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Keadaan klinis dimana terjadi peningkatan volume cairan pada ruang interstitial,ditandiai adanya pembengkakan oleh sejumlah cairan. Anasarka adalah edema yang besar, tersebar luas.
Patogenesis Edema
Kerusakan membran basal pada glomerulus Proteinuria masif Hipoalbumin (<35g/dl)
Tekanan onkotik menurun Caian berpindah dari tekanan rendah ke tinggi Cairan berpindah dari intravaskuler ke interstitial Edema
Ginjal
1.
Ed
Hati
Furosemid
Jenis diuretika yang berkerja pada loop henle Contoh lain : AS. ETAKRINAT BUMETANID
mekanisme kerja furosemid dengan memblok reabsi aktif NaCl pada bagan ascenden loop henle sehingga mencegah air ditarik ke bagian capiler. kerja cepat, kadar puncak per-oral 1 jam Intravena 30 menit
Contraindications : 1. Severe Na+ and volume depletion 2. Hypersensitivity to sulfonamides 3. Anuria unresponsive to a trial dose of loop diuretic.
Glucocorticoids
Glucocorticoids lyse (in some species) and induce the redistribution of lymphocytes, causing a rapid, transient decrease in peripheral blood lymphocyte counts. To effect longer-term responses, steroids bind to receptors inside cells; either these receptors, glucocorticoidinduced proteins, or interacting proteins regulate the transcription of numerous other genes (see Chapter 59). Additionally, glucocorticoid- receptor complexes increase IB expression, thereby curtailing activation of NF-B, which increases apoptosis of activated cells (Auphan et al., 1995). Of central importance, key proinflammatory cytokines such as IL-1 and IL-6 are downregulated. T cells are inhibited from making IL-2 and proliferating. The activation of cytotoxic T lymphocytes is inhibited. Neutrophils and monocytes display poor chemotaxis and decreased lysosomal enzyme release.
Efek samping : 1. growth retardation in children 2. avascular necrosis of bone 3. osteopenia 4. increased risk of infection 5. poor wound healing 6. cataracts 7. hyperglycemia 8. Hypertension Pengobatan SN dengan Kontra-Indikasi Steroid : 1. Tekanan darah tinggi 2. Peningkatan ureum dan kreatinin 3. Infeksi berat
Glucocorticoids
Efek steroid menyebakan hipertensi 1. Cardiovascular effects ; they increase sensitivity to pressor agents such as catecholamines and angiotensin II while reducing nitric oxide (mediated endothelial dilatation)
a. increase peripheral resistance. c. increase cardiac contractility
2. Angiotensinogen synthesis is increased by glucocorticoids, so can act on the distal nephron to cause sodium retention
Glucocorticoids increase blood pressure by a variety of mechanisms involving actions on the kidney and vasculature.[143] In vascular smooth muscle, they increase sensitivity to pressor agents such as catecholamines and angiotensin II while reducing nitric oxidemediated endothelial dilatation. Angiotensinogen synthesis is increased by glucocorticoids.[144] In the kidney, depending upon the activity 11-HSD2, cortisol can act on the distal nephron to cause sodium retention and potassium loss (mediated via the MR).[121] Elsewhere across the nephron, glucocorticoids increase glomerular filtration rate, proximal tubular epithelial sodium transport, and free water clearance.[145] This latter effect involves antagonism of the action of vasopressin and explains the dilutional hyponatremia seen in patients with glucocorticoid deficiency
complication of albumin therapy is Symptomatic volume overload, with hypertension and heart failure therapy mandates close monitoring of volume status, serum electrolyte balance, and renal function.