Which Would Antibacterial Agent Be Effective in the Therapy of Mr. Bts Urinary Tract Infection - Assignment Example

Pharmacology 2 PART A - (Total 15 marks) 1. Which would antibacterial agent(s) be effective in the therapy of Mr. BT’s urinary tract infection? (4 marks) Urinary tract infections abbreviated as UTIs is one among the most infectious disease in the world, with statistics indicating that about 10% of the people suffer from the UTIs in their lifetime. These infections can either be symptomatic or asymptomatic (Kistorp et al. 2005). The major causative agents are bacteria though there are other causative agents such as fungi and virus. Examples of anti-bacterial agents for UTI therapy includes: i. Nitrofurantoin ii. Auranofin iii. Cephalosporins iv. Fosfomycin 2. State the mechanisms of action of each of these agents. (4 marks) i. Nitrofurantoin This is a drug which is a strong resistance to the development bacterial. The resistance to bacterial development is as a result of multiplicity action. It also inhibits synthesis of, RNA, DNA, cell wall and proteins. This drug is under the activation of bacterial flavoprotein. ii. Auranofin It has the ability to inhibit multiple biosynthetic pathways. These include the bacterial protein synthesis and DNA synthesis. When the auranofin Surprise the synthesis of the bacterial proteins methicillin production is greatly reduced iii. cephalosporins The mode of action of this drug is that it inhibits synthesis of a cell wall; it bides with penicillin binding proteins thus blocks peptidoglycan transpeptidation reaction. iv. Fosfomycin This is an antibiotic that concentrates in the bladder and the kidney. This drug is useful particularly to treat uncomplicated UTIs. It is known to reduce the ototoxity and nephrotoxity of platinum that contains anti-tumor agents (Barnes, 2010). Fosfomycin works by inhibiting enolpyruvate transferase (MurA). By inhibiting MurA then N-acetylmuramic acid formation is prevented. Just as other anti-bacterila agents; fosfomycin works against gram-positive bacteria e.g. staphylococcus aureus and gram-negative bacteria e.g. pseudomonas aeruginosa. 3. Outline the pathophysiology underlying Mr. BT’s hypersensitivity to penicillin (4 marks) The main problem in the use of penicillin is a hypersensitivity reaction. This reaction will lead to the following; vomiting, pruritus, urticaria, laryngeal and cardiovascular collapse. The spread of multiple drug resistance bacteria will be slowed down by the allergic condition of penicillin. It is also important to note that all forms of synthetic and natural penicillins can cause allergy. The hypersensitivity in penicillin cannot be predicted and has been found that individuals who tolerated penicillin in the past are likely to show allergy on succeeding penicillin administration. 4. Given the fact that Mr. BT is allergic to penicillins, is cephalexin therapy contraindicated here? (3 marks) Cephalexin therapy is contradicted in the case of Mr. BT. This is because it is a medical precaution that anyone who is allergic to penicillin should not take cephalexin. Most patients who are allergic to penicillin are also found to be allergic to Cephalexin. The doctor should closely monitor Mr. BT since there is an increased risk that he will be allergic to cephalosporin antibiotics. PART B: (Total 30 marks) Answer the following questions: 1. Describe the mechanism of action of the corticosteroids and indicate the adverse effects that require monitoring during treatment with these drugs. (6 marks) Corticosteroid is a class of steroid hormones. There are two classes of Corticosteroids which includes; glucocorticoids, and mineralocorticoids. Glucocorticoids will affect metabolism activity. Generally, Corticosteroid is released by the adrenal cortex. Hypothalamic-pituitary-adrenal axis is the one responsible for the control of the plasma concentration of corticosteroids. These drugs for long have been used as an immunosuppressive drug and also as an the inflammatory drug. This drug has been used in the treatment of the following diseases since the early 50s; rheumatoid arthritis, allergies, asthma, and also dermatological disorders. The mechanism of action is that it will inhibit cyclooxygenase-2 and 5-lipoxygenase. In the alleviation of inflammatory disorders, there is glucocorticoids efficacy. This efficacy will result from glucocorticoid receptors’ pleiotropic effects. The drug will also induce IkB and MAPK phosphate I which is an anti-inflammatory protein. It will block NF-KB; this is by inflammatory protein synthesis inhabitation. Most of the patients who receive high doses of corticosteroids commonly show the following disorders; psychosis, mania, depression, and this wil require pharmacological treatment (Dantze et al. 2008). The psychiatric symptoms, however, are reversible when this therapy is discontinued. The following are the adverse side effect: a) Retarded growth in children b) Hyperglycemia c) Suppression of the immune system d) Osteoporosis e) Glaucoma f) Metabolic disturbances g) Hypertension 2. To which cytotoxic drug groups does each of the drugs in the case study belong? (5 marks) There is a classification of drugs according to how they can seriously cause necrosis when extravagated; neutral drugs have the least damage while vesicant drugs may cause necrosis of the tissue. Table A Neutral cytotoxic Inflammitants cytotoxic Irritant cytotoxic Exfoliants cytotoxic Vesicants cytotoxic cytarabine methotrexate Daunorubicin- liposomal vincristine The cytotoxic agents can be classified as following in the table bellow Table B Alkylating agents Anti-metabolites Mitotic inhibitors antibiotics Others Methotrexate Vincristine Daunorobicin L-Asparaginase 3. Describe the mechanism of action of each of the drug groups identified in question Antibiotic Type Cytotoxic Agent (5 marks) Mechanism of action of: i. Antibiotic agents e.g. Daunorubicins: some compounds that occur naturally were found to have antibiotic activities. They were developed into an anticancer agent. There are several examples as Daunorubicins in question. Others include; bleomycin, dactinomycin, doxorubicin among others. To consider the mechanism of these antibiotic agents we consider the mechanism of Daunorubicins; these antibiotics will inhibit cell wall synthesis and affect the permeability of some agents into the cell by inhibiting the cell membrane. They also inhibit protein synthesis by affecting ribosomal activities. They also work by blocking the metabolic process of the microorganisms. Finally, the antibiotics will interfere with the synthesis of nucleic acid. However, due to mutation, it has been found that the bacteria have been developing some resistance ii. Anti-metabolites e.g. Methotrexate, among the first chemotherapeutic effective drugs to be discovered were the antimetabolites. The metabolite agents include; pyrimidine, purine analogues, and folic acids. Their structures are similar to those of the molecules useful in both DNA and RNA synthesis. These antimetabolites are comparable to the compounds used in biochemical activities. They will prompt the death of a cell during the cell growth at the S phase of growth. These agents inhibit the enzymatic activities useful in the production of nucleic acid. iii. Alkylating agents, alkylating are classified as the first non-hormonal drugs administered to the treatment of cancer. These agents are found to be very reactive with biological molecules which are rich in electrons. They interfere with the process of cell division. They are also found to be toxic to another cell since they interfere with their normal cell division process. A good example of the frequently dividing cells are those found in; testicles, in the bone marrows and other organs. iv. This is a drug that will inhibit the process of mitosis. When cell division starts, microtubules are destructed and the cell is not able to divide. The reason why these inhibitors are useful in cancer treatment is that cancer cell through the process of mitosis they can spread over the whole body. It is should be noted that cancer cells have an abnormal growth and division. Therefore they are adversely affected by mitotic inhibitor than the normal body cells, thus preventing cancerous cell growth. 4. What are the common immediate and delayed adverse reactions associated with cytotoxic drugs? (4 marks) Cytotoxic cells are in opposition to reach all parts of the body. As they kill cancer cells they will also kill the normal body cells. Treatments will cause; nausea, fatigue and loss of hair. Damage to the pharynx and the mouth, diarrhea is also another side effect. The bone marrows will be destroyed since the blood cells have their site of formation in the bone marrow. The hands and the soles of the feet become numb, they are hypersensitivity, premature menopause and the finger and toenail changes frequently. 5. Describe the clinical management of a client with increased susceptibility to infection. (5 marks) During chemotherapy, the body produces very few white blood cells. This implies that the immune system will be weak. The viruses, fungi, and bacteria that surround you are likely to get into your body with less or no destruction of the white blood cells. These surrounding may include; the skin, the colon, the mouth, the genitals etc. the chances of being infected with a disease is very high due to the weakened immune system. The following precautions should be taken into place; a) Treating the infections using antibiotics b) In the case of high fever transfusion may be used though it is not recommendable to patients with a low neutrophil. It can be administered to patients who also have low or no response to fungal infections. c) Medical staff and those who visit the patient should always wash their hands and also observe other precautions in order to prevent themselves from exposing to infection-causing agents. Wearing of masks, gloves also would help to prevent exposure to the infection causing agents. d) Meticulous cleaning of the catheter by the caregiver in case of chemotherapy. 6. To which antimicrobial drug group does doxycycline belong? Is it considered a bactericidal or bacteriostatic agent? Explain. (3 marks) Doxycycline acts against both aerobic and anaerobic positive and gram-negative bacteria. An antimicrobial can be defined as any agent that will kill the microorganism. The disease-causing microorganisms can be classified according to the micro-organisms in which they will act against. I.e. antifungal are used to fight against fungi, antibiotic fights against bacteria. The other mode of classifying them is according to how they will function. I.e. microbicidal – kills microbes, and biostatic will inhibit the growth of the microbes. Doxycycline acts by inhibiting bacterial protein synthesis. Basing on the mode of action it is, therefore, a biostatic since it inhibits bacterial growth. Basing on the microorganism that it acts against it is an antibiotic. 7. Define the term ‘antimicrobial drug spectrum of activity’. What is the spectrum of activity of doxycycline? Why choose a drug with this spectrum of activity? (2 marks) Antimicrobial drug spectrum of activity can be defined as the range of objectives against which a drug is biologically active mainly in relations to medical effectiveness. Doxycycline is an antibiotic. The antibiotic’s spectrum of activity can be described as the variety of bacteria against which the antibiotic is effective. The spectrum can be divided into narrow spectrum antibiotic, implying that only a few number of bacteria, or broad spectrum. A broad spectrum of activity is advantageous in there a capability to treat presumptively. PART C - (Total 35 marks) 1. What is the rationale for the use of fibrinolytic drugs in acute myocardial infarction (AMI)? Are there any constraints regarding the timing of administration of these drugs in AMI? (4 marks) Formation of thrombus leads to the formation of acute coronary thrombosis. Fibrinolytic therapy was introduced to treat myocardial infarction. The modern fibrinolytic drugs are used to activate the fibrinolytic system. It is composed of plasminogen which is infused into the bloodstream through intravenous. It should be noted that, while using fibrinolytic therapy to treat anyone suffering from AMI the dose and timing are very important. A slight deviation in timing will have an adverse effect on the patients’ health. The medication outcome is likely to be negatively affected. 2. Compare and contrast the mechanisms of action of the fibrinolytic drugs streptokinase and aspirin. (3 marks) Fibrinolytic drugs stimulate the dissolution of the blood clot. It is therefore very useful under a condition where the patient is under heart attack, especially when a patient suffers from coronary thrombosis. The blood clot that forms and blocks coronary artery is dissolved and blood circulation is restored. Aspirin improves vasodilation thus reducing thrombosis. 3. What adverse reactions should be monitored during and after fibrinolytic drug therapy? (3 marks) Hemorrhage is the following thrombosis; the excessive bleeding may keep on increasing as therapeutic time increases. The other adverse reaction associated with fibrinolytic drug is kidney diseases, very high blood pressure, due to bleeding in the brain, it may result in hemorrhagic stroke. 4. Describe the mechanism of action of the antidysrhythmic agent amiodarone. To which Vaughan Williams antidysrhythmic drug class does it belong? (4 marks) antidysrhythmic drug acts by correction of the abnormal functioning of the cardiac. It is divided into four classes. I. Class I this will work on sodium channels. II. Class II they are beta-adrenergic blockers. They reduce stimulation of the sympathetic nervous system. This help in the reduction of impulse transmission into the heart. III. Class III they work by increasing the APD through prolonged repolarization.\ IV. Class IV in this channel, calcium channel is blocked. This will help to reduce the movement of calcium ions. 5. Compare and contrast the actions of heparin and streptokinase (3 marks) Heparin is used in the prevention or blood clotting. Clotting is prevented from occurring to people with certain medical conditions (Tavazzi et al. 2008). It is also used to stop the growth of the clot which might have formed in the blood vessels. However, heparin could not stop the size of the clots that already formed. It is also used to prevent blood clotting in the catheter. It is in the medical class of anticoagulants (Antman et al. 2006). On the other hand, streptokinase is used in the breakdown of clots. Therefore two compare in that, they work against blood clotting in the blood vessels. The difference is that, as streptokinase break down the clots, heparin prevents the growth of the blood clots; it cannot reduce the size of the clots that has already formed in the blood vessels. 6. Outline the pathophysiology of heart failure (4 marks) Heart failure can be described as a clinical syndrome which occurs when the heart is unable to supply enough blood in order to meet the required blood for metabolic activity (MICHOTTE, & STRIK, 2010). The following are the adverse effects of heart failure, i. Weak and thread pulse ii. Oliguria and nocturia iii. Hepatojugular reflux iv. Acute pulmonary edema v. Rales vi. Radiographic cardiomegaly vii. Circulation time of 25 times viii. Nocturnal cough 7. Describe the mechanism of action of ACE inhibitors and indicate why they are a drug of choice in heart failure (4 marks) Angiotensin-converting enzymes, inhibitors are very crucial in the management of heart failure. They are useful in that they reduce the blood pressure by relaxing blood vessels. This help in the improvement of blood flow throughout the body (Nicolle, 2013). This helps the heart to supply blood to the rest part of the body without much struggle. The following are few examples of ACE, benazepril, ramipril, quinapril, fisinopril, among etc. ACE has a number of side effects which includes: dizziness, persistent coughing, salty metallic taste and low sensitivity to tastes, unusual bruising, confusion, swelling on the; neck, tongue, face etc. 8. Pulmonary oedema is caused by alterations in fluid distribution between pulmonary blood vessels and the lung tissue. Using fluid dynamics and changes in fluid pressure, explain the link between heart failure and pulmonary oedema. (3 marks) From the definition, can be described as a situation whereby there is fluid accumulation in the lungs. In the case of heart failure, the heart is not in a position to pump blood quickly at the required pace. Therefore, since the blood does not return to the heart through the veins as fast as possible, the left ventricle will cause blood to accumulate in the pulmonary vein. This results in a severe high blood pressure (Hooton et al. 2010) 9. Compare and contrast the actions of the loop and thiazide diuretics (4 marks) Loop diuretics obstruct sodium potassium chloride in the transporter. Only the 25% of the sodium load is reabsorbed (Piras et al. 2008). Distal tubular concentration of sodium may increase as a result of the inhabitation. There are a reduced hypertponicity and less water reabsorption in the collecting duct. Thiazide diuretic will inhibit sodium chloride transporter in the distal tubule (Lohr, 2008). About 5% of the filtered sodium is reabsorbed. The two increases sodium delivery to the distal segment and contribute to the loss of potassium. 10. At what stages do the diuretics and the peripheral vasodilators interrupt the pathophysiology of heart failure? (3 marks) Peripheral vasodilators and diuretics will interrupt stage C of heart failure. This is a stage characterized by systolic heart failure (Cantor et al. 2009). The symptoms in this stage are; less ability to exercise, short breath, fatigue. The recommended treatment is; beta-blockers and ACE inhibitors, diuretics, hydralazine/nitrate. PART D - (Total 10 marks) Compare and contrast the general characteristics of the following drug groups: a. the TCAs and the SSRIs Both TCAs and SSRIs prolongs neurotransmitter’s effect TCAs raise the level of neurotransmitter norepinephrine and serotonin in the brain by slowing the rate of reabsorption by the nerve cells. It is a strong inhibitor in the reabsorption of both norepinephrine and serotonin (Gershlick et al. 200t5). SSRIs are highly selective and will work as weak inhibitors in norepinephrine reabsorption and strong inhibitor to the reabsorption of serotonin. b. the non-selective MAOIs and the RIMAs MAOIs and RIMAs have the same properties. The difference is that in MAOIs there is selectivity in the inhibitor while in RIMAs there is the property of reversibility of the inhibitors. I.e. MAOIs will permanently bind with the monoamine oxidase enzyme while RIMA they bind in a reversible manner (Logan et al. 2007). c. the TCAs and the tetracyclic antidepressants Both work by affecting brain chemicals to ease the symptoms of depression (McMurrayet al. 2012). Cyclic blocks reuptake of serotonin and makes their concentration be high in the blood stream. d. the TCAs and the non-selective MAOIs TCA is a strong inhibitor of the reabsorption of norepinephrine and serotonin, while MAOIs inhibits monoamine oxidase enzyme which is responsible for the breakdown of dopamine, serotonin and norepinephrine. The similarities are that they reduce the concentration of norepinephrine and serotonin in the blood stream (Weitz, Hirsh, & Samama, 2008). e. the SSRIs and the SNRIs The similarities between the two are that the two drugs will affect the reabsorption of serotonin while SNRI will, in addition, affect the level of norepinephrine in the brain. References Nicolle, L. E. (2013). 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The role of pro-inflammatory cytokines in cancer treatment-induced alimentary tract mucositis: pathobiology, animal models and cytotoxic drugs. Cancer treatment reviews, 33(5), 448-460. MICHOTTE, A., & STRIK, H. (2010). The role of cytotoxic drugs in the treatment of central nervous system gliomas. Acta Neurol. Belg, 110, 1-14. Weitz, J. I., Hirsh, J., & Samama, M. M. (2008). New antithrombotic drugs: American College of Chest Physicians evidence-based clinical practice guidelines. CHEST Journal, 133(6_suppl), 234S-256S. Piras, A. M., Chiellini, F., Fiumi, C., Bartoli, C., Chiellini, E., Fiorentino, B., & Farina, C. (2008). A new biocompatible nanoparticle delivery system for the release of fibrinolytic drugs. International journal of pharmaceutics, 357(1), 260-271. Cantor, W. J., Fitchett, D., Borgundvaag, B., Ducas, J., Heffernan, M., Cohen, E. A., & Lazzam, C. (2009). Routine early angioplasty after fibrinolysis for acute myocardial infarction. New England Journal of Medicine, 360(26), 2705-2718. Gershlick, A. H., Stephens-Lloyd, A., Hughes, S., Abrams, K. R., Stevens, S. E., Uren, N. G., & Baumbach, A. (2005). Rescue angioplasty after failed thrombolytic therapy for acute myocardial infarction. New England Journal of Medicine, 353(26), 2758-2768. Antman, E. M., Morrow, D. A., McCabe, C. H., Murphy, S. A., Ruda, M., Sadowski, Z., & White, H. D. (2006). Enoxaparin versus unfractionated heparin with fibrinolysis for ST-elevation myocardial infarction. New England Journal of Medicine, 354(14), 1477-1488. Read More