if u can explain .answer this question - super99

[ArchivalUser]

. A 56 yr old male is admitted to ER with sever chest pain. His initial BP is 240/130 mmhg andHR 100/m. A beta blocker and nitroprusside infusion is started. Several hrs after admission the patient seems confused and disoriented.U noticed that nitroprusside infusio rate is higher than recommended.Supplyin whcih of the folowing elemetn would help reverse the patients condition?>
a. Oxygen
b. Phosphorus
c. Sulfur
d. Sodium
e. Potassium
f. Hydrogen

AGAIN ,I NEED EXPLANATION

[ArchivalUser]

CC
Sulphur( in the form of sodium thiosulphate)
S forms thiosulphate with Cyanide ion in the liver to form soluble thiocyanate ion which gets excreted by the kidney.
This is a question from UW, answer might have been better explained there.

[ArchivalUser]

SOME RELATED QUESTIONS
1-WHAT IS THE MECHANISM OF ACTION OF NA nitroprusside?USES?IS IT VENULAR OR ARTERIOLAR VASODILATOR OR BOTH?
AND WHY SOME SIDE EFFECT APPEAR WITH IT'S USE?
2-WHAT IS THE EFFECT OF CYANIDE TOXICITY ON MITOCHONDRIA?
3-WHAT IS THE MANGEMENT OF CYANIDE TOXICITY?


GOOOD TOPIC FOR DISCUSSION
GL

[ArchivalUser]

1) both. it acts by releasing NO (and CN)---stimulates soluble guanylate cyclase---> inc. in cGMP--->inc. in PKG----> phosphorylation (and therefore, inactivation) of MLCK---> dephos. and inactivation of myosin light chain----> relaxation

2)dizziness, flushing, tachycardia, throbbing headache, abd pain, nausea.

(i looked this up) s/s of thiocynate toxixity: Ataxia, blurred vision, delirium, dizziness, headache, loss of consciousness, nausea and vomiting, SOB, tinnitus.

cyanide toxicity: coma, absent reflexes, distant heart sounds, hypotension, feeble pulse, met. acidosis, pink color, very shallow breating, widely dilated pupils

3) prevents o2 utiliztion

4)...i'm asking a Q on this

[ArchivalUser]

the correct ans:C
Sodium thiosulfate by donating sulfur to liver rhodanase to enhance conversion of cynaide to thiocyanite ion (less toxic than cyanide and excreted by kidney)

and your questions:


1-WHAT IS THE MECHANISM OF ACTION OF NA nitroprusside?USES?IS IT VENULAR OR ARTERIOLAR VASODILATOR OR BOTH?
it can act both on ARTERIOL and VASODIL

2-WHY SOME SIDE EFFECT APPEAR WITH IT'S USE?
because of CYANIDE TOXICITY effect!
NA nitroprusside is initially metabolized to cyanide and nitric oxide.(we actually just need to nitric oxide effect for it's antihypertensive effect in treatment)
Cyanide has a high affinity to bond to Hb .....> dec distribution of o2 to tissues from Hb

3-WHAT IS THE EFFECT OF CYANIDE TOXICITY ON MITOCHONDRIA?
cyanide inhibits complex IV of ETC in mitochondia........>dec. ATP production

4-WHAT IS THE MANGEMENT OF CYANIDE TOXICITY

The United States standard cyanide antidote kit first uses a small inhaled dose of amyl nitrite, followed by intravenous sodium nitrite, followed by intravenous sodium thiosulfate.[citation needed] Alternative methods of treating cyanide intoxication are used in other countries.

[ArchivalUser]

THANKS enhancer73 AND SAMO
U ARE RIGHT

[ArchivalUser]

thanks a lot for your good question!