Free Sample on Pathophysiology Case Study

Question: Discuss about the Case Study for Pathophysiology. Answer: Case study 1 1. The patient is having primary aldosteronism or hyperaldosteronism or Conns Syndrome. Additionally, the high level of sodium and potassium in blood indicates hypernatremia and hyperkalemia. It is caused by the hyperaldosteronism (Ashton Acton 2012). 2. The condition is primary; thus, the patient is having a symptom of primary hyperaldosteronism. The symptoms of the patient are indicating that the patient is having an irregular blood aldosterone and rennin ratio. The primary aldosteronism includes the common features including hypertension, hypokalemia and alkalosis. The laboratory tests would reveal high serum aldosterone, low serum rennin, high blood pressure and high-resolution CT abdomen. The patient is having high serum aldosterone and low rennin with high potassium and low sodium in urine (Ashton Acton 2012). Additionally, the bradycardia with depressed ST segment in ECG report is also indicating hypertension that is a symptom of primary hyperaldosteronism. Additionally, the patient is facing frequent urination which is also a sign of the primary disorder. Low rennin concentration is the major indicator of primary hyperaldosteronism. 3. The ST depression in ECG result is causing due to coronary insufficiency. This is due to the changes in electrolyte level in blood serum. Decreased extracellular potassium causes myocardial hyperexcitability. The changes or imbalance in the electrolyte, especially, potassium increases the amplitude of U wave and T wave flattens, ST depression occurs. Therefore, ECG changes are mainly due to changes in potassium level in blood serum (Ashton Acton 2012). 4. In Conns syndrome, blood aldosterone level enhances that enhances the activity of sodium-potassium ATPase in the basolateral membrane of kidney and epithelial sodium and potassium channels, thereby increasing sodium reabsorption and potassium secretion. The symptoms lead to increased extracellular sodium and reduced extracellular potassium. 5. While assessing muscle strength, the patient showed the grade of 3 bilaterally. The bilateral muscle weakness indicates weakness occurring on both sides of the body. The grade 3 muscle weakness refers to the movement against gravity, but no movement against added resistance that is a sign of muscle weakness (Ashton Acton 2012). The proper balance of electrolytes in blood is important for proper functioning of muscles. The low serum potassium level causes muscle weakness. The low potassium level and electrolyte imbalance in the blood leads to osmosis and low acidity in blood are the major cause of muscle weakness, as potassium is important for nerve impulse transmission and muscle contract. 6. A cross-sectional analysis revealed that plasma aldosterone is related to high BP. In hyperaldosteronism, the extracellular sodium level increases with decreased potassium. Increased salt increases the blood pressure with low potassium level. Sodium reabsorption and retention lead to high blood pressure. 7. In the hyperaldosteronism, the increase in aldosterone enhances the activity of sodium-potassium channels and ATPase, thereby increases sodium reabsorption and potassium secretion. The sodium retention increases blood pressure. High blood pressure increases glomerular filtration rate and release of potassium through urine (Ashton Acton 2012). 9. The ABG diagnosis of the patient indicates Alkalosis. Patient's pH is 7.5, that is 7.45 and CO2 is 35. Also, the patient's HCO3- is 26, i.e. 32. Therefore, the signs indicate metabolic alkalosis. It is one of the symptoms of primary hyperaldosteronism. 10. The excess secretion of aldosterone enhances the permeability of sodium and potassium through the membrane channels; sodium level enhances more than the level of potassium loss. It leads to alkalosis and more sodium ion (cation) elevates blood pH (Ashton Acton 2012). 11. The patient has the syndrome due to potassium imbalance; therefore, potassium-sparing diuretic would be suitable, i.e. Spironolactone, as this medicine will help to increase body fluid and prevent too much loss of potassium. 12. The first recommendation would be to consume salt-free diet. The second recommendation would be to consult with an expert physician like endocrinologist. 13. Potassium-sparing medication, aldosterone antagonists and angiotensin-converting enzyme (ACE) inhibitorscan help the patient to reduce his symptom related to the Conns syndrome. In the further case, surgery can be suggested (Ashton Acton 2012). Case study 2 1. The patient is going through the stage 3 intracranial hypertension with the sustained increase of ICP with small changes. At this stage, the CPP decreases with increased systolic pressure and dilated blood vessels in the brain. The results lead to increase cerebral blood volume with high leukocytes and protein level. Lowered CPP led to unconsciousness due to reduced cerebral blood flow (Myers 2012). 2. The Biots breathing pattern was identified in the patient. The patient was diagnosed with low breathing rate, 30/minute with no crackles and 61bpm heart rate. The symptoms were related to the respiratory pattern that can be characterized by the clusters of rapid respiration of equal depth followed by regular apnea. Based on the breathing pattern, it can be said that the damage is in medulla oblongata due to uncal or tentorial herniation (Myers 2012). 3. The patient is having small purple rashes on his arms, legs and check. This rash is known as the purpura which is red or purple and arises due to the bleeding into the skin. These rashes do not blanch with pressure, indicating meningitis rashes. 4. The Brain edema increases intracranial pressure leading to brain injury. The meningitis mechanism is indicating that crossing blood-brain barrier leads to vasogenic edema and then the huge amount of white blood cells enter in CSF and the inflammation leads to interstitial edema. The cytotoxic edema also occurs due to decreased blood flow (Myers 2012). The breakdown of tight endothelial junction allows intravascular proteins to penetrate the barrier and the edema spreads with the entry of water into gray matter, thereby swelling occurs. The activation of the immune system enhances the secretion of immune mediators, leading to inflammation. 5. The organism when crossing the blood-brain barrier, it causes the activation of the immune system leading to inflammation. The swelling leads to increased pressure within the skull and enhanced ICP; it lowers CPP. Lowered CPP enhances the blood pressure (Myers 2012). 6. Meningitis leads to the inflammation or swelling of the brain leading to increased intracranial pressure. After crossing the blood-brain barrier, the organism activates the immune system and enhances the secretion of various mediators; it influences the entrance of white blood cells in CSF, thereby enhancing pressure in CSF leading to intracranial pressure. 7. pH is 7.56 that is higher than the normal rate and it indicates the alkalosis. On the other hand, the pCO2 is 25 mmHg that is lower than the normal rate; normal range is 35-45. The normal rate of pHCO3 is 22-28 mEq/L. Therefore, the HCO3 level is normal in patients blood. Overall, respiratory alkalosis is found (Myers 2012). 8. The doctor preferred lumbar puncture instead of a blood test because the bacteria Neisseria meningitides spread and divide in cerebral spinal fluid and the immune response against the organism also occurs in the CSF. The organism would not be found in blood; therefore, to isolate the organism lumber puncture was done (Myers 2012). Case study 3 1. Ms. Myocardium experienced acute myocardial infarction or heart attack due to the blockage of left anterior artery. In this condition, the patient had undergone shock that is known as the cardiogenic shock. It is the condition when the heart is unable to pump blood needs by the body. 2. Ms. Myocardium experienced heart attack due to 95% occlusion of left anterior artery. It is a major hindrance in normal blood flow through the circulatory system. At this condition, due to major blockage, the heart becomes unable to pump enough blood to cells through the blood vessels. Therefore, blood flow reduces. It leads to low blood pressure (Hjemdahl et al. 2012). 3. Due to 95% blockage of left anterior artery, the heart becomes unable to pump blood through the blood vessels. The amount of blood and red blood cells reduces in the blood vessels; thus, the patient looks pale. For the similar reason, the patients body is cold (Fryar et al. 2012). 4. The blood test found the presence of creatine phosphokinase-MB (CPK-MB) which is the most specific and sensitive indicator of acute myocardial infarction or heart attack. The LDH2 is also a significant cardiac marker as it indicates hemolysis or tissue breakdown. The presence of blood myoglobin indicates very recent injury to the heart or skeletal muscle, therefore, the chance of occurrence of heart attack (Hjemdahl et al. 2012). 5. The presence of creatine kinase (CK-MB) indicates heart muscle injury instead of skeletal muscle damage. A high level of LDH2 indicates the occurrence of myocardial infarction. However, myoglobin is not much specific for myocardial infarction. Its presence indicates muscle tissue damage (Fryar et al. 2012). 6. The Q wave indicates the normal left-to-right interventricular depolarization. It indicates an artery of heart is blocked. The ST segment indicates the ventricular depolarization. However, ST elevation in myocardial infarction indicates the full thickness elevation of the affected area (Hjemdahl et al. 2012). 7. The TPA is the most common drug used for the therapy of thrombolytic patient such as a heart attack patent. It is important for dissolving the blood clot in the anterior left artery which led to the blood clot. IT would help to clear the blockage (Fryar et al. 2012). 8. The ejection fraction is 30%. It indicates the heart failure is Systolic heart failure. 9. Indigestion- Blockage of fatty deposits in an artery reduces the blood supply to the heart. Blockage leads to poor blood circulation that can signal abdomen leading to indigestion, for poor oxygen supply (Fryar et al. 2012). Pain between shoulder blades- The damaged tissue in heart or pain in blocked artery sends the signal to the spinal cord leading to shoulder pain. Tachycardia- It is characterized by left ventricular dilation and systolic dysfunction due to the myocardial infarction (Hjemdahl et al. 2012). Reference List Fryar, C.D., Chen, T. and Li, X., 2012. Prevalence of uncontrolled risk factors for cardiovascular disease: United States, 19992010.NCHS data brief,103, pp.1-8. Hjemdahl, P., Rosengren, A. and Steptoe, A., 2012. Stress and cardiovascular disease. London: Springer-Verlag London Ltd. Myers, T., 2012. Meningitis. Cork: Publish on Demand Global LLC. Ashton Acton, P., 2012. Advances in Hyperaldosteronism Research and Treatment: 2012 Edition. ScholarlyEditions.