Congestive Heart Failure and Peptic Ulcers Diseases - Assignment Example

Pathophysiology and Pharmacology Pathophysiology and Pharmacology Pathophysiology Pneumonia Pneumonia is an infectious process resulting from the microbial invasion of the lung parenchyma evoking exudative solidification of the lung tissues. Its causative agents include bacteria, viruses, fungi, parasites or chemicals. Inhalation exposes the respiratory airways and alveoli to hazardous dusts, chemicals, and microorganisms (Lowe & Stevens, 200). The lung has potent defense mechanisms that clear or destroys any bacteria, and other microorganisms inhaled with air. These defense mechanisms include nasal clearance by sneezing or blowing, tracheobronchial clearance by mucociliary action and alveolar clearance where alveolar macrophages phagocytize bacteria or solid particles. Impairment of these mechanisms results in pneumonia. It may also occur when the resistance of the host is lowered. Congestive Heart Failure (CHF) Congestive Heart Failure arises when the heart is unable to circulate enough blood to meet the body’s metabolic demands. Heart failure is caused by damage or overloading of the myocardium (Hosenpud & Greenberg, 1994). It is, therefore, associated with systolic or diastolic overloading and with myocardial weakness. Various conditions cause heart failure. Such conditions include hypertension, myocardial infarction, and amyloidosis. Overtime physiologic stress on the myocardium causes the contractility of the muscle to reduce and cardiac output declines. However, venous input to the ventricle remains constant or increases and is responsible for cardiac overload. There is also increased heart rate, hypertrophy and enlargement of the ventricles. Tuberculosis Tuberculosis is a highly infectious disease that infects one-third of the world population. It is often fatal killing about three million people yearly. It usually caused by Mycobacterium tuberculosis transmitted by inhalation of infective droplets and Mycobacterium bovis transmitted by milk from infected cows. The primary phase of M. tuberculosis infection starts with inhalation in the lower segment and middle lobes of the lung (DYER, 2010). Alveolar macrophages then phagocytize the mycobacterium and transported it to hilar lymph nodes. However, naïve macrophages are unable to kill the Mycobacterium that lyses the cell upon multiplication. Other macrophages are infected, and dissemination through the blood to other parts of the body occurs. The active disease years later, Reactivation TB, results from the proliferation of dormant Mycobacterium seeded during the primary phase. Peptic Ulcers Diseases (PUD) Peptic ulcer disease is the breach of the gastrointestinal tract mucosal layer. There are two forms of PUD; gastric and duodenal peptic ulcer diseases (ESCOTT-STUMP, 2008). They occur in areas of GI tract exposed to acid-pepsin secretions. Development of GI mucosal ulceration is as a result of various predisposing factors. One such factor is increased level of mucosal aggressive; that is hydrochloric acid and pepsin. The production is influenced by the hormone gastrin and neural stimulations. The other factor is the inability of the mucosal barrier to resist the destructive action of the gastric secretions. The integrity of the mucosal surface depends on adequate blood flow and intact mucosal barriers. Increased permeability of the epithelial layer of the stomach to hydrogen ion is seen in patients with gastric-peptic ulcers. Diabetes Insipidus (DI) Deficiency of production or secretion or a decreased renal response to ADH result in a condition called Diabetes insipidus (FLEISHER, 2006). ADH is produced by the hypothalamus and stored in the pituitary gland. It regulates the amount of fluid in the body. Diabetes insipidus results in fluid and electrolyte imbalances caused by increased urinary output and increased plasma osmolality. This condition is characterized polydipsia and polyuria. Hypernatremia causes elevated serum osmolality as a result of water loss in the kidney. Patients tend to drink large amounts of water so that serum osmolality is normal. Nocturia causes fatigue with patients often complaining of generalized weakness. Hashimotos thyroiditis Hashimotos thyroiditis is an autoimmune thyroid disease that causes significant morbidity. The thyroid gland cells are destroyed by an immunologic process. The distinctive pathophysiological feature of Hashimoto’s thyroiditis is lymphocytic infiltration of thyroid follicles resulting in autoimmune glandular destruction. The pathogenesis involves genetic, environmental and immunological factors (Chistiakov, & Trukulov, 2003). This disorder causes hypothyroidism. However, a hyperthyroid state may develop mid-course in the disease as a result of leakage of preformed thyroid hormone from damaged cells of the gland. The signs and symptoms include bradycardia, slowed speech, delayed reflexes, constipation, bile reflux, and ascites. At critical level myxedema coma occurs. In children, it is the main cause goiter and hypothyroidism. Cushing’s syndrome Cushing’ syndrome is as a result of chronic elevation in glucocorticoid hormones. It is as a result of increased ACTH production (BRONSTEIN, 2011). Cushing’s syndrome can result from excessive secretion of adrenocorticotropic hormone caused by increased adrenocortical activity. Other causes include the use of corticosteroid medication, primary hyperplasia and ectopic production of ACTH. Pituitary form of Cushing’s syndrome results from excessive production of ACTH by a tumor of the disease cases, and it is called Cushing’s disease. An adrenal tumor causes an adrenal form of Cushings syndrome. Ectopic Cushing’s is due to an ACTH- producing tumor such as in some bronchogenic cancers. The major manifestations of Cushing’s syndrome include hypertension, truncal obesity, moon face, buffalo hump, peptic ulcers, and hyperglycemia. Meningitis This is the inflammation of the meninges affecting pia mater, arachnoid mater and subarachnoid space. It is caused mainly by infection with bacteria, viruses, and other microorganisms and sometimes chemicals. Bacterial meningitis is caused by Haemophilus influenza, Neisseria menengitidis, and Streptococcus pneumonia. The microbe reaches the meninges by contact with the nasal cavity and skin or through the bloodstream. The pathogens replicate and induce inflammation (MYERS, 2012) A pathophysiological hallmark or this infection is the recruitment of activated leukocytes into the CSF. Symptoms and signs of meningitis include fever and chills caused by the release of inflammatory mediators and endotoxins, headache, photophobia and nausea due to raised ICP as the result of inflamed meninges and neck pain and stiffness. Pharmacology Analgesics Analgesics are drugs that provide pain relief. There are two categories of analgesics; narcotic and non-narcotic. Narcotic analgesics are derived from opium. They bind to delta, kappa, mu and sigma opioid receptors. These receptors are situated in the nervous system and are involved in pain signaling and control (LUSSIER & BEAULIEU, 2015). Opioid analgesics block nociceptive signals to the brain. They also act at higher brain centers where they control affective components of pain. Non-narcotic analgesics, on the other hand, are over-the-counter analgesics used to treat mild to moderate pain. In addition to the analgesic activity, they are antipyretic and anti-inflammatory. They act in peripheral tissues inhibiting the formation of pain-producing substances. NSAIDs inhibit cyclooxygenase hence blocking prostaglandin production. Anesthetics Anesthetics are drugs that cause anesthesia that refers to the elimination of sensation. They are mainly used during surgical procedures and in dentistry (BURGDORF, 2014). There are two types of anesthetic; general anesthetics ad local anesthetics. General anesthetics cause total loss of consciousness. They target biological factors involved in neuronal pathways. Effects of general anesthetics also include analgesia, amnesia, inhibition of sensory and autonomic reflexes and skeletal muscle relaxation. Local anesthetics, on the other hand, cause loss of sensation in a region of the body without loss of consciousness. In addition, local anesthetics act by binding to fast sodium channels and hence preventing transmission of nerve impulses. Steroids Steroid drug are designed to mimic natural hormones that regulate certain functions. These drugs treat a wide variety of conditions. Corticosteroid drugs are based on hormones produced by the adrenal gland (LAU, 2008). They are used to treat inflammation. They reduce inflammation, as well as suppressing the immune system. Corticosteroids treat conditions including asthma, atopic eczema, allergic rhinitis, chronic obstructive pulmonary disease and lupus. They are also used in hormone replacement such as in Addisons disease. Side effects of long-term treatment with Corticosteroid include acne, diabetes, high blood pressure, osteoporosis and withdrawal symptoms. Anabolic steroids, often abused by athletes, act to increase proteins in the cells especially those of the skeletal muscle. Barbiturates Barbiturates drugs are a group of drugs derived from barbituric acid. These drugs are used as anxiolytic, sedatives, antiepileptic, hypnotics and weak analgesics. They act by suppressing the central nervous system. They act as positive allosteric modulators and at high levels as agonists of GABA receptors of the central nervous system. Their classification is according to the duration of action. Long-acting last up to 24 hours such as barbital. Intermediate act for 6 to 12 hours an example is amobarbital. Short-acting include pentobarbital used to treat insomnia (GOLAN, 2008). Ultrashort-acting such as thiamylal are used in surgery to induce unconsciousness. Barbiturates are highly addictive causing physical dependence and withdrawal syndrome. Anthelmintic Anthelmintics are drugs used against parasitic worms. They can be classified into three categories; cestode anthelmintic, nematode anthelmintic, and trematode anthelmintic. Cestode anthelmintic are used to expel tapeworms. Albendazole acts by inhibiting glucose uptake by the helminths. This, therefore, disrupts energy production of the parasite. Praziquantel is a broad-spectrum anthelmintic that acts by causing tetanus-like contraction of the musculature of the parasite. Nematode anthelmintic treat roundworms. Nematodes cause infection of the blood and tissue. Mebendazole acts by binding and interfering with the synthesis and by decreasing glucose uptake (ACTON, 2012). Trematode anthelmintic treat fluke. These are leaf-shaped flatworms that infect the liver, lungs, intestines and blood. Antibiotics Antibiotics drugs are used to treat bacterial infections. These drugs act by inhibiting growth or killing the bacteria. They are used for, bacterial infections, protozoan infections, immunomodulation and prevention of infection during surgery. These drugs have various mechanisms of action. They may act by targeting the bacterial cell wall or cell membrane. These have bacterial activity and include penicillin, cephalosporin sand polymyxin. Some such as quinolones and sulfonamides interfere with bacterial enzymes affecting metabolic processes such as protein synthesis. Side effects include diarrhea when they affect intestinal flora, nausea, fever, photodermatitis, and anaphylaxis (GALLAGHER & MACDOUGALL, 2012). Yeast infections may occur when they interfere with vaginal flora causing overgrowth of Candida yeast. Antineoplastic Antineoplastic drugs used to inhibit the development of a neoplasm. They are classified as cytotoxic drugs that act directly on the cell, hormones, which are mainly steroid in nature acting to suppress hormone secretions or antagonize hormone action and miscellaneous. One mode of action is by distracting DNA synthesis. Some of these drugs are structural analogs of bases or nucleosides of intermediate metabolites (LEDNICER, 2015). They are converted to ribotides by enzymes of nucleotide metabolism, which then act as inhibitors of nucleotide synthesis. Some of the ribotides are incorporated into DNA, which is inactive. Other antineoplastic drugs act as chelating agents inhibiting DNA double strand dissociation. Antineoplastic drugs may also act by activation of endonuclease and inhibition of topoisomerase causing DNA scission and apurinic acid formation. Antiarrhythmic drugs These are drugs used control cardiac arrhythmias. They are divided into five classes on the basis of their action. Class I used in the treatment of conditions such as ventricular arrhythmias act on the sodium channel. Class II act at beta-adrenergic receptor’s blocking catecholamine effect hence decreasing sympathetic activity (BILLMAN, 2010). Propranolol, a beta blocker with sodium channel blocking action is commonly used to decrease myocardial infarctions deaths. Potassium channel are blocked by class III resulting in enhanced repolarization. Class IV is calcium channel blockers resulting in decreased contractility of the myocardium. Drugs whose mechanism of action are not well defined such as digoxin are classified in class V. Bibliography ACTON, Q., 2012, Anthelmintics: advances in research and application: Scholarly Paper. http://alltitles.ebrary.com/Doc?id=10549821 BILLMAN, G., 2010, Novel therapeutic targets for antiarrhythmic drugs, Hoboken, N.J., John Wiley & Sons. BRONSTEIN, M. D., 2011, Cushings syndrome: pathophysiology, diagnosis, and treatment, New York, Humana Press. BURGDORF, S., 2014, Anesthetics, Minneapolis, MN: ABDO Publishing Company. Chistiakov, D., & Trukulov, R., 2003, “CTLA4 and its role in autoimmune thyroid disease”, Journal of Molecular Endocrinology, 3, (August, 2003), pp.(21-36), doi:10.1677/jme.0.0310021 DYER, C., 2010, Tuberculosis. Santa Barbara, Calif, Greenwood. ESCOTT-STUMP, S., 2008, Nutrition and diagnosis-related care, Philadelphia, Wolters Kluwer Health/Lippincott Williams & Wilkins. FLEISHER, L. A., 2006, Anesthesia and uncommon diseases, Philadelphia, PA, Elsevier/Saunders. GALLAGHER, J., & MACDOUGALL, C., 2012, Antibiotics simplified, Sudbury, MA, Jones & Bartlett Learning. GOLAN, D., 2008, Principles of pharmacology: the pathophysiologic basis of drug therapy, Philadelphia, Lippincott Williams & Wilkins. HOSENPUD, J. D., & GREENBERG, B. H., 1994, Congestive heart failure pathophysiology, diagnosis, and comprehensive approach to management, New York, Springer-Verlag. LAU, D., 2008, Steroids, New York, Rosen Central. LEDNICER, D., 2015, Chemistry of antineoplastic agents, Hoboken, John Wiley. Lowe, J. F., Stevens, A., 2000, Pathology, St. Louis: Mosby LUSSIER, D., & BEAULIEU, P., 2015, Adjuvant analgesics, New York: Oxford University Press. MYERS, T., 2012, Meningitis, Cork, Publish on Demand Global LLC. Read More