Therapeutics-2 Case Presentation Retroviral disease with Meningitis By

HISTORY OF PRESENT ILLNESS: SENARIO : Here is a 35yrs old female hospitalized for 10days. Chief Complaints: Fever since 15days. Headache and vomiting since 7 days. HISTORY OF PRESENT ILLNESS: Patient was apparently normal 15 days back then she developed fever since 15 days. Low grade fever, not associated with chills and rigors and sweat. Headache since 7days present in frontal region, and vomiting since 7 days.

PAST MEDICATION HISTORY: PAST MEDICAL HISTORY: k/c/o RVD since 2yrs. PAST MEDICATION HISTORY: Tb.Nevirapine 200mg 1-0-1 Tb.Levotin LABORATORY INVESTIGATIONS: CBC 21/7 WBC 11,300 Neutrophils 90 Lymphocytes 10 ESR 70

TEMPERATURE CHART: DATE 1 2 3 4 5 6 7 8 9 10 TEMP 39 38 37

GENERAL PHYSICAL EXAMINATION: Signs of Meningial initiation. Neck rigidity (+) Kernig’s sign (+) NVBS (+) SOAP NOTE Subjective: here is a 35 yrs old female patient presenting with complaints of fever since 15 days. Headache and vomiting since 7 days. Headache in frontal region.

Neutrophils-90 increased due to meningitis. Objective: WBC-11,300 decreased due to inflammation/infection. Neutrophils-90 increased due to meningitis. Lymphocytes-10 decreased due to RVD ESR-70 increased due to infection Tests Lab value Normal Range WBC 11,300 4000-11000 cumm Neutrophils 90 40-60% Lymphocytes 10 20-60% ESR 70 <20 mm/hr

DIAGNOSIS: Retroviral Disease with Meningitis. ASSESSMENT: Problem-1 fever: Its occurs due to the presence of pyrogens which are the toxic substances released from the disease causing organisms Problem-2 Vomiting:Due to the toxic substances (drug) present in the stomach which triggers the CTZ zone in the brain, as a result vagus nerve (cranial nerve-9)stimulates nd vomiting occurs. Problem-3 Headache (frontal): due to the current usage of RVD drug( nevirapine ) Due to the presence of pathogenic organism in meninges. Problem-4 Meningitis: Due to inflammation of meninges caused by meningococci.

PLAN: Vomiting: Fever: T. Dolo: Paracetamol MOA: It blocks prostaglandin synthesis by (COX)cyclooxygenase pathway. Inhibits thromboxane A2 formation in platelets reducing platelet aggregation. Vomiting: T.Zofer stat, inj.vomikind iv 1-1-1 Ondansetron: It antagonises 5-HT3 receptor in CNS. Meningitis: Inj.Ofloxacin: It is a broad-spectrum antibiotic that is active against both Gram-Positive and Gram-Negative bacteria. It functions by Inhibiting DNA-gyrase, a type-2 topoisomerase and topoisomerase4

Which is an enzyme necessary to seperate replicated DNA, there by inhibiting bacterial cell division. Inj.Amphotericin-B: IT is a polyene antifungal antibiotic which alters cell membrane permeability by binding to ergosterol, thus causing leakage of cell components and subsequent cell death. Inj.Dexona : dexamethasone is a synthetic GC which decreases inflammation by inhibiting the migration of leukocytes and reversal of increased capillary permeability.It suppresses normal immune response. T.Akurit-4: :[ isoniazid ,rifampicin,pyrazemide,etambutanol ]

: Isoniazid : It acts by inhibition of mycolic acid synthesis and Disruption of the cell wall in susceptible organism. : Rifampicin: A semisynthetic broad-spectrum bactericidal antibiotic, Inhibits bacterial RNA synthesis by binding strongly to the beta subunit of DNA-dependent RNA polymerase, preventing attachment of the enzyme to DNA, and thus blocking initiation of RNA transcription. :Ethambutol :. It inhibits the synthesis of certain metabolites Subsequently impairing cell metabolism leading to cell death. Inj.kefazone: cefoperazone binds to one or more of the penicillin- binding proteins (PBPs) which inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell wall, thus inhibiting biosynthesis and arresting cell wall assembly resulting in bacterial cell Death.

Others: Inj.mannitol: It is an osmotic diuretic reduces intracranial pressure and enhances cerebral blood flow Inj.Dynapar: Diclofenac has potent anti-inflammatory analgesic and antipyretic actions. It inhibits the enzyme cycloxygenase, thus resulting in reduced synthesis of prostaglandin precursors. Inj.Pantocid: Pantoprazole inhibits the proton pump (H+ K+ ATPase) Functioning to suppress acid production and thus heals the ulcers.

T.Lamivudine& tenofavir 0-0-1 S.No Brand Name Generic Name Dose 21/7 22/7 23/7 24/7 25/7 26/7 27/7 28/7 29/7 30/7 1 T.Nevirapine 1-0-1 nevirapine 200 mg Y 2 T.Lamivudine& tenofavir 0-0-1 300mg 3 Inj.kefazone cefoperazone 1gm 4 Inj.pantocid 1-0-0 pantoprazole 40mg 5 Inj.vomikind 1-1-1 Ondansetron 1amp 6 Inj.Dexona dexamethasone 2c 7 Inj.Mannitol 100ml 8 T.Zofer stat ondansetron 4mg

Brand Name Generic Name Dose 21/7 22/7 23/7 24/7 25/7 26/7 27/7 28/7 S.No Brand Name Generic Name Dose 21/7 22/7 23/7 24/7 25/7 26/7 27/7 28/7 29/7 30/7 9 Inj.Dynapar 1-0-1 Diclofenac 1amp Y 10 Syp.Cremaffin 0-0-1 2tsp 11 Inj.oflox ofloxacin 10ml 12 Inj.Amphotericin-b 1-0-1 35mg 13 T.Akurit-4 2-0-0 HRZE 14 T.Flucos 0-1-0 fluconazole 100mg 15 T.Dolo paracetamol 650mg

Drug interaction MAJOR 1.Rifampicin- Isoniazid Effects liver(may cause fever,chills,joint pains)-need drug adjustment if hepatic damage occurs. Rifampicin alters metabolism of isoniazid and increases toxic metabolities. 2.Amphotericin-B-Tenofavir : nephrotoxicity 3.Rifampicin-Nevirapine : decreases plasma concentrartion of nevirapine.Induction of metabolism 4.Ofloxacin-Dexamethasone : Increase risk of tendonitis. 5.Rifampicin-Pyrizinamide : increases liver injury. 6.Diclofenac-Tenofavir : nephrotoxicity.

MODERATE: 1.Amphotericin-B-Dexamethasone : Hypokalemia 2.Rifampicin-Dexamethasone : reduces therapeutic effect of Dexamethasone. 3.ofloxacin-Diclofenac : Increases GI disturbances 4.Ethambutol-INH : Peripheral neuropathy risk MINOR: 5.INH-Dexamethasone : decreases corticosteroid level.

DISCHARGE DRUGS: T.Nevirapine-200mg- 1-0-1 T.Lamivudine+Tenofavir-300mg- 0-0-1 T.Pantocid-40mg- 1-0-0 X 5-days T.Akurit-4- 2-0-0 X 2 weeks T.Flucos-100mg – 0-1-0 X 2 weeks PATIENT COUNCELLING: T.Pantocid should be taken before breakfast. ART therapy should be continued without skipping.