Fatigue and Weakness Flashcards
normal serum osmolarity
- what is the limit of hyponatremia
normal: 280-290
hyponatremia: <135
osmotic stimuli for ADH
increases in serum osmolality detected by osmoreceptors
non-osmotic stimuli for ADH
- decrease in BP detected by baroreceptors
- nausea
- hypoxia
- pain
- mediations (opiates, antipsychotics, antidepressants)
hyponatremia results primarily from:
increase in total body water
if pt has hypo-osmotic hyponatremia, what should you measure
random urine sodium level and urine osmolality
- obtain serum uric acid if suspecting SIADH
low serum uric acid is associated w/
SIADH
what is hyperglycemic sodium correction
Na decreases 1.6 mEq/L for every 100 mg/dL increase in glucose
what must you rule out when diagnosing SIADH
cortisol deficiency and hypothyroidism
essential diagnostic criteria for SIADH
- decreased ECF osmolality
- inappropriate urine concentration
- clinical euvolemia
- elevated urine Na+ under normal salt and water intake
most common malignancy associated with ectopic ADH prodcution
small cell lung cancer
what drugs are associated w/ causing SIADH
- antidepressants
- anticonvulsants
- anticancer drug cyclophosphamide
- opiates
- MDMA (ectasy)
sx of hyponatremia (when serum sodium gets to <125)
- HA
- fatigue/lethargy
- dizziness
- nausea
- confusion
- gait instability
- psychosis
- seizures
- coma from cerebral edema
complications of hyponatremia
- increased falls
- death
- osmotic demyelination syndrome
why does osmotic demyelination occur
rapid serum Na+ correction in chronic hyponatremia
general rule of thumb for tx hyponatremia
serum Na+ should be corrected over same time period it took to become low
tx for acute hyponatremia (less than 48 hrs)
can have rapid correction of serum sodium w/ little risk of ODS
tx for chronic hyponatremia (more than 48 hrs or unknown)
- be careful of rapid correction b/c risk of ODS
- raise serum Na+ by 8-10 mEq/day with no more than 18 in first 48 hours
tx for symptomatic pts w/ hyponatremia
- 100 mL IV bolus hypertonic saline over 10 mins
- continuous IV hypertonic saline
sx of osmotic demyelination syndrome (ODS)
- dysarthria
- dysphagia
- paraparesis or quadriparesis
- behavioral disturbances
- pseudobulbar palsy
- seizures
- lethargy
- confusin
- coma
- death
preferred imaging modality for dx ODS
MRI of head
pathophysiology of ODS
too fast Na+ correction –> axonal shear damage occurs –> disruption of BBB –> demyelination
what cells are in charge of secretion and reabsorption of K+
secretion: principle cells
reabsorption: a-intercalated cells
describe potassium transport along the nephron
PCT: 65% reabsorption
TAL: 25% reabsorption
DCT: 0-120% secretion
Collecting Duct: 5% reabsorption
clinical manifestations hyperkalemia
- cardiac arrhythmias
- skeletal muscle weakness
- metabolic acidosis
- decreased ammoniagenesis and decreased ammonium excretion in kidneys
describe the electrophysiology of why potassium causes cardiac arrhythmias and neuromuscular weakness/paralysis
long term hyperkalemia –> resting membrane potential remains more positive than normal –> leads to inactivation of sodium channels –> net decrease in membrane excitability –> impaired cardiac conduction and/or neuromuscular weakness/paralysis
ECG changes at 6-7 mmol/l K+
peaked T waves
ECG changes at 7-8 mmol/l K+
- flattened P wave
- prolonged PR
- depressed ST
- peaked T wave
ECG changes at 8-9 mmol/l K+
- atrial standstill
- prolonged QRS
- peaked T wave
ECG changes at >9 mmol/l K+
sinusoid wave pattern (v fib)
what meds can cause hyperkalemia
- B2 blockers
- a1 agonists
- digoxin
- succinylcholine
- minoxidil
what extrinsic events can cause cells to release intracellular potassium leading to hyperkalemia
- burns
- trauma
- radiation
- tumor lysis syndrome
- rhabdomyolysis
how does insulin deficiency cause hyperkalemia
insulin stimulates Na/K ATPase and drive K+ intracellularly, so without it you’ll have excess K+ outside the cell
how does aldosterone affect K+ levels
low aldosterone –> hyperkalemia
high aldosterone –> ^^potassium secretion (hypokalemia)
how does GFR affect K+ levels
low GFR –> hyperkalemia
how does a ureterojejunostomy affect K+ levels
bowel reabsorbs K+ excreted in the urine –> hyperkalemia
causes of pseudohyperkalemia
- RBC hemolysis during venipuncture
- sampling clotted blood samples
- leukocytosis
how does leukocytosis cause pseudohyperkalemia
leukemia pts have fragile WBCs which can then rupture during centrifugation and release K+
how does fractional excretion of K+ determine renal or extrarenal etiology
FEK < 10%: renal
FEK > 10%: extrarenal
tx for peaked T waves caused by hyperkalemia
calcium gluconate
tx for transcellular shift of K+ causing hyperkalemia
- insuline and dextrose
- B2 agonist
- bicarbonate infusion
tx for potassium removal in pts w/ hyperkalemia
- loop diuretic or thiazide
- exchange resins
- hemodialysis
compare central and obstructive sleep apnea
central: caused by failure of respiratory center in brainstem
obstructive: upper airway obstruction resulting in decreased air flow
how does OSA lead to heart disease
OSA –> decreased PO2 and increased PCO2, increase BP, oxidative stress, inflammation, intrathoracic pressure, LV wall tension, decreased myocardial O2 delivery –> heart dz
how do diagnose OSA
polysomnography
compare apnea and hypopnea
apnea: complete obstruction for 10 seconds
hypopnea: partial obstruction for 10 seconds
compare mild, moderate, and severe OSA
mild: AHI 5-14 events/hour
moderate: AHI >15-29 events/hour
severe: AHI >30 events/hour
calculating AHI
adding all the apneas and hypopneas and dividing by total sleep time
tx OSA
- weight loss
- cpap
compare systolic and diastolic HF
systolic: EF < 40%
diastolic: EF > 50%
