6:00 am: TB meds, 3 tabs. 30 tablets left, 10 days.
10 days before I go back to RITM, to DOTS... To what I understand, I would be doing a sputum test again... if it shows that I still have TB, then we are looking at Multi-Drug Resistant (MDR) TB... which would be much difficult to treat, I might be referred to Lung Center already...
Note to self: I should also pay for my PhilHealth... as much as possible for at least 6 months... a full year would be great... but since money is still very tight... I guess would have to settle for just 3 months...
The TB med is 150mg/75mg tablet Rifampicin and Isoniazid.
Rifampicin was introduced in 1967, as a major addition to the cocktail-drug treatment of tuberculosis and inactive meningitis, along with isoniazid, ethambutol, pyrazinamide and streptomycin. It requires a prescription in North America. It must be administered regularly daily for several months without break; otherwise, the risk of drug-resistant tuberculosis is greatly increased. In fact, this is the primary reason that it is used in tandem with the three aforementioned drugs, particularly isoniazid. This is also the primary motivation behind directly observed therapy for tuberculosis.
Rifampicin resistance develops quickly during treatment and rifampicin monotherapy should not be used to treat these infections — it should be used in combination with other antibiotics.
Rifampicin is also used in the treatment of cholestatic pruritus.
Isoniazid (Laniazid, Nydrazid), also known as isonicotinylhydrazine (INH), is an organic compound that is the first-line anti tuberculosis medication in prevention and treatment. It was first discovered in 1912, and later in 1951 it was found to be effective against tuberculosis by inhibiting its mycolic acid (wax coat). Isoniazid is never used on its own to treat active tuberculosis because resistance quickly develops. Isoniazid also has an antidepressant effect, and it was one of the first antidepressants discovered. Isoniazid can also be used in the treatment of a BCG-oma.
The compound was first synthesised in the early 20th century, but its activity against tuberculosis was first reported in the early 1950s and three pharmaceutical companies attempted unsuccessfully to simultaneously patent the drug (the most prominent one being Roche, who launched their version, Rimifon, in 1952). With the introduction of isoniazid, a cure for tuberculosis was first considered reasonable.
Isoniazid is available in tablet, syrup, and injectable forms (given intramuscularly or intravenously). Isoniazid is available worldwide, is inexpensive and is generally well tolerated. It is manufactured from isonicotinic acid, which is produced from 4-methylpyridine.
One of the adverse side effect of Isoniazid is Peripheral Neuropathy, which I am suffering from right now. It is due to pyridoxine (vitamin B6) depletion, but are uncommon at doses of 5 mg/kg. Persons with conditions in which neuropathy is common (e.g., diabetes, uremia, alcoholism, malnutrition, HIV-infection), as well as pregnant women and persons with a seizure disorder, may be given pyridoxine (vitamin B6) (10–50 mg/day) with isoniazid.
My ARV Cocktail includes: Zidovudine and Lamivudine, combined in one tablet, taken at 8 in the morning and again 8 in the evening, this time with Efavirenz.
Zidovudine (INN) or azidothymidine (AZT) (also called ZDV) is a nucleoside analog reverse-transcriptase inhibitor (NRTI).
AZT was the first approved treatment for HIV, sold under the names Retrovir and Retrovis. AZT use was a major breakthrough in AIDS therapy in the 1990s that significantly altered the course of the illness and helped destroy the notion that HIV/AIDS was a death sentence. AZT slows HIV spread significantly, but does not stop it entirely. This allows HIV to become AZT-resistant over time, and for this reason AZT is usually used in conjunction with other NRTIs and anti-viral drugs. In this form, AZT is used as an ingredient in Combivir and Trizivir, among others. Zidovudine is included in the World Health Organization's "Essential Drugs List", which is a list of minimum medical needs for a basic health care system.
AZT works by inhibiting the action of reverse transcriptase, the enzyme that HIV uses to make a DNA copy of its RNA. Reverse transcription is necessary for production of the viral double-stranded DNA, which is subsequently integrated into the genetic material of the infected cell (where it is called a provirus).
The azido group increases the lipophilic nature of AZT, allowing it to cross cell membranes easily by diffusion and thereby also to cross the blood-brain barrier. Cellular enzymes convert AZT into the effective 5'-triphosphate form. Studies have shown that the termination of the formed DNA chains is the specific factor in the inhibitory effect.
The triphosphate form also inhibits DNA polymerase used by human cells to undergo cell division, but has approximately 100-fold greater affinity for viral reverse transcriptase. Because of this selectivity, in vitro studies have shown that AZT inhibits HIV replication without affecting the function of normal T cells. The cellular DNA polymerase used by mitochondria to replicate is more sensitive to the inhibitory effects of AZT, accounting for its toxic effects on cardiac and skeletal muscles, causing myositis.
Chronic, high-dose therapy with AZT is associated with significant side effects, including anemia, neutropenia, hepatotoxicity, cardiomyopathy, and myopathy. Damage to muscle cells is reversible upon cessation of AZT treatment. It has been attributed to several possible causes including depletion of mitochondrial DNA, sensitivity of the γ-DNA polymerase in the cell mitochondria, the depletion of thymidine triphosphate, oxidative stress, reduction of intracellular L-carnitine or apoptosis of the muscle cells. Anemia due to AZT can be treated using erythropoietin to stimulate red blood cell production. Drugs that inhibit hepatic glucuronidation, such as indomethacin, acetylsalicylic acid (Aspirin) and trimethoprim, decrease the elimination rate and increase the toxicity of the drug. Minor side effects include nausea and vomiting, headache, changes in the distribution of body fat, sleep disruption and loss of appetite while less common but potentially serious side effects include discoloration of fingernails and toenails, mood changes, tingling or numbness of the hands or feet, easy bruising or bleeding and seizures. Serious allergic reactions are rare.
Lamivudine (2',3'-dideoxy-3'-thiacytidine, commonly called 3TC) is a potent nucleoside analog reverse transcriptase inhibitor (nRTI).
Lamivudine has been used for treatment of chronic hepatitis B at a lower dose than for treatment of HIV. It improves the seroconversion of e-antigen positive hepatitis B and also improves histology staging of the liver. Long term use of lamivudine unfortunately leads to emergence of a resistant hepatitis B virus (YMDD) mutant. Despite this, lamivudine is still used widely as it is well tolerated.
Lamivudine is an analogue of cytidine. It can inhibit both types (1 and 2) of HIV reverse transcriptase and also the reverse transcriptase of hepatitis B. It is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis. The lack of a 3'-OH group in the incorporated nucleoside analogue prevents the formation of the 5' to 3' phosphodiester linkage essential for DNA chain elongation, and therefore, the viral DNA growth is terminated.
Lamivudine is administered orally, and it is rapidly absorbed with a bio-availability of over 80%. Some research suggests that lamivudine can cross the blood-brain barrier. Lamivudine is often given in combination with zidovudine, with which it is highly synergistic. Lamivudine treatment has been shown to restore zidovudine sensitivity of previously resistant HIV. Lamivudine showed no evidence of carcinogenicity or mutagenicity in in vivo studies in mice and rats at doses from 10 to 58 times those used in humans
Efavirenz is used to treat HIV infection. It is never used alone and is always given in combination with other drugs. The decision on when to start treatment should take into account CD4 count, HIV viral load, treatment history, resistance profiles and patient preference.
Since the preliminary publication of the results of the ACTG 5142 trial in 2006 which compared efavirenz against lopinavir, efavirenz has been used as first line treatment in preference to the protease inhibitors. The ACTG 5095 trial showed that the potency of efavirenz is maintained at all CD4 counts and HIV viral loads.
Efavirenz falls in the NNRTI class of antiretrovirals. Both nucleoside and non-nucleoside RTIs inhibit the same target, the reverse transcriptase enzyme, an essential viral enzyme which transcribes viral RNA into DNA. Unlike nucleoside RTIs, which bind at the enzyme's active site, NNRTIs act allosterically by binding to a distinct site away from the active site known as the NNRTI pocket.
Efavirenz is not effective against HIV-2, as the pocket of the HIV-2 reverse transcriptase has a different structure, which confers intrinsic resistance to the NNRTI class.
As most NNRTIs bind within the same pocket, viral strains which are resistant to efavirenz are usually also resistant to the other NNRTIs, nevirapine and delavirdine. The most common mutation observed after efavirenz treatment is K103N, which is also observed with other NNRTIs
Side effects may include Psychiatric symptoms, including insomnia, nightmares, confusion, memory loss, and depression, are common, and more serious symptoms such as psychosis may occur in patients with compromised liver or kidney function.
Rash, nausea, dizziness and headache may occur
A general guideline about efavirenz and pregnancy states that efavirenz can cause birth defects and should not be used in women who might become pregnant. A later study, however, found no increased risk of overall birth defects among women exposed to efavirenz during the first trimester of pregnancy compared with exposure to other antiretroviral drugs.
Safety in children has not been established
Use of efavirenz can produce a false positive result in some urine tests for marijuana.
Plus, I take a prophylaxis: Co-trimoxazole.
Trimethoprim/sulfamethoxazole or co-trimoxazole (abbreviated SXT, TMP-SMX, TMP-SMZ or TMP-sulfa) is a sulfonamide antibiotic combination of trimethoprim and sulfamethoxazole, in the ratio of 1 to 5, used in the treatment of a variety of bacterial infections.
The synergy between trimethoprim and sulfamethoxazole was first described in a series of in vitro and in vivo experiments published in the late 1960s. Trimethoprim and sulfamethoxazole have a greater effect when given together than when given separately; the reason is because they inhibit successive steps in the folate synthesis pathway.
It is unclear whether this synergy occurs at doses used in humans, because, at the concentrations seen in blood and tissues, the ratio of trimethoprim to sulfamethoxazole is 1:20, which is less than the 1:5 ratio needed in vitro for synergy to occur.
Sulfamethoxazole acts as a false-substrate inhibitor of dihydropteroate synthetase. Sulfonamides such as sulfamethoxazole are analogues of p-aminobenzoic acid (PABA) and, thus, are competitive inhibitors of the enzyme, inhibiting the production of dihydropteroic acid.
Trimethoprim acts by interfering with the action of bacterial dihydrofolate reductase, inhibiting synthesis of tetrahydrofolic acid.
Folic acid is an essential precursor in the de novo synthesis of the DNA nucleosides thymidine and uridine. Bacteria are unable to take up folic acid from the environment (i.e., the infection host) and, thus, are dependent on their own de novo synthesis - inhibition of the enzyme starves the bacteria of two bases necessary for DNA replication and transcription.
Trimethoprim/sulfamethoxazole may have the following adverse reactions:
- Allergic – Stevens–Johnson syndrome, toxic epidermal necrolysis, anaphylaxis, allergic myocarditis, erythema multiforme, exfoliative dermatitis, angiodema, drug fever, chills, Henoch–Schönlein purpura, serum sickness-like syndrome, generalized allergic reactions, generalized skin eruptions, photosensitivity, conjunctival and scleral injection, pruritus, urticaria and rash. In addition, periarteritis nodosa and systemic lupus erythematosis have been reported.
- Endocrine – The sulfonamides bear certain chemical similarities to some goitrogens, diuretics (acetazolamide and the thiazides), and oral hypoglycemic agents. Cross-sensitivity may exist with these agents. Diuresis and hypoglycemia have occurred rarely in patients receiving sulfonamides.
- Gastrointestinal – Hepatitis, including cholestatic jaundice and hepatic necrosis, elevation of serum transaminase and bilirubin, pseudo-membranous enterocolitis, pancreatitis, stomatitis, glossitis, nausea, emesis, abdominal pain, diarrhea, anorexia.
- Genitourinary – Renal failure, interstitial nephritis, BUN and serum creatinine elevation, toxic nephrosis with oliguria and anuria, and crystalluria.
- Hematologic – Agranulocytosis, aplastic anemia, thrombocytopenia, leukopenia, neutropenia, hemolytic anemia, megaloblastic anemia, hypoprothrominemia, methemoglobinemia, eosinophilia.
- Metabolic – Hyperkalemia, hyponatremia.
- Musculoskeletal – Arthralgia and myalgia.
- Neurologic – Aseptic meningitis, convulsions, peripheral neuritis, ataxia, vertigo, tinnitus, headache.
- Psychiatric – Hallucinations, depression, apathy, nervousness.
- Respiratory System – Cough, shortness of breath, and pulmonary infiltrates.
- Miscellaneous – Weakness, fatigue, insomnia.
***hot guy on pic have no connect to the article, pantangal umay lang kasi ang haba eh... lolz
8:00 pm: arv: zido/lami, efav. prophylaxis: Cotrimoxazole
hot
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