role of 1,25 OH vit D
absorption of calcium and phosphate
cause of low 1,25 OH vit D
malabsorption
hypocalcemia and hypophosphatemia
1,25 OH vit d deficiency
quid of winter foormula
to see if metabolic acidosis has respiratory compensation
expected PACO2 in metabolic acidosis with good respiratory compensation
1,5(hco3-)+8 +-2
calculation of anion gap acidosis
Nacl-(cl +Bicarb)
Normal anion gap
quid CO2 acid ou basique
acide
respiratory compensation in alkalosis metabolic
Increase of co2
clue for respiratory acidosis
increase of co2
compensation of respiratory acidosis
increase bicarb to compensate
quid of bicarb acid ou base
basique
what happen in metabolic acidosis(2)
decreased HCO3
CO2 decreases to compensate
what happen in respiratory alkalosis(2)
co2 decreased
bicarb decreased to compensate
what happen in metabolic alkalosis(2)
bicarb increased
increase co2 to compensate
pregnant women with bicarb 44 PH 7,49 why
hyperemesis gravidarum causing metabolic alkalosis
physiopatho of high bicarb in vomiting(2)
Perte de H+ in vomiting
stimulation of RAA —>retention d’eau de sodium et de HCO3 -
causes of metabolic alkalosis(3)
vomiting
excess of mineralocorticoid
diuretic use
hypocalcemia in patient receiving large amount of blood
chelation of calcium by citrate in blood product
when to suspect hypocalcemia
in any case of massive transfusion
why hypomagnesemia can mimic hypocalcemia(2)
because it causes low PTH
decrease peripheral responsiveness to PTH
clue for alveolar hypoventilation
high Paco2 in a context of acidosis
Normal Pao2
75-105
normal PaCO2
33-45 mm de Hg
cause of alveolar hypoventilation and respiratory acidosis(4)
pulmonary thoracic disease
neuro muscular disease
drug induced hypoventilation
primary central nervous system dysfunction
pulmonary thoracic disease causing alveolar hypoventilation(4)
COPD
obstruction sleep apnea
scoliosis
obesity hypoventilation
neuro muscular disease causing alveolar hypoventilation(3)
Myastheni gravis
lambert eaton syndrome
GB syndrome
drugs induced alveolar hypoventilation(3)
sedatives
narcotics
anesthetics
primary nervous system disease causing hypoventilation(3)
brainstem lesion
infection
stroke
how’s A-A nin hypoventilation syndrome
normal
cause of hypoxemia(5)
reduced inspired o2 tension hypoventilation diffusion limitation shunt V/q mismatch
abnormal acid base disturbance in house fire
metabolic acidosis
why metabolic acidosis in house fire(2)
low o2 delivery in tissue
accumulation of lactic acid
what happen in metabolic acidosis in house fire
it’s carbon monoxyde poisonning
quid of Type A lactic acidosis(2)
co poisonning
circulatory failure
why co poisonning causes acid lactic accumulation
because 02 delivery is decreased in tissues
hypotension in a context of TB and hypereosinophilia
primary adrenal insufficiency
acid base disturbance in primary adrenal insufficiency(4)
acidose metabolic with normal anion gap
hyponatrmia
hyperkaliemia
hypercalcemia
cause of primary adrenal insufficiency(4)
autoimmune
infection
metastatic
hemorragic infarction
infection causing primary adrenal insufficiency(3)
TB
cryptococus
HIV
patinet seen with hypotension,hyperpigmentation of skin on palamr creases what metabolic problem you expect to find ?
hyperkaliemia
the most common electrolytes abnormality in adrenal insufficiency
hyponatremia
patient with PCP develops hyperkaliemia why
rx with TMS
why TMS causes high K+
by blocking the epithelial sodium channelin the collecting tubule
what other drug has the same action than TMS in the physiopatho of HyperK+
K+ sparing diuretic
why Creat can be high during TMS intake
it inhibits renal tubular of creat secretion
side effect of lithium
diabetes insipidus
clue for DI
plasma osmolarity > urine osmolarity
clue for central DI(4)
Trauma
hemorrage
infection
tumors
cause of renal DI(4)
Lithium
hypercalcemia
hypokaliemia
tubulointersticial disease
drugs causing nephrogenic DI(5)
lithium memeclocycline foscarnet cidofovir amphotericin B
rx of lithium induced DI(2)
salt restriction
stop lithium
rx of vomiting induce metabolic alkalosis
NACL 0,9%
plus
K+
why HCO- is elevated during vomiting(2)
retention of Hco3- in blood
stimulation of RAA
why you have retention of HCO3 - in blood(2)
acid stimulates pancreas to release HCO3- in intestinal lumen
vomiting—–>no Hcl —>no pancreas stimulation
quid of generation phase(2)
acid stimulates pancreas to release HCO3- in intestinal lumen
vomiting—–>no Hcl —>no pancreas stimulation
quid of maintenance phase of HCO3- (2)
stimulation of RAA system
retention of HCO3_
how they call alkalosis induce by vomiting
contracting alkalosis
edema and red blood cells cast and HTA
acute nephritic syndrome
cause of edema in acute nephritic syndrome
decrease filtration rate
retention of Na+ and H2O by kidneys
primary mechanism in nephritic syndrome
primary glomerular damage
patient with exacerbation of COPD ,what medication can be used to treat hyperkaliemia in this patient
succinylcholine
action succcinyl choline(2)
K+ release
neuromuscular blocker depolarising
patient for whom we can’t use succinylcholine(3)
crush injury or burn injuries >8 H
demyelinating syndrome like GBS
tumor lysis syndrome
crush injury or burn injuries >8 H
demyelinating syndrome like GBS
tumor lysis syndrome
med can be used to rx hyperkaliemia in this patients(2)
vecuronium
rocuronium
electrolyte problem in alcoholism
hypophosphatemia
hypokaliemia
hypomg++
rebellious hypokaliemia in alcoholic next step
rx hypomagnesemia
why hypo Mg++ causes rebelious hypokaliemia
Mg++ is a cofactor of K+ intake
what to do in rx of hypokaliemia in patient alcoholic
check Mg++ level
other cause of hypoMg++
diuretics
patients with severe abdominal pain develops lactic acidosis with anion gap
bowel ischemia
whe to suspect bowel ischemia(2)
any patient with AFIB or atherosclerosis
and abdominal pain
main symptom of hyponatremia
seizures
what rate should be used inthe rx of hypokaliemia
hypertonic saline or 3%
rate no more 0,5meq/l /h
why hyponatremia should be corrected slowly
to avoid osmotic demyelinating syndrome
what will happen if you correct hyponatremia too quickly
cerebral edema will occur
most common cause of cushing syndrome
iatrogenic use of corticosteroid
electrolyte problem in cushing(2)
hypokaliemia
hypernatremia
corticoid=aldosterone
quid of normal anion gap
6-12
cause of normal anion gap
presence of acid molecule
quid of acid molecule(4)
protein
citrate
phosphate
sulfate
most common cause of high anion gap metabolic acidosis(6)
lasctic acidosis ketoacidosis methanol formaldehyde ingestion ethylene glycol ingestion salycilate poisonning uremia
acid found in ketoacidosis
b hydroxybutyrate
acetoacetic acid
why uremia is marked by acidosis in end stage renal disease
impaired excretion of ion H+
first thing to check in front of metabolic acidosis
check the anion gap
why anion gap metabolic acidosis in post seizure
accumulation of lactic acid in blood
what to in metabolic acidosis after seizure
do nothing
recheck after 60-90 mn(2 hours )
electrolyte problem in vomiting
low chlore
low H+
high HCO3_
low K+
why hypochloremia in vomiting
GI loss
why low K+(2) in vomiting
stimulation of RAA
aldosterone causes secretion of H+ et K+
cause of ketoacidosis(3)
diabete type 1
starvation
alcoholism
acid accumulation in formaldehyde ingestion
acid formic
substance causing primary metabolic acidosis with high anion gap and primary respiratory alkalosis
salycylate
acid causing anion gap acidosis in glycolene ethylene ingestion(2)
acid oxalic
acid glycolic
salycilate intox clue(3)
fever
tinnitus
tachypnea
vomiting
metabolic problem ion salycilate ingestion(3)
Normal PH
low PAco2
low HCO3-
best indicator to talk about metabolic acidosis(2)
HCO3-
not the PH
why primary respiratory alkalosis in aspirin toxicity
increase respiratory drive
cause of metabolic acidosis in aspirin intox(2)
increase production of acid
decrease renal clearance of organic acids
what’s the appropriate respiratory compensation in front of metabolic alkalosis
1 meq rise of hco3-=0,77 mm de hg rise of co2
compensation ina cute respiratory alkalosis
decrease serum HCO3- de 2 meq/l for every 10mm de HG decrease of Paco2
the most common cause of hypernatremia
hypovolemia
people at risk for hypovolemia(2)
debilitated
unconscious
proof of severe hypernatremia
altered mental status
rx of severe hypernatremia
o,9 normal saline
rx of moderate hypernatremia
d/s 0,45
calculation of PH
6,1+log(hco3-/0,03*paco2
logic of rx of metabolic alkalosis
increase excretion of HCO3-
classification of metabolic alkalosis(2)
saline responsive
saline resistant
cause of saline responsive metabolic alkalosis(5)
vomiting gastric suctionning diuretics laxative abuse low oral fluid intake
saline resistant alkalosis(4)
primary hyperaldosteronism
cushing
severe hypokaliemia
action of NACL during rx of saline responsive metabolic alkalosis(3)
increase of chlore
restore arterial volume
increase bicarb excretion
complication of tumor lysis syndrome
hyper K+
3 ways in Rx Hyper K+
stabilization of the membrane with IV gluconate de calcium
shift K intracelularly
decrease K+ in the body
best way to shift K+ intra cellularly
insulin plus glucose
patient with metabolic acidosis develops lethargy and high PCO2 why
hypoventilation
high PCO2 in a context of metabolic acidosis Dx
hypoventilation
cause of accumulation of CO2(2)
confusion
lethargy
good compensation of metabolic acidosis(2)
tachypnee
low co2
clue for SIADH(5)
euvolemic hyponatremia low serum osmolarity high urine osmolarity increassed sodium excretion failure to correct with normal saline infusion
clue for chloride sensitive metabolic alkalosis
urine chloride
clue for chloride resistant metabolic alkalosis
urine chloride > 20
2 grandes cause of hyponatremia(2)
SIADH
primary polydipsia
hyponatremia plus low urine osmolarity
primary polydypsia
malnutrition(beer potomania)
patient at risk for primary polydypsia
psychiatric conditions (schizophrenia)
consequence of hyponatremia(4)
lethargy
confusion
convulsion
psychosis
role of B2 agonist in rx of hyperkaliemia
shift K+ intracellurlarly
medication used tor x hyperkaliemia(3)
insulin/glucose
sodium bicarb
B2 agonist
patient after breakup develops orthostatic hypotension,hypokaliemia hyponatremia,high K+ and Na+ in Urine why
diuretic abuse
most common cause of hyperkaliemia(5)
renal failure acute or chronic medication disruption of SRAA axis hyperglycemia tumor lysis syndrome
symptom of hyperkaliemia
flaccid paralysis
medication causing hyper k+(6)
Non B2 adrenergic blockers ACE inhibitor ARBS K+ sparing diuretics cardiac glycosid NSAIDS
patient with cirrhosis develops metabolic alkalosis with high creat and hypok+ cause
loop diuretic use
what to do when creat is high
determine if it ‘s prenal or renal failure
IR induce d by loop diuretics
prerenal problem
2 things to do in front of any metabolic acidosis(2)
1-calculation of anion gap
2-winter formula
patient with COPD exacerbation and right ventricular failure how will be the PH
PH
for the patient with COPD exacerbation and right ventricular failure furosemide is given ,ph is 7,31(avant 7,32) bicarb: 18 why decrease of bicarb
because of uremia=metabolic acidosis
the patient on diuretics develop hypokaliemia and renal failure why
because of the diuretics given
action of diuretics
diuretic loops cause high excretion of NA+ et K+
causes metabolic alkalosis
but when you have high BUN,you can have a drastic decrease of Hco3_causing metabolic acidosis
acute renal injury caused by diuretic consequence and why
metabolic acidosis will develop
defaut d’excretion d’ion H+
level of BUN to have metabolic acidosis in acute kidney failure
a partir de 60mg/dl
reflexes in hypomagnesemia
decreased tendon reflexes
GBS
guillain barre
mechanism of heparin induced hyper K+
block aldosterone production
mechanism of NSAIDS induced hyper K+
decreased renal perfusion causes decrease K+ delivery in the collectinf tubules
mechanism of succynilcholine induced hyper K+
cause extracellular leakage of K+ through acetylcholine receptor
mechanism of cyclosporine induced hyper K+
blocks aldosterone activity
mechanism of digitalis induced hyper K+
inhibition of NA+K-ATPASE pump
mechanism of ACE inhibitor induced hyper K+
inhibition of aldosterone or the ENAC channel
mechanism of b blocker induced hyper K+
interferes with b2 mediated intracellular k+ intake
Patient with cirrhosis and vomitind developsmetabolic alkalosis,best next step
volume resucitation to rx alkalosis
mechanism of edema(4)
increased capillary hydrostatic pressure
decreased capillary oncotic pressure
increased capillary permeability
lymphatic obstruction/increased intersticial oncotic pressure
cause of increased capillary hydrostatic pressure(3)
heart failure
primary brenal sodium retention (renal disease)
venous obstruction
cause of venous obstruction(2)
cirrhosis
venous insufficiency
cause of decreased capillary oncotic pressure(2)
protein loss
decreased albumin synthesis
cause of protein loss(2)
SN
protein losing enteropathy
cause of decreased protein synthesis(2)
cirrhosis
malnutrition
cause of increased capillary permeability(4)
burn trauma sepsis
allergic rx
ARDS
malignant ascites
cause of lymphatic obstruction and increased intersticial oncotic presure(3)
malignant ascites
hypothyroidism
lymph node dissection
risk factor for bowel ischemia(2)
AFIB
PAD
acid base disturbance in bowel ischemia
metabolic acidosis
symptom of severe hypernatremia
neurologic symptom
envelope shaped crystals in ethylene glycol poisonning
calcium oxalate crystals
quid of hypotension plus hypovolemia
hypovolemic hyponatremia
cause of hypovolemic hyponatremia(4)
volume depletion
primary adrenal insufficiency
GI losses
renal losses
why hyponatremia in hypovolemia(3)
hypovolemia causes stimulation of Renine AA axis
-relargage of ADH
ADH causes retentionn of water and sodium dilution
inappropriate ADH elevation(2)
hypervolemic hyponatremia
euvolemic hyponatremia
cause of hypervolemic hyponatremia(4)
cirrhosis
haert failure
chronic kidney disease
SN
euvolemic hyponatremia(4)
SIADH
primary polydipsia
secondary adrenal insufficiency
hypothyroidism
fever a 40 plus hypotension
septic shock
acid base disturbance in septic shock
anion gap metabolic acidosis
rx of anion gap metabolic acidosis caaused by shock
IV 0,9% saline solution
metabolic acidosis with low urine excretion
chlorine sensitive metabolic acidosis
quid of low urine Na+ excretion
cause of chlorine sensitive metabolic acidosis
volume contraction
quid of volume contraction(2)
vomiting
diarrhee
patient with metabolic acidosis develops high PACO2 ,more than normal compensation according to winter formula DX
mixed respiratory and metabolic acidosis
acid base in loop diuretic (3)
Metabolis alkalosis
hypokaliemia
high creat
condition to have metabolic acidosis during loop diuretic failure
when loop diuretics cause acute kidney injury with uremia >60
