1. Susceptibility
2. Asymptomatic disease
3. Clinical Disease
4. Disability

The stage of a disease where pathologic changes are not detectable but risk factors are

Note: primary prevention is relevant

stage of a disease where symptoms have not appeared but pathologic changes or indicators are detectable

Note: secondary prevention/early intervention is relevant

The stage of a disease where symptoms have appeared and a diagnosis is possible if a physician is consulted. The patient may or may not be significantly disabled, depending on the patient

Note: interventions resulting in iatrogenic disease must be prevented

The significant phase of disease in which it interferes with the performance of one or more of the patient’s valued roles

Note: Tertiary prevention ( control of disability and rehabilitation) is relevant

athere = "gruel” referring to the lipid accumulation

sclerosis = “hardening” referring to the thickening of the arterial intima

also secretes substances like prostacyclin that inhibits platelet aggregation and   Factor VIII that is necessary for clotting

insult to the endothelium that initiates plaque buildup.

Insult can be due to metabolic, mechanical or immunologic

This causes loss of endothelial cells to function normally, or to attach to each other, or to attach to underlying connective tissue

How can hemodynamic forces influence the cellular events that initiate atherosclerotic lesions and explain their focal distribution at certain sites predetermined by altered blood flow

Sites of predilection for forming atherosclerotic lesions, e.g. branch points, often have disturbed laminar flow and are unable to suppress VCAM-1 expression

Lipid accumulation and the propensity to form atheroma will ensue if the amount of lipid entering the artery wall exceeds that exported by mononuclear cells or other pathways

Formation of fibrous cap and lipid core:

Macrophages loaded with modified lipoproteins, like intrinsic vascular wall cells, may elaborate cytokines and growth factors that can stimulate smooth muscle cell proliferation and production of extracellular matrix

No, not all the time. The lipid in the fatty streak is mainly  cholesterol oleate. It is usually sessile and causes no obstruction or symptoms 

True or False?

Arrival of smooth muscle cells and their elaboration of extracellular matrix probably provides a critical transition, yielding a fibrofatty lesion in place of a simple accumulation of macrophage derived foam cells

Rupture of plaque and cause thrombus. In advanced fatty streaks, microscopic breaches in endothelial integrity may occur. Microthrombi rich in platelets can form at such sites of limited endothelial denudation, due to exposure of the highly thrombogenic extracellular matrix of underlying basement membrane  

Activated platelets release numerous factors that can promote the fibrotic response and alter smooth muscle function.

Most microthrombi resolve without clinical manifestation by a process of local fibrinolysis, resorption and endothelial repair

palpably elevated areas of intimal thickening and are the most characteristic lesion of advancing atherosclerosis          

Plaque cholesterol ester composition differs from fatty streaks but resembles plasma lipoproteins                       

Hemorrhage and Calcium Deposit:

Atherosclerotic plaques also accumulate calcium. Proteins specializing in binding of calcium, such as osteocalcin, osteopontin and bone morphogenetic proteins, also occur in atherosclerotic lesions  

With increasing necrosis and accumulation of extracellular lipid, the arterial wall progressively weakens and ruptures of the intima can occur, causing aneurysm and hemorrhage 

The hypoxic stimulus of repeated bouts of ischemia characteristically induces the formation of collateral vessels, such as the coronary arteries  

In addition to modified lipoproteins, what other factors can regulate the expression of adhesion molecules for leukocyte recruitment in fatty streaks?

Upper outer quadrant – 50%

  Central portion – 20%

  Medial quadrants – 20%

  Lower outer quadrant – 10%

Breast Self Examination

Colorectal cancer

Note: Second highest mortality for both male and female in US

Sigmoid colon tumor present with obstruction from circumferential growth and gross blood per rectum observes

Tumors in the rectum exhibit rectal pain, gross blood per rectum, tenesmus with a feeling of incomplete rectal evacuation

Adenocarcinoma 

Breast self exam – starting in the early 20s

Clinical breast exam – every 3 yrs, ages 20-39

       annually, starting at age 40*

  Mammography – annually, starting at age 40

For men and women over age 50:

  Flexible Sigmoidoscopy – every 5 years, starting at age 50

  FOBT or FIT           -   annually, starting at age 50 

  Colonoscopy            -  every 10 years, starting age 50

  Double Contrast Barium Enema – every 5 years, starting at age 50  

  Computed Tomography Colonography – every 5 years, starting age 50

Digital rectal exam (DRE) and PSA annually

For women 18+

Pap test should begin app. 3 yrs after a woman begins having intercourse, but no later than age 21.

Screening should be done every year with conventional Pap tests or every 2 yrs using liquid-based Pap tests.

At or after age 30, women who have had 3 normal Paps in a row may get screened every 2 to 3 yrs.

Women age 70 and older who have had 3 or more normal Paps and no abnormal Paps in the last 10 yrs and women who have had a total hysterectomy may choose to stop cervical cancer screening

Incidence rates and death rates for prostate cancer are much higher in which of the following minorities?