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94 Cards in this Set
- Front
- Back
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Hypoplasia-
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Tissue that is smaller than normal got that way by never growing or by growing and then shrinking. This tissue is hypoplasia which means that less cells make up the tissue. Not all hypoplasia or atrophy is abnormal.
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HYPERPLASIA
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more cells more tissue bigger organ. Not all of this is abnormal in some tissue pregnancy-uterus and breast tissue will have this.
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Metaplasia-
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away from something or beyond something. Away from the form Cells begin to change and develop along a different pattern. This can be in response to an insult. Chronic yeast infection=metaplasia
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Dysplasia-
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Dys means bad and plasia means form. Dysplasia means bad form. This is an abnormality in differentiation and proliferation. Not only do we have cells that have moved from the original pattern of development but they have also increased their rate or reproduction
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Neoplasms-
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is a new growth or new mass of cells. Tumor is the same thing.
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BENIGN
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neoplasm is a localized affair, it is surrounded by normal cells. It is confined to a certain area. They can push other cells out of the way. Some may be very small or some may be very large.
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MALIGNANT
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neoplasm means wicked or evil having an evil influence. Abnormal group of tissue that invades other cells and continuously invading.
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Adenoma-
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An adenoma is a benign glandular growth.
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Carcinoma-
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Carcinomas tell that the neoplasm is malignant and arises from epithelial tissue. Sometimes the tissue is known.
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Adenocarcinoma-
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Adeno carcinomaà malignant glandular neoplasm.
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Fibroma-
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A fibroma is a benign growth in fibrous tissue
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Sarcoma-
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If the malignancy arises from supporting tissue, the correct name is sarcoma. Sarcoma means malignant and located in supporting tissue.
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Fibrosarcoma-
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fibro sarcomaà malignant fibrous tissue neoplasm.
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Osteosarcoma-
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Osteo sarcomaà malignant bone neoplasm
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LYMPHOMA
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benign growth in lymphoid tissue what we really means is malignant lymphoma.
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ANGINA
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is a symptom which is chest pain caused by not enough oxygen. Heart is 100% dependent on oxygen. The tissue will die without oxygen.
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ORTHOPNEA
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difficulty breathing when lying down. This is not an acute problem it is chronic.
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PALPITATIONS
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are being aware of your heart beat. We have to change rate, regularity, force of contraction then you are aware and you can tell you are palpating.
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EDEMA
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swelling or fluid in the interstitial space. Peripheral edema
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Fatigue and weakness—
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can I walk up stairs, across the room? If they can’t there is decreased CO, decreased perfusion.
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Define stroke volume.
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A nice, bounding pulse means good stroke volume. Stroke volume is normally 70 mL. Stroke volume is the amount of blood pumped out with each left ventricle contraction. If the pulse is thready and weak then it could mean that 70 mL is not being kicked out due to loss of muscle from MI, loss of blood volume, or due to vasodilation.
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Korotkoff sounds
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sounds heard during auscultatory determination of blood pressure.
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When is BP considered hypertensive. .
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If diastolic >90 and systolic >140 then this is hypertension. The numbers previously were diastolic >95 and systolic >160.
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Define and explain calculation of pulse pressure.
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Simply the difference between the systolic and diastolic pressure. Patient has 120/80 BP then the pulse pressure is 40
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Explain how pulse pressure is influenced by stroke volume and peripheral resistance.
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To a great extent, it is influenced by stroke volume and peripheral resistance. Acutely, it more influenced by stroke volume. Ex: Patient with falling BP, narrow pulse pressure, this is an ominous sign of sudden increase in peripheral resistance or loss of stroke volume. Pulse pressure narrows because they have suddenly lost muscle in the left ventricle (myocardial infarction).
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Explain Kussmaul’s sign. .
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A paradoxical increase in venous pressure when a patient inspires, this is known as Kussmaul’s sign. It tells that there is an impediment in blood return to the right side of the heart. What is probably going on is some degree of right side heart failure. The CV system is a closed system so you have to look uphill and downhill to determine what is going on. When there is failure in the right side of the heart, that puts pressure on the venous system entering into it and trying to empty and there is incoming pressure trying to fill a chamber (the right side) that hasn’t emptied.
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Explain correlation of 1st and 2nd heart sounds.
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Normal heart sounds are the results of vibrations of the blood and blood volume and the valves closing. Blood going into the chambers and the valves closing behind is what we hear. Typically talk about as lub dub. First sound is lub. This is correlated with the closing of the AV valves (bicuspid and tricuspid). The second is correlated with the semilunar valves closing. Here the 1st sound at the onset of ventricle systole. As the ventricles to start contract, they get smaller, and increase pressure in the ventricles, and causes pressure to be greater than that in the atrium, thus causing the AV valves to close. An abnormal bicuspid valve sound is heard during ventricle systole. The 2nd heart sound is audible at the beginning of ventricle relaxation. The ventricle is relaxed because it is filling again, has pushed the blood out into the pulmonary and aorta system, the blood starts to run backwards and catches on the semilunar valves and closes them. Backflow actually closes the valve. 2nd heart sound is slightly split because normally the aortic valve closes slightly before the pulmonary valve. If the split is extended, that possibly means that the pulmonary valve is closing before the aortic valve.
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Explain gallop rhythm.
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Two additional heart sounds are occasionally heard. These sounds are termed gallop rhythm.
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Explain 3rd and 4th heart sounds.
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The 3rd sound is called ventricle gallop. What causes it is rapid ventricle filling or an increase in ventricle filling, blood rushing into the ventricle. The 4th sound is atrial gallop. Atrial gallop when there is an increase in ventricle resistance to atrial filling.
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Explain extra cardiac sounds such as friction rub.
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These are extra stuff. They often have to do with valves. Normally when a valve opens it is silent. If the valve is thick, stenotic, when that valve opens it isn’t silent. It opens with a snap to it. The friction rub, fibropurulent exudates in the pericardial sac and the rubbing sound is an extracardiac sound.
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Heart murmurs
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1. Turbulent flow within chambers or vessels. This is turbulence you don’t normally hear. You hear a stream because of increase flow or because it is going over and around rocks. The reason you hear a sound is because the quickness of flow or over and around structurally things. If you are right over an area it is not as loud as if you are “down stream”
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P Wave-
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The P wave represents atrial depolarization. Depolarizing means the electrical charge is lost. If the P wave is wider than normal and maybe even the amptitude is increased, it tells us that it is taking longer for the atria to depolarize. This occurs when the atria is hypertrophied, it is too big. If the P wave is inverted, then this means that origination of the electrical stimulus in the heart did not occur in the SA node. Normally we go SA node, AV node, bundle of HIS, bundle branches. If the P wave is inverted, the electrical event started somewhere other than the SA node and then we would expect a decreased heart rate. This is because the SA node fires the most frequently. If the SA node isn’t firing, something else is, and the other areas don’t fire nearly as much.
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PR Interval-
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The PR interval represents the current’s transmission time through the atria and then the slight delay of the impulse at the AV node. Normally what happens is that the impulse is slightly delayed at the AV node. This is normally like 0.1 or 0.2 seconds. If the PR interval is a little longer, this tells us that there is a heart block. The length determines the degree of heart block. Heart block means that the conduction system is blocked and the muscle isn’t doing what we want it to. This can only be gauged from the PR interval.
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QRS complex
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The QRS complex is not very long but is tall. It is 0.1 seconds or less. It represents the ventricle depolarizing and at the same time the atria are repolarizing. It picks up the ventricle depolarizing. It is tall because there is more muscle in the ventricle. If the QRS is wider, the ventricle is hypertrophied.
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ST segment-
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The ST segment is the interval between ventricular depolarizing and repolarizing, thus the ventricle is isoelectric. This is important to look at in comparison to the baseline. If the ST segment is depressed, or below baseline, this is correlated with myocardial ischemia. If the ST segment is elevated above the baseline, this is correlated with myocardial infarction. There are drugs that can cause this segment to bounce—digitalis. Electrolyte disturbances can also do this.
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T wave-
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The T wave represents the ventricle repolarizing. It is normally wider than the QRS because the ventricle repolarizes more slowly than it depolarizes. If the T wave is spiked, peaked, or narrow, this means the ventricle is repolarizing quickly. This can be caused by increased potassium. Potassium levels can get so high that the ventricle doesn’t repolarize and it stops beating. Always think hyperkalemia when the T wave is peaked.
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Explain the development of atheroscierotic lesions and give most likely location of development.
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The most common reason is atherosclerosis. The reason the vessels are sclerotic is an increase in lipids, fibrous tissue, plaque. This is generally a very slow process. The body is very accommodating. A vessel that is 40% occluded is not even obvious to a person. A rule of thumb is that until a vessel is more than 75% occluded, the person will not know it. After this, there are symptoms of the myocardial tissue not being oxygenated. Occlusion does not happen overnight but there are no symptoms because the body is accommodating. When we give stress tests, we increase the heart rate, and put the body in a position where the heart is not being oxygenated. Then the muscle starts cramping causing angina. Stress tests are stopped once a person reaches angina. The less the occlusion, the higher the heart rate has to go to determine that there is occlusion. Plaque typically doesn’t develop in the straightaway of a vessel, it normally develops where a vessel turns, curves, or branches.
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Identify the risk factors of coronary artherosclerosis.
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A. Age likelihood increases with age. Significant occlusion is really unlikely before the age of 40.
B. Race this is more common in African Americans than the white population. C. Family this tends to runs in the family so it suggests genetics. D. Sex- females are relatively immune until after menopause. It is the number one killer of females after this time. |
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LDL
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LDL (low density lipoprotein) LDL are the bad stuff because they are a lot of fat and not a lot of protein. So increases in LDL are correlated with increasing risk of coronary artery disease.We want total cholesterol less than 180, LDL really low, and HDL really high. There are people with cholesterol at 150, high HDL, low LDL and coronary artery disease. Some people with cholesterol of 400, high LDL, and low LDL with no problems
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HDL
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HDL (high density lipoprotein). HDL are the good stuff because they are a lot of protein and very little fat. Increase in HDL is correlated with decreasing risk. We want total cholesterol less than 180, LDL really low, and HDL really high. There are people with cholesterol at 150, high HDL, low LDL and coronary artery disease. Some people with cholesterol of 400, high LDL, and low LDL with no problems.
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VLDL
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increase triglyceride
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HYPERLIPIDEMIA
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fat and water do not mix. Lets connect fat to protein and move it around.
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Bacterial Pneumonia-
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Bacterial pneumonias can be seen as consolidation on the chest film. What you see is the pus from the WBC coming into the area. The bacteria that is the most common cause of pneumonia is a species of Strep. The pneumonia vaccine is against Strep. This bacteria has a capsule around it (so does the Strep that causes tooth decay) that is sticky. They pulled a protein out of the capsule and it is injected into people. They develop their own antibody to the protein in the capsule so that when the bacteria is presented, the antibody inactivates the protein in the capsule by pokes holes in the capsule so that the WBC have access and can phagocytize the bacteria.
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Viral Pneumonia-
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With viral pneumonias there is no consolidation because WBC can’t phagocytize the viruses and therefore there is no pus that can be seen on the chest film.
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Aspiration pneumonia-
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Aspiration pneumonias are nasty. Aspiration pneumonia is why people shouldn’t be on their back and vomiting because they can aspirate the vomit back into their lungs. pH of the stomach is 2-3, and then the vomit goes into the mouth where there is bacteria, and then it goes into the lungs and then the acidity from the stomach kills the lung tissue and the bacteria from the upper respiratory tract infects the tissue. These people end up with gangrenous lung tissue and bacterial infected lung tissue. This can also be seen in near-drownings in chlorinated swimming pools. Chlorine is very acidic.
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Hypostatic Pneumonia-
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Hypostatic pneumonias develop in the low bases of the lungs when they are not being aerated. Most seen in nursing home patients or patients not being turned or moved. Patient laying on their back for 3 weeks is not aerating the lungs. Also this can be seen in a patient who is having surgery because they are constantly on their back and aren’t being moved. Want people post-surgery to sit up, cough, and deep breathe. Sitting all day can cause this and deep vein thrombophlebitis
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Explain pectus excavatum.
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A condition is called pectus excavatus. This is on a continuum. It means the chest is caved in. In the most severe cases, kids are born with the lower end of the sternum fused to their thoracic spine. The chest is completely caved in. This makes breathing very difficult. These kids usually die at birth. The caved in appearance is on a continuum. Marfan’s syndrome—Abe Lincoln, tall and lanky, eye problems, mitral valve problems, higher incidence of aortic aneurysms, and higher incidence of pectus excavatus.
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Pickwickian-
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is named after a series of short stories written by Charles Dickens. Extreme obesity. These people usually cannot lie down because they cannot breathe. People with this will have sleep apnea.
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--Sleep apnea
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these people will stop breathing when they are asleep. Every hour or so they are awake because they quit breathing. More common in males, snoring, and overweight. Children is correlated with swollen tonsils and adenoids. Give them a respiratory to force them to breathe at night.
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Cystic fibrosis
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--1 in 2000 births in the white population
--Increase viscid secretions This is in the white population and it is a disease that has to deal with secretions. Thick and viscous secretions->lung, liver. Sweat glands not thick and are really salty. This is a sign of this disease. In the lungs the goblet cells are producing really thick secretions, coughing up cylindrical plugs of jello. |
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Bronchiectasis
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this is a chronic irritation/inflammation/infection of bronchi and bronchioles. This is seen in children this is developed after upper respiratory flu or virus. These children can cough up as much as 200ml/day. This is really nasty and may be that way for a long time. Right side heart failure pneumonia can kill them. It reflects incompetent parents. At this point it may or not be treatable. If it is caught early enough on it can be treated with antibiotics.
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Centrilobular Emphysema-
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selectively affects the respiratory bronchiolus. This is the transition part where there are a few alveoli. A little bit of alveoli involved. This is more common in males than females and very seldomly seen in non smokers.
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--Panlobular Emphysema-
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all of the alveoli, alveolar ducts and sacs. Everything. These can get blown up reducing the availability of gas exchange. This also has to do with loss of elasticity in the alveoli in the lungs.
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Explain chronic bronchitis and explain the role of goblet cells.
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inflammation of the bronchi. Acutely it means an infection that is causing inflammation. We treat this with antibiotics if it is bacterial. Chronic bronchitis is a hypertrophy and increase in the number of goblet cells. Goblet cells produce mucus which is why people cough. The only way the lungs can deal with something is to get us to cough it up. When lungs are infected and inflamed, mucus is created to cough it up. The GI can only deal by diluting it out and diarrhea. Coughing is a defensive response. The main etiological correlate to chronic bronchitis is air pollution. There is more in urban areas then. Sometimes chronic bronchitis is a prelim of emphysema, which is oftentimes what people are saying when they say COPD
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Asthma-allergic
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Allergic in children. Antigen antibody reactions which equals a spasm in bronchi. Increase 3-5% per year here.
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Idiopathic-asthma
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Idiopathic no clear cut reason. This happens in people usually over 40 and this is not a good sign. This is a preliminary sign of emphysema.
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Mixed-asthma
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Mixed some antigens and some idiopathic reasons.
Six gene sites that are very highly correlated with asthma particularly allergic asthmas. |
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Define COPD.
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This is a category of diseases characterized by an increase in the resistance to air flow in the respiratory system. Air isn’t moving in the respiratory system. There are a number of diseases under this heading.
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Define varicose veins
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Varicose veins means veins are elongated and dilated. These are typically in the legs. Varicose veins run in the family and have to do with a profession where you are on your feet a lot as well. Generally this is more of a cosmetic issue more than anything, they can be lasered but will probably get more.
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Explain superficial thrombophlebitis.
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Superficial thrombophlebitis (clot in vein inflammation). Typically seen in upper and lower extremities. In the arms this is most likely the result of acidic or hypertonic IV solutions. In the lower extremities, this is commonly due to varicose veins, although it could be due to trauma. Typically they are not a big deal.
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Define thromboembolic venous disease and explain 3 categories of contributing factors often present.
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reflects a relationship between thrombus (clotting) and embolus (blocked vessel). Most likely the vessels are blocked due to clotted blood. IN this case a vein is blocked by clotted blood. 3 things happen simultaneously: a stasis of blood, injury to endothelium of the blood vessel, and a hypercoagulative state. When the clot happens, if it stays in the vein that is fine, but if it moves, it will head towards the right side of the heart, then is pumped out of the left side to the pulmonary system. Pulmonary embolisms kill. This is what people on combination birth control pills accentuate.
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Explain deep vein thrombosis and give 3 veins most often affected.
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More concerning is deep vein thrombophlebitis. These are usually in the lower extremities. Usually involves veins around calf—popliteal, superficial femoral, illeofemoral. People who have these will complain of legs aching. This is not terribly excruciating pain just aching pain.
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Pleural effusion
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extra fluid in space
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Hemothorax
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Blood in the pleural space
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Pnuemothorax
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Air in the pleural space
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Tension pneumothorax
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With only one lungs ability to expand, these people are air hungry. We put a chest tube in the pleural space to drain out the air. Put the other end in water and you can’t suck water in. Instantly, people feel better once there is a chest tube in. On a chest film, you can see the air filling the pleural space. Sometimes this happens without injury. It is called a spontaneous pneumothorax. Most commonly in tall and lanky teenage males. The cause of this is unknown—it could be a growth spurt.
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Explain cardiac shock.
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This is seen in massive MI. It causes a decrease in the ability to perfuse because blood pressure is down. MAP = CO x TPR is what governs tissue perfusion. Most cardiogenic shock is due to a decrease in MAP. This decrease in MAP if most likely due to a decrease in CO.
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Mitral Regurgitation-
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-Permits a backwask of blood flow from the left ventricle to the left aorta due to a sloppy valve.
-Chronic or acute -Atria not as compliant as ventricles. -Sudden regur. can be life threatening |
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Aortic stenosis-
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-Stiff valve.
-Obstructs blood flor from the left ventricle to the aorta during ventricle systole. -Vent. has to hyperthrophy the muscle which can lead to decrease flexibility. -Seen on ECG as a spiked and wider QRS complex=vent repolarizing. |
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Aortic regurgitation-
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-Reflux of blood from the aorta into the left vent during vent relaxation.
-Blood coming from atria and backflowing so that the left vent has to get larger and dilate. -50% results from rheumatic heart disease. |
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Tricuspid Valve Disease-
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-More likely to have stenosis
-Restricts blood flow from right atrium into the right vent during diastole. -Stiff valves increases workload of right atrium. -Cause hyperthrophy which make it thinner -EKG wider P wave=atiral depolarization |
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1st degree heart block.
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PR interval is little extended
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2nd degree heart block
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PR interval is more extended
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3rd degree heart block
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No conduction getting through to vent. from SA node so the vent is contracting due to impulses from somewhere else in the conduction system.
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Preload-
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Defined as the pressure generated in the left ventricle at the end of diastole. Preload is determined by two factors: the amount of venous return to the ventricle and the blood left in the ventricle after systole (end-systolic volume)
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Afterload-
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Defined as the resistance to ejection of blood from the left ventricle. Aortic systolic pressure is a good index of afterload. Decreased afterload enables the heart to contract more rapidly and increased afterloads slow contraction and cause higher workloads against which the heart must function so it can eject less blood.
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Contractility-
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Contractility is the degree of myocardial fiber stretching. Myocardial infarction is the most common cause of decreased contractility
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Explain how the following contribute to heart failure:
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Stroke volume is influenced by contractility, preload, and afterload. Decreased contractility, increased preload, and increased afterload all play a role in the progression of left heart failure.
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Define fusiform and saccular aneurysm.
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2 forms of aneurysms- fusiform and sacular. Sacular means one side of the blood vessel and fusiform means both sides. Most likely these develop in the abdominal aorta more than in the chest. The first symptom of abdominal aortic aneurysm is the funeral. When these rupture, it is a hole in the abdominal aorta, and unless you are on the operating table you are going to die. There are no symptoms until it ruptures. Dissecting aortic aneurysm means they blow a tiny hole and blood seeps out slowly.
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Premature beats
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A. Premature activation other than the SA node. On occasion this is ok, but this can lead to ventricular tachycardia, vent flutter, and then vent fibrillation. You have to shock the heart which turns off autoryhtmicity. The heart has the ability to excite itself.
B. Atrial premature beat which can lead to atrial tachycardia, atrial flutter, and atrial fibrillation. |
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Ischemia
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Cells are deprived of blood supply
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Most common cause of decreased coronary blood flow and resulting in myocardial ischemia
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Athersclerotic Plaques
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How long does it take a myocardial cell to become ischemic?
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10 seconds
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Infarctions are in two categories Transmural and Subendocardial
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Trans-full thickness of myocardial tissue
Sub-halfway into myocardial tissue |
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What will an ECG/EKG look like with ischemia?
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ST depresion and inverted T wave because of an increase in potassium and lowering of pH.
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How long are cardiac cells viable for under ischemic conditions?
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20 minutes
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Symptoms of ischemia
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Angina or chest pain
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What area is most vulnerable to ischemia or MI?
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Left ventricle
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Major Determinants of Myocardial O2 Demand?
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Increase heart rate
Increase contracile force Increased muscle mass Ventricle wall tension-the amount of tension when the vent contracts. |
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Relationship of hypertension to coronary atherosclerosis
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Hyper-affects 25% of pop.
Problem is subtle. Increase in pressure damages lining of blood vessels=plaque build up eventually |
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Relationship of ischemia, anaerobic metabolism, and decrease in pH.
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Ischemia=heart in anaerobic environment->anaerobic environment=lactic acid= lowered pH and causes angina.
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Diagnostic criteria of MI
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Chest pain, Increase in cardica enzymes (CPK, SGOT, LDH), CK-MB begins to rise 4-6 hrs after an MI, Troponin-protein peaks 4-6 hrs
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Congestive Heart Failure
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when you can no longer move blood around the heart. Ventricle involved tells you where congestion will be.
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Ventricular Septal Defect
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-Complication of MI
-Multiple vessel occlusion -Problems=differences in pressure -Dead tissue in the middle the ventricles poke holes in the septum and blood flows between the ventricles. |
