Patho (the cell)

Atrophy

Decrease in cell size

* If atrophy affects a sufficient number of cells, the affected organ shrinks in size.
* Occurs mostly in:
* skeletal muscle
* Heart muscle
* secondary sex organs
* the brain

Physiologic Atrophy

\-Occurs with early development

* Thymus gland during childhood, the atrophy is a normal event
* Age related atrophic changes to the gone occur secondary to decreases in hormonal stimulations
* The ovaries atrophy in postmenopausal women secondary to a lack of estrogenic stimulation. Aging result in atrophic changes to Brain cells.

Pathologic Atrophy

* Occur in organs as a result of decreases in workload, pressure, use, blood supply, nutrition, hormonal stimulation, neural stimulation
* Disuse atrophy -
* Occurs with prolonged bed rest or other immobilization

Describe Atrophic muscle cells :

Atrophic muscle cells contain less endoplasmic reticulum (ER), fewer mitochondria, and fewer myofilaments (the contractile components of the muscle fiber) compared with normal cells.

What causes Muscle Atrophy

Decreased neural stimulation, results in reduced oxygen consumption and decreased amino acid uptake

Hypertrophy

Increase in cell size

* Occurs in response to mechanical load or stress

Hypertrophy common triggers:

What organ cells are particularly prone to enlargement?

* Repetitive stretching
* Chronic pressure
* Volume overload
* Heart
* Kidneys

Hypertrophy is an adaptive réponse that occurs in the :

Striated muscle cells of both the heart and skeletal muscles

* Cardiac muscle hypertrophy: (LVP) left ventricular hypertrophy

Physiological Hypertrophy definition & example

\-Results from a demand, stimulation by hormones, and growth factors

* Enlargement secondary to aerobic exercise or “runners” heart
* No pathology is present and function is preserved

Pathologic Hypertrophy

\-Results from chronic hemodynamic overload ( such as from Hypertension or heart valve dysfunction)

* LVH (left heart ventricular hypertrophy)
* When LVH occurs secondary to hypertension, its *Pathologic hypertrophy*
* The initial adaptation comes in the form of cardiac enlargement with dilated ventricles, short lived
* Prolonged cardiac hypertrophy progresses into contractile dysfunction and ultimately into heart failure.
* Pathological hypertrophy is associated with increased interstitial fibrosis, cell death, and abnormal cardiac function.

Compensatory Hypertrophy Example

* After a unilateral nephrectomy (removal of one kidney) compensatory hypertrophy occurs in the remaining kidney, which preserves renal structure and function.

Hyperplasia

Increase in cell number, response to cell injury

* Resulting from an increased rate of cellular division
* Hyperplasia requires for the cell to undergo mitosis

Main mechanism for hyperplasia is :

The production of growth factors WHICH stimulate the remaining cells after injury or cell loss to synthesize new cell components and ultimately to divide

* typically occurs bc of
* Skin loss compensation
* Chronic inflammatory response
* Hormonal dysfunctions
* Compensation for damage or disease elsewhere

Compensatory Hyperplasia (Physiological/normal)

Adaptive mechanism that enables organs to regenerate.

* Removal of part of the liver leads to rapid hyperplasia of the remaining hepatocytes (liver cells)
* Even with removal of 70% of liver mass, regeneration is complete in about 2 weeks
* Significant compensatory hyperplasia readily (without hesitation) occurs in epidermal and intestinal epithelia, hepatocytes, bone marrow cells, and fibroblasts '
* To a lesser extent hyperplasia occurs in bone, cartilage and smooth muscle cells.
* A callus (thickening of the skin) is an example of compensatory hyperplasia in response to injury from a mechanical stimulus or response to wound healing (after inflammation process )

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Hormonal Hyperplasia

\-Occurs in organs that respond to endocrine hormonal stimulation

* EX: during follicular phase of the menstrual cycle, estrogen secretion by the ovary results in hyperplasia and endometrial proliferation

\-Hormonal secretion from endocrine organs maintains normal structure and function of target organs and function of target organs.

Pathologic Hormonal Hyperplasia (Not normal)

\-ABNORMAL proliferation of normal cells, usually in response to excessive hormonal stimulation or to the action of growth factors on target cells

* A common example is pathologic hyperplasia of the uterine endometrium (lining of the uterus) that occurs from an imbalance between estrogen and progesterone levels
* The resulting endometrial hyperplasia commonly presents as erratic or excessive uterine bleeding, known as dysfunctional uterine bleeding
* Left unchecked can result in endometrial cancer
* Another examples is Benign prostatic hyperplasia (BPH). The incidence of BPH increases with age, secondary to age-related hormonal imbalances that result in epithelial and stratal proliferation or impaired apoptosis.
* Similarly to thyroid enlargement, including thyroid goiters, can result from excessive levels of pituitary thyroid stimulating hormone (TSH)

\-In the absence of malignant transformation, when presupposing factors are corrected, pathologic hyperplasia will typically regress.

Dysplasia

Deranged cellular growth, is not considered a true cellular adaptation but rather atypical hyperplasia

* Abnormal Changes in the size, shape, and organization of mature cells
* Often referred as atypical hyperplasia
* DYSPLASIA DOES NOT REFER TO CANCER
* Dysplastic Changes are common in the epithelial tissue of the $uterine cervix$, the $endometrium$ and $gastrointestinal$ and r$espiratory tract mucosa$

Metaplasia

==**reversible**== replacement of one mature cell type by another, less mature cell type OR a change in cell phenotype

* Found in association with tissue damage, repair, regeneration

\-It is an adaptive response in which the new cell type may be better suited to withstand an adverse environment, usually the change is not beneficial

Metaplasia Example:

Long-term cigarette smoker, the chronic irritation from smoke causes the normal ciliated columnar epithelial cells of the trachea and bronchi to become replaced by stratified squamous epithelial cells.

* The newly formed squamous epithelial cells do not secret mucus or have cilia, causing a loss of critical protective mechanism

Cellular Injury

occurs when the cell is unable to maintain homeostasis

injury to cells → injury of tissues → injury of organ

* Reversible injury= cell can recover
* Irreversible injury= cellular death

Reversible cell Injury

\-Loss of ATP

\- cellular swelling

\-Detachment of ribosomes

\-Autophagy of lysosomes

Irreversible Cell injury

“point of no return”

* Vacuolization of mitochondria occurs and Ca++ moves into cell

Necrosis

\-Type of cell death

\-Severe cell swelling and breakdown of organelles

Apoptosis (programmed cell death)

Cellular self-destruction for elimination of unwanted cell population

Autophagy

\-EATING OF SELF

\-Cytoplasmic vesicles engulf cytoplasm and organelles

\-Recycling factory

Chronic Cell injury ( Subcellular alterations)

* Persistant stimuli repose may involve only specific organelles or cytoskeleton (eg. Phagocytosis of bacteria)

Accumulations/ Infiltrations

* Water
* pigments
* Lipids
* glycogen
* proteins

Pathologic Calcification

Dystrophic and metastatic calcification