Critical Thinking Question

Custom Student Mr. Teacher ENG 1001-04 5 January 2017

Critical Thinking Question

1. Explain the differences between bacterial meningitis, aseptic meningitis, fungal meningitis, and tubercular meningitis. Bacterial meningitis is a primary infection of the pia mater, arachnoid and subarachnoid space, ventricular system and the CSF of the brain. The subarachnoid space is accessed either by a systemic, bloodstream or direct extension infection. Common causes of bacterial meningitis after the neonatal period are Meningococcus (Neisseria meningitidis) and pneumococcus (Streptococcus pneumonia).

For neonates, pneumococcus and gram-negative enteric bacilli are common agents. Aseptic meningitis (viral meningitis, nonpurulent meningitis, lymphocytic meningitis) is an inflammation which is thought to be localized to the meninges. The population at risk depends of the virus. A variety of symptoms are caused by a plethora of viruses such as enteroviral (most common), mumps, herpes simplex types 1 and 2,, St. Lus encephalitis virus, West Nile virus, California encephalitis virus, Venezuelan equine encephalitis, Colorado tick fever, lymphocytic choriomeningitis virus, Epstein-Barr virus, and influenza virus types A and B. Fungal meningitis is a chronic, much less common condition than bacterial or viral meningitis. It most frequently occurs in persons with impaired immune systems or those with altered normal flora.

Development is insidious and usually occurs over days to weeks. Also associated with chronic meningitis are syphilis, tuberculosis and Lyme disease. Tubercular meningitis is the most common and most serious form of CNS tuberculosis, and is found mostly in those with acquired immunodeficiency syndrome (AIDS). Miliary tubercules form in the brain and meninges, later eroding in the pia mater with mycobacteria entering in the CSF producing a hypersensitivity reaction which causes purulent exudate to the basal meninges, cerebrum and spinal nerves. Vasculitis occurs causing cerebral ischemia and infarction. Symptoms include headache, low-grade fever, stiff neck, nausea and vomiting, irritability, difficulty sleeping and fatigue.

These signs and symptoms lead to increase to confusion, stiff neck, significant behavioral changes, and seizures. Additionally, hydrocephalus and cranial nerve palsies or cerebral infarcts may occur. Early diagnosis and treatment with proper antituberculosis may cause a 90% recovery rate.

2. A neonate has a harsh, loud, systolic murmur shortly after birth. This is best heard at the left lower sternal border. The neonate is acyanotic and has no other symptoms. What type of congenital heart disorder does this infant have? Explain why the neonate is not cyanotic. When could the infant become cyanotic? These symptoms describe a ventricular septal defect (VSD). This type of defect is a left to right shunt of blood flow through the septum of the heart and symptoms depend on the size of the shunt. Because of the increase in blood from the right ventricle (RV) into the pulmonary artery (PA), the PA, left atrium (LA) and left ventricle (LV) become enlarged.

A large VSD causes a large amount of pulmonary volume. Over time, the smooth muscle layer of the arteriolar wall thickens and a decrease in diameter of the pulmonary vessels occurs which causes resistance to the new blood flow. An increase in pulmonary vascular resistance causes a reverse shunting through the VSD causing cyanosis from deoxygenated blood flowing through systemic circulation. This phenomenon is termed Eisenmenger syndrome.

3. How does defective gastric secretion of intrinsic factor (IF) cause anemia? What is this type of anemia called, and how does a person get it? Intrinsic factor (IF) is a mucoprotein that is produced by the parietal cells. It is responsible for absorption of vitamin B12 in the ileum. Decreased amounts of IF causes a lack of absorption of B12 resulting in pernicious anemia. IF deficiency may be congenital or from adult onset gastric mucosal atrophy and parietal cell destruction. In older adults, failure to absorb IF is the cause of almost all vitamin B12 deficiencies. Congenital IF disorder is caused by an autosomal recessive inheritance pattern which is a genetic disorder. Gastric atrophy may be autoimmune and occurs along with type A chronic gastritis.

4. Discuss the pathophysiologic relationship between cirrhosis and portal hypertension. Cirrhosis is an inflammatory disease of the liver that disrupts its structure and function. Fibrous bands are formed causing nodular regeneration giving the liver a bumpy appearance. The liver is smaller or larger than normal and is hard when palpated. Parenchyma of the liver becomes distorted and the biliary channels become obstructed causing jaundice. Shunting is formed in new vascular channels bypassing blood from the liver. Obstruction in the portal veins also causes abnormal high blood pressure in the system from resistance of the blood flow from the obstruction. This is termed portal hypertension. Cirrhosis of the liver is the most common cause of portal hypertension.

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  • Subject:

  • University/College: University of California

  • Type of paper: Thesis/Dissertation Chapter

  • Date: 5 January 2017

  • Words:

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