1.

Potensial adverse effects (renal) ( disuruh buat ppt) pelajar tentang obat inflasmasi

2. Patofisiologi hipertensi yg kemarin no 3, penjelasan lengkapnya

Clinical Presentation & Pathophysiology

Hypertensive emergencies include hypertension associated with
vascular damage (termed malignant hypertension) and hypertension
associated with hemodynamic complications such as heart
failure, stroke, or dissecting aortic aneurysm. The underlying
pathologic process in malignant hypertension is a progressive arteriopathy
with inflammation and necrosis of arterioles. Vascular
lesions occur in the kidney, which releases renin, which in turn
stimulates production of angiotensin and aldosterone, which further
increase blood pressure.
Hypertensive encephalopathy is a classic feature of malignant
hypertension. Its clinical presentation consists of severe headache,
mental confusion, and apprehension. Blurred vision, nausea and
vomiting, and focal neurologic deficits are common. If untreated,
the syndrome may progress over a period of 12–48 hours to convulsions,
stupor, coma, and even death

3. Medicinal plant coumarin

a. Fraxinus excelsior
Tumbuhan ini merupakan bagian dari keluarga Oleaceae. Di dalamnya terkandung
komponen fenolic, yang sebagian besar adalah iridoid dan glikosida sekoiridoid.
Kumarin terdapat di bagian daun (16% - 28%). Daunnya dapat dibuat menjadi obat
anti hipertensive.
b. Aesculus hippocastanum
Tumbuhan ini bagian dari keluarga Hippocastanaceae. Selain kumarin, tumbuhan ini
juga mengandung asam galat dan asam tanik yang digunakan di dalam industri.
Daunnya mengandung hydroxycoumarin heterosides (esculosid, fraxoside).
Komponen ini digunakan sebagai treatment penyakit jantung.
c. Justicia pectoralis
Tumbuhan ini dapat berperan dalam anti-inflamasi, actionsEffects on central
nervous systemIn the evaluation of the effects on the central nervous system(CNS),
the aqueous extract from the leaves of J. pectoralis reducedthe aggressive conduct
and the exploratory activity in rats, andblocked the excitation induced by
phencyclidine (NMDA receptorantagonist). However, it was unable to prevent
seizures induced byGABAergic antagonists (pentilenotetrazole and picrotoxin),
unlikediazepam, which showed neuroprotection, suggesting that theanxiolytic
action of the plant does not occur via a benzodiazepine-mediated mechanism (Saad
et al., 1987; Fernández et al., 1989).Furthermore, it was found that intraperitoneal
administration ofthe aqueous extract of the plant was not able to reverse the
effectsof apomorphine (dopaminergic agonist), showing no antidopamin-ergic
activity similar to typical neuroleptics