unit 1 - disease, cells, inflammation

pathology

the study of disease, changes to cells and tissues associated with disease

physiology

the normal functions of living organisms, their organs and systems, mechanisms of human body functioning

pathophysiology

the abnormal functioning of diseased organs with the application of diagnosis, treatment, and patient care, the study of functional or physiologic changes in the body that result from disease process

importance of pathophysiology

if healthcare professionals can understand the causes and mechanisms of a disease, then they can find the way to influence them rationally

health

a state of complete physical, mental, and social well being and not merely the absence of disease

life expectancy

the number of years a person can expect to live

quality of life

the degree of overall satifsaction that a person gets form life, involves all aspects of health

homeostasis

maintenance of a relatively stable internal environment regardless of external changes, maintained by the nervous and endocrine system

stimulus

any disruption that changes a controlled condition

disease

the failure to maintain homeostatic conditions, the functional impairment of cells, tissues, organs, and organ systems

local disease

in one spot: a boil on the neck

systemic disease

throughout the body: toxic shock, massive edema

focal disease

usually confined to a part of a particular organ: liver abscess

diffuse disease

disease is throughout the organ, corrhosis of the liver

etiology

the cause of the disease (risk factor, types)

causes of disease

genetics, congenital, acquired, microorganisms

idiopathic

etiology is unknown

iatrogenic

etiology is caused by treatment, procedure, or error by a health professional

nosocomial

originating in a hospital

pathogenesis

the development of a disease, description of how etiologic factors are thought to alter physiologic function and lead to the development of clinical manifestations that are observed in a disease

clinical manifestations

indications of illness, signs and symptoms

symptoms

subjective, sensations that the patient feels and can describe

signs

objective, something a doctor can observe

precipitating factors

factors that promote the onset of clinical manifestations

syndrome

characteristic combination of signs and symptoms asociated with a particular disease

nephrotic syndrome

leakage of protein into urine, low serum protein, edema

chinese restaurant syndrome

MSG, chest pain, flushing, numbness, burning in/around mouth, headache, giddiness, sweating, abdominal pain, urticaria

acute

radip onset, usually short duration

chronic

may occur slowly and remain for long periods

remissions

decrease in severity, may indicate disease is cured

exacerbations

sudden increase in severity

complications

new additional problems that arise during the disease

sequelae

the after effect of a disease, a condition resulting from a previous disease state

diagnosis

characterization of the affliction and probable cause, determination of the disease, cause may be unknown, leads to treatment or therapy

differential diagnosis

the process of differentiating between two or more conditions which share similar symptoms

specific treatment

directed at underlying cause

symptomatic treatment

alleviates symptoms but does not influence course of disease

epithelial tissue

covers body surfaces, lines hollow organs and cavities, forms glands

connective tissue

connects, supports, and protects body organs while distributing blood vessels to other tissues: cells, fibers, ground substance

muscular tissue

contracts to make body parts move, generate heat: smooth, skeletal, cardiac muscle

nervous tissue

carries information through the body using nerve impulses: neurons, neuroglia

central nervous system

astrocytes, oligodendrocytes, microglia, ependymal cells

peripheral nervous system

schwann cells, satellite cells

cellular adaptation

changes to cellular size or number, induction of alternative matabolic pathways or organelle changes to meet cellular demand: protection against injury

atrophy

decrease in cell size, minimizes energy and nutrient consumption

physiologic atrophy

diminished function (thymus, female reproductive), senile (old age)

pathologic atrophy

disuse (cast), endocrine (cryptorchidism, steroids), denervation (Carpal Tunnel), inadequate nutrition

hypertrophy

increase in cell size, commonly seen in tissues that are unable to mitotically divide

physiological hypertrophy

incresed workload, hormone-induced (pregnant/gravid uterus)

pathologic hypertrophy

response to stress/disease (hypertrophic cardiomyopathy)

hypertropic cardiomyopathy

increased pressure in outflow of left ventricle leads to hypertrophy of muscle fibers

hyperplasia

increase in number of cells, occurs in tissues capable of mitotic division, increases functional capabilities (labile/stable cells)

physiologic hyperplasia

hormonal (breasts during pregnancy), compensatory (liver after donation, RBCs in bone marrow)

pathologic hyperplasia

hormonal (endometrial, BPH), chonic injury

endometrial hyperplasia

overabundance of cells lining the uterus, continuous stimulation by estrogen, generally considered precancerous condition for endometrial cancer

endometrial hyperplasia signs and symptoms

heavy bleeding during menstruation, erratic bleeding during periods, abnormal/heavy bleeding durin menopause

benign prostatic hyperplasia

estrogen of dihydrotestosterone (DHT), hyperplasia regresses if hormonal stimulation is eliminated

benign prostatic hyperplasia signs and symptoms

frequent urination, trouble starting to urinate, weak stream, inability to urinate, loss of bladder control

metaplasia

reversible, one cell type is replaced by another cell type, allows for substitution of cells that are better able to survive when a more fragile cell type might succumb to injusry from insult

gastroesophageal reflux disease (GERD)

lower esophageal sphincter is weakened and allows atomach acid to reflux into lower esophagus (squamous → intesinal-like epithelium)

tobacco smoke

squamous metaplasia in the respiratory tract

dysplasia

cells vary in size, shape, and organization → strongly implicated as a precursor of cancer, usually in response to chronic irritation and inflammation, potentially reversibel

anaplasia

loss of cellular differentiation and structure

neoplasia

the formation of new, abnormal growth of tissue

cytochrome P450 (CYP450) hepatic enzymes

essential for production of cholesterol, steroids, prostacyclines, and thromboxane A2, essential for the detoxification of foreign chemicals and metabolism of many medications/drugs

exogenous material

anthracosis: severe anthracosis seen in the lungs and bronchial lymph nodes of people who work in coals mines (air pollution and cigarette smoking can also cause)

endogenous metabolites

hemosiderin, lipids, lipofuscin

hemosiderin

accumulation of blood-derived brown pigment, usually derived from hemolyzed blood, hemosiderans in liver develop in people who have received many blood transfusions or in those with hemolytic anemia, hereditary hemchromatosis

alcoholic fatty liver

triglycerides in the liver form, alcohol stimulation acculumatlion of fat in the liver → decreased utilization of triglycerides due to inhibition of enzymes, alcohol inhibits apoptorein synthesis and export of fat form the liver in the form of lipoproteins

lipofuscin

finely granular yellow-brown pigment granules composed of lipid-containing residues of digestion → “liver spots”

oxygen deprivation

hypoxia causes cells to switch to anaerobic glycolysis for ATP production

hypoxia

reduced availability of oxygen

anoxia

complete lack of oxygen

oxygen deprivation causes

inadequate supply of oxygen, obstruction of the airways, inhibition of blood oxygenation in the blood, inadequate transport of oxygen, inadequate perfusion of blood in the tisue, blockage of cellular respiration

physical agents

mechanical trauma, heat or cold, ionizing or UV radiation, electric shock

hyperthermia

too hot, denaturation of tisue proteins

hypothermia

too cold, ice crystal formation

ionizing radiation

production of free radicals that react with other cellular components/DNA, ionizes atoms and molecules → direct cell membrane/organelle damage

UV radiation

formation of pyrimidine dimers, disrupts cellular conds with the formastion of reactive oxygen species (ROS)

external pressure

loud noise leads to internal ear damage, blunt force leads to bruises or contusion

internal pressure

tumors, cysts, pus, pressure on nerves/blood vessles, inhibits mitosis and blood flow

parasites, bacteria, and viruses

destory cells by lysis, enzymatic erosion or ingestion

herpes

causes physical lesions due to cell destruction

infectious microbes

can replicate once they gain access to cells or tissues, range form protein molecules to microscopic parasites

immune defect

antigen-antibody interactions

deficiency

lacking sufficient nutrients (nutritional imbalances)

primary deficiency

lacking a vitamin or precursor

primary deficiency example

anecephaly resulting from a lack of maternal dietary folic acid during fetal brain development

secondary deficiency

nutrient is present but can’t be absorbed or utilized

secondary deficiency example

pernicious anemia: individual present with low hemocrit, stomach fails to produce intrisic factos (B12 not absorbed), vitamin K is not absored due to bile insufficiency

intoxication

poinsoning by toxins (chemicals, drugs, bacterial toxins)

genetic defect (intoxication)

endogenous metabolite becomes toxic due to genetic defect (PKU, liver failure, congenital erythropoeitic porphyria)

phenylketonuria (PKU)

individuals lack the enzyme necessary to metabolize phenylalanine → concentreation increases and becomes toxic

congenital erythropoietic porphyria

faulty porphyrins react with UV light and cause skin destruction via “burning” and blistering

liver failure

NH3 (ammonia) not converted to urea (hepatic coma)

ATP depletion

anything that decreases the supply of oxygen and other nutrients to the cell or that damages mitochondria directly halts aerobic respiration, leads to rapid deltion of ATP, cells switch to protein and lipid metabolism

membrane damage

increased permeability of cellular and organellar membranes, mitochondria injury leads to loss of calcium homeostasis

disruption of biochemical pathways

protein synthesis (enzymes, structural proteins)

intracellular accumulations

physical changes in cells due to injury

hydropic change

cellular swelling, buildup of water within the cytoplasm of the cell and organelles → loss or reduction of ATP synthesis, failure of Na/K pump, pressure inside cell builds up, water moves in via osmosis, lysis of cell