Sx Nefrítico

Question 1

¿Cuál es la presentación clínica del sx nefritico?

Answer 1

hematuria, proteinuria, and often arterial

hypertension and renal failure.

Question 2

¿Cuáles son los principales tipos de glomerulonefritis proliferativa?

Answer 2

1. Glomerulonefritis endocapilar proliferativa
2. Glomerulonefritis membranoproliferativa
3. Glomerulonefritis endo y extra capilar

Question 3

¿Cómo clasifico histologicamente las glomerulonefritis?

Answer 3

Proliferativas y no proliferativas

Question 4

¿Cuál es la mas común de la no proliferativa?

Answer 4

Glomerulonefritis membranosa

Question 5

¿Cuales son las 2 glomerulonefritis que solo puedes diagnosticar con inmunofluorescencia?

Answer 5

Glomerulonefritis Anti-MBG

Glomerulonefritis por IgA

Question 6

¿cómo es el edema ?

Answer 6

Periférico-Anasarca a diferencia del nefrotico que es periorbital/facial

Question 7

Sintomas de glomerulonefritis aguda

Answer 7

1. fever
2. headache,
3. and abdominal pain, or more progressive, with 4.peripheral edema, weight gain, and asthenia

Question 8

¿Cómo resulta la hematuria del sx nefritico?

Answer 8

Es una hematuria no selectiva que se puede presentar con oliguria a diferencia del sx nefrotico que es albuminuria

Question 9

Evaluación del paciente con sospecha de glomerulonefitis

Answer 9

1. Complement levels (CH50, C3, C4)
2. Antistreptolysin O, anti-DNAse B, antistreptokinase, anti-NADase,
3. antihyaluronidase antibodies
4. IgA
5. Antinuclear antibodies, anti-DNA antibodies
6. ANCA
7. Anti-GBM antibodies
8. Serology for EBV and hepatitis B and C
9. Renal biopsy with light microscopy and immunofl uorescence

Question 10

several features suggest a diagnosis

of acute poststreptococcal glomerulonephritis:

Answer 10

1. a throat or
skin infection in previous weeks
2. an increase in the antistreptolysin
O and anti-DNAse antibody titers, 
3. and a marked but
transient reduction of C3 and C4.

Question 11

Dosis de Furosemida

Answer 11

1mg/kg inicialmente

maximo 40mg

Question 12

Dosis de nifedipino

Answer 12

0.5-2microgramos/kg min

Question 13

Mecanismo de acción furosemida

Answer 13

Furosemide, a loop diuretic, inhibits water reabsorption in the nephron by blocking the sodium-potassium-chloride cotransporter (NKCC2) in the thick ascending limb of the loop of Henle. This is achieved through competitive inhibition at the chloride binding site on the cotransporter, thus preventing the transport of sodium from the lumen of the loop of Henle into the basolateral interstitium. Consequently, the lumen becomes more hypertonic while the interstitium becomes less hypertonic, which in turn diminishes the osmotic gradient for water reabsorption throughout the nephron. Because the thick ascending limb is responsible for 25% of sodium reabsorption in the nephron, furosemide is a very potent diuretic.

Question 14

mecanismo de accion nifedipino

Answer 14

Nifedipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the influx of calcium ions through L-type calcium channels. Calcium ions entering the cell through these channels bind to calmodulin. Calcium-bound calmodulin then binds to and activates myosin light chain kinase (MLCK). Activated MLCK catalyzes the phosphorylation of the regulatory light chain subunit of myosin, a key step in muscle contraction. Signal amplification is achieved by calcium-induced calcium release from the sarcoplasmic reticulum through ryanodine receptors. Inhibition of the initial influx of calcium inhibits the contractile processes of smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. The vasodilatory effects of nifedipine result in an overall decrease in blood pressure.