Final Exam Study Guide NURS 261 Pathophysiology II

P. 311-312- Know Natriuresis and ANP Final Exam Study Guide NURS 261 Pathophysiology II Chapter 15- Arterial Disorders ○ Natriuresis is a natural diuresis promoted by the heart and brain. The heart releases atrial natriuretic peptide (ANP), brain (BNP) in response to excess water in the bloodstream. The natriuretic peptides act at the nephrons to release water into the urine. Natriuresis decreases the water content in the blood, and sodium follows water out of the urine. P. 319-Complication section. Know how HTN affects the heart ○ When HTN is not well controlled, it contributes to the development of heart disease, heart failure, and renal failure. It is also the major contributing factor to fatal intracerebral hemorrhage. HTN is the most common predisposing factor of heart failure. ○ Long term HTN often leads to left ventricular myocardial ischemia and infarction. As the left ventricle hypertrophies, the enlarged muscle protrudes into the left ventricular chamber, reducing the chambers capacity. ○ HTN weakens the walls of the arteries, increasing susceptibility to development of aneurysms, causing turbulent blood flow that is subject to rupture. It places pressure on cerebral arteries causing cerebral hemorrhage. HTN contributes to the development of hypertensive encephalopathy (cerebral edema). P. 319-320-Complications of HTN. Know the 3 organs damaged by HTN ○ HTN is responsible for damage to target organs which includes the heart, retina, kidney, brain, and peripheral arteries. P. 320-Etiology of Atherosclerosis ○ Endothelial injury serves as the precursor of atherosclerosis. The injury stimulates the inflammatory reaction, a chain of events that involves the WBCs, platelets, clotting factors, cytokines, and other inflammatory mediators. The developmet of arteriosclerotic plaque is an inflammatory process that includes LDL→ an added constituent to the other inflammatory mediators for endothelium. P. 322-Formation of Foam Cells ○ Injured endothelial cells attract and bind circulating WBCs to the endothelium of arterial vessels, then are incorporated into the layer underneath the endothelium. WBCs differentiate into macrophages that engulf and ingest LDL. These LDL-laden macrophages become what is known as foam cells. P. 323-Figure 15-9, increased risk for stroke ○ Endothelial injury occurs, LDL deposits on injured area, FOAM cells (macrophages & oxidized LDL) accumulate, Atherosclerotic plaque forms, smooth muscle wall of artery and begins hypertrophy, vasodilation capacity decreases, plaque calcifies with time, fissures easily and pieces of plaque break off, traveling, creating an embolism. Chapter 16- Ischemic Heart Disease and Conduction Disorders P. 353- Pathophysiology of Acute MI. How long before irreversible damage occurs to the heart ○ Acute MI occurs when the heart tissue endures prolonged ischemia without recovery. Prolonged ischemia of longer than 30 minutes usually causes irreversible damage and necrosis. Chapter 17- Heart Failure P. 384-Know the Alert Box ○ Diminished perfusion of the kidney is particularly significant in LVF; it stimulates the secretion of renin from the juxtaglomerular apparatus of the nephron which initiates cycling of the RAAS. P. 391- Know the peripheral edema section ○ Venous congestion within the lower body causes high hydrostatic pressure within all the capillary beds of the extremities and leads to edema. Edematous fluid accumulation is influenced by gravitational pull. If patient is on bedrest, sacral edema increases the skins fragility and can lead to skin breakdown. Chapter 19-Disorders of the Venous System P. 426-427- Deep Venous Thromboembolism - know the side effects ○ DVT occurs when a thrombus develops in a deep leg vein accompanied by inflammation. The thrombus can travel as an embolism within the venous system, then enter the lungs, becoming a pulmonary embolism (PE). Chapter 20- Respiratory Inflammation and Infection P. 440-Know the Clinical Concept Box on top of Right Column ○ It is important that all functioning alveoli have adequate perfusion. Ventilation-perfusion mismatching occurs when air cannot flow into an alveolus or blood flow around an alveolus is altered. One of the most common etiologies for this is a blood clot in the lung, also called a pulmonary embolism (PE). The clot prevents blood flow to the alveolus and gaseous exchange cannot take place. P. 452- Know the Pathophysiology R/T TB ○ TB is passed via droplets down the airway, settling in the bronchial tree. Tissue inflammation occurs as pulmonary macrophages and WBCs migrate to the infected area. The lesion (tubercle), is a granulomatous accumulation of WBC, bacilli, and fibrotic tissue. Eventually scar tissue grows around the tubercle. The lesion in TB is referred to as Ghon’s, when calcified it is called a Ranke complex. Chapter 21-Restrictive and Obstructive Pulmonary Disorders P. 464- Know the Pathophysiology of Asthma ○ Asthma is a chronic inflammatory disease that causes episodes of spastic reactivity in the bronchioles. T-Lymphocytes (Th1 and Th2) are active during asthma. Th1 cells are stimulated by allergens to assist B-cells, producing IGE that bind to mast cells, releasing histamine. Th2 cells attract mast cells, eosinophils, and basophils, which promote inflammation. ○ Allergy is the most common stimulus of asthma. They trigger the immune system, causing bronchoconstriction. Asthma is also triggered by viral respiratory infections, exercise, inhaled chemicals, GERD, and circadian rhythm changes at night. ○ A degranulation of the mast cells* P. 476-Know the pulmonary edema section ................................................continued.........................................................