Generation of toxic metabolites such as
conversion of CCl4 to CCL3* free radicals in
the SER of the liver

A

Chemical Agents

70
Q

Causes of Cellular Injury

Infectious Agents

A

ViBaFuRiBaFuPa

a) Viruses
b) Bacteria
c) Fungi
d) Rickettsiae
e) Bacteria
f) Fungi
g) Parasites

71
Q

direct effects of
bacterial toxins; cytopathic effects of

A

Infectious agents

72
Q

-interfering with DNA,RNA, proteins, cell
membranes or
-inducing apoptosis.
-indirect effects via the host immune reaction.

A

infectious agents

73
Q

anaphylaxis, loss of
immune tolerance leading to autoimmunity

A

Immune System -

74
Q

sickle cell
disease, inborn errors of metabolism

A

Genetic Abnormalities

75
Q

vitamin deficiencies, obesity leading to type II DM, fat leading to atherosclerosis

A

Nutritional imbalances

76
Q

degeneration as a result of
trauma, intrinsic cellular senesence

A

Aging

77
Q

causes of cell injury

A

Hypoxic Cell injury
Free Radical Injury
Physical Agents
Chemical Agents
Infectious Agents
Immune System
Genetic Abnormalities
Nutritional imbalances
Aging

78
Q

2 ways of cell death

A

necrosis
apoptosis

79
Q

-produced by enzymatic digestion of dead
cellular elements
-irreversible injury

A

necrosis

80
Q

eliminate unwanted cells–an internally programmed series of events effected

A

Apoptosis

81
Q

-Morphologic expression of cell death
-disintegration of cell structure
-initiated by overwhelming stress
-elicits an acute inflammatory cell
response

A

Necrosis

82
Q

types of necrosis

A

CoLiCaGaFiFa

coagulative
liquefactive
caseous
gangrenous
fibrinoid
fat

83
Q

seen in hypoxic environments
the outline of the dead cells are maintained the tissue is somewhat firm.

◼Example: myocardial infarction

A

Coagulative necrosis

84
Q

dead cells undergo disintegration and affected tissue is liquified

associated with cellular destruction
and pus formation

ischemia in the brain

Example: cerebral infarction

A

Liquefactive necrosis

85
Q

ischemia

A

restriction of blood supply

86
Q

form of coagulation (cheese-like)
caused by mycobacteria

Example: tuberculosis lesions.

A

Caseous necrosis

87
Q

(secondary to ischemia)
usually with superimposed infection

Example: necrosis of distal limbs, usually foot
and toes in diabetes.

A

Gangrenous Necrosis

87
Q

(secondary to ischemia)
usually with superimposed infection

Example: necrosis of distal limbs, usually foot
and toes in diabetes.

A

Gangrenous Necrosis

88
Q

by immune-mediated vascular damage.
by deposition of fibrin-like proteinaceous material in arterial walls
smudgy and eosinophilic

A

Fibrinoid necrosis

88
Q

by immune-mediated vascular damage.
by deposition of fibrin-like proteinaceous material in arterial walls
smudgy and eosinophilic

A

Fibrinoid necrosis

89
Q

release of powerful enzymes which damage fat by the production of soaps

chalky white

A

fat necrosis

89
Q

release of powerful enzymes which damage fat by the production of soaps

chalky white

A

fat necrosis

90
Q

fat necrosis types

A

Traumatic fat necrosis
Enzymatic fat necrosis

91
Q

necrosis of fat by pancreatic enzymes.

A

Enzymatic fat necrosis

92
Q

is restricted to necrosis involving spirochaetal infections (e.g. syphilis).

A

Gummatous necrosis

93
Q

blockage of the venous drainage (e.g. in
testicular torsion).

A

Haemorrhagic necrosis

94
Q

-Regulated suicide program
-Controlled by specific genes.
-Fragmentation of nucleus, DNA
-Blebs form and apoptotic bodies are released.
-Apoptotic bodies are phagocytized.
-No neutrophils.

A

Apoptosis

95
Q

n cells produced =n cells die
Development and morphogenesis
Homeostasis
Deletion of damaged/ dangerous cells

A

apoptosis

96
Q

 During limb formation separate digits evolve
 Ablation of cells no longer needed (tadpole)

A

Apoptosis: Development and morphogenesis

97
Q

 Immune system
 >95% T and B cells die during maturation
(negative selection)

A

apoptosis: Homeostasis

98
Q

Examples of Apoptosis

A

removal of excess cells during embryogenesis
maintain cell population (skin)
eliminate immune cells
remove damaged cells
eliminate cells with DNA damage
Hormone-dependent involution
Cell death in tumours.

99
Q

causes of apoptosis

A

◼ Physiologic
◼ Pathologic

100
Q

Physiologic Apoptosis

A

Embryogenesis and fetal development
Hormone dependent involution - mens
Cell loss in proliferating cell populations
Elimination of self-reactive lymphocytes
Death of cells
programmed cell destruction in
embryogenesis

101
Q

Pathologic Apoptosis

A

DNA damage due to radiation
misfolded proteins
viral infections hiv
Organ atrophy after duct obstruction

Anaphy Lec (13 decks)

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