what is the difference between the clinical manifestations of Lower and Upper Respiratory Tract Infection?

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In simplistic terms upper respitory infections are those of the ears, nose and throat. Fever, ear pain, post nasal drip, sinus pain....there are many different sypmtoms. Lower respitory infections involve the lungs and trachea. Fever, coughing, wheezing, chest pain...these are the usual symptoms. Sometimes people will have both.  (+ info)

explain the pathophysiology of artherosclerosis and its clinical manifestations?

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Atherosclerosis is patchy intimal plaques (atheromas) in medium and large arteries; the plaques contain lipids, inflammatory cells, smooth muscle cells, and connective tissue. Risk factors include dyslipidemia, diabetes, cigarette smoking, family history, sedentary lifestyle, obesity, and hypertension. Symptoms develop when growth or rupture of the plaque reduces or obstructs blood flow; symptoms vary by artery affected. Diagnosis is clinical and confirmed by angiography, ultrasonography, or other imaging tests. Treatment includes risk factor and dietary modification, physical activity, and antiplatelet drugs.

Atherosclerosis can affect all large and medium-sized arteries, including the coronary, carotid, and cerebral arteries, the aorta, its branches, and major arteries of the extremities. It is the leading cause of morbidity and mortality in the US and in most Western countries. In recent years, age-related mortality attributable to atherosclerosis has been decreasing, but in 2001, coronary and cerebrovascular atherosclerosis still caused > 650,000 deaths in the US (more than cancer and almost 6 times more than accidents). Atherosclerosis is rapidly increasing in prevalence in developing countries, and as people in developed countries live longer, incidence will increase. By 2020, atherosclerosis is expected to be the leading cause of death worldwide.

Pathophysiology
The hallmark of atherosclerosis is the atherosclerotic plaque, which contains lipids (intracellular and extracellular cholesterol and phospholipids), inflammatory cells (eg, macrophages, T cells), smooth muscle cells, connective tissue (eg, collagen, glycosaminoglycans, elastic fibers), thrombi, and Ca deposits. All stages of atherosclerosis—from initiation and growth to complication of the plaque—are considered an inflammatory response to injury. Endothelial injury is thought to have a primary role.

Atherosclerosis preferentially affects certain areas of the arterial tree. Nonlaminar or turbulent blood flow (eg, at branch points in the arterial tree) leads to endothelial dysfunction and inhibits endothelial production of nitric oxide, a potent vasodilator and anti-inflammatory molecule. Such blood flow also stimulates endothelial cells to produce adhesion molecules, which recruit and bind inflammatory cells. Risk factors for atherosclerosis (eg, dyslipidemia, diabetes, cigarette smoking, hypertension), oxidative stressors (eg, superoxide radicals), angiotensin II, and systemic infection and inflammation also inhibit nitric oxide production and stimulate production of adhesion molecules, proinflammatory cytokines, chemotactic proteins, and vasoconstrictors; exact mechanisms are unknown. The net effect is endothelial binding of monocytes and T cells, migration of these cells to the subendothelial space, and initiation and perpetuation of a local vascular inflammatory response. Monocytes in the subendothelium transform into macrophages. Lipids in the blood, particularly low density lipoprotein (LDL) and very low density lipoprotein (VLDL), also bind to endothelial cells and are oxidized in the subendothelium. Uptake of oxidized lipids and macrophage transformation into lipid-laden foam cells result in the typical early atherosclerotic lesions called fatty streaks. Degraded erythrocyte membranes that result from rupture of vasa vasorum and intraplaque hemorrhage may be an important additional source of lipids within plaques.

Macrophages elaborate proinflammatory cytokines that recruit smooth muscle cell migration from the media and that further attract and stimulate growth of macrophages. Various factors promote smooth muscle cell replication and increase production of dense extracellular matrix. The result is a subendothelial fibrous plaque with a fibrous cap, made of intimal smooth muscle cells surrounded by connective tissue and intracellular and extracellular lipids. A process similar to bone formation causes calcification within the plaque.

Atherosclerotic plaques may be stable or unstable. Stable plaques regress, remain static, or grow slowly over several decades until they may cause stenosis or occlusion. Unstable plaques are vulnerable to spontaneous erosion, fissure, or rupture, causing acute thrombosis, occlusion, and infarction long before they cause stenosis. Most clinical events result from unstable plaques, which do not appear severe on angiography; thus, plaque stabilization may be a way to reduce morbidity and mortality.

The strength of the fibrous cap and its resistance to rupture depend on the relative balance of collagen deposition and degradation. Plaque rupture involves secretion of metalloproteinases, cathepsins, and collagenases by activated macrophages in the plaque. These enzymes digest the fibrous cap, particularly at the edges, causing the cap to thin and ultimately rupture. T cells in the plaque contribute by secreting cytokines. Cytokines inhibit smooth muscle cells from synthesizing and depositing collagen, which normally reinforces the plaque.

Once the plaque ruptures, plaque contents are exposed to circulating blood, triggering thrombosis; macrophages also stimulate thrombosis because they contain tissue factor, which promotes thrombin generation in vivo. One of 5 outcomes may occur: The resultant thrombus may organize and be incorporated into the plaque, changing the plaque's shape and causing its rapid growth; the thrombus may rapidly occlude the vascular lumen and precipitate an acute ischemic event; the thrombus may embolize; the plaque may fill with blood, balloon out, and immediately occlude the artery; or plaque contents (rather than thrombus) may embolize, occluding vessels downstream.

Plaque stability depends on multiple factors, including plaque composition (relative proportion of lipids, inflammatory cells, smooth muscle cells, connective tissue, and thrombus); wall stress (cap fatigue); size and location of the core; and configuration of the plaque in relation to blood flow. By contributing to rapid growth and lipid deposition, intraplaque hemorrhage may play an important role in transforming stable into unstable plaques. In general, unstable coronary artery plaques have a high macrophage content, a thick lipid core, and a thin fibrous cap; they narrow the vessel lumen by < 50% and tend to rupture unpredictably. Unstable carotid artery plaques have the same composition but typically cause problems through severe stenosis and occlusion, not rupture. Low-risk plaques have a thicker cap and contain fewer lipids; they often narrow the vessel lumen by > 50% and produce predictable exercise-induced stable angina.

Clinical consequences of plaque rupture depend not only on plaque anatomy but also on relative balance of procoagulant and anticoagulant activity in the blood and on the vulnerability of the myocardium to arrhythmias.

A link between infection and atherosclerosis has been suggested to explain the serologic associations between infections (eg, Chlamydia pneumoniae, cytomegalovirus) and coronary artery disease. Putative mechanisms include indirect effects of chronic inflammation in the bloodstream, cross-reactive antibodies, and inflammatory effects of infectious pathogens on the arterial wall.

Risk Factors
Dyslipidemia (high total, high LDL, or low high density lipoprotein [HDL] cholesterol), hypertension, and diabetes promote atherosclerosis by amplifying or augmenting endothelial dysfunction and inflammatory pathways in vascular endothelium.

In dyslipidemia, subendothelial uptake and oxidation of LDL increases; oxidized lipids stimulate production of adhesion molecules and inflammatory cytokines and may be antigenic, inciting a T cell–mediated immune response and inflammation in the arterial wall. HDL protects against atherosclerosis via reverse cholesterol transport (see Lipid Disorders: Exogenous (dietary) lipid metabolism); it may also protect by transporting antioxidant enzymes, which can break down and neutralize oxidized lipids. The role of hypertriglyceridemia in atherogenesis is complex, and whether it has an effect independent of other lipid abnormalities is unclear.

Hypertension may lead to vascular inflammation via angiotensin II–mediated mechanisms. Angiotensin II stimulates endothelial cells, vascular smooth muscle cells, and macrophages to produce proatherogenic mediators, including proinflammatory cytokines; superoxide anions; prothrombotic factors; growth factors; and lectin-like oxidized LDL receptors.

Diabetes leads to the formation of advanced glycation end products, which increase the production of proinflammatory cytokines from endothelial cells. Oxidative stress and reactive oxygen radicals, generated in diabetes, directly injure the endothelium and promote atherogenesis.

Cigarette smoke contains nicotine and other chemicals that are toxic to vascular endothelium. Smoking, including passive smoking, increases platelet reactivity (possibly promoting platelet thrombosis) and plasma fibrinogen levels and Hct (increasing blood viscosity). Smoking increases LDL and decreases HDL; it also promotes vasoconstriction, which is particularly dangerous in arteries already narrowed by atherosclerosis. HDL increases by about 6 to 8 mg/dL within 1 mo of smoking cessation.

Hyperhomocysteinemia increases risk of atherosclerosis, although not as much as the above risk factors. It may result from folate deficiency or a genetic metabolic defect. The pathophysiologic mechanism is unknown but may involve direct endothelial injury, stimulation of monocyte and T-cell recruitment, LDL uptake by macrophages, and smooth muscle cell proliferation.

Lipoprotein(a) is a modified version of LDL that has a cysteine-rich region homologous with plasminogen. High levels may predispose to atherothrombosis, but mechanism is unclear.

A high level of small, dense LDL, characteristic of diabetes, is highly atherogenic. Mechanism may include in  (+ info)

What are the manifestations of food allergy symptoms?

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research
Anaphlyaxis - burning in GI tract, diarrhoea, hives, shortness of breath, facial and tongue swelling, stridor, low blood pressure, unconscious, death

Intolerance - bloating, diarrhoea/constipation, rashes, feeling tired, lethargy, nausea

coelic disease - unsure of all the symptoms  (+ info)

Are oral canker sores and cold sores different manifestations of the same herpes virus?

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Yes and no.

Cold sores are HSV-1, canker sores can be HSV-1 or they can be bacteria after an injury for instance.

HSV-2 is the kind people call genetal herpes. They are a different *strain* of the herpes virus.

They are both still a retrovirus and work in a very similar fashion.

Either one can be spread to other people and both have other complications beyond what most people know about, such as spreading to other parts of the body.

Wikipedia has a good article on it but it is quite long but not overly technical.  (+ info)

What are varicose viens? What veins are commonly affected? What are the clinical manifestations?

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its enlarged vein that looks like spider veins all over your legs or arms.. its not attractive, so a lot of ppl hides it or pay huge amount of money to remove it.. I believe it cost 100 dollars a shot per vein.. so its costy.. its caused by vary reasons.. some are by inherited characteristics... being overweight or pregnant usually develop that too.. if you have it in your legs, then your legs will feel swollen and heavy and painful.. its not comfortable.. a lot of people use the stocking to prevent those to develop, it is proven that stocking works..
here is the link with best explanation about varicose veins, anything you wana know, they got it.. http://health.yahoo.com/other-other/varicose-veins-topic-overview/healthwise--hw113840.html  (+ info)

what are the allergic manifestations on the skin of mitomycinc when given intravesically?

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This is a tough one. From all that I read here, it appears that it is a cancer fighting drug. I gave you a link so that you could see what it all involves.
If this is you or one of your loved ones, I hope that this works. It sounds pretty involved and serious.  (+ info)

Anyone have genetic memory manifestations in dreams, deja vu feelings, inexplicable attachment to any places?

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I used to dream of white stone houses with black grill balconies or trim. In one dream I was a little boy with a Caucasian grandmother, watching a religious procession from a black grill balcony (I'm Asian). Then I traced my greatgreatgrandmother's ancestry as possibly, Mexican Jew starting back to Valencia, Spain. When I saw a TV feature on Valencia I was startled to see the white stone houses with black balconies I had seen in dreams.
I've had deja vu. I recommend Sylvia Browne's books to you. She is an awesome psychic in our lifetime. Check her books out at the library or in the bookstores.  (+ info)

Impaired skin integrity and skin manifestations are common in persons with chronic renal failure...?

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Pale skin and subcutaneous bruising are often present as a result of...

thrombocytopenia
anticoagulant therapy
increased vascular volume
impaired platelet function

me an a couple friends have no idea about this one and its our last question...can you please help? if you could explain why its the answer would be great too...thanks!
it's impaired platelet function. mostly because of reduced granule content, and there is less ADP and serotonin in the granules. hypercalcemia and PTH can also alter platelet function.  (+ info)

what are the manifestations of a newborn who has hyperbilirubinemia or jaundice??

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what are also its diagnostic exams/tests????????????
They have yellowish tinge skin that starts from forehead down to the extremities.Sclera is yellow. Test include total bilirubin,direct and indirect,CBC is also taken to check if infection was the caused of jaundiced and blood typing to check for ABO incompatibility.  (+ info)

is weight gain, one of the manifestations of liver cirrhosis?

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signs and symptoms of liver cirrhosis
If your liver isnt functioning, like when you have cirrhosis, you are far more likely to lose weight then gain it. Look for yellowing of the eyes, itching, tiredness.  (+ info)

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