Cellular patho (1b) Flashcards
Homeostasis and point of no return
If demands excess cells ability to adapt, cell may hit point of no return
Reversible injury
Cell responds but stays in range of homeostasis, cell will return to original state.
Induced by toxins, brief hypoxia, anoxia
Reversible Injury effects on the cell
The membrane gradient is disturbed, Na+ Cl- enter cell, so does water and accumulates in mitochondria
Cytoplasm swells
What happens to the cell in irreversible injury
Nucleus ruptures, cell loses integrity, membrane ruptures, minimal energy produced, cell contents released into ECF
Causes of cellular injury
Hypoxia/anoxia Free radicals Chemical agents Biological Agents Radiation Physical Agents Nutritional imbalances Inflammation & Immunity Genetic & Metabolic Disturbances
Hypoxia/Anoxia results in
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
4 types of hypoxia
Hypoxic Hypoxia
Anemic Hypoxia
Circulatory Hypoxia
Histotoxic Hypoxia
Hypoxic Hypoxia
Low alveolar PO2 -airway obstruction -hypoventilation -high altitudes -Less than 21% O2 Diffusion impairment -Pulmonary edema -Alveolar consolidation V/Q mismatch -Pulmonary Emboli
Anemic Hypoxia
Reduced RBC O2 carrying capacity
- Low hemoglobin
- Inability of hemoglobin to carry O2 (CO)
Circulatory Hypoxia
Inadequate blood
- Stagnant hypoxia
- Hypovolemic shock
- Arterial venous shunting
Histotoxic Hypoxia
Inability of cell to use O2
-Cyanide
Free radicals
Unpaired electron in valence shell, allows nonspecific reactions, and can create chain reactions (generating new free radicals)
ROS reactive oxygen species
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
Two types of chemical agent cell injury
direct (mercury) indirect (carbon tetrachloride)
Microbial agents cell damage
Bacteria produce toxins
Virus kill from within or integrate on cell genome
Parasite - malaria
Non-ionizing radiation
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
Ultra-violet radiation
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
Physical agents of cell injiry
Trauma, temp, electricity
Temperature cell damage
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
Electrical injuries
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.
Nutritional imbalances
Anemia, scury, rickets, pellagra, beriberi
Inflammation cell damage
Lymphokines, cytokines and complements may kill bodies own cell
Genetic and metabolic examples of cell damage
Disturb metabolism or cause accumulation of toxins
Diabetes and tay-sachs
6 types of cellular adaptations
Atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia, intracellular accumulations.
Brought on by chemical messengers and do not affect housekeeping genes
Atrophy
Decrease in size of cell tissue or organ because smaller = less nutrients and finite nutrient sources get distributed to cells being used
Types of atrophy
Physiologic (age) 5 pathologic types: Disuse Denervation Loss of endocrine stim Lack of nutrition Ischemia
Hypertrophy
Increased size of tissue or organs
Patho or physiologic
LVH could be either
Hyperplasia
Increase number of cells (increases size) due to hormone stimulation. Can have hypertrophy with hyperplasia
Metaplasia
Change in cell type
From chronic irritation/inflammation
Columnar cells of bronchial mucosa to stratified squamous epithelium
Dysplasia
Disorderly arrangement of cells and nuclear atypia
May be reversible
Intracellular accumulations
From -metabolites or exogenous material -disturbances preventing excretion -normal cell secretions Coal (anthracosis) blood pigment (hemosidrosis)
Apoptosis (autolysis)
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
4 types of necrosis
Coagulative, liquefactive, caseous, fat
Coagulative necrosis
Caused by hypoxia (loss of blood supply)
Acidosis denatures proteins, leaving a firm gray mass
Liquefactive necrosis
Cell dies by catalytic enzymes continue to destroy cell components leaving a liquid like medium. Common in the brain
Caseous necrosis
A result of the immune response, dead cells persist indefinitely as soft cheese-like debris
Seen in TB granuloma
Fat necrosis
Saponification - fat converted to soap, common around pancreas
Gangrene
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
Ionizing radiation
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)
UV radiation
From the sun
