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Pathophysiology > Altered Cellular Biology > Flashcards

Altered Cellular Biology Flashcards

1
Q

Cellular Adaptation

A

Changes made by a cell in response to adverse or varying environmental changes.

Can be normal (physiologic) or abnormal (pathologic)

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2
Q

Atrophy

A

Decrease in cell size.

b. Ex. Skeletal muscle, cardiac muscle, brain, secondary sex organs
USE IT OR LOSE IT

c. Thymus gland atrophies from children to adulthood because you no longer need it.

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3
Q

Hypertophy elements

A
  1. Increase in cell size-
    a) caused by mechanical signals - stretching
    b) trophic factors (growth factors)

ex. sustained weight bearing exercises

Patho: Heart muscle growth due to HTN

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4
Q

Hyperplasia elements and types

A
  1. Increase in the number of cells - secondary to mitosis or cell division

a) Compensatory hyperplasia - tissue regeneration - epithelial surfaces (skin cells, mouth, bone, marrow)

b) Hormonal hyperplasia - organs that depend on estrogen (pregnancy, hyperplasia of uterine cells)

Patho: endometriosis (more endometrial cells than necessary)

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5
Q

Metaplasia elements

A
  1. One cell type is replaced by another, usually a less-differentiated cell
  2. Can be reversible ,more undifferentiated, more likely to become dangerous ( ex. cancer)
  3. Worst cancer cells are undifferentiated
  4. Metaplastic cells can turn into dysplastic cells if the irritant is not removed

ex. bronchiole cells can convert from mucus secreting to incapable of mucus secretion due to exposure to irritants like cig. smoke.

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6
Q

Dysplasia

A
  1. abnormal change in cell shape, size or organization
  2. progression of hyperplasia
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7
Q

Cellular Injury

A

Changes to a a cell by continuous stress from internal and external environments.

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8
Q

Cell Death Types

A
  1. Apoptosis - controlled cell death. Cells shrink and breaks off into pieces taken up by the immune system (spleen). No effect on the surrounding tissue.
  2. Necrosis - cell explodes causing inflammation and effects other surrounding cells.
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9
Q

Three mechanisms from injury in a cell

A
  1. Hypoxic
  2. Chemical
  3. Free Radical
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10
Q

Hypoxic Injury elements

A
  1. Inadequate flow of oxygen and nutrients to the cell.
  2. ATP levels drop
  3. Cell functions cannot maintain themselves
  4. If enough time passes in this state it will lead to cell death.

Symptoms : pins and needles, coolness cyanosis, AMS

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11
Q

Complete deprivation of of oxygen supply

A

(Anoxia)

ex. CO exposure

Reperfusion injury -
result of blood flow restoration to tissues that have been ischemic or hypoxic.
The restoration of blood flow must be gradual because too fast will introduce calcium into cells and create cytotoxic damage. Ischemia damages mitochondria, when oxygen is added suddenly can cause free radicals.

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12
Q

Chemical cell injury

A
  1. Direct damage to cells by caustic agents or toxins
    a) typically target plasma membrane or mitochondria where the damage is done.

(If PM is damaged it will have difficulty generated action potentials, keeping resting membrane potentials, and messes up ion channels.

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13
Q

Free Radicals - How they develop

A
  1. By product of chemical processes. Some are essential to transform food and air into energy.
  2. Waste products from chemical reactions in the cell, that when built up harm other cells of the body.
  3. Molecular species with a single unpaired in outer orbital. Steal electrons randomly.
  4. Highly reactive and very nonspecific.
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14
Q

Effects of Free Radicals

A
  1. Widespread derangement of cellular components
  2. Normal biological functions can’t be performed.
  3. Associated with cancer, atherosclerosis, Parkinson’s, Alzheimer’s and more.
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15
Q

Where Free Radicals can come from

A
  1. Fried foods, alcohol, air pollutants
  2. Intensive oxidative distress from unusual aerobic exercise

** Antioxidants - prevent free radicals from taking electrons.
Body produces its own but not enough. Beta carotene, Vit C, Vit E, lycopene (tomatoes) .

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16
Q

Unintentional Cellular Injuries

A
  1. Blunt force trauma
  2. Contusion
  3. Abrasion
  4. Laceration
  5. Puncture wounds ( most common is nail in foot of diabetics)
  6. Gunshot wounds
  7. Asphyxiation (unintentional)
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17
Q

Degeneration

A
  1. Can be non-lethal if injury subsides’
  2. If injury persists it can create structural and biochemical changes that = necrosis.
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18
Q

Necrosis

A
  1. Uncontrolled cell death
  2. Swelling of the organelles, membranes will rupture, and all cellular content will be spilled into surrounding tissues causing tissue damage to the surrounding areas.
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19
Q

Types of Necrosis

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Fat
  5. Fibroid
  6. Gangrenous
  7. Dry
  8. Wet
  9. Gas
20
Q

Coagulative necrosis

A
  1. Usually caused by ischemia or infarction.
  2. Cell-architecture is conserved for a few days
  3. Usually does not occur in the brain.
21
Q

Liquefactive necrosis

A
  1. When inflammatory cells release proteolytic enzymes that destroy surrounding tissue.
  2. Usually happens in tissues that contain high amount of lipids, or prone to abscess.

ex. Brain, lungs - common cause- bacterial infection

22
Q

Caseous necrosis

A
  1. Cell death that causes tissues to appear “cheese-like”
  2. Most common - TB

**preventable and treatable.

23
Q

Fat necrosis

A
  1. Inflammation causes a decrease in oxygen and blood supply to fat cells which results in cell death.
  2. Usually occurs after injury, surgery, or radiation.

ex. Breast tissue - v. common.

24
Q

Fibroid Necrosis

A
  1. Dead cells of blood vessels form fibrin - a fibrous material that can block blood flow through the vessels.
  2. Usually after Very high BP. Can cause knicks, fibrin build up, or clotting which blocks blood flow.

**Irreversible - ex. Vasculitis

25
Q

Gangrenous necrosis

A
  1. Circumferential cell death around digit or extremity
  2. Discoloration, pain, numbness, foul-smelling discharge
  3. 3 Types
26
Q

Dry Necrosis

A
  1. Peripheral vascular disease
  2. Usually arterial

(common in the arterioles of the feet)

27
Q

Wet Necrosis

A
  1. Poor prognosis
  2. Decreased blood flow, cannot be returned up via venous
  3. Stagnant (venous) blood promotes growth of bacteria that rapidly spreads → amputation to salvage the limb

-

28
Q

Gas Necrosis

A
  1. Infection producing gas between tissues
  2. MOST FATAL
29
Q

Apoptosis definition and process

A
  • Controlled/programmed cell death
  • Used to rid the body of cells that are beyond repair
  • DOES NOT CAUSE INFLAMMATION
  1. Cells shrink
  2. Within shrunken cell, cell fragments are put into blebs are formed
  3. Nucleus and organelles collapse → cannot function
  4. Apoptotic bodies form
  5. Cell releases apoptotic bodies to macrophages to get rid of them
30
Q

Cellular Aging

A
  1. Aka senescence
  2. Permanent cell growth arrest
  3. Caused by oxidative stress, DNA damage

After so many cell divisions, eventually there will be an error in the division, and it will stop making a new copy of itself

  • Can also be caused by decline of autophagy – cell’s ability to recycle damaged parts
31
Q

Inflammation

A
  • nonspecific response to tissue injury
  1. Brings phagocytes and plasma proteins to invaded or injured area
  2. No matter what the triggering event is, inflammatory response will be the same
  3. Tissue macrophages → cause redness (increased blood flow to the site or localized vasodilation), swelling (more fluid with more antibodies), interstitial clots, immigration of leukocytes, purulent material will form under the surface sometimes, heat (increased local metabolism).
32
Q

Inflammation and Repair

A
  1. Resident macrophages
  2. localized vasodialation
  3. Leukocyte immigration
  4. Histamine released (increase capillary permeability)
  5. Arterioles dilate
  6. Plasma proteins can leave the blood and enter the area
33
Q

Types of Inflammation

A
  1. Serous - exudate
  2. -Suppurative -
    Secondary to bacterial infection
    Hemotoxins are produced by bacterial → dense accumulation in neutrophils
  3. Membranous
  4. Granulomatous
34
Q

Four classic signs of inflammation

A
  • Leakage of plasma proteins and fluid from the blood (localized edema)
  • The fluid accumulation causes the 4 classic signs of inflammation
    1. Heat (calor) - CAY-lore
    2. Pain (dolor) - Doh-lore
    3. Redness (rubor) - ROO-bore
    4. Swelling (tumor) - TOO-more
35
Q

Repair aspects from inflammation cont…

A
  • Fibrin formation walls off the area from surrounding tissues
  • Neutrophils or monocytes emigrate from the blood into the area and form…
    1. Margination: adhere to surface of capillaries
    2. Diapedesis: neutrophils enter the interstitial space (start to squeeze through)
    3. Chemotaxis: neutrophils are guided to the areas that they are needed
    Within a few hours of the inflammatory response, there is a leukocyte proliferation
36
Q

Repair aspects from inflammation 3

A

Neutrophils will increase 4-5x their size
Monocytes increase at a slower rate
Bacteria will be marked for destruction by opsonins → more susceptible to phagocytosis → complement system activated → allows phagocytes to determine what is foreign vs. normal
- Leukocytes destroy bacteria by phagocytosis

37
Q

Mediation of inflammatory response

A
  1. Nitric oxide
  2. Lactoferrin
  3. Histamine
  4. Etcetc
    - Repairs the tissues
  • Can be perfect → replacing all lost cells with same kind of cells
    Certain non-regenerative tissue will be replaced by scar tissue
38
Q

Neoplasia

A

The formation or presence of a new, abnormal, growth of tissue
Cell adaptations again
1. Hyperplasia
2. Hypoplasia: arresting development of organ or tissue
2. Hypertrophy
▪ Ex. Pregnancy. Uterus will get larger
a)Atrophy

39
Q

Anaplasia

A
  • Loss of specialize cell feature
  • Usually seen in a malignant tumor
40
Q

Carcinogens

A
  • Chemical carcinogens
  • Physical carcinogens
  • Radiation, asbestos
  • Infectious pathogens (viral)
    HPV, Epstein-Barr virus, Hep B (hepatocellular carcinoma)
41
Q

Malignancy

A
  • Cells that grow uncontrollably
  • Spread through bloodstream and lymphatic system
  • Cancerous and spread rapidly
  • Most common: breast, brain, bone, liver
42
Q

Types of malignant tumors

A
  • Carcinoma: epithelial cell origin
  • Sarcoma: mesenchymal cell origin
43
Q

Ocogene

A
  • Mutated gene with gene POTENTIAL to cause cancer
  • Breast cancer gene (BRCA1, BRCA2)
  • Most normal cells undergo programmed, rapid cell death when critical functions are altered
44
Q

Tumor classification -

A
  1. By tissue/organ/system - I
  2. Specific Type - II
  3. Grading according to who classification - III
  4. Spread according to the tumor node metastasis (TNM) system – IV
    a. Amount of spread and where it spread
    b. T = size of primary tumor
    c. N = degree of lymph node involvement
    d. M = presence of different metastasis.
45
Q

Paraneoplastic syndrome

A
  • Disease or symptom that is a consequence of cancer, but not due to the cancer cells

All of a sudden you can be a 35 year old healthy male, difficulty walking and swallowing, slurred speech, memory loss, vision problems, seizures, loss of motor coordination → no idea that you have a tumor somewhere

Usually occur BEFORE tumor is discovered

46
Q

paraneoplastic syndromes examples

A

Pathophysiology (11 decks)

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