Cellular patho (1b) Flashcards

1
Q

Homeostasis and point of no return

A

If demands excess cells ability to adapt, cell may hit point of no return

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2
Q

Reversible injury

A

Cell responds but stays in range of homeostasis, cell will return to original state.
Induced by toxins, brief hypoxia, anoxia

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3
Q

Reversible Injury effects on the cell

A

The membrane gradient is disturbed, Na+ Cl- enter cell, so does water and accumulates in mitochondria
Cytoplasm swells

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4
Q

What happens to the cell in irreversible injury

A

Nucleus ruptures, cell loses integrity, membrane ruptures, minimal energy produced, cell contents released into ECF

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5
Q

Causes of cellular injury

A
Hypoxia/anoxia
Free radicals
Chemical agents
Biological Agents
Radiation
Physical Agents
Nutritional imbalances
Inflammation & Immunity
Genetic & Metabolic Disturbances
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6
Q

Hypoxia/Anoxia results in

A
Cessation of energy
Brain 2-3 minutes
Heart 1-2 hours
Connective tissue 1 day
Oxygen radicals can form during hypoxic episodes and damage tissue
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7
Q

4 types of hypoxia

A

Hypoxic Hypoxia
Anemic Hypoxia
Circulatory Hypoxia
Histotoxic Hypoxia

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8
Q

Hypoxic Hypoxia

A
Low alveolar PO2
-airway obstruction
-hypoventilation
-high altitudes
-Less than 21% O2
Diffusion impairment
-Pulmonary edema
-Alveolar consolidation
V/Q mismatch
-Pulmonary Emboli
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9
Q

Anemic Hypoxia

A

Reduced RBC O2 carrying capacity

  • Low hemoglobin
  • Inability of hemoglobin to carry O2 (CO)
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10
Q

Circulatory Hypoxia

A

Inadequate blood

  • Stagnant hypoxia
  • Hypovolemic shock
  • Arterial venous shunting
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11
Q

Histotoxic Hypoxia

A

Inability of cell to use O2

-Cyanide

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12
Q

Free radicals

A

Unpaired electron in valence shell, allows nonspecific reactions, and can create chain reactions (generating new free radicals)

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13
Q

ROS reactive oxygen species

A

Free radicals with oxygen
May be normal endogenous (phagocytosis) or from radiation.
ROS may be important signalling molecules for healthy cells to regulate normal activity

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14
Q

Two types of chemical agent cell injury

A

direct (mercury) indirect (carbon tetrachloride)

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15
Q

Microbial agents cell damage

A

Bacteria produce toxins
Virus kill from within or integrate on cell genome
Parasite - malaria

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16
Q

Non-ionizing radiation

A

Causes vibration and rotation of atoms and molecules, eventually converted to thermal energy.
Typically thermal injury, involving dermal and sub q tissues
From infrared light, ultrasound, microwaves, friggin lasers

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17
Q

Ultra-violet radiation

A

From sun
Caused by ROS and melanin-producing processes
Causes pyrimidine dimers (insertion of two identical pyrimidines)
Xeroderma pigmentosum has no enzyme to reverse p-dimers, 2000X higher risk for skin CA

18
Q

Physical agents of cell injiry

A

Trauma, temp, electricity

19
Q

Temperature cell damage

A

43-46 degrees (2nd degree burn, severe heat stroke) is vascular injury, faster cell metabolism, inactivating enzymes, disrupting cell membrane
More heat causes coagulation of blood
Cold increases blood viscosity, vasoconstriction, ice crystals causing stasis and lack of perfusion

20
Q

Electrical injuries

A

High voltage and AC are most dangerous
Think of path electricity took to determine damage
More resistance is more heat so more damage. Highest resistance in order - bone fat tendons skin muscles blood nerves.

21
Q

Nutritional imbalances

A

Anemia, scury, rickets, pellagra, beriberi

22
Q

Inflammation cell damage

A

Lymphokines, cytokines and complements may kill bodies own cell

23
Q

Genetic and metabolic examples of cell damage

A

Disturb metabolism or cause accumulation of toxins

Diabetes and tay-sachs

24
Q

6 types of cellular adaptations

A

Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, intracellular accumulations.
Brought on by chemical messengers and do not affect housekeeping genes

25
Q

Atrophy

A

Decrease in size of cell tissue or organ because smaller = less nutrients and finite nutrient sources get distributed to cells being used

26
Q

Types of atrophy

A
Physiologic (age)
5 pathologic types:
Disuse
Denervation
Loss of endocrine stim
Lack of nutrition
Ischemia
27
Q

Hypertrophy

A

Increased size of tissue or organs
Patho or physiologic
LVH could be either

28
Q

Hyperplasia

A

Increase number of cells (increases size) due to hormone stimulation. Can have hypertrophy with hyperplasia

29
Q

Metaplasia

A

Change in cell type
From chronic irritation/inflammation
Columnar cells of bronchial mucosa to stratified squamous epithelium

30
Q

Dysplasia

A

Disorderly arrangement of cells and nuclear atypia

May be reversible

31
Q

Intracellular accumulations

A
From
-metabolites or exogenous material
-disturbances preventing excretion
-normal cell secretions
Coal (anthracosis) blood pigment (hemosidrosis)
32
Q

Apoptosis (autolysis)

A

Programmed cell death which doesn’t allow cell contents to leak out
For old cells or also physiologic (menstruation)
Interference can lead to cancer
Can be internally (mitochondria) or externally (cell receptors) driven

33
Q

4 types of necrosis

A

Coagulative, liquefactive, caseous, fat

34
Q

Coagulative necrosis

A

Caused by hypoxia (loss of blood supply)

Acidosis denatures proteins, leaving a firm gray mass

35
Q

Liquefactive necrosis

A

Cell dies by catalytic enzymes continue to destroy cell components leaving a liquid like medium. Common in the brain

36
Q

Caseous necrosis

A

A result of the immune response, dead cells persist indefinitely as soft cheese-like debris
Seen in TB granuloma

37
Q

Fat necrosis

A

Saponification - fat converted to soap, common around pancreas

38
Q

Gangrene

A

Wet or dry
Dry is a form of coagulative and from poor arterial flow
Wet is a form of liquefaction and related to poor venous return

39
Q

Ionizing radiation

A

Causes ionization of molecules either by directly hitting molecules or producing free radicals.
Damages DNA so rapidly dividing cells are more susceptible
Usually caused by localized irradiation for cancer (whole body preceding bone marrow transplants)

40
Q

UV radiation

A

From the sun