Fluid and Electrolytes/Acid Base Flashcards
major determinant of LV filling volume, CO, MAP
intravascular volume
diagnostic hallmark of decrease EABV
Urine sodium < 15
principal anion lost in diarrhea
bicarbonate
acid base in diarrhea
hyperchloremic acidosis
acid base in diuretics, bartter, Gitelman
hypokalemic alkalosis
K and acid base in adrenal insufficiency
hyperkalemia and met acidosis
urine parameters in hypovolemia
u.spg > 1.020, Una < 10, Uosm > 400 mOsm/Kg
Feureia of hypvolemia with diuretics less than 30-35%
Fena of hypovolemia less than 1%
clilnical detection of edema occurs when interstitial fluid is
>2 to 3 L
sine qua non for Na and water retention in cirrhosis with portal hypertension
intrasinusoidal hypertension > 12 mmHg
halmark of fluid retention in cirrhosis peripheral arterial vasodilation with vasoconstriction
treatment of choice for HRS liver transplantation
standard of care for heart failure
B blocker
daily insensible water loss 8-10 ml/kg
8-10 ml/kg
primary determinant of free water excretion in regulation of H20
ADH
most important stimulus of AVP secretion
hypertonicity, oncotic pressure of plasma
absolute level of Posm at which a person develops a conscious urge to drink osmotic thirst threshold
Osmotic thirst threshold 295 mOsm/kg/H20
lack of osmoreceptors that regulate thirst and impaired osmoregulation of AVP
osmoreceptor dysfunction
hallmark of osmoreceptor dysfunction abnormal thirst response
enzyme enhanced in gestational DI
oxycytocinase and vasopressinase
resistance of ADH due to defect within the kidney
nephrogenic DI
most common cause of drug induced NDI
lithium
characteristic clinical symptom of DI
polyuria, polydipsia
solute excretion rate in solute diuresis
> 15 mOsm
diabetes insipidus central vs nefrogenico
fluid deprivation test
increase in U Osm after vasopressin
CDI
<10% increase in Uosm after vasopressin
NDI
drug of choice for acute and chronic CDI
desmopressin
paradoxic antidiuretic effect in NDI
Thiazide
major comploication of desmopressin
hyponatremia
hyponatremia, normal osm
pseudohyponatremia, factitious hyponatremia
potent stimulus to AVP secretion
volume depletion
most common of hospitalized hyponatremia
SIADH
Uosm in sIADH > 100 mOsm/Kg H20
most common malignancy with sIADH
bronchogenic Ca and small cell lung cancer
Na increase in 100 ml hypertonic saline
2 to 4 mmol/L
most dreadful complication in acute hyponatremia
brain herniation
allowable increase in Na in 24 hours in high risk ODS
8 mmol/L
max daily rate of increase in Na
10-12 mmol/L
TTKG 2-3
redistributive hypokalemia
TTKG>4
renal K wasting
Urine K/Crea signifying poor dietary intake
< 13 meq/g Crea
Most common cause of hypokalemia in hospitalized
GI losses, diuretics, hypomagnesemia
renal compression by subscapular mass or hematoma causing increase in renin
page kidney
unusual presentation of renal artery stenosis and renal ischemia
hyponatremic hypertensive syndrome + hypokalemia
Familial Hyperaldosteronism Type I
Glucocorticoid remediable hyperaldosteronism
suppresion of aldosterone after dexamethasone suppression test: FH I
< 4 ng/dL
Findings in primary hyperaldosteronism after saline loading test
UNa > 200 mmol/day, Ualdo > 33 mmol/day
PAC in PA
> 277 pmol/L
preferred surgical management for APA or PAH
laparoscopic adrenalectomy
Most common cause of hyperKalemia in the ER
Renal Failure
combined alpha and betablocker common to cause hyperkalemia
Labetalol
most common cause of adrenalitis in hiv disease
cmv
loss of function mutation in mineralocorticoid receptor: unc in aldosterone, ang II and renin; Asymptomatic in adulthood
Pseudohypoaldosteronism (PHA-1) autosomal dominant
recessive form of pha-1, mutation
EnaC
PHA-II, gain of function in NCC
Gordon syndrome
Htn, hyperK, Nagma, suppressed pra and aldosterone, hypercalciuria reduced bone density
Gordon syndrome
Tx Gordon syndrome
Thiazide
first line drug in Er management of hyperkalemia
Calcium IV
vasoconstrictor of choice for liver cirrhosis
terlipressin
most constant and reliable medication to induce redistribution of K
Insulin with glucose
transporters affected by B agonists
Na K ATPase and NKCC1
preferred mode when rapid correction of hyperkalemic episode is desired
Hemodialysis
low plasma K can alter the rate of tissue metabolism, decrease tissue oxygen consumption, promoting arteriolar constriction, reduce efficiency of hd
Solandt Effect
Excess of this hormone is responsible for hyperca of malignancy
PTHrp
Most common cause of hypercalcemia in hospitalized patients
Malignancy
Most common cause of hypercalcemia in outpatient clinic
PHPT
positive family history, hypercalcemia at a young age, low Uca
Familial hypocalciuric hypercalcemia
excessive and incompletely regulated secretion of pth with hypercalcrmia and hypophosphatemia
primary hyperparathyroidism
Cause of PhPT in 80-85% of cases
Parathyroid adenoma
classic bone lesion in phpt
osteitis fibrosa cystica
standard therapy for phpt
surgery
most popular and most sensitive technique to localize pth glands
sestamibi scanning
endocrine tumors in 2 of 3: Parathyroid gland, pituitary gland, enteropanxreatic tissue; most common form of familial phpt
MEN1
syndrome of heritable predisposition to medullary thuroid carcinoma, pheochrokocytoma and phpt
Men 2A
glycoprotein that inhibits wnt b catenin signaling
sclerostin
fully humanized monoclonal antibody that prevents bunding of rank to rankl
denosumab
most common granulomatous disease with hypercalcemia
sarcoidosis
most effective therapy for hypercalcemia in hematologic malignancies
glucocorticoids
most common causes of hypocalcemoa in the nonacute setting
hypoparathyroidisn, hypomagnesemia, ckd and vitamin d deficiencies
pth resistance with short stature, round face, mental retardation, brachydactyly, lack of phosphaturic response to parathyroid extract
albright hereditart osteodystrophy
php with complete resistance to effects if pth
PHP-1
php without hypocalcemia and endocrine dysfunction
pseudohypoparathyroidism
php with reduced phosphaturic response to pth but normal increase in urinary camp levels
php-2
most common cause of acquired hypoparathyroidism in adults
surgical removal or damage to the pth glands
prolonged hypocalcemia after parathyroidectomy
hungry bone or recalcification syndrome
best indicator of vitamin d status
25 (OH)D
tumor lysis
hyperphos, hyperuric
hypocalcemia
best test of overall magnesium status
magnesium tolerance test
FeMg suggestive of magnesium wasting
>24 mg per day
earliest manifestation of hypermg
hypotension
rare autosomal recessive disorder characterized by hyperphos and progressive deposition pf ca phos crystals
familial tumor calcinosis
acquired paraneoplastic syndrome of kidney phos wasting - hypophos, normal serum calcium, pth levels, low calcitriol, decreased bone mineralization
tumor induced osteomalacia
First line of defense against acid or base
buffers
second line of defense against acid base respiratory system
3rd line of defense renal
major buffer system in the body
CO2/Hco3
most common cause of drug induced respiratory alkalosis
salicylates
surrugate for ammonium excretion
urine anion gap
principal defect in acidification of advanced renal failure
reduced ammoniagenesis, impaired NH4 accumulation
most common cause of acquired pRTA
multiple myeloma
most common drug causing of acquired pRTA
ifosfamide
acid base in fanconi syndrome
chronic hyperchloremic metabolic acidosis
Type 1 RTA
classical distal RTA
Type 2 RTA
proximal RTA
hallmark of cDRTA
hypokalemia distal RTA
reliable marker for cDRTA
nephrocalcinosis
Type 4 RTA
hyperkalemic RTA
HIPOALDOSTERONISMO=
principal= nefropatia diabetica
tbm associado a =cni, aines, nefrite intersticial cronica, e glomerulonefrite aguda
suspeitar em casos de hipercalemia sem etiologia aparente
glucocorticoid and mineralocorticoud deficiency
addison’s disease
most common congenital adrenal defect
21 hydroxylase deficiency
most frequently associated renal disease with hyporeninimic hypoaldosteronism
DM nephropathy and tubulointerstitial disease
drugs that inhibits EnaC
amiloride, triamterene
inhibited by cyclosporine and tacrolimus
Na K ATPase, ROMK channel,enac
target hco3 concentration
> 22 meq/L
PHA-2
Gordon syndrome
most common lactic acidosis
L-lactic
most widely reported drug that can cause lactic acidosis metformin
lactic acidosis from tissue hypoperfusion
Type A
most common cause of type A acidosis
bowel ischemia
treatment for salicylate activated charcoal
activated charcoal
treatment for ethylene glycol fomepizole
mutation in Bartter Syndrome
NKCC2
Gitelman
NCC DCT
Gitelman vs Barter
hypocalciuria and hypomagnesemia for Gitelman
mutation in Liddle
Enac principal cells CCD
diabetes insipidus central
destruicao dos neuronios da neurohipofise ou mutacoes do adh
diminuicao da liberacao do adh
diabetes insipidus gestacional
atividade excessiva da vasopressinase placentaria
quebra o adh
treatment of gestational DI
vasopressin
RESPOSTA A DESMOPRESSINA
OSMOLARIDADE URINARIA aumenta menos de 15%para um valor menor que <300 mosmol/kg = di nefrogenico completo
osm urinaria aumenta de 15 a 45% para um vamor <300 = di nefrogenico parcial
osm urinaria mais que dobra >100% = di central completo
osm urinaria aumenta 15-100 % para um valor > 300 = di central parcial
minimo ou sem aumento e valor >300 = nao diagnostico
quando é nao diagnostico é pq é polidipsia primaria ou di central parcial
diabetes insipidus nefrogenico
resistencia a acao do adh no nefron
acidose metabolica
AG= na -cl+bic = 10 +-2
> 12- anion gap aumentado
AG corrigido = AG calculado + 2,5 x (valor de referência da albumina – albumina mensurada)
GOLDMARK=
Glicois, oxoprolina,l-lactato, d-lactato, metformina, metanol,
aas, renal, kad
paraldeido,cetoacidose alcoolica, jejum
tto= reversao das causas base
gap osmolar
2xna +glicose/18 +ureia /6
delta/delta.
Colocando de forma matemática (variação do AG) / (variação do bicarbonato) = 1 é o normal (ou seja, variações iguais).
Como assumimos valor normal do ânion gap como 10 e do bicarbonato como 24, temos que:
(AG calculado – 10) / (24 – HCO3–medido ) = 1
Se esse cálculo resultar em < 1, quer dizer que o denominador (bicarbonato) variou muito em relação ao numerador (AG). Portanto, possivelmente há acidose metabólica com AG elevado e acidose metabólica hiperclorêmica coexistindo.
Se o resultado é > 2, quer dizer que apesar de o AG ter variado, o bicarbonato variou muito pouco. Uma explicação para isso é que junto com a acidose metabólica de AG elevado, há uma alcalose metabólica (algo que causou um relativo aumento no HCO3–, evitando que ele caia proporcionalmente ao aumento do AG).
acidose metabolica com ag normal ou hipercloremica
diarreia ou rta
ag urinario se ag negativo = diarreia