front 1 What does the circulatory system do? | back 1 Delivers oxygen & nutrients needed for metabolic processes to the tissues, carries waste products away from cellular metabolism to kidneys and other excretory organs for elimination, and circulates electrolytes & hormones needed to regulate body functions |
front 2 What are the 2 parts of the circulatory system? | back 2 Pulmonary Circulation (AKA central circulation) Systemic circulation (AKA peripheral circulation) |
front 3 What does the pulmonary circulation consist of? | back 3 Right side of heart, the pulmonary arteries, the pulmonary capillaries, and the pulmonary veins (Moves blood thru the lungs and creates a link for gas exchange) |
front 4 What does the systemic circulation of? | back 4 The left side of the heart, the aorta, and its branches, the capillaries that supply the brain and peripheral tissues, and the systemic venous system and vena cava. (moves blood throughout all other tissues of the body) |
front 5 What are the 3 factors that affect blood flow thru vessels? | back 5 Pressure, resistance, flow/velocity. |
front 6 Pericardium | back 6 Outer cover of heart. Visceral pericardium- faces the organ parietal pericardium - faces away from organ. |
front 7 What is the cardiac conduction system? | back 7 The SA Node : functions as the pacemaker of the heart The AV Node: connects the atrial and ventricular conductive systems |
front 8 What is the cardiac cycle? | back 8 The ryhthmic pumping action of the heart. Divided into 2 parts: Systole & Diastole |
front 9 Systole | back 9 Period when ventricles are contracting Ventricles contract blood pushes against AV valves & they shut Blood pushes thru semilunar valves into aorta and pulmonary trunk Cardiac emptying |
front 10 Diastole | back 10 Period when ventricles are relaxed and filling with blood Ventricles relaxed Blood enters atria blood flows thru AV Valves into ventricles Semilunar valves are closed. Cardiac filling |
front 11 What is stroke volume? | back 11 EDV - ESV (End Diastolic volume - end systolic volume) the amount of blood the heart pumps out in a single beat. |
front 12 What is cardiac Output | back 12 Stroke Volume X heart rate Amount of blood pumped out of heart per minute |
front 13 What is formula for blood pressure? | back 13 Cardiac Output X Peripheral resistance Helps to understand blood pressure: if Peripheral resistance is high, then BP is high & vice versa |
front 14 what is the formula for Ejection Fraction? | back 14 Stroke volume/ End diastolic volume The percent of blood pumped out |
front 15 Hyperlipidemia | back 15 Elevated levels of lipids or fats in the blood. Cholesterol and triglycerides are insoluble in plasma and are encapsulated by special fat carrying proteins called lipoproteins for transport in blood LDL is main carrier of cholesterol |
front 16 Lipid Transportation | back 16 Dietary lipids absorbed from intestines as chylomicrons, which adipose & muscle cells take up, but chylomicrons remnants are intermediate-density lipoproteins. IDLs become LDL's and delivers fat to the liver and other tissues |
front 17 Form of Hyperlipidemia: Primary Hypercholesterolemia | back 17 Independent of other causes, no known cause often genetic |
front 18 Form of hyperlipidemia: Secondary Hypercholesterolemia | back 18 Associated with other health conditions
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front 19 Treatment for hyperlipidemia | back 19 Dietary, Therapeutic, medication ( decrease cholesterol production or absorption, remove cholesterol from blood stream) |
front 20 Arteriosclerosis | back 20 Are blood vessels that carry oxygen and nutrients from your heart to the rest of your body, but when there is too much pressure the arteries become thick and harden, which can restrict flow |
front 21 Artherosclerosis | back 21 a type of arteriosclerosis, refers to build up of fats in and on artery walls (plaques) which can cause vessel stenosis and restrict blood flow. It is considered a heart problem, but it can occur anywhere. |
front 22 Atherosclerosis formation | back 22 Lipids get into vascular endothelium (proportional to LDL Levels) Macrophage tries to clear them away, then macrophage turns into a foam cell. WBS & vascular endothelium release growth factors that promote plaque formation Plaques block the arteries. |
front 23 What are the lesions associated with atherosclerosis? | back 23 Fatty Streak The fibrous atheromatous plaque The complicated lesion |
front 24 Fatty streak | back 24 the earliest lesion, which is present in children, lesions result from collections of macrophage that phagocytize and accumulate fat within their cytoplasm (Foam Cells) |
front 25 Fibrous Atheromatous plaque | back 25 basic lesion of clinical atherosclerosis; characterized by accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells, formation of scar tissue and calcification. |
front 26 what are the clinical manisfestations of atherosclerosis (depends on extent and vessels involved | back 26 1. Stenosis of the vessel (Narrowing) and ischemia. 2. sudden vessel obstruction due to plaque hemorrhage or rupture 3. Thrombosis and formation of emboli resulting from damage to the vessel endothelium. 4. Aneurysm formation due to weakening of vessel wall. |
front 27 Thrombosis Formation | back 27 The most important complication of atherosclerosis bc it causes acute blockage of arteries. It is caused by slow and turbulent blood flow in the region of the plaque and ulceration of the plaque. * may cause acute vessel occlusion
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front 28 Where is the most frequent sites of atherosclerosis | back 28 The Abdomen |
front 29 Peripheral Arterial Disease | back 29 Atherosclerosis changes that result in tissue ischemia (low blood) Most common in men in 60s & 70s Risk factors include: Smoking, diabetes |
front 30 Ischemic Symptoms of Peripheral Arterial Disease | back 30 Gradual onset of intermittent claudication (pain in calf when walking) Atrophic changes of the skin (pale bc skin is not getting oxygen) Rest pain, only if severe, ulceration, and gangrene can develop (when blood flow no longer meets minimal needs) |
front 31 Treatment for PAD | back 31 avoidance of injury,walking program, reduce risk factors, antiplatelet agents, surgery, Diagnose by: Inspection, check pulses(DP & PT), ankle brachial index |
front 32 Raynauds Phenomenon | back 32 Functional disorder of arteries & arterioles of the skin - there are intense spasms of arteries & arterioles in the fingers and less often in the toes in response to stimuli. its aggravated by cold or emotional stress. More common in feet and in middle-aged women |
front 33 Treatment of Raynauds Phenomenon | back 33 avoidance of triggering events, no smoking, use of vasodilator drugs. |
front 34 Aneurysm | back 34 An abnormal localized dilation of a blood vessel or wall of the heart., which may rupture or hemmorhage. Most common in abdominal aorta can occur in arteries or veins |
front 35 Causes of aneurysm | back 35 atherosclerotic plaque formation (most common) congenital abnormality or arterial wall Trauma Infection |
front 36 locations of Aneurysms | back 36 Aorta (most common)
Cerebral artery ( at circle of willis) Femoral and popliteal arteries |
front 37 Complications of aneurysms | back 37 Rupture - risk increases with increasing size pressure on adjacent structures * involving large vessels in critical locations |
front 38 what are the four forms of aneurysms | back 38 Saccular
Fusiform Dissecting ( most common in ascending aorta) |
front 39 Abdominal Aortic Aneurysms | back 39 can go undetected for long periods of time bc they are asymptomatic. A pulsating mass found on routine abdominal examination may be first evidence. Develop in Men after 50 90% occur below renal artery Diagnostic signs: ultra sound, echocardiography, CT, MRI, surgical repair |
front 40 Dissecting aneurysm | back 40 an abrupt presence of excrutiating pain, described as tearing or ripping, high mortality rate. |
front 41 Arterial Blood Pressure | back 41 the rythmic ejection of blood from the left ventricle into the aorta. It rises as left ventricle contracts and falls as it relaxes. The highest pressure is systolic and the lowest is Diastolic |
front 42 Normal blood pressure | back 42 Systolic <120/ Diastolic <80 |
front 43 Prehypertension | back 43 S 120-139 D 80-89 |
front 44 Stage 1 Hypertension | back 44 S 140-159 D 90-99 |
front 45 Stage 2 Hypertension | back 45 S >160 D>100 |
front 46 Hypertension | back 46 most common of all health problems in adults and leading risk factor for cardiovascular disorders and is usually asymptomatic. When symptons do occur its usually related to long-term afects on the organ systems. |
front 47 Essential Hypertension | back 47 90% of hyepertenssive patients unknown cause More frequent in Males, Black, Poor, Older, Obese |
front 48 Secondary Hypertension | back 48 10% of hypertensive patients Cause is known- most common cause is Renal Disease |
front 49 Risk Factors of Hypertension | back 49 Constitutional factors
Lifestyle factors
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front 50 Most common sites of HT organ damage | back 50 Kidney- Renal Failure Brain- Cerebral Vascular accident (stroke) CVA, TIA0 transient ischemic accident (a smaller stroke) Heart - chest pain (angina), LVH (left ventricle hypertrophy), CAD, CHF Eyes - retinopathy blood vessels - peripheral vascular disease(PVD), arteriosclerosis |
front 51 Hypertension Diagnosis | back 51 you treat patients to live longer, not feel better. Must take repeated BP measurements to be diagnosed with HT |
front 52 Orthostatic Hypotension | back 52 AKA postural Hypotension, an abnormal drop in BP upon standing. Symptoms: Dizziness & Syncope (fainting) Causes: Reduce blood volume, Drug induced, aging, immobility |
front 53 Diagnosis & treatment for Orthostatic Hypotension | back 53 Diagnosis: sitting and standing BP measurements Tilt Table Treatment: alleviate the cause(ie if it is due to dehydradtion, then rehydrate), education, adjusting meds, support hose |
front 54 The venous system | back 54 Low-pressure system, pumped by skeletal muscles to return blood to hear and has venous valves to prevent retrograde flow 2 components: Deep Veins ( these return blood to the heart) & Superficial Veins |
front 55 What are the Disorders of Venous Circulation | back 55 Varicose Veins Venous Insufficiency Venous Thrombosis |
front 56 Varicose Veins | back 56 Dilated, tortuous veins, engorged with blood resulting from improper venous valve function. Most common in legs; edema of calves, leg heaviness, dull aching of lets
2 types: Primary & Secondary Complications include: Chronic Venous insufficiency & blood clots secondary to venous stasis Treatment: Treat underlying cause, anti-embolism socks, exercise, surgical stripping |
front 57 Primary Varicose Veins | back 57 Originates in superficial veins |
front 58 Secondary Varicose Veins | back 58 Result from impaired flow in the deep venous channels The most common cause is DVT Deep Vein Thrombosis |
front 59 Chronic Venous Insufficiency | back 59 a condition in which the incompetent venous valves result in an ineffective venous pump. THe pump causes tissue congestion and impaired nutrition resulting in atrophy of the skin and fat necrosis. Brown pigmentation occurs bc of hemosiderin deposits resulting from the break down of RBCs Stasis dermatitis & ulcers |
front 60 Venous thrombosis | back 60 acute development of a blood clot that may cause vessel occlusion or embolization
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front 61 The triad that can cause Venous Thrombosis | back 61 Venous Stasis: bed rest, immobility, shock, airplane rides, long car rides, AMI (Acute Mycardial infarction) Hypercoagulability of blood - pregnancy, child birth, BCPs, dehydration, cancer Vascular Trauma - venous catheters, surgery, massive trauma, hip fracture, orthopedic surgery |
front 62 Pericarditis | back 62 Inflammation of the pericardium as a result of systemic or cardiac diseases
Associated with fluid collection within the pericardial space ( pericardial effusion) |
front 63 Pericarditis Pathological changes | back 63 when the pericardial becomes inflammed the serous fluid becomes inflammed as well Pericardial friction run & sharp substernal pain shallow rapid respirations due to associated pleurisy mild fever from inflammation dyspnea, orthopnea, tachycardia |
front 64 Pericardial effusion | back 64 accumulation of fluid in pericardial cavity; may occur as a result of inflammatory processes, infection, neoplasms, cardiac surgery, trauma. Major threat is compression of the heart chambers with resultant reduction in ventricular filling and cardiac output. Testing: CXR shows a widened mediastinum & echnocardiogram shows pericardial fluid Treatment: Pericardiocentesis; Pericardial window; Pericardiectomy |
front 65 Cardiac Tamponade | back 65 Rapid compression of the heart due to accumulation of fluid, pus, or blood in pericardiarl space. Could be due to infection, inflammation, trauma, or rupture of ventricular wall. THe compression of the heart results in a decrease in ventricular filling, which ultimately results in a decrease stroke volume & a diminished or absent pulse |
front 66 EKG | back 66 a rapid, accurate and widely used method of evaluating pericardial effusion. |
front 67 Coronary Artery Disease | back 67 Impaired Coronary blood flow
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front 68 Acute coronary syndromes | back 68 acute ischemic heart diseases Unstable Angina Acute Myocardial Infarction (aka, heart attack) |
front 69 Unstable Angina | back 69 Intermediate of stable angina and myocardial infarction. Often ischemia is not severe enough to cause permanent myocardial damage Worst than stable angine, but not quite MI Due to atherosclerotic plque disruption --> platelet aggregation --> Hemostasis |
front 70 Acute Myocardial infarction | back 70 Occurs when a portion of the myocardium loses its blood supply and the tissue infarcts(dies) The onset is usually abrupt pain at significant symptom, GI complaints common The extend depends on location & extent of occlusion, amount of heart tissue supplied by the vessel, duration of the occlusion, metabolic needs of the affected tissue, extent of collateral circulation, & other factors like heart rate. Ischemic death of myocardial tissue sudden onset --> pain |
front 71 Myocardial Infarction | back 71 reduced blood flow thru one or more coronary arteries causing myocardial ischemia & necrosis |
front 72 Complications of myocardial infarction | back 72 heart failure
Cardiogenic Shock Pericarditis thromboembolism rupture of heart ventricular aneurysms cardiac arrthythmias
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front 73 Myocardial Ischemia | back 73 occurs when the ability of the coronary arteries to supply oxygen is inadequate to meet the metabolic demands of the heart. 3 types of chronic ischemic heart disease |
front 74 Chronic Stable Angina | back 74 Pain when hearts oxygen demand increases Fixed coronary artery obstruction that produces a disparity b/w coronary blood flow and the metabolic demands of the myocardium. Pain is described as constricting, squeezing, suffocation. pain relieved by anti-platelet aspirin or nitroglycerin |
front 75 Variant Angina | back 75 Pain when coronary arteries spasm Prinzmetals angina (vasopastic angina) Intermittent coronary vasospasms (at rest) |
front 76 Silent Myocardial ischemia | back 76 myocardial ischemia without pain unknown eitology but found in diabetic patients |
front 77 Cardiomyopathies | back 77 a group of disorders that affect the myocardium & are usually associated with disorders of myocardial performance which may be mechanical(heart failure) or electrical (arrhythmias) They can be primary or secondary |
front 78 Primary cardiomyapothies | back 78 disorders of the heart muscle that are confined to the myocardium. |
front 79 Secondary cardiomyopathies | back 79 conditions in which there is a cardiac muscle disease in the presence of a multisystem disorder |
front 80 what are the 3 categories of primary cardiomyopathy? | back 80 Genetic Mixed Acquired |
front 81 Genetic Cardiomyopathy | back 81 Hypertrophic cardiomyopathy, most common, genetic, ppl dont' know they have it
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front 82 Mixed Cardiomyopathy | back 82 Dilated Cardiomyopathy: extensively damaged myocardium reduces contractility causing a decline in systolic function and cardiac output (heart failure). There is left ventricular dysfuncion characterized by thinning of the ventricular wall. (still hypertrophied, but it's stretched out) Restrictive Cardiomyopathy: Fibrosis and stiffening of the ventricle reducing the ability to relax and fill during diastole resulting in a decrease in cardiac output. Least common |
front 83 Aqcuired Cardiomyopathy | back 83 Termed myocarditis or inflammatory cardiomyopathy. Its inflammation of the heart muscle and conducting systemw/o evidence of myocardial infarction Focal or diffuse inflammation of the cardiac muscle which may be acute or chronic
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front 84 Causes of Myocarditis | back 84 Infection(bacterial, viral); radiation therapy, hypersensitivity immune reaction, toxins such as lead, chemicals, & cocaine, chronic alcoholism most common cause is viral Treatment- most cases are transient and resolve within several months |
front 85 Complications of myocarditis | back 85 Arrhythmias & sudden death Chronic valvulititis dilated cardiomyopathy heart failure pericarditis cardiac rupture thromboembolism |
front 86 Infective Endocarditis | back 86 infection of the endocardium, heart valves or cardiac prosthesis. relatively uncommon, life-threatening
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front 87 Causes of infective Endocarditis | back 87 Bacterial (most common) or fungal invasion predisposing factors
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front 88 S/SX & Diagnosis of endocarditis | back 88 S/Sx: fever, chills due to bacterial infection heart murmur due to turbulent blood flow (over valves that have been damaged by endocarditis) diagnosis: positive blood cultures (most definitive & essential guide to treatment) blood cultures can identify causitive agent & sensitivity testing to make antibiotics elevated WBC Count |
front 89 Complications of endocarditis | back 89 acute renal failure brain abscess (from septic emboli) cardiac arrhythmia cerebral emboli heart failure meningitis death |
front 90 Rheumatic heart fever | back 90 an acute immune mediated, systemic, inflammatory disease of childhood that develops after infections with group A streptococcus.
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front 91 Rheumatic Heart Disease | back 91 The cardiac and valvular manifestations of rheumatic fever & is associated w acute inflammation of the myocardium, pericardium, and heart valves
Patients who develop acute rheumatic heart disease are not actively infected w Group A Streptococci but rather develop S/Sx weeks after infection has cleared |
front 92 Pathophysiology of Rheumatic Heart Disease | back 92 GAS infection leads to autoimmune reaction in which antibodies produced to combat GAS affect connective tissues of the body Antibodies may attack healthy body cells by mistake bc the bacterial antigens are similar to the bodys own cells molecular mimicry |
front 93 Pathophysiologic changes of RHD | back 93 polyarthritis caused by inflammation firm movable subcutaneous nodules Erythema marginatum skin rash found on trunk Carditis with dyspnea and chest pain sydenhams chorea is a CNS manisfestation |
front 94 Complications of RHD | back 94 destruction of mitral and aortic valves pancarditis (Inflammation of heart) heart failure infection |
front 95 Treatment of RHD | back 95 prompt treatment of GAS with antibiotics salicylates(aspirin) to relieve fever & pain corticosteroids for carditis corrective surgery |
front 96 Valve Stenosis | back 96 Narrowing of heart valve opening
often results in decreased cardiac output and left ventricular hypertrophy. there is a heart murmur as blood is forced thru the narrow opening |
front 97 Valve Incompetence | back 97 occurs when heart valve leaflets don't completely close
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front 98 what is a murmur/? | back 98 blood going thru a valve |
front 99 Heart Failure | back 99 syndrome that occurs when the heart cannot pump enough blood to meet the bodys needs (pump failure)
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front 100 Left sided heart failure | back 100 Pumping ability of left ventricle fails cardiac output falls blood backs up into left atrium |
front 101 right-sided heart failure | back 101 Pumping ability of right ventricle fails blood backs up into right atrium and peripheral circuation peripheral edema develops |
front 102 what are 2 most common causes of heart failure? | back 102 Hypertension myocardial infarction |
front 103 Acute Pulmonary edema | back 103 most dramatic symptom of left heart failure. A life-threatening condition in which capillary fluid moves into the interstitial and causes lung stffness, makes lung expansion more difficult & decreases gas exchange in lungs |
front 104 Shock | back 104 an acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply resulting in cellular hypoxia |
front 105 Cardiogenic shock | back 105 Diminished cardiac output that severely impairs tissue perfusion (pump failure)
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front 106 Causes of Cardiogenic shock | back 106 acute myocardial infarction (most common) end stage cardiomyopathy cardiac tamponade myocardial ischemia Ventricular arrhythmias |
front 107 Hypovelemic Shock | back 107 Circulatory dysfunction and inadequate tissue perfusion caused by reduced intravascular blood volume. venous return is reduced and cardiac output fails
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front 108 Causes of hypovelemic Shock | back 108 blood loss; burns; GI fluid loss pathophysiologic changes: tachycardia restlessness; reduced urine output; hypotension; cyanosis treatment: oxygen, fluids, blood replacement |
front 109 Obstructive Shock | back 109 Mechanical obstruction of blood flow
causes: aortic aneurysm; pneumothorax; pulmonary embolism (most common) |
front 110 Distributive Shock | back 110 inqadequate tissue perfusion and circulatory collapse in response to infection caused by loss of blood vessel tone and enlargement of vascular compartment capacity of vascular compartment expands such that normal blood volume will not fill the circulatory system |
front 111 Causes of Distributive Shock | back 111 decreased sympathetic activity: neurogenic
vasodilator substances in blood
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front 112 Pathopysiologi changes of distributive shock | back 112 chills & fever due to infection tachycardia reduced urine output cyanosis |
front 113 complications and treatment of distributive shock | back 113 death, heart failure, renal failure test with blood cultures treatment: antibiotics therapy, medications to increase cardiac output oxygen |
front 114 What are the primary functions of the Respiratory System? | back 114 Oxygenation of blood Removal of CO2 Carbon Dioxide |
front 115 What are the secondary functions of the Respiratory System? | back 115 Protection (ciliary blanket, macrophage0 Metabolism |
front 116 What 2 zones is respirator broken down into? | back 116 Conducting Airways - consists of nasal passage, mouth, & pharynx, larynx, trachea, bronchi, bronchioles Respiratory tissue - area distal to the terminal bronchi and consists of respiratory bronchioles, alveolar ducts and alveoli |
front 117 What are the components of the conducting airways? | back 117 Outer layer- supporting connective tissue layer- provides support and protection Middle Layer - Smooth muscle layer that circle the airway Inner Layer - Mucosal Lining, pseudostratified columnar epithelium with hair like projections called cilia intermingled are goblet cells that secrete mucus. mucus forms ciliary blanket |
front 118 Type 1 Alveolar cell | back 118 95% of surface, primary function is gas exchange |
front 119 Type 2 Alveolar cell | back 119 secrete surfactant |
front 120 Surfactant | back 120 1. lowers surface tension within the alveoli therby keeping the alveoli open 2. Increases lung compliance or the ease of inflation 3. Provides stability and more even inflation of the alveoli 4. assists in preventing pulmonary edema by keeping alveoli dry |
front 121 Pleura | back 121 encases the lungs; the pleura is thin, transparent, double layered serous membrane, Functions to reduce friction during breathing |
front 122 What is involved with the transportation & exchange of gasses | back 122 Ventilation, perfusion, diffusion |
front 123 Ventilation | back 123 The movement of air bw the atmosphere and the alveoli of the lungs |
front 124 Perfusion | back 124 Process of blood flowing thru lungs |
front 125 Diffusion | back 125 The actual movement of gas b/w alveoli & blood |
front 126 How is Oxygen & CO2 transported? | back 126 Oxygen: can be carried as a dissolved gas in plasma or in combination with hemoglobin (98%) CO2 - carried in blood but is converted to bicarbonate and transported in that form |
front 127 What is partial pressure? | back 127 when oxygen and CO2 are dissolved in plasma. Normal partial pressure for Oxygen is 80-100 mmhg Normal partial pressure for CO2 is 35-45 mmhg |
front 128 Pulse Oximetry | back 128 has become preferred method to measure PO2 in arterial blood gas. It measures total percent of O2 that is saturated with oxygen (SpO2)and the PO2 is determined using the Oxygen-Hemoglobin Dissociation Curve. This is an INDIRECT measure of PO2 and PO2 must be calculated. |
front 129 How is CO2 transported in blood? | back 129 As dissolved CO2 (10%) Attached to Hemoglobin (30%) As Bicarbonate, HCO3 (60%) |
front 130 Hypoxemia | back 130 PO2 <60 mmHg Cyanosis Impaired function of vital centers
Activation of Compensatory mechanisms
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front 131 HyperCapnia | back 131 PCO2 > 50 mmHg Respiratory Acidosis
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front 132 Where is the respiratory Center | back 132 Medulla (the rate) & Pons (how deep your breath is) |
front 133 Regulation of breathing : Chemoreceptors | back 133 monitor oxygen & cabon dioxide & pH Central Chemoreceptors - hypercapnic drive- located in brain stem
Peripheral Chemoreceptors - hypoxemic drive
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front 134 Regulation of breathing: lung & chest wall receptors | back 134 monitors breathing patterns and lung function Lung receptors: Stretch Receptors: located in smooth muscle of conducting airways & responds to changes in airway pressure Irritant receptors: Located bw the airway epithelial cells, stimulated by irritants, like smoking Juxtacapillary: J Receptors: located in alveolar wall & sense lung congestion |
front 135 Influenza | back 135 caused by a virus & has 3 distinct types: A B or C 36,000 deaths annually in US A&B can cause epedemics bc they can mutate C cannot Antigenic Drift- minor mutation (epedemic) Antigenic Shift - Major Mutation (pandemic) |
front 136 Pneumonia | back 136 an acute inflammation of the parenchyma of the lungs (alveoli & bronchioles). Leading cause of morbidity & mortality world wide. The interstitial tissues & alveolar spaces become infiltrated & filled with exudative fluid, leukocytes, and local macrophages |
front 137 Development of pneumonia | back 137 1. Virulence of organism 2. size of innoculum 3. effectiveness of host defense |
front 138 Classification of pneumonia | back 138 Type of Agent
Anatomic Pattern (distribution)
Setting
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front 139 Pneumonia Type of Agent- TYPICAL | back 139 Bacteria in the alveoli
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front 140 ATYPICAL | back 140 Viral, mycoplasma and chlamydia infections of alveolar septum or interstitium |
front 141 Lobar Pneumonia | back 141 Affects entire Lung |
front 142 Bronchopneumonia | back 142 Affections patchy distributions over more than one lobe |
front 143 What is the mos common cause of bacterial pneumonia? | back 143 Streptococcus or Pneumococcal gram positive virulence factors- capsule prevents or delays digestions by phagocytes Spleen is helpful in clearing bacteria from blood Immunization for preventioin |
front 144 Legionnaires Disease | back 144 Bacteria, Acquired from the environment gram negative rod warm stagnant waters incubation period is 2-10 days, abrupt onset of malaise, weakness, diarrhea, high fever & cough Treatment- quick antibiotics |
front 145 Tuberculosis | back 145 Worlds foremost cause of deat from a single infectious agent. Caused by myobacterium which are acid fast with a waxy cell wall. |
front 146 Gohn Foci | back 146 Lesions that contain macrophage, T Cells and INACTIVE TB. |
front 147 Diagnosis of TB | back 147 Definitive Diagnosis: Bacterial culture (can take up to 12 weeks) M. TUberculsosis DNA amplification technique Sputum identification (nonspecific) skin test (PPD) - cannot distinguish bw active & latent |
front 148 Treatment for Active TB | back 148 4 drugs: isoniazid, rifamycin, pyrazinamide, ethambutol |
front 149 4 types of lung cancer | back 149 Adenocarcinoma Squamous cell carcinonma Small Cell Carcinoma Large cell carcinoma |
front 150 Lung cancer therapeutically classified as: | back 150 Small cell carcinoma & non-small cell carcinoma |
front 151 Small cell Carcinoma | back 151 Metastasizes early infiltrate widely rarely resectable death within 3 months w/o treatment cant do surgery usually, only chemo |
front 152 Non-small cell carcinoma | back 152 Adenocarcinoma- most common (in women & non smokers) Squamous cell- most common in men, smokers |
front 153 Viral Croup | back 153 Parainfluenza virus, in children under 5, a "cold gone bad" upper airway infection, primarily with vocal chords barking cough, worsens at night |
front 154 Epiglottitis | back 154 Upper airway infection; etiologic agent: historically- haemophilus influenza now: streptococcus or staphylococcus Very sudden onset that can be life threatening bc airways become occluded Cherry-red epiglottis, drooling, chin thrust forward, sick looking |
front 155 Acute Bronchiolitis | back 155 Lower airway infection, occurs in children less than 2 yrs old etological agent: Respiratory Syncytial Virus (RSV) Preceede by stuffy nose, cold symptoms may progress to respiratory failure but usually slower onset |
front 156 Pleuritis | back 156 Inflammation of the pleura Parietal Pleura - abrupt onset, unilateral Causes: neoplasm, Inflammation (pneumonia) Must differentiate: Musculoskeletal Pain and Heart pain (angina) |
front 157 Pleural effusion | back 157 fluid accumulation in pleural space |
front 158 Hydrothorax | back 158 Serous, water like fluid |
front 159 Empyema | back 159 Pus cells & infectious fluids |
front 160 Chylothorax | back 160 milky fluid |
front 161 Hemothorax | back 161 bloody fluid |
front 162 Pneumothorax | back 162 Air in pleural space partial or complete collapse of the affected lung Types: spontaneous, traumatic (open or tension) |
front 163 Traumatic Pneumothorax (Open) | back 163 Penetrating chest injury or surgery, air flows into pleural space |
front 164 Traumatic Pneumothorax (Tension) | back 164 Intrapleural pressure exceeds atmospheric pressure. air enters pleural space but cannot exit |
front 165 Spontaneous Pneumothorax | back 165 Bleb ruptures (or a blister0 |
front 166 Obstructive Asthma Disorders | back 166 Bronchial Asthma (acute) Chronic Obstructive airway disease
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front 167 Asthma | back 167 Episodic acute airway narrowing
Basically- inflammatory airway disease, causes spasm, excessive mucous production & edema causes obstruction |
front 168 Extrinsic (Atopic) Asthma | back 168 type 1 hyersensitivities (childhood, allergies) Mast cells inflammatory mediators cause acute response within 10-20 minutes Airway inflammation causes late phase response in 4-8 hrs. Caused by External factors- pollen, |
front 169 Intrinsic (non-atopic) asthma | back 169 Respiratory infections (epitheleal damage, IgE production) Caused by internal factors- exercise, cold air |
front 170 Chronic obstructive pulmonary disorders Mechanisms | back 170 inflammation and fibrosis of bronchial wall hypertrophied mucus glands, excess mucus (obstructs airway flow) loss of alveolar tissue (decreased surface area for gas exchange) Loss of elastic lung fibers (airway collapse, obstructed exhalation) 4th leading cuase of death in US |
front 171 Emphysema | back 171 Enlargement of air spaces and destruction of lung tissue defined anatomically: abnormal permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of the walls of the alveoli w/o fibrosis |
front 172 Chronic Obstructive Bronchitis | back 172 Increased mucus production and obstruction of small airways clinical terms: condition in which chronic productive cough is present for 3 months per year for at least 2 consectutive years and the absence of other causes of chronic cough |
front 173 Bronchiectasis | back 173 uncommon, secondary condidtion infection and inflammation destroy smooth muscle airways, causing permanent dilation of airways |