SEARCH RESULTS FOR: renal
Nephrotic Syndrome: Pathogenesis and Clinical Findings
3.5g/day*? Ability of blood to retain fluids within vessels ? fluid leaks into extra-vascular spaceInjury to glomerular endothelium and epitheliumImmune complexes deposit into glomerulusDamaged glomerulus ? abnormally permeable to proteins within the blood ? plasma proteins are thus excessively filtered out? Oncotic pressure signals liver to ? albumin synthesis, only to have it filtered out by the kidneys? anabolic activity of liver ? ? lipoprotein synthesisHyperlipidemia*:(? serum LDL, VLDL, and TGs)Lipiduria(lipid/fatty casts; "Maltese cross" sign under polarized light)Since counter-balancing anticoagulant proteins are lost, clotting factors (i.e. 1, 7, 8, 10) now have more activityThrombo-embolic diseaseBlood becomes hyper-coagulable? Lipids are filtered into renal tubules, end up in urineMembranoproliferative Glomerulonephritis (MPGN)Lupus Glomerulonephritis Post-infectious GlomeruloneprhitisIgA NephropathyDamages podocytes on epithelial side of glomerulus ("podocyte effacement"; foot processes flattening)Diabetes MellitusChronic hyperglycemia damages glomeruliDeposition of Immunoglobulin light chains in glomerulusAmyloidosisAnasarca(If generalized)Peri-orbital edema (classic sign)Focal Segmental Glomerular Sclerosis (FSGS)Membranous GlomeruloneprhitisAntibodies attack podocytes, thickening glomerular basement membraneOverflow of immunoglobulin light chains into urine (More filtered than can be reabsorbed)Proteinuria >3.5g/day*The Anion Gap is mostly due to the negative charge of plasma albumin? Anion GapNotes: The four classic features (*) of Nephrotic Syndrome are PEAL (Proteinuria (>3.5 g/day), Edema, hypo-Albuminemia, and hyperLipidemia)For each 10 g/L drop in albumin below 40:Add 2.5 to the calculated anion gap (AG) to get the "correct" AG valueAdd 0.2 mmol/L to total calcium or get an ionized calcium, which is unaffected50% of serum Ca2+ is albumin-bound, so total serum calcium ? Serum total Ca2+ does not reflect ionized Ca2+ ? Blood oncotic pressure" title="Destroys charge barrier to protein filtrationNephrotic Syndrome: Pathogenesis and Clinical FindingsAuthor: Yan YuReviewers:Alexander ArnoldDavid WaldnerSean SpenceStefan Mustata** MD at time of publicationLegend:Published August 19, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsExcessive ("Nephrotic-range") loss of albumin in the urineHypo-albuminemia*Loss of anti-coagulant proteins (Antithrombin, Plasminogen, and proteins C and S) in urineMinimal Change Disease (MCD)"Underfill" edema*Proteinuria >3.5g/day*? Ability of blood to retain fluids within vessels ? fluid leaks into extra-vascular spaceInjury to glomerular endothelium and epitheliumImmune complexes deposit into glomerulusDamaged glomerulus ? abnormally permeable to proteins within the blood ? plasma proteins are thus excessively filtered out? Oncotic pressure signals liver to ? albumin synthesis, only to have it filtered out by the kidneys? anabolic activity of liver ? ? lipoprotein synthesisHyperlipidemia*:(? serum LDL, VLDL, and TGs)Lipiduria(lipid/fatty casts; "Maltese cross" sign under polarized light)Since counter-balancing anticoagulant proteins are lost, clotting factors (i.e. 1, 7, 8, 10) now have more activityThrombo-embolic diseaseBlood becomes hyper-coagulable? Lipids are filtered into renal tubules, end up in urineMembranoproliferative Glomerulonephritis (MPGN)Lupus Glomerulonephritis Post-infectious GlomeruloneprhitisIgA NephropathyDamages podocytes on epithelial side of glomerulus ("podocyte effacement"; foot processes flattening)Diabetes MellitusChronic hyperglycemia damages glomeruliDeposition of Immunoglobulin light chains in glomerulusAmyloidosisAnasarca(If generalized)Peri-orbital edema (classic sign)Focal Segmental Glomerular Sclerosis (FSGS)Membranous GlomeruloneprhitisAntibodies attack podocytes, thickening glomerular basement membraneOverflow of immunoglobulin light chains into urine (More filtered than can be reabsorbed)Proteinuria >3.5g/day*The Anion Gap is mostly due to the negative charge of plasma albumin? Anion GapNotes: The four classic features (*) of Nephrotic Syndrome are PEAL (Proteinuria (>3.5 g/day), Edema, hypo-Albuminemia, and hyperLipidemia)For each 10 g/L drop in albumin below 40:Add 2.5 to the calculated anion gap (AG) to get the "correct" AG valueAdd 0.2 mmol/L to total calcium or get an ionized calcium, which is unaffected50% of serum Ca2+ is albumin-bound, so total serum calcium ? Serum total Ca2+ does not reflect ionized Ca2+ ? Blood oncotic pressure" />
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2nd gen antipsychotics (Slovenian translation) - FINAL VERSION
BMR (Slovenian translation) - FINAL VERSION
Bupropion (Slovenian translation) - FINAL VERSION
NAT), ki proizvaja aktivne metabolite. Natan'6en mehanizem delovanja (se) ni znan.
znak/simptom/laboratorijska najdba
DA in NE posledi6no ostaneta v sinapsah dlje Casa in okrepita 2iv6ni prenos
neieleni udnki
glavobol
suha usta
4, tel. tee nespeEnost slabost zaprtie
tahikardija
epileptiEni napadi
faringitis
omotica hipertenziia agitacija
prevedel in priredil: Jan Kejiar, dr. med., specializant psihiatrije pregledala: doc. dr. Brigita Novak Sarotar, dr. med., spec. psih.
eliminacija poteka preko jeter in ledvic
prilagoditev odmerka v primeru bolezni jeter in/ali ledvic
bupropion lahko inhibira jetrni citokrom P4502D6 in povzrod interakcije med zdravili
kontraindiciran pri boleznih, ki zmanIgajo epileptogeni prag: anoreksija/bulimija nervoza, epilepsija, odtegnitev alkohola, odtegnitev benzodiazepinov
zaplet Objavljeno 30. junija 2017 na www.thecalgaryguide.com.
" title="Bupropion (atipiEni antidepresiv): Mehanizem delovanja in neieleni utinki
potenten antidepresiv v monoterapiji all kot dodatno zdravilo pri zdravljenju razpoloienjskih motenj
okrajgave: 5-HT - serotonin DA - dopamin DAT - prenagalec DA NA - noradrenalin NAT - prenagalec NA SSRI - selektivni zaviralec ponovnega privzema 5-HT
Legenda:
bupropion
farmakologija
antidepresivni udnki uporaben pri zdravljenju "zmaniganega pozitivnega afekta"
nima pomembnelgih 5-HT udnkov povzraa spolne disfunkcije v primerjavi s SSRI; lahko celo odpravi omenjeni neieleni udnek (povzraen s strani SSRI)
dodatek pri zdravljenju odvisnosti od nikotina preko T iive'nega prenosa DA v nagrajevalni poti
energije preko T 2ivbega prenosa NA
patofiziologija mehanizem
farmakokinetika
farmakodinamika
avtorica: JoAnna Fay, Sara Meunier pregledala: Jojo Jiang, Alexander Arnold, Aaron Mackie*
* dr. med. ob objavi
Nizkoafiniteten zaviralec ponovnega privzema DA in NA (DAT>NAT), ki proizvaja aktivne metabolite. Natan'6en mehanizem delovanja (se) ni znan.
znak/simptom/laboratorijska najdba
DA in NE posledi6no ostaneta v sinapsah dlje Casa in okrepita 2iv6ni prenos
neieleni udnki
glavobol
suha usta
4, tel. tee nespeEnost slabost zaprtie
tahikardija
epileptiEni napadi
faringitis
omotica hipertenziia agitacija
prevedel in priredil: Jan Kejiar, dr. med., specializant psihiatrije pregledala: doc. dr. Brigita Novak Sarotar, dr. med., spec. psih.
eliminacija poteka preko jeter in ledvic
prilagoditev odmerka v primeru bolezni jeter in/ali ledvic
bupropion lahko inhibira jetrni citokrom P4502D6 in povzrod interakcije med zdravili
kontraindiciran pri boleznih, ki zmanIgajo epileptogeni prag: anoreksija/bulimija nervoza, epilepsija, odtegnitev alkohola, odtegnitev benzodiazepinov
zaplet Objavljeno 30. junija 2017 na www.thecalgaryguide.com.
" />
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