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BIO 235 FINAL
YOU CAN DO IT. I BELIEVE.
| Question | Answer |
|---|---|
| What are the three tunics of the artery wall? | Adventitia, media, interna |
| What is included in the adventitia? | the vaso vasorum and nerves |
| What is part of the media? | external elastic muscle and smooth muscle |
| What is part of media? | lamina propria, basement membrane, endothelium, internal elastic membrane |
| Which part of the artery is most affected by atherosclerosis? | The tunica media and intima -> changes in smooth muscle and endothelial cell lining of the endothelium, basement membrane |
| What is atherosclerosis? | hardening of paste or mushy texture if the inside lining of the blood vessels; fatty deposits and inflammation of the intima, gradual hardening of deposits into plaqu |
| What might atherosclerosis cause? | heart disease, renal failure, stroke |
| What is atheroma? | a focal hardening of the tunica intima |
| What happens in atheroma? | deposition of lipid and CT, proliferation of smooth muscle cells, progressive reduction in lumen diameter and vessel elasticity |
| What are risk factors for atherosclerosis? | men, postmenopause, family, tabacoo, ^fat, ^alcohol, ^salt, obesity, ^stress, low exercise, diabetes, systemic hypertension |
| Why is obesity a risk factor for atherosclerosis? | fats accumulate in adipose cells causing release of proinflammatory cytokines that are similar to having an infection, the tunica intima responds and plaque builds up |
| Why might diabetes be a risk factor for atherosclerosis? | hyperinsulinemia/hyperlipidemia cause an increase in LDL; hyperglycemia cause glycation of LDLs & basement membrane of arteries |
| How is atherosclerosis developed? | LDL accumulation > Fatty streak > Plaque formation |
| What happens when LDL accumulates | LDL undergoes chemical changes and signals the endothelial cells to latch onto WBC ciculating in the blood. These immune cells penetrate the intima and trigger an inflammatory response, devouring LDLs to become fat-laden foam cells |
| What is happening when fatty streaks are appearing in the artery? | focal proliferation of smooth muscle, lipid accumulates in these cells causing yellow colouring, asymptomatic |
| What happens in the plaque phase? | plaque continues to grow and forms a fibrous cap, substance released by foam cells may destabilize the cap, allowing it to rupture, causing a blood clot which can block blood flow and trigger a heart attack |
| At what point does a fatty streak turn into a plaque? | when it starts to push and occlude |
| What are complications of lesions? | calcium deposit build up in plaque from inflammation process; thrombosis causing ischemic heart attack, stroke; emboli |
| When foam cells release proteolytic enzymes causing a destabilization of the fibrous cap, what is released? What does this do? Why is the fibrous cap so dangerous? | Tissue factors are released; these a blood clotting factors that initiate thrombin formation; fibrous cap is dangerous because it not only occludes, but also releases enzyme that ^ formation of blood clots |
| What factors may initiate atherogenesis? | Injury, increased permeability of endothelium, Diet, smoking, obesity, homocysteine |
| What causes injury to the endothelial lining? | stretch and recoil of pressure pulsations, turbulence at branch points, inflammation from infections and obesity, hypertension, toxic agents |
| What toxic agents injury the endothelial lining? | smoke and environmental pollution |
| How do toxic agents cause injury to the endothelial lining? | Carbon monoxide creates ischemia by reduction the amount of bound O2 in vessels; This causes vascular spasm which constricts smooth muscle & reduces blood flow, increased LDL intake into intima, ^platelet aggregation |
| How does ASA reduce the risk of a thrombus formation? | anti-inflammatory action reduces formation of plaque; ASA inhibits thromboxina A2 (TA2) which increases platelet aggregation |
| What increases the permeability of the endothelium? | platelet and monocy aggregation, adherence to the injury site, release of growth factors and cytokines into the tunica intima |
| What growth factors and cytokines are released into the tunica intima? What does this do? | platelet-derived growth factore, IL-1, CRP; ^monocyte (precursor of macrophage) migration, ^ lipid uptake by the endothelium, stimulates cholesterol synthesis by the smooth muscle |
| How is CRP involed in atherosclerosis? | it is a marker of inflammation and is released by the inflammatory cells in the plaque |
| What type of diet is an increased risk of atherogenesis? | hyperlipidemia |
| What is the optimum total plasma cholesterol? | < 5.1mM (<200mg/dl) |
| What is the optimum triglyceride intake? | 15-35% of total daily calories |
| What does a typical lipid look like? | 3 fatty acids attached to one glycerol |
| What transports cholesterol and lipids in the blood? | lipoproteins |
| Which one is bad, LDL or HDL? | LDLs |
| What do LDLs do? | they carry lipids to all tissues, glands, and arterial endothelial cells; thus, they deposit cholesterol and lipids into foam cells |
| What is the relationship between LDL and coronary heart disease? | more LDL, more foam cells, more risk CHD |
| What is the optimum LDL level? | <4.1mM (160mg/dl) |
| What do HDLs do? | HDLs remove excess cholesterol and lipid from adipose cells |
| What is the relationship between HDL and coronary heart disease? | low HDL, more risk |
| What is the optimum HDL level? | >1mM (40mg/dl) |
| Which fat is better, saturated or unsaturated? | Unsaturated fat |
| What are saturated fats? | straight chains of carbon atoms linked by single covalent bonds; these easily form plaque |
| What are unsaturated fats? | carbon chains with a variable amount of double bonds; these are less likely to form plaque |
| What are cis bonds? | hydrogens are on the same side, thus, kink the chain -> these are better |
| What are trans bonds? | straight chains which easily stack up |
| What are PUFA? What do these have? Where can we get these? Which type of PUFA is food, which is bad? | poly unsaturated fatty acids; these have may double bonds; seen in corn oil (omega-6) and olive oil/fish oil (omega-3); omega 3 is good, omega 6 is bad |
| What does omega 6 do? | breaks down and form leukotrienes and prostaglands (PGs) which are made from lipids in membranes of our cells -> they ecentuate proinflammatory cytokines |
| What damages LDLs? Why is this process bad? What can stop oxidation? | LDLs are damaged by oxidation; oxidized LDLs are more rapidly taken into macrophages to create foam cells, also are proinflammatory and release cytokines so more monocytes invade; oxidation can be prevented by antioxidants and HDL |
| What is the relationship between vitamins and oxidized LDL? | high diet in vitamin = low oxidized LDL = less LDL in BV tissue |
| What are examples of anti-oxidants? | vitamin E, C, B-complex, betacarotene |
| What does smoking cause in the cell? | smoking causes the synthesis of endothelial cell monocyte-chemotatic protein |
| What does monocyte-chemotactic protein do? | ^ migration of monocytes into tunica intima, increases inflammation of vessel |
| Besides fats, what other dietary factorrs increase the risk of atherosclerosis? | alcohol, salt |
| Approximately how many people are obese? | 15% |
| How does losing weight reduce risk? | it lowers LDL, cholesterol, diabetes, and HTN |
| What is homocysteine? What does it do? | a metabolic derivative of an amino acid; it promotes blood clot formation and possibly damages the endothelium but promoting LDL* and inhibiting Tissue plasminogen activator |
| What does tissue plasminogen activator do? | breaksdown clots |
| What does atherosclerosis do to large vessels? | atherosclerosis weaks the wall of large vessels causing a bulging or aneurism which is at risk of a rupture OR can cause dissecting aneurism |
| Where are atherosclerostic aneurisms common? | common at the aorta because of the high pressures |
| How are areteriosclerotic aneurisms diagnosed? | by ultrasound |
| How are arteriosclerotic aneurisms treated? | treated by grafted bypass via open surgical repair graft or endovascular repair graft |
| What is a dissecting aneurism? Why is this bad? | large vessels with multiple layers of tunica media; the layers separate and can fill with blood; risk of blood clot formation withing vessel wall and impairs flow throgh vessel |
| What is heart disease mostly related to? | Cardiac Output |
| What are different types of CO defects? | changes in blood volume, blood composition changes, ventricular pumping problems, structural defects in the heart |
| What are causes of a change in blood volume? | dehydration, hemorrhage |
| What are causes of blood composition changes? | anemia |
| What are causes of ventricular pumping probles? | congestion of venous blood - decreased pre-load |
| What are different structural defects in the heart? | ASD, VSD, Coarctation (narrowing) of major arteries, patent ductus arterious, valvular stenosus, regurgitation, prolapse, tetralogy of fallot, transposition of great arteries |
| What is tetralogy of Fallot? | ventricular septal defect, pulmonary stenosis, malformed aorta (enlarged), hypertrophy of right ventricle |
| What is meant by transposition of great arteries? | pulmonary artery and aorta are revered |
| What is the foramen ovale? | the hole between the septum of the atria; creates an ASD shunting |
| What is a left to right ASD shunt? | pulmonary venous return flows into the right atrium instead of the left; increases the preload on the right side; right ventricle will hypertrophy to deal with the extra blood |
| When does a right to left ASD shunt occur? | in cases of increased afterload on the right (ex. COPD); will increase pressure in the right atrium and ventricle d/e ^resistance in lungs; ^cyanosis due to blood by-pass of pulmonary circulation |
| What is a patent ductus artereosis? | the hole between the aorta and pulmonary artery |
| What is the definition of Heart failure? | the failure of the pumping function of the heart |
| What are causes of Heart Failure? | myocardial diseases, valvular heart disease, |
| What are tyes of myocardial diseases? | cardiomyopathy, myocarditis |
| What is a myocardial disease? | a disease of heart muscle |
| What is cardiomyopathy? What are the different types? How is treated? Which is more common? What are other causes? | an inherited condition; hypertrophy and dilation of the ventricles; hypertrophic tx by betablockers, ACEI, surgery to remove excess tissue in septum (decreases workload of heart); dilated more common and can be caused by ischemia, ETOH, drugs, infections |
| What is myocarditis? What is the usual cause? Is this resolved? How? | inflammation of the myocardium; usually d/t viral infections; yes, resolved with rest and treatment |
| What are causes of valvular heart disease? | rheumatic fever, infective endocarditis |
| What is a cause of rheumatic fever? What does this cause in the heart? | Group A streptococcus/strep throat; can cause hypersensitivity to subsequent infection, scarring or heart murmur |
| What are two types of infective endocarditis? What are causes of each? What might be presecribed? What might happen to the heart? | Subacute infection vs Acute infection; Subacute infection can result from dental procedures, prophylactic abx to prevent; Acute infaction from a staph. aureus infection can cause "vegetations" on heart valves, stenosis regurgitant valves. |
| What is congestive heart failure? | HF accompanied by systemic or pulmonary venous congestion |
| What is the pathophysiology of congestive heart failure? | a combination forward failure and backward failure |
| What is forward failure? | poor perfusion of kidneys > retention of salt and water in blood > increased blood volume |
| What is backward failure? | inadequate CO causes retention of blood in venous circulation, increase venous pressure, edema |
| What happens in right side failure? | pumping into the pulmonary circulation is restricted causing an accumulation in the systemic circulation |
| What are signs of right side HF? | edema in lower limbs when upright when upright; edema in sternal, head & neck when supine; impaired digestion, abdominal discomfort, liver failure; weight gain due to fluid accumulation > 2lbs/2 hours |
| What happens in left side failure? | pumping into systemic circulation is restriced (decreased CO) causing an accumulation of blood in pulmonary circulation (pulmonary edema) |
| When is left sided HF most prevalent? | occurs most often at night when patient is reclining; fluid in limbs is redistributed |
| What are manifestations of CHF? | depends on balance of RHF vs LHF; edema, nocturia, SOB, cough, blood in sputum, fatigue, cyanosis, limited exercise tolerance |
| What happens in systolic heart failure? | normal ejection fraction is about 60% and can drop to 20%; CO drops, tissue perfusion is inadequate |
| What happens in diastolic heart failure? | lower end diastolic volume; lower stroke volume; normal ejection fraction; CO drops, perfusion is inadequate |
| What is circulatory failure? What are the types of shock? | any time CO is reduced to the point where there is inadequate perfusion to the brain, organs; hypovolemic shock, cardiogenic shock, anaphylactic shock, septic shock |
| What is hypovolemic shock? What are causes of hypovolemic shock shock? | acute blood loss of 15-20% of blood volume; loss of whole blood from hemorrhage, loss of plasma from severe burns, loss of extracellular fluid from vomiting and diarrhea |
| When are compensatory mechanisms activated in hypovolemic shock? What do these mechanisms maintain? What are the mechanisms | Compensatory mechanisms activated in initial 0-15% blood loss; maintains BP; ^HR, contraction force, vasoconstriction to nonessential organs, redistribution of blood from organs to general circulation |
| What happens in the body during hypovolemic shock? | SNS system is activated; fight or flight occurs causing coronary arteries and cerebral arteries to vasodilate, while the rest constricts |
| Besides SNS activation in hypovolemic shock, what other system is activated? | RAAS to reabsorb sodium and water to increase blood volume |
| In hypovolemic shock, when does MAP begin to fall? | after 20% loss |
| When are CO and MAP at zero? | at about 35-45% loss of blood |
| What are the stages of hypovolemic shock? | initial, compensatory, decompensated, irreversible |
| What is the initial stage of hypovolemic shock? | starting phase with no serious clinical effects |
| What happens in the compensatory stage of hypovolemic shock? | BP and perfusion are still sufficient |
| What happens in the decompensated stage of hypovolemic shock? | sympathetics insufficient to prevent cell damage; blood flow to heart and brain decreased enough to impair function; patient can still be saved by increasing fluid volume |
| What happens in the irreversible stage of hypovolemic shock? | even if perfusion is restored the VS won't recover |
| What are the treatments of hypovolemic shock? | transfusions and/or blood expanders (has osmotic characteristics) (ex. dextran sulfate or colloidal albumen), redistribute fluids (elevate lower extremities) |
| What are the osmotic characteristics of transfusions and blood expanders? | pulls water by osmosis from cells into the blood vessels to maintain blood volume or holds blood fluid in the vessels instead of leaking out into other places of the body |
| What is cardiogenic shock? What are causes? | Heart's cannot pump; HF, MI, pulmonary embolism (blocking the pulmonary artery); cardiac tamponade (pericardial cavity filled w/ unwanted space which takes up potential space and prevents the heart from dilating to fill properly); pneumothorax |
| What is anaphylactic shock? | a severe allergic reaction |
| What happens in anaphylactic shock? | allergen causes release of histamine into the blood; systemic edema, bronchospasm, laryngeal edema, GI cramps; emergency airway obstruction |
| Why does bronchospasm occur? | histamine attaches to smooth muscle to cause contraction |
| Why does laryngeal edema occur? | histamine causes blood vessels to release their fluid through leaky spaces |
| What are treatments for anaphylactic shock? | epinephrine injection, antihistamines, corticosteroids, oxygen, ice compress if the cause is topical |
| What is septic shock? Who is most at risk for severe sepsis? What happens in spetic shock? | a severe bacterial or fungal infection; immunocompromised patients (HIV/Aids, organ transplant); bacterial endotoxins cause arterial and venous dilation causing hypotension |
| What are the treatments for septic shock? | aggressive antibiotics, vasopressive drugs to redistribute blood volume out of the vessels and into the tissue |
| What happens in ischemic heart disease? What are the usual causes of ischemic heart disease? | reduced oxygenation due to reduced arterial supply; myocardial ischemia most often due to atherosclerosis, vasospasm, thrombosis |
| What is an infarction? | impairment of blood flow causing cells to eventually die because not enough oxygen |
| Why might vasospasm cause ischmeic heart disease? | it causes a sudden decrease in blood flow |
| Why might a thrombosis cause ischemic heart disease? | it blocks the coronary arteries |
| What is angina? | paroysmal CP or pressure sensation associated with myocardial ischemia |
| What are the s/s of angina? | s/s for up to 5 minutes; SOB; nausea; pain in the sternal region, left chest, ulnar side of left arm & forearm, right if severel ocasional pain in the jaw, epigastric, centre of back |
| Why is there referred pain in angina? | nociceptor synapse on the same path of skin > left side and heart fo to the same pain pathway |
| What are the different types of angina? | stable, unstable |
| When does stable angina occur? | when you exercise or put a demand on the heart because more oxygen is used up than when you are at rest; occurs with anything that increases metabolic activity |
| What is the cause of stable angina? | fixed atherosclerotic occlusion of the cornary arteries |
| What might induce the onset of angina if it is stable? | physical exertion, exposure to cold, stress |
| How can stable angina be treated? | treat with nitroglycerin |
| When does unstable angina occur? | unpredictable; can occur at rest or not at rest |
| What is unstable angina usually a sign of? | usually a sign of potential heart attack |
| What is the cause of unstable angina? | probably associated with disruption of unstable atheromatous plaque, may involve thrombus formation |
| Can nitroglycerin be used to treat unstable angina? | it doesn't respond well to it |
| What are non-pharmacologic treatments of MI? | pacing of exercise, avoid smoking, stress, cold exposure, weight reduction, when attack occurs stop activity |
| What are pharmacologic treatments of MI? | vasodilating drugs such as nitroglycerin, isosorbide dinitrate |
| On onset of attack, what should you avoid doing? | avoid lying down because it increases preload because fluid goes to the heart instead of the extremities |
| How does nitroglycerin work? | very fast acting vasodilator which dilates a lot of the arterial system |
| How does isosorbide dinitrate work? | causes the release of nitric oxide which is released bu endothelial cells of arteries |
| What does nitric oxide do? | causes vasodilation at the local level, does not work on the CNS, counteracts endothelin which causes vasoconstriction at the local level |
| Wait substances locally control vascular perfusion? | nitric oxide and endothelin and andrenergic receptors |
| What causes increased endothelin release? What does this cause in the body? | smoking, bacterial toxins, hypoxia, oxidized LDL, inflammation; causes endothelin release and subsequent vasoconstriction, HTN, CHD, angina |
| How do vasodilators work? | they act systemically on veins (decrease preload) and arterioles (afterload) to reduce the work of the heart |
| What meds are used for ischemia? | betablockers, Ca++ channel blockers, aspirin, reperfusion treatments |
| How do beta blockers work? | The are B1 antagonists on SA/AV nodes and myocardia; they reducte the heart's O2 consumption |
| How do Ca++ channel blockers work? | slows heart rate and force, dilates arterioles, increases coronary perfusion |
| How does aspirin work? | antiplatelet drugs; inhibits thromboxane A2 which stimulates platelet aggregation |
| What are types of reperfusion treatments? | angioplasty, stenting, bypass surgery |
| What is an example of angioplasty? What happems? | PTCA - percutaneous transluminal coronary angioplasty; coronary atherosclerotic occlusion dilation and possible insertion of a stent |
| What does a stent do? | prevents re-stenosis |
| What happens in a bypass surgery? | saphenous vein graft, or re-directed internal thoracic cavity |
| What are the reversible changes of an acute MI? | cardiac dysrhythmias, loss of muscle function |
| When there are cardiac dysrhthmias, what is seen? | ECG changes observed after 30 to 60 seconds |
| Why is there a loss of muscle function in AMI? What might help prevent this? HOw long can isschemic myocardial cells survive? | No oxygen in the cells = death; glycolysis can continue to make ATP; Can survive about 20 minutes on ATP, glycogen reserves |
| In moderate ischemia/angina, what ECG's are seen? How is it treated? | ST depression that returns to normal at the end of angina; treat with vasodilators, anticoagulants |
| In Non-ST elevation AMI what is seen? How is it treated? | ST depression, troponin elevated (no CK); treate with anticoagulants and possible angioplasty |
| In ST elevation AMI, what is seen? How is it treated? | ST elevation, troponin and CK are both elevated; Treat with immediate angioplasty and/or thrombolytic drugs (clot busters) |
| In AMI, when do irreversible changes occur? What are the irreversible changes? | after 20 to 40 minutes, myocardial death occurs |
| What are the 3 zones of damage in AMI? Explain each | area of necrosis (nearest endocardium), area of injury (some perfusion may exist), ischemic zones (cells recover if perfusion is re-established) |
| How might necrosis be prevented? When should this occur? | necrosis prevented if re-perfusion withing 15 to 20 minutes of onset |
| What happens to necrotic tissue in the heart? What happens to the function of the heart? Describe the phases of wound healing in terms of MI? | necrotic area is gradually replaced by scar tissue; function is permanently lost; acute inflammation for 2-3 days so dead cells can be removed by macrophages, after 4-7 days the infarct area is soft and yellow, by 7 weeks scarring is complete |
| What serum proteins are used to diagnose AMI? | myoglobin, troponin, creatining kinase |
| When are myoglobins seen? | 3-4 hours post MI |
| What are troponin subunits? Describe this? | cardiac contractile protein; rise more slowly than myolobin; most sensitive and appears with partial MI |
| What is creatine kinase? What is the peak time of this mark? Describe it | Creatine Kinase are enzymes that peak at 24 hours; some are highly specific to MI; test less sensitive and appears after a full occlusion |
| What increases the risk of a stroke? | HTN, DM 2 or smoking |
| What are the four types of stroke? | thrombic, TIA, embolic stroke, hemorrhagic |
| What is the cause of thrombotic stroke? | Atherosclerosis > thrombus forms at the plaque site, fragments dislodge causing a stroke |
| What are TIAs? What changes might occur? When does this resolve? Is it common? | transient ischemic attacks from temporary decreases in blood flow from platelet clumps, and vessel spasm > may see changes in vision, speech, motor function, dizziness, and a loss of consciousness |
| What are embolic strokes? | strokes caused by thrombus fragments, fat, air, or tumor fragments |
| What are causes of hemorrhagic stroke? What happens? What is the survival prognosis like? | d/t HTN, ruptured aneurism, and vascular malformation; expanding blood pool compresses the brain; poor survival rate if large but smaller ones can reabsorb via astroglia, microglia, phagocytosis leaving a cavity surrounded by glial scar |
| What are the different manifestations of a stroke? | depending on cerebral artery affected it can be numbness, weakness, generalized headaches that may be severe, dysphagia, partial to complete paralysis, paresis, unconsciousness, cerebral edema can be fatal |
| What are the pleural membranes? | visceral and parietal |
| What is the visceral pleural membrane? | the lining of the lung |
| What is the parietal pleural membrane? | the lining of the chest wall |
| What is the normal intrapleural pressure of the lungs? | normally negative |
| What is a pneumothorax? | a collapsed lung because of something filling the pleural space; Usually the pleural space is negative but when it is filled the pressure of the space becomes positive which stops the lungs from expanding |
| What are the causes of pneumothorax? | Lung puncture and spontaneous rupture of blebs |
| What is a tension pneumothorax? | It is when air enters the pleural space and cannot leave during expiration |
| Why is a tension pneumothorax dangerous? | The tension can cause of shift in the mediastinen away from the pneumothorax causing lung collapse on the other lung |
| What is atelectasis? | a collapse of the lung; when the alveoli within the lung become deflated |
| What are causes of atelectasis? | collapse of the lung, obstructions, compression |
| What is an obstructive cause of atelectasis? | bronchial tube is blocked causing absorption of air in the lung distal to the block (no air = no filling of the lung); mediastinum shift towards the obstruction |
| What is a compressive cause of atelectasis? | pleural cavity partially filled with fluid, blood or air |
| What is bronchial asthma? | a chronic inflammatory disease of the airways that is associated with reversible bronchospasm; it is a chronic condition with acute exacerbations that resolves spontaneously or with treatment |
| What age are people affected by bronchial asthma? Where does bronchial asthma usually occur? | all ages are affected, reported in 10% of children; incidence is on rise in industrial countries |
| What increases risk of bronchial asthma? | indoor allergens - dust mites, air-tight housing, animal dander, insulation, furniture allergens, pollution; airways develop increased sensitivity to this |
| What is a bronchial spasm? | smooth muscle in bronchial artery will contract and the diameter will decrease |
| What are triggers to bronchospastic asthma? | cold exposure, exercise, emotional upset, bronchial irritants/smoke |
| What are triggers to inflammatory asthma? | immune reactions (inflammation and hyper responsiveness to non allergenic stimuli, increases immune reactivity and makes you more susceptible to inflammation); allergen exposure |
| What are the phases of Asthma response? | Early response and late response |
| What happens in the earl response? | immediate bronchoconstriction on exposure to allergen or irritant; IgE sensitized mast cells release histamine |
| How quickly does this develop? What are manifestations of this development? When does this recover? How can this response be inhibited | Develops withing 10 to 20 minutes; manifests as bronchospasm, pulmonary edema, mucous secretion; spontaneous recovery within 60 to 90 minutes; response inhibited or reveresed by B2-agonists |
| What are the steps of early asthma response? | antigen enters airway > mast cell degranulates, releases medatiors, and causes gaps to form in adjacent tissue > mediators increase mucous secretion, leakage of vascular fluid, airway smooth muscle contstriction |
| When does the delayed response occur? For how long? How is this manifested? | occurs 4 to 8 hours after exposure to trigger and may last days to weeks; manifested as inflammation and increased airway responsiveness AND dyspnea, and increased effort in breathing |
| What happens in the delayed response? | macrophages and mast cells release histamine cytokines, bradykinins, and leukotrienes. This causes migration and activation of basophils, neutrophils, and eosinophils damaging the airway and increasing bronchospasm and mucous secretion |
| What is a complication of delayed response? | chronic remodelling |
| What is chronic remodelling? | irreverstible damage to distal airways allowing eosinophils to migrate in causing smooth muscle hypertrophy and fibrosis |
| How is increased effort in breathing displayed as? | flared nostrils, pursed lip breathing, accessory respiratory muscles, cyanosis, wheezing, NP cough from bronchospasm, hyerinflation, reduced FEV1 and PEFR |
| What is FEV1? | forced expiratory volume |
| What is PEFR? | peak expiratory flow rate |
| How is asthma prevented? | ID allergens and remove from home, avoid high altitudes |
| What is the treatment for acute symptoms of asthma? | albuterol, short acting |
| What is the treatment for long term control of asthma? | steroids (prednisone), leukotriene inhibitors (reduce inflammation and work slower and longer, having chemotactic effect), Anti-IgE antibody |
| What is emphysema? | destruction of septa of alveoli causing an enlargement of the alveoli but decrease in number of alveoli; loss of elasticity; destruction of alveolar capillaries |
| What are causes of emphysema? | smoking, a-1 antitrypsin deficiency |
| What protects the lung | a-1 antitrypsin |
| How does smoking cause emphysema? | smoking stimulates inflammatory cells into the alveoli > neutrophils, macrophages and mast cells activated and release elastase > elastase decreases a-1 antitrypsin activity |
| What can cause a-1 antitrypsin deficiency? | respiratory infection and smoking (reduces plasma stores); hereditary condiftion |
| What does a-t antitrypsin deficiency cause? | decrease in elasticity |
| What are manifestations of emphysema? | pink puffer |
| What is pink puffer? | fight to maintain oxygenation from hyper inflation of the lung with typical onset at 40 to 50 years |
| What are manifestations of pink puffer? | barrel chest, severe weight loss, wheezing and abset rhonchi, absent sputum, absent cyanosis, normal Blood gas until advanced, right side HF in advanced, plycythemia in advanced, slow debilitating prognosis |
| What are the treatment options for emphysema? | no smoking, oxygen supplementation, surgical removal of most severely affected lobes |
| What is chronic obstructive bronchitis? What does this cause? What might cause this? | obstruction of large & small airways caused by inflammation; causes edema, hypersecretion of submucous glands, chronic P cough; smokign and recurrent infections are causative |
| What is the manifestation of chronic obstructive bronchitis? | blue bloaters, frequent infection, abundant purulent sputum, dramatic cyanosis, hypercapnea, hypoxemia, rt side HF with peripheral edema, polycythemia frequent (pulmonary HTN), finger clubbing, life-threatening episodes |
| Describe blue bloater | unable to compensate for lack of ventilation with an onset in 30 to 40 year |
| What is the manifestion of a blue bloater? | normal weight, dyspnea prominent early in disease, worsening with exercise; prominent rhonchi |
| What is rhonichi? | loud, low-pitched noises from large airways |
| What is AIDS? | the syndrome of indicator disease associated with end stage HIV infection |
| What causes mortality in HIV/AIDS? | opportunistic infections |
| How many new cases of HIV in 2011? How many cases of HIV related deaths? Where is AIDS most prominent? | 2.5 million new cases, 1. million HIV related deaths, women represent 50% of HIV infections; leading cause of death by infections and 4th cause of death worldwide; most prominent in sub-saharan africa |
| What increases risk of HIV | drug injection/sharing and not using condoms |
| What is HIV? What does it infect? | a retro virus; infects subset of lymphoctes that contain the CD4 protein |
| What is the structure of HIV? | gp120 docking glycoprotein connected to dp41 transmembrane glycoprotein that covers and goes around the lipid membrane which covers a matrix that covers the capsid that holds the RNA |
| Describe the HIV RNA | they are 2 identical copies of a single stranded viral RNA with 9 genes coding for viral core and envelope proteins, replicating enzymes and regulatory proteins |
| Describe gp120 | a viral surface protein that binds to CD4 membrane and co-receptor; HIV target cells will have both and binding will cause recognition and penetration |
| What does viral uncoating do? | liberates reverse transcriptase; synthesis of double stranded cDNA copy of viral genome |
| What does integrase do? | inserts the viral cDNA into host DNA; dormant provirus |
| Does the provirus infect immediately? How is it protected? What phase might it enter? | provirus can remain latent for a long period (makes no new virus particles to infect other cells); protected from immune destruction or anti-retroviral meds; can enter a lytic phase |
| Describe the lytic phase | viral cDNA is transcribed to make many copies of single-stranded viral genomic RNA; 9 viral genes are transcribed into mRNA to make 9 viral proteins and are cut by protease to activate |
| How is HIV transmitted? | exposure to infected blood, semen, vaginal secretions; enntry via mucous membranes, injection, cuts, sexual intercourse, oral sex, donor insemination, infected mother to baby (in utero, delivery, breast feeding), blood transfusion, organ transplants |
| Can HIV be transmitted via insect bites, casual contact, saliva, tears, nasal secretions? | NO |
| How is HIV diagnosed? | seroconversion, window period, polymerase chain reaction, T4 cell count, symptomatology |
| What is seroconversion? | when a specific antibody becomes detectable in the blood, and the corresponding antigen becomes undetectable |
| What is the window period? | occurs before seroconversion; infected blood donor may not be screened; risk of transmission is high because patient isn't aware of infection; can last 6 to 14 months |
| Describe the polymerase chain reaction? | detects viral DNA, rather than antibodies; used in infants of HIV positive mothers |
| Describe T4 cell counts? | T4 is based on 3 categories |
| What is Category 1 of T4 cell counts? | >/= 500 cells per ul blood |
| What is Category 2 of T4 cell counts? | 200 - 499 cells per ul |
| What is Category 3 of T4 cell counts? | <200 cells per ul |
| What is the normal T4 cell count? | 1000cells/ul |
| Describe symptomatology? | 4 stages: acute (primary) HIV infection, latent (asymptomatic), chronic, AIDS |
| What are the manifestations of the Acute (primary) HIV infection stage? What happens in the body? Is the patient infectious? How long does this last? | fever, sore throat, malaise, nausea, lethargy, headache, swollen lymph nodes; latently infected cells are seeded in lymphoid organs; rapid viral replication temporaily lowers T4 count; patient highly infections; 2-8 weeks |
| How long does the latent (asymptomatic) period last? What happens in the body? | Lasts several years (avg 11); immune system controls viral replication; T4 counts decline; HIV antibodies are present (seroconversion has occured) |
| How long does the chronic symptomatic HIV stage last? What happens in the body? | lasts months to years; T4 drops to <200/ul; viral counts rise; immunes system fails and opportunistic diseases appear |
| What happens in AIDS? | serious immunodeficiency, QOL impaired, life-threatening illness |
| What opportunistic inections and diseases show up with AIDS? | pneumocystis pneumonia, myobacterium TB, toxoplasma gondii, cytomegalovirus, malignancies, candidiasis, wasting syndrome, |
| Describe pneumocystis pneumonia? | most common resp disease in AIDS; fungus, non-pathogenic in healthy individuals |
| Descrive TB? | drug resistance high in AIDs patients, mortality rate high in (70-90%) in 4 to 16 weeks |
| Describe toxoplasma gondii? | a protozoa that infects CNS in about ⅓ of AIDs patients; a brain abscesses |
| Describe cytomegalovirus? | pneumonia, brain, eyes, liver |
| Describe malignancies? | Kaopsi's sarcoma; cancer of BVs, dark skin lesions, plaques |
| Describe candidiasis? | fungus |
| Describe wasting syndrome? | severe wt loss, fever, diarrhea, fatigue |
| How is HIV/AIDS treated? | HAART: multi-cocktail formations of reverse transcriptase inhibitors, protease inhibitors, HIV entry inhibitors, Integrase inhibitors, HIV vaccines |
| What does HAART stand for? | highly active anti retroviral therapy |
| What do reverse transcriptase inhibitors do? | nucleoside analogues are competitive inhibitors of RT enzyme (ex. azidodideoxythymidine mimicks thymidine); non-nucleoside drugs are non-competitive inhibitors of the RT enzyme |
| Do HIV vaccines work? | poor results d/t high mutaton rate |
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db5k
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