Test 3 Mini

A progressive bone disease where bones lose density become thin brittle and prone to fracture

Alterations in bone remodeling with aging osteoclast activity exceeds osteoblast activity

Metabolic Bone disease characterized by inadequate mineralization of bone tissue

Starts with vitamin D deficiency results in thinning of spongy bone and weakening of compact bone

Accelerated remodeling of bone tissues that lead to bone deformity and fractures

First you see an increase in osteoclastic activity causing bone resorption than the formation of new abnormal bone

Bone infection usually caused by bacterial infection

Pathogen is transported through the bloodstream to the Bone or pathogen spreads from adjacent infection tissues. The infection and inflammation cause damage to the Bone tissue leading to abscesses and necrosis

Osteoarthritis is a chronic degenerative and inflammatory disease affecting synovial joints

Enzymatic degradation of articular cartilage and wear and tear. inflammation causes joint cartilage to soften flake and fissures appear. Leads to the collapse of joint space and the development of osteophytes

A chronic systemic autoimmune disease that affect synovial joints and other body systems

Trigger stimulates an autoimmune response involving B & T cells. Antibodies and TC cells cause damage to synovial tissues

Inflammatory syndrome caused by excess of uric acid in the blood and synovial fluid

Urate crystal deposition and inflammatory response

The rapid breakdown of muscle tissue leading to release of intercellular contents into the bloodstream

Skeletal muscle cells lyse resulting in the release of intracellular molecules including potassium and myoglobin hyperkalemia can lead to cardiac arrhythmias myoglobin accumulates in the glomerulus causing renal ischemia

Fatigue weakness irritability confusion paresthesias pallor chest pain heart failure increase rate and depth of respiration dyspnea abdominal pain nausea vomiting decreased bowel movement

A mycotic hypochromic anemia

Gradual depletion of iron stores in liver and bone marrow manifested by a decrease in plasma ferritin levels later see a decrease in plasma iron levels. In iron deficient electrophoresis begins and small hemoglobin deficient red blood cells enter circulation manifested by a decrease in the mean cell volume of red blood cells and a decrease in hemoglobin and hematocrit development of microcytic hypochromic anemia. Eventually leading to low red blood cell count

A macrocytic normochromic anemia. Vitamin B12 Anemia has historically been known as pernicious anemia. Meaning destruction

Role of vitamin B12 and folate in electrophoresis both vitamins are coenzymes necessary for DNA synthesis and the developing red blood cell. Vitamin B deficiency results in a decrease in rate of cell division of developing red blood cells combined with the normal rate of growth.

A decrease in the number of red blood cells produced by the bone marrow low hematocrit low hemoglobin and production of unusually large stem cells that mature into unusually large erythrocytes

Milan degradation loss of neurons in the spinal cord and peripheral nerve degradation

Folate deficiency manifested by low plasma folate levels results in a decrease in the rate of cell division of developing red blood cells combined with the normal rate of growth same patho as Vitamin B12 deficiency

Premature accelerated destruction of otherwise normal erythrocytes

Binding of any buddies and complement proteins to red blood cell membrane called opsonization. Hopsin eyes red blood cells are phagocytes toast by macrophages as they migrate through the narrowing capillaries in the spleen. Following hemolysis excessive amounts of hemoglobin are released from red blood cells and broken down by macrophage resulting in unconjugated bilirubin released into the plasma

Sickle cell disease is a genetic disorder that results in the presence of abnormal form of hemoglobin

Presence of abnormal hemoglobin s, hemoglobin s reacts to hypoxemia and dehydration, the red blood cells take on a Ridgid sickle-shaped and normal flexibility of red blood cell is lost. Sickling in is reversible but after repeated episodes the cells are permanently damaged

Bone marrow failure associated with production of red blood cells white blood cells and platelets

Reduction in number or absence of bone marrow stem cells or stem cell abnormalities resulting in an inadequate production of red blood cells white blood cells and platelets

Spp 140 to 159 and DBP 90 to 99

SBP 160 +, DBP over 100

Vasoconstriction of systemic arteries and arterioles such as arterial to skin and digestive tract

Increase heart rate and increase strength of ventricular contraction which increases cardiac output

An increase in blood pressure results in release of renin by the kidney combined with angiotensinogen results in Angiotensin 1 combined with Ace results in Angiotensin 2 causing vasoconstriction in the arteries and stimulating the adrenal cortex to release aldosterone which results in sodium and water re-absorption increasing blood pressure

Increase in systemic vascular resistance with normal cardiac output, increased workload on the left ventricle, turbulence of high pressure blood causes Shear stresses on vascular endothelium

Increased levels of catecholamines and Angiotensin II causes reorganization hypertrophy and hyperplasia of vascular smooth muscle in arteries leading to narrowed arterial lumen

Atherosclerosis, heart failure, chronic renal failure, aneurysm, nocular changes

Elevated LDL low HDL elevated cholesterol elevated triglycerides

Chronic disease of the arteries involving abnormal thickening and hardening of the blood vessel wall caused by endothelial injury and dyslipidemia

Elevated C-reactive protein predictor of atherosclerosis mi in other cardiovascular diseases

Partial blockage of one or more branches of the left or right coronary artery

Coronary atherosclerosis results in myocardial ischemia when plaque buildup in the coronary arteries lumen sizes decrease and it's unable to relax and visit dilate. Oxygen demand of ventricles exceeds oxygen supply in the coronary arteries when there's not enough oxygen there can't be enough ATP to maintain cell activity

Severe reduction of coronary artery blood flow leading to myocardial cell death

Infarction cessation of blood photo of an anther sclerotic coronary artery generally occurs due to the following circumstances a thrombus forms on the rough surface of the plaque, wall of the atherosclerotic coronary artery ruptures, long-term obstruction of coronary artery by plaque, plaque embolus obstructs coronary artery

Hypoxic injury, inflammation, reperfusion injury, repair and resolution

Troponin 1 and T are proteins unique to myocardial muscle cells and their only released into circulation after myocardial cell injury elevated troponin levels are considered diagnostic of an acute MI

Phase of the cardiac cycle where the ventricles contract and pump blood into the arteries

Phase of the cardiac cycle where ventricles relax and fill

Volume of blood ejected from The ventricle with each contraction

Stroke volume x heart rate

Stroke volume divided by end-diastolic volume

Pressure generated in The ventricle at the end of diastole. Factor affecting preload are changes in blood volume. Increase blood volume increase preload

Resistance or impedance in arteries leading from ventricle. Factors affecting afterload are pressures in the aorta and pulmonary arteries

It increases left ventricular afterload

Increase in right ventricular afterload

Valve leaflets do not close completely

Sephora calcified valve leaflets prevent the valve from opening completely

Regurgitation of the blood into the left ventricle during diastole

Regurgitation of the blood into the left atrium during systole

Reduction of blood flow through the aortic valve during systole

Reduction of blood flow through the mitral valve during diastole

The inability of the ventricles to contract against a load resulting in decreased ejection fraction and increase left ventricular end-diastolic volume

An impairment in left ventricular filling which results in decreased cardiac output

Left ventricle is unable to generate an adequate stroke volume and cardiac output causing increase residual volumes in the left ventricle which causes an increased left ventricle preload and ventricular dilation. The pressure backs up into the left atrium and eventually pulmonary veins. Increase pressures in pulmonary capillaries leads to pulmonary edema

Decreased cardiac output leads to a job in arterial blood pressure with activate several mechanisms including the sympathetic nervous system and the renal compensation system

And left ventricular failure BNP secretion is stimulated by the ventricles stretch dilation caused by the increased left ventricular residual volume preload and renal retention of fluids. Elevated plasma levels of BNP is a laboratory indicator of heart failure

Systolic dysfunction which is abnormal muscle contraction, diastolic dysfunction which is a failure of The ventricle to fully relax and fill, limited ventricular filling volume overload

Tachycardia cool extremities decreased urine output hypoxemia tachypnia dyspnea auscultation of respiratory crackles in the bases of the lungs cough low blood pressure signs of organ ischemia and failure