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Kaplan Qbank USMLE



Author7 Posts
  #1

What is the proposed mech of action of Lithium, and does your patient have hyper or hypothyroidism? What about poly- or oligouria?

  #2

Mech of action is not established; possibly related to inhibition of phosphoinositol casade(inhibition of conversion of IP2 to IP1 this results in dec IP3 production) . It also uncouples ADH and TSH receptors from adenyl cyclase that leads to dec cAMP. It causes dec release of thyroid hormones, blocks peripheral conversion of T4 to T3, goiter, polyuria, polydipsia, NDI

  #3

MOA: inhibits dephosphorylation of IP2 and IP1.
Also decrease cAMP .

it causes hypothyroidism and nephrogenic Diabetis insipidus..

  #4

produce inhibition of the phosphatidylinositol cycle, by inhibition of the dephosphorylation of IP2 to IP 1and IP1 to IP decreasing the recycling of inositol
It also produce Hypotiroidism by inhibition of 5' deiodinnse, and polyuria by coupled to ADH receptor ( nephrogenic Diabetes insipidus)

  #5

which protein kinase is involoved in here ?

1. protein kinase A
2. kinase M
3. kinase G
4. tyrosine kinase
5. kinase C

  #6

Since the MOA is still controversial that would not be the q .The q would lean more towards, indications, T.I., adverse rxns, drug-drug intereactions, [toxicity-(sodium polystyrene sulfonate)charcoal does nothing] some of the weird side effects-nephrogenic diabetes insipidus, hypothroidism, depressed t waves, leukocytosis, Seizures.
In answer to the q I saw phospholipse C mentioned in Goodman/Gillman

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  #7

kaplan says it is via protein kinase C







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