Reduced RBC O2 carrying capacity - Low hemoglobin - Inability of hemoglobin to carry O2 (CO)

Inadequate blood - Stagnant hypoxia - Hypovolemic shock - Arterial venous shunting

Cellular patho (1b) Flashcards by Samborg Thedestroyer

Homeostasis and point of no return

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

How well did you know this?

Not at all

Perfectly

Reversible injury

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

How well did you know this?

Not at all

Perfectly

Reversible Injury effects on the cell

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

How well did you know this?

Not at all

Perfectly

What happens to the cell in irreversible injury

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

How well did you know this?

Not at all

Perfectly

Causes of cellular injury

Hypoxia/anoxia
Free radicals
Chemical agents
Biological Agents
Radiation
Physical Agents
Nutritional imbalances
Inflammation &amp; Immunity
Genetic &amp; Metabolic Disturbances

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

4 types of hypoxia

Hypoxic Hypoxia
Anemic Hypoxia
Circulatory Hypoxia
Histotoxic Hypoxia

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Anemic Hypoxia

Reduced RBC O2 carrying capacity

Low hemoglobin
Inability of hemoglobin to carry O2 (CO)

How well did you know this?

Not at all

Perfectly

Circulatory Hypoxia

Inadequate blood

Stagnant hypoxia
Hypovolemic shock
Arterial venous shunting

How well did you know this?

Not at all

Perfectly

Histotoxic Hypoxia

Inability of cell to use O2

-Cyanide

How well did you know this?

Not at all

Perfectly

Free radicals

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Two types of chemical agent cell injury

direct (mercury) indirect (carbon tetrachloride)

How well did you know this?

Not at all

Perfectly

Microbial agents cell damage

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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