Case studies - This is a document containing the answers and questions for a lot of the case studies we go over in class PDF

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This is a document containing the answers and questions for a lot of the case studies we go over in class....

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Cardiovascular Case Histories - Case 1 A 56-year old man has come to the emergency room complaining of fatigue, weakness, dyspnea, and exercise-induced chest pain that radiates to his left arm and neck (angina). His history indicates that, in the past couple of years, he has had several minor episodes of angina during periods of sudden exertion. Recently, he has awakened several times at night with the feeling that he cannot breathe; however, these sensations has gone away after a few minutes of sitting up in bed. A physical examination shows a relatively low blood pressure of 110/80 mm Hg, a weak pulse, and heart rate of 100 beats per minute. The patient has swollen ankles (edema), and the jugular veins in his neck are visibly distended. An ECG analysis indicates the electrical activation of hi heart is proceeding normally from the atria to the ventricles (normal sinus rhythm). The ECG does indicate an elevated ST segment. The physician performs and echocardiography examine of the heart and notices the patient’s heart is dilated and contains more blood than does a normal heart. To visualize the coronary arteries, a dye which is visible on a portable X-ray screen is injected into the coronary arteries. The dye is introduced through a catherter that is inserted into a femoral artery. The imaging of the arterial tree indicates significant narrowing of several segments of the coronary arteries. The patient was treated with bed rest, digitalis and a diuretic. After three months, the patient was admitted for coronary artery bypass surgery. 1. What is the underlying physiological problem for this patient?

2. What is dyspnea and why does the patient experience dyspnea while sleeping; why do the symptoms disappear after he sits up in bed?

3. What is the cause of the peripheral edema and the distending veins?

Cardiovascular Case Histories - Case 2 A 32-year-old nurse who had rheumatic fever as a child noticed a persistent tachycardia and light-headedness. Upon examination, chest x-rays showed an enlarged left atrium and left ventricle. ECG analysis showed atrial fibrillation. There was also mild pulmonary congestion. Cardiac evaluation resulted in the following information: Cardiac output (CO) 3.4 L/min Blood pressure (BP) 100/58 mmHg Left atrial pressure (LAP) 16 mmHg Right ventricular pressure (RVP) 44/8 mm Hg Heart sounds revealed valvular regurgitation. 1. Based on the information provided, which A-V valve is incompetent, allowing the regurgitation?  The A-V valve that is incompetent, allowing the regurgitation, is the mitral valve. 2. Which heart sound would be pronounced and lengthened?  The first heart sound would be pronounced and lengthened for mitral incompetence. 3. Describe, using surface anatomy, the location at which this valvular disorder could best be heard.  This valvular disorder could best be heard at the left midclavicular line at the fifth intercostal space. 4. If the other A-V valve were incompetent instead of this one, would the CO, BP, LAP, and RVP be different? If so, how?  If the tricuspid valve were incompetent instead of the mitral valve, the LAP and RVP would be different. They both would be normal or near normal. 5. What are the causes of the tachycardia, light-headedness, and mild pulmonary congestion?  The tachycardia is a reflex response (sympathetic) to the lowered systemic blood pressure. The light-headedness is from reduced blood pressure (100/58). The mild pulmonary congestion is due to regurgitation of blood through the mitral valve from the left ventricle into the left atrium during left ventricular contraction. This “reverse flow” through the incompetent mitral valve elevates the left atrial pressure and increases the pulmonary capillary pressure, resulting in fluid accumulation in the lungs (pulmonary congestion). 6. Calculate the pulse pressure (PP) and mean arterial pressure (MABP) for this individual. a. PP = 42 mm Hg b. MABP = 72 mm Hg

Cardiovascular Case Histories - Case # 3 Tom Smith is an 80-year-old retired carpenter who still does “odd jobs” for friends and neighbors. His wife has pleaded with him to relax, but he ignores her. Despite having chest pains (angina) and periods of confusion, Tom doesn’t trust doctors and has stubbornly refused to have a check-up. Recently, though, after several episodes of syncope (fainting) while he was hauling lumber, Tom grudgingly agreed to see a physician. On Physical examination, the physician noted a murmur during systole, a palpable S4, and a significantly diminished aortic component of S2 (second heart sound). An electrocardiogram (ECG) was consistent with left ventricular hypertrophy. His carotid pulse was weak. The physician ordered a cardiac catheterization which showed a pressure gradient of 100 mm Hg between the left ventricle and the aorta during systole consistent with aortic stenosis. 1. In aortic stenosis, there is significant narrowing of the aortic valve opening. Why does this narrowing cause a murmur?

2. In aortic stenosis, the murmur occurs during systole. Why?

3. Why does left ventricle hypertrophy occur in aortic stenosis?

4. What is the likely reason for Tom’s fainting during physical exertion?

5. Congestive heart failures is one consequence of aortic stenosis. Which ventricle fails in aortic stenosis, and where is edema likely to occur?

Cardiovascular Case Histories - Case 4 A 54-year-old Type-A male business executive had been experiencing migraine like headaches. One afternoon he also experienced light-headedness, slurred speech and mildly impaired motor function on his right side. One of his colleagues rushed him to the emergency room of a nearby hospital where blood pressure, blood gases, electrolytes, and an ECG were run. His blood pressure was 195/100 mm Hg, which he said was typical of what he had experienced during the past two years. Blood gases and electrolytes were normal. The ECG showed no arrhythmias but did demonstrate a left axis deviation. The gentleman was admitted to the hospital and a cerebral angiogram was performed which showed left cerebral hemorrhaging. 1. What is the diagnosis of this individual's disorder?  This individual has had a stroke (or cerebral vascular accident (CVA)). 2. What are the major contributing factors to this disorder?  The major contributing factors include chronic hypertension and a probable stressfilled profession. 3. What could have been done to prevent this problem?  Regular exercise and proper diet are important in helping to control blood pressure. If necessary, pharmacological intervention may be necessary to help return blood pressure back to normal. Agents that are vasodilators, beta-blockers and ACEinhibitors are helpful in controlling hypertension. 4. What are the early warning symptoms prior to the complication?  Elevated blood pressure and headache are early warning symptoms prior to strokes. 6. Why was there impaired motor function on the right side from cerebral hemorrhaging on the left side?  There was impaired left side motor function following right cerebral hemorrhaging because of the damage/lack of blood flow to the motor neurons in the right precentral gyrus which cross over in the corpus callosum to innervate the left side of the body.

Muscle Case 1 Chief Complaint: A 26-year-old woman with muscle weakness in the face. History: Jill Rothman, a 26-year-old gymnastics instructor, presents with complaints of muscle weakness in her face that comes and goes, but has been getting worse over the past two months. Most notably, she complains that her "jaw gets tired" as she chews and that swallowing has become difficult. She also notes diplopia ("double vision") which seems to come on late in the evening, particularly after reading for a few minutes. At work, it has become increasingly difficult to "spot" her gymnasts during acrobatic moves because of upper arm weakness. On physical examination, she has notable ptosis ("drooping") of both eyelids after repeated blinking exercises. When smiling, she appears to be snarling. Electromyographic testing revealed progressive weakness and decreased amplitude of contraction of the distal arm muscles upon repeated mild shocks (5 shocks per second) of the ulnar and median nerves. Both her symptoms and electromyographic findings were reversed within 40 seconds of intravenous administration of edrophonium (Tensilon), an acetylcholinesterase inhibitor (i.e. an "anticholinesterase"). Blood testing revealed high levels of an antiacetylcholine receptor antibody in her plasma, and a diagnosis of myasthenia gravis was made. Jill was treated with pyridostigmine bromide, which is a long-acting anticholinesterase drug, and was also started on prednisone, which is a corticosteroid drug. She also underwent occasional plasmapheresis when her symptoms became especially severe. She was given a prescription of atropine as needed to reduce the nausea, abdominal cramps, diarrhea, and excessive salivation she experienced as side effects of the anticholinesterase drug. Questions: 1. Why is this young woman experiencing difficulty chewing and double vision?  The muscles of her face and eyes are weakening due to the lack of impulse transmission. 2. How are the anti-acetylcholine receptor antibodies interfering with her normal skeletal muscle activity?  By damaging the acetylcholine receptors on the sarcolemma, these antibodies are causing interference with normal contraction impulse transmission between the motor neurons and muscle fibers. Acetylcholine can’t bind to the muscle cell, so an action potential can’t develop and contraction won’t occur. 3. How do the anticholinesterase drugs act to improve Jill's skeletal muscle function?  As mentioned above, acetylcholinersterase is a naturally-occurring chemical that breaks up the acetylcholine in the synaptic cleft after impulse transmission. An anticholinersterase drug will prevent release of acetylcholinesterase, so the acetylcholine in the synaptic cleft will not be broken down. Having the acetylcholine linger in the gap will increase the chance of contraction impulse being transmitted in the presence of fewer functioning acetylcholine receptors on the muscle fiber. 4. Why are nausea, abdominal cramps, diarrhea, and excessive salivation all side effects of the anticholinesterase drug she is taking?  The drug will affect all junctions, including junctions between neurons and smooth muscles. These smooth muscles will then be essentially over-stimulated and will contract excessively, leading to the cramps, etc.

5. Why is atropine beneficial in treating the gastrointestinal side effects mentioned in question #4?  Atropine is a drug that specifically blocks and inactivates the muscarinic type of ACh receptor without blocking the nicotinic type of ACh receptor. It is therefore an ideal drug to treat the gastrointestinal side effects caused by pyridostigmine bromide. However, atropine is not without side effects, principally caused by the widespread inhibition of parasympathetic nerve activity. 6. Why does repetitive nerve stimulation result in decreased amplitude of the muscle contractions?  The muscles will become fatigued with repetitive stimulation. 7. How will the corticosteroid prednisone benefit this patient?  It should slow down the destruction of the acetylcholine receptors on the sarcolemma. 8. Why must Jill undergo plasmapheresis when her symptoms become especially severe?  Replacing part of the patient’s plasma will reduce the concentration of the antibodies that are destroying the acetylcholine receptors. 9. Jill's doctor advises her that she is at increased risk for respiratory failure. Explain why this is so.  If the patient’s diaphragm and intercostals muscles are affected the she will experience respiratory failure.

Muscle Case 2 Chief Complaint: 19-year-old non-ambulatory male with pneumonia. History: James Fenlow, a 19-year old male, is immobile and hospitalized for pneumonia. He has a long history of progressive weakening of his muscles. In the first year of his life, James reached many gross motor skill milestones, such as holding his head up, rolling over, sitting, and standing, at normal times. However, he did not walk until age 16 months, and by age two, started to assume a lordotic posture while standing but not while sitting. A Gower's sign was noted by age four, as was a Trendelenberg gait. Over the next several years, he suffered progressive muscle weakness, most notably in the proximal musculature of the arms, pelvis, and legs. By age 9, he required orthotic braces to assist his walking, and by age 11, he was confined to wheelchair ambulation. In his early teen years, James was still able to use eating utensils, write, and type on a keyboard, though these functions have declined over the past year. At 16, he was hospitalized with bronchitis requiring antibiotic treatment, but recovered. Throughout the years, James has had no history of muscle pain or spasm, chest pain, or irregular heartbeat. He was diagnosed with a learning disability in the fourth grade, but has progressed through the grades with tutorial assistance. The only medications that he normally takes are calcium and fluoride supplements. James has a younger sister in good health and a younger brother (age 10) who is confined to a

wheelchair with problems similar to James's. No other immediate or distant family members have musculoskeletal difficulties. Physical Examination: On examination, James appeared fatigued and short of breath. Vital signs: (1) heart rate = 104 beats per minute, (2) respiratory rate = 28 breaths per minute, (3) temperature (oral) = 102.4 degrees F, and (4) blood pressure = 138 / 74. Pupils were normal and reactive to light, with ocular movements intact. No dysarthria or facial muscle weakness was noted. Percussion of the thorax suggested pulmonary infiltrates in the lower lung fields bilaterally. Breath sounds were reduced, with significant inspiratory rales heard over both lungs. His cough was very weak, but productive of green sputum. Heart sounds were normal, with no murmur. Bowel sounds were normal. Musculoskeletal exam revealed a scoliotic deformity of the spine when James sat up. Upper chest, shoulder, and thigh muscles were significantly atrophied, but the calf muscles appeared enlarged. Bilateral elbow contractures limited elbow extension to 80 degrees. Bilateral Achilles contractures were also present. Muscle strength was reduced in the biceps and triceps brachii muscles bilaterally (+2 on a scale from 0 to +5, +5 being normal), deltoids (+1), and he was not able to move either thigh into flexion or extension. Muscle stretch reflexes (rated on a scale from 0 to +4, +2 being normal) were as follows: right and left biceps and triceps brachii (+1), right and left brachioradialis (+1), right and left patellar reflexes (0), and right and left ankle jerks (+1). Questions: 1. James suffers from a condition called Duchenne muscular dystrophy. Explain the full meaning of this name.  This hereditary X-linked recessive disease characterized by progressive muscular weakness is Duchenne-type muscular dystrophy. 2. At age 4, James underwent a biopsy of the right gastrocnemius muscle. The pathologist's report noted histopathologic changes suggestive of Duchenne muscular dystrophy. Describe in detail the typical microscopic changes noted in the muscle tissue of someone with Duchenne's muscular dystrophy.  Dystrophy means defective nourishment. In muscular dystrophy there is death to muscle and replacement by fat and connective tissue, with concomitant metabolic defects. 3. Which muscles are most severely affected by this disease process?  Muscles involved in walking “on the toes” are the gastrocnemius and the soleus. The tibialis anterior muscles are “weakening,” failing to pull the toes up (opposing the gastrocnemius muscles). 4. Why did James's calves appear enlarged? What is this condition called?  Many muscles start to degenerate and adipose and collagen replace muscle tissue. There is a build-up of connective tissue in the calf muscle that causes them to enlarge because the viable cells try to compensate for the cells that are dead.

The trunk muscles that weaken in certain cases of lordosis and abdominal protuberance are the following: Lordosis: quadratus lumborum and iliocostalis lumborum Abdominal protuberance: external oblique, internal oblique, transversus abdominis, and rectus abdominis 5. At the time of diagnosis, James had an elevated serum creatine kinase (i.e. creatine phosphokinase) level of 26,000 IU / L (normal level is...