Fisiopato Parcial 1 Flashcards
Sodio IC vs. EC
EC: 135-145
IC: 10-14
K+ IC , EC
EC: 3.5-5
IC: 140-150
Cl- IC, EC
EC: 98-106
IC: 140-150
Bicarbonato IC, EC
EC: 24-31
IC:7-10
Calcio IC, EC
EC: 8.5-10.5
IC:
Fosforo IC, EC
EC: 2.5-4.5
IC: variable
Mg IC, EC
EC: 1.8-3.0
IC: 40mEq/kg (20mmol)
Bomba Na+/K+-ATPasa
3 Na+ afuera
2 K+ adentro
plasma glucosa
entre 180-380mg/dL
Cuando niveles de glucosa son mas de 380mg/dL
glucosuria
Plasma Creatinina
0!!!!
No hay reabsorción, no debe haber en sangre pero si en orina
*Niveles de creatinina en suero se utilizan para estimar TFG
Gasto urinario obligado
300-500ml/dia
sodio of body weight
60
Sistema de Renina-Angiotensina
receptores sensibles a cambios en preseion @ arteriolas afferentes principalmente responden a cambios en presion arterial estimulando SNS + liberando renina
renina responde a cambios en presion arterial, TFG, y # de Na+ en filtrado
renina entra a torrente sanguinea done ayuda convertir angiotensinogeno –> angiotensina I
angiotensina I se convierte en angiotensina II por la enzima (ACE) en el pulmon
angiotensina II interactua directamente en los tubulos renales para aumentar reabsorcion de sodio
Tambien provoca constriccion de vasos renales diminuyendo flujo renal –> menos Na+ se filtra y mas se reabsorbe
TFG aumenta a nivel normal
Angiotensina II tambien regula aldosterona
aldosterona
una hormona secretada por la corteza adrenal
actua @ nivel de tubulo collector cortical para aumentar reabsorcion de Na+ y eliminacion de K+
diureticos que bloquean acciones de aldosterona (K+ sparing)
spironolactone
amiloride
triamterene
diureticos que suprimen liberation de renina
beta-adrenergic blocking drugs
diureticos que inhiben conversion de angiotensina I –> II
inhibidores ACE
drogas que blouean acion de angiotensina II en su receptor
ARBs
En tx que tiene prioridad , volumen o electrolitos?
VOLUMEN
que provoca deshidratacion celular
aumento de osmolalidad EC
que sucede @ volumen sanguineo baja + presion sanguinea bajja
aumenta angiotensina II
que provoca la sensacion de sed?
deshidratacion celular por aumento de osmolalidad EC
disminucion de volumen de sangre
Hipodipsia
falta de sed
Polidipsia
demasiado sed
3 categorias de polidipsia
sintomatica/verdadera
(estimulado por deshidratación celular por aumento de la osmolalidad EC + Disminución de la volemia + angiotensina II)
falsa
compulsivo
Porque diabetes insipidus y melliltus causan sed verdadera?
Diabetes mellitus is a disorder of blood glucose regulation, which results from a deficiency in the action of the hormone insulin. This may be due to autoimmune destruction of the insulin-secreting cells of the pancreas (type 1 diabetes mellitus) or it may result from a problem in the responsiveness of tissues to insulin, known as insulin resitance (type 2 diabetes mellitus). With either disorder, the result is hyperglycemia, or high levels of glucose in the plasma.
In a diabetic that has hyperglycemia, the filtered load of glucose (amount of glucose filtered) can exceed the capacity of the kidney tubules to reabsorb glucose, because the transport proteins become saturated. The result is glucose in the urine. Glucose is a solute that draws water into the urine by osmosis. Thus, hyperglycemia causes a diabetic to produce a high volume of glucose-containing urine.
Diabetes Insipidus tambien resulta en perdida de agua por deficiencia de ADH (neurogenico) o falta de respuesta a ADH (nefrogenico)
que causa aumenta de angiotensina II
nivel aumenta en respuesta a volumen sanguíneo baja pression sanguínea baja)
funcion de angiotensina II
actua sobre tubulos aumentando reabsorción de sodio, estrecha (constricts) vasos sanguíneos renales, reduce TFG, enlentece flujo sangineo renal Na+ filtra menos y se reabsorbe mas.
ADH
Sintetizado por celulas en nucleo supraoptico y paraventricular @ hipotálamo –> posterior pituitary gland (neurohipófisis) almacena aquí –> circulación
Forma aquaporina 2
–> aumenta permeabilidad y reabsorcion para agua
en que condiciones se libera ADH?
released by the pituitary in response to sensors that detect an increase in blood osmolality or decrease in blood volume
que son factores que aumentan TFG?
increased glomerular capillary filtration
coefficient
increased blood flow into glomerulus
increased glomerular capillary hydrostatic pressure
increased arterial pressure
increased resistance of efferent arterioles (constriction)
decreased resistance of afferent arterioles (dilation)
Endothelial-derived nitric oxide
Prostaglandins
Manifestaciones de SIADH
dilutional hyponatremia.
no edema + headaches
Urine osmolality is high and serum osmolality is low.
Urine output decreases despite adequate or increased fluid intake.
Hematocrit and the plasma sodium and BUN levels are all decreased because of the expansion of the ECF volume.
causas de polidipsia
deficit de agua, tobaco, antipsicoticos
Sustancias y farmacos que disminuyen los niveles o la accion de la ADH
anfotericina B demeclociclina etanol foscarnet litio antagonistas de la morfina
sustancias y farmacos que aumentan los niveles o la accion de la ADH
antineoplasicos (vincristina y ciclofosfamida) carbamazepina clorpropamida clofibrato anestesicos generales narcoticos (morfina y meperidina) nicotina AINES antipsicoticos fenotiacinicos inhibidores selectivos de la recaptacion de serotonina diureticos tiacidicos (clorotiazida) tiotixeno (antipsicotico) antidepresivos triciclicos
Tx para diabetes insipidus central
acetato de desmopresina, clorpropamida
los dos tipos responden a ii. Diuréticos tiazidicos (hidroclorotiaziada) – aumentan excreción de sodio, disminuyendo la TFG y aumenta reabsorción de agua en Tubulo proximal
Causas de deficit del volumen isotonico
Inadequate Fluid intake (trauma, impaired thirsts)
Excessive GI fluid lossis (diarrea, vomito)
Excessive Renal Losses (terapia diuretica, hiperglicemia, addisons disease)
excessive skin loss (fever, burns)
third space losses (intestinal obstruction, edema, ascitis)
Que es la enfermedad de Addison?
the adrenal glands are underactive, resulting in a deficiency of adrenal hormones
A deficiency of aldosterone in particular causes the body to excrete large amounts of sodium and retain potassium, leading to low levels of sodium and high levels of potassium in the blood. The kidneys are not able to retain sodium easily, so when a person with Addison disease drinks too much water or loses too much sodium, the level of sodium in the blood falls, and the person becomes dehydrated. Severe dehydration and a low sodium level reduce blood volume and can lead to shock
Manifestaciones de deficit de volumen isotonicos
perdida de peso (mas de 8% severo)
Compensatory increase in ADH (decrease urine)
Aumento de osmolalidad (sed, aumento en Ht + BUN)
increased urine osmolality
fiebre
Disminuye volumen vascular (hipotension, tachycardia, shock)
Disminuye volumen EC (sunken eyes and soft eyeballs)
Impaired temperature regulateion (elevated T)
hipotension postural
Causas de excesso del volumen isotonico
inadequate sodium and water elimination (fallo cardiaco, fallo renal, aumento de niveles de corticosteroids, hiperaldoseronism, enfermdedad de cushing, fallo hepatico()
Excessive Na+ ingestion (dieta)
Excessive fluid intake
que son corticoesteroides
are produced in the adrenal cortex of vertebrates as well as the synthetic analogues of these hormones.
Glucocorticoids such as cortisol control carbohydrate, fat and protein metabolism, and are anti-inflammatory by preventing phospholipid release, decreasing eosinophil action and a number of other mechanisms.[1]
Mineralocorticoids such as aldosterone control electrolyte and water levels, mainly by promoting sodium retention in the kidney.
what is BUN?
A common blood test, the blood urea nitrogen (BUN) test reveals important information about how well your kidneys and liver are working. A BUN test measures the amount of urea nitrogen that’s in your blood.
Here’s how your body typically forms and gets rid of urea nitrogen:
Your liver produces ammonia — which contains nitrogen — after it breaks down proteins used by your body’s cells.
The nitrogen combines with other elements, such as carbon, hydrogen and oxygen, to form urea, which is a chemical waste product.
The urea travels from your liver to your kidneys through your bloodstream.
Healthy kidneys filter urea and remove other waste products from your blood.
The filtered waste products leave your body through urine.
A BUN test can reveal whether your urea nitrogen levels are higher than normal, suggesting that your kidneys or liver may not be working properly.
what is Cushings diesase?
Excess cortisol interacts with mineralocorticoid receptors leading to:
Sodium retention causing hypertension (in 70-80%).
Potassium loss: hypokalemic alkalosis in 20% of cases
Manifestaciones de isotonic fluid volume excess?
Aumento de peso
Aumento de volumen intesticial (edema)
Aumento de volumen vascular (venous distenstion, full pulse, dispnea por edema pulmonar)
osmolalidad serica
275-295m
Osm/kg
tipos de hiponatremia
Hipertonica por hiperglucemia
hipovolemic Hipotonica hiponatremia (+)
pueder ser :
hipovolemica (mas Na+ se pierde que agua)
euvolemica (SIADH)
hipervolemica (por trastornos que causan edema –> liberacion de ADH)
Causas de hiponatremia hipotonica
hipovolemia ingestion de soluciones sin sodio perdida GI diureticos enfermedad de addison
causas de euvolemic hiponatremia
aumenta ADH trauma SIADH diurticos deficiency de glucocorticoide hipotiroidismo polidipsia psicogenico ejercicio MDMA
causas de hiponatremia hipervolimico
fallo cardiaco
fallo hepatico
fallo renal
causas de hiponatremia hipertonica (IC–>EC)
hiperflicemia
manifestaciones de hiponatremia
serum sodium 280mOsmo/kg
cramps, weakness, headache depresion, personality changes, lethhargy, coma (agua entra a neuronas)
anorexia, nausea, vomito, diarrea
aumenta IC –> fingerprint edema
causas de hipernatremia
perdida de agua excessiva (diarrea aguada, sweating, increased respirations, diabetes insipidus)
decreased water intake (trauma, impaired thirs)
excessive sodium intake (ocean drowning)
manifestaciones de hipeprnatremia
Na+ > 145
aumento de Ht y BUN
high urine specific gravity
Sed, aumento de ADH –> polidipsia, oliguria, anuria
Deshidratacion IC –> dry skin, decreased tissue turgor, rough tongue, disminucion de salivacion and lacrimacion
Agua sale de neuronas (cefalea, agitation, disminucion de reflejos, convulsiones , coma
Deshidratacion EC,
tacicardia, weakpulse, hipotension, vascular collapse
Peso corporal de postasio en adultos
50mEq/kg (K+)
Potasio ingerido por dia
50-100mEq
40-60 se elimina en heces
cuanto potasio se elimina por rinon
80-90%
factores que alteran distribucion de K+
osmolalidad de suero, trastornos acido-base, insulina, estimulacion beta-adrenergica, ejercicio
que estimula la bomba ATPasa y la entrada de K+ en la celula?
insulina
adrenalina
que provoca hiperpotasemia en excitivilidad
hipolarizacion, potencial de membrana de reposo mas positivo
closer to threshold
prolonged depolarization that can decrease excitability.
more rapid repolarization
que provoca hipopotasemia en excitibilidad
PMR mas negativo = hiperpolarizacion y se aleeje del umbral para que se produzca la excitacion
Thus, it takes a greater stimulus to reach threshold and open the sodium channels that are responsible for the action potential
slower repolarization
que determina el potencial de membrana de reposo
K+ IC: EC
Causas de hipokalemia
inadequate intake (dieta, inconsciencia)
excessive renal loss (terapia diuretica, fallo renal, increased mineralocorticoid levels, hiperaldosteronism, tx con corticosteroid drugs)
excessive GI losses (vomit, diarrea)
transcompartmental shift (beta-adrenergic agonist, insulina, alkalosis)
manifestaciones de hipokalemia
poliuria
orina no concentrada
polidipsia
anorexia, nausea, vomito
constipation,
muscle fatigue, cramps, paresthesias, paralisis
hipotension postural, cambios en ECG, disrithmias
confusion, depresion
alkalosis metabolica
takicardia y disrimias
que puede aumentar perdida renal de K+
thiazide diuretics
metabolic alkalosis
magnesium deplesion (causes renal K+ wasting)
aumento en aldosterona + cortisol
Cortisol binds to aldosterone receptors and exerts aldosterone-like effects on potassium elimination.
Other rare, genetic disorders that can also result in hypokalemia are the Bartter, Gitelman, and Liddle syndromes.
cambios en ECG @ hipokalemia
PR prolongado
ST depression
T flattened
U prominante
U>T
Hypokalemia reduces the permeability of the cell membrane to potassium
tasa de repolarizacion prolongada, perioodo refractorio prolongada
bradicardia
causas de hiperkalemia
excessive ingestion
release from IC (trauma, burns, extreme excercise, siezures)
inadequate elimination (fallo renal, enfermedad de addison, potassium-sparing diuretics, tx with ACE inhibitors or ARBs)
manifestaciones de hiperkalemia
suero > 5mEq
nausea, vomito , cramps, diarrea
paresthesia, weakness, cramps, dizziness
cambios en ECG (more cardiac than neurological)
cambios en ECG @ hipercalemia
peaked T waves
shortened !T
widened QRS
PR interval prolonged
P waves disappear
Que Tx se puede usar para hipekalemia
Calcium antagonizes the potassium-induced decrease in membrane excitability, restoring excitability toward normal. The protective effect of calcium administration is usually short-lived (15 to 30 minutes), and it must be accompanied by other therapies to decrease the ECF potassium concentration
Sodium bicarbonate, b-adrenergic agonists (nebulized albuterol) or insulin distributes K+ into ICF and decreases ECF (IV insulin + glucose)
3 formas de calcio EC
unidos a proteinas (40%)
o ionizados libres (50%)
complejado con citrato, fosfato, sulfato (10%)
funcion de calcio ionizados
excitacion neuromuscular y cardiaco, reacciones enzimaticas, contraccion del musculo, liberacion de hormonas, NTs, mensajeros quimicos, contractilidad cardiaca, coagulacion
regulacion de [calcio ] EC
PTH y renal, alteraciones en albumina + pH
sitio regulatorio de absorcion de calcio
tubulo distal convoluted:
PTH, Vitamina D, thiaziade diuretics, fosfato, glucosa, e insulina regulan aqui
causas de hipocalemia
Perdida de habilidad de movilizar calcio del hueso (hipoparatiroidismo, resistencia a PTH, hipomagnesemia)
Perdida anormal de calcio por riñones (fallo renal + hiperfosfatemia)
decreased intake or absorption (malabsorcion, deficiencia de vitamina D, fallo de activacion de vitamina D por fallo hepatico o renal)
Aumento de unión con proteínas o chelation –> mas proporciones de calcio en forma noionizado (aumento en pH, aumento en AGs, transfusion de sangre citrado)
Sequestracion por tejidos blandos (pancreatitis aguda)
TFG normal
120-130
como el pH afecta calcio
pH acido
disminuye union de calcio con proteína –> aumentando Ca2+ ionizado (plasma calcio total no cambia)
pH alkalino aumenta union con proteina –> tetany
que es tetany?
Tetany is a symptom characterized by muscle cramps, spasms or tremors. These repetitive actions of the muscles happen when your muscle contracts uncontrollably
caused by low levels of calcium in the body
como los AGs afecta Calcio?
AGs aumentan union de calcio con albumina
elevados por estres, heparina, beta-adrenergic drugs (epinefrina, isoproterenol, NE) y alcohol
que provoca el estres?
elevación de AGlibres, epinefrina, glucagón, hormona de crecimiento , y adrenocortocotropic hormone
manifestaciones de hipocalcemia
calcio en suero osteomalacia, bone pain, deformities + fractures
Muscle cramps, pins and needle sensation around the mouth/lips, and unexplained bruising
while abdominal spasms and hyperactive reflexes are more likely consequences of low calcium levels
personality changes
ventricular arrythmias
Hypocalcaemia may be evidenced by personality changes and neuromuscular irritability along with tremors, choreiform movements, and positive Chvostek or Trousseau signs. Cardiovascular manifestations include tachycardia, hipotension, and ventricular dysrhythmias.
como es que la pancreatits aguda provoca hipocalcemia
a. Ca2+ se une con acidos grasos libres liberados por lipolisis en el páncreas –> soaps + removing Ca2+ de la circulación
Chvostek sign
taping face below temple @ nervio VII –> spasm of lip, nose face = +
causas de hipercalcemia
aumenta de absorcion intestinal (excessive Ca en dieta, excessive vitamin D, milk-alkali syndrome)
Aumento de Resorcion Osea (aumento de PTH, neoplasias, immobilizacion prolongada)
falta de eliminacion de calcio (diureticos thiazide, terapia con lithium)
de malignancy (PTH suppresed)
manifestaciones de hipercalcemia
suero > 10.5mg/dL
inabilidad de concentrar orina (poliuria, polidipsia, dolor, fallo renal, calculos renales)
(anorexia, nausea, vomito, constipation)
disminucion en excitibilidad neuromuscular (debilidad musculoar, atrocity, ataxia)
osteopenia, osteoporosis
lethargy, cambios en personalidad, coma
hipertension
QT shortening with atrioventricular block on ECG
Polydipsia, polyuria, anorexia, lethargy, and stupor
what is milk-alkali syndrome?
ingestion excesiva de calcio (leche) _ antacidos absorbables
drogas que causan hipercalcemia?
lithium, thiazide diuretics
distribucion de fosforo en el cuerpo
85% en hueso
14% iC
1% EC
formas de fosforo en el cuerpo
organica (90% de fosforo IC - acidos nucleicos, fosfolipidos, ATP)
inorganica (principal forma circulante - el que se mide en laboratorio)
funciones de fosforo
Formación de hueso
Esencial para procesos metabólicos
Formación de ATP + enzimas usadas en metabolismo de glucosa, grasa, y proteína
Comonente de celulas (acidos nucleico, fosfolípidos, )
Amortiguador @ EC + ecreccion renal de H+
Delivery de Oxigeno por GR depende de fosforo organico en ATP y 23DPG
Función de GBs y plaquetas
sustancias que se unen al fosforo e inhiben su absorcion?
magnesio, calcio, alumino
fosforo se une a proteinas en plasma?
NO ! todo se filtra
causas de hipofosfatemia
disminucion de absorcion intestinal (antacids = calcio y aluminum, diarrea, ausencia de vitamina D)
aumento de eliminacion renal (alkalosis, hiperparatiroidismo, diabetic ketoacidosis, renal tubular absorption defects)
Malnutricion + IC shifts (alcoholismo, total parenteral hiperalimentation, insulina)
manifestaciones de hipofosfatemia
Phosphate is necessary for the normal function of platelets and the excretion of hydrogen ions that contribute to acidosis. Phosphate replacement would be unlikely to resolve ascites and cardiac anomalies,
Neural Manifestations Intention tremor Ataxia Paresthesias Confusion, stupor, coma Seizures
Muscle weakness Joint stiffness Bone pain Osteomalacia Blood Disorders Hemolytic anemia Platelet dysfunction with bleeding disorders Impaired white blood cell function
porque antacidos causan hipofosfatemia?
Antacidos que contienen aluminum hydroxide, alimunim carbonate, and calcium carbonate se unen con fosfato –> perdida en heces
causas de hiperfosfatemia
laxatives and enemas
IC –> EC shift por (trauma, heat stroke, seizures, rhabdomiolisis, deficiencia de K+)
fallo renal, hipoparatiroidismo
manifestaciones de hiperfosfatemia
suero >4.5 en adultos y mas de 5.4 en ninos
dismiucion de calcio en suero (paresthesias, tetania)
hipotension , arrithmias
distribucion de magnesio en el cuerpo
50-60% stored en hueso
39-49% en celulas del cuerpo
15-30% se puede intercambiar con EC
1% EC
20-30% unido a proteína (EC)
[Mg] normal en plasma
1.8-3mg/dL
funciones de Mg
Cofactor en reacciones (generación ATP de ADP, replicación, tramscripcion, tradducion)
Metaboloismo
Bomba ATPasa Estabilización de membrana Conducion de nercvio
Trasnporte ion
Actividad de canales de Ca2+ y K+
Smooth muscle relaxant – anticonvulsante
trata eclampsia en embarazadas
agente neuroprotector para infantes
causas de hipomagnesemia
difunction de absorcion (alcoholismo, malnutricion, malabsorcion, dieta alta en calcio sin magnesio)
perdida de Mg por terapia diuretica, hiperparatiroidismo, hiperaldosteronismo, diabeteic ketoacidosis,
manifestaciones de hipomagnesemia
Serum magnesium level below 1.8 mg/dL (0.75 mmol/L) Personality change Athetoid or choreiform movements Nystagmus Tetany Positive Babinski, Chvostek, Trousseau signs Tachycardia Hypertension Cardiac arrhythmias
causas de hipermagnesemia
ingestion excessiva (para tratamiento de preeclampsia)
fallo renal, glomerulonefriis disminuyen excreccion
manifestaciones de hipermagnesemia
mg en suero > 3mg/dL
lethargia, hiporeflexia, confusion, coma, hipotension, arritmias
que es preeclampsia
Formerly called toxemia, preeclampsia is a condition that pregnant women develop. It is marked by high blood pressure and a high level of protein in the urine. Preeclamptic women will often also have swelling in the feet, legs, and hands.
a result of a placenta that doesn’t function properly
no cure
Mg se usa para tratar
hipercalcemia + eclampsia
causas de obstruction del tracto urinario
@ pelvis renal: calculos renales, necrosis papilar
@ ureter: calculos, embarazo, tumores que comprimen ureter, trastornos congenitos
@ vejiga/uretra : CA, calculos, trastornos congenitas
componentes de calculos renales
sales de calcio, acido urico, magnesimu ammonium phosphate, cystine
inhibidores de calculos renales
Mg+ citrato
4 tipos de calculos renales
calcio (oxalate and phosphate - 75-80%)
mg ammonium phosphate (struvite) (15%)
uric acid (urate-7%)
cystine
factores que causan calculos de calcio
@ ph alta –> calcium phosphate
@ pH baja –> calcium oxalata
hipercalcemia, hipercalcuria, immobilizacion, hiperparatiroidismo, intoxicacion con vitamina D, diffuse bonde disease, milk-alkali syndrome, hiperoxaluria,
oxalate crystals from ethylene glycol, vitamin C abuse, Crohn disease
factores que causan calculos de Mgammoniumphosphate
urea splitting
infeccion por bugs ureasa positivo (proteus, staph, kliebsella) that hydrolisan urea –> ammonia –> urine alkalinization
UTIs
aumento de pH
factores que causan calculos de acido urico
pH 5.5
high purine diet
low urine volume, arid climates, acidic pH
hiperuricemia (gout)
leukemia
factores que causan calculos de cystine
low pH
cistinuria (genetico , trastrono de metabolismo de AAs)
tx de calculos de calcio
trata underlying condition
increase fluid intake
thiazide diuretics + citrate
dieta sin oxalate
tx de calculos de Mg/Am/Fos
tratar UTI (eradicacion de infecion )
acidify orina
increase fluid intake
surgical removal of stone
tx calculos de acido urico
increase fluid intake
allopurinol for hyperuricosuria
alkalinzation of urine
tx calculos de cysteina
increase fluid intake
alkalinzation of urine
que es osteoporosis
debilita los huesos y aumenta la posibilidad de fracturas.
que forma de calcio se debe medir?
ionico
tipos de obstruccion:
Insidious, parcial, complete, unilateral, bilateral
causas de de obstruccion:
Anormalidades congenitales, calculi urinaria (stones), embarazo, hiperplasa prstatica benigna, scar tissue de infección + inflmacion, tumores, trastronos neurológicos,
danos causados por uropatias obstructivas
Stasis of urine (stoppage of flow) –> infeciones y pierdras
Dilatación progressiva de ducto colectores renales y estructuras tubulares destrucion + atrofia del tejido renal
en que pH precipita mas facilmente sales de calcio?
in stagnant alkaline urine
que es hidronefrosis
dilatacion de pelvis renal + calyces por obstruccion de tracto urinario (calculos renales, CA cervical, trauma en ureter, retroperitoneal fibrosis, vesicoureteral reflux)
only impairs renal function if bilateral
causa compression atrophy of renal cortex and medulla
manifestaciones de hidronefrosis
Silent, or pain
complete Bilateral= (below the level of the ureterovesical junction): olguria (less urine ) + anuria
parcial: fallo renal, perdida de habilidad de concentrar orina –> poliuria , nocturia
Hipertensión
focal
solo afectan algunos glomérulos
difuso
compromete todos los glomérulos + todas las partes
segmental
solo comprometen un segmento especifico de cada glomérulo
mesangial
solo afectan cel. Mesangiales
2 mecanismos inmunitarios que provocan trastornos glomerulares
Lesión por anticuerpos que reaccionan contra antígenos glomerulares fijos
Lesión por immunocomplejos atrapados en la membrana glomerular
alteraciones histologicas en glomerulopatias
Proliferativos: aumento en componentes celulares
Escleroticos: aumento en componentes no celulares
Membranosos: aumento en espresor de pared capilar
Glomerulonefritis Proliferativa Aguda
- Proceso inflamatoria producida por reacción inmune que se desencadena cuando los complejos inmunes circulantes quedan atrapados en la membrana capilar glomerular.
- se observa proliferación de las celulas endoteliales que tapizan los capilares glomerulares y de las celulas mesangiles
- La membrana capilar se edematiza y se torna permeable a las proteínas plasmáticas y celulas de la sangre –> proteinuria , hematuria
- Disminuye TFG –> oliguria
- Aumenta retención de Na+ y H2O hipertensión y edema
azotemia
Deposición de IgG, IgM y C3 --> aparencia granular en tincion Inmunocomplejos
en ninos
se resuelve
Glomerulonefritis Rapidamente Progresiva
- Prolif. Focal + segmentaria de cel. Glomerulares + reclutamiento de monocitos y macrófagos estructuras en forma de medialuna que obliteran espacio de Bowman
linear
causada por sindrome de goodpasure
mal pronostico
Sindrome de goodpasture
antricuerpos contra MBG y membrana basal alveolar
Hemorragia pulmonar
anemia ferropenica
glomerulonefritis
Goodpasture syndrome is a form of glomerulonephritis; treatment includes plasmapheresis to remove circulating anti-GBM antibodies and immunosuppressive therapy to inhibit antibody production.
sindrome nefrotico
aumento de permeabilidad glomerular
Proteinuria masiva (>3.5 g/dia)
Hipoalbuminemia
The pathophysiology of the nephrotic syndrome involves damaged glomeruli becoming increasingly permeable to protein, allowing more protein into the glomerular filtrate. Massive proteinuria results, leading to hypoalbuminemia. Generalized edema, which is the hallmark of nephrotic syndrome, results from the loss of colloidal osmotic pressure of the blood with subsequent accumulation of fluid in the interstitial tissues.
Glomerulonefritis membranoso
causa mas frecuente de sinfrome nefrotico in whites
Engrosamiento difuso de MBG y capilares por immunocomplejos
granular
Causas:- Idiopático o asociado con anti-fosfolipasa A2 receptor, drogas (AINES) infecciones, SLE, tumores, alteraciones metabolicas
50% –> fallo renal
Enfermedad con cambios minimos (nefrosis lipoidea)
- Perdida difusa/fusion de los podocitos
Niños
Causa desconocido (infecion, immunizacion, linfoma de hodkin)
Respuesta excelente a tratmiento con corticoesteroides
Glomerulosclerosis segmentaria y focal
- Esclerosis segmental y hyalinosis
Hipertensión
perdida de funcion renal
causa mas comun de sind. nerfrotico en hispanos y afroamericanos
causas: - Idiopático , ↓ O2 en sangre, VIH, abuso de drogas IV, secundario, obesidad, tx IFN
Enf. de Berger
causa sind. nefritico
Deposito de IgA en mesangio –> proliferación mesangial –> inflamación
infecion respiratorio + gastroenteritis o asintomatico
hematuria (2-6 dias)
no tx
Immunoglobulin A (IgA) nephropathy (Buerger disease) is a primary glomerulonephritis characterized by the presence of glomerular IgA immune complex deposits. It can occur at any age, but most commonly occurs with clinical onset in the second and third decades of life. It is more common in males than in females and is the most common cause of glomerular nephritis in Asians. There is no satisfactory treatment for IgA nephropathy.
Henoch –Schonlein purpura
ninos vasculitis de vasos pequentos erupcion palpable artralgias dolor abdominal,
asociado con IgA nefropatia
sindrome nefrotico, nefritico o combinado
recuperacion
Sind. de Alport
Defecto hereditario de MBG por mutacion en tipo IV colágeno –>thinning and splitting of glomerular basement membrane –> fallo renal
defectos en ojos oidos
hematuria
proteinuria
glomerulonefritis
Heavy microscopic hematuria, proteinuria, and sensorineural deafness and eye disorders are characteristic of Alport syndrome. This symptomatology is less characteristic of systemic lupus erythematosus glomerulonephritis, Henoch-Schönlein purpura nephritis, or immunoglobulin A nephropathy.
lesiones glomerulares de SLE
Tipo I: normal Tipo II: proliferación mesangial Tipo III: proliferación focal y segmental Tipo IV: proliferación difusa Tipo V: proliferación membranosa
Diabetic glomerulosclerosis
thicenking of glomerular capillary basement membrane + diffuse increase in mesangial matrix ; this impinges on capillary lumen reducing glomerular filtration
Kimmelstiel-Wilson syndrome
- Nodular glomerulosclerosis
nodular deposition of hyaline in mesangial portion of glomerulus –> obliteration
in nodular glomerulosclerosis, also known as Kimmelstiel-Wilson syndrome, there is nodular deposition of hyaline in the mesangial portion of the glomerulus. As the sclerotic process progresses in the diffuse and nodular forms of glomerulosclerosis in many cases, early changes in glomerular function can be reversed by careful control of blood glucose levels. Control of high blood pressure and smoking cessation are recommended as primary and secondary prevention strategies in persons with diabetes
microalbuminuria
urinary albumin excretion of 30 to 300 mg in 24 hours (predicts future diabetic nephropathies)
que provoca hipertension en glomerulos
sclerotic changes in renal arterioles and small arteries, referred to as benign nephrosclerosis –> bilateral, kidneys smaller, narrowed arterioles, thicken and scarring, –> less blood flow to nephron –>patchy tubular atrophy, interstitial fibrosis
2 tipos de trastornos tubulointerstitial
AGUDA –> edema intersticial
CRONICA –> fibrosis intersticial, atrofia, infiltrado mononuclear; primeros asintomaticos
causan imbalancia de fluido + electrolitos
ACIDOSIS RENAL TUBULAR
defectos tubulares en reabsorción de HCO3- o excreccion de H+ –> acidosis metabolica
Tipos de renal tubular acidosis
I (distal, ph >5.5) = defecto en secrecion de H+ –> no new HCO3- generated
asociado con hipokalemia
II (proximal pH se elimina en orina
asociado con hipokalemia –> aumenta riesgo de hipofosfatemic rickets
IV ( hiperkalemic pH 5.5) - dificiencia de aldosterona o resistencia , hiperkalemia, no se elimina H+
sindrome de fanconi
(wilsons disease)
asociado con proximal renal tubular acidosis
defecto en reabsorcion de glucosa, AAs, fosfato, y acido urico –> retraso de crecimiento, rickets, osteomalacia, metabolismo anormal de vitamina D + acidosis
Tipos de Pyelonefritis
infección de parénquima de rinon + pelvis renal
Aguda y cronica
pielonefritis aguda
affects cortex
UTI superior, catherter, cesicouretral reflux, embarazo
white cell casts
disuria, fever, costovertebral tenderness, nausea, vomiting
can cause renal papillary necrosis in px with diabetes or px with obstructtion
tx: antibioticos
Manifestations of acute pyelonephritis include pain, frequency, urgency, dysuria, nausea, and vomiting. s.
pielonefritis cronica
from reccurent pielonefritis aguda
scarring + deformation of calyxes renales
Chronic rather than acute pyelonephritis is often caused by hypertension, while most cases are caused by ascending bacteria, not systemic infections. Scarring is more commonly a result of chronic pyelonephritis
Nefropatieas relacionadas a drogas
acute interstitial renal inflamation
piuria (eosinofilia) , azotemia, fiebre, rash, hematuria, costovertebral angle tenderness, or asintomatico
1-2 semanas after
drogas: diureticos, penicilin derivatives, sulfonamides, rifampin, AINes)
50% fallo renal
locacion de rinones
- Fuera del peritoneal cavity @ back of upper abdomen
T12 a L3
a donde se encuentran los glomerulos
en corteza exterior
porque niveles de HCO3- sanguineo cambian mas facilemente que niveles de HCO3- en LCR?
porque HCO3- has lag entry across blood-brain barrier
que mecanismo de regulacion de pH es mas rapido?
respiratorio
3 maneras de control renal
- Excreccion de H+ de acidos metabolisados
- Reabsorpcion de HCO3- filtrado
- Produccion de HCO3- liberada en sangre
Bicarbonato se filtra @ glomerulo?
SI, 4300mEq/dia
y se reabsorbe
cual es lipid soluble, ammonia o ammonium?
ammonia NH3 = lipid solube and can diffuse across collecting duct cells
Once in the tubular fluid, NH3 combines with secreted H+ to form NH4+. NH4+ is not lipid soluble, and thus is trapped in the tubular fluid and excreted in urine.
normalmente Cl- se absorbe con ?
Na+
trastornos tubulointersticiales se clasifican en
aguda –> edema interstical
y cronica –> fibrosis intersticial, atrofia, infiltrado mononuclear
primeroos manifestaciones de trastornos tubulointersticiales
imbalancia de fluido y electrolitos
pH EC
7.35-7.45
que es acido carbonico y su funcion principal?
H2CO3 (hecho de CO2 + HCO3-)
contribuye a pH sanguineo
dos tipos de acidos
volatile (en equilibrio) H2CO3 eliminado por polmon
Nonvolatile (fijados) (sulfuric, HCl,, eliminados por rinon)
cuanto CO2 se produce por dia
15,000mmol
que es un amortiguador
un base leve con su acido conjugado o vice versa
trades a strong acid for weak or strong base for weak
3 formas que se transporta CO2 en circulacion
como gas en plasma (10%) –>pulmon
como bicarbonato en GRs cuando hay exceso de CO2; en GRs (70%)
(anhidrasa carbonica convierte H2CO3 en H+ + HCO3-(goes into plasma); H+ + Hb
20% carbaminohemoglobina – CO2 en GRs que queda + Hb para formar HbCO2
pH se regula por 3 mecanismos
amortiguadores químicas
(bicarbonato , proteínas, H+/K+ transcellular )
pulmones que eliminan Co2
riñones que eliminan H+ y reabsorbe/genera HCO3-
sistema de regular pH mas poderoso
HCO3-
sistema de regular pH mas grande
proteinas
como es el hueso un amortiguador?
40%
H+ se cambia por Na+ y K+ @ superficie de hueso –> liberación de CaCO3 + NaHCO3 al espacio EC puede amortiguar acidos
Provoca demineralizacion del hueso y predispone a formación de cálculos renales por aumento en excreción urinario de calcio.
aumento de ventilacion provoca
disminucion de PCO2
cuando H+ aumenta ventilacion…
aumenta
cual es mas rapido control renal or respiratorio?
respiratorio
cual crusa mas facilmente la barrera heamto-encefalica CO2 o HCO3-
CO2
3 funciones de control renal
Excreccion de H+ de acidos metabolisados
- Reabsorpcion de HCO3- filtrado
- Produccion de HCO3- liberada en sangre
Describe el intercambio de H+ y HCO3- @ TP
85%-90% de secreción de H+ y reabsorción de HCO3- occure aqui
H+ secretado se combina con HCO3- filtrado –> H2CO3 –> CO2 + H2O (catalizado por anhidrasa carbonica) –>crusan membrana luminal y entran celula tubular –> adentro de la celula las reacciones occuren en reversa –> CO2 + H2O (catalizado por anhidrasa carbonica) –> H2CO3 –> HCO3- + H+.
HCO3- se reabsorbe en sangre con Na+ y H+ secretado , comienza de nuevo
pH minimo en filtrado
4.5 (en este pH secreccion de H+ stops)
2 amortiguadores intratubulares que forman HCO3-
fosfato
ammonia
Describe intercambio de H+/K+ @ tubulo distal
transporte activo reabsorbe K+ y secreta H+ (@ hipokalemia)
plasma K+ –> eliminacion de H+ y vice versa
como influye H+ la aldosterona?
Normally, Cl− is absorbed along with Na+ throughout the tubules. In
@ tubulo colector influye secreccion de H+ indirectamente por secreccion de K+ y reabsorcion de Na+
Sodium absorption generates a more lumen-negative potential that drives both potassium secretion by principal cells as well as proton secretion by type A intercalated cells.
entonces hiperaldosteronismo –> alkalosis metabolica
cuando se utiliza el intercambio de Cl-/HCO3-
cuando hay deplecion de volumen , rinones substituyen HCO3- por Cl- aumentando absorcion de HCO3-
alkalosis hipocloremico
por disminucion en Cl- hay un aumento excesso en reabsorcion de HCO3-
acidosis hipercloremico
aumento de Cl- disminuye HCO3- y pH
PCO2 normal
35-45mmHg
HCO3- normal
venous normal = 24-31mEq/L
arterial = 22-2mEq/
2 tipos de trastorno acido-base
metabolico (altera HCO3-) y respiratorio (altera PCO2)
acidosis respiratorio
diminuye pH, ventilación y aumento de PCO2 (>45mmHg)
compensacion renal: mas H+ excrecion y mas reabsorcion de HCO3- (acute = 0.1, chronic 0.3)
accompanied by renal adaptation with a more marked increase in plasma HCO3– and a lesser decrease in pH. Her pH is likely below 7.35, and the likely renal response involves the reabsorption of HCO3– and secretion of H+. Excess
alkalosis respiratorio
aumenta pH, por aumento de ventilación y disminución en PCO2 (
Bajo condiciones de disminución de la perfusión o el aumento de la estimulación del sistema nervioso simpático, el flujo sanguíneo
se redistribuye lejos de la corteza hacia la médula. Esta redistribución del flujo sanguíneo disminuye la filtración glomerular mientras se mantiene la capacidad de concentración de la orina de los riñones, un factor que es importante durante las condiciones tales como choque
BP normal
(120/80)
BP es 88/53 = hipotension
Frecuencia cardiaca normal
60 to 100 beats a minute
frecuencia respiratorio normal
12 to 20 breaths
characteristicas de celulas mesangiales
Mesangial cells possess phagocytic properties and remove macromolecular materials that enter the intercapillary spaces. Mesangial cells also exhibit contractile properties in response to neurohumoral substances and are thought to contribute to the regulation of blood flow through the glomerulus. Mesangial hyperplasia and increased mesangial matrix occur in a number of glomerular diseases
que tipo de medicamentos pasan por el TP?
The proximal tubule secretes exogenous organic compounds such as penicillin, aspirin, and morphine. Many of these compounds can be bound to plasma proteins and are not freely filtered in the glomerulus. Therefore, excretion by filtration alone eliminates only a small portion of these potentially toxic substances from the body.
@hipotension que causa vasoconstriccion?
El aumento de la actividad simpática causa la constricción de la arteriolas aferentes y eferentes y por lo tanto una marcada disminución en el flujo sanguíneo renal. La estimulación simpática intenso puede producir disminuciones en el flujo sanguíneo renal y la TFG marcada. Sustancias humorales, incluyendo la angiotensina II, ADH, y endotelinas, producen vasoconstricción del flujo sanguíneo renal.
que tipo de medicamento puede inducir hipokalemia?
A common side effect of thiazide diuretics is increased potassium losses in the urine, which may necessitate potassium supplementation. Aldosterone antagonists, loop diuretics, and osmotic diuretics are less likely to induce hypokalemia.
Thiazide diuretics increase the loss of potassium in urine. Because calcium is actively reabsorbed in the distal convoluted tubule, it is likely that her calcium level will go up, especially if she takes it for a long time.
24h urine test vs. single
Twenty-four–hour urine tests are often used to quantify the amount of substances, such as proteins, that an individual’s kidneys are spilling. Single urine samples are able to assess more parameters than just the presence of bacteria, and they are sufficient in quantity to detect numerous substances such as glucose.
algunas observaciones en un rinon que no funciona bien?
Increased creatinine and BUN are associated with abnormalities in renal function, as is the presence of glucose in a urine sample
acidosis metabolica
disminucion de pH y HCO- (
alkalosis metabolico
aumento de pH y HCO3- (>26mEq/l)
compensacion respiratorio: disminucion de ventilacion
aumento de PCO2 (0.7)
compensacion renal:
disminucion de excreccion de H+ y reabsorcion de HCO3-
causas de acidosis metabolico
excess metabolic acids (increased anion gap)
(excessive production of metabolic acids, lactic acidosis from strenuous excercise, diabetic ketoacidosis, alcoholic ketoacidosis, starvation, poisoning)(impaired elimination of metabolic acids por fallo renal)
excessive HCO3- loss (normal anion gap)
(loss of intestinal secretions, diarrea, renal losses por renal tubular acidosis, carbonic anhydrase inhibitors, hypoaldosteronism)
Increased chloride levels (normal anion gap)
(excessive reabsorption of Cl- by kidney,
heavy alcohol use and renal failure are associated with acidosis.
Manifestaciones de acidosis metabolico
disminuye pH
HCO3- (primario) disminuye
PCO2 (compensatorio) disminuye
anorexia, nausea, dolor abdominal, vomito
lethargy, confusion, coma, depresion of vital functions
decreaesed heart rate, arrythmias
decreaseled alertness
warm flushed skin
bone disease
COMPENSACION: Kussmaul breathing (increased rate and depth of respiration)
hiperkalemia, orina acido, increased ammonia in urine
renal tubular acidosis vs chronic kiney disease
in RTA only tubular function is compromised vs. both tubular and glomerular funciont
causas de alkalosis metabolico
excessive gain of HCO3- or alkali (acetate, lactate, citrate)
Excessive loss of H+ (vomiting, K+ deficit, hiperaldosteronismo, milk-alkali syndrome)
Increased HCO3- Retention
(loss of Cl-)
Volume contraction (diuretics)
Ingestion of bicarbonate, gastric suction, and vomiting are causes of metabolic alkalosis.
manifestaciones de alkalosis metabolico
pH increased
HCO3- (primary) increased
PCO2 (compensatory) increased
confusion, hyperactive reflexes, tetany, convulsions
hipotension, arrithymias
respitory acidosis (decreased rate)
increased urine pH
Causas de acidosis respiratorio
depression of respiratory center (drug overdose, trauma)
Lung disease (asma, emfisema, edema,etc)
Obstrucion (paralisis de musculus respiratorios, trauma, obesidad, paralisis, kyphoscoliosis)
breathing aire with high CO2 content
manifestaciones de acidosis respiratorio
pH decreased
PCO2 (primary) increased
HCO3- (compensatory) increased
dilation of cerebral cessels, depresion, headache, behavior changes, tremors, paralysis, coma
skin warm and flushed
Carbon dioxide readily crosses the blood–brain barrier, exerting its effects by changing the pH of brain fluids. Elevated levels of CO2 produce vasodilation of cerebral blood vessels, causing headache, blurred vision, irritability, muscle twitching, and psychological disturbances
acid urine
accompanied by renal adaptation with a more marked increase in plasma HCO3– and a lesser decrease in pH. Her pH is likely below 7.35, and the likely renal response involves the reabsorption of HCO3– and secretion of H+. Excess
diferencia en acidosis respiratorio aguad vs. cronica?
Aguda: rapid rise in PCO2 arterial >45mmHg, with minimal increase in plasma HCO3-, and large decrease in pH
causas de alkalosis respiratorio
ventialcion excessiva (anxiety, hypoxia or lung disease with reflex ventilation, stimulation of respiratory center, elevated blood ammonia, salicylate toxicity, enceefalitis, fiebre, mechanical ventialtion)
manifestaciones de alkalosis respiratorio
pH increased
PCO2 (primario) decreased
HCO3- (compensatory) decreased
constriction of cerebral vessels and increased neuronal excitiability, dizziness, panic, tetany, numbness and tingling of fingers and toes, +++ Chvostek and Trousseau signs
Seizures
arritmias
Renal compensation for respiratory alkalosis involves decreased bicarbonate reabsorption
soluciones hipertonico
3%-5% sodium chloride
10% dextrose in water
soluciones isotonicos
0.9% NaCl
5% dextrose
solucion hipotonico
0.45% NaCl o 0.33% NaCl
que provoca ascitis
Ascites is characterized by an accumulation of fluid in the transcellular component of the ECF, not ICF.(Third-spacing) The fluid is not categorized as belonging to the plasma component of the ECF.
Como se puede formar edema
Right-sided heart failure, burns, and low levels of plasma proteins are all associated with the development of edema.
droga para tratar tratar diabetes insipidus
Desmopressin acetate (DDAVP)
manifestaciones de diabetes insipidus
Elevated blood glucose levels, dry mucous membranes, and severe projectile vomiting
se utuliza tx IV para hiperkalemia
NO
Regular insulin infusion, rate dependent on lab values
Feedback:The administration of sodium bicarbonate, -adrenergic agonists, or insulin distributes potassium into the ICF compartment and rapidly decreases the ECF concentration
Sequencia de Vitamin D
esta presente @ piel o intestino
se concentra @ higado
se transporta a kidney
se produce calcitriol
absorcion de calcio del intestino aumenta
tratamiento de hipercalcemia
The bisphosphonates (e.g.,pamidronate, zoledronate), which act mainly by inhibiting osteoclastic activity, provide a significant reduction in calcium levels with relatively few side effects. Calcitonin also inhibits osteoclastic activity. Gallium nitrate is highly effective in the treatment of severe hypercalcemia associated with malignancy. Prednisone, a corticosteroid, inhibits bone resorption.
Mg deficiency occurs in conjunction with
low calcium levels
H+/Na+ intercambio regula acido-base?
NO
relation between anion gap and acidosis?
Increased CO2 levels, an increased anion gap, and a base deficit are all associated with an acidotic state. Base excess, low oxygen, high potassium, high ammonia, and decreased anion gap would not suggest acidosis
D-lactic acidosis
Feedback:A unique form of lactic acidosis, called D-lactic acidosis, can occur in persons with intestinal disorders that involve the generation and absorption of D-lactic acid. D-lactic acidosis can occur in persons with jejunoileal bypass, in which there is impaired reabsorption of carbohydrate in the small intestine. Persons with D-lactic acidosis experience episodic periods of metabolic acidosis often brought on by eating a meal high in carbohydrates. Manifestations include confusion, cerebellar ataxia, slurred speech, and loss of memory. They may complain of feeling (or may appear) intoxicated.
ethelyn glycol
y OD tx
Ethylene glycol is found in products ranging from antifreeze and deicing solutions to carpet and fabric cleaners. It tastes sweet and is intoxicating—the factors that contribute to its abuse potential. A lethal dose is approximately 100 mL. It is rapidly absorbed from the intestine, making treatment with either gastric lavage or syrup of ipecac ineffective. Fomepizole, with specific indications for ethylene glycol poisoning, was recently approved by the U.S. Food and Drug Administration
aspirin OD provoca
The salicylates cross the blood–brain barrier and directly stimulate the respiratory center, causing hyperventilation and respiratory alkalosis. The blood pressure is at normal range, and the urine output is normal or excessive depending on fluid intake. Bilateral crackles (fluid) in the lungs `are usually a sign of heart failure.
lactic acidosis es que tipo de acidosis
metabolico
tx de alkalosis metabolica
IV KCl solucion
tx de acidosis respiratorio
ventilacion mecanico
como se puede utilizar alkalosis respiratorio como tratamietno?
Respiratory alkalosis is seen as a treatment with the ventilator with intubated people experiencing high intracranial pressure (ICP) in order to attempt to lower the ICP.
trastornos renales en infantes
Renal hypoplasia, cystic dysplasia, and horseshoe kidney are more common diagnoses in infants. Renal cell carcinoma is not a congenital condition or one that often manifests in infancy.
que cicrunstancias predisponen a obstructiones urinarios
Pregnancy, BPH, renal calculi, and neurogenic bladder are all identified contributors to urinary obstructions.
que cambios en electrolitos provoca la malnutricion
hipofosfatemia
hipomagnesemia
BPH causa
dolor y hidroureter, distention of distal ureter
que tipo de dolor es provocado por los colicos
Excruciating pain in the flank and upper outer quadrant of the abdomen that radiates to the bladder area
Classic ureteral colic is manifested by acute, intermittent, and excruciating pain in the flank and upper outer quadrant of the abdomen on the affected side. The pain may radiate to the lower abdominal quadrant, bladder area, perineum, or scrotum in the man
que tipo de dieta se debe modificar en px con calculos de calcio-oxlato
Individuals with calcium oxalate stones often need to avoid high-oxalate foods like nuts, cocoa, and chocolate. Extracorporeal shock-wave lithotripsy treatment may be used to fragment larger renal calculi. It would not be necessary to avoid calcium intake, and fluid intake should encouraged, not curbed. Medications can reduce the potential for stone formation but are not a common treatment modality
sindrome de nefritico
In its most dramatic form, the acute nephritic syndrome is characterized by sudden onset of hematuria, variable degrees of proteinuria, diminished GFR, oliguria, and signs of impaired renal function. Inflammatory processes damage the capillary wall. This damage to the capillary wall allows RBCs to escape into the urine and produce a decrease in GFR. Extracellular fluid accumulation, hypertension, and edema develop because of the decreased GFR.
most common cause of primary nephrosis in adults
membranous glomerulonephritis is the most common cause of primary nephrosis in adults, most commonly those in their sixth or seventh decade. It is treated with corticosteroids.
cationes que medimos
Na+=136
aniones que medimos
Cl- = 100 HCO3= 24
124
Na+ - (Cl- + HCO3-) =
12
por cada 1mEq/l HCO3 - perdido comensa con
disminucion de 1.2 mmHg pCO2
por cada 1mEq/l HCO3- ganado
aumento de 0.7mmHgpCO2
por cada 10 mmHg pCO2 ganado
aguda: aumenta 1 mEq/l HCO3-
Cronica: aumenta 3.5 mEq/l HCO3-
por cada 10 mmHg pCO2 perdido
aguda: disminuye 2 mEq/l HCO3-
cronica: disminuye 5 mEq/l HCO3-
MUDPILES
metanol, uremia, diabetic, pildoras, iron, lactic acidosis, etilen glicol, salicilatos
anion gap
pCO2 normal
40***
pCO2 = 1.5(HCO3) + 8 (+/-2)
if close together = acidosis metabolica + alcalosis resp. compensatorio (pCO2 = 16, HCO3=5, pH=7.11)
a que cambios responde la renina
renina responde a cambios en presion arterial, TFG, y # de Na+ en filtrado
Decreased Anion Gap for differential dx of metabolioc acidosis
(
Increased Anion Gap @ ddx of metabolic acidosis
(>16mEq/L)
Presence of unmeasured metabolic anion Diabetic ketoacidosis Alcoholic ketoacidosis Lactic acidosis Starvation Renal insufficiency Presence of drug or chemical anion Salicylate poisoning Methanol poisoning Ethylene glycol poisoning
Normal anion gap @ ddx of metabolic acidosis
Loss of bicarbonate Diarrhea Pancreatic fluid loss Ileostomy (unadapted) Chloride retention Renal tubular acidosis Ileal loop bladder Parenteral nutrition (arginine, histidine, and lysine)
causas de edema
Increased Capillary Pressure Increased vascular volume Heart failure Kidney disease Premenstrual sodium retention Pregnancy Environmental heat stress Thiazolidinedione (e.g., pioglitazone, rosiglitazone) therapy Venous obstruction Liver disease with portal vein obstruction Acute pulmonary edema Venous thrombosis (thrombophlebitis) Decreased arteriolar resistance Calcium channel–blocking drug responses Decreased Colloidal Osmotic Pressure Increased loss of plasma proteins Protein-losing kidney diseases Extensive burns Decreased production of plasma proteins Liver disease Starvation, malnutrition Increased Capillary Permeability Inflammation Allergic reactions (e.g., hives) Malignancy (e.g., ascites, pleural effusion) Tissue injury and burns Obstruction of Lymphatic Flow Malignant obstruction of lymphatic structures Surgical removal of lymph nodes
Effects of changes in plasma K+ on resting membrane e potential, activation, and opening of Na+ channels at threshold and rate of repolarization during nerve action potential
Normal: starts at rest goes up and down a lil below resting and back to resting
Hyperkalemia: closer to threshold potential, farther up from resting membrane potential, doesn’t go all the way back down to it
Hypokalemia: starts below resting goes up down way below resting and back up way below as well
Normally, potassium leaves the cell during the repolarization phase of the action potential, returning the membrane potential to its normal resting value. Hypokalemia produces a decrease in potassium efflux that prolongs the rate of repolarization and lengthens the refractory period. The U wave normally may be present on the ECG but should be of lower amplitude than the T wave. With hypokalemia, the amplitude of the T wave decreases as the U-wave amplitude increases.
Distribution of Ca+ between bone and ICF and ECF
Bone 99%,
1% ICF,
0.1—0.2% ECF
(ECF divides into 50% free, 10% complexed, 40% protein bound)
immunodeficiency virus (HIV) infection is an established cause of …..
name illness + 5 cardinal features
immunodeficiency virus (HIV) infection is an established cause of SIADH (e.g., related to associated infections, tumors, drugs).
Its 5 cardinal features
Hypotonic hyponatremia
Natriuresis (excretion of sodium in the urine)
High urine osmolality and low plasma osmolality
Absence of edema and volume depletion
Normal renal, adrenal, and thyroid function
Relationship between cancer and hypercalcemia
hypercalcemia is a common complication of malignancy.
Some tumors destroy the bone, but others produce humoral agents that stimulate osteoclastic activity, increase bone resorption, or inhibit bone formation.
80% of patients with hypercalcemia of malignancy produce PTH-related protein (PTH-rP). PTH and PTH-rP have marked homology, or structural similarity, at their amino terminal ends, with 8 of the first 13 amino acids in the same positions. This homology results in both PTH and PTH-rP binding to the same receptor (PTH/PTH-rP receptor). PTH-rP is produced by several tumors, including cancers of the lung, breast, kidney, head and neck, and ovary.
Your answer should include that the following additional tests may also be completed:
Tests for renal function: BUN, creatinine, urine specific gravity
Tests of bone density in regard to osteoporosis
Tests for cardiac involvement: ECG, blood pressure
Tests for hydration levels: electrolytes
Tests for serum PTH levels to rule out hyperparathyroidism
On a mixed diet, pH is threatened by
On a mixed diet, pH is threatened by the production of strong acids (sulphuric, hydrochloric, and phosphoric) mainly as the result of protein metabolism. These strong acids are buffered in the body by chemical buffer bases, such as extracellular fluid (ECF) bicarbonate (HCO3−).
When the ratio of bicarbonate (HCO3−) to carbonic acid (H2CO3, arterial CO2 × 0.03) = 20:1, the pH =
7.4
pH = 6.1 + log10 (ratio HCO3–: H2CO3)
Metabolic acidosis with a HCO3−:H3CO3 ratio of 10:1 and a pH of 7.1.
Respiratory compensation lowers the H3CO3 to 0.6 mEq/L and returns the HCO3−:H3CO3 ratio to 20:1 and the pH to 7.4.
Respiratory alkalosis with a HCO3−:H3CO3 ratio of 40:1 and a pH of 7.7.
Renal compensation eliminates HCO3−, reducing serum levels to 12 mEq/L, returning the HCO3−:H3CO3 ratio to 20:1 and the pH to 7.4. Normally, these compensatory mechanisms are capable of buffering large changes in pH but do not return the pH completely to normal
Henderson-Hasselbalch equation
This equation is utilized for explaining the calculation of pH. It should be noted that it is the ratio rather than the absolute values for bicarbonate and dissolved CO2 that determines the pH. For example, when the ratio is 20:1 (bicarbonate to carbon dioxide), the serum pH equals 7.4. Plasma pH decreases when the ratio is less than 20:1, and it increases when the ratio is greater than 20:1. In this stated scenario, the pH is 7.1 and the reported serum bicarbonate is 12 mEq/L. Utilizing Figure 40.2, the ratio is 10:1, and the decreased pH is documented. Calculating for PCO2, the value would be 40.
Hydrogen ion (H+) secretion and bicarbonate ion (HCO3−) reabsorption in a renal tubular cell
Carbon dioxide (CO2) diffuses from the blood or urine filtrate into the tubular cell, where it combines with water in a carbonic anhydrase (CA)–catalyzed reaction that yields carbonic acid (H2CO3). The H2CO3 dissociates to form H+ and HCO3−. The H+ is secreted into the tubular fluid in exchange for Na+. The Na+ and HCO3− enter the ECF. (ATP, adenosine triphosphate.)
The renal phosphate buffer system
The monohydrogen phosphate ion (HPO42–) enters the renal tubular fluid in the glomerulus. An H+ combines with the HPO42– to form H2PO4− and is then excreted into the urine in combination with Na+.
Acidification along the nephron.
The pH of tubular urine decreases along the proximal convoluted tubule, rises along the descending limb of the Henle loop, falls along the ascending limb, and reaches its lowest values in the collecting ducts. Ammonia (NH3 + NH4) is chiefly produced in proximal tubule cells and is secreted into the tubular urine. NH4 is reabsorbed in the thick ascending limb and accumulates in the kidney medulla. NH3 diffuses into acidic collecting duct urine, where it is trapped as NH4.
H+ and NH3+ secreted @ PT
@ ascending thick: na reabsorbed,NH4+ reabsorbed H+ secreted (NH4+, Na, 2Cl- cotransport) H+ secreted
@ collecting duct: H+ secreted, NH3 as well NH4+ excreted
anion gap
Normal anion gap = 12
Acidosis anion gap = 25 ( low bicarbonate – like 14) = excess organic acids
Acidosis anion gap: 12, high chloride leves, low bicarbonate
The anion gap in acidosis due to excess metabolic acids and excess plasma chloride levels. Unmeasured anions such as phosphates, sulfates, and organic acids increase the anion gap because they replace bicarbonate. This assumes there is no change in sodium content.
vomiting
K+ depletion from vomiting –>HCO3- reabsorption @ intercalated cells only??!/ –>alkalosis metabolica
EC fluid depletion DECREASES GFR : increases renin release , aldosterone increases HCO3- reabsorption, (electrical gradient) –> alkalosis
also DGFR decreases HCO3- filtration –> alkalosis
Vomit –>Cl depleted absorbs HCO3- reabsorbed –> alkalosis
as acidosis progresses, the skin vessels become
as acidosis progresses, the skin vessels become less responsive to sympathetic stimulation and lose tone. Acidosis depresses neuronal excitability and decreases binding of calcium to plasma proteins so that more free calcium is available to decrease neural activity. This results in a decreased level of consciousness, stupor, and ultimately, coma.
Anti-GBM Glomerulonephritis
Circulating anti-GBM antibodies with linear GBM staining for IgG
with lung hemorrage –> good pasutre
without lung hemorrage –> anti-GBM glomerulonefritis
Immune Complex Glomerulonephritis
Glomerular immune complex localization with granular capillary wall and/or mesangial staining
IgA dom and no vasculitis –> IgA nefropathy
IgA dom + systemic vasculitis –> henoch-schonlein purpura
SLE –> leupus nefritis
Acutre strep –> acute glomerulonefritis
thick capillary walls and endocapullary hypercelularity (acute post strep glomerulonefritis)
subepithelial dense deposits –> membranous glomerulopathy
other
ANCA Glomerulonephritis
Circulating ANCA with paucity of glomerular immunoglobulin staining
without lung hemorrage —-> ANCA glomerulonephritis
vascultis with no asma or granulomas –> microcopic polyangitis
granulomas no asma –> wegener granulomatosis
eosinophilia, asma, granulomas
–> churg strauss syndrome
