3 - therapeutics for gordons syndrome Flashcards
examples of thiazide diuretics
chlorothiazide (diuril)
chlorothalidone
hydrochlorothiazide (microzide)
outcome of thiazide diuretics
increase renal excretion of Na+, K+ and H+
decrease renal excretion of Ca2+
why is it important to excrete excess H+
causes metabolic acidosis
mechanism of thiazide diuretics
compete for Cl- binding site on Na+Cl- co-transporter in DCT
therefore inhibit transport of ions and decrease intracellular Na+
increased delivery of Na+ to collecting duct
effect of decreased intracellular Na+
causes decreased intracellula Ca2+ due to Na/Ca2+ exchange on basolateral membrane
effect of increased Na+ in collecting duct
stimulates efflux of K+ leading to hypokalemia
surgical therapeutic options
Correct physical abnormalities e.g. clubfoot, camptodactyly
Potential reconstruction of cleft palate
physical therapy
o Increase range of motion in hands, arms and legs
o Braces/splints used
lifestyle therapy
change diet to have less salt
e.g. DASH diet
increase potassium and calcium in diet
general function of thiazides
NCC antagonist
competitive inhibitors
other drug therapies than thiazides
- Acetazolamides
- Furosemide
- Potassium sparing diuretics (Amiloride/Spironalide)
why is systolic blood pressure more important to look at
it is a better indicator of cardiovascular disease
what conditions are commonly presented with gordons hypertension syndrome
metabolic acidosis
hyperkalemia
Suppressed plasma renin activity and hyperchloremia also common
what causes hyperkalemia and metabolic acidosis
impaired K+ excretion
decreased urinary H+ excretion
what alternative conditions could NO be used to treat
tendinopathy –> supplementary NO could enhance tendon wound healing
Hypoxic respiratory failure in neonates-
AHF (acute hepatic failure)
