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NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Asthma Basic Pharmacotherapy • Source Session/Topic 21 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 21: Pharmacotherapy of Asthma Learning Objectives By the end of this session students are expected to be able to: Define asthma Explain pathophysiology of asthma Explain the clinical presentation of asthma Outline diagnosis asthma Describe pharmacological treatment of asthma Describe the monitoring of asthma Activity: Buzzing What is Asthma ? Definition of Asthma Asthma is a common, chronic respiratory disease of the airways of the lung characterized by either the intermittent or persistent presence of highly variable degrees of airflow obstruction from airway wall inflammation and bronchial smooth muscle constriction. People with asthma experience episodes of wheezing, breathlessness and chest tightness due to widespread narrowing of the airways. The cause of Asthma is unknown but the risk if associated with genetics and environmental factors. Genetic factors account for 60% to 80% of the susceptibility. Asthma represents a complex genetic disorder in that the asthma phenotype is likely a result of polygenic inheritance or different combinations of genes Definition of Asthma Cont.….. Environmental risk factors for the development of asthma include; S ocioeconomic status, F amily size, E xposure to secondhand tobacco smoke in infancy and in utero, A llergen exposure U rbanization , R espiratory syncytial virus infection, and E xposure to common childhood infectious agents List of agents and events Triggering Asthma Pathophysiology Of Asthma The major characteristics of asthma include a variable degree of airflow obstruction (related to bronchospasm, edema, and mucus hypersecretion) and airways inflammation To understand the pathogenetic mechanisms that underlies the many phenotypes of asthma, it is critical to identify factors that initiate, intensify, and modulate the inflammatory response of the airways and to determine how these processes produce the characteristic airway abnormalities . Pathophysiology Of Asthma Cont …. The immunohistopathologic features of asthma include inflammatory cell infiltration: Neutrophils (especially in sudden-onset, fatal asthma exacerbations; occupational asthma, and patients who smoke) Eosinophils Lymphocytes Mast cell activation Epithelial cell injury P athophysiology of Asthma cont. … Airway inflammation contributes to airway hyper responsiveness, airflow limitation, respiratory symptoms, and disease chronicity. In some patients, persistent changes in airway structure occur, including sub-basement fibrosis, mucus hypersecretion, injury to epithelial cells, smooth muscle hypertrophy, and angiogenesis. Gene-by-environment interactions are important to the expression of asthma. Atopy, the genetic predisposition for the development of an immunoglobulin E ( IgE )-mediated response to common aeroallergens, is the strongest identifiable predisposing factor for developing asthma . Viral respiratory infections are one of the most important causes of asthma exacerbation and may also contribute to the development of asthma Clinical Presentation And Diagnosis Of Asthma Clinical Presentation is divided into Acute Asthma Chronic asthma Acute asthma General An episode can progress over several days or hours (usual scenario) or progresses rapidly over 1 to 2 hours . Clinical Presentation And Diagnosis Of Asthma Acute asthma….. Symptoms The patient is anxious in acute distress and complains of severe dyspnea , shortness of breath, chest tightness, or burning and wheezing sound The patient is only able to say a few words with each breath. Symptoms are unresponsive to usual measures ( shortacting inhaled β 2 –agonist administration). Clinical Presentation And Diagnosis Of Asthma Cont … Acute asthma….. Signs Signs include expiratory and inspiratory wheezing on auscultation (breath sounds may be diminished with very severe obstruction), D ry hacking cough, T achypnea , T achycardia , P ale or cyanotic skin, Hyper inflated chest with intercostal and supraclavicular retractions, and Hypoxic seizures if very severe Clinical Presentation And Diagnosis Of Asthma Cont … Acute asthma…… Laboratory PEF(peak expiratory flow) and/or FEV(Forced expiratory volume 1) less than 40% of normal predicted values. Decreased arterial oxygen ( PaO 2 ), and O 2 saturations by pulse oximetry ( SaO 2 less than 90% on room air is severe). Increased arterial or capillary CO 2 if mild, but in the normal range or increased in moderate to severe obstruction . Clinical Presentation And Diagnosis Of Asthma Cont … Acute asthma… Other Diagnostic Tests Blood gases to assess metabolic acidosis (lactic acidosis) in severe obstruction. Complete blood count if there are signs of infection (fever and purulent sputum). Serum electrolytes as therapy with β 2 -agonist and corticosteroids can lower serum potassium, magnesium, and phosphate, and increase glucose. Chest radiograph if signs of consolidation on auscultation Clinical Presentation And Diagnosis Of Asthma Cont … Chronic Asthma General Asthma is a disease of exacerbation and remission, so the patient may not have any signs or symptoms at the time of exam. Symptoms The patient may complain of episodes of dyspnea, chest tightness, coughing (particularly at night), wheezing, or a whistling sound when breathing. These often occur in association with exercise, but also occur spontaneously or in association with known allergens . Clinical Presentation And Diagnosis Of Asthma Cont … Chronic Asthma…. Signs Expiratory wheezing on auscultation, dry hacking cough, or signs of atopy (allergic rhinitis and/or eczema) may occur. Laboratory Spirometry demonstrates obstruction (reduced FEV 1 /FVC(forced vital capacity) with reversibility following inhaled β 2 -agonist administration (at least a 12% improvement in FEV 1). Clinical Presentation And Diagnosis Of Asthma Cont … Chronic Asthma….. Other Diagnostic Tests A fall in FEV 1 of at least 15% following 6 minutes of near maximal exercise. Elevated eosinophil count and IgE concentration in blood. Positive methacholine challenge (PC 20 FEV 1 less than 12.5 mg/mL) or mannitol challenge (FEV 1 decrease of at least 15% from baseline after 635 mg or less ). Activity : Small Group Discussion What is the treatment of Asthma ? Pharmacological Treatment of Asthma Acute Severe Asthma The primary goal is prevention of life-threatening asthma by early recognition of signs of deterioration and early intervention. The principal goals of treatment include: Correction of significant hypoxemia ( A low

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Vulvovaginal Candidiasis Basic Pharmacotherapy • Source Session/Topic 20 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 20: Pharmacotherapy of Vulvovaginal Candidiasis Learning Objectives By the end of this session students are expected to be able to: Define vulvovaginal candidiasis Explain pathophysiology of vulvovaginal candidiasis Explain the clinical presentation of vulvovaginal candidiasis Outline diagnosis of vulvovaginal candidiasis Describe pharmacological treatment of vulvovaginal candidiasis Describe the monitoring of vulvovaginal candidiasis therapy Activity: Buzzing What is Vulvovaginal Candidiasis ? Definition of Vulvovaginal Candidiasis Vulvovaginal Candidiasis Vulvovaginal candidiasis (VVC) refers to infections in individuals with or without symptoms who have positive vaginal cultures for Candida species. Depending on episodic frequency, VVC can be classified as either; Sporadic or Recurrent. This classification is essential to understanding the pathophysiology, as well as the pharmacotherapy of VVC. Definition of Vulvovaginal Candidiasis Cont.… VVC may also be classified as; uncomplicated, which refers to sporadic infections that are susceptible to all forms of antifungal therapy regardless of the duration of treatment, or Complicated, in which consideration of factors affecting the host, microorganism, and pharmacotherapy all have an essential role in successful treatment. Complicated VVC includes recurrent VVC, severe disease, non– Candida albicans candidiasis, and host factors, including diabetes mellitus, immunosuppression, and pregnancy Pathophysiology of Vulvovaginal Candidiasis Candida albicans is the major pathogen responsible for VVC, accounting for 80% to 92% of symptomatic episodes. The remainders are caused by non– C. albicans species, with Candida glabrata dominating. The number of cases of non– C. albicans candidiasis appears to be increasing, possibly related to the use of nonprescription vaginal antifungal preparations and short-course therapy and/ or the increased use of long-term maintenance therapy in preventing recurrent infections. Candida species can act as commensal members of the vaginal flora. Asymptomatic colonization with Candida species has been found in 10% to 20% of women of reproductive age. Pathophysiology of Vulvovaginal Candidiasis Cont … Candida organisms are dimorphic; blastospores are believed to be responsible for colonization (transmission and spread), whereas Germinated Candida forms are associated with tissue invasion and symptomatic infections. To colonize the vagina, Candida species must be able to attach to the mucosa. The attachment process is complex. Not only are candidal surface structures important for attachment, but appropriate receptors for attachment must be present in the epithelial tissue. Pathophysiology of Vulvovaginal Candidiasis Cont.… Not all women have the same range of receptors, which may explain variation in colonization. Changes in the host’s vaginal environment or response are necessary to induce a symptomatic infection. Unfortunately, in most cases of symptomatic VVC, no precipitating factor can be identified C linical presentation of Vulvovaginal candidiasis General Often involves both the vulva and the vagina Symptoms Intense vulvar itching, soreness, irritation, burning on urination, and dyspareunia Signs Erythema, fissuring (crack), curdy “cheese”-like discharge, satellite lesions, edema Laboratory tests Vaginal pH—normal, saline and 10% KOH microscopy— blastospores or pseudohyphae Other diagnostic tests Candida cultures not recommended unless classic signs and symptoms with normal vaginal pH and microscopy are inconclusive or recurrence is suspected Activity : Small Group Discussion What is the treatment of Vulvovaginal Candidiasis ? Treatment of Uncomplicated Vulvovaginal candidiasis Pharmacological Treatment of Vulvovaginal Candidiasis Complicated Vulvovaginal Candidiasis Complicated VVC occurs in patients who are immunocompromised or have uncontrolled diabetes mellitus and pregnant. These individuals need a more aggressive treatment plan. Current recommendations are to lengthen therapy to 10 to 14 days regardless of the route of administration. Therapeutic options include those listed in Table however , regimens should be continued for 10 to 14 days. It is also recommended to repeat 150 mg dose of fluconazole 72 hours after the initial dose for better therapeutic outcomes Pharmacological Treatment of Vulvovaginal Candidiasis Cont.…. Antifungal-Resistant Vulvovaginal Candidiasis Resistance to azole antifungals should be considered in individuals who have persistently positive yeast cultures and fail to respond to therapy despite adherence to prescribed regimens. These infections can be treated with; Boric acid Boric acid administered as a 600 mg intravaginal capsule daily for 14 days of induction therapy, followed by a maintenance regimen of one capsule intravaginal twice weekly. Boric acid should not be administered orally, as it is toxic. OR 5-Flucytosine cream is administered vaginally, 1,000 mg inserted nightly for 7 days. Pharmacological Treatment of Vulvovaginal Candidiasis Cont.…. Monitoring of Vulvovaginal Candidiasis Therapy Efficacy of the antifungal agent is partly influenced by patient adherence to the medication regimen. Patients must be counseled on proper administration and dosing Safety end points include monitoring for occurrence of the relevant drug side effects and drug interactions It is still prudent to monitor for hypersensitivity reactions and side effects that might occur with any medication. Monitoring of Vulvovaginal Candidiasis Therapy Cont.….. GI intolerance is more associated with the oral azoles. Hepatotoxicity can occur when azole therapy is prolonged beyond 7 to 10 days or high doses are used. Periodic monitoring of liver enzymes (alanine transaminase and aspartate amino-transferase) should be considered, especially if prolonged therapy (longer than 21 days) is anticipated. Patients who are receiving IV amphotericin B require daily monitoring by the pharmacist. Key Points Vulvovaginal candidiasis (VVC) refers to infections in individuals with or without symptoms who have positive vaginal cultures for Candida species Symptoms include intense vulvar itching, soreness, irritation, burning on urination, and dyspareunia Azole antifungals and other topical antifungals are drug of choice for culvovaginal candidiasis Evaluation What is Vulvovaginal Candidiasis? What is the pathophysiology of Vulvovaginal Candidiasis? What are the signs and symptoms of Vulvovaginal Candidiasis? How is the treatment of Vulvovaginal Candidiasis? References Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6 th Ed). New York, NY: McGraw-Hill. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed ): New York, NY: McGraw-Hill. Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles & Practice Study Guide:

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Folliculitis, Furunculosis and Carbuncles Basic Pharmacotherapy • Source Session/Topic 19 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 19: Pharmacotherapy of Folliculitis, Furunculosis and Carbuncles Learning Objectives By the end of this session students are expected to be able to: Define folliculitis, furunculosis and carbuncles Explain pathophysiology of folliculitis, furunculosis and carbuncles Explain the clinical presentation of folliculitis, furunculosis and carbuncles Outline diagnosis of folliculitis, furunculosis and carbuncles Describe pharmacological treatment of folliculitis, furunculosis and carbuncles Describe the monitoring of folliculitis, furunculosis and carbuncles therapy Activity: Buzzing What are Folliculitis, Furunculosis and Carbuncles? Definition of Folliculitis, Furunculosis and Carbuncles Folliculitis , Furunculosis and Carbuncles Folliculitis is inflammation of the hair follicle and is caused by physical injury, chemical irritation, or infection. Infection occurring at the base of the eyelid is referred to as a stye. Folliculitis is a superficial infection with pus present only in the dermis , Furuncles and carbuncles occur when a follicular infection extends from around the hair shaft to involve deeper areas of the skin. A furuncle, commonly known as an abscess or boil, is a walled-off mass of purulent material arising from a hair follicle. Definition of Folliculitis, Furunculosis and Carbuncles The lesions are called carbuncles when they coalesce and extend to the subcutaneous tissue . This aggregate of infected hair follicles forms deep masses that generally open and drain through multiple sinus tracts. S. aureus is the most common cause of folliculitis, furuncles, and carbuncles. Inadequate chlorine levels in whirlpools, hot tubs, and swimming pools have been responsible for outbreaks of folliculitis caused by P. aeruginosa . Pathophysiology of Folliculitis, Furunculosis and Carbuncles The skin and subcutaneous tissues normally are extremely resistant to infection but may become susceptible under certain conditions. Even when high concentrations of bacteria are applied topically or injected into the soft tissue, resulting infections are rare. Several host factors act together to confer protection against skin infections. Because the surface of the skin is relatively dry and has a pH of approximately 5.6, it is not conducive to bacterial growth. Continuous renewal of the epidermal layer results in the shedding of keratocytes , as well as skin bacteria. In addition, sebaceous secretions are hydrolyzed to form free fatty acids that strongly inhibit the growth of many bacteria and fungi. Pathophysiology of Folliculitis, Furunculosis and Carbuncles Conditions that may predispose a patient to the development of skin infections include H igh concentrations of bacteria (>10 5 microorganisms), E xcessive moisture of the skin, I nadequate blood supply, A vailability of bacterial nutrients, and Damage to the corneal layer allowing for bacterial penetration. The majority of Skin and Soft Tissue Infections result from the disruption of normal host defenses by processes such as skin puncture, abrasion, or underlying diseases (e.g., diabetes). The nature and severity of the infection depend on both the type of microorganism present and the site of inoculation Clinical presentation and diagnosis of Folliculitis, Furunculosis and Carbuncles Folliculitis Pruritic, erythematous papules typically appear within 48 hours (range: 6 to 72 hours) of exposure to large numbers of organisms. Papules evolve into pustules that generally heal in several days. Systemic signs such as fever and malaise are uncommon, although they have been reported in cases caused by P. aeruginosa Clinical presentation and diagnosis of Folliculitis, Furunculosis and Carbuncles Cont.… Furuncles/ Furunculosis Furuncles can occur anywhere on hairy skin but generally develop in areas subject to friction and perspiration. Furuncles are discrete lesions, whether occurring as singular or multiple nodules. The lesion starts as a firm, tender, red nodule that becomes painful and fluctuant. Lesions often drain spontaneously. Lesions caused by CA-MRSA often have necrotic centers characteristic of “spider bites.” Culture of lesion for laboratory investigation to conform the presence and the type of the pathogen Clinical presentation and diagnosis of Folliculitis, Furunculosis and Carbuncles Cont.… Carbuncles Carbuncles are broad, swollen, erythematous, deep, and painful follicular masses. Carbuncles commonly develop on the back of the neck and are more likely to occur in patients with diabetes. Unlike folliculitis and furuncles, carbuncles are commonly associated with fever, chills, and malaise. Bacteremia with secondary spread to other tissues is common Culture of lesion for laboratory investigation to conform the prensence and the type of the pathogen Activity : Small Group Discussion What is the treatment of Folliculitis, Furunculosis and Carbuncles? Pharmacological treatment of Folliculitis, Furunculosis and Carbuncles Treatment of folliculitis generally requires only local measures, such as warm moist compresses or topical therapy (e.g., clindamycin, erythromycin, mupirocin , or benzoyl peroxide). Topical agents generally are applied two to four times daily for 7 days. Small furuncles generally can be treated with moist heat, which promotes localization and drainage of pus. Large and/or multiple furuncles and carbuncles require incision and drainage. Systemic antibiotics are usually not necessary unless accompanied by fever or extensive cellulitis. Treatment of more severe infections generally consists of a penicillinase-resistant penicillin (such as dicloxacillin ) or a first-generation cephalosporin (such as cephalexin) for 5 to 10 days Drug Treatment Monitoring of Folliculitis , Furuncles and Carbuncles Therapy Many follicular infections resolve spontaneously without medical or surgical intervention. Lesions should be incised if they do not respond to a few days of moist heat and nonprescription topical agents. Following drainage, most lesions begin to heal within several days without antimicrobial therapy. Any patient who is unresponsive to several days of therapy with a penicillinase-resistant penicillin or first-generation cephalosporin should have a culture and sensitivity Performed because of the increasing frequency of MRSA. Key Points Folliculitis is inflammation of the hair follicle and is caused by physical injury, chemical irritation, or infection Symptoms of Folliculitis include Pruritic, erythematous papules typically appear within 48 hours (range: 6 to 72 hours) of exposure to large numbers of organisms Treatment of folliculitis generally requires only local measures, such as warm

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Urinary Tract Infections Basic Pharmacotherapy • Source Session/Topic 18 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 18: Pharmacotherapy of Urinary Tract Infections Learning Objectives By the end of this session students are expected to be able to : Define urinary tract infections Explain pathophysiology of urinary tract infections Explain the clinical presentation of urinary tract infections Outline diagnosis of urinary tract infections Describe pharmacological treatment of urinary tract infections Describe the monitoring of urinary tract infections therapy Activity: Buzzing What is Urinary Tract Infections? Definition of Urinary Tract Infections Urinary Tract Infections (UTI ) UTI is defined as the presence of microorganisms in the urinary tract that cannot be accounted for by contamination. The organisms present have the potential to invade the tissues of the urinary tract and adjacent structures. Infection may be limited to the growth of bacteria in the urine, which frequently may not produce symptoms. A UTI can present as several syndromes associated with an inflammatory response to microbial invasion and can range from asymptomatic bacteriuria to pyelonephritis with bacteremia or sepsis. Definition of Urinary Tract Infections Cont.…. UTIs are classified by lower and upper urinary tract infections. Upper tract infection include pyelonephritis (an infection involving the kidneys) represents Lower tract infections correspond to cystitis (bladder), Also, UTIs are designated as uncomplicated or complicated. Uncomplicated infections occur in individuals who lack structural or functional abnormalities of the urinary tract that interfere with the normal flow of urine or voiding mechanism. Definition of Urinary Tract Infections Cont.…. These infections occur in females of child-bearing age (15 to 45 years) who are otherwise normal healthy individuals. Complicated UTIs are the result of a predisposing lesion of the urinary tract, such as a congenital abnormality or distortion of the urinary tract, a stone, indwelling catheter, prostatic hypertrophy, obstruction, or neurologic deficit that interferes with the normal Classification of UTI Pathophysiology of Urinary Tract Infections The bacteria causing UTIs usually originate from bowel flora of the host. Although virtually every organism is associated with UTIs, certain organisms predominate as a result of specific virulence factors. The most common cause of UTIs is Escherichia coli , which accounts for 80% to 90% of community-acquired infections. Additional causative organisms in uncomplicated infections include Staphylococcus saprophyticus , Klebsiella pneumoniae, Proteus spp., Pseudomonas aeruginosa , and Enterococcus spp. Pathophysiology cont … Pathogenic organisms have differing degrees of pathogenicity (virulence), which play a role in the development and severity of infection. Bacteria that adhere to the epithelium of the urinary tract are associated with colonization and infection The mechanism of adhesion of gram-negative bacteria, particularly E. coli, is related to bacterial fimbriae that are rigid, hair-like appendages of the cell wall These fimbriae adhere to specific glycolipid components on epithelial cells The most common type of fimbriae is type 1, which binds to mannose residues present in glycoproteins Pathophysiology Cont. … Glycosaminoglycan and Tamm- Horsfall protein are rich in mannose residues that readily trap those organisms that contain type 1 fimbriae, which are then washed out of the bladder. Other fimbriae are mannose resistant and are associated more frequently with pyelonephritis, such as P fimbriae, which bind avidly to specific glycolipid receptors on uroepithelial cells These bacteria are resistant to washout or removal by glycosaminoglycan and are able to multiply and invade tissue, and causing infection Clinical Presentation of UTIs Signs and symptoms Lower UTI: dysuria, urgency, frequency, nocturia , suprapubic heaviness Gross hematuria Upper UTI: flank pain, fever, nausea, vomiting, malaise Physical examination Upper UTI: costovertebral tenderness Clinical Presentation of UTIs Cont … Laboratory tests Bacteriuria Pyuria (white blood cell count >10/mm 3 ) Nitrite-positive urine (with nitrite reducers) Leukocyte esterase-positive urine Antibody-coated bacteria (upper UTI ) Diagnosis of UTIs Symptoms alone are unreliable for the diagnosis of bacterial UTIs. The key to the diagnosis of UTI is the ability to demonstrate significant numbers of microorganisms in an appropriate urine specimen to distinguish contamination from infection. Diagnosis of UTIs Cont.… Urine testing The gold standard for a urine test is to perform a bacteriological urine culture, with identification of the pathogen, with quantification and sensitivity testing. To test whether the patient has a UTI at all, orientating indirect methods are often used in practice to detect the bacteria or inflammation (dip sticks). The bacterial count may be assessed by urine microscopy and immersion culture media. Midstream urine is normally collected Diagnosis of UTIs Cont.… Dip sticks Urine dip sticks are one of the most frequently used instruments for diagnostic testing if there is clinical evidence that a patient is suffering from UTI. Multistix are most often used, which may be able to detect nitrite (a metabolic product of typical pathogens of the urinary tract), leukocyte esterase, protein and blood (as a marker of inflammation ). Diagnosis of UTIs Cont.… Dip sticks…… If nitrite is detected, this increases the probability of a urinary tract infection, with a likelihood ratio [LR] of 2.6 to 10.6. However, the sensitivity is relatively low. In contrast, the detection of leukocyte esterase increases the probability to a lesser degree (LR 1.0 to 2.6). The detection of blood is admittedly highly sensitive, but the specificity is low. Activity : Small Group Discussion What is the treatment of UTI ? Pharmacological Treatment of UTIs The management of a patient with a UTI includes; Initial evaluation, Selection of an antibacterial agent and duration of therapy, and Follow-up evaluation. The initial selection of an antimicrobial agent for the treatment of UTI is based primarily on; The severity of the presenting signs and symptoms, The site of infection, and Whether the infection is determined to be uncomplicated or complicated. Other considerations include antibiotic susceptibility, side-effect potential, cost, and the comparative inconvenience of different therapies . Empirical Treatment of UTIs Treatment of UTI according to Pathogen Monitoring of UTI Therapy In

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Genital Herpes Basic Pharmacotherapy • Source Session/Topic 17 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 17: Pharmacotherapy of Genital Herpes Learning Tasks By the end of this session students are expected to be able to: Define genital herpes Explain pathophysiology of genital herpes Explain the clinical presentation of genital herpes Outline diagnosis of genital herpes Describe pharmacological treatment of genital herpes Describe the monitoring of genital herpes therapy Activity: Buzzing • What is Genital Herpes? Definition of Genital Herpes Genital Herpes Genital herpes is a common sexually transmitted infection caused by the herpes simplex virus (HSV). Sexual contact is the primary way that the virus spreads. There are two types of Herpes Simplex viruses; herpes simplex virus type 1 (HSV-1) and herpes simplex virus type 2 (HSV-2). HSV-1 is associated most commonly with oropharyngeal disease, and HSV-2 is associated most closely with genital disease; However, each virus is capable of causing clinically indistinguishable infections in both anatomic areas. Definition of Genital Herpes Cont.…. Humans are the sole known reservoir for HSV. Infection is transmitted via inoculation of virus from infected secretions onto mucosal surfaces (e.g., urethra, oropharynx, cervix, and conjunctivae) or through abraded skin. The cycle of HSV infection occurs in five stages: primary muco-cutaneous infection, infection of the ganglia, establishment of latency, reactivation, and recurrent infection Pathophysiology Of Genital Herpes After viral inoculation, HSV infection is associated with cytoplasmic granulation(condensed areas of cellular material that may be bounded by a membrane), ballooning degeneration of cells (cells undergoing this form of death increase in size(balloon), and production of mononucleated giant cells ( cells formed by fusion of monocytes/macrophage) Initially, the cellular response is predominantly polymorph nuclear, followed by a lymphocytic response. Replication occurs with viral spread to contiguous cells and peripheral sensory nerves. Latency then is established in sensory or autonomic nerve root ganglia. Latency appears to be lifelong, interrupted only by reactivation of the viral infection. It is unclear what factors are important in maintaining latency, but immune responses and emotional and physical stresses appear important in reactivating latent virus. Clinical Presentation Of Genital Herpes The signs and symptoms of genital herpes infection are influenced by many factors, including previous exposure to HSV, viral type, and host factors such as age and site of infection. High percentage of initial and recurrent infections are asymptomatic, Viral shedding can occur in the absence of apparent lesions or symptoms A summary of the clinical presentation of genital herpes is provided in Table Diagnosis Of Genital Herpes A presumptive diagnosis of genital herpes commonly is made based on the presence of dark-field negative , vesicular, or ulcerative genital lesions. A prior history of similar lesions or recent sexual contact with an individual with similar lesions also is useful in making the diagnosis Viral culture. This test involves taking a tissue sample or scraping of the sores for examination in the laboratory . Diagnosis Of Genital Herpes Cont …. Polymerase chain reaction (PCR) test. PCR is used to copy patient DNA from a blood sample, tissue from a sore or spinal fluid. The DNA can then be tested to establish the presence of HSV and determine which type of HSV you have. Blood test. This test analyzes a sample of blood for the presence of HSV antibodies to detect a past herpes infection. Several serologic tests capable of distinguishing HSV-1 and HSV-2 antibodies are available. These tests detect antibodies to type-specific HSV-1 and HSV-2 proteins gG-1 and gG-2, respectively Activity : Small Group Discussion What is the treatment of Genital Herpes? Pharmacological Treatment of Genital Herpes The most achievable goals in the management of genital herpes are to relieve symptoms and to shorten the clinical course, to prevent complications and recurrences, and to decrease disease transmission. Although research has focused primarily on the treatment of active infection and suppression of recurrences, increasing emphasis is being placed on various approaches, including immunotherapy that might provide protection from disease transmission or possibly eliminate established latency. . Pharmacological Treatment of Genital Herpes Oral formulations of acyclovir, famciclovir , and valacyclovir have demonstrated efficacy in reducing viral shedding, duration of symptoms, and time to healing of first-episode genital herpes infections, with maximal benefits seen when therapy is initiated at the earliest stages of infection Pharmacological Treatment of Genital Herpes Monitoring of Genital Herpes Therapy Available antiviral compounds are of greatest benefit in patients experiencing first-episode primary infections, immunocompromised patients, and patients with frequent or severe recurrent infections. Antivirals, however, are palliative and not curative, and patients receiving these agents should be monitored closely for adverse drug effects. Discontinuation of suppressive therapy after 1 year should be considered to assess for possible changes in the patient’s intrinsic pattern of recurrence. In many patients, decreases in recurrence rates and the severity of symptoms occur over time. However, it is also preferred to continue suppressive therapy indefinitely because it significantly reduces asymptomatic viral shedding, a potential benefit in reducing the risk of disease transmission to uninfected sexual partners Key Points Genital herpes is a common sexually transmitted infection caused by the herpes simplex virus (HSV). Infection is transmitted via inoculation of virus from infected secretions onto mucosal surfaces (e.g., urethra, oropharynx, cervix, and conjunctivae) or through abraded skin The signs and symptoms of genital herpes infection are influencedby many factors, including previous exposure to HSV, viral type, and host factors such as age and site of infection Oral formulations of acyclovir, famciclovir , and valacyclovir have demonstrated efficacy in the treatment of genital herpes Evaluation What is genital herpes? What is the pathophysiology of genital herpes? What are the signs and symptoms of genital herpes? How is the treatment of genital herpes? References Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6 th Ed). New York, NY: McGraw-Hill. DiPiro JT, Talbert RL, Yee GC,

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Chlamydial Genital Tract Infections Basic Pharmacotherapy • Source Session/Topic 16 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 16: Pharmacotherapy of Chlamydial Genital Tract Infections Learning Tasks By the end of this session students are expected to be able to : Define chlamydial genital tract infections Explain pathophysiology of chlamydial genital tract infections Explain the clinical presentation of chlamydial genital tract infections Outline diagnosis of chlamydial genital tract infections Describe pharmacological treatment of chlamydial genital tract infections Describe the monitoring of chlamydial genital tract infections therapy Activity: Buzzing What is Chlamydial Genital Tract Infections? Definition of Chlamydial Genital Tract Infections Chlamydial Genital Tract Infections Chlamydial Genital Tract Infections is a sexually transmissible infection caused by bacterium Chlamydia t rachomatis Persons infected with the bacterium may not have symptoms of infection but can still transmit the bacterium. Chlamydia can affect the urethra (the urine passage), cervix (the neck of the womb), rectum and anus, throat, and eyes . Pathophysiology of Chlamydial Genital Tract Infections C. trachomatis is an obligate intracellular parasite that shares properties of both viruses and bacteria. Like viruses, chlamydiae require cellular material from host cells for replication; however, unlike viruses, chlamydiae maintain their cellular identity throughout development. Although C. trachomatis lacks a cell-wall peptidoglycan, its major outer membrane is similar to gram-negative bacteria. At least 18 serovars (subspecies) of C. trachomatis exist, of which only the lymphogranuloma venereum strains produce potentially invasive infections. The remaining serovars are involved primarily with superficial infection of epithelial cells . Pathophysiology of Chlamydial Genital Tract Infections Cont .. Chlamydia have the ability to establish long-term associations with host cells. When an infected host cell is starved for various nutrients such as amino acids (for example, tryptophan), iron, or vitamins, this has a negative consequence for Chlamydiae since the organism is dependent on the host cell for these nutrients. The starved Chlamydiae enter a persistent growth state wherein they stop cell division and become morphologically aberrant by increasing in size. Persistent organisms remain viable as they are capable of returning to a normal growth state once conditions in the host cell improve and causing chronic Clinical Presentation of Chlamydial Genital Tract Infections In comparison with gonorrhea, chlamydial genital tract infections are more frequently asymptomatic, and when present, symptoms tend to be less noticeable. Urethral discharge usually is less profuse and more mucoid or watery than the urethral discharge associated with gonorrhea. Diagnosis of Chlamydia Genital tract infection A sample of urine can be collected and analyzed in the laboratory to investigate the presence of this infection. A swab of the discharge can be collected for culture or antigen testing for chlamydia. Nucleic Acid Amplification Tests (NAAT), such as Polymerase Chain Reaction (PCR ), Transcription Mediated Amplification ( TMA), and the DNA Strand Displacement Amplification (SDA) now are the mainstays. NAAT for chlamydia may be performed on swab specimens sampled from the cervix (women) or urethra (men), on self-collected vaginal swabs, or on voided urine Activity : Small Group Discussion What is the treatment of Chlamydial Genital Tract Infections? Pharmacological treatment of Chlamydial Genital Tract infection Monitoring of chlamydial Genital Tract Infections Therapy Treatment of chlamydial infections with the recommended regimens is highly effective; therefore, post-treatment laboratory testing is not recommended routinely unless symptoms persist or there are other specific concerns (e.g., pregnancy). Post-treatment tests should not be performed for at least 3 weeks following completion of therapy. When post-treatment tests are positive, they usually represent noncompliance, failure to treat sexual partners, or laboratory error rather than inadequate therapy or resistance to therapy. Infants with pneumonitis should receive follow-up testing because erythromycin is only 80% effective, and a second course of therapy can be necessary Key Points Chlamydia is a sexually transmissible infection caused by bacterium Chlamydia t rachomatis Persons infected with the bacterium may not have symptoms of infection but can still transmit the bacterium. Azithromycin is drug of choice for the treatment of chlamydia infection Evaluation What is Chlamydia infection? What is the pathophysiology of Chlamydial infection? What are the signs and symptoms of Chlamydia infection? How is the treatment of Chlamydia Infection? References Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6 th Ed). New York, NY: McGraw-Hill. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed ): New York, NY: McGraw-Hill. Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles & Practice Study Guide: A Case-Based Care Plan Approach : New York, NY: McGraw-Hill. Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused Approach (7 th ed ): New York, NY: McGraw-Hill. ← Previous TopicNext Topic →View all Basic Pharmacotherapy topicsOpen Complete Full Notes PDF / OFFLINE NOTES Unataka kutumiwa notes hizi kupitia WhatsApp?Kwa notes zilizopangiliwa vizuri kwa kusoma offline au PDF, bonyeza kitufe hapa chini. Ujumbe wenye Level, Semester, Module na Topic utaandaliwa moja kwa moja.TUMIWA NOTES WHATSAPP WhatsApp: 255620339260

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Syphilis Basic Pharmacotherapy • Source Session/Topic 15 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 15: Pharmacotherapy of Syphilis Learning Task By the end of this session students are expected to be able to: Define syphilis Explain the clinical presentation of syphilis Outline diagnosis of syphilis Describe pharmacological treatment of syphilis Describe the monitoring of syphilis therapy . Activity: Buzzing • What is syphilis?? Definition of Syphilis Syphilis Syphilis is an infectious venereal disease caused by the spirochete Treponema pallidum . Syphilis is transmissible by sexual contact with infectious lesions, from mother to fetus in utero, via blood product transfusion, and occasionally through breaks in the skin that come into contact with infectious lesions. If untreated, it progresses through 4 stages: primary, secondary, latent, and tertiary Clinical Presentation Primary Syphilis The primary stage, characterized by the appearance of a chancre on cutaneous or mucocutaneous tissue exposed to the organism, is highly infectious. Even without treatment, chancres persist only for 1 to 8 weeks before healing spontaneously. Because syphilitic chancres can be confused with other infectious etiologies, appropriate diagnostic testing is important . Clinical Presentation Cont … Secondary Syphilis The secondary stage of syphilis is characterized by a variety of mucocutaneous eruptions resulting from widespread hematogenous and lymphatic spread of T. pallidum . Skin lesions can be either generalized or localized to a small portion of the body and, with the exception of follicular lesions, are nonpruritic . Generalized lymphadenopathy also is seen in the majority of patients, as are nonspecific symptoms such as mild and transitory malaise, fever, pharyngitis, headache, anorexia, and arthralgia. If untreated, secondary syphilis disappears in 4 to 10 weeks; however, lesions can recur at any time within 4 years. Clinical Presentation Cont … Latent Syphilis These are persons with a positive serologic test for syphilis but with no other evidence of disease. Latent syphilis is further divided into early and late latency. During early latency, the patient is considered potentially infectious. Early latency is defined as 1 year from the onset of infection, up to 2 to 4 years. Late latency is considered noninfectious, although the patient remains a host. Most untreated patients with late latent syphilis have no further sequelae; however, approximately 25% to 30% progress either to neurosyphilis or to late syphilis with clinical manifestations other than neurosyphilis. Treatment of all patients with latent syphilis is essential because there is no way to predict which patients will have progression of their disease Clinical Presentation Cont … Tertiary Syphilis and Neurosyphilis If left untreated, syphilis can slowly produce an inflammatory reaction in virtually any organ in the body. Manifestations of this disease progression are referred to as tertiary syphilis. These clinical manifestations are differentiated into two subgroups based on the presence or absence of central nervous system (CNS) involvement which are neurosyphilis or tertiary syphilis (i.e., gumma and cardiovascular syphilis). The gumma, a nonspecific granulomatous lesion, is the classic lesion of late syphilis and develops in 50% of patients with disease progression. These chronic, destructive lesions characteristically infiltrate the skin, bone, soft tissue, and liver but can be found in any organ or tissue. Gummas of critical organs, such as the heart or brain, can be fatal Clinical Presentation Of Syphilis Diagnosis Of Syphilis Syphilis diagnosis is based on the; patient’s history, physical examination, laboratory testing and Radiology Diagnosis of Sphilis Cont … The available laboratory tests for diagnosis of syphilis include D irect detection methods (i.e. dark field microscopy, direct fluorescent antibody test and nucleic acid amplification test), S erology tests such as; Treponemal tests which include the Treponema pallidum haem- agglutination assay (TPHA), the Treponema pallidum particle agglutination assay (TPPA) and the fluorescent treponemal antibody absorbed (FTA-ABS) tests Non-treponemal tests (the microscopic Venereal Diseases Research Laboratory -VDRL and the macroscopic rapid plasma reagin –RPR tests), Examination of cerebrospinal fluids Rapid diagnostic tests (RDTs) for treponemal antibodies in syphilis infection Activity : Small Group Discussion • What is the treatment of Syphilis ? Pharmacological Treatment Parenteral penicillin G is the treatment of choice for all stages of syphilis. Because T. pallidum multiplies slowly, single doses of short- or intermediate-acting penicillins do not provide the prolonged, low-level exposure to penicillin required for eradication of the treponeme . A result, benzathine penicillin G is the only penicillin effective for single-dose therapy. The recommended treatment for syphilis of less than 1 year’s duration is benzathine penicillin G 2.4 million units as a single dose. Units can be administered once a week for 2 consecutive weeks. In patients with syphilis of longer than 1 year’s duration and normal CSF examination, benzathine penicillin G is administered weekly for three successive doses Monitoring Of Syphilis Therapy Non treponemal tests should be performed at 6 and 12 months in all patients treated for primary and secondary syphilis and at 6, 12, and 24 months for early and late latent disease. More frequent monitoring of HIV-infected individuals (i.e., 3, 6, 9, 12, and 24 months after therapy) should be done In general, the time to reach seronegativity is proportional to the duration of the disease. Despite adequate therapy, some patients can remain seropositive based on non- treponemal test results. In these cases, stabilization of low antibody titers is indicative of adequate therapy. For women treated during pregnancy, monthly quantitative non-treponemal tests are recommended in those at high risk of reinfection. Key Points Syphilis is a systemic disease from the outset and is caused by the spirochaete , Treponema pallidum (T. pallidum) The infection can be classified as congenital (transmitted from mother to child in utero) or acquired (through sex or blood transfusion) Acquired syphilis is divided into early and late syphilis Early syphilis comprises the primary, secondary and early latent stages while late syphilis refers to late latent syphilis, gummatous , neurological and cardiovascular syphilis Long-acting benzathine

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Gonorrhoea Basic Pharmacotherapy • Source Session/Topic 14 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 14: Pharmacotherapy of Gonorrhea Learning Objective By the end of this session students are expected to be able to: Define gonorrhoea Explain pathophysiology of gonorrhoea Explain the clinical presentation of gonorrhoea Outline diagnosis of gonorrhoea Describe pharmacological treatment of gonorrhoea Describe monitoring of gonorrhoea therapy Activity: Buzzing •What is Gonorrhoea ? Definition of Gonorrhea Gonorrhea is a sexually transmitted disease ( STD) caused by infection with the bacterium Neisseria gonorrhoeae . It tends to infect warm, moist areas of the body, including the: U rethra (the tube that drains urine from the urinary bladder) E yes T hroat V agina A nus F emale reproductive tract (the fallopian tubes, cervix, and uterus) Definition of Gonorrhea Gonorrhea is transmitted from person to person through unprotected oral, anal, or vaginal sex. People with numerous sexual partners or those who don’t use a condom are at greatest risk of infection . Pathophysiology of Gonorrhea On contact with a mucosal surface lined by columnar, cuboidal, or noncornified squamous epithelial cells, the gonococci attach to cell membranes by means of surface pili and are then pinocytosed . The virulence of the organism is mediated primarily by the presence of pili and other outer membrane proteins. After mucosal damage is established, polymorphonuclear (PMN) leukocytes invade the tissue, submucosal abscesses form, and purulent exudates are secreted . Clinical Presentation of Gonorrhea Individuals infected with gonorrhea can be; symptomatic or asymptomatic, have complicated or uncomplicated infections, and Have infections involving several anatomic sites. Complications associated with untreated gonorrhea appear more pronounced in women, because most of them are asymptomatic As a result, most of these patients develop serious complications, such as; pelvic inflammatory disease (PID), Infertility and ectopic pregnancies. In other patients the gonococci invade the bloodstream and produce disseminated disease Diagnosis of Gonorrhea Diagnosis of gonococcal infections can be made by ; gram-stained smears, culture, or Methods based on the detection of cellular components of the gonococcus such as Enzyme immunoassay, DNA probe techniques, and nucleic acid amplification techniques (NAATs) are also used in clinical specimens. Various stains have been used to identify gonococci microscopically, with the Gram stain the most widely used in clinical practice. Gram-stained smears are positive for gonococci when gram-negative diplococci of typical kidney bean morphology are identified within PMN leukocytes. Activity : Small Group Discussion What is the treatment of Gonorrhoea? Pharmacological treatment of gonorrhea Uncomplicated gonococcal infection Recommended Regimen Ceftriaxone 250mg IM in a single dose PLUS Azithromycin 1g orally in a single dose Alternative regimen If ceftriaxone is not available. Cefixime 400mg orally in a single dose plus Azithromycin 1g orally in a single dose Treatment of various forms of Gonorrhea Infection Monitoring Of Gonorrhea Therapy It is recommended to obtain follow-up cultures at least 3 days after treatment However the combination gonorrhea and chlamydial therapy rarely results in treatment failures, and routine follow-up of patients treated with a regimen is not necessary. Persistence of symptoms following any treatment requires culture of the site(s) of gonorrheal infection, as well as susceptibility testing if gonococci are isolated. Monitoring Of Gonorrhea Therapy Cont.. In most cases, the presence of gonococci indicates reinfection rather than treatment failure and reflects the need for improved patient education and sex partner referral. Persistence of symptoms also can be caused by other infectious causes, such as C. trachomatis Key Points Gonorrhea is a sexually transmitted disease (STD). It’s caused by infection with the bacterium Neisseria gonorrhoeae Gonorrhea passes from person to person through unprotected oral, anal, or vaginal sex. First line drug treatment with Cetriaxone and Azithromycin is recommended Evaluation What is Gonorrhoea? What is the pathophysiology of Gonorrhoea? What are the signs and symptoms of Gonorrhoea? How is the treatment of Gonorrhoea? References Wells BG, DiPiro J, Schwinghammer T (2013), Pharmacotherapy Handbook (6 th Ed). New York, NY: McGraw-Hill. DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey ML, (2008): Pharmacotherapy: A Pathophysiologic Approach (7 th ed ): New York, NY: McGraw-Hill. Katz M D., Matthias KR., Chisholm-Burns M A., Pharmacotherapy(2011) Principles & Practice Study Guide: A Case-Based Care Plan Approach : New York, NY: McGraw-Hill. Schwinghammer TL, Koehler JM (2009) Pharmacotherapy Casebook: A Patient-Focused Approach (7 th ed ): New York, NY: McGraw-Hill. ← Previous TopicNext Topic →View all Basic Pharmacotherapy topicsOpen Complete Full Notes PDF / OFFLINE NOTES Unataka kutumiwa notes hizi kupitia WhatsApp?Kwa notes zilizopangiliwa vizuri kwa kusoma offline au PDF, bonyeza kitufe hapa chini. Ujumbe wenye Level, Semester, Module na Topic utaandaliwa moja kwa moja.TUMIWA NOTES WHATSAPP WhatsApp: 255620339260

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Schistosomiasis Basic Pharmacotherapy • Source Session/Topic 13 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 13: Pharmacotherapy of Schistosomiasis Learning tasks By the end of this session students are expected to be able to: Define schistosomiasis Explain pathophysiology of schistosomiasis Explain the clinical presentation of schistosomiasis Outline diagnosis of schistosomiasis Describe pharmacological treatment of schistosomiasis Describe monitoring of schistosomiasis therapy Activity: Buzzing What is Schistosomiasis ? Definition of Schistosomiasis Schistosomiasis Schistosomiasis is an acute and chronic parasitic disease caused by blood flukes (trematode worms) of the genus Schistosoma . Definition of Schistosomiasis Cont … There are 2 major forms of schistosomiasis which are intestinal and urogenital caused by 5 main species of blood fluke as follows ; Definition of Schistosomiasis Cont …. Infection happens when larval forms of the parasite released by freshwater snails penetrate the skin during contact with infested water. Transmission occurs when infected individual from schistosomiasis contaminate freshwater sources with their excreta containing parasite eggs, which hatch in water. In the body, the larvae develop into adult schistosomes . Adult worms live in the blood vessels where the females release eggs. Some of the eggs are passed out of the body in the faeces or urine to continue the parasite’s lifecycle. Others become trapped in body tissues, causing immune reactions and progressive damage to organs . Pathophysiology and Symptoms of Schistosomiasis In schistosomiasis, adult worms reside in the mesenteric and pelvic venules in various sites where they lay eggs These sites tend to be specific for each species (e.g. S. japonicum prefers the superior mesenteric veins draining to the small intestine, while S. mansoni prefers the superior mesenteric veins of the large intestine) Many eggs are carried upstream where they get lodged in various organs, especially in the liver, bowel, and genitourinary tract Acute disease may trigger a cell-driven inflammatory response (involving tumour necrosis factor, interleukin-1, and interleukin-6 cytokines) and cause febrile illness Pathophysiology and Symptoms of Schistosomiasis Cont.. As mature female worms lay eggs, products of worm and egg metabolism induce formation of immune complexes resulting to a serum like-sickness called Katayama syndrome In chronic disease, eggs are the cause of pathology; they evoke a Thelper type 2 (Th2) cell-driven granulomatous reaction (involving interleukin-4, interleukin-5, and interleukin-13 cytokines) resulting in tissue fibrosis and chronic morbidity Gastrointestinal schistosomiasis due to S. mansoni , S. japonicum and S. mekongi can cause bowel lesions such as ulceration, pseudopolyps (masses of scar tissue during healing), and microabcesses . These manifest clinically as abdominal pain, altered bowel habits, and blood in stools Pathophysiology and Symptoms of Schistosomiasis Cont … The classic sign of urogenital schistosomiasis is haematuria and is specifically noted with S. haematobium Bladder, ureter fibrosis and kidney damage are sometimes seen in advanced cases The urogenital form may present with genital lesions (e.g. vulvar nodules), vaginal bleeding, dyspareunia(painful intercourse) , and fallopian tube damage (in the late stages) in females Genital infection in males may result in damage to seminal vesicles, prostate and other related organs; this may lead to irreversible infertility Clinical Presentation of Schistosomiasis Symptoms of schistosomiasis are caused by the body’s reaction to the worms' eggs. Intestinal schistosomiasis can result in abdominal pain, diarrhoea , and blood in the stool. Liver enlargement is common in advanced cases, and is frequently associated with an accumulation of fluid in the peritoneal cavity and hypertension of the abdominal blood vessels. In such cases there may also be enlargement of the spleen. The classic sign of urogenital schistosomiasis is haematuria (blood in urine). Clinical Presentation of Schistosomiasis Cont … Fibrosis of the bladder and ureter, and kidney damage are sometimes diagnosed in advanced cases. Bladder cancer is another possible complication in the later stages. In women, urogenital schistosomiasis may present with genital lesions, vaginal bleeding, pain during sexual intercourse, and nodules in the vulva. In men, urogenital schistosomiasis can induce pathology of the seminal vesicles, prostate, and other organs. This disease may also have other long-term irreversible consequences, including infertility. Diagnosis of Schistosomiasis Schistosomiasis is diagnosed through the detection of parasite eggs in stool or urine specimens Antibodies and/or antigens detected in blood or urine samples are also indications of infection For urogenital schistosomiasis, a filtration technique using nylon, paper or polycarbonate filters is the standard diagnostic technique Children with S. haematobium almost always have microscopic blood in their urine which can be detected by chemical reagent strips Diagnosis of Schistosomiasis Cont … The eggs of intestinal schistosomiasis can be detected in faecal specimens through a technique using methylene blue-stained cellophane soaked in glycerine or glass slides, known as the Kato-Katz technique For people living in non-endemic or low-transmission areas, serological and immunological tests may be useful in showing exposure to infection and the need for thorough examination, treatment and follow-up Activity : Small Group Discussion • What is the treatment of Schistosomiasis? Pharmacological Treatment of Schistosomiasis Praziquantel (PO) 40mg/kg as a single dose or in 2 divided doses The control of schistosomiasis is based on large-scale treatment of at-risk population groups, access to safe water, improved sanitation, hygiene education, and snail control. The WHO strategy for schistosomiasis control focuses on reducing disease through periodic, targeted treatment with praziquantel through the large-scale treatment (preventive chemotherapy) of affected populations. It involves regular treatment of all at-risk groups. Groups targeted for treatment are: School-aged children in endemic areas. Pharmacological Treatment of Schistosomiasis Cont … Adults considered to be at risk in endemic areas, and people with occupations involving contact with infested water, such as fishermen, farmers, irrigation workers, and women whose domestic tasks bring them in contact with infested water. Entire communities living in highly endemic areas. In high-transmission areas, treatment may have to be repeated every year for a number of years. Monitoring is essential to determine the impact of control interventions . Monitoring Of Schistosomiasis

NTA Level 6 • Semester 1 • PST06106 Pharmacotherapy of Trypanosomiasis Basic Pharmacotherapy • Source Session/Topic 12 Full source-text version: all educational wording from the extracted learning source is retained; only presenter/tutor metadata and web-layout noise are removed, while formatting is improved for readability. PST 06106 Basic Pharmacotherapy Session 12: Pharmacotherapy of Trypanosomiasis Learning objectives By the end of this session students are expected to be able to: Define trypanosomiasis Explain the clinical presentation of trypanosomiasis Outline diagnosis of trypanosomiasis Describe pharmacological treatment of trypanosomiasis Describe monitoring of trypanosomiasis therapy Activity: Buzzing What is Trypanosomiasis? Definition of Trypanosomiasis Two distinct forms of the genus Trypanosoma occur in humans. One is associated with African trypanosomiasis (sleeping sickness) and the other with American trypanosomiasis (Chagas disease) Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne parasitic disease. The parasites concerned are protozoa belonging to the Trypanosoma genus. They are transmitted to humans by tsetse fly ( Glossina genus) bites which have acquired their infection from human beings or from animals harbouring the human pathogenic parasites Definition of Trypanosomiasis Cont … Two forms of the disease exist. The slow-progressing form, caused by Trypanosoma brucei gambiense , is found in Western and Central Africa. The faster progressing form, caused by T. b. rhodesiense , is found in Eastern and Southern Africa Mother-to-child infection: the trypanosome can cross the placenta and infect the fetus . Mechanical transmission through other blood sucking insects is possible. Accidental infections have occurred in laboratories due to pricks from contaminated needles. Clinical presentation of Trypanosomiasis In the first stage, the trypanosomes multiply in subcutaneous tissues, blood and lymph. This is known as a haemolymphatic phase, which entails bouts of fever, headaches, joint pains and itching. After their inoculation, parasites proliferate at the site of infection, leading to an inflammatory nodule or ulcer. This trypanosomal chancre arises in about 50% of all rhodesiense—but rarely in gambiense—infections. After 3–4 weeks, the chancre usually heals with overlying desquamation, sometimes with altered pigmentation. Parasites spread to the draining lymph node and reach the bloodstream, initiating the haemolymphatic stage of the disease. This stage is characterised by general malaise, headache, and fever of an undulating type. In rhodesiense infection, with its more acute course, pancarditis with congestive heart failure, pericardial effusion, and pulmonary oedema can cause fatalities at this early stage, whereas gambiense infection shows a more insidious development that is frequently unrecognised or misdiagnosed. A typical sign of gambiense human African trypanosomiasis is generalised lymphadenopathy that develops after several weeks, frequently in the posterior triangle of the neck Clinical presentation of Trypanosomiasis cont. … In the second stage the parasites cross the blood-brain barrier to infect the central nervous system. This is known as the neurological phase. In general this is when more obvious signs and symptoms of the disease appear: changes of behaviour, confusion, sensory disturbances and poor coordination. Disturbance of the sleep cycle, which gives the disease its name, is an important feature of the second stage of the disease. Diagnosis of Trypanosomiasis The diagnosis of African Trypanosomiasis is made through laboratory methods, because the clinical features of infection are not sufficiently specific. The diagnosis rests on finding the parasite in body fluid or tissue by microscopy. The parasite load in T. b. rhodesiense infection is substantially higher than the level in T. b. gambiense infection. T. b. rhodesiense parasites can easily be found in blood. Diagnosis of Trypanosomiasis Cont … They can also be found in lymph node fluid or in fluid or biopsy of a chancre. The classic method for diagnosing T. b. gambiense infection is by microscopic examination of lymph node aspirate, usually from a posterior cervical node. It is often difficult to detect T. b. gambiense in blood. Concentration techniques and serial examinations are frequently needed. Serologic testing is available outside the U.S. for T. b. gambiense ; however, it normally is used for screening purposes only and the definitive diagnosis rests on microscopic Diagnosis of Trypanosomiasis Cont … All patients diagnosed with African trypanosomiasis must have their cerebrospinal fluid examined to determine whether there is involvement of the central nervous system, since the choice of treatment drug(s) will depend on the disease stage. The World Health Organization criteria for central nervous system involvement include increased protein in cerebrospinal fluid and a white cell count of more than 5. Trypanosomes can often be observed in cerebrospinal fluid in persons with second stage infection . Activity : Small Group Discussion What is the treatment of Trypanosomiasis? Pharmacological treatment of Trypanosomiasis The type of treatment depends on the stage of the disease. The drugs used in the first stage of the disease are of lower toxicity and easier to administer. The earlier the disease is identified, the better the prospect of a cure. Treatment success in the second stage depends on a drug that can cross the blood-brain barrier to reach the parasite. Such drugs are toxic and complicated to administer. Monitoring of Trypanosomiasis Therapy Monitor clinically and by using laboratory test In both early- and late-stage trypanosomiasis, symptoms usually resolve after treatment, and the parasitemia clears on repeat blood smears. Patients who have recovered from late-stage East African trypanosomiasis should undergo lumbar punctures every 3 months for the first year. Patients who have recovered from West African trypanosomiasis should undergo lumbar punctures every 6 months for 2 years . Monitoring of Trypanosomiasis Therapy Cont …. If symptoms return, the CSF WBC count is higher than 20/µL, CSF pleocytosis occurs((presence of an abnormally large number lymphocytes in cerebrospinal fluid), or trypanosomes are still present in blood or CSF, a relapse is suggested. However, a persistently elevated CSF WBC count may also be observed in recovering patients; thus, the change (increase or decrease) in the WBC count is more diagnostically helpful than the count by itself. If a relapse is noted, repeat treatment with melarsoprol or eflornithine may be considered Key Points Human African trypanosomiasis, also known as sleeping sickness, is a vector-borne parasitic disease. It is caused