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Pathology > Week 2: Cell Injury > Flashcards

Week 2: Cell Injury Flashcards

1
Q

Rudolf Virchow

A

Father of cellular pathology
19th century German scientist
“Diseases arise in CELLS, not tissues or organs. Every cell comes from another cell like it”

Revolutionized how we define disease/treat it

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2
Q

Pathogenesis

A

Mechanism/development of disease

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3
Q

Aortic valve stenosis

A

Because the valve does not work, the heart must pump HARDER which causes myocytes to become super big.

This adaptation of the heart = injury

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4
Q

Disease

A

Results when adaptive mechanisms fail OR become harmful

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5
Q

Vulnerable cell components

A

Cell membrane (critical for ionic/osmotic homeostasis)
Mitochondria (generation of energy via ATP)
Protein synthesis
Cellular DNA

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6
Q

What is atrophy? State its causes.

A

Decrease in mass due to decrease in cell size

Due to: decreased blood supply, decreased endocrine stimulation, decreased innervation, workload, aging

Lysosomes and ubiquitin-proteasome pathway play a role too; autophagy (the recycling of cellular components)

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7
Q

What is hypertrophy? State its causes and provide a few examples.

A

Increase in cell size due to the synthesis of organelles/proteins

Due to: Increasing functional demand, hormone stimulation

Uterus in pregnancy, aortic valve stenosis, cardiomegaly

Occurs in conjunction with hyperplasia

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8
Q

Hyperplasia

A

Increase in cell number

Due to: increased cell division

Breast during pregnancy (hormonal), liver if you cut some of it out (compensatory)

If there is too much estrogen, you make too many cells and cells become unresponsive to cues

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9
Q

Metaplasia

A

Change to a different cell type

Results in decreased function or increased chances of malignancy (in resp. system, ciliated columnar –> squamous with injury; doesn’t respond to cell signals)

Tissue usually reverts to its resting state if you remove the stimulus

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10
Q

Dysplasia

A

Abnormal cells from hyperplasia (more division and proliferation) and metaplasia (more change means more room for DNA replication mistakes) that CAN become cancerous

ALWAYS PATHOLOGIC

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11
Q

Duration of Injury vs. Effect

A

After cell death –> ultrastructural changes –> light micro changes –> gross morphological changes

If someone dies very fast of heart attack, heart will appear normal

If someone dies slowly, you will see necrosis

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12
Q

Reversible Injury

A

Acute/mild stress or stimulus that is reversible if the stimulus is removed (reduced oxphos, ATP depletion, cellular swelling)

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13
Q

Reversible Injury - Hydropic Swelling

A

Increase in cell volume. Large, pale cytoplasm, normally located nucleus

Causes: chemical/biological toxin, viral/bacterial infections, ischemia/hypoxia, excessive heat/cold –> causes ion imbalance –> swelling

Impairment of cellular volume regulation causes mitochondria to swell, ER cisternae dilation, blebs on PM

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14
Q

Reversible Injury - Fatty Change (Steatosis)

A

Disruptions in fatty metabolism following hypoxia/chemical poisoning. Abnormal accumulation of fats

Cause: A) increased delivery of fat (starvation), B) fat metabolism impairment (alcoholism), C) decreased synthesis of transport proteins (CCl4 deficiency)

Alcohol = most common cause (alteration in uptake of fatty acids)

Big vacuoles that push the nucleus out of the way; small vacuoles of fat appear throughout cytoplasm (or form one large vacuole)

Liver, heart, kidney, skeletal muscle

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15
Q

Explain the causes of intracellular accumulations and give an example.

A

Causes: inadequate rate of metabolism, genetic defects in metabolism, and the presence of abnormal exogenous substances

Steatosis/fatty change

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16
Q

State the causes of intracellular accumulations and provide an example

A

Due to: Genetic/acquired defects in metabolism

Proteins accumulate if you cannot break them down, causing tissues to break down from too many misfolded proteins

17
Q

Intracellular Accumulations - Pigments

A

Can be exogenous or endogenous

Endogenous pigments:
-Lipofuscin (wear and tear)
-Hemosiderin (blood broken down)
-Melanin (skin colour; protects from UV)

Exogenous pigments:
-Smoke (lungs; macrophages gobble up smoke)
-Tattoos (skin; macrophages gobble up ink)

18
Q

What is ischemia? State some of its causes

A

Reduced blood flow to tissues downstream. Injures you FASTER than hypoxia (because waste products are not removed/circulated away)

Can lead to hypoxia and cellular swelling

Causes:
-Hypotension
-Vasoconstriction
-Thrombus/embolus
-Atherosclerosis (plaque)

19
Q

Hypoxia

A

Reduced state of oxygen availability. Glycolytic energy production continues during hypoxia because it is anaerobic.

20
Q

Ischemic and Hypoxic Cell Injury Effects

A

Decreased Oxygen
Decreased ATP (cannot pump ions; sodium accumulates; lactic acid accumulates)
Pump failure (increases calcium = enzymes that attack cellular proteins)
Increased Sodium (rupture cell PM, blebs)
Decreased pH (causes ribosomes to detach from RER, less protein synthesis)

21
Q

Ischemia-reperfusion Injury

A

Continued injury AFTER reperfusion (opening up the vessel) due to:
1. Influx of calcium
2. Oxygen free radicals from damaged mitochondria
3. Compromised antioxidant defense mechanisms
4. Inflammation
5. Activation of complement pathway

22
Q

Irreversible Cell Injury

A

Acute, severe stress OR prolonged, unrelieved stress

Inability to reverse mitochondrial dysfunction, severe disruption of membrane function

23
Q

Necrosis

A

Necrosis is ONLY PATHOLOGICAL insult

Severe/prolonged injury; cell cannot adapt

Morphological changes: eosinophilia, nuclear changes (pyknosis, karyorrhexis, karyolysis), inflammatory infiltration

24
Q

Pyknosis

A

Shrinkage of nucleus

25
Q

Karyorrhexis

A

Breakup of nuclear material

26
Q

Karyolysis

A

Dissolution of the nucleus

27
Q

Coagulative Necrosis

A

Most common type of necrosis

Due to: Ischemic injury

Found in: Heart and kidneys because they are closely related to blood flow

Appearance: Pink, pyknosis, karyorrhexis, karyolysis -> ghost cells (no nuclei)

Texture: Firm

28
Q

What is liquefactive necrosis? State some of its causes and the resulting texture of the tissue.

A

Digestion of dead cells due to inflammatory response (like basic necrosis) -> only here is there a rapid loss of tissue architecture; the cell turns into mush

Due to: Ischemic injury, bacterial damage -> hydrolytic enzymes act

Found in: CNS, lungs, or in the presence of bacteria

Tissue texture: Mushy

29
Q

Caseous Necrosis

A

Cheese-like (goat cheese)
-soft and friable
-Found in tuberculosis!!!!

30
Q

Fat Necrosis

A

Enzymes digest fat, which then combines with calcium = white, chalky deposits

Found in: Pancreatitis, breast tissue damage
Enzymes from pancreas leak out

31
Q

Fibrinoid Necrosis

A

Fibrin in the blood seeps out the walls of the blood vessel, destroying it

Found in: blood vessels

32
Q

Gangrenous Necrosis

A

Occurs in the limbs!!
Is due to compromised vascular supply
-wet gangrene - liquefactive component
-dry gangrene - mummified tissue (dry)

33
Q

Apoptosis

A

Programmed cell death that can be physiologic OR pathologic
-ATP dependent process
-uses caspases and endogenous endonucleases to break down cell nucleus and cytoskeleton
-apoptotic cells are engulfed by phagocytic cells
-TIGHTLY regulated

Characterized by nuclear dissolution without complete loss of membrane integrity (cell contents are broken down with the membrane still intact)

34
Q

Necrosis vs. Apoptosis

A

-Severe damage = necrosis
-Immune-mediated damage = apoptosis
-ATP gets too low = necrosis
-Fast cell loss/turnover = necrosis

35
Q

Intrinsic Mechanism of Apoptosis

A

Mitochondrial pathway (BCL2 activation)

36
Q

Extrinsic Mechanism of Apoptosis

A

Death receptor pathway (TNF, executioner caspases, phagocytes)

37
Q

Calcification

A

Physiologic or pathologic; could be malignant or dystrophic if pathologic

38
Q

Dystrophic Calcification

A

-Deposition of calcium in necrotic or degenerative tissue
-You can have normal calcium levels in the blood because the problem is that the calcium is even going to those tissues in the first place, not the amount of calcium

39
Q

Malignant Calcification

A

-Deposition of calcium in normal tissue
-High blood calcium levels (problem is with the very high CALCIUM levels, not the TISSUE)
-E.g. happens due to increased parathyroid hormone

Pathology (7 decks)

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