front 1 A patient presents to the emergency department with a diastolic blood pressure of 132 mm Hg, retinopathy, and symptoms of an ischemic stroke. This symptomology is likely the result of | back 1 hypertensive crisis. |
front 2 Which serum biomarker(s) are indicative of irreversible damage to myocardial cells? | back 2 Elevated CK-MB, troponin I, and troponin T |
front 3 While hospitalized, an elderly patient with a history of myocardial infarction was noted to have high levels of low-density lipoproteins (LDLs). What is the significance of this finding? | back 3 Increased LDL levels are associated with increased risk of coronary artery disease. |
front 4 Critically ill patients may have parenterally administered vasoactive drugs that are adjusted according to their _____ pressure. | back 4 mean arterial |
front 5 A loud pansystolic murmur that radiates to the axilla is most likely a result of | back 5 mitral regurgitation. |
front 6 After being diagnosed with hypertension, a patient returns to the clinic 6 weeks later. The patient reports “moderate” adherence to the recommended lifestyle changes and has experienced a decreased from 165/96 to 148/90 mm Hg in blood pressure. What is the most appropriate intervention for this patient at this time? | back 6 Continue lifestyle modifications only. |
front 7 Primary treatment for myocardial infarction (MI) is directed at | back 7 decreasing myocardial oxygen demands. |
front 8 A patient has a history of falls, syncope, dizziness, and blurred vision. The patient’s symptomology is most likely related to | back 8 hypotension |
front 9 TRUE/FALSE, The ingestion of certain drugs, foods, or chemicals can lead to secondary hypertension. | back 9 True |
front 10 Patent ductus arteriosus is accurately described as a(n) | back 10 communication between the aorta and the pulmonary artery. |
front 11 What compensatory sign would be expected during periods of physical exertion in a patient with limited ventricular stroke volume? | back 11 Tachycardia |
front 12 Myocarditis should be suspected in a patient who presents with | back 12 acute onset of left ventricular dysfunction. |
front 13 An elderly patient’s blood pressure is measured at 160/98. How would the patient’s left ventricular function be affected by this level of blood pressure? | back 13 Left ventricular workload is increased with high afterload. |
front 14 Restriction of which electrolytes is recommended in the management of high blood pressure? | back 14 Sodium |
front 15 The most reliable indicator that a person is experiencing an acute myocardial infarction (MI) is | back 15 ST-segment elevation. |
front 16 Aortic regurgitation is associated with | back 16 diastolic murmur. |
front 17 Which blood pressure reading is considered to be indicative of prehypertension according to the JNC-7 criteria? | back 17 128/82 |
front 18 The prevalence of high blood pressure is higher in | back 18 non-Hispanic black adults |
front 19 Rheumatic heart disease is most often a consequence of | back 19 β-hemolytic streptococcal infection. |
front 20 A middle-aged patient has a follow up visit for a recorded blood pressure of 162/96 mm Hg taken 3 weeks ago. The patient has no significant past medical history and takes no medications, but smokes 1 1/2 packs of cigarettes per day, drinks alcohol regularly, and exercises infrequently. The patient is about 40 lbs. overweight and admits to a high-fat, high-calorie diet. At the office visit today, the patient’s blood pressure is 150/92 mm Hg. What is the least appropriate intervention for this patient at this time? | back 20 Begin antihypertensive drug therapy. |
front 21 Tumor necrosis factor α and interleukin-1 contribute to shock states because they induce production of | back 21 nitric oxide. |
front 22 In which stage of shock is a patient who has lost 1200 mL of blood, who has normal blood pressure when supine, but who experiences orthostatic hypotension upon standing? | back 22 Class II, Compensated Stage |
front 23 The progressive stage of hypovolemic shock is characterized by | back 23 tachycardia. |
front 24 Hypotension associated with neurogenic and anaphylactic shock is because of | back 24 peripheral pooling of blood. |
front 25 Hypertrophy of the right ventricle is a compensatory response to | back 25 pulmonary stenosis |
front 26 Low cardiac output in association with high preload is characteristic of ________ shock. | back 26 cardiogenic |
front 27 First-degree heart block is characterized by | back 27 prolonged PR interval. |
front 28 Second-degree heart block type I (Wenckebach) is characterized by | back 28 lengthening PR intervals and dropped P wave |
front 29 TRUE/FALSE A type of shock that includes brain trauma that results in depression of the vasomotor center is cardiogenic | back 29 False A type of shock that includes brain trauma that results in depression of the vasomotor center is neurogenic shock |
front 30 TRUE/FALSE Disseminated intravascular coagulation is a serious complication of septic shock characterized by abnormal clot formation in the microvasculature throughout the body. | back 30 True |
front 31 In which dysrhythmias should treatment be instituted immediately? | back 31 Atrial fibrillation with a ventricular rate of 220 beats/minute |
front 32 Which dysrhythmia is thought to be associated with reentrant mechanisms? | back 32 Preexcitation syndrome tachycardia (Wolf-Parkinson-White syndrome) |
front 33 Administration of which therapy is most appropriate for hypovolemic shock? | back 33 Crystalloids |
front 34 The majority of tachydysrhythmias are believed to occur because of | back 34 reentry mechanisms. |
front 35 A patient who was involved in a fall from a tree becomes short of breath. The lung sounds are absent on one side. This patient is experiencing ________ shock. | back 35 obstructive |
front 36 Patients with structural evidence of heart failure who exhibit no signs or symptoms are classified into which New York Heart Association heart failure class? | back 36 Class I |
front 37 Administration of a vasodilator to a patient in shock would be expected to | back 37 decrease left ventricular afterload. |
front 38 Improvement in a patient with septic shock is indicated by an increase in | back 38 systemic vascular resistance |
front 39 The effect of nitric oxide on systemic arterioles is | back 39 vasodilation. |
front 40 A laboratory test that should be routinely monitored in patients receiving digitalis therapy is | back 40 serum potassium. |
front 41 A measurement of blood pressure in which it represents the peak pressure during cardiac_______. This is _________ __________ _________. 120/72 | back 41 Systole, systolic blood pressure |
front 42 A measurement of blood pressure in which it represents the lowest pressure during cardiac ________. This is __________ ___________ _________. 120/72 | back 42 Diastole, diastolic blood pressure. |
front 43 What is the most accurate method for measuring blood pressure? | back 43 Direct measurement of blood pressure. |
front 44 Where is the catheter in direct measurement of blood pressure commonly placed? | back 44 radial artery |
front 45 What auscultation of Korotkoff sound is heard during systolic blood pressure (SBP)? | back 45 Onset of Korotkoff sounds. |
front 46 What auscultation of Korotkoff sound is heard during diastolic blood pressure (DBP)? | back 46 Disappearance of Korotkoff sounds. |
front 47 What are the determinants of systemic blood pressure (SBP and DBP)? | back 47 Cardiac output (CO), and the resistance to the ejection of blood from the heart. |
front 48 End-Diastolic volume is the..... | back 48 preload |
front 49 In End-Diastolic volume~preload, what is the amount of blood returned to the heart called? | back 49 Venous return. |
front 50 Systemic vascular resistance (SVR) us the..... | back 50 afterload |
front 51 Systemic vascular resistance is determined by.... | back 51 the radius of arteries and degree of vessel compliance. |
front 52 Mechanism of BP regulation: in short-term regulation of systemic blood pressure, changes in BP are mediated through activation of the _______ __________ ___________. | back 52 Sympathetic nervous system: epinephrine and norepinephrine |
front 53 What are the 3 effect of Beta 1 in the heart | back 53 Stimulating SA node, ~cause increase in HR Increase conduction time in AV node ~cause increase in HR Increased contractility in the heart muscle. |
front 54 Long Tem Regulation of Systemic BP-1: In RAAS angiotensin I when in contact with ACE activates..... | back 54 Angiotensin II |
front 55 Long Term Regulation of Systemic BP-1: What are the two effects of Angiotensin II.... | back 55 Potent vasoconstriction (afterload) and stimulates the release of aldosterone. |
front 56 Everytime constriction happens what happens to BP? | back 56 It goes up. |
front 57 Long Term Regulation of Systemic BP-1 When aldosterone is released, sodium and water retention caused an ________ in blood pressure. | back 57 increase |
front 58 Long Term Regulation of Systemic BP- RAAS and fluid volume is regulated by ________, _________, __________. | back 58 neural, hormonal. renal |
front 59 Long Term Regulation of Systemic BP-RAAS & fluid volume: Increase in extracellular fluid volume (preload) = ________ CO and SVR= _____________. | back 59 Increased, elevated BP. |
front 60 Long Term Regulation of Systemic BP-RAAS & fluid volume: Increased serum sodium level = _________osmolarity =___________ADH secretion. | back 60 Increased, increased |
front 61 Where are baroreceptors located? | back 61 Aorta arch and carotid sinus. |
front 62 What do baroreceptors sense? | back 62 Osmolarity |
front 63 Increased serum sodiun level = increased osmolarity = increased ADH secretion causes _______ ____ _______ ______/________ _________. | back 63 kidneys to reabsorb water/increase preload. |
front 64 Long-Term Regulation of Systemic BP--2: Causes kidney to increase sodium and water excretion by increasing the glomerular filtration rate (resulting in a decrease in preload). | back 64 Atrial natriuretic peptides/ANP |
front 65 Adult Blood Pressure: Normal BP: | back 65 SBP: < 120 DBP: < 80 |
front 66 Adult Blood Pressure Prehypertension: | back 66 SBP: 120-139 DBP: 80-89 |
front 67 Adult Blood Pressure: Stage 1 hypertension | back 67 SBP: 140-159 DBP: 90-99 |
front 68 Adult Blood Pressure: Stage 2 hypertension | back 68 SBP: > 160 DBP: >100 |
front 69 Primary Hypertension: What subtype is presented when systolic BP is >140mm Hg while diastolic pressure remains <90mm Hg? | back 69 Isolated systolic hypertension |
front 70 Primary Hypertension: What subtype is presented when diastolic pressure is >90mm Hg with a systolic pressure of <140mm Hg? | back 70 Isolated diastolic hypertension |
front 71 Primary Hypertension: What subtype is presented when both systolic and diastolic exceed prehypertension levels? | back 71 Combines systolic and diastolic hypertension |
front 72 TRUE/FALSE The highest reading will determine the degree of hypertension | back 72 True |
front 73 Primary Hypertension: End organ damage causes ______ ______ ________ __________. | back 73 Renal failure, stroke, heart disease |
front 74 Primary Hypertension: In end-organ damage, damage to arterial system and acceleration of atherosclerosis leads to ________ ___________. | back 74 Cardiovascular disease. |
front 75 Primary Hypertension: In end-organ damage, increased myocardial work results in ______ _______. | back 75 Heart failure |
front 76 In Primary Hypertension, what results from end-organ damage and glomerular damage _______ _________, | back 76 Kidney failure |
front 77 In primary hypertension end-organ damage affects ___________ ___ _____ ________. | back 77 microcirculation of the eyes. |
front 78 In primary Hypertension, end-organ damage increases pressure in cerebral vasculature that can result in _______. | back 78 Hemorrhage |
front 79 What are the non-modifiable risk factors in primary hypertension? | back 79 family history, age, ethnicity and genetics. |
front 80 Primary hypertension is also called ________ ________. | back 80 Essential hypertension |
front 81 What are modifiable risk factors in primary hypotension? | back 81 dietary factors, sedentary lifestyle, obesity/weight gain, metabolic syndrome, elevated blood glucose levels/ diabetes, elevated total cholesterol, alcohol and smoking. |
front 82 In treatment for primary hypertension, what non-medical modification can be made as a form of treatment? | back 82 Weight loss, exercise, DASH diet, alcohol moderation, decrease sodium intake. |
front 83 Treatment for primary hypertension affects _____ _______ _______. | back 83 heart rate, SVR, and/or stroke volume |
front 84 What type of hypertension is most common from in infants and preschool children? | back 84 secondary hypertension |
front 85 The most common cause for childhood secondary hypertension is relation to ______ _______ _____ ____ _____ _______. | back 85 renal disease, and coarctation of the aorta (aortic narrowing). |
front 86 A hypertensive emergency is a........ | back 86 sudden increase in either systolic or diastolic pressure with evidence of end-organ damage. |
front 87 Hypertensive urgency is....... | back 87 blood pressure elevation without evidence of end-organ damage. |
front 88 High blood pressure increases the workload of the left ventricle, because it increases | back 88 afterload |
front 89 Hypertension with a specific, identifiable cause is known as ____ hypertension. | back 89 Secondary |
front 90 TRUE/FALSE Lactated Ringer solution and normal saline are commonly used crystalloid solutions that contain electrolytes. | back 90 True |
front 91 An erroneously low blood pressure measurement may be caused by | back 91 Positioning the arm above the heart level |
front 92 TRUE/FALSE A patient is diagnosed with cardiogenic shock. The patient is hyperventilating and is therefore at risk for the respiratory complication of respiratory acidosis. | back 92 False A patient diagnosed with cardiogenic shock who is hyperventilating is at risk for respiratory alkalosis |
front 93 Angina caused by coronary artery spasm is called _____ angina. | back 93 Prinzmetal variant |
front 94 Patients presenting with symptoms of unstable angina and no ST-segment elevation are treated with | back 94 Antiplatelet drugs |
front 95 Constrictive pericarditis is associated with | back 95 Impaired cardiac filling |
front 96 An elderly patient’s blood pressure is measured at 160/98. How would the patient’s left ventricular function be affected by this level of blood pressure? | back 96 Left ventricular workload is increased with high afterload. |
front 97 Hypotension, distended neck veins, and muffled heart sounds are classic manifestations of | back 97 Cardiac Tamponade |
front 98 Hypertension is closely linked to | back 98 obstructive sleep apnea |
front 99 What results when systemic blood pressure is increased? | back 99 vasoconstriction |
front 100 Increased preload of the cardiac chambers may lead to which patient symptom? | back 100 Edema |
front 101 Cor pulmonale refers to | back 101 Right ventricular hypertrophy secondary to pulmonary hypertension. |
front 102 A patient is diagnosed with heart failure with normal ejection fraction. This patient is most likely characterized by a(n)Correct! | back 102 Elderly woman without a previous history of MI. |
front 103 The majority of cases of anaphylactic shock occur when a sensitized individual comes in contact with | back 103 Antibiotics |
front 104 Cardiogenic shock is characterized by | back 104 Reduced cardiac output |
front 105 Sepsis has been recently redefined as | back 105 A systemic inflammatory response to infection |
front 106 TRUE/FALSE Chronic elevation of myocardial wall tension results in atrophy. | back 106 FALSE Chronic elevation of myocardial wall tension results in hypertrophy |
front 107 Beta-blockers are advocated in the management of heart failure because they | back 107 Reduce cardiac output |
front 108 Tachycardia is an early sign of low cardiac output that occurs because of | back 108 Baroreceptor activity |
front 109 Heart Failure | back 109 Is the inability of heart to maintain sufficient cardiac output |
front 110 Heart Failure results | back 110 Congestion of blood flow in the systemic (RHF) or Pulmonary (LHF) venous circulation |
front 111 What is the short term compensatory mechanism of Heart failure | back 111 SNS activation - Heart rate and contractility increase |
front 112 What is the long term compensatory mechanism of heart failure | back 112 RAAS system - increases preload thus increasing cardiac output |
front 113 Which ventricular failure is the most common? | back 113 Left Ventricular failure |
front 114 What are the clinical manifestations of Heart Failure | back 114 Forward failure= insufficient cardiac pumping manifested by poor CO/hypoxia Backward failure = congestion of blood behind the pumping chamber/ede,a |
front 115 What is the underlying issue of Heart failure | back 115 90% is due to ischemic issues 10% is due to hypertension or valvular disease |
front 116 What are the forward effects of heart failure | back 116 Systemic Hypoxia and SNS activation: Fatigue, oliguria, anxiety, confusion, HR increase, faint pulses, restlessness |
front 117 What are the backward effects of LHF | back 117 Pulmonary congestion and edema dyspnea on exertion, orthopnea and paroxysmal nocturnal dyspnea cough, respiratory crackles, hypoxemia, and high left-atrial pressure, cyanosis, S3 sound |
front 118 What are the backward effects of RHF | back 118 Congestion in the systemic venous system/systemic edema Edema, ascites, jugular veins distended, impaired mental functioning, hepatomegaly, splenomegaly |
front 119 Coronary heart disease is characterized by.... | back 119 Insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries (CAD) |
front 120 Sequelae of CHD include... | back 120 Angina pectoris (myocardial infarction), dysrhythmias, heart failure, and sudden cardiac death. |
front 121 99% of cases of coronary heart disease are associated with.... | back 121 Atherosclerosis |
front 122 In ischemia, what are the two main factors that determine oxygen demand? | back 122 Rate of coronary perfusion and myocardial workload. |
front 123 Coronary perfusion can be altered by? | back 123 Large, stable atherosclerotic plaque, vasospasm, failure of autoregulation by the microcirculation, poor perfusion pressure, acute platelet aggregation, and thrombosis. |
front 124 Chronic occlusion of a coronary vessel results in... | back 124 Stable angina |
front 125 Plaque disruption and thrombus formation result in unstable angina or MI called? | back 125 Acute occlusion |
front 126 Angina pectoris results in.... | back 126 Chest pain associated with intermittent myocardial ischemia. |
front 127 What type of angina is chronic occlusion of a coronary vessel? | back 127 Stable angina |
front 128 What type of angina is associated with plaque disruption and thrombus formation? | back 128 Unstable angina/MI |
front 129 Myocardial ischemia may also uncommonly be caused by? | back 129 Coronary vasospasm-prinzmental or variant angina Hypoxemia and low perfusion pressure from volume depletion or shock |
front 130 What type of pattern angina pectoris? - Most common (Classic) - Onset of anginal pain is generally predictable and elicited by similar stimuli each time. -Relieved by rest and nitroglycerin -Characterized by stenotic atherosclerotic coronary vessels. | back 130 Stable or typical angina |
front 131 What type of pattern angina pectoris? - No relief without medical help - May progress to MI or acute ischemia | back 131 Unstable or crescendo angina |
front 132 What type of pattern angina pectoris? - Unpredictable -Onset of symptoms is unrelated.to physical or emotional exertion, heart rate, or other obvious causes of increased myocardial oxygen demand. -Characterized by vasospasm, atherosclerosis-included, hyper contractility, abnormal secretion of a vasospastic chemical by local mast cells, abnormal calcium influx across vascular smooth muscle. | back 132 Prinzmetal or variant angina |
front 133 Acute coronary syndromes/unstable or crescendo angina causes.... | back 133 plaque rupture with acute thrombus development |
front 134 What are sign and symptoms of acute coronary syndromes | back 134 Severe chest pain, last longer than 15 minutes and is not relieved by rest or nitroglycerin. |
front 135 When diagnosing acute coronary syndrome what must be elevated? | back 135 specific marker proteins in the blood |
front 136 TRUE/FALSE In acute coronary syndrome, electrocardiographic changes are seen. | back 136 True |
front 137 TRUE/FALSE The following sign and symptoms are seen when diagnosing acute coronary syndrome: severe crushing, excruciating chest pain that may radiate to the arm, shoulder, jaw or back accompanied by nausea, vomiting, diaphoresis, shortness of breath. | back 137 True |
front 138 Finish the acute coronary syndrome pathway signs and symptoms of cardiac ischemia -> ACS -> ST elevation -> +biomarkers -> | back 138 STEMI |
front 139 Finish the acute coronary syndrome pathway signs and symptoms of cardiac ischemia -> ACS ->NO ST elevation -> -biomarkers -> | back 139 Unstable angina |
front 140 Finish the acute coronary syndrome pathway signs and symptoms of cardiac ischemia -> ACS ->NO ST elevation -> +biomarkers -> | back 140 NSTEMI |
front 141 What serum makers will increase within 24 hours in diagnosing myocardial infarction? | back 141 CK-MB and troponin I and T |
front 142 In a typical ECG which pattern represents ventricle repolarization? | back 142 T wave |
front 143 In a typical ECG which pattern represents depolarization of atria in response to SA node triggering? | back 143 P wave |
front 144 In a typical ECG what represents the delay of AV node to allow filling of ventricles? | back 144 PR interval |
front 145 In a typical ECG what represent the depolarization of ventricle triggers main pumping contractions? | back 145 QRS complex |
front 146 In a typical ECG what represent the beginning of ventricle repolarization and should be flat? | back 146 ST segment |
front 147 A patient with chest pain and evidence of acute ischemia will show _________ ___________ in ECG. | back 147 ST-segment elevation |
front 148 What type of therapy could be used when there is evidence of ST-segment elevation? | back 148 acute reperfusion therapy |
front 149 A patient presenting with symptoms of unstable angina and no ST elevation on the ECG will show _______ _______. | back 149 non-STEMI (NSTEMI) |
front 150 Patients with NSTEMI are candidates for _______________ drugs. | back 150 antiplatelet |
front 151 In acute coronary syndrome MI leads to drop in CO, triggering _________ ___________. | back 151 compensatory responses |
front 152 What leads to increase myocardial workload by increasing heart rate, contractility,and blood pressure. | back 152 Sympathetic nervous system activation |
front 153 What are the clinical treatments for Acute coronary syndrome? | back 153 Morphine, Oxygen, Nitroglycerin, Anticoagulants |
front 154 What are the three treatment principles for acute coronary syndrome? | back 154 Decreasing myocardial oxygen demand, increasing myocardial oxygen supply, and monitoring and managing complications (SNS activation). |
front 155 Common factor among all types of shock is..... | back 155 Hypoperfusion and impaired cellular oxygen utilization. |
front 156 What does hypoperfusion mean? | back 156 oxygen supply is going down |
front 157 Inadequate cellular oxygenation may result from.... | back 157 decreased cardiac output, maldistribution of blood flow, reduced blood oxygen content |
front 158 Pump failure causes..., | back 158 Cardiogenic issues- MI, valves are not working, cardiomyopathy |
front 159 Hypovolemia causes.... | back 159 Bleeding (internal or external) |
front 160 Vasodilation causes.... | back 160 septic shock |
front 161 What type of shock causes the following: -MI. -Cardiomyopathy. -Valvular heart disease -Ventricular rupture. -Congenital heart defects -Papillary muscle rupture. | back 161 Cardiogenic shock |
front 162 What type of shock causes the following: -Pulmonary embolism. -Cardiac tamponade. -Tension pneumothorax -Dissecting aortic aneurysm | back 162 Obstructive shock |
front 163 What type of shock causes the following: -Acute hemorrhage. -Dehydration from vomiting & diarrhea -Overuse of diruetics. -Burns. -Pancreatitis | back 163 Hypovolemic shock |
front 164 Macrophage induction will release.... | back 164 cytokines producing: Alpha TNF, IL1 That can attack blood vessel walls, and cause vasodilation. Alpha TNF can cause coagulation leading to clot formation |
front 165 What type of shock causes the following: -Anaphylaxis. -Neurotrauma. -Spinal cord trauma -spinal anesthesia. -sepsis | back 165 Distributive shock |
front 166 Lack of oxygen causes several outcomes and.... | back 166 Reperfusion injury |
front 167 During shock, your heart rate _________. your urine output___________. your respiratory rate ____________. | back 167 Increase, decrease, increase |
front 168 During shock your level of consciousness _____________. Your blood pressure _____________. Specific gravity_________________. | back 168 Decrease, decreases (hypotension), increase. |
front 169 TRUE OR FALSE During shock constriction of splanchnic vessels cause nausea and abdominal pain? | back 169 True |
front 170 During shock a decrease in capillary refill causes.... | back 170 clammy cool skin, and a blush gray color to the skin. |
front 171 What is released during shock? | back 171 Cortisol and aldosterone |
front 172 The following clinical findings distinguish which type of shock? -Hypotension. -High vascular resistance -Low cardiac output -High cardiac preload -Low venous oxygen saturation -Low urine output. -Cool skin temperature -Myocadiac muscle dysfunction -HF management | back 172 Cardiogenic |
front 173 The following clinical findings distinguish which type of shock? -Hypotension -High systemic vascular resistance. -Low cardiac output -Low cardiac preload. -Low venous oxygen saturation -Low urine output. -Cool skin temperature -Fluid resurrection | back 173 Hypovolemic |
front 174 The following clinical findings distinguish which type of shock? -Hypotension -Low systemic vascular resistance. -High cardiac output -Low cardiac preload. -High venous oxygen saturation -Low urine output. -Warm skin temperature -excessive vasodilation -Anti-infection + FR | back 174 Septic |
front 175 What type of distributive shock? Mast cells release vasodilatory mediators such as histamine that will result in severe hypotension | back 175 Anaphylactic shock- Type 1 hypersensitivity |
front 176 What type of distributive shock? Loss of sympathetic activation of arteriolar smooth muscle. | back 176 Neurogenic shock |
front 177 What type of distributive shock? Severe systemic inflammatory response to infection (NO and Kinin) | back 177 Septic shock |
front 178 TRUE OR FALSE Complications in shock DO NOT cause inflammation. | back 178 False, complications in shock causes inflammation in nature, |
front 179 What type of complication of shock is the following? - Commonly associated with septic shock -Development of refractory hypoxemia, decreased pulmonary compliance and pulmonary edema. | back 179 Acute respiratory distress syndrome (ARDS) |
front 180 What is the cause of death in ARDS? | back 180 multiple organ failure |
front 181 TRUE or FALSE in ARDS exudate leaks in the interstitial spaces and alveoli of the lung. | back 181 True |
front 182 What type of complication of shock is the following? -Wide spread clot formation consumes platelets and clotting factors. -Usually occurs in septic shock -Activation of the clotting cascade -Platelet count and fibrinogen levels are low, and fibrin degradation-producing D dimer is elevated. | back 182 DIC - Disseminated intravascular coagulation |
front 183 What type of complication of shock is the following? -Acute tubular necrosis (ATN) is associated with decreased urinary exertion of waste products (creatinine and urea). -Kidneys undergo long periods of hypoperfusion. -Vasoconstriction causes decreased glomerular blood flow, reduced hydrostatic pressure and filtration causing low urine output. | back 183 Acute renal failure. |
front 184 What type of complication of shock is the following? - Mostly in sepsis -Initiated by immune mechanisms that are overactive and destructive. -Cytokines affect endothelium, recruit neutrophils, and activate inflammation in vascular beds, leading to tissue destruction and organ dysfunction. | back 184 MODS- Multiple organ dysfunction syndrome |