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218 Cards in this Set
- Front
- Back
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Endothelial cells
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-form inner layer of blood vessels and veins
-maintain homeostasis of flow -keep blood in liquid form w/o allowing clots to form -secrete substances to control vascular tone |
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Smooth muscle cells
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relax and contract to control vascular tone
-help distribute blood to different organ systems -produces fibrous tissue ( forms matrix of blood vessels) |
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What are the 3 levels that blood vessels are divided in
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1. Intima
2.Media 3. adventita |
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Intima
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-thin
-predominately endothelial cells -may change character, and thicken with age and injury |
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Media
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-mainly smooth muscle cells
-organized into layers(particularly in arteries) * allows arter |
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adventita
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outtermost structure of the blood vessel
-acts as protective coat and is comprised mainly of fibrous tissue -nerve endings interact with blood vessels at this layer -location of vasa vasorum ( blood supply to nourish cells in the blood vessel) |
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Large arteries
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transport blood directly from the heart and distribute it to major blood vessels in circulatory system
-many muscle layers to absorb pulsatility and control flow -distribute into smaller arterial structures |
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arterioles
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-thin layer of smooth muscle cells and endothelial lining
-merge into capillaries |
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capillaries
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single layer vessel of endothelial tissue
-semi-permeable membrane -leak more fluid than gain back -excess fluid carried away by lymph system -blood in capillaries is low flow, low pressure system |
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Blood returns from organ systems into
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venules
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veins
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-no direct pulsatility or force
-blood propelled through veins by outside movements such as muscles groups -one way valves that maintain flow in direction towards heart -drain into great vessels that return blood to the right side of the heart |
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Primary difference between veins and arteries
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Veins have much less smooth muscle, so appear to be stiffer
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atherosclerosis
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-placement of lipoproteins on intimal layer of blood vessels
-cause white blood cells to aggregate/accumulate -tend to form plaques in branch areas that have more turbulent flow |
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Foam cells
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white blood cells evolve into macrophages that take up lipoproteins as foam cells
-can replicate once in artery and take up more lipid -more inflammation -smooth muscle cells migrate from media to intima |
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Risk factors for artherosclerosis
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Diet, smoking tobacco, high blood pressure, physical activity , weight, diabetes, alcohol, gender, chronic inflammation
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Coronary Artery disease
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-plaques build up and reduce total capacity of blood flow through the artery
-chest pain (exertional angina) - |
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myocardial infartion
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artery totally occludes due to ruptured plaque
-causes acute symptoms of MI |
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atherosclerotic carotid artery disease
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-built up plaques, remain asymptomatic
-stroke symptoms if flow is severely compromised -transiet ischemic attacks: last for short period * alternative cause could be ruptured plaque that ejects debris downstream into the brain capillaries * causes transient plugging of small arteries |
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Most prominent risk factors for carotid artery disease
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hypertension, smoking, diabetes, hypercholesterolemia
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Peripheral artery disease
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-plaques build up over time and are asymptomatic
-intermittent claudication: reduce blood flow to certain muscle groups -acute onset of pain , usually in form as cramp in calve or thigh -limbs mainly affected |
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Prominent risk factors for Peripheral artery disease
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-diabetes, smoking, high cholesterol
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aneurysms
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enlargement of an artery at least 50% of normal diameter
-generally not caused by plaque buildup -may be due to focal enlargement of artery or abnormal collagen formation that weakens the artery wall |
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aortic dissection
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tear of intimal layer of artery
-necrosis of medial layer -pts with aneurysms, inflammatory disease, and inherited diseases of collagen are more likely to have this |
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vasculitis
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localized disease of groups of arteries
-local inflammation of the artery ---> deterioration of vessel, bleeding, compromise of lumen -abnormal antibody and antigen formation diseases may be cause of inflammation |
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telangelectasias
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-localized dilations of small veins of the skin, loss of integrity of valves w/in veins
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varicose veins
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dysfunction of larger, superficial veins
-venous function deteriorates --> poor blood flow, swelling, clot formation - |
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Chronic venous insufficiency
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-disease of larger and sometimes deeper veins associated with poor flow and reflux
-failure of venous valves, stasis, edema, deterioration of skin, or ulceration of skin - |
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venous thrombosis
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altered blood flow(stasis), endothelial injury to artery or vein, presence of alterations in blood clotting system
-stasis and poor flow w/ reduced activity |
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One of most common places for plaques to develop
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larger arteries supplying blood to cardiac muscle
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Causes of angina
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-demand is increased, coronary flow is unable to deliver oxygen downstream of obstruction
-emotional upset or stress -disruption of previously stable arthersclerosis plaque |
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typical angina
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-patient develops pressure sensation, heaviness, deep pain in chest
-radiation of pain to arm, jaw, neck, shoulder, back -relief of stress causing pain = pain goes away( 5 min or less) |
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acute coronary artery disease
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-prolonged pain of 20 mins or greater usually results in permanent damage to artery ( necrosis of Myocardial tissue)
-acute coronary lesions from plaque rupture expose injured tissue--> attracts and activates platelets--> reduced flow due to aggregation of platelets---> triggers clotting cascade--> occlusion of artery--> MI |
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electrocardiogram
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-can indicate changes in ischemia through tracing
-often used in conjunction with a stress test -increases specificity and sensitivity from just symptoms |
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echocardiagram
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evaluate mechanical function of the heart in response to exertion
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Nuclear perfusion agent
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-taken up by heart muscle cells
-exercise-induced ischemic cardiac muscle cells do not take up -allows you to see differences in perfusion between normal and abnormal portions of the heart |
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angiogram
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direct imaging picture of coronary arteries
-shows exact location of blockages -allows for mechanical therapy such as placement of stents |
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valvular stenosis
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max opening of valve is reduced --> increased resistance to forward flow---> higher ejection pressures
- leads to pressure overload hypertrophy ( increase in size of left ventricle) |
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valve insufficiency
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valve looses ability to close tightly due to damage
-allows blood to flow in both directions -backflow of blood into chamber due to valve leak -output must be increased to maintain normal flow of blood -heart enlarges to accommodate more volume in chambers ( eccentric hypertrophy) |
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pressure overload
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causes walls of left ventricle to thicken
-chamber size stays normal -pump function preserved -increase in diameter and volume density of myocytes in wall of left ventricle |
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volume overload
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-from insufficiency of valve
-left ventricle responds with enlargement of chamber -myocytes lengthen in response to increased volume in chamber --> continue at normal levels of performance |
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rheumatic heart disease
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cause direct injury and inflammation to the valve
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Mechanisms of aortic stenosis
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-oxidized low density lipids, enzymes, macrophages-->growth factors and regulator proteins transform cells from fibrocytes to osteoblasts -->calcium nodules form --> stiffening of valve leaflet-->increases force to open valve--> stenosis
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exertional angina pectoris
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-substernal chest pain
-inadequate blood supply to portions of left ventricular myocardium during exercise -increase in workload and blood pressure causes higher oxygen demand that is not met |
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exertional syncope
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-fainting
-caused by 1) dilation of vessels w/o increase in flow and 2) reflex responses that respond to high pressures in left ventricle reflexes reduce contraction of heart-->vasodilation-->slow down heart rate -factors may cause sudden drop of pressure= fainting |
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heart failure
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impaired ability of heart to fill due to thickened walls
-cannot meet needed demand during exercise -ventricular stiffness causes blood to go back to lungs and leads to lung congestion |
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Treatment for aortic stenosis
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-none to make go away
-surgery to replace valve if little calcification -insert prosthetic device |
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etiology of mitral stenosis
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majority of cases caused by rheumatic heart disease
-leads to fusion of portions of leaflet and thickening of other areas, if progresses, calcium build up as well |
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Mitral stenosis
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-limits ability of left ventricle to fill
blood unable to pass w/o limitation to left ventricle -increase in pressure in left atrial chamber |
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cardiac dyspnea stage 1
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-pressure in left atrium rises, translated back to lung capillaries
-high pressure in capillaries causes fluid from blood to leak in interstitial space -lymphatic system evacuates blood back to bloodstream -lungs are more filled with blood and get shortness of breath |
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cardiac dyspnea stage 2
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-continued exercise causes pressures to continue to rise in capillaries causing greater fluid leak into interstitial space.
-lymphatic system cannot compensate and fluid builds up |
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cardiac dyspnea stage 3
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-pressure continues to rise
-interstitial space becomes full and fluid bulges around air sacs and invades them -air sacs collapse, no longer able to exchange gas -gasping breath, could lead to death |
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Mitral insufficiency etiology
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-any disease process that disrupts the functional anatomy of the mitral valve can cause it to leak
-rheumatic heart disease: scars leaflets and reduces size -mitral valve prolapse: oversized leaflets that do not close properly -diseases that cause papillary muscles or chordae tendinae to rupture |
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symptoms of mitral valve insufficiency
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-medical emergency
-shortness of breath -quickly go through stages of cardiac dyspnea -chronic insufficiency may show no symptoms until no longer to adapt |
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pulmonic stenosis
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most causes related to congenital heart problems
-tricuspid valve stenosis= rheumatic heart disease( less common) |
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tricuspid insufficiency
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occurs as secondary consequence of enlargement of right ventricular or right atrial chambers
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First heart sound, S1
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generated by deceleration of blood and closure of mitral valve
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Second heart sound S2
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generated by deceleration of blood and closure of aortic valve
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3rd heart sound
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-indication of disease state
-rapid filling of ventricle...abnormally large amount of blood or higher than normal pressure - |
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4th sound
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-indication of diseased state
-left atrium contracts and forces blood across mitral valve into left ventricle -makes a sound when at it's peak flow |
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heart murmur
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sound generated by turbulent blood flow
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bacterial endocarditis
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infectious source commonly low grade organism present in the flora or gastrointestinal system
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acute endocarditis
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-caused by more virulent organisms
-S. aureus or beta hemolytic streptococcal species -fast downhill progression -could lead to heart failure - |
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atrial septal defect
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a hole in the atrial septum dividing the two atrial chambers
-normally no communication between these two chambers -oxygenated blood needlessly passes back to lungs |
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ventricular septic defect
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-hole in ventricular septum that separates 2 ventricles
-shunt is from left to right -most produce loud murmur |
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ductus arteriosus
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communication between aorta and pulmonary artery in developing fetus
-allows blood to bypass lungs ( not developed yet) -results in failure of this vessel to close after birth |
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non-cyanotic heart disease
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when left to right shunt is only problem present
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cyanotic heart disease
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-flow across shunt lesion goes from right side to left side
-non-oxygenated blood is pumped into left sided circulation -results in reduction of oxygen saturation -usually more severe and common |
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tetralogy of fallot
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most common cause of cyanotic congenital heart disease
-results from 4 abnormalities 1.obstruction of outflow of blood from right ventricle 2.right ventricular hypertrophy 3. ventricular septal defect 4. abnormal positioning of the aorta |
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pericarditis
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inflammation of the pericardial sac
-commonly caused by viral infection in young -usually treated and resolved with anti-inflammatory meds - |
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pericardial effusion
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-fluid accumulates within pericardial space
-may be caused from persistence of viral pericarditis -other causes include severe infections such as Tuberculosis -usually runs its' course or ends when underlying problem is treated -if continues, get increased pressure in the pericardial sac and causes heart to be pushed inward and chambers ( particularly right side) may be reduced in volume |
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constrictive pericarditis
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chronic inflammation--> chronic fibrosis-->formation of shell around heart---> calcifies if left untreated
-constriction on heart, becomes less responsive to normal variation of filling, and chamber volume decreases -severely limits ability to exercise -treatment: removal of pericardium |
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primary cardiomyopathies
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-group of diseases where predominant disorder is caused by abnormality of myocytes and other structural elements of ventricular chamber
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secondary cardiomyopathies
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result of a response of myocytes to other disease processes
-ischemic heart disease is most common cause |
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Dilated cardiomyopathy etiology
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-etiology is failure of myocytes
-most common type of myopathy |
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Dilated cardiomyopathy Characteristics
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systolic dysfunction: cardiac muscle contracts less vigorously than normal. reduction in systolic performance of the ventricle, reduced pump capacity, reduced cardiac reserve---> loss of exercise capacity
Ventricular enlargement: neurohormonal system tries to maintain normal cardiac cardiac output and normal responsiveness to exercise. |
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Hypertrophic cardiomyopathy
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-unique disorder of the sarcoplasmic reticulum
-mutations in sarcoplasmic reticulum -genetic...autosomal dominant pattern -inappropriate hypertrophy is hallmark of disease process -asymmetry in development of hypertrophy -septum thickened, ventricular chamber reduced, left atrial chamber enlargement( persistent high filling pressures) -bizzare mycoadrial architecture called myocardial disarray( microscopic hallmark of disease process) |
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restrictive cardiomyopathy
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-stiffness and non compliant during relaxation and ejection beats
-caused by diseases that cause abnormal material to be stored between the heart muscle cells. -production of protein called amyloid in West is common cause -abnormality of diastole or filling -takes more pressure to fill heart |
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arrhythmogenic right ventricular cardiomyopathy
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predominant problem is in right ventricle
-myocytes replaced with fatty tissue, resulting in enlargement, reduced function, fatal arrhythmias |
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heart failure
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result of structural or functional disorders that impair the ability of the heart to fill or eject blood to meet cardiac output needs of body
common symptoms: dyspnea( SOB) and fatigue, fluid retention |
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Diuretics
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-Do not prolong life in chronic heart failure
-eliminate congestion and fluid overload |
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ACE I and angiotensin receptor blockers (ARB)
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reduce excessive stimulation of renin angiotensin system
-help reduce congestion and increase output -reduce likelihood of cardiac fibrosis and enlargement - improve survival and reduce hospitalizations |
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beta blockers
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inhibit excessive stimulation of catcholamine system in HF
-improve survival, reduce sudden death, improve function and over time reverse some of remodeling that occurs -affect changes at myocyte level -powerful when combined with ACE I |
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digoxin
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weak stimulant
-causes modest increase in pump performance -reduction in symptoms, but no effect on mortality |
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aldosterone antagonists
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-neurohormone inhibiting drug
-inhibits excessive levels of aldosterone in the circulation -reduces amount and tendency of myocytes to hypertrophy or the fibrocyte to hypertrophy -have anti-remodeling effect |
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pumps
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-called left ventricular assistance devices
-placed in series with left ventricle of heart |
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acute kidney injury
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any process that happens rapidly ( hours to days) that prevents clearance of waste products from the blood
-loss of the steady state -reversible |
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oliguric
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when urine output is less than 500 cc a day
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anuric
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patients urine output is less than 100 cc a day
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azotemia
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build of nitrogenous waste products in the blood
-detected by rise in BUN -look at serum creatine( builds up if kidneys not functioning properly and better indicator than BUN) |
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uremia
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build up of waste products as a result of kidney dysfunction
-fatigue, lassitude, nausea , etc -neuropathy, pericarditis, -indication for dialysis |
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Causes of acute kidney injury
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-low blood flow to kidney,
-blockage so urine cannot flow properly -issues in glomeruli, tubules, or interstitium -in elderly, prost |
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Acute interstitial nephritis -AKI
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-represents inflammation of the interstitium(space between the tubules)
-caused by infections, auto immune diseases, medications that elicit hypersensitivity reaction -WBCs in urine |
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glomerulonephritis-AKI
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-inflammation of the glomeruli
-blood and protein in urine -caused by immune complex etiologies ex post streptococcal GN -non immune complex mediated ex Wegener's granulomatosis |
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Acute tubular necrosis-AKI
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continuum of hypo perfusion and ischemia
-supply of oxygen and nutrients to kidney nutrients and tubules is insufficient to meet metabolic demands ex septic shock |
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How long does kidney damage need to be present to be classified as chronic
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more than 3 months
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Stage 1 CKD
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kidney damage with normal or increased GFR> 90 ml/min
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Stage 2 CKD
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kidney damage with midely decreased GFR 60-89 ml/min
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stage 3 CKD
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kidney damage with moderately decreased GFR 30-59 ml/min
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stage 4 CKD
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kidney damage w/ severely decreased GFR 15-29 ml/min
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stage 5 CKD
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kidney failure GFR < 15 ml/min or dialysis/ transplantation
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What leads to loss of functional nephrons in the kidney
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destruction of glomeruli or renal tubules
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How does renal tissue adapt?
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undamaged nephrons takes on more of workload and maintains body's balance of salts and water.
-adaption can occur until less than 20% of normal nephrons left |
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uremic syndrome
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-kidneys no longer able to maintain a balance
-waste products of metabolism accumulate and alter the function of normal |
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Symptoms of uremia
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fatigue, increased irritability, difficulty breathing & concentrating, nausea, loss of appetite, itching, fluid retention
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typical signs/ altered lab values are
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hypertension, peripheral edema, anemia, acidosis, low serum calcium, high setup phosphate and or potassium, high levels of nitrogen waste in the blood such as urea
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Medications that protect kidney
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ACE-inhibitors and ARBs( angiotensin receptor blockers)
-help lessen back pressure on glomerulus at level of efferent arterioles -lessened pressure helps alleviate hemodynamic stress in glomerulus ---> can slow disease progression over time |
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Most common causes of CKD in descending order
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diabetes mellitus, hypertension, glomerular diseases and polycystic kidney disease
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Complications stage 1 CKD
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none typically present
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complications of CKD stage 2
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high blood pressure due to CKD and or mild lab abnormalities such as anemia
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Complications CKD stage 3
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high blood pressure and lab abnormalities more consistently found, clinical symptoms such as edema or fatigue
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complications stage 4 CKD
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lab abnormalities and high blood pressure become more common, clinical symptoms more present
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Proteinuria
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the major risk factor for progression of CKD and independent risk factor for cardiovascular events ACE inhibitors and ARBs help reduce proteinuria and slow progression of protein uric CKD
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pyelonephritis
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inflammation of the kidney, particularly due to bacterial infection
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Routes of infection of pyelonephritis
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1. Hematogenous- uncommon, seen in endocarditis or septicemia, Staphylococcus or some fungi
2. Ascending- more common |
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Clinical presentation of acute pyelonephritis
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fever, costovertebral angle pain, dysuria( painful urination), frequency, urgency
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Risk factors for pyelonephritis: Gender and age
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infants-mostly boys
infancy-40 y.o. mostly girls/ women beyond age 40 men and women -urinary obstruction -neurogenic bladder: improper filling and emptying of bladder due to abnormal function of nerves -instrumentation of bladder(catheter) -pregnancy -diabetes -immunosuppression -vesicoureteral reflux( shortening of urethra) |
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Most common organisms
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E.Coli - about 85% of infections
- Proteus sp, Klebsiella sp, Enterobacter sp- normally found in GI -S. epidermidis, Enterococcus- skin organisms -Mycoplasma sp- may be seen in patients with catheters |
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Urinalysis of pyelonephritis
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cloudy urine, pyuria(white blood cells in urine), hematuria(red blood cells in urine), proteinuria, high pH, leukocyte cast
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Leukocyte cast
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formed when white blood cells are present in large numbers within renal tubules--> stick to each other and form cylindrical shape
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Signs of acute pyelonephritis
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-neutrophilic inflammation of renal tubules and the spaces between them
-may form abscess -glomeruli usually Uninvolved, except in advanced cases |
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What happens after the acute phase of pyelonephritis
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replacement of neutrophils by macrophages, plasma cells, and lymphocytes
-fibrous scar that involves underlying calyx and pelvis - most cases due to ascending infection |
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Signs of chronic pyelonephritis
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important cause of end stage renal disease
-small, shrunken kidneys -scarring on surface tubular dilation and atrophy -chronic inflammation |
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cyst
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fluid filled cavity with an epithelial cell lining
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Cystic Kidney Disease: simple cyst
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very common at any age
-multiple, thin walled cysts on surface of kidney -microscopically: cyst lined by flat epithelial cells -usually asymptomatic w/ no complications |
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Cystic Kidney Disease: Autosomal Dominant Polycystic Kidney Disease= Adult Polycystic Kidney Disease
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fairly common( 1/400 to 1/1000 live births)
-autosomal dominant -always bilateral w/ loss of renal fxn in 30s or 40s -may be asymptomatic prior to kidney failure, hematuria, pain due to pressure or passage of blood clots |
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Signs of Adult Polycystic Kidney Disease
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-kidneys become enlarged
-hundreds of cysts( epithelial lined) -fibrotic tissue in between cysts |
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Pathogenesis of Adult polycystic kidney disease
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-PKD1 gene accounts for 85% of cases
-PKD2 gene accounts for 15% -overactive proliferation of tubule cells, overactive secretion of fluid, fibrosis of space between tubule cells |
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Clinical outcome and complications of adult polycystic kidney disease
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-10% of all renal failure pts have this
-intracranial aneurysms, mitral valve prolapse, asymptomatic cysts in other organs(mainly liver) |
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Autosomal Recessive Polycystic Kidney Disease= Childhood Polycystic Kidney Disease
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-rare (1/4000 births)
-autosomal recessive -always bilateral -renal failure in infancy and childhood |
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Signs of Childhood Polycystic Kidney disease
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enlarged kidneys with smooth surface
-hundreds of cysts originating in distal tubules and collecting ducts -cysts are lined by cuboidal cells |
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Pathogenesis of Childhood Polycystic Kidney Disease
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-mutations of PKHD1 gene( encodes protein fibrocystin)
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clinical outcome and complications of Childhood Polycystic Kidney disease
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-usually cysts on liver
-child may develop liver fibrosis and failure |
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Transplantation
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process of removing cells, tissues, or organs( graft) from an individual and placing back into same or another individual
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orthotopic transplantation
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graft is transplanted into its usual anatomical location
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heterotopic transplantation
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graft is transplanted into a site other than its usual anatomic location.
ex transplanted kidney placed into lower abdomen rather than usual location |
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autologous transplantation (autograft)
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graft is transplanted back into the same individual
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allogeneic transplantation ( allograft)
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graft is transplanted into a genetically different individual of the same species
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syngeneic transplantation
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graft is transplanted into a genetically identical individual
ex: transplant between identical twins |
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xenogeneic transplantation ( xenograft)
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graft is transplanted between individuals of different species
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Hyperacute rejection
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-graft turns pale and fails
-due to pre-existing antibodies in the recipients blood stream---> recognize proteins in graft as foreign--> causes graft to become ischemic and fail(b/c binding occurs in blood vessels) |
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Acute Rejection
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capacity of T-cells to discriminate between cells from self and non-self
-MHC or HLA(in humans) unique to each individual...T-cells have specific receptors for each one -foreign MHC recognized as non self and targeted for destruction -highest risk is about 3 months after transplant |
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Chronic Rejection
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- T cell mediated
-response leads to chronic inflammation in the graft -chronic inflammatory state activates tissue repair mechanisms that result in scarring and fibrosis of graft |
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Reducing graft rejection
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1. immunosuppression of host by drugs
2. minimizing immunogenicity of graft by minimizing differences in blood type antigens(ABO matching) and MHC patterns (HLA matching) between graft and host |
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Classes of drugs given to suppress immune system after transplantation
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cyclosporines, corticosteroids,
antiproliferative agent- inhibit DNA replication in dividing cells--> prevents proliferation of activated T cells, but effects not specific to T cells, prevent all cells from proliferating and effects bone marrow where blood cells produced |
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Important viral infections that affect transplant recipients
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EBV----> malignant lymphoma
CMV--> graft dysfunction and immunosuppresion BK--> kidney graft failure |
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Fungal infections seen in immunosupressed patients
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-pneumonia secondary to pneumocystis jiroveci
-meninigitis due to Cryptococcus neoformans -soft tissue abscess due to Nocardia -tissue destruction due to Aspergillus |
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Immunosuppression and cancer
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Immunosuppression increases risk for cancer
-primarily skin cancer and lymphoma - |
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Post transplant lymphoproliferative disorder
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when lymphoma develops in a transplant recipient
-most common in small bowel transplants -likely due to EBV and immunosuppression |
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Bone marrow transplant (allogenic)
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-replaces native B & T cells w/ B&T cells derived from graft
-recognizes host as foreign and attacks (GVHD graft versus host disease) *mostly affects skin, mucosal lining to GI, liver |
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Pituitary gland : anterior lobe
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aka adenohypophysis
--comprises 80% of gland -derived from ectoderm of fetus -corticotropes are cells that secrete ACTH--> stimulates adrenal glands -lactotropes secrete prolactin-->causes milk production -somatotropes secrete growth hormone -thyrotropes secrete TSH -gonadotropes secrete FSH |
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Pituitary gland: posterior lobe
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-does not make hormones
-stores hormones -oxytocin and vasopressin are made in the hypothalamus and secreted from pituitary |
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hypopituitarism
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deficiency of one or more pituitary hormone
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panhypopituitarism
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deficiency of all pituitary hormones
-caused by tumor, infarction, surgery, radiation, trauma, disease, or genetic syndromes |
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benign craniopharyngioma
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common pituitary tumors in childhood
-congenital cyst like tumor that causes symptoms by pressure and destroying some or all hormone producing cells in pituitary |
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diabetes insipidus
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-pituitary disorder
-caused by vasopressin deficiency -cannot concentrate urine and drink water constantly |
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nontoxic goiter
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enlarged thyroid that is not hypo functioning or hyper functioning .
-adolescence, pregnancy, viral or autoimmune thyroiditis |
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hypothyroidism
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underproduction of thyroid hormones
-may occur with or without a goiter -caused by congenital lesions, hashimoto thyroiditis, surgery, viruses, drugs such as lithium |
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symptoms of hypothyroidism
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bradycardia, constipation, cold intolerance, dry skin, hair loss, and edema
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Hashimoto thyroiditis
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autoimmune thyroid disease
-common in families with autoimmune diseases and in children and adults with down's syndrome -lymphocytic destruction and circulating antibodies -Pathology: lymphocytic infiltrates, gland destruction, and metaplasia of follicular epithelial cells |
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hyperthyroidism
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over production of thyroid hormone
-Graves disease(autoimmune) *antibodies bind to TSH receptors on thyroid and stimulate thyroid hormone production * more common in females and down syndrome -Pathology: enlarged gland w/ hyperplastic and hypervascular appearance |
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parathyroid glands
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usually located on back of thyroid gland.
-4 to 12 glands that secrete parathormone to control calcium metabolism |
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hypoparathyroidism
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-caused by decrease PTH secretion that leads to low calcium levels
-Symptoms: cramps, seizures, tingling, stridor -Causes: surgery, autoimmune disease and congenital syndromes of absence of parathyroid glands |
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hyperparathyroidism
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caused by excess PTH production causing high Ca++ levels
-symptoms: kidney and pancreatic duct stones, psychiatirc illness and abdominal pain -causes: benign tumors, cancer, or hyperplasia of parathyroid glands |
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adrenal cortex: congenital adrenal hyperplasia
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-genetic
-missing enzyme in adrenal cortex pathway--> cortisol deficiency --->body produces high levels of ACTH--> enlarged adrenal gland and overproduction of unneeded hormones( androgens and sex hormones -most common form is 21-hydroxylase deficiency --> salt wasting and ambiguous genitalia in girls and salt wasting in boys |
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Addison disease
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adrenal cortex insufficiency
signs and symptoms: hypoglycemia, vomitting, weight loss, shock, low sodium and high potassium -life threatening, must be treated with glucocorticoids immediately( prednisone, hydrocortisone, dexamethosone) |
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cushing syndrome
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-excess adrenal cortex hormones
symptoms due to excess cortisol -can be caused by adrenal tumors, taking large doses of prednisone, hydrocortisone, or dexamethasone -signs: obese trunk w/ thin arms and legs, purple striae on abdomen, thinning of skin, hypertension, osteoporosis |
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cushing disease
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excess adrenal cortex hormones are result of pituitary overproduction of ACTH
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autoimmune polyglandular syndromes (APS)
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-3 different kind exist
-autoimmune disease result of destruction of endocrine glands by antibodies and lymphocytic damage -result in hypo function or hyper function of endocrine glands |
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APS 1
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triad of Addison disease, hypoparathyroidism, and mucocutaneous canidiasis( skin and mucous membrane infection )
-autosomal recessive defect in Chromosome 21 in AIRE gene |
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APS 2
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Addison disease + diabetes mellitus type 1, thyroid disease( Hashimoto or Grave's) and or pernicious anemia
-involves HLA antigens |
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APs 3
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type 1 diabetes + autoimmune thyroid disease
-occurs in about 20% of people with diabetes type 1 |
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T or F: When one autoimmune is diagnosed in a patient, you must screen for other autoimmune diseases
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True!
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Type I Diabetes Melitus
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aka insulin dependent or juvenile onset( peak incidence of less than 20 years)
-loss of >80% insulin producing beta cells -95% have HLA alleles -coud be caused by vacor, alloxan, streptozotocin, and cyclosporine drugs |
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pathology of type I diabetes
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lymphocytic infiltrate around islets. contains macrophages and neutrophils that gradually disrupt islet architecture
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Type II diabetes
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-insulin resistance
-beta cells don't meet the demands of the body, but insulin levels can still be normal or high -most common after age 40, but occurs in childhood |
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Defect in type II diabetes
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impaired insulin secretion and decreased insulin uptake
-deficiency of GLUT-2 in beta cells( disrupts how beta cells sense and respond to glucose) |
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gestational diabetes
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-especially seen in women predisposed to diabetes 2
-controlled w/ diet or insulin -leads to very large infants w/ hypoglycemia, jaundice, respiratory failure, or calcium problems if untreated |
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steroid induced diabetes
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-occurs in some patients on high dose glucoccorticoids such as prednisone
-treated w/ insulin until steroid lowered or D/C |
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Other causes of diseases
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chemotherapy
-chronic diseases such as cystic fibrosis, hemachromatosis, damage of islets |
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complications of diabetes
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- caused by severity and chronicity of hyperglycemia
-early diagnosis critical for type 2 diabetes -atherosclerosis, diabetic nephropathy, neuropathy, retinopathy, infection |
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langerhans cells
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-reside in outter layer of skin
-present foreign antigen derived from intruders to immune system |
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1st degree burns
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only epidermis is damaged. redness and mild pain
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2nd degree burns
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injury extends into or through the dermis. results in blister and pain
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3rd degree burns
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injury extends through the dermis and into the subcutis. Charred skin and little pain
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4th degree burns
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injury extends beyond the subcutis to underlying muscle or bone
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burn shock
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burn patients develop this: immediate systemic inflammatory response to burn injury
-vessels adjacent to burnt skin dilate and become permeable-->fluid & heat loss -vessels going to organs constrict-->ischemic, organ damage--> kidney fxn drops, impaired heart contractility, bowls ischemic and more prone to bacteria and infection -bronchoconstriction |
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pemphigus vulgaris
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-autoimmune disorder
-antibodies destroy a protein that keeps squamous cells of epidermis stuck together -blisters, exposed dermis -loss of fluids, eroded surfaces let in infectious organisms -treatment is immunosuppressive drugs |
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Staphylococcal scalded skin syndrome
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-caused by toxins produced by staphylococcal bacteria
-->cause sloughage on top of epidermis -usually affects babies and immunocompromised people -skin sloughage can lead to fluid loss -treatment directed to underlying infection |
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toxic epidermal necrolysis
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reaction to certain drugs(sulfonamides, PCN, ASA, APAP, phenytoin, valproic acid)
-skin and mucous membranes of oral cavity and gastrointestinal tract are affected -sloughage of epidermis and mucous membranes -treatment: stopping drug, reversing process, and electrolyte imbalance |
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Melanoma
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malignant neoplasm that arises from melanocyte of epidermis
-related to sun exposure, arises in younger population and spread widely throughout body -black growth |
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nevus
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collection of cells that are present in an unusual location or in excessive number
-melanocytic nevus: collection of benign melanocytes at base of epidermis and or in dermis |
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ABCDE criteria of Melanoma
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A-assymetry. Lesions not mirror images
B-border irregularity C-color. not uniformly black. can be mixtures of red, brown, black, blue, white D-Diameter> 6mm E-evolution or change in size, color, or border over time |
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Most prognostic factors of melanoma
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-thickness( how far it penetrates into dermis) and whether or not it is ulcerated
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important predictive factors of melanomas
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lymph node metastases and distant metastases
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Acne vulgaris
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caused by infection of plugged sebaceous glands
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cellulitis
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infection of the skin caused by staph or streptococcal baceria
-can result in skin necrosis, bacteremia, and septic shock |
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albinism
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-genetic skin disease
-autosomal recessive disorder--> involves genes controlling production or transportation of melanin |
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dermatitis
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inflammation of the skin--> reaction pattern to causes of inflammation
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Psoriasis
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autoimmune disease in which T cells stimulate rapid production of squamous cells--> not sloughed at same rate produced
-thick scales, itchy |
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acute mastitis of breast
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-almost exclusively in lactating women in first several months of post pardum
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pathogenesis of acute mastitis in breast
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-occurs in presence of milk stasis ( obstruction of a milk duct)
-could be from poor positioning of infant, skipped feedings, tight bras, etc -milk accumulates in breast and potentially released in surrounding breast tissue--> inflammatory response -could lead to bacteria growth primarily by staph or strept -could result w/o stasis if bacteria entered through cracked or damaged nipples |
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clinical presentation of acute mastitis in breast
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pain, tenderness, swelling, redness,and warmth of breast as well as low grade fever and malaise
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microscopic findings of acute mastitis in breast
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-biopsy rarely done, if done shows necrotic breast tissue w/ many neutrophils
treatment: drainage of milk from breast, antibiotics, warm compress complications: may progress to abscess |
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duct ectasia
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large ducts near the nipple become dilated
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epidemiology of duct ectasia
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older women who have multiple children
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clinical presentations of duct ectasia
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nipple discharge and nipple retraction. fibrosis around dilated ducts, sub areolar mass, mimicking carcinoma
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microscopic findings of duct ectasia
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dilated ducts surrounded by chronic inflammation, become filled with macrophages and debris
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fibroadenoma
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benign tumors of the breast composed of proliferating stromal and epithelial cells
-usually in women 20s-30s |
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pathogenesis of fibroadenoma
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usually present in women of child bearing age--> response to estrogen stimulation in tissue
-polyclonal proliferation of cells |
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clinical presentation of fibroadenoma
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mobile, round mass less than 1cm to around 4cm , occasionally much larger
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microscopic findings
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round, or lobulated lesions composed of spindle cell stroma with slit like spaces lined y epithelial cells
benign so no treatment needed |
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Fibrocystic change
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-occur more commonly in pre menopausal women
-mass formation, calcification, mamographic abnormality |
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Risk factors for breast cancer
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gender
Age-rare before 25 y.o., risk increases with age Genetic factors-family history, BRCA 1 or 2 mutation Estrogen exposure- high levels, post-menapous Radiation exposure- |
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invasive carcinoma
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cancer cells invade beyond normal confines of ducts, and spreads by lymphatic channels
-usually forms mass lesion |
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prognostic factor: stage
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tumor size, lymphatic spread(curable), distant metals( incurable)
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prognostic factor: grade
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assigned based on how abnormal cells look, not as powerful prognosis as stage
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common sites of metastasis
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auxillary lymph nodes
-distant metastasis *lungs, bones, liver, adrenals, brain |
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immunohistochemical assays
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apply antibodies against an antigen of interest. if the antigen is there , will bind to it. color bound so can see where antigen of interest is
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