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1. INFECTIOUS / INFLAMMATORY DISORDERS

2. What is Inflammation? Response to injury (including infection) Reaction of blood vessels leads to: Accumulation of fluid and leukocytes in extravascular tissues Destroys, dilutes, or walls off the injurious agent Initiates the repair process Fundamentally a protective response

3. Cont …… May be potentially harmful Hypersensitivity reactions to insect bites, drugs, contrast media in radiology Chronic diseases: arthritis, atherosclerosis Disfiguring scars, visceral adhesions Consists of two general components Vascular reaction Cellular reaction Controlled by a variety of chemical mediators Derived from plasma proteins Derived from cells inside and outside of blood vessels

4. Cont ….. four cardinal signs of acute inflammation: Rubor (erythema [redness]): vasodilatation, increased blood flow Tumor (swelling): extravascular accumulation of fluid Calor (heat): vasodilatation, increased blood flow Dolor (pain)

5. Types of Inflammation Acute inflammation Short duration Edema Mainly neutrophils Granulomatous inflammation Distinctive pattern of chronic inflammation Activated macrophages ( epithelioid cells) predominate Chronic inflammation Longer duration Lymphocytes & macrophages predominate Fibrosis New blood vessels (angiogenesis)

6. Acute Inflammation Three major components: Increase in blood flow (redness & warmth) Edema results from increased hydrostatic pressure (vasodilation) and lowered intravascular osmotic pressure (protein leakage) Leukocytes emigrate from microcirculation and accumulate in the focus of injury Stimuli: infections, trauma, physical or chemical agents, foreign bodies, immune reactions

7. Systemic Manifestations Leukocytosis: increased leukocyte count in the blood Neutrophilia : bacterial infections Lymphocytosis: infectious mononucleosis, mumps, measles Eosinophilia: Parasites, asthma, hay fever Leukopenia: reduced leukocyte count Typhoid fever, some viruses, rickettsiae , protozoa

8. Chronic Inflammation Inflammation of prolonged duration (weeks or months) Active inflammation, tissue destruction, and attempts at repair are proceeding simultaneously May follow acute inflammation or begin insidiously and often asymptomatically Persistent infections, exposure to toxic agents such as silica (silicosis), or by autoimmunity

9. Chronic Inflammation Persistent infections Treponema pallidum [syphilis], viruses, fungi, parasites Exposure to toxic agents Exogenous: silica (silicosis) Endogenous: toxic plasma lipid components (atherosclerosis) Autoimmunity Rheumatoid arthritis, systemic lupus erythematosus

10. Chronic Inflammation Histological features Infiltration with mononuclear cells (macrophages, lymphocytes, and plasma cells) Tissue destruction (induced by the inflammatory cells) Healing by replacement of damaged tissue by connective tissue (fibrosis) and new blood vessels (angiogenesis)

11. MENINGITIS Inflammation of the meninges of the brain and spinal cord Bacterial Aseptic (other infective agents—usually viral)

12. CLINICAL MANIFESTATIONS Classic symptoms: Nuchal rigidity Brudzinski’s sign Kernig’s sign Photophobia Other: fever, tachycardia, h/a, prostration, chills, nausea, vomiting May be irritable at first with progression to confusion, stupor, and semiconsciousness

13. Seizures may occur Petechial or hemorrhagic rash may develop CSF is cloudy with bacterial

14. BRUDZINSKI’S SIGN

15. KERNIG’S SIGN

16. DIAGNOSIS Lumbar puncture: Bacterial: increased protein, decreased glucose, cloudy, increased leukocytes Viral: increased protein, normal glucose, clear, increased lymphocytes May culture other areas: blood, wounds, sinuses, etc .

17. TREATMENT Isolate until results of CSF analysis are obtained. Bacterial is very contagious antibiotics Anticonvulsants Fluid and electrolyte replacement Monitor for increased ICP Provide quiet environment Analgesics may be avoided if they have CNS depressant actions—will mask CNS changes

18. ENCEPHALITIS Inflammation of the parenchyma of the brain and spinal cord. Usually caused by a virus. Arbovirus encephalitis (transmitted by ticks and mosquitoes) Herpes simplex virus encephalitis may occur as a complication of measles, chickenpox, or mumps .

19. CLINICAL MANIFESTATIONS Fever Headache Seizures Nuchal rigidity Altered LOC Disorientation Agitation Restlessness or lethargy Drowsiness Photophobia N/V

20. BRAIN ABSCESS A collection of either encapsulated or free pus within brain tissue arising from a primary focus elsewhere (ear, mastoid process, sinuses, heart, distal bones, lungs, bacteremia, etc).

21. MANIFESTATIONS Headache Lethargy Drowsiness Confusion Depressed mental status Symptoms of infection Fever Chills

22. Heart disorders

23. Functions of the Heart Pumps oxygenated and nutrient-rich blood to the body through blood vessels Pumps deoxygenated blood, containing wastes, to the lungs, where gas exchange to the outside environment occurs

24. Anatomy of the Heart Located under rib cage and in between the lungs Size varies depending on age, size, and condition of the heart On average, the heart is about the size of that person’s clenched fist

25. Valves 4 Heart Valves Tricuspid Valve Pulmonary Semilunar Valve Mitral ( Biscuspid ) Valve Aortic (Semilunar) Valve Purpose : prevent backflow of blood, keep blood flowing in one direction

26. Flow of Blood 1. Deoxygenated blood from the upper and lower body flows through the superior and inferior vena cava .

27. Flow of Blood 2. The superior and inferior vena cava empty blood into the right atrium .

28. Flow of Blood 3. Blood from the right atrium passes through the tricuspid valve .

29. Flow of Blood 4. Blood passes through the tricuspid valve into the right ventricle .

30. Flow of Blood 5. Blood from the right ventricle passes through the pulmonary semilunar valve .

31. Flow of Blood 6. Blood flows through the pulmonary semilunar valve into the right and left pulmonary arteries.

32. Flow of Blood 7 . Pulmonary arteries take blood to the lungs for gas exchange. In the lung capillaries, blood picks up oxygen and transfers carbon dioxide to the lungs for exhalation. Blood becomes oxygenated .

33. Flow of Blood 8 . Right and left p ulmonary veins bring the blood back to the heart.

34. 9. Pulmonary veins empty blood into the left atrium . 10. The blood from the left atrium flows through the mitral (or bicuspid) valve 11. After passing through the mitral valve, blood enters the left ventricle . 12) Blood from the left ventricle passes through the aortic semilunar valve 13. After passing through the aortic semilunar valve, the blood enters the aorta and is then pumped to the rest of the body. Pulmonary circuit : movement of blood from the heart to the lungs and back to the heart

35. Contraction Systole - contract Atrial Systole: when the atria contract and pump blood into the ventricles Ventricular Systole: when the ventricles contract and pump blood out of the heart to the lungs or body Diastole - relax When the atria and ventricles relax and start to fill with blood

36. Electrical System AKA the Cardiac Conduction System Consists of three parts: 1. Sinoatrial (SA) node 2. Atrioventricular (AV) node 3. Bundle of His and Purkinje fibers

37. Electrical System 1. Electrical signal starts at the SA node as blood fills the right atrium. This signal causes the atrium to contract. The SA node sets the pace of the heart, so it is also called the pacemaker . 2. Signal arrives at the AV node as blood fills the ventricles. 3. Signal moves along the Bundle of His and along the walls of the ventricles. The Bundle of His divides into right and left branches and then to Purkinje fibers . The v entricles contract.4) Signal passes and ventricles relax.

38. CONGENITAL HEART DISEASES

39. MEANING Congenital heart disease is a defect in the structure of the heart and great vessels that is present at birth.

40. CONGENITAL HEART DISEASE

41. Cont ….. ACYANOTIC Increased pulmonary Obstruction to blood blood flow flow from ventricle ASD 1. Coartation of aorta VSD 2. Aortic stenosis PDA 3. Pulmonic stenosis Atrio ventricular canal

42. ETIOLOGY 90% of the etiology of congenital cardiac defects is unknown. Most are thought to be a result of multifactorial inheritance . Fetal exposure to drugs such as phenytoin and lithium and radiation. Maternal viral infections such as rubella. Maternal metabolic disorders such as phenylketonuria and insulin-dependent diabetes mellitus

43. Risk factors Maternal complications of pregnancy such as increased age and antepartum bleeding. Maternal dietary deficiencies. Genetic factors Chromosomal abnormalities like Turner syndrome, Down syndrome and Trisomy 13 and 18 .

44. Cont ……… ACYANOTIC HEART DISEASES

45. Refers to disorders that causes flow of blood from arterial to venous system. These defects have normal level of oxyhemoglobin saturation in systemic circulation. DEFINITION

46. DEFECTS WITH INCREASED PULMONARY BLOOD FLOW Intra cardiac communications abnormal connection between the great arteries Increased blood to flow from the high-pressure left side of the heart to the low-pressure right side of the heart increases pulmonary blood flow

47. ATRIAL SEPTAL DEFECT (ASD)

48. DEFINITION An atrial septal defect (ASD) is an abnormal opening between right and left atria resulting in left-to-right shunt of blood.

49. CAUSES unknown. Atrial septal defects occur when the partitioning process does not occur completely, leaving an opening in the atrial septum . defect in a gene a chromosome abnormality Drugs – alcohol, lithium Infections- rubella

50. PATHOPHYSIOLOGY

51. CLINICAL FEATURES Asymptomatic Dyspnea Murmer Bulging of chest Poor weight gain Child tired easily when playing Fatigue Sweating

52. DIAGNOSIS Physical assessment- murmers Chest X-ray —heart -enlarged Electrocardiogram (ECG or EKG) —shows abnormal rhythms (arrhythmias or dysrhythmias ) Two-dimensional echocardiogram with Doppler study and color flow mapping - To identify the site of the ASD and associated lesions and document left-to-right flow across the atrial septum.

53. Cont.. Cardiac Catheterization Cardiac Magnetic Resonance Imaging (MRI) Medical Management -- Many children have no symptoms and require no medications, however some children may need to take medications to help the heart work better, since the right side is under strain from the extra blood passing through the ASD

54. Cont.. . Medication that may be prescribed includes the following: Digoxin Diuretics Infection Control: Children with certain heart defects are at risk for developing an infection of the inner surfaces of the heart known as bacterial endocarditis . SURGICAL REPAIR Ideal age for surgery is in between 2- 5 yrs. With the use of hypothermia, patients are being operated below the age of 2 yrs without any risk.

55. SURGICAL REPAIR The surgical closure of an ASD is carried out through an incision in the middle of the chest. A heart-lung machine is used to do the work of the heart while the heart is cooled, stopped, emptied and opened through the right atrium. The hole in the wall between the right and left atrium is closed with stitches if it is small,

56. Cont ,,, if too large, with a patch of thin leather-like material called pericardium, which makes up the sac covering the heart, cow (bovine) pericardium, or rarely, a manmade material, Dacron patch . The right atrium is then closed and the heart is restarted as the heart-lung machine is withdrawn.

57. COMPLICATIONS CHF (rare). Infective endocarditis. Embolic stroke. Pulmonary hypertension. Atrial arrhythmias.

58. PROGNOSIS Although the prognosis is excellent in asymptomatic people, it's poor in those with cyanosis caused by large, untreated defects.

59. 2. VENTRICULAR SEPTAL DEFECT (VSD)

60. DEFINITION Ventricular Septal Defect is a congenital disorder in which blood moves from left ventricle to right ventricle through a defective ventricular septum . It may vary in size from very small defects (Roger’s defect) to very large defect.

61. CLASSIFICATION It may be classified according to location:- Membranous VSD- the defect is located high in the membranous portion of the ventricular septum with a variable extension to the adjoining muscular part of the septum. Anatomically 90% of the VSD are located in the membranous part of the ventricular septum.

62. Cont …… Muscular VSD- It is located in the muscular portion of the septum i.e. toward middle and lower portion of the septum. It has multiple apparent channels. It can be at central, apical, marginal and “Swiss cheese” septum- large number of muscular defects.

63. Classification based on size :- Restricted VSD- It is a small VSD or other words, pinhole VSD. Non- restricted VSD- Large VSD or some times, there may be even absence of septum.

64. PATHOPHYSIOLOGY Due to etiological factors Defect in the septum of the ventricle Due to high pressure in the left ventricle, and more resistance in systemic arterial circulation than pulmonary circulation and also due to contraction of the left ventricle before right ventricle,

65. oxygenated blood shunts from the left ventricle to the right ventricle. Declining left ventricular pressure and become lower than aortic pressure .

66. Cont.. Closure of aortic valve. Continuation of left to right ventricular shunting. Blood accumulate in the right ventricle and more amount of blood flows to the pulmonary artery. More blood reaches Increased blood volume the lung . in the right ventricle.

67. More blood reaches the lung. Pulmonary hypertension. Pulmonary edema. Long standing pulmonary over circulation. Increased pulmonary vascular resistance. Reverse shunt from right to left, aloes known as Eisenmenger’s complex (it is a sever condition, in which there is a combination of pulmonary hypertension with bidirectional or reversal shunting through a VSD or ASD)

68. Increased blood volume in the right ventricle. Increased thickness and hypertrophy of muscles of the right ventricle. Right ventricular enlargement. Inadequate emptying of the right atrium. Pooling of blood in systemic circulation. Peripheral edema.

69. CLINICAL MANIFESTATIONS Only 15% of VSDs are large enough to cause symptoms. Small VSD usually asymptomatic; high spontaneous closure rate during the first year of life. Large VSDs. CHF: tachypnea , tachycardia, excessive sweating associated with feeding, hepatomegaly . Frequent Upper Respiratory Infections. Poor weight gain, failure to thrive. Feeding difficulties. Decreased exercise tolerance.

70. DIAGNOSTIC EVALUATION Auscultation : harsh systolic regurgitant murmur heard best at the lower left sternal border (LLSB); systolic thrill felt at LLSB, narrowly split S 2 . Chest X-ray: varies; normal or cardiomegaly and increased pulmonary vascular markings. ECG: varies; normal to biventricular hypertrophy. Two-dimensional echocardiogram with Doppler study and color flow mapping to identify the size, number, and sites of the defects, estimate pulmonary artery pressure, and identify associated lesions.

71. Cont ….. Cardiac catheterization usually not needed for initial diagnosis; may be needed to calculate the size of the shunt or to assess PVR . May be performed if defect can be closed using a ventricular occlusion device (device can be used only in muscular defects). It is also helps to find out O 2 saturation and pressure in the right ventricle.

72. MANAGEMENT It has been estimated that, about 70-80% of all VSD become smaller in size or disappear entirely, and is known as spontaneous closure . In almost 90% of the patient with spontaneous closure occurs by the age of 3yrs, though it may occur as late as 25 yrs or more. Treatment is conservative when no signs of congestive heart disease or pulmonary hypertension are present.

73. SMALL VSD Medical management: Usually no anticongestive therapy is needed. Infective endocarditis prophylaxis for 6 months after surgical implantation of a ventricular occlusion device. Cardiac catheterization for placement of a ventricular occlusion device for muscular defects Surgical intervention is usually not necessary.

74. MODERATE TO LARGE VSD Medical Management: CHF management: digoxin and diuretics ( furosemide , spironolactone ) and afterload reduction. Avoid oxygen; oxygen is a potent pulmonary vasodilator and will increase blood flow into the PA. Increase caloric intake : Infective endocarditis prophylaxis for 6 months after surgery/ventricular device occluder . Cardiac catheterization for placement of a ventricular occlusion device for muscular defects

75. COMPLICATIONS OF VSD CCF Recurrent respiratory tract infections Infective endocarditis Eisenemenger’s syndrome Pulmonary stenosis Pulmonary hypertension Failure to thrive, poor weight gain

76. 4. ATRIOVENTRICULAR CANAL  

77. MEANING Atrioventricular canal refers to a combination of defects in atrial and ventricular septa and portions of tricuspid and mitral valves. This defect is associated with Down’s syndromes. The most complex AV canal malformation results in one AV valve and large septal defects between both atria and ventricles.

78. CLINICAL MANIFESTATIONS Severity of symptoms depends on amount of mitral regurgitation. Congestive heart failure Poor growth Repeated respiratory failure Systolic murmur Mild cyanoses

79. DIAGNOSTIC EVALUATION Chest x-ray – appears large and pulmonary vascular markings are present. Echocardiogram – presence of septal defects and details of valvular malformations. Cardiac catheterizations – performed to evaluate pulmonary hypertension and pulmonary resistance.

80. MEDICAL MANAGEMENT Surgery is performed during infancy to prevent pulmonary vascular disease. Oxygen may be required until surgery.

81. SURGICAL MANAGEMENT PALLIATIVE Pulmonary artery banding for infants with severe symptoms that are caused by increased pulmonary blood flow in some centers . Most centers perform complete repair in infancy. COMPLETE REPAIR Surgical repair consists of patch closure of the septal defects and reconstruction of the AV valve tissue. If the mitral valve defect is severe, a valve replacement may be needed.

82. POSTOPERTAIVE COMPLICATIONS Heart block Congestive heart failure Mitral regurgitation Dysrhythmias Pulmonary hypertension

83. PREVENTION OF CONGENITAL HEART DISEASES Preventing preterm deliveries Get early prenatal care, even before becoming pregnant Eat a balanced diet. Exercise regularly. Avoid risks. Avoid infections. Keep diabetes under control.

84. Valvular heart disease Function of normal Valves – Unidirectional blood flow, one-way flow of blood from the atria to the ventricles to the arteries. Name of heart valves – 1.Two atrioventricular valves: Mitral valve: Left heart - “Bicuspid valve” . Tricuspid valve: Right heart -“tricuspid” 2. Two semilunar valves: Aortic valve: Left heart . Pulmonary valve: Right heart.

85. definition HVD is groups of critical clinical conditions involve heart valves, leading to different pattern of dysfunction . HVD come to clinical attention – because impose: Hemodynamic instability . Increase susceptibility to infection (infective endocarditis ). Why hemodynamic burden precipitated? 1. Stenosis (Obstruction) 2. Insufficiency (Regurgitation or incompetence). 3. Both

86. Cont ….. 1 Valve Stenosis Obstruction to valve flow . 2. Valve Regurgitation/ Insufficiency/ Incompetence Inadequate valve closure---  back leakage . 3. A single valve can be both stenotic and regurgitant ; but both lesions cannot be severe !! 4. Combinations of valve lesions can coexist 5. Atresia

87. Cont … Stenosis is the failure of a valve to open completely , which obstructing forward flow. Etiology   Almost caused by chronic primary cuspal abnormalities- (1) Calcification or (2)Valve scarring. Stenosis of the mitral valve is a common complication of  rheumatic fever. Definition of Valvular Regurgitation ? Insufficiency results from failure of a valve to close completely , thereby allowing reversed flow .

88. Cont ….. Etiology (1 ) Intrinsic disease of the valve cusps= destruction . ( 2) Distortion of supporting structure

89. Classification Based on etiology can be classified into: 1. Congenital valvular heart disease e.g. Septal defect, Atresia, mal-position 2. Acquired valvular heart disease . Endocarditis– MR & AR Post-inflammatory healed scar (Rheumatic heart disease) MS+MR & AS+AR Senile calcific aortic stenosis- AS Myxomatous - Mitral valve Prolapse- MR

90. Clinical manifestation The clinical consequences depend on : Type of valve involved. Degree of impairment. How fast it develops. (Acute form and chronic form) Rate of compensatory mechanism . Clinical Outcomes : 1) Stenosis leads to pressure overload in the heart. 2 ) Insufficiency leads to volume overload in the heart.

91. Assessment for Valve Dysfunction Murmurs, rales General malaise Dyspnea on exertion Dizziness Chest pain or discomfort Prior history of rheumatic heart disease Orthopnea Pink-tinged sputum Complications: Hemodynamic instability Heart failure Angina Syncope Death Diagnosis : ECG Chest x-ray Cardiac catheterization Echocardiogram

92. Mitral stenosis

93. Treatment Close monitoring No treatment for mild cases just regular check-up Lifestyle changes Eating a health-healthy diet Maintaining a health weight Regular physical activity Quitting smoking Managing stress Medication ; to control symptom and support heart function Diuretics ACE inhibitors Beta blockers Blood thinners

94. Cont ……. Interventional procedure Balloon valvuloplasty;a procedure to open a narrowed valve Transcathetervalve repair /replacement Devices are delivered the heart through catheter to repair Surgery ; valve repair ,valve replacement

95. Peripheral Vascular Diseases

96. Arteries are thick-walled vessels that transport 0 2 and blood via the aorta from the heart to the tissues 3 Layers of Arteries inner layer of endothelium (intima) middle layer of connective tissue, smooth muscle and elastic fibers (media) outer layer of connective tissue (adventitia) have smooth muscles that contracts & relaxes to respond changes in blood volume.

97. Veins are thin-walled vessels that transport deoxygenated blood from the capillaries back to the right side of the heart 3 Layers – intima, media, adventitia there is little smooth muscle & connective tissue  makes the veins more distensible  they accumulate large volumes of blood Major veins, particularly in the lower extremities, have one-way valves --- allow blood flow against gravity Valves allow blood to be pumped back to the heart but prevent it from draining back into the periphery

98. Peripheral Vascular Diseases charac . by a reduction in blood flow and hence 0 2 through the peripheral vessels when the need of the tissues for 0 2 exceeds the supply, areas of ischemia and necrosis will develop Factors that can contribute to the development of peripheral vascular disorders : atherosclerotic changes thrombus formation embolization  coagulability of blood hypertension inflammatory process/infection

99. Arterial Insufficiency there is a deceased blood flow toward the tissues, producing ischemia pulses one usually diminished or absent sharp, stabbing pain occurs because of the ischemia, particularly with activity there is interference with nutrients and 0 2 arriving to the tissues, leading to ischemic ulcers and changes in the skin .

100. Cont …… Venous Insufficiency there is deceased return of blood from the tissues to the heart leads to venous congestion and stasis of blood pulses are present lead to edema , skin changes and stasis ulcers

101. Comparison of characteristics of Arterial & Venous Disorders Arterial Disease Venous Disease Skin cool or cold, hairless, dry, shiny, pallor on elevation, rubor on dangling warm, though, thickened, mottled, pigmented areas Pain sharp, stabbing, worsens w/ activity and walking, lowering feet may relieve pain aching, cramping, activity and walking sometimes help, elevating the feet relieves pain Ulcers severely painful, pale, gray base, found on heel, toes, dorsum of foot moderately painful, pink base, found on medial aspect of the ankle Pulse often absent or diminished usually present Edema infrequent frequent, esp. at the end of the day and in areas of ulceration

102. Risk Factors Age (elderly) – blood vessels become less elastic, become thin walled and calcified –  PVR –  BP Sex (male ) Cigarette smoking nicotine causes vasoconstriction and spasm of the arteries –  circulation to the extremities C0 2 inhaled in cigarette smoke reduces 0 2 transport to tissues Hypertension – cause elastic tissues to be replaced by fibrous collagen tissue  arterial wall become less distensible   resistance to blood flow   BP Hyperlipedimia – atherosclerotic plaque

103. Risk Factors (cont.) 6 Obesit y – places added burden on the heart & blood vessels excess fat contribute to  venous congestion Lack of physical activity Physical activity – promotes muscle contraction   venous return to the heart aids in development of collateral circulation Emotional stress – stimulates sympathetic N.S. - peripheral vasoconstriction   BP Diabetes mellitus – changes in glucose & fat metabolism promote the atherosclerotic process Family history of arthrosclerosis

104. Arteriosclerosis Obliterans is a disorder in which there is an arteriosclerotic narrowing or obstruction of the inner & middle layer of the artery most common cause of arterial obstructive disease in the extremities the lower extremities are involved more than upper extremities common site of disease – femoral artery , iliac arteries , popliteal arteries in a diabetic, the disease becomes more progressive, affects the smaller arteries and often involves vessels below the knee

105. Pathophysiology Plaque formation on the intimal wall that causes partial or complete occlusion Calcification of the medial layer and a gradual loss of elasticity  weakens the arterial walls predisposes to aneurysm, dilation or thrombus formation  artery is unable to transport an adequate blood volume to the tissues during exercise or rest Symptoms appear when the blood vessels can no longer provide enough blood to supply 0 2 and nutrients and remove metabolic waste products

106. Clinical Manifestations Intermittent claudication – most common pain in the extremity that develops in a muscle that has an inadequate blood supply during exercise the cramping pain disappear w/in 1-2 mins . after stopping the exercise or resting the femoral artery is often affected – pain in the calf muscle – common symptom pain at rest is indicative of severe disease gnawing, burning pain, occur more frequently at night feelings of coldness, numbness , tingling sensation advanced arteriosclerosis obliterans  ischemia may lead to necrosis, ulceration and gangrene – toes and distal foot advanced arteriosclerosis obliterans  ischemia may lead to necrosis, ulceration and gangrene – toes and distal foot

107. Diagnostic Tests Doppler ultrasonography – high frequency sound waves directed to artery or veins through a hand-held transducer moved evenly across skin surface audible tone produced in proportion to blood velocity measure blood flow through vessels

108. Management – directed toward prevention of vessel occlusion use of vasodilators Surgical intervention – in advanced disease – ischemic changes and pain severely impairs activity Embolectomy removal of a blood clot, done when large arteries are obstructed

109. Mgt ….. Endarterectomy is removal of a blood clot and stripping of atherosclerotic plaque along with the inner arterial wall. Arterial by-pass surgery an obstructed arterial segment may be bypassed by using a prosthetic material (Teflon) or the pt’s . own artery or vein (saphenous vein)

110. Management Percutaneous Transluminal Angioplasty The balloon tip of the catheter is inflated to provide compression of the plaque Amputation with advanced atherosclerosis & gangrene of extremities toes are the most often amputated part of the body The surgical goal is the remove the least amt. of tissue possible and create a stump adequate for the fitting of a prosthesis

111. Nursing Interventions prevent further progression of existing disease Acute care monitor the limb distal to the affected site for changes in color or temperature  arterial flow – pale & cool (initially)  bluish/darker  tissue become necrotic & black activities that cause pain should be avoided give vasodilators if prescribed – relaxation of vascular smooth muscle  decreases the pain comfort measures – proper body positioning to dec. pressure on affected area

112. Arterial Embolism blood clots floating in the circulating arterial blood. the embolus is frequently a fragment of arterioscherotic plaque loosened from the aorta emboli will tend to lodge in femoral or popliteal arteries , blood flow is impaired and ischemia develops

113. Clinical manifestations: S/ Sx depends on the size of the embolus, the presence of collateral circulation and if it is close to a major organ abrupt onset of severe pain from the sudden cessation of circulation muscular weakness and burning, aching pain occur distal pulses are absent and extremity becomes cold, numb and pale symptoms of shock may develop if the embolus blocks a large artery

114. Medical Management bed rest anticoagulants – prolong the clotting time of the blood and are used to prevent clot extension and new clot formation Ex. 1. heparin – inhibits thrombin action – prevents clotting IV or SQ, antidote – Protamine sulfate 2. Warfarin sodium – inhibits Vit . K dependent clotting factor synthesis,  prothrombin activity - oral (10-15 mg/day) antidote – Vit . K

115. Mgt …… Fibrinolytics or thrombolytics – are useful for dissolving existing thrombus or clot when rapid dissolution of the clot is required to preserve organ and limb function Ex. Streptokinase, Urokinase IV side effect - bleeding Embolectomy – surgical removal of a blood clot, when large arteries are obstructed must be performed w/in 6-10 hrs. to prevent muscle necrosis and loss of the extremity

116. Venous Disorders alteration in the transport/flow of blood from the capillary back to the heart changes in smooth muscle and connective tissue make the veins less distensible with limited recoil capacity valves may malfunction, causing backflow of blood Virchow’s triad: blood stasis, vessel wall injury, and altered blood coagulation

117. Thrombophlebitis inflammation of the veins caused by thrombus or blood clot Factors assoc. with the devt . of Thrombophlebitis venous stasis damage to the vessel wall hypercoagulability of the blood – oral contraceptive use common to hospitalized pts. , undergone major surgery (pelvic or hip surgery), MI

118. Cont ….. Pathophysiology develops in both the deep and superficial veins of the lower extremity deep veins – femoral, popliteal, small calf veins superficial veins – saphenous vein Thrombus – form in the veins from accumulation of platelets, fibrin, WBC and RBC

119. Medical Management Superficial thrombophlebitis bed rest with legs elevated apply moist heat NSAID’s ( Non – steroidal anti-inflammatory drugs) - aspirin Deep vein thrombosis requires hospitalization bed rest w/ legs elevated to 15-20 degrees above heart level ( knees slightly flexed, trunk horizontal (head may be raised) to promote venous return and help prevent further emboli and prevent edema

120. Mgt Cont ……. application of warm moist heat to reduce pain, promotes venous return elastic stocking or bandage anticoagulants, initially with IV heparin then coumadin fibrinolytic to resolve the thrombus vasodilator if needed to control vessel spasm and improve circulation

121. Surgery if the thrombus is recurrent and extensive or if the pt. is at high risk for pulmonary embolism Thrombectomy – incising the common femoral vein in the groin and extracting the clots Vena caval interruption – transvenous placement of a grid or umbrella filter in the vena cava to block the passage of emboli

122. Assessment characteristic of the pain onset & duration of symptoms history of thrombophlebitis or venous disorders color & temp. of extremity edema of calf of thigh - use a tape measure, measure both legs for comparison

123. Varicose Veins are abnormally dilated veins with incompetent valves, occurring most often in the lower extremities usually affected are woman 30-50 years old. Causes : congenital absence of a valve incompetent valves due to external pressure on the veins from pregnancy, ascites or abdominal tumors sustained  in venous pressure due to CHF, cirrhosis Prevention wear elastic stockings during activities that require long standing or when pregnant moderate exercise, elevation of legs

124. Pathophysiology the great and small saphenous veins are most often involved weakening of the vein wall  does not withstand normal pressure  veins dilate , pooling of blood  valves become stretched and incompetent  more accumulation of blood in the veins

125. Clinical Manifestations Primary varicosities – gradual onset and affect superficial veins, appearance of dark tortuous veins S/ sx – dull aches, muscle cramps, pressure, heaviness or fatigue arising from reduced blood flow to the tissues Secondary Varicosities – affect the deep veins occur due to chronic venous insufficiency or venous thrombosis S/ sx – edema, pain, changes in skin color, ulcerations may occur from venous stasis

126. Trendelenburg test assess competency of venous valves through measurement of venous filling time the pt. lies down with the affected leg raised to allow for venous emptying a tourniquet is then applied above the knee and the pt. stands. The direction and filling time are recorded both before & after the tourniquet is removed * Incompetent valves are evident when the veins fill rapidly from backward blood flow

127. Surgical Intervention indicated or done for prevention or relief of edema, for recurrent leg ulcers or pain or for cosmetic purposes Vein ligation and stripping the great sapheneous vein is ligated (tied) close to the femoral junction the veins are stripped out through small incisions at the groin, above & below the knee and at the ankles. sterile dressing are placed over the incisions and an elastic bandage extending from the foot to the groin is firmly applied

128. Autoimmune disease

129. The immune system (IS) Main physiologic role: - primary role of IS is to discriminate self from nonself and to eliminate the foreign substance - finely tuned network that protects the host against forein antigens, particularly infection agents

130. Hypersensitivity 1) Exaggerated activity against environmental antigens (allergy) 2) Misdirected activity against host’ s own cells (autoimmunity) 3) Activity directed against benefitial foreign tissues, e.g. transfusion, transplants (isoimunity ) Hyposensitivity 1) Activity insufficient for protection of the body (immune deficiency) Main forms of inappropriate reactions of immune system

131. Cont …. Condition in which the body’s own immunologically competent cells or antibodies act against its self-antigens resulting in structural or functional damage Normally immune system does not react to its own antigens due to a protective mechanism called tolerance. Any breach in tolerance mechanisms predispose to several autoimmune diseases Mediated by two broad mechanisms: Central tolerance Peripheral tolerance

132. Central tolerance Refers to the deletion of self-reactive T and B lymphocytes during their maturation in central lymphoid organs (i.e., in the thymus for T cells and in the bone marrow for B cells ). In thymus : During the T cell development in thymus  any self-antigens are encountered  processed and presented by thymic antigen presenting cells (APCs) in association with self-MHC. Any developing T cell that expresses a receptor for such self-antigen is negatively selected (i.e. deleted by apoptosis).

133. Peripheral tolerance Back-up mechanisms that occur in the peripheral tissues to counteract the self-reactive T cells that escape central tolerance . Ignorance - Self-reactive T cells might never encounter the self-antigen which they recognize. Anergy : Defined as unresponsiveness to antigenic stimulus. The self-reactive T cells interact with the APCs presenting the self antigen, but the co-stimulatory signal is blocked. The B7 molecules on APC bind to CTLA-4 molecules on T cells instead of CD28 molecules.

134. MECHANISMS OF AUTOIMMUNITY Breakdown of T-Cell Anergy : In the presence of tissue necrosis and local inflammation express co-stimulatory molecules (B7) . Multiple sclerosis, rheumatoid arthritis and psoriasis Failure of AICD - Failure of the auto reactive activated T cells to undergo activation induced cell death (AICD) SLE (systemic lupus erythematosus)

135. MYASTHENIA GRAVIS A chronic, progressive autoimmune disease characterized by fatigue and severe muscle weakness of the skeletal muscles, that worsens with exercise and improves with rest Manifestations result from a loss of Ach receptors in the postsynaptic neurons of the neuromuscular junction

136. CLINICAL MANIFESTATIONS Primary feature: increasing weakness with sustained muscle contraction Ptosis (drooping of upper eyelid) Diplopia (double vision) Facial weakness (snarls when smiling) Dysphagia dysarthria

137. Weakness and fatigue Decreased function of hands, arms, legs, and neck muscles Weakening of intercostals Decreased diaphragmatic movement Breathlessness and dyspnea Poor gas exchange Inability to chew and swallow Decreased ability to move tongue

138. DIAGNOSIS Based on clinical presentation and response to anticholinesterase drugs TENSILON TEST

139. TREATMENT Anticholinesterase drugs Pyridostigmine ( mestinon ) Neostigmine ( Prostigmine ) Immunosuppressive therapy (corticosteroids) Plasmaphoresis Thymectomy

140. COMPLICATIONS Myasthenic crisis: caused by undermedication Sudden marked rise in B/P due to hypoxia Increased heart rate Severe respiratory distress and cyanosis Absent cough and swallow reflex Increased secretions, increased diaphoresis, increased lacrimation Restlessness, dysarthria Bowel and bladder incontinence

141. Cholinergic Crisis: caused by excessive medication Weakness with difficulty swallowing, chewing, speaking and breathing Apprehension N/V/D/abdominal cramps Increased secretions and saliva Sweating, lacrimation, fasciculations , and blurred vision

142. NURSING CARE Airway management Suction at bedside ABGs Endotracheal intubation if ventilatory support is needed Administer edrophonium chloride ( Tensilon ) to determine type of crisis Monitor electrolytes, I&O, daily weight Tube feeding if unable to eat

143. CEREBROVASCULAR ACCIDENT (CVA OR STROKE ) Neurological deficits occur as a result of decreased blood flow to a localized area of the brain. Risk factors: Hypertension Diabetes Mellitus CV disease, a-fib Hyperlipidemia Cigarette smoking, alcohol consumption, cocaine use Obesity

144. ISCHEMIC CVA Occurs when blood supply to a part of the brain is interrupted or occluded. Causes: Spasm: caused by irritation Thrombosis: platelets adhere to irregular plaque surfaces Embolism: traveling clot which becomes lodged in a narrow lumen

145. HEMORRHAGIC CVA Occurs in only 10 % of cases, usually women Results from rupture of a cerebral blood vessel that results in bleeding into the brain tissue or the subarachnoid space

146. CLINICAL MANIFESTATIONS H/A Vomiting Seizures AMS Fever ECG changes Manifestations related to area of injury

147. Motor deficits: Hemiplegia Hemiparesis Flaccidity Spasticity Rigidity Dysphagia Elimination disorders Bowel bladder

148. Sensory perceptual deficits Hemianopia Agnosia Apraxia Language disorders Aphasia Dysarthria Cognitive and behavioral changes Intellectual: memory and judgment changes

149. Right sided CVA Impulsive Over estimate their abilities Have decreased attention span Left sided weakness

150. Left sided CVA Slow, cautious, and disorganized Right sided weakness Spatial perceptual defects: denial of illness or non functioning body parts; erroneous perception of self; agnosia; apraxia

151. DIAGNOSIS CT MRI Doppler ultrasound Cerebral angiogram Lumbar puncture if not contraindicated

152. TREATMENT Acute phase (first 12 – 72 hours): If not hemorrhagic: anticoagulant Thrombolytics, if not hemorrhagic Calcium channel blockers Hyperosmolar solutions Diuretics Anticonvulsants Decadron Antipyretics

153. Monitor Neurologic Status LOC Pupilary response Movement, strength of extremities Babinski Decorticate/decerebrate posturing Changes in LOC

154. Monitor CV status Assess for fluid overload (rales, SOB, dyspnea) Fluid restriction (if CO is low, increase fluid based on ADH and aldosterone levels) Prevent thrombosis of lower extremities (ROM, antiembolic hose, pneumatic compression sleeves Monitor Neuro status Monitor temp (risk for hyperthermia Monitor for seizures (place on precautions)

155. Sensory perceptual Keep environment clutter free Well lighted environment Bed in low position Wheels locked Side rails up Keep needed objects of the unaffected side