NURS 110 PATHOPHYSIOLOGY EXAM TWO
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- Describe the difference between atherosclerosis and arteriosclerosis
- (page 640) "Arteriosclerosis is a chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls. Atherosclerosis is a form of arteriosclerosis in which soft deposits of intraarterial fat and fibrin on the vessels wall harden over time."
- Describe the etiology of both atherosclerosis and arteriosclerosis.
- (page 640)Arteriosclerosis;"Although heses changes may be part of normal aging, pathophysiologic conditions such as high blood pressure, insufficient perfusion of tissues, or weakening and outpuching of arterial walls can be exacerbated." Atherosclerosis: "begins with injury to the endothelial cells that line artery walls. Possible causes of endothelial injury include smoking, hypertension, diabetes (insulin resistance), hyperhomocystinemia, hyperdyslipidemia, autoimmune phenomena, and infection.
- In atherosclerosis at what % of occlusion does symptoms generally appear
- (page 641) "Atherosclerotic lesions generally cause no symptoms until 60% or more of the tissue's blood supply is occluded."
- Explain how arteriosclerosis raises blood pressure
- (page 646) (in my own words) Because it causes the vessels to become stiff and unable to constrict and dilate.
- Define normal blood pressure for adults age 18 or older
- (page 645) "⬦toward the new goal of 120/80⬦"
- Differentiate between primary and secondary hypertension
- (pages 646-648) "Primary hypertension is the result of an extremely complicated interaction of genetics and the environment mediated by a host of neurohumoral effects. Most common kind. 90%. Secondary hypertension is caused by a systemic disease process that raises peripheral vascular resistance or cardiac output. Examples include renal vascular or parenchymal disease, adrenocortical tumors, adrenomedullary tumors (pheochromocytoma), and drugs (oral contraceptives, corticosteroids, antihistamines.)
- Describe the mechanisms of organ damage secondary to sustained hypertension
- (pages 648-649) "Complicated hypertension commonly compromises the structure and function of the vessels themselves: the heart, aorta, kidneys, eyes, brain, and lower extremities. The two majormechanisms of tissue damage are ischemia and edema. Ischemia deprives tissuesof the oxygen and nutrients needed for survival and function. Leakage of fluids into the interstitial space, and even hemorrhage, are caused by high pressures in the vessels."
- Describe etiology, manifestations of orthostatic hypotension
- (pages 650-651) "Orthostatic hypotension is often accompanied by dizziness, blurring or loss of vision, and syncope or fainting caused by insufficient vasomotor compensation and reduction of blood flow through the brain⬦Orthostatic hypotension is caused when the normal regulatory mechanisms are sluggish as a result of (1) anatomic variation, (2) altered body chemistry, (3) drug action (e.g., antihypertensives, antidepressants), (4) prolonged immobility caused by illness, (5) starvation, (6) physical exhaustion, (7) any condition that produces volume depletion (e.g., massive diuresis, potassium or sodium depletion), or (8) venous pooling (e.g., pregnancy, extensive varicosities of the lower extremities). Chronic orthostatic hypotesnion may be (1) secondary to a specific disease or (2) idiopathic or primary.
- Discuss aneurysms; including location of majority, types requiring emergency surgeries
- (pages 651-652) "An aneurysm is a localized dilation or outpouching of a vessel wall or cardiac chamber. The aorta is particularly susceptible to aneurysm formation because of constant stress on the vessel wall and the absence of penetrating vasa vasorum in the media layer.
- Explain the difference between a thrombus, embolus and thromboembolus
- (pages 652-653) "A thrombus is a blood clot that remains attached to a vessel wall. A detached thrombus is a thromboembolus⬦Embolism is the obstruction of a vessel by an embolus-a bolus of matter circulationg in the bloodstream. The embolus may consist of a dislodged thrombus; an air bubble; an aggregate of amniotic fluid; an aggregate of fat, bacteria, or cancer cells; or a forein substance."
- Explain the pathophysiology of thrombus formation
- (page 652) "Thrombi tend to develop wherever intravascular conditions promote activation of the coagulation, or clotting, cascade (e.g., intimal irritation, roughening, inflammation [including surgical procedures], traumatic injury, infection, low blood pressures or obstructions that cause blood stasis and pooling within the vessels.) In the arteries, activation of the coagulation cascade is usually caused by roughening of the tunica intima by atherosclerosis. Invasion of the tunica intima by an infectious agent also roughens the normally smooth lining of the artery, causing platelets to adhere readily." (SEE ALSO PAGE 526)
- Discuss pulmonary embolism; including etiology, s/s, most likely originating site
- (page 775-776) "Pulmonary embolism is occlusion of a portion of the pulmonary vascular bed by an embolus, which can be a thrombus (blood clot) tissue, fragment, lipids (fats), or an air bubble. The most common emboli are thrombi dislodged from deep veins in the thigh. "More than 90% of pulmonary emboli result from clots formed int he veins of the legs and pelvis. Deep vein thrombosis is often asymptomatic and clinical examination has low sensitivity for the presence of clot, especially in the thigh. Pulmonary embolism without infarction is the most common type and is the most difficult to evaluate. The individual usually presents with the sudden onset of tachypnea, tachycardia, dyspnea, and unexplained anxiety. Occasionally syncope (fainting) or pleural pain occurs...Manifestations of emboli that cause infarction are pleural pain, dyspnea, pleural friction rub, pleural effusion, hemoptysis, fever, and leukocytosis."
- Discuss Raynauds disease; including pathophysiology, trigger events, s/s
- (page 653-654) "Raynaud phenomenon and Raynaud disease both are characterized by attacks of vasospasm in the small arteries and arterioles of the fingers and, less commonly, the toes⬦Raynaud disease is a primary vasospastic disorder of unknown origin; however, endothelial damage and platelet activation do play a role. It tends to affect young women and to consist of vasospastic attacks triggered by brief exposure to cold or by emotional stress. Genetic predisposition may play a role in its development. The clinical manifestations of the vasospastic attacks of either disorder are changes in skin color and sensation caused by ischemia. Vasospasm occurs with varying frequency and severity and causes pallor, numbness, and the sensation of cold in the digits...Stimuli that trigger attacks (e.g., cold, emotional stress) are avoided, and cigarette smoking is stopped to eliminate the vasoconstricting effects of nicotine."
- Discuss varicose veins; including common etiologies
- (page 654) "A varicose vein is a vein in which blood has pooled, producing distended, tortuous, and palpable vessels. Causes include (1) trauma to the saphenous veins that damages one or more valves or (2) gradual venous distention caused by a combination of standing for long periods, which diminishes the action of the muscle pump, and the pull of gravity on blood within the legs."
- Discuss chronic venous insufficiency; including etiology and manifestations
- (page 654) "Chronic venous insufficiency (CVI) is inadequate venous return over a long period⬦It causes pathologic changes as a result of ischemia in the vasculature, skin, and supporting tissues. Symptoms include chronic pooling of blood in the veins of the lower extremities and hyperpigmentation of the skin of the feet and ankles. Edema in these areas may extend to the knees."
- Differentiate between myocardial ischemia, necrosis and hypertrophy and etiologies of all.
- (page 655-???) "The earliest lesions of the continuum are those of coronary artery disease-any vascular disorder that narrows or occludes the coronary arteries; the most common cause of conronary obstruction is athersclerosis. CAD can diminish the myocardial blood supply until deprivation impairs myocardial metabolism enough to cause ischemia, a local state in which the cells are temporarily deprived of blood supply. The remain alive but cannot function normally." Necrosis is the death of the cells. Hypertrophy is the increase in cell size generally due to increase workload/demand. (my own words)
- Describe modifiable and non-modifiable risk factors for CAD
- (page 655-65?)
- Describe what is happening in the heart that causes angina pectoris
- (page 658) "Stable angina: Angina pectoris is chest pain caused by myocardial ischemia. The discomfort usually transient, lasting approximately 3 to 5 minutes. If blood flow is restored, no permanent change or damage results⬦Stable angina is caused by gradual luminal narrowing and hardening of the arterial walls, so that affected vessels cannot dilate in response to increased myocardial demand associated with physical exertion or emotional stress..."
- Differentiate between stable, unstable and prinzmetal angina
- (page 658-662) "Stable angina: Angina pectoris is chest pain caused by myocardial ischemia. The discomfort usually transient, lasting approximately 3 to 5 minutes. If blood flow is restored, no permanent change or damage results. Prinzmetal angina is chest pain attributable to transient ischemia of the myocardium that occurs unpredictably and almost exclusively at rest. Pain is caused by vasospasm of one or more major coronary arteries with or without associated atherosclerosis. The pain often occurs at night during rapid-eye-movement sleep and may have a cyclic pattern of occurence. Unstable angina is a form of acute coronary syndrome that results from reversible myocardial ischemia. It is important to recognize this syndrome because it signals that the atherosclerotic plaque has become complicated, and infarction may soon follow. Unstable angina occurs when a fairly small fissuring or superficial erosion of the plaque leads to transient episodes of thrombotic vessel occlusion and vasoconstriction at the site of plaque damage. Unstable angina presents as new onset angina, angina that is occuring at rest, or angina that is increasing in severity or frequency."
- How long can cardiac cells withstand ischemic conditions before damage is permanent
- (page 663) "Cardiac cells can withstand ischemic conditions for about 20 minutes before cellular death takes place. After only 30 to 60 seconds of hypoxia, electrocardiographic changes are visible. Yet even if cells are metabolically altered and nonfunctional, they can remain viable if blood flow returns within 20 minutes."
- Describe the goal(s) of therapy in managing myocardial ischemia
- (page 665-666) "Acute myocardial infarction requires admission to the hospital, often directly into a coronary care unit. The individual should be placed on supplemental oxygen and given an aspirin immediately. Pain relief is of utmost importance and involves the use of sublingual nitroglycerin or morphine sulfate. Continuous monitoring of cardiac rhythms and enzymatic changes is essential, because the first 24 hours after onset of symptoms is the time of highest risk for sudden death. Individuals who are in shock require aggresive fluid resuscitation and possible emergent invasive procedures (see p. 689)." ****MONA****
- Describe how myocardial infarction can lead to ventricular impairment
- (page 663) " The severity of functional impairment depends on the size of the lesion and the site of the infarction. Functional changes can include (1) decreased cardiac contractility with abnormal wall motion, (2) altered left ventricular compliance, (3) decreased stroke volume, (4) decreased ejection fraction, (5) increased left ventricular end-diastolic pressure, and (6) sinoatrial nod malfunciton. Life-threatening dysrhytmias and heart failure often follow myocardial infarction."
- Explain why fever often occurs soon after myocardial infarction
- (page 664) "Fever may develop in the first 24 hours and persist for 1 week because of inflammatory activity within the myocardium."
- Discuss pericarditis; including complications of pericardial effusion, related condtions
- (pages 667-669) "Pericardial disease is often a localized manifestation of another disorder, such as infection (bacterial, viral, fungal, rickettsial, or parasitic); trauma or surgery; neoplasm; or a metabolic, immunologic, or vascular disorder (uremia, rheumatoid arthritis, systemic lupus erythematosus, periarteritis nodosa)....Acute pericarditis is commonly caused by infection (viral or bacterial), uremia, neoplasm, myocardial infarction, surgery, or trauma. The pericardial membranes become inflamed and roughened, and an exudate may develop. Symptoms include sudden onset of severe chest pain that worsens with respiratory movements and with lying down. Although the pain may radiate to the back, it is generally felt in the anterior chest and may be confused initially with the pain of acute myocardial infarction. May have pericardial friction rub. Pericardial effusion-the accumulation of fluid in the pericardial cavity-can occur in all forms of pericarditis. Pericardial effusion, even in large amounts, is not necessarily clinically significant, except that it indicates an underlying disorder, such as systemic lupus erythematosus. If the fluid creates sufficient pressure to cause cardiac compresion, a serious condition known as tamponade exists...The danger is that pressure exerted by the pericardial fluid eventually will equal diastolic pressure within the heart chambers." (READ MORE ON 667-669)
- Describe complication that is possibility in all forms of heart valve dysfunction
- (pages 670-671) "The usual cause of acquired valvular dysfunction is inflammation of the endocardium secondary to acute rheumatic fever or infective endocarditis. In valvular stenosis, the valve orifice is constricted and narrowed, so blood cannot flow forward and the workload of the cardiac chamber "in front" of the diseased valve is in creased. Pressure rises in the chamber to overcome resistance to flow through the valve, causing the myocaardium to work harder and producing myocardial hypertrophy. In valvular regurgitation (also called insufficiency or incompetence), the valve leaflets, or cusps, fail to shut completely, permitting blood flow to continue even when the valve is supposed to be closed."
- Differentiate between valvular regurgitation, insufficiency, and stenosis
- (page 671) "In valvular stenoisis, the valve orifice is constricted and narrowed, so blood cannot flow forward and the workload of the cardiac chamber "in front" of the diseased valve is increased. Pressure (intraventricular or atrial) rises in the chamber to overcome resistance to flow through the valve, causing the myocardium to work harder and producing myocardial hypertrophy. In valvular regurgitiation (also called insufficiency or incompetence), the valves leaflets, or cusps, fail to sut completely, permitting blood flow to continue even when the valve is supposed to be closed. Valvular regurgitation increases the volume of blood the heart must pump and increases the workload of both atrium and ventricle."
- Identify the valve disorder commonly resulting in R sided heart failure
- (page 673)"Tricuspid regurgitation is more common than tricuspid stenosis and is usually associated with failure and dilation of the right ventricle secondary to high blood pressure in the pulmonary circulation or right ventricle."
- Identify the most common cardiac valve disease most prevalent in young women
- (page 703) "Mitral valve prolapse (MVP) is a common finding especially in young women. Although not grossly abnormal, the mitral valve leaflets do not position themselves proplerly during systole. Mitral valve prolapse may be a completely asymptomatic condition or could result in severe subjective symptoms. Afflicted valves may be at greater risk for developing infective endocarditis."
- Describe the etiology, pathophysiology and s/s of rheumatic heart disease
- (page 674-677) "Rheumatic fever is a diffuse, inflammatory disease caused by a delayed immune response to infection by the group A beta-hemolytic streptococcus in genetically predisposed individuals. In its acute form, rheumatic fever is a febrile illness characterized by inflammation of the joints, skin, nervous system, and heart. If untreated, rheumatic fever can cause scarring and deformity of cardiac structures, resulting in rheumatic heart disease...This is because the strains of the microorganism that affect the skin do not have the same antigenic molecules in their cell membranes as those that cause pharyngitis and, therefore, do not elicit the same kind of immune response. Acute rheumatic fever affects the heart, joints, central nervous system, and skin through an abnormal humoral and cell-mediated immune response to grou A streptococcal cell membrane antigens called M proteins. These antigens can bind to receptors on heart, muscle, and brain cells and have an affinity for membrane receptors within synovial joints, where they trigger an autoimmune response...Many common clincila manifestations of acute rheumatic fever-fever, lyphadenopathy, arthralgia, nausea, vomiting, epistaxis, abdominal pain, and tachycardia...The major specific manifestations of acute rheumatic fever are carditis, acute migratory polyarthritis, chorea, and erythema marginatum,...(SEE PAGE 676 FOR DESCRIPTION)
- Define the type of microbe most often responsible for infective endocarditis
- (page 677) "The most common cause of infective endocarditis is staphylococcus aureus, followed by viridans streptococci."
- Describe how chronic HTN can lead to L heart failure
- (page 685; Figure 23-36) Increased systemic vascular resistance leads to; increased force of LV contraction leads to; increased LV oxygen demand leads to; LV hypoxia leads to; Ventricular remodeling (hypertrophy) leads to; decrease for of LV contraction..."
- Describe how decreased perfusion to kidneys from heart failure can aggravate the problem
- (page 687) "As cardiac output fall, renal perfusion diminshes with activation of the renin-angiotensin-aldosterone system, which acts to increase PVR and plasma volume, thus increasing afterload and preload further. In addition, baroreceptors in the central circulation detect the decrease in perfusion and stimulate the sympathetic nervous system to cause more vasoconstriction and the hypothalamus to produce antidiuretic hormone. It is believed that angiotensin and the catecholamines not only disturb cardiac hemodynamis but also are directly cardiotoxic...This vicious cycle of decreasing contractility, increasing preload, and increasing afterload causes progressive worsening of left heart failure." (FIGURE 23-38; PAGE 686)
- In heart failure what is the pathophysiology that results in pulmonary symptoms
- (pages 687-688) "Individuals with diastolic dysfunction present with dyspnea on exertion, fatigue, evidence of pulmonary edema (rales on auscultation, pleural effusions), and evidence of underlying coronary disease, hypertension, or valvular disease." (my own words: Basicly it's when the heart backs up, generally starting with LV dysfunction, then LA...then backing up into the lungs.)
- Identify the common cause of R heart failure
- (page 688) "Right heart failure can result from left heart failure caused by an increase in left ventricular filling pressure that is reflected back into the the pulmonary circulation. As pressure in the pulmonary circulation rises, the resistance to right ventricular emptying increases...When right heart failure occurs iin the absence of left heart failure, it is caused most commonly by diffuse hypoxic pulmonary disease such as chronic obstructive pulmonary disease (COPD), cystic fibrosis, and dult respiratory distress syndrome (ARDS).
- Differentiate between the s/s of R and L heart failure
- (from notes) "Right side failure: fatigue, ascites, liver and spleen engorgement, distended jugular veins (JVD), dependent edema⬦Left sided failure: exertional and nocturnal proximal dyspnea, blood tinged sputum, orthopnea, cough, cyanosis, decreased urinary output, rales, fatigue, S3 gallop."
- In shock what leads to the impairment in cellular metabolism
- (pages 689-690) "Without oxygen, the cell shifts from aerobic to anaerobic metabolism. Anaerobic metabolism is a less efficient method of extracting energy from carbon bonds, and the cell begins to use its stores of ATP faster than stores can be replaced." (LACK OF O2)
- Differentiate between the etiology and patho, s/s of cardiogenic, hypovolemic, anaphylactic and septic shock
- (pages 691-697) "Shock is classified by cause as cardiogenic (caused by heart failure), hypovolemic (caused by insufficient intravascular fluid volume), neurogenic (caused by neural alterations of vascular smooth muscle tone), anaphylactic (caused by immunologic processes), or septic (caused by infection).
- What major injury can result in 3 rd spacing. What type of shock is this?
- (from notes) "hypovolemic shock-third spacing??
- What is the underlying process occurring that results in the pale cool skin that often occurs in hypovolemic shock
- (page 692-693) (in my own words) It is a compensatory mechanism of the shifting of interstitial fluid into the vasculard compartment.
- Describe the etiology of neurogenic shock
- (pages 692-693) "Neurogenic shock (sometimes called vasogenic shock) is a widespread and massive vasodilation that results from parasympathetic overstimulation or sympathetic understimulation. The loss of vascular tone results in "relative hypovolemia." Neurogenic shock can be caused by any factor that stimulates parasympathetic or inhibits sympathetic stimulation of vascular smooth muscle. Trauma to the spinal cord or medulla and conditions that interrupt the supply of oxygen or glucose to the medulla can cause neurogenic shock by interrupting sympathetic activity. Depressive drugs, anesthetic agents, and severe emotional stress and pain are other causes."
- Describe the most common cause of Multiple organ dysfunction syndrome (MODS)
- (page 698) "Multiple organ dysfunction syndrome (MODS) is the progressive dysfunction of two or more organ systems resulting from an uncontrolled inflammatory response to a severe illness or injury. The organ dysfunction can progress to organ failure and death. Although sepsis and septic shock are the most common causes, MODS can be initiated by any severe injury or disease process that activates a massive systemic inflammatory response in the host."
- Which organ of the body is often the first to fail in MODS
- (page 700) "The lung is often the first organ to fail, resulting in adult respiratory distress syndrome (ARDS)."