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Mechanisms of Disease > Cell Adaptation, Injury & Death > Flashcards

Cell Adaptation, Injury & Death Flashcards

1
Q

Anatomic pathology

A

Medical specialty - diagnose disease by its morphology, as seem in lab

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2
Q

Clinical pathology

A

Medical specialty - focusing on other aspects of the lab

-hematology, clinical chem, blood banking, UA,

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3
Q

Pathogenesis

A

The story of a disease

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4
Q

Functional disease

A

May not have a known morphological correlate

ie. schizophrenia, lbp, migraine

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5
Q

Becker’s nevus

A

Skin on the trunk that is extra-sensitive to testosterone

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6
Q

Incidence

A

number of new cases per unit time

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7
Q

Prevalence

A

number sick at any time

= Incidence x average duration

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8
Q

Risk

A

How much your unusual situation increases your chance of getting the disease

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9
Q

Biopsy

A

tissue from the living

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10
Q

Closed biopsy

A

tissue obtained for diagnosis without making a real surgical incision

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11
Q

Open biopsy

A

getting tissue by surgery

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12
Q

Incisional biopsy

A

a piece of tissue was take for diagnosis from a larger structure that is diseased

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13
Q

Excisional biopsy

A

The entire mass/organ was taken for diagnosis

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14
Q

Syndrome

A

A group of symptoms and/or signs with a common underlying pathophysiology but many different underlying diseases
ex. Meniere’s syndrome

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15
Q

Pathognomonic

A

A particular abnormality is found in only one disease or condition
Ex. fetal heartbeat when you are preggers

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16
Q

Forme fruste

A

A mild variant of a longstanding, typically much more severe disease
ie. scar vs. cleft lip

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17
Q

Aplasia/agenesis

A

Complete failure of an organ to form

ie. anencephaly

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18
Q

Atresia

A

A lumen completely failed to form

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19
Q

Occlusion

A

Once open, now closed

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20
Q

Hypoplasia

A

Failure of an organ to grow into normal size along wight he rest of the body

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21
Q

Syn- and holo-

A

Both mean things didn’t separate

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22
Q

Hamartoma

A

The right stuff in the right place, but wrong arrangement/mix
ie. vascular hamartoma - aka stork bite or tuberous sclerosis

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23
Q

3 conditions necessary for a cyst

A

Fluid filled
Epithelially lined
Closed
ie. mucocele - mucous cyst in the mouth

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24
Q

Choristomas

A

Good stuff in the wrong place

ie. Fordyce granules

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25
Q

Fordyce granules

A

Sebaceous glands in the mouth

type of choristomas

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26
Q

Fistula

A

Abnormal, epithelially lined communication between two surfaces.
ie. piercing

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27
Q

Pathological sinus

A

One end is a sack - leads to nowhere

Most familiar is pilonidal cyst/sinus

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28
Q

True diverticulum

A

Includes the muscle

Ex. Meckel’s, normal appendix

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29
Q

Pseudodiverticulum

A

Through the muscle

ie. Zenker’s esophageal, common colon ‘ticks’

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30
Q

Atrophy

A

Organ shrinkage due to cell loss

-usually irreversible

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31
Q

Cachexia

A

Wasting of the entire body as a result of cytokine activity/cancer
-selectively destroys muscle over fat

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32
Q

Hypertrophy

A

Increase in the sizes of cells and hence the size of the organ
Sometimes helpful - body builder
Sometimes not - heart

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33
Q

What is an example of an organ that undergoes hypertrophy and hyperplasia?

A

Pregnant uterus

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34
Q

How thick should the left ventricle be in a non-athlete?

A

Not thicker than 1.5 cm

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35
Q

Hallmark of myocardial hypertrophy

A

Many more than the normal 92 chromosomes

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36
Q

Hyperplasia

A 
The organ gets bigger because it now has more cells
--ie. you are a medical student studying for this new crazy class that the powers that be dreamed up. You suddenly die during your final exam. During the autopsy they find your adrenal cortex is ~ 30 grams vs. 8 grams found in a nursing student. Why is the dead student doctor's adrenal cortex so large? Hyperplasia due to stress and overuse
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37
Q

Prayer mark

A

Hyperplasia of the epidermis

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38
Q

What do most goiters result from?

A

Hyperplasia of thyroid epithelium

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39
Q

Endometrial hyperplasia

A

Hyperplasia driven by genetic mutation

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40
Q

Metaplasia

A

One adult type tissue component replaces another

ie. pseudo stratified epithelium of the big airways by a more protective stratified squamous epithelium

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41
Q

Anaplasia

A

Cells that are bizarre, unlike any normal cells

ie. in a pap smear, topsy-turvy cells with huge, dark, wrinkled nuclei - warn of developing CA

42
Q

Dysplasia

A 
Anaplasia confined (for now) to an epithelium 
-this change precedes the development of many cancers
43
Q

Necrosis

A

Death of cells due to injury, prior to the death of the organism
Visible and/or microscopic evidence

44
Q

Reversible cell injury

A

May or may not lead to necrosis

45
Q

The ways in which cell death might occur

A 
Apoptosis due to illness
Hypoxia/denaturation
Hydrolysis of proteins
Mass apoptosis
Saponified
46
Q

What tells you whether the cells have died?

A

Nuclei

47
Q

Pyknosis

A

Nuclei are dark and condensed

48
Q

Karyorrhexis

A

Nuclear dust

49
Q

Ischemic hypoxia

A

Loss of arterial blood flow

50
Q

How fast do the brain and heart die without blood flow?

A

Adult brain will be permanently damaged after a few seconds
Neurons will die after a few minutes
Heart myocytes usually die after about 30 minutes

Other organs can survive hours

51
Q

Shock

A

total body ischemic hypoxia

52
Q

Hypoxemia

A

Aka - hypoxic hypoxia

hypoxia due to too little oxygen in the blood

53
Q

Anemia

A

Aka - anemic hypoxia

Hypoxia due to too little oxygen carrying capacity

54
Q

Histotoxic hypoxia

A

cytochrome failure

55
Q

What happens when a cell is deprived of oxygen

A

Anaerobic glycolysis kicks in and pH goes down - this changes tertiary structure of protein molecules

Cell membrane becomes too permeable to sodium = hypoxic cells swell with water (this causes most of the electrical chaos in the heart when deprived of O2)

Potassium leaks out

Calcium leaks in and intracellular calcium is displaced by H+ ions from proteins. Deadly

56
Q

What color is necrosis?

A

Yellow, like fat, free lipid takes yellow pigment

57
Q

Free radicals

A

Species with an unpaired electron
Electron gets passes from molecule to molecule producing a cascade of damage
Tends to produce apoptosis or coagulation necrosis, depending on severity

58
Q

Examples of free radical damage

A

Ionizing radiation
Tylenol poisoning
Sunburn

59
Q

H2O + radiation =

A

H2 + OH’ (hydroxyl radical)

60
Q

H2O2 + anything =

A

OH’ + OH’

61
Q

O2-‘

A

Superoxide

62
Q

Pus

A

Tissue liquified by enzymes produced by your own neutrophils

63
Q

What do you see histologically for apoptosis?

A

Blebs coming off the edge

64
Q

Caseous

A

Stroma is destroyed, the whole region becomes a fine powder, not quite solid, not quite liquid
Ie. cheese

65
Q

What is the best known cause of caseous necrosis?

A

Tuberculosis

-easier to cough up the virus and infect others

66
Q

How does the death angel toadstool kill ya?

A

Scrambles ribosomes

67
Q

Inclusion bodies

A

Masses of virus in nucleus and/or cytoplasm

68
Q

Councilman body

A

Liver, apoptotic cell

69
Q

Ichthyosis

A

Apoptotic cells are not shed from the skin

70
Q

Early in a brain infarct

A

Brain swells and softens

ALL the major cell types must die, and even then takes about a week to liquefy

71
Q

Abscess

A

Pus in a confined space

72
Q

Dry gangrene

A

The tissue dried out before the clostridia got there

73
Q

Wet gangrene

A

The clostridia got there before it dried out

74
Q

Trench mouth

A

Ulcerative/necrotizing gingivitis

75
Q

Noma

A

Necrosis of the mouth in malnutrition

76
Q

Fournier’s gangrene

A

Testis all fucked up

77
Q

Fibrinoid necrosis

A

When the wall of a muscular artery dies for whatever reason, it becomes rich in plasma proteins

78
Q

Syphilitic gummas

A

Can progress to necrosis/gangrene

79
Q

How does lack of oxygen/blood flow kill tissues?

A

By the effects of lack of oxphos

80
Q

What mediates the signals for apoptosis?

A

Mitochondria

81
Q

What causes damage in reperfusion injury?

A

Influx calcium into cell

82
Q

What does injured mito generate?

A

Free radicals

83
Q

Necroptosis

A

Triggered by TNFR1

-morphology more like common necrosis

84
Q

Pyroptosis

A

Triggered by caspase 1 which yields IL-1b

-morphology more like common necrosis

85
Q

If death is sudden, do you see necrosis in the body?

A

No

86
Q

Livor mortis

A

Post-mortem lividity

87
Q

Cadaveric spasm

A

ie. ivy grabbed during a fatal fall

88
Q

Putrefaction

A

the familiar series of events during the days to months following death

89
Q

Fatty change

A

Accumulation of neutral fat in cells
ie. fatty liver - alcohol abuse
fatty heart - diphtheria

90
Q

Xanthoma

A

Cholesterol accumulation

-in skin around eyes, strawberry seeds in wall of gallbladder

91
Q

Hyaline

A

Generic term for masses of a single protein, staining homogeneously pink

92
Q

Tau

A

in the neurofibrillary tangles of Alzheimer’s

93
Q

Amyloid

A

Beta-pleated protein that accumulates in a variety of local and systemic illnesses

94
Q

Lipofuscin

A

The breakdown product of long-gone membranes stored in lysosomes

95
Q

Melanin

A

seen in cancer

Alerts clinician that this is a malignant melanoma

96
Q

Hemosiderin

A

The compact storage form of iron

-ie. seen at a site of repeated small bleeds from overloaded venules

97
Q

Dystrophic calcification

A

Accumulation of calcium at sites of disease

–necrosis need not be present

98
Q

Metastatic calcification

A

Precipitation of calcium phosphate

In healthy tissues due to elevated blood calcium, elevated blood phosphate, or both

99
Q

Hayflick phenomenon

A

Clonal senescence

100
Q

What cells bear the greatest burden in aging?

A

Brain, CT

-both are postmitotic

101
Q

Who is gonna kick some pathological ass?!

A

WE AREE!!!!!

Mechanisms of Disease (8 decks)

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