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Pathophysiology

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the study of underlying changes in body physiology that result from disease or injury.

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Etiology

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study of the cause of disease

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Clinical manifestations

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s/s, evidence of disease, local and systemic

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Risk factors

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predisposing) increase disease probability, but do not cause.

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Complications

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onset of disease while having an existing disease

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Hypertrophy

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increase in the size of cells which results in enlargement of the organs, tissue or muscle (Mostly seen in cells that cannot divide)

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Metaplasia

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transformation or replacement of one adult cell type to another adult cell type (respiratory tract, distal esophagus) (usually results from chronic irritation)

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Dysplasia

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deranged cell growth that results in cells that vary in size, shape and organization.

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Hyperplasia

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increased # of cells in an organ or tissue (may sometimes co-exist with hypertrophy. Physiologic, hormonal, compensatory, pathologic)

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Atrophy

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shrinkage of cells (physiologic and pathologic)

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Physiologic Atrophy

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occurs with early development, thymus gland undergoes during childhood

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Pathologic Atrophy

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Result of decrease in workload, pressure, use, blood supply, nutrition, hormonal stimulation, and nervous stimulation

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Physiologic Hypertrophy

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Growth of uterus and mammary glands in response to pregnancy

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Pathologic Hypertrophy

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Growth of Heart secondary to hypertension or diseased heart valves *Cells of the heart and kidney are particularly prone

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physiologic Hyperplasia Compensatory

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Adaptive mechanism that enables certain organs to regenerate: Removal of part of the liver

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Hormonal Hyperplasia

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Increase in cells in Estrogen dependent organs of uterus and breast

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Pathologic Hyperplasia

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Pathologic endometrial hyperplasia-excessive menstrual bleeding, cells undergo malignant transformation

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Dysplasia

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Epithelial tissues of the cervix and repiratory tract where they are strongly associated with common neoplastic growths/Found adjacent to cancer cells

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Metaplasia

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Replacement of normal columnar ciliated epithelial cells in bronchial airway by stratified squamous

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Suffocation

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Choking asphyxiation, Blockage of external airways, Failure of oxygen to reach blood

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Strangulation

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Compression and closure of the blood vessels and air passages resulting from external pressure on the neck

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Lead poisoning

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Children absorb more readily. Worse when nutrition is compromised, effects nervous system

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Carbon Monoxide poisoning

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odorless, colorless, undetectable, causes oxygen deprivation by forming carboxyhemoglobin.

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mercury poisoning

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peripheral neuropathy, skin discoloration, swelling and desquamation (shedding of skin), sweating, tachycardia, hypertension

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Carbon tetrachloride poisoning

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increase of fatty liver, decrease ph, cellullar swelling, cellular auto digestion, destruction of rough ER and plasma membrane

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Apoptosis

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vital process that helps to eliminate unwanted cells. Internally programmed series of events affected by dedicated gene products

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Necrosis

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irreversible injury changes produced by enzymatic digestion of dead cellular elements.

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Necrosis: Coagulative

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Necrosis of kidneys, heart, and adrenal glands. Protein denaturation.

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Necrosis: Liquefactive

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Necrosis of neurons and glial cells of the brain. Hydrolytic enzymes, bacterial infection.

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Necrosis Caseous

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Necrosis: tuberculous pulmonary infection, combination of coagulative and liquefactive necrosis.

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Necrosis Fat

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Necrosis of breast, pancreas, and other abdominal organs. Action of lipases.

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Gangrenous Necrosis

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death of the tissue from severe hypoxic injury

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Dry Gangrenous Necrosis

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aka senile gangrene. Mainly due to arterial occlusion. Actually a form of coagulative necrosis

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Wet Gangrenous Necrosis

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occurs in naturally moist tissue and organs such as the mouth, bowel, lungs, cervix, and vulva. Tissue is infected by saprogenic microorganisms (Clostridium perfringens or Bacillus fusiformis, for example).

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Ischemia

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restriction in blood supply to tissues, causing a shortage of oxygen and glucose needed for cellular metabolism (to keep tissue alive) (decreased mitochondrial oxygenation, decreased ATP)

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Anoxia

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results when oxygen is not being delivered to a part of the body. Reperfusion injury: tissue damage when blood flow returns after being gone for a while.

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primary intention wound healing

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Wounds that heal under conditions of minimal tissue loss involves epidermis and dermis without total penetration of dermis healing by process of epithelialization

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Secondary intention wound healing

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wound is allowed to granulate. Surgeon may pack wounds with gauze or drainage system.

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livor mortis

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settling of the blood in the lower (dependent) portion of the body, causing a purplish red discoloration of the skin: when the heart is no longer agitating the blood, heavy red blood cells sink through the serum by action of gravity

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Algor mortis

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the reduction in body temperature following death. This is generally a steady decline until matching ambient temperature, although external factors can have a significant influence.

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Rigor mortis

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: one of the recognizable signs of death, caused by chemical changes in the muscles after death, causing the limbs of the corpse to become stiff and difficult to move or manipulate.

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functions of α receptors

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Vasoconstriction of arteries to heart (coronary artery).Vasoconstriction of veins.Decrease motility of smooth muscle in gastrointestinal tract

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actions of the β1 receptor

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Increase cardiac output by increasing heart rate and stroke volume. Increase renin secretion from juxtaglomerular cells of the kidney.Increase ghrelin secretion from the stomach.

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Generalized Adaption Syndrome: Alarm Stage

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G.A.S. Stressor triggers the hypothalamic-pituitary-adrenal (HPA) axis. Activates sympathetic nervous system

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Generalized Adaption Syndrome Resistance stage

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G.A.S. Begins with the actions of adrenal hormones

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Generalized Adaption Syndrome Exhaustion stage

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G.A.S. Occurs only if stress continues and adaptation is not successful

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After initial exposure to antigen

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there is latent or lag period (antigen processing & B cell differentiation occurs)

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Primary response: characterized by initial production of IgM followed by

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production of IgG against same antigen, IgG is same as or less than concentration of IgM

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Secondary response: characterized by

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more rapid production of a larger amount of antibody than primary response; IgG production predominately increases

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Active acquired immunity

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immunity produced by an individual either after natural exposure to antigens or after immunization. Long lived.

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Passive acquired immunity

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immunity that does not involve the host's immune response at all. It occurs when preformed antibodies or T cells are transferred from a donor or recipient. Only temporary.

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Passive acquired immunity

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During pregnancy, when maternal antibodies cross placenta to fetus

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Passive acquired immunity

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Artificially; when antibodies are injected to fight specific disease

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Histamine role

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cause temporary, rapid constriction of smooth muscle and dilation of postcapillary venules, which result in increased blood flow into microcirculation

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Histamine affects cells by binding to

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to histamine H1 and H2 receptors on target cell surface

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Antihistamines

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block binding of histamine to its receptors, resulting in decreased inflammation.

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Histamine Action

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cause increased vascular permeability & increased adherence of leukocytes to endothelium

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Eosinophils: 2 Special Functions

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1. Serve as body's primary defense against parasites, and 2. They help regulate vascular mediators released from mast cells

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secondary role of eosinophils

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helps limit and control inflammation

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Mast cells produce

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eosinophil chemotactic factor-A (ECF-A), which attracts eosinophils to site of inflammation.

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Neutrophils pprimary role

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The primary roles of ______are removal of debris and dead cells in sterile lesions, such as burns, and destruction of bacteria in nonsterile lesions.

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Lymphocytes

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generate acquired immune response, the production of family of cytokines, they guide development of a subset of T cells (helper cells) that coordinate the development of functional B and T cells. T lymphocytes are active during the proliferative phase of wound healing.

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Macrophages and wound healing

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orchestrate wound healing process by cleaning up site of injury by phagocytosis, promoting angiogenesis, releasing cytokines and growth factors that promote epithelial cell division, activating fibroblasts and promoting synthesis of extracellular matrix and collagen formation.

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inflammation acute symptoms

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symptoms swelling, pain, heat and redness

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inflammation acute duration

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:self-limiting, it continues only until the threat to host is eliminated (8-10 days)

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chronic inflammation duration

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lasts 2 weeks or longer, regardless of cause

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chronic inflammation symptoms

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symptoms characterized by a dense infiltration of lymphocytes and macrophages. If macrophages are unable to protect the host from tissue damage, the body attempts to wall off and isolate the infected area, thus forming a granuloma

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Complement system

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Activation produces proteins that can directly destroy pathogen or activate activity of many other components of inflammatory and adaptive immune response

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Complement system Most important function

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activation of C3 & C5, which results in molecules such as 1. Opsonins, 2. Chemotactic factors, 3. Anaphylatoxins

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Opsonins

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coat surface of bacteria and increase their susceptibility to being phagocytized and killed by inflammatory cells (neutrophils & macrophages

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Chemotactic factors

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diffuse from site of inflammation and attract phagocytic cells to that site

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Anaphylatoxins

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induce rapid degranulation of mast cells (i.e. release of histamine that induces vasodilation and increases capillary permeability)

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Activation of components C5b through C9 (MAC) results in a complex that

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complex that creates pores in the outer membranes of cell or bacteria; pores disrupt the cell's membrane and permit water to enter, causing the cell to burst and die or at least prevent its reproduction

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classical pathway that controls the activation of complement

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pathway that controls the activation of complement mainly activated by antibodies (acquired immune system), which bind to antigens of bacteria activates C1 other components C3 & C5

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alternative pathway that controls the activation of complement

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pathway that controls the activation of complement activated by substances found on surface of infectious organisms (ex: endotoxin on bacterial surface). Uses unique proteins to form complex that activates C3 C5 activation & convergence with classical pathway

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lectin pathway that controls the activation of complement

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activation of complement activated by plasma proteins (Mannose-binding lectin) - similar to C1 converges with classical

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clotting system

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group of plasma proteins that, when activated sequentially, form a blood clot.

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clotting system functions

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Clots: 1. Plug damaged vessels and stop bleeding, 2. Trap microorganisms and prevent their spread to adjacent tissues, 3. Provide framework for future repair and healing

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tissue factor (extrinisic) pathway

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activated when there is tissue injury and membrane-bound or soluble tissue factor (released by damaged endothelial cells in blood vessels) reacts with activated factor VII

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contact activation (intrinsic) pathway

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activated when there is an abnormal vessel wall and Hageman factor (factor XII) in plasma contacts negatively charged subendothelial substances

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Final product of kinin system bradykinin

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causes dilation of blood vessels, acts with prostaglandins to induce pain, causes smooth cell contraction and increases vascular permeability

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Humoral immunity

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activation of a variety of inflammatory mediators that will destroy pathogens, by antibodies binding to antigen, B cells.

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Cell-mediated immunity

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T cells, that differentiate, Acts directly with cells or activates leukocytes or cytokines that act directly

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Cell-mediated immunity & Humoral immunity

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both contribute to the acquired immune response both activators can act directly or indirectly to produce immune response both produce memory cells (remember sp. Antigens to respond more rapidly)

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Anaphylaxis Systemic symptoms

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Symptoms: pruritus, erythema, vomiting, abdominal cramps, diarrhea and breathing difficulties

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Anaphylaxis Systemic symptoms Severe

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Symptoms: contraction of bronchial smooth muscle, edema of the throat, breathing difficulties, decreased BP, shock and death

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Anaphylaxis Cutaneous Sypmtomrs

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local symptoms such as pain, swelling and redness

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type I reactions, GI allergy

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Symptoms: vomiting, diarrhea or abdominal pain

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skin manifestation of allergic reaction

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Characterized by wheals (white fluid-filled blisters) surrounded by area of redness (flares). Also accompanied by pruritus (itching).

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hypersensitivity Type I

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Alergy mediated by antigen-specific IgE and the products of tissue mast cells: Food, oral drugs, pollens, dust, molds

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hypersensitivity Type II

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generally reactions against a specific cell or tissue:ingestible drugs, injectable drugs

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hypersensitivity Type III

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caused by antigen-antibody (immune) complexes that are formed in the circulation and deposited later in vessel walls or other tissues

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hypersensitivity Type IV

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mediated by T lymphocytes and do not involve antibody (unlike Type I,II, III) Contact dermatitis with poison ivy and metals

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Autoimmune Disorder

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results from breakdown of tolerance of his or her own antigens

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Systemic lupus erythematosus

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Autoimmune Disorder: large variety of autoantibodies, 1. Facial rash confined to cheek, 2. Discoid rash, 3. Photosensitivity, 4. Oral or nasopharyngeal ulcers, 5. Non-erosive arthritis of at least two peripheral joint, 6. Serositis, 7. Renal disorder

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Alloimmunity

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two individuals may have different antigens on their tissues, and be able to therefore establish an immune response against each other's tissues

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effect of bacteria

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exotoxins that damage cell membranes, activate second messengers and inhibit protein synthesis,vasoactive peptides and cytokines that affect blood vessels, producing vasodilation, which reduces BP, causes decreased O2 delivery and produces subsequent cardiovascular shock.

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Viruses effect

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host cell DNA, RNA or protein synthesis, disrupt lysosomal membranes, promotes apoptosis, fusion of infected, adjacent host cells, alteration of antigenic properties, transformation of host cells into cancerous cells, promotion of secondary bacterial infection. They usually spread cell-to-cell.

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Fungi:

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invade the skin, hair or nails b/c they digest keratin, and adapt to host environment (wide temperature variation, low oxygen).

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symptoms of immunodeficiency

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Early stage: influenza, night sweats, swollen lymph glands, diarrhea or fatigue

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Identify the target cells of HIV/AIDS

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T helper cells; necessary for the development of both plasma cells and cytotoxic T cells.

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Interleukins

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Cytokine types produced primary by macrophages and lymphocytes in response to a pathogen or stimulation by other products of inflammation

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Interferon

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Cytokine types protects against viral infections. Produced and released by virally infected host cells in response to viral double stranded RNA

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Tumor necrosis factor-alpha

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Cytokine types secreted by macrophages in response to PAMP and toll-like receptor regonition; induces fever by acting as an endogenous pyrogen; increases synthesis of inflammatory serum proteins; causes muscle wasting and intravascular thrombosis.

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Kinin system (bradykinin): causes

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Causes pian among other things. Swelling during inflammation causes pain b/c the swelling pushes against the nerves

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Inflammatory and immune responses to parasitic infection

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Eosinophils (mildly phagocytic) defend against parasites (as well as regulate vascular mediators). Eosinophils are a type of granulocyte WBC.

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why elderly and pediatric patients are at risk for dehydration

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Water volume of elderly is 55% and infants 80% means they are at risk for

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Aldosterone

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hormone from adrenal cortex: Increased reabsorption of sodium and water retention

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