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FISIO II > Fisiopato Parcial 1 > Flashcards

Fisiopato Parcial 1 Flashcards

1
Q

Sodio IC vs. EC

A

EC: 135-145
IC: 10-14

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2
Q

K+ IC , EC

A

EC: 3.5-5
IC: 140-150

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3
Q

Cl- IC, EC

A

EC: 98-106
IC: 140-150

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4
Q

Bicarbonato IC, EC

A

EC: 24-31
IC:7-10

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5
Q

Calcio IC, EC

A

EC: 8.5-10.5
IC:

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6
Q

Fosforo IC, EC

A

EC: 2.5-4.5
IC: variable

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7
Q

Mg IC, EC

A

EC: 1.8-3.0
IC: 40mEq/kg (20mmol)

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8
Q

Bomba Na+/K+-ATPasa

A

3 Na+ afuera

2 K+ adentro

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9
Q

plasma glucosa

A

entre 180-380mg/dL

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10
Q

Cuando niveles de glucosa son mas de 380mg/dL

A

glucosuria

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11
Q

Plasma Creatinina

A

0!!!!

No hay reabsorción, no debe haber en sangre pero si en orina

*Niveles de creatinina en suero se utilizan para estimar TFG

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12
Q

Gasto urinario obligado

A

300-500ml/dia

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13
Q

sodio of body weight

A

60

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14
Q

Sistema de Renina-Angiotensina

A

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

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15
Q

aldosterona

A

una hormona secretada por la corteza adrenal

actua @ nivel de tubulo collector cortical para aumentar reabsorcion de Na+ y eliminacion de K+

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16
Q

diureticos que bloquean acciones de aldosterona (K+ sparing)

A

spironolactone
amiloride
triamterene

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17
Q

diureticos que suprimen liberation de renina

A

beta-adrenergic blocking drugs

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18
Q

diureticos que inhiben conversion de angiotensina I –> II

A

inhibidores ACE

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19
Q

drogas que blouean acion de angiotensina II en su receptor

A

ARBs

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20
Q

En tx que tiene prioridad , volumen o electrolitos?

A

VOLUMEN

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21
Q

que provoca deshidratacion celular

A

aumento de osmolalidad EC

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22
Q

que sucede @ volumen sanguineo baja + presion sanguinea bajja

A

aumenta angiotensina II

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23
Q

que provoca la sensacion de sed?

A

deshidratacion celular por aumento de osmolalidad EC

disminucion de volumen de sangre

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24
Q

Hipodipsia

A

falta de sed

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25
Q

Polidipsia

A

demasiado sed

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26
Q

3 categorias de polidipsia

A

sintomatica/verdadera
(estimulado por deshidratación celular por aumento de la osmolalidad EC + Disminución de la volemia + angiotensina II)

falsa

compulsivo

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27
Q

Porque diabetes insipidus y melliltus causan sed verdadera?

A

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)

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28
Q

que causa aumenta de angiotensina II

A

nivel aumenta en respuesta a volumen sanguíneo baja pression sanguínea baja)

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29
Q

funcion de angiotensina II

A

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.

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30
Q

ADH

A

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

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31
Q

en que condiciones se libera ADH?

A

released by the pituitary in response to sensors that detect an increase in blood osmolality or decrease in blood volume

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32
Q

que son factores que aumentan TFG?

A

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

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33
Q

Manifestaciones de SIADH

A

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.

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34
Q

causas de polidipsia

A

deficit de agua, tobaco, antipsicoticos

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35
Q

Sustancias y farmacos que disminuyen los niveles o la accion de la ADH

A 
anfotericina B
demeclociclina
etanol
foscarnet
litio
antagonistas de la morfina
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36
Q

sustancias y farmacos que aumentan los niveles o la accion de la ADH

A 
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
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37
Q

Tx para diabetes insipidus central

A

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

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38
Q

Causas de deficit del volumen isotonico

A

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)

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39
Q

Que es la enfermedad de Addison?

A

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

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40
Q

Manifestaciones de deficit de volumen isotonicos

A

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

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41
Q

Causas de excesso del volumen isotonico

A

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

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42
Q

que son corticoesteroides

A

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.

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43
Q

what is BUN?

A

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.

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44
Q

what is Cushings diesase?

A

Excess cortisol interacts with mineralocorticoid receptors leading to:
Sodium retention causing hypertension (in 70-80%).
Potassium loss: hypokalemic alkalosis in 20% of cases

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45
Q

Manifestaciones de isotonic fluid volume excess?

A

Aumento de peso

Aumento de volumen intesticial (edema)

Aumento de volumen vascular (venous distenstion, full pulse, dispnea por edema pulmonar)

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46
Q

osmolalidad serica

A

275-295m

Osm/kg

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47
Q

tipos de hiponatremia

A

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)

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48
Q

Causas de hiponatremia hipotonica

A 
hipovolemia
ingestion de soluciones sin sodio
perdida GI
diureticos
enfermedad de addison
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49
Q

causas de euvolemic hiponatremia

A 
aumenta ADH
trauma
SIADH
diurticos
deficiency de glucocorticoide
hipotiroidismo
polidipsia psicogenico
ejercicio
MDMA
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50
Q

causas de hiponatremia hipervolimico

A

fallo cardiaco
fallo hepatico
fallo renal

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51
Q

causas de hiponatremia hipertonica (IC–>EC)

A

hiperflicemia

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52
Q

manifestaciones de hiponatremia

A

serum sodium 280mOsmo/kg

cramps, weakness, headache depresion, personality changes, lethhargy, coma (agua entra a neuronas)

anorexia, nausea, vomito, diarrea

aumenta IC –> fingerprint edema

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53
Q

causas de hipernatremia

A

perdida de agua excessiva (diarrea aguada, sweating, increased respirations, diabetes insipidus)

decreased water intake (trauma, impaired thirs)

excessive sodium intake (ocean drowning)

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54
Q

manifestaciones de hipeprnatremia

A

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

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55
Q

Peso corporal de postasio en adultos

A

50mEq/kg (K+)

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56
Q

Potasio ingerido por dia

A

50-100mEq

40-60 se elimina en heces

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57
Q

cuanto potasio se elimina por rinon

A

80-90%

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58
Q

factores que alteran distribucion de K+

A

osmolalidad de suero, trastornos acido-base, insulina, estimulacion beta-adrenergica, ejercicio

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59
Q

que estimula la bomba ATPasa y la entrada de K+ en la celula?

A

insulina

adrenalina

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60
Q

que provoca hiperpotasemia en excitivilidad

A

hipolarizacion, potencial de membrana de reposo mas positivo

closer to threshold

prolonged depolarization that can decrease excitability.

more rapid repolarization

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61
Q

que provoca hipopotasemia en excitibilidad

A

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

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62
Q

que determina el potencial de membrana de reposo

A

K+ IC: EC

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63
Q

Causas de hipokalemia

A

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)

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64
Q

manifestaciones de hipokalemia

A

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

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65
Q

que puede aumentar perdida renal de K+

A

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.

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66
Q

cambios en ECG @ hipokalemia

A

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

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67
Q

causas de hiperkalemia

A

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)

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68
Q

manifestaciones de hiperkalemia

A

suero > 5mEq

nausea, vomito , cramps, diarrea

paresthesia, weakness, cramps, dizziness

cambios en ECG (more cardiac than neurological)

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69
Q

cambios en ECG @ hipercalemia

A

peaked T waves

shortened !T

widened QRS

PR interval prolonged

P waves disappear

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70
Q

Que Tx se puede usar para hipekalemia

A

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)

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71
Q

3 formas de calcio EC

A

unidos a proteinas (40%)

o ionizados libres (50%)

complejado con citrato, fosfato, sulfato (10%)

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72
Q

funcion de calcio ionizados

A

excitacion neuromuscular y cardiaco, reacciones enzimaticas, contraccion del musculo, liberacion de hormonas, NTs, mensajeros quimicos, contractilidad cardiaca, coagulacion

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73
Q

regulacion de [calcio ] EC

A

PTH y renal, alteraciones en albumina + pH

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74
Q

sitio regulatorio de absorcion de calcio

A

tubulo distal convoluted:

PTH, Vitamina D, thiaziade diuretics, fosfato, glucosa, e insulina regulan aqui

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75
Q

causas de hipocalemia

A

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)

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76
Q

TFG normal

A

120-130

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77
Q

como el pH afecta calcio

A

pH acido
disminuye union de calcio con proteína –> aumentando Ca2+ ionizado (plasma calcio total no cambia)

pH alkalino aumenta union con proteina –> tetany

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78
Q

que es tetany?

A

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

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79
Q

como los AGs afecta Calcio?

A

AGs aumentan union de calcio con albumina

elevados por estres, heparina, beta-adrenergic drugs (epinefrina, isoproterenol, NE) y alcohol

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80
Q

que provoca el estres?

A

elevación de AGlibres, epinefrina, glucagón, hormona de crecimiento , y adrenocortocotropic hormone

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81
Q

manifestaciones de hipocalcemia

A

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.

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82
Q

como es que la pancreatits aguda provoca hipocalcemia

A

a. Ca2+ se une con acidos grasos libres liberados por lipolisis en el páncreas –> soaps + removing Ca2+ de la circulación

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83
Q

Chvostek sign

A

taping face below temple @ nervio VII –> spasm of lip, nose face = +

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84
Q

causas de hipercalcemia

A

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)

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85
Q

manifestaciones de hipercalcemia

A

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

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86
Q

what is milk-alkali syndrome?

A

ingestion excesiva de calcio (leche) _ antacidos absorbables

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87
Q

drogas que causan hipercalcemia?

A

lithium, thiazide diuretics

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88
Q

distribucion de fosforo en el cuerpo

A

85% en hueso
14% iC
1% EC

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89
Q

formas de fosforo en el cuerpo

A

organica (90% de fosforo IC - acidos nucleicos, fosfolipidos, ATP)

inorganica (principal forma circulante - el que se mide en laboratorio)

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90
Q

funciones de fosforo

A

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

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91
Q

sustancias que se unen al fosforo e inhiben su absorcion?

A

magnesio, calcio, alumino

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92
Q

fosforo se une a proteinas en plasma?

A

NO ! todo se filtra

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93
Q

causas de hipofosfatemia

A

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)

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94
Q

manifestaciones de hipofosfatemia

A

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

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95
Q

porque antacidos causan hipofosfatemia?

A

Antacidos que contienen aluminum hydroxide, alimunim carbonate, and calcium carbonate se unen con fosfato –> perdida en heces

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96
Q

causas de hiperfosfatemia

A

laxatives and enemas

IC –> EC shift por (trauma, heat stroke, seizures, rhabdomiolisis, deficiencia de K+)

fallo renal, hipoparatiroidismo

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97
Q

manifestaciones de hiperfosfatemia

A

suero >4.5 en adultos y mas de 5.4 en ninos

dismiucion de calcio en suero (paresthesias, tetania)
hipotension , arrithmias

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98
Q

distribucion de magnesio en el cuerpo

A

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)

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99
Q

[Mg] normal en plasma

A

1.8-3mg/dL

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100
Q

funciones de Mg

A

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

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101
Q

causas de hipomagnesemia

A

difunction de absorcion (alcoholismo, malnutricion, malabsorcion, dieta alta en calcio sin magnesio)

perdida de Mg por terapia diuretica, hiperparatiroidismo, hiperaldosteronismo, diabeteic ketoacidosis,

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102
Q

manifestaciones de hipomagnesemia

A

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

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103
Q

causas de hipermagnesemia

A

ingestion excessiva (para tratamiento de preeclampsia)

fallo renal, glomerulonefriis disminuyen excreccion

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104
Q

manifestaciones de hipermagnesemia

A

mg en suero > 3mg/dL

lethargia, hiporeflexia, confusion, coma, hipotension, arritmias

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105
Q

que es preeclampsia

A

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

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106
Q

Mg se usa para tratar

A

hipercalcemia + eclampsia

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107
Q

causas de obstruction del tracto urinario

A

@ pelvis renal: calculos renales, necrosis papilar

@ ureter: calculos, embarazo, tumores que comprimen ureter, trastornos congenitos

@ vejiga/uretra : CA, calculos, trastornos congenitas

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108
Q

componentes de calculos renales

A

sales de calcio, acido urico, magnesimu ammonium phosphate, cystine

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109
Q

inhibidores de calculos renales

A

Mg+ citrato

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110
Q

4 tipos de calculos renales

A

calcio (oxalate and phosphate - 75-80%)

mg ammonium phosphate (struvite) (15%)

uric acid (urate-7%)

cystine

111
Q

factores que causan calculos de calcio

A

@ 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

112
Q

factores que causan calculos de Mgammoniumphosphate

A

urea splitting
infeccion por bugs ureasa positivo (proteus, staph, kliebsella) that hydrolisan urea –> ammonia –> urine alkalinization
UTIs
aumento de pH

113
Q

factores que causan calculos de acido urico

A

pH 5.5

high purine diet

low urine volume, arid climates, acidic pH
hiperuricemia (gout)
leukemia

114
Q

factores que causan calculos de cystine

A

low pH

cistinuria (genetico , trastrono de metabolismo de AAs)

115
Q

tx de calculos de calcio

A

trata underlying condition
increase fluid intake
thiazide diuretics + citrate

dieta sin oxalate

116
Q

tx de calculos de Mg/Am/Fos

A

tratar UTI (eradicacion de infecion )
acidify orina
increase fluid intake
surgical removal of stone

117
Q

tx calculos de acido urico

A

increase fluid intake
allopurinol for hyperuricosuria
alkalinzation of urine

118
Q

tx calculos de cysteina

A

increase fluid intake

alkalinzation of urine

119
Q

que es osteoporosis

A

debilita los huesos y aumenta la posibilidad de fracturas.

120
Q

que forma de calcio se debe medir?

A

ionico

121
Q

tipos de obstruccion:

A

Insidious, parcial, complete, unilateral, bilateral

122
Q

causas de de obstruccion:

A

Anormalidades congenitales, calculi urinaria (stones), embarazo, hiperplasa prstatica benigna, scar tissue de infección + inflmacion, tumores, trastronos neurológicos,

123
Q

danos causados por uropatias obstructivas

A

Stasis of urine (stoppage of flow) –> infeciones y pierdras

Dilatación progressiva de ducto colectores renales y estructuras tubulares  destrucion + atrofia del tejido renal

124
Q

en que pH precipita mas facilmente sales de calcio?

A

in stagnant alkaline urine

125
Q

que es hidronefrosis

A

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

126
Q

manifestaciones de hidronefrosis

A

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

127
Q

focal

A

solo afectan algunos glomérulos

128
Q

difuso

A

compromete todos los glomérulos + todas las partes

129
Q

segmental

A

solo comprometen un segmento especifico de cada glomérulo

130
Q

mesangial

A

solo afectan cel. Mesangiales

131
Q

2 mecanismos inmunitarios que provocan trastornos glomerulares

A

Lesión por anticuerpos que reaccionan contra antígenos glomerulares fijos

Lesión por immunocomplejos atrapados en la membrana glomerular

132
Q

alteraciones histologicas en glomerulopatias

A

Proliferativos: aumento en componentes celulares

Escleroticos: aumento en componentes no celulares

Membranosos: aumento en espresor de pared capilar

133
Q

Glomerulonefritis Proliferativa Aguda

A
  • 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

134
Q

Glomerulonefritis Rapidamente Progresiva

A
  • 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

135
Q

Sindrome de goodpasture

A

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.

136
Q

sindrome nefrotico

A

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.

137
Q

Glomerulonefritis membranoso

A

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

138
Q

Enfermedad con cambios minimos (nefrosis lipoidea)

A
  • Perdida difusa/fusion de los podocitos

Niños

Causa desconocido (infecion, immunizacion, linfoma de hodkin)

Respuesta excelente a tratmiento con corticoesteroides

139
Q

Glomerulosclerosis segmentaria y focal

A
  • 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

140
Q

Enf. de Berger

A

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.

141
Q

Henoch –Schonlein purpura

A 
ninos
vasculitis de vasos pequentos 
erupcion palpable
artralgias
dolor abdominal,

asociado con IgA nefropatia

sindrome nefrotico, nefritico o combinado

recuperacion

142
Q

Sind. de Alport

A

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.

143
Q

lesiones glomerulares de SLE

A 
Tipo I: normal
Tipo II: proliferación mesangial
Tipo III: proliferación focal y segmental
Tipo IV: proliferación difusa
Tipo V: proliferación membranosa
144
Q

Diabetic glomerulosclerosis

A

thicenking of glomerular capillary basement membrane + diffuse increase in mesangial matrix ; this impinges on capillary lumen reducing glomerular filtration

145
Q

Kimmelstiel-Wilson syndrome

A
  1. 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

146
Q

microalbuminuria

A

urinary albumin excretion of 30 to 300 mg in 24 hours (predicts future diabetic nephropathies)

147
Q

que provoca hipertension en glomerulos

A

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

148
Q

2 tipos de trastornos tubulointerstitial

A

AGUDA –> edema intersticial

CRONICA –> fibrosis intersticial, atrofia, infiltrado mononuclear; primeros asintomaticos

causan imbalancia de fluido + electrolitos

149
Q

ACIDOSIS RENAL TUBULAR

A

defectos tubulares en reabsorción de HCO3- o excreccion de H+ –> acidosis metabolica

150
Q

Tipos de renal tubular acidosis

A

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+

151
Q

sindrome de fanconi

A

(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

152
Q

Tipos de Pyelonefritis

A

infección de parénquima de rinon + pelvis renal

Aguda y cronica

153
Q

pielonefritis aguda

A

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.

154
Q

pielonefritis cronica

A

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

155
Q

Nefropatieas relacionadas a drogas

A

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

156
Q

locacion de rinones

A
  1. Fuera del peritoneal cavity @ back of upper abdomen

T12 a L3

157
Q

a donde se encuentran los glomerulos

A

en corteza exterior

158
Q

porque niveles de HCO3- sanguineo cambian mas facilemente que niveles de HCO3- en LCR?

A

porque HCO3- has lag entry across blood-brain barrier

159
Q

que mecanismo de regulacion de pH es mas rapido?

A

respiratorio

160
Q

3 maneras de control renal

A
  1. Excreccion de H+ de acidos metabolisados
  2. Reabsorpcion de HCO3- filtrado
  3. Produccion de HCO3- liberada en sangre
161
Q

Bicarbonato se filtra @ glomerulo?

A

SI, 4300mEq/dia

y se reabsorbe

162
Q

cual es lipid soluble, ammonia o ammonium?

A

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.

163
Q

normalmente Cl- se absorbe con ?

A

Na+

164
Q

trastornos tubulointersticiales se clasifican en

A

aguda –> edema interstical

y cronica –> fibrosis intersticial, atrofia, infiltrado mononuclear

165
Q

primeroos manifestaciones de trastornos tubulointersticiales

A

imbalancia de fluido y electrolitos

166
Q

pH EC

A

7.35-7.45

167
Q

que es acido carbonico y su funcion principal?

A

H2CO3 (hecho de CO2 + HCO3-)

contribuye a pH sanguineo

168
Q

dos tipos de acidos

A

volatile (en equilibrio) H2CO3 eliminado por polmon

Nonvolatile (fijados) (sulfuric, HCl,, eliminados por rinon)

169
Q

cuanto CO2 se produce por dia

A

15,000mmol

170
Q

que es un amortiguador

A

un base leve con su acido conjugado o vice versa

trades a strong acid for weak or strong base for weak

171
Q

3 formas que se transporta CO2 en circulacion

A

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

172
Q

pH se regula por 3 mecanismos

A

amortiguadores químicas
(bicarbonato , proteínas, H+/K+ transcellular )

pulmones que eliminan Co2

riñones que eliminan H+ y reabsorbe/genera HCO3-

173
Q

sistema de regular pH mas poderoso

A

HCO3-

174
Q

sistema de regular pH mas grande

A

proteinas

175
Q

como es el hueso un amortiguador?

A

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.

176
Q

aumento de ventilacion provoca

A

disminucion de PCO2

177
Q

cuando H+ aumenta ventilacion…

A

aumenta

178
Q

cual es mas rapido control renal or respiratorio?

A

respiratorio

179
Q

cual crusa mas facilmente la barrera heamto-encefalica CO2 o HCO3-

A

CO2

180
Q

3 funciones de control renal

A

Excreccion de H+ de acidos metabolisados

  1. Reabsorpcion de HCO3- filtrado
  2. Produccion de HCO3- liberada en sangre
181
Q

Describe el intercambio de H+ y HCO3- @ TP

A

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

182
Q

pH minimo en filtrado

A

4.5 (en este pH secreccion de H+ stops)

183
Q

2 amortiguadores intratubulares que forman HCO3-

A

fosfato

ammonia

184
Q

Describe intercambio de H+/K+ @ tubulo distal

A

transporte activo reabsorbe K+ y secreta H+ (@ hipokalemia)

plasma K+ –> eliminacion de H+ y vice versa

185
Q

como influye H+ la aldosterona?

A

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

186
Q

cuando se utiliza el intercambio de Cl-/HCO3-

A

cuando hay deplecion de volumen , rinones substituyen HCO3- por Cl- aumentando absorcion de HCO3-

187
Q

alkalosis hipocloremico

A

por disminucion en Cl- hay un aumento excesso en reabsorcion de HCO3-

188
Q

acidosis hipercloremico

A

aumento de Cl- disminuye HCO3- y pH

189
Q

PCO2 normal

A

35-45mmHg

190
Q

HCO3- normal

A

venous normal = 24-31mEq/L

arterial = 22-2mEq/

191
Q

2 tipos de trastorno acido-base

A

metabolico (altera HCO3-) y respiratorio (altera PCO2)

192
Q

acidosis respiratorio

A

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

193
Q

alkalosis respiratorio

A

aumenta pH, por aumento de ventilación y disminución en PCO2 (

194
Q

Bajo condiciones de disminución de la perfusión o el aumento de la estimulación del sistema nervioso simpático, el flujo sanguíneo

A

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

195
Q

BP normal

A

(120/80)

BP es 88/53 = hipotension

196
Q

Frecuencia cardiaca normal

A

60 to 100 beats a minute

197
Q

frecuencia respiratorio normal

A

12 to 20 breaths

198
Q

characteristicas de celulas mesangiales

A

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

199
Q

que tipo de medicamentos pasan por el TP?

A

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.

200
Q

@hipotension que causa vasoconstriccion?

A

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.

201
Q

que tipo de medicamento puede inducir hipokalemia?

A

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.

202
Q

24h urine test vs. single

A

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.

203
Q

algunas observaciones en un rinon que no funciona bien?

A

Increased creatinine and BUN are associated with abnormalities in renal function, as is the presence of glucose in a urine sample

204
Q

acidosis metabolica

A

disminucion de pH y HCO- (

205
Q

alkalosis metabolico

A

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-

206
Q

causas de acidosis metabolico

A

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.

207
Q

Manifestaciones de acidosis metabolico

A

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

208
Q

renal tubular acidosis vs chronic kiney disease

A

in RTA only tubular function is compromised vs. both tubular and glomerular funciont

209
Q

causas de alkalosis metabolico

A

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.

210
Q

manifestaciones de alkalosis metabolico

A

pH increased
HCO3- (primary) increased
PCO2 (compensatory) increased

confusion, hyperactive reflexes, tetany, convulsions

hipotension, arrithymias

respitory acidosis
(decreased rate)

increased urine pH

211
Q

Causas de acidosis respiratorio

A

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

212
Q

manifestaciones de acidosis respiratorio

A

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

213
Q

diferencia en acidosis respiratorio aguad vs. cronica?

A

Aguda: rapid rise in PCO2 arterial >45mmHg, with minimal increase in plasma HCO3-, and large decrease in pH

214
Q

causas de alkalosis respiratorio

A

ventialcion excessiva (anxiety, hypoxia or lung disease with reflex ventilation, stimulation of respiratory center, elevated blood ammonia, salicylate toxicity, enceefalitis, fiebre, mechanical ventialtion)

215
Q

manifestaciones de alkalosis respiratorio

A

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

216
Q

soluciones hipertonico

A

3%-5% sodium chloride

10% dextrose in water

217
Q

soluciones isotonicos

A

0.9% NaCl

5% dextrose

218
Q

solucion hipotonico

A

0.45% NaCl o 0.33% NaCl

219
Q

que provoca ascitis

A

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.

220
Q

Como se puede formar edema

A

Right-sided heart failure, burns, and low levels of plasma proteins are all associated with the development of edema.

221
Q

droga para tratar tratar diabetes insipidus

A

Desmopressin acetate (DDAVP)

222
Q

manifestaciones de diabetes insipidus

A

Elevated blood glucose levels, dry mucous membranes, and severe projectile vomiting

223
Q

se utuliza tx IV para hiperkalemia

A

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

224
Q

Sequencia de Vitamin D

A

esta presente @ piel o intestino

se concentra @ higado

se transporta a kidney

se produce calcitriol

absorcion de calcio del intestino aumenta

225
Q

tratamiento de hipercalcemia

A

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.

226
Q

Mg deficiency occurs in conjunction with

A

low calcium levels

227
Q

H+/Na+ intercambio regula acido-base?

A

NO

228
Q

relation between anion gap and acidosis?

A

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

229
Q

D-lactic acidosis

A

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.

230
Q

ethelyn glycol

y OD tx

A

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

231
Q

aspirin OD provoca

A

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.

232
Q

lactic acidosis es que tipo de acidosis

A

metabolico

233
Q

tx de alkalosis metabolica

A

IV KCl solucion

234
Q

tx de acidosis respiratorio

A

ventilacion mecanico

235
Q

como se puede utilizar alkalosis respiratorio como tratamietno?

A

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.

236
Q

trastornos renales en infantes

A

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.

237
Q

que cicrunstancias predisponen a obstructiones urinarios

A

Pregnancy, BPH, renal calculi, and neurogenic bladder are all identified contributors to urinary obstructions.

238
Q

que cambios en electrolitos provoca la malnutricion

A

hipofosfatemia

hipomagnesemia

239
Q

BPH causa

A

dolor y hidroureter, distention of distal ureter

240
Q

que tipo de dolor es provocado por los colicos

A

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

241
Q

que tipo de dieta se debe modificar en px con calculos de calcio-oxlato

A

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

242
Q

sindrome de nefritico

A

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.

243
Q

most common cause of primary nephrosis in adults

A

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.

244
Q

cationes que medimos

A

Na+=136

245
Q

aniones que medimos

A 
Cl- = 100
HCO3= 24

124

246
Q

Na+ - (Cl- + HCO3-) =

A

12

247
Q

por cada 1mEq/l HCO3 - perdido comensa con

A

disminucion de 1.2 mmHg pCO2

248
Q

por cada 1mEq/l HCO3- ganado

A

aumento de 0.7mmHgpCO2

249
Q

por cada 10 mmHg pCO2 ganado

A

aguda: aumenta 1 mEq/l HCO3-
Cronica: aumenta 3.5 mEq/l HCO3-

250
Q

por cada 10 mmHg pCO2 perdido

A

aguda: disminuye 2 mEq/l HCO3-
cronica: disminuye 5 mEq/l HCO3-

251
Q

MUDPILES

A

metanol, uremia, diabetic, pildoras, iron, lactic acidosis, etilen glicol, salicilatos

anion gap

252
Q

pCO2 normal

A

40***

pCO2 = 1.5(HCO3) + 8 (+/-2)

if close together = acidosis metabolica + alcalosis resp. compensatorio (pCO2 = 16, HCO3=5, pH=7.11)

253
Q

a que cambios responde la renina

A

renina responde a cambios en presion arterial, TFG, y # de Na+ en filtrado

254
Q

Decreased Anion Gap for differential dx of metabolioc acidosis

A

(

255
Q

Increased Anion Gap @ ddx of metabolic acidosis

A

(>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

256
Q

Normal anion gap @ ddx of metabolic acidosis

A

Loss of bicarbonate Diarrhea Pancreatic fluid loss Ileostomy (unadapted) Chloride retention Renal tubular acidosis Ileal loop bladder Parenteral nutrition (arginine, histidine, and lysine)

257
Q

causas de edema

A 
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
258
Q

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

A

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.

259
Q

Distribution of Ca+ between bone and ICF and ECF

A

Bone 99%,
1% ICF,
0.1—0.2% ECF
(ECF divides into 50% free, 10% complexed, 40% protein bound)

260
Q

immunodeficiency virus (HIV) infection is an established cause of …..

name illness + 5 cardinal features

A

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

261
Q

Relationship between cancer and hypercalcemia

A

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

262
Q

On a mixed diet, pH is threatened by

A

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−).

263
Q

When the ratio of bicarbonate (HCO3−) to carbonic acid (H2CO3, arterial CO2 × 0.03) = 20:1, the pH =

A

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

264
Q

Henderson-Hasselbalch equation

A

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.

265
Q

Hydrogen ion (H+) secretion and bicarbonate ion (HCO3−) reabsorption in a renal tubular cell

A

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.)

266
Q

The renal phosphate buffer system

A

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+.

267
Q

Acidification along the nephron.

A

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

268
Q

anion gap

A

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.

269
Q

vomiting

A

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

270
Q

as acidosis progresses, the skin vessels become

A

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.

271
Q

Anti-GBM Glomerulonephritis

A

Circulating anti-GBM antibodies with linear GBM staining for IgG

with lung hemorrage –> good pasutre

without lung hemorrage –> anti-GBM glomerulonefritis

272
Q

Immune Complex Glomerulonephritis

A

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

273
Q

ANCA Glomerulonephritis

A

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

FISIO II (5 decks)

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