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Pathology I > Cell Function & Dysfunction > Flashcards

Cell Function & Dysfunction Flashcards

1
Q

Homeostasis

A

The control of composition of immediate environment and intracellular Millie within a narrow range of physiological parameters

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2
Q

Adaptation

A

Can occur when cells are under physiological or pathological (injury) stimuli; cells achieve a new steady sate that is compatible with their viability in a new environment

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3
Q

Reversible injury

A

Cell is able to adapt or heal from injury.

Cells can either adapt to stress or die.

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4
Q

Irreversible injury

A 
Injury is too severe; affected cells die
An acute stress cannot be overcome.
Common causes are:
Viruses, ischemia, radiation, toxic chemicals, extreme temperatures.
Usual series - coagulative necrosis
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5
Q

Cell injury

A

Occurs when adaptive mechanisms aren’t sufficient to maintain homeostasis.
Results when environmental insults raise beyond ability of cell to adapt
Not an “all or nothing” response

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6
Q

Causes of cell stress/injury

A
  1. Hypoxia
  2. Ischemia
  3. Chemical insult
  4. Infections
  5. Immunological
  6. Genetic
  7. Nutritional
  8. Endocrine
  9. Physical
  10. Aging
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7
Q

Hypoxia injury

A

Deficient oxygen levels; lack of O2 cells.
Especially organ transplants.
Big deal for mitochondria
*expensive tissues (cardiac, kidney, nervous, muscle)

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8
Q

Ischemia injury

A

Deficient blood flow.
Since arterial vessels bring O2 to cells, pathways.
Especially organ transplants

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9
Q

Chemical insult injury

A

Drugs, alcohol, heavy metals
Liver is often affected
Ex: acetaminophen (hepatic necrosis)
alcohol (fatty liver, hepatitis, cirrhosis)

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10
Q

Infection injury

A

Viruses, bacteria, parasites, fungi

May operate through release of toxins or cause long term inflammation

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11
Q

Immunological injury

A

Damage caused by immune reactions. Anaphylaxis & loss of immune tolerance results in auto-immune disorders. Stressful on the body overall. Act on cell and release histamine.

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12
Q

Genetic injury

A

Gene defects, chromosomal anomalies.
Heritable or environment damage to genes and chromosomes.
Can be chronic
Ex: sickle cell

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13
Q

Nutritional injury

A

Deficiency or excess in nutrients (too little iron, vitamin deficient, protein deficient, calorie deficient, excess lipid intake - increase atherosclerosis).
Can be chronic

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14
Q

Endocrine injury

A

Increases or decreases in hormonal activity.
Stress hormones, growth factors.
Ex: cortisol (diverts glucose from brain to skeletal muscle = limiter memory)
Can be chronic

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15
Q

Physical injury

A

Mechanical trauma, thermal damage, radiation damage.
Ex: UV rays
Can be chronic

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16
Q

Aging injury

A

Injury occurs via programmed cell death or toxin build up. Failure of components, free radical build up, etc.
Cells become less and less efficient as they age.
Is more chronic

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17
Q

Labile

A

Epithelium tissues that replace themselves quickly

Ex: tongue cells

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18
Q

Cellular respnose to stress/injury

A

Results when environment insults raise beyond ability of cell to cope.
Cell attempts to respond (not an all or nothing)
The stronger/longer the injury = more damage done
Response of cell depends on type, status, genetic makeup. (ex: ischemia in muscle, cardiac = 20 mins, skeletal = 2 hours)
Either reversible (allows repair) or irreversible (cell necrosis)
Cellular swelling always occurs

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19
Q

Types of reversible cell injury

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
  4. Metaplasia
  5. Dysplasia
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20
Q

Cellular swelling

A

Cytoplasmic volume increases due to increased water volume as a response to injury.
Cell becomes incapable of controlling ion concentrations
Loss of homestasis occurs
Ex: at the organ level, this appears as pallor or weight increase

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21
Q

Cellular swelling

A

Also called “hydropic change”.

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22
Q

Atrophy

A

Shrinkage on size of the cell by loss of substance.
Clinically, decreased size or function level of structure.
Reflects in size decrease at cellular level.
Occurs in regions of persistent injury.
*A retreat to smaller size in attempt to survive
Ex: brain tissue in Alzheimer’s dementia
Frequent in heart, brain, skeletal, muscle, kidneys

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23
Q

Hypertrophy

A

Increase in cell size with heightened functional capacity.
Response to trophic (growth) signals or increased demands.
Clinically, increased size of organ.
Results from increased synthesis of structural proteins and organelles
“Good hypertrophy” - normal physiological response to demand
“Bad hypertrophy” - pathological response to injury

24
Q

Causes of atrophy

A

Occurs in regions of persistent injury (chronic inflammation, vascular insufficiency, disuse, incomplete ischemia, reduced blood flow, denervation of muscles, interruption of hormones to cells)

25
Q

Hyperplasia

A

Increase in cell number, often seen with hypertrophy.
Hormonal stimulation usually influences.
Ex: gravid uterus, estrogen levels at puberty yield hyperplasia of endometrial uterine cells; glandular epithelium of great cells), tumors.
Mostly occurs due to excessive growth factor stimulation, but can also be normal growth (like an embryo).
(warts due to viruses, wound healing, callus, etc.)

26
Q

Metaplasia

A

Conversion of an already differentiated cell the to a different cell type due to injury.
A cell type sensitive to a particular stress is replaced by a cell type that is better adapted to handle it.
Ex: tobacco irritation in bronchi - bronchi normally lined with ciliated columnar epithelium, then replaced by squamous epithelium to provide protection
(occurs as a precursor of neoplastic conversions)

27
Q

Dysplasia

A

Change in cell size, shape, and organization.
Ex: Most frequently occurs hyper plastic squamous epithelia (epidermal actinic keratosis from sunlight) squamous metaplasia (bronchus).
Progresses from metaplasia
A preneoplastic phase prior to cancer

28
Q

Causes of hypertrophy

A

Results from increased synthesis of structural proteins and organelles

29
Q

Causes of hyperplasia

A

Hormonal stimulation usually influences.

Mostly occurs due to excessive growth factor stimulation.

30
Q

Causes of metaplasia

A

When a cell cannot handle the adaptions of a stressor or injury.

31
Q

Neoplastic conversions

A

Occurs in cells as a conversion of the immortalized cells to tumorigenic cells.
Seen in cancers of lung, cervix, stomach, bladder

32
Q

Causes of dysplasia

A

Cells become abnormal in features due to such high stressors.

33
Q

Neoplastic conversions

A

Occurs in cells as a conversion of the immortalized cells to tumorigenic cells.
Seen in cancers of lung, cervix, stomach, bladder

34
Q

Coagulative necrosis

Generally

A

Common sequence leading to cell death from insults
Histologic characteristics similar regardless of causes
Normally, cytosol calcium ion concentration is hypotonic relative to the extracellular environment, but here - an influx of Ca2+ occurs causing necrosis.

35
Q

Irreversible cell injury

Point of no return

A

Eventually, injury affects oxidative phosphorylation and thus stops supplies of ATP synthesis.
Plasma membrane is affected.
1. Inability to reverse mitochondrial dysfunction
2. Profound losses in plasma membrane function
These injuries can take minutes or hours, depending on cell type

36
Q

Coagulative necrosis

Steps & mechanisms

A

Ca2+ influx sets stage for destruction of organelles by lysosomes.
1. cell injury
2. loss of plasma membrane integrity
3. influx of Ca2+ (calcium homeostasis disrupted)
4. lysosomal digestion of the cell & it’s organelles
5. denaturation of proteins in the cell
The outline of cell remains, but it is dead.
Typical mechanism of cell death = MI & hypoxic cell death

37
Q

Calcium homeostasis for cell injury

A

*flowchart
SO IMPORTANT!

The cystolic free Ca++ concentration is kept about 10x lower than the concentration of Ca++ in the extracellular environment.
Most intracellular Ca++ is kept sequestered in mitochondria and in E.R.
During cell injury, come is released into the cytosol and causes damage to the organelles.

38
Q

Types of irreversible cell injury

A
  1. coagulative necrosis
  2. liquefactive necrosis
  3. fat necrosis
  4. caseous necrosis
  5. fibrinoid necrosis
  6. apoptosis
39
Q

Liquefactive necrosis

A

Clinical result is commonly abcess
Same sequence of events as coagulative necrosis, BUT result is digestion of dead cells.
Typically seen in brain
Occurrences in large areas can yield cavities or cysts

40
Q

Fat necrosis

A

Specifically seen in adipose tissue
Most common in pancreatitis or trauma
Unique feature - presence of triglycerides; digestive enzymes that are normally only in pancreatic duct and small intestine.
The triglycerides are released from injured pancreatic acinar cells and ducts into the extra-cellular spaces.
Digestion of pancreas and surrounding adipose cells ensues.

41
Q

Caseous necrosis

A

Lesions seen in tuberculosis
Dead cells remain indefinitely in tissue as:
amorphous, coarse, granular, eosinophilic debris.
Unlike coagulative necrosis, the cells do not retain cellular outlines but they also don’t liquify.

42
Q

Fibrinoid necrosis

A

In injured blood vessels, accumulation of plasma proteins causing intensely eosinophilic epithelial walls.

43
Q

Apoptosis

A

Programmed cell death.
Activation of a genetically programmed “suicide pathway”
Ex: fetal hands and feet, apoptosis results in separation of web-like paddles into distinguished fingers/toes

44
Q

Calcification

A

A normal event during bone formation.
Ca ion entry to dying cells is also frequent.
Two major types: dystrophic & metastatic

45
Q

Types of calcification

A
  1. Dystrophic calcification

2. Metastatic calcification

46
Q

Dystrophic calcification

A

Localized manifestation
Macroscopic deposition of calcium salts in injured tissues.
Occurs with Ca deposition from circulation or intestinal fluid into injured cells.
Grossly as sandlike grains or rock hard material.
May occur in mitral or aortic valves. The inflexibility leads to impeded blood flow;
Ex: atherosclerotic coronary arteries this lead to narrowing of lumen

47
Q

Metastatic calcification

A

Systemic manifestation via blood
Deranged calcium metabolism.
Associated with hypercalcemia or increased serum calcium concentration.
Can cause calcification of alveolar septa of lung, renal tubules, blood vessels.
Ex: hyperparathyroidism (PTH increases Ca ion levels) or
Vitamin D intoxication (promotes Ca ion uptake)

48
Q

Cellular aging

A

Normal process but represents progressive accumulation of sublethal injury that compromises cellular function.
May lead to cell death or a diminished capacity to respond to injury.

49
Q

Cellular aging

Causes & effects

A

A number of processes decline with age:
Mitochondrial oxidative phosphorylation
Protein synthesis (ribosomes detach from rough ER)
Repair of chromosomal damage.
Free radical damage
*Due to both internal molecular clock AND extrinsic stressors (wear and tear).

50
Q

Free radical damage

A

Free radicals are chemical species with a single, unpaired electron in the outer orbit.
They cause aging/injury by:
Causing lipid changes in the plasma membrane
Modifying protein synthesis
Cause lesions in DNA (DNA usually dictates protein synthesis)

51
Q

Free radical “debate”

A

Whether they can be neutralized or not.
Evidence exists they can be neutralized by antioxidants (vitamins A & E), but does this actually add up to a decrease in the rate of cellular aging?

52
Q

Effects of Ca2+ imbalances or irregulation

A

ATP decrease
plasma membrane loss
chromatin damage
cytoskletetal disassembly

53
Q

Mitochondrial oxidative phosphorylation

A

effect/causes of cellular aging

54
Q

protein synthesis

A

effect/causes of cellular aging

ribosomes detach from rough endoplasmic reticulum

55
Q

repair of chromosomal damage

A

effect/causes of cellular aging

Pathology I (9 decks)

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