1. Therapeutics-2 Case Presentation Retroviral disease with MeningitisBy

2. 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.

3. 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

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

5. 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.

6. 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
cumm
Neutrophils 90
40-60%
Lymphocytes 10
20-60%
ESR 70
<20 mm/hr

7. 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.

8. 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

9. 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 ]

10. : 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.

11. 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.

12. 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
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

13. 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

14. 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.

15. 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.

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