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Summary NUR 3032 - Patho Final Exam Study Guide 2.
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NUR 3032 - Patho Final Exam Study Guide 2/ NUR 3032 - Patho Final Exam Study Guide 2.
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1Patho Final 1. Cancer (4)
Pathophysiology of Cancer
Cancer is a disorder of altered cell differentiation and growth
Second leading cause if death in the US
Originates in almost any organ
Inhibits apoptosis
Increases with age
Proto-oncogene: a normal gene mutates into proto-oncogene and eventually contributes to cancer
Characteristics
The hallmark of cancer is the loss of cell differentiation and the generate their vasculatures to feed
itself (angiogenesis)
Disorder of altered cell differentiation and growth
oResults in neoplasia (“new growth”)
Growth is uncoordinated and relatively autonomous
oLacks normal regulatory controls over cell growth and division
oTends to increase in size and grow after stimulus ceases or needs of the organism are met
Components of Tissue Renewal and Repair
Cell Proliferation process of cell division
oInherent adaptive mechanism for replacing body cells
oProcess of increasing cell numbers by mitotic cell division
oIn normal tissue; regulated
# of cells actively dividing= # cells dying Cell Differentiation process of specialization
oNew cells acquire the structure and function of cells they replaces
oProcess by which proliferating cells become more specialized
oResults in fully differentiated adult cells Limited in division and reproduction
Stimuli to induce mitosis become more limited as cells become more highly differentiated (ex. Neurons)
Apoptosis a form of programmed cell death to eliminate unwanted cells
Differences between malignant and benign tumors
Malignant grow fast, differentiated, disorganized, uncontrollable cell replication, cells tend to break and scatter everywhere. Malignant neoplasms, which invade and destroy nearby tissue and spread to other parts of the body, tend to grow rapidly and spread widely and have the potential to cause death. Benign grow slow, well differentiated, surrounded by capsules, regularly apoptosis. They can become malignant, but don’t really metastasize. Well differentiated cells that are clustered together in a single mass
2. Different hyperplasia’s
Number (plasia) # of cell/multiplication of cells
Hyperplasia
Increase in the number of cells in an organ of tissue
Occurs in tissue with cells capable of mitotic division (neurons are not capable of this; happens in response to a stimulus and stops when stimulus is removed.)
Physiologic:
oHormonal: breast and uterine enlargement during pregnancy 2
oCompensatory: regeneration of the liver after partial hepatectomy
Non-physiologic: due to excessive hormonal stimulation or effects of growth factors on target tissues (endometrial hyperplasia)
Example gigantism (pathological, because endocrine disorder); with pregnancy there is an increase in hormones and causes an enlarged uterus (physiological, to meet the demands of the baby)
Metaplasia
Reversible
Can become malignancy
On type of cell becomes another type of cell mature form of cell to a less mature form
Occurs in response to chronic irritation and inflammation it allows for substitution of cells that are better able to survive under circumstances in which a more fragile cell type might succumb
Barrett Esophagus most common cause of metaplasia
oPremalignant condition that occurs in the esophagus of people with chronic gastroesophageal reflux disease (GERD)
oCharacterized by normal stratified squamous epithelium in the lower esophagus transforming into ciliated columnar-lined epithelium
Replaces a more mature form of the cell to a less mature form of cell
Primary risk factor for developing esophageal adenocarcinoma Dysplasia
Deranged cell growth which results in cells that vary in size, shape, and organization
Potentially reversible after irritating cause has been removed
May also become malignant Chronic irritation/inflammation
Cells are irregular, a typical, and disorganized Cervical dysplasia in women *Cardiovascular (16) *
3. Peripheral Vascular Disease
Defined as those conditions that interfere with blood flow to or from extremities
Disorders of circulation in the extremities Can be arterial or venous in origin
Disorders that affect the arteries in the extremities are the same as those affecting the coronary and cerebral arteries
Causes include cardiovascular disease, thrombi, prolonged immobility, excess standing, and pulmonary disease
Clinical Manifestations
Ischemia
Pain
Impaired function
Infarction
Tissue necrosis
4. Differences between peripheral arterial disease and peripheral venous disease Peripheral Arterial Disease Chronic condition (partial or total arterial occlusion). Deprives lower extremities of O2 and nutrients
Any reduction in blood supply compromises O2 supply
Result of systemic atherosclerosis distal to the aortic arch 3
Most common in men 60-70 years old Risk Factors
Cigarette smoking
Diabetes mellitus
Pathophysiology
Reduced blood flow which does not meet needs to muscle and nerve
Clinical Manifestations
Intermittent claudication (pain in calf when walking)
Thinning of the skin and weak pulses
If you cant find it use the Doppler
Calf pain (highest O2 consumption)
Vague aching
Numbness
Trophic changes (thick toe nails, hair loss)
Stasis ulcers Poor circulation
Decreased or absent pedal pulse blockage somewhere else Peripheral Venous Disease Can be acute (thromboembolism) or chronic (varicose veins)
Blockage within venous system may occur in system of superficial veins or deep veins
Proper function depends on veins being open with competent valves; assistance of surrounding muscle to pump blood toward heart
If not functioning properly venous distention
Three problems alter venous blood flow
1. Varicose veins Dilated and tortuous veins that result from a sustained increase in pressure that causes the venous valves to become incompetent, allowing for reflux of blood and vein
Superficial vein that is twisted and enlarged, causes incompetence of vein valves
Engorged veins distended caused by trauma or long term venous distention 2. Venous insufficiency Impaired blood flow in the venous system leads to tissue congestion, edema, and eventual impairment of tissue nutrition
3. Venous thrombosis Refers to thrombus formation and the accompanying inflammatory response that occurs in veins. Deep vein thrombosis may be a precursor to pulmonary embolism You see edema with these patients. * KEY WORD: EDEMA *
Clinical Manifestations
Discoloration of lower extremities
Edema
Ulcers
Tenderness in legs
Calf pain on dorsiflexion of foot Comparison of Arterial and Venous Insufficiency Arterial Venous 4
Description of pain Intermittent claudication, relived by dependent positionAching, cramping, relieved by elevation
Pulse assessment Diminished or absent Present
Ulcer characteristics Deep, pale; located on toes, feet, or other area of skinSuperficial, pink; over inner or outer ankle
Skin characteristics Dependent rubor; pallor upon elevation; dry, shiny skin; cool or cold temperature; edema mild if present at allThick and tough; brawny (brown) pigment; skin normal temperature; may have edema
Complications Gangrene Poor healing 5. Pathophysiology of atherosclerosis Thickening or hardening of arterial wall. Associated with aging but diet also
Formation of plaque with arterial wall, wall looses elasticity, so it becomes calcified and porcelain like. Can rupture of plaque becomes unstable and clotting can occur
Every time you rupture a plaque the lumen will have scar tissue and it will no longer be able to do its job like it used to
oPatho of plaque: unstable plaque: large central lipid core, inflammatory infiltrate, thin fibrous cap increased risk of rupture
The major risk factor is hypercholesterolemia, which can be modified
Most common cause of CAD
Associated more with lifestyle diet and high cholesterol
Usually associated with larger arteries (coronary, aorta, carotid, vertebral, renal, iliac, femoral)
Blood vessel damage inflammatory response
Blocked flow can lead to infarction, dead bowls and stroke
Stable or unstable plaques can develop Atherosclerosis raises the systolic blood pressure by: decreasing arterial distensability and
lumen radius or diameter Risk Factors
Hypercholesteremia
Increasing age
Male gender in women after menopause, it equalizes with men
Cigarette smoking
Obesity
Hyperlipidemia (increased LDL)
Diabetes
Inflammation (CRP) c-reactive proteins plasma concentration increase or decrease by 25% or more during inflammatory disorders Endothelial damage
6. Who is at most risk for hypertension? What population, Asians, African Americans, etc.?
The risk is increased in blacks
7. Risk factors of coronary artery disease (modifiable and non-modifiable)
Nonmodifiable
Age
Male gender (more at risk)
Genetic disorders of lipid metabolism
Family history
Ethnicity
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