GENERAL PATHOLOGY

Pathos

suffering

Logos

study

Pathos

suffering

Logos

study

Pathology

study of the structure, biochemical, and functional changes in cells, tissues, and organs that underline disease

Rudolf Virchow

father of modern pathology

proposed that injury to the smallest living unit of the body, the cell, is the basis of all disease

General pathology

concern with the basic reaction of cells and tissues to abnormal stimuli that underlie the disease

Systemic pathology

examines the specific responses of specialized organs to defined stimuli

Etiology

the cause

can be genetic or acquired but most commonly multifactorial

Pathogenesis

mechanism

sequence of events that follow after injury

Morphologic changes

Structural alterations

remains a diagnostic cornerstone

Clinical manifestations

functional consequences

the end result of the disease process

Manifestation

observable or measurable characteristics associated with a specific type of pathology

Sign

objective observation that can be seen or measured

Symptom

subjective report that can be perceived only by the person affected

Disease

a specific set of sings and symptoms seen together frequently and become the basis for diagnosis

Disorder

disruption of the disease to the normal or regular functions in the body

Syndrome

disease or disorder that has more than one identifying feature or symptoms

Adaptations

reversible changes in the size, number, phenotype, metabolic activity, or functions of cells in response to changes in their development

Hypertrophy

Hyperplasia

Atrophy

Metaplasia

types of adaptations

are very critical for maintaining homeostasis and allowing the boy to respond to changes in its environment

Hypertrophy

increase in cells size, leading to overall organ enlargement

Cells capable of division

may show hypertrophy with hyperplasia

Cells incapable of division

are post-mitotic

tissue mass increases only by hypertrophy

Physiologic hypertrophy

caused by increased functional demand or stimulation by hormones or growth factors

Pathologic hypertrophy

caused by chronic hemodynamic overload

leads to hypertrophy of myocardial fibers

Hyperplasia

an increase in the size of an organ or tissue caused by an increase in a number of cells

Physiologic hyperplasia

due to hormonal or growth factor stimulation

often occurs together with hypertrophy

Pathologic hyperplasia

caused by excessive or inappropriate hormonal or growth factor stimulation

Atrophy

defined as a reduction in the size of an organ or tissue

due to a decrease in cell size and number

Physiologic atrophy

common during normal development

a normal and reversible process

Pathologic atrophy

abnormal atrophy due to a disease or dysfunctional process

can be local or generalized

Diminished blood supply

a reduction in the blood flow can lead to ischemia which results in the lack of oxygen and nutrient needed for tissue maintenance

Marasmus

a condition of severe malnutrition

often seen in children with inadequate caloric intake

Cachexia

leads to muscle wasting and atrophy

occurs due to a combination of poor nutrition and the body’s increased metabolic demands in response to the disease

Metaplasia

reversible changes where one differentiated cell type is replaced by another

adaptive response to environmental stress or injury

Columnar to squamous

in response to chronic irritation or inflammation

most common epithelial metaplasia

Squamous to columnar

may lead to adenocarcinoma

Connective tissue metaplasia

formation of cartilage, bone, or adipose tissue in tissues that don’t normally contain these elements

Cell injury

occurs when adaptive limits are exceeded by injurious agents or stress

can also occur due to nutrient deprivation or mutations affecting essential cellular components

Embryogenesis

helping shape developing organs by eliminating unnecessary cells

Organ development

ensuring organs form properly by removing excess cells

homeostasis maintenance

balance cell numbers by removing damaged or agent cells and allowing tissue renewal

Necrosis

always a pathologic process

Apoptosis

serves many normal functions

Reversible cell injurt

Due to:

• decreased ATP generation

• loss of cell membrane integrity

• defects in protein synthesis

• cytoskeletal damage

• DNA damage

Plasma membrane bleb

structural weakening

Mitochondrial swelling

disturbances in iron balance but still functional

Nuclear clumping

a sign of stress on genetic material but without complete breakdown

Cellular swelling

caused by failure to maintain ionic and fluid homeostasis

Fatty change

occurs in hypoxic injury or due to a toxic or metabolic activity

manifested by lipid vacuoles in the cytoplasm

Irreversible cell injury

result of two major processes:

• denaturation of intracellular proteins

• enzymatic digestion of the cell

Pyknosis

Karyolysis

Karyorrhexis

Nuclear changes that reflect the progressive breakdown and death of the cell

are classic markers that are looked for identifying necrotic cells under the microscope

Pyknosis

nuclear shrinkage and increased basophilia

stains darker blue with hematoxylin

due to the condensation of your chromatin inside the nucleus

Karyorrhexis

the pyknotic or partially pyknotic nucleus undergoes fragmentation

is a sign that the cell is progressing further into irreversible injury

Karyolysis

basophilia of the chromatin may fade

the nucleus eventually disappears due to the action of your DNA-degrading enzymes

Coagulative necrosis

one of the most common patters of tissue necrosis

the architecture of dead tissues is preserved for a span of at least some days

Infarct

a localized area of coagulative necrosis

Liquefactive necrosis

tissue transformation into a liquid, viscous mass due to digestion of dead cells

common in bacterial or fungal infections

characterized tissue breaking down into a liquid, usually caused by infections or lack of oxygen in the brain and is marked by pus-liie material in the tissue

Gangrenous necrosis

not a specific pattern of cell death

commonly used in clinical practice to describe certain types of tissue death

often associated with the loss of blood supply

Dry gangrene

applied to limb that has lost blood supply

characterized by coagulative necrosis where the tissue becomes dry, shriveled, and darkened or appears black

Wet gangrene

undergone coagulative necrosis but with superimposed bacterial infection becomes liquefactive necrosis making the tissues appear wet and foul smelling

Caseous necrosis

most commonly encountered in tuberculosis infection

tissue takes on a cheese-like appearance

Fat necrosis

refers to focal areas of fat destruction

fat tissue is being broken down in certain spots rather than throughout an entire area

composed of triglyceride and calcium

involves the focal destruction of fat often caused by pancreatic lipases

Fibrinoid necrosis

special form of necrosis usually seen in immune reaction involving blood vessels

referred to as “fibrinoid” by pathologists

gives a bright pink and amorphous appearance under the microscope

Mitochondrial permeability

the membrane of the mitochondria becomes leaky, which disrupts the cells energy production

Depletion of ATP

reduced blood supply or nutrients, mitochondrial damage

Apoptosis

often referred to as programmed cell death

greek term for “falling away from”

induced by a tightly regulated suicide program in which cells are destined to die

Physiologic apoptosis

happens naturally and is essential for normal development and maintenance of healthy tissues

Pathologic apoptosis

occurs when apoptosis is triggered by abnormal conditions or stress within the body

Necroptosis

a hybrid that shares aspects of both necrosis and apoptosis

Pyroptosis

occurs in cells infected by microbes

Autophagy

process in which a cell eats its own contents

Intracellular accumulation

refers to the buildup of abnormal amounts of various substances inside the cell

Steatosis

accumulation of intracellular triglycerides causes include alcohol abuse, diabetes, and obesity

Atherosclerosis

the accumulation of cholesterol within macrophages, and smooth muscle cells

Xanthomas

intracellular accumulation of cholestero within macrophages found in the skin and tendons of linked to hyperlipidemia

Exogenous pigments

come from outside the body

pigment deposited in the skin

Endogenous pigments

produced inside the body

Inflammation

response of vascularized tissues to infections and damaged tissues

bring cells and molecules of host defense

Rubor

Calor

Dolor

Tumor

Functio Laesa

five cardinal signs of inflammation

Rubor

redness

increased blood flow due to vessel dilation

Calor

warmth

increased blood flow

Dolor

pain

caused by chemical mediators and pressure from swelling

Tumor

swelling

leakage of fluid from blood vessels into tissue

Functio Laesa

loss of function

combination of pain and swelling

limits movements or function

Margination

peripheral positioning of the leukocytes along the endothelial surface

results from slower blood flow due to vessel dilation

Rolling

transient, weak binding, and detachment of leukocytes to the endothelium

mediated by selectins

Adhesion

permanent, firm adhesion of leukocytes to endothelium

Mediated by CD31/PECAM-1

Chemotaxis

movement towards a chemotactic signal

most common exogenous product: N-formylmethionine