Pathophysiology

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Cellular Adaptation

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Cells are able to adapt to their environment in order to escape and protect themselves from injury.

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Most common adaptations

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atrophy, hypertrophy, hyperplasia, metaplasia, dysplasia.

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Atrophy

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A decrease or shrinkage in cellular size.

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Types of atrophy:

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Physiologic atrophy
Pathologic atrophy
Disuse atrophy

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Physiologic atrophy:

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occurs with early development; thymus gland in children

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Pathologic atrophy

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occurs with decreases in use, nutrition, vascularization, nervous stimulation, etc

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Disuse atrophy

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example of decrease in use of muscle cells

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Hypertrophy

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An increase in size of cell and of an organ as a result

Can also be physiologic or pathologic and is caused by INCREASED FUNCTIONAL DEMAND

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Hypertrophy is triggered by 2 types of signals:

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Mechanical signals like the stretching of a cell
Trophic signals such as hormones, growth factors, etc.

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Hyperplasia

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an increase in the number of cells resulting from an accelerated rate of cell division.

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Hyperplasia types

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Compensatory hyperplasia,
Hormonal hyperplasia
Pathologic hyperplasia

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Hormonal hyperplasia occurs

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when hormone sensitive tissues are stimulated (LIKE UTERUS AND BREAST)

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Compensatory hyperplasia,

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which is a mechanism of adaptation that allows organs to regenerate (LIKE THE LIVER)

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Pathologic hyperplasia

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is the abnormal proliferation of normal cells, normally as a result of hormonal stimulation or growth factors on target cells.

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Dysplasia is

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AN ABNORMAL CHANGE IN SIZE, SHAPE, AND ORGANIZATION OF MATURE CELLS.

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Metaplasia is .

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THE REVERSIBLE REPLACEMENT OF ONE MATURE CELL TYPE BY ANOTHER

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Mechanisms of Injury

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Hypoxia injury.
Ischemia:
Anoxia:

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Anoxia:

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total lack of oxygen; not well tolerated

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Ischemia:

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reduction in blood supply; cause of hypoxia.

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Hypoxia: .

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lack of sufficient oxygen; most common cause of cellular injury

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Free radicals

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A free radical is an uncharged atom with an unpaired electron. This makes the molecule unstable.to stabilize the molecule, it “steal” an electron from another molecule or give one up.
can injure cell membranes.

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3 ways free radicals are initiated within a cell

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Absorption of extreme energy sources (UV light, radiation)
Redox reactions in which oxygen is reduced to water
Enzymatic metabolism of exogenous chemicals or drugs

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Two general chemical mechanisms in cellular damage

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Direct toxicity in which the chemical combines with a component of the cell membrane or organelles and disrupts function

Formation of reactive free radicals and lipid peroxidation (destruction of polyunsaturated lipids, causing membrane damage)

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chemical injury agents:

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LEAD, CARBON MONOXIDE, ETHANOL, DRUGS (STREET DRUGS SUCH AS COCAINE).

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Carbon monoxide causes injury due to

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HYPOXIA.

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Symptoms of carbon monoxide poisoning

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headache, giddiness, tinnitus, nausea, weakness, and vomiting.

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Acute ethanol ingestion (acute alcoholism) first affects

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central nervous system. The liver is also forced to metabolize the alcohol

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Blunt force:

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caused by the application of mechanical energy to the body resulting in tearing, shearing, or crushing of tissues.

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Unintentional and Intentional Injuries

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Blunt force
Contusion
Hematoma
Abrasion
Laceration
Fractures
Sharp force injuries
Gunshot wounds

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Contusion:

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bleeding into the skin and/or underlying tissues as a result of a blow that squeezes or crushes the soft tissues and ruptures blood vessels without breaking the skin.

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Hematoma:

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collection of blood in soft tissues or an enclosed space.

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Abrasion

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results from removal of superficial layers of the skin caused by friction between the skin and another object.

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Laceration:

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a tear or rip resulting when the tensile strength of the skin is exceeded. NOT an incision; much more jagged and irregular.

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AVULSION

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is an extreme laceration in which a wide area of tissue is pulled away, creating a flap.

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Sharp force injuries

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Incised wound:
Stab wound:
Puncture wound:
Chopping wound:

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Two types of Gunshot wounds

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penetrating (bullet stays in) or perforating (bullet leaves).

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Asphyxial injuries caused by a

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failure of cells to receive or utilize oxygen. Can occur with hypoxia or anoxia.

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Asphyxial injuries types

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Suffocation
Strangulation
Chemical
Drowning

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probability of getting an Infected injury

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depend on the ability of a microorganism to invade and destroy cells, produce toxins, and cause damaging hypersensitivity reactions.

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manifestations of cellular injury include

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accumulations of water, lipids, carbohydrates, glycogen, proteins, pigments, hemosiderin, bilirubin, calcium, and urate.

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Accumulation of WATER can cause

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cellular swelling when more water is drawn into the cell due to a failure of transport mechanisms. The cell becomes distended and large vacuoles are formed to isolate water from cytoplasm. Unfortunately, this usually leads to oncosis, a type of cell death resulting from cell swelling.

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cell damage by Accumulations

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Lipids and carbohydrates, glycogen, proteins, and pigments are all organic substances that can accumulate in the cell

: It is the ABNORMAL accumulation of these substances within the cell that can cause injury. These accumulations also occur in normal cells.

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Accumulations are caused by disorders in which

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Cellular uptake of a substance is more than the cells ability to digest or use it
Cellular synthesis of a substance is more than the cells ability to use or secrete it

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Calcium salts accumulate in both

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injured and dead tissues. Damage occurs when calcium salts clump and harden, interfering with normal cellular structure and function.

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Damage occurs from Calcium when

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calcium salts clump and harden, interfering with normal cellular structure and function.

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Dystrophic calcification (accumulation of calcium salts) is always a sign of

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pathologic change because it occurs in dying and dead tissues

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Metastatic calcification occurs in

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undamaged normal tissues

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Metastatic calcification consists of

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mineral deposits that result from hypercalcemia (too much calcium in the bloodstream).

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URATE can accumulate when .

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there are disturbances in urate metabolism.

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disturbances in urate metabolism. leads to

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hyperuricemia and deposit of sodium urate crystals in tissue. This leads to a disorder called gout

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hyperuricemia and deposit of sodium urate crystals in tissue leads to a disorder called

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gout

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Cellular death eventually leads to

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cellular dissolution or NECROSIS.

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NECROSIS is the sum of

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cellular changes after local cell death and the process of cellular self-digestion (autolysis).

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The stages of necrosis include

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pyknosis and karyolysis

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4 types of necrosis:

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coagulative:
Liquefactive:
Caseous:
Fat:

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coagulative:

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occurs primarily in kidneys, heart, adrenal glands; most often results from hypoxia due to severe ischemia

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Liquefactive: usually results from

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ischemic injury to neurons and glial cells in brain

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Caseous is combination of

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coagulative and liquefactive; most often results from TB infection

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Fat: occurs in

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breast, pancreas, and other abdominal structures.

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gangrenous necrosis refers to

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tissue death

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Gangrenous necrosis is caused by

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hypoxia and subsequent bacterial invasion.

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Gas gangrene is a type of gangrene caused by

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Clostridium infection. Bubbles of gas form inside muscle cells.

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Manifestations of somatic death include:

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Cessation of respiration and circulation
Gradual lowering of body temperature (algor mortis)
Pupil dilation
Blood settling in the most dependent tissues causing a purple discoloration (livor mortis)
Muscle stiffening (rigor mortis) within 6 hours after death
Signs of putrefaction are obvious about 24 to 48 hours after death

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Mast cells develop in the ______, move through the_____, and mature in ____

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bone marrow
bloodstream
tissue

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Mast cells activate the inflammatory response through:

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Synthesis:
Degranulation:

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Synthesis:

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making certain mediators in response to a stimulus

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Degranulation:

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releasing preformed granular contents into the extracellular matrix

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Mast cells synthesize 2 important inflammatory mediators

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Leukotrienes:
Prostaglandins:

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Leukotrienes:

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act slower than histamines and are important in later stages of response

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Prostaglandins:

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increase vascular permeability and smooth muscle contraction; also cause pain

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Inflammation is also mediated by 3 key plasma protein systems:

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The complement system
The clotting system
The kinin system

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The Complement System Can be activated by:

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The classic pathway: The alternative pathway:

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The alternative pathway:

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occurs when stimulated by biologic substances such as bacterial or fungal cell wall polysaccharides

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The classic pathway:

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occurs when an antigen-antibody complex reacts with C1 (the first component in the cascade)

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The Clotting System can be activated by 2 different pathways:

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Can be activated by 2 different pathways:
Extrinsic pathway: usually injured cells
Intrinsic pathway: by collagen or other activators

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The primary kinin is

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bradykinin

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Two main classes of leukocytes to carry out inflammatory processes:

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Granulocytes
Monocytes/macrophages

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Platelets

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Interact with components of the coagulation cascade to stop bleeding.
Degranulate, releasing biochemical mediators such as serotonin, which has vascular effects like histamine.

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Local Manifestations of Acute Inflammation

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Serous exudate:
Fibrinous exudate:
Purulent exudate:
Hemorrhagic exudate:

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Serous exudate:

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watery and clear looking; usually occurs in early or mild inflammation.

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Fibrinous exudate:

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thick and clotted; occurs in severe or advanced inflammation.

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Purulent exudate:

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consists of pus; occurs if leukocytes and bacterial infection are present.

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Hemorrhagic exudate:

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filled with erythrocytes, occurs with bleeding

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three primary systemic changes associated with acute inflammation are

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fever, leukocytosis (an increase in the circulating number of leukocytes), and an increase in circulating plasma proteins

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Resolution:

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the restoration of original structure and physiologic function. This is the best possible outcome.

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Repair:

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the replacement of destroyed tissue with scar tissue composed of collagen, which fills the lesion and restores tensile strength, but cannot carry out physiologic function of normal tissue.

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Types of healing of wounds:

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Primary intention
Secondary intention:

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Secondary intention:

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occurs with an open wound that requires epithelialization, scar formation, and contraction. This process takes longer, obviously.

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Primary intention:

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occurs when a wound heals under conditions of minimal tissue loss; cuts or surgical wounds that have been sutured

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Ischemia:

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reduction in blood supply; cause of hypoxia.

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Anoxia:

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total lack of oxygen; not well tolerated.

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ANEMIA is

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a reduction in the total number of circulating erythrocytes or a decrease in the quality of quantity of hemoglobin.

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ANEMIA Can be caused by what 3 factors

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1.Altered production of erythrocytes
2.Blood loss
3.Increased erythrocyte destruction
Combination of the above 3

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Pernicious anemia is a type of

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macrocytic anemia caused by vitamin B12 deficiency.

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Gangrenous necrosis is caused by

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hypoxia and subsequent bacterial invasion.