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30:718:409 Study Guide - Midterm Guide: Dobutamine, Cardiac Muscle, Cyclic Adenosine Monophosphate

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peachtiger667
27 Dec 2018
School
Rutgers University
Department
Pharmacology and Toxicology
Course
30:718:409
Professor
Dr. Lavoie and Dr. Chakalamanil

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Document Summary

Inotropes used for the treatment of congestive heart failure. Increase of camp in vascular sm and in myocardium. Block degradation of camp to amp: pde inhibs. Pah: disease state, an elevation of bp in the pulmonary artery causing heart strain, progressive, life threatening, types of pah. Idiopathic (ipah): familial (fpah), associated (apah): an unknown cause. Abnormal narrowing in the pulmonary veins and/or capillaries and may or may not include arteries. These associated conditions include: pulmonary veno-occlusive disease (pvod, pulmonary capillary hemangiomatosis, persistent pulmonary hypertension of the newborn, epidemiology, women > men. Ipah most commonly occurs in women in their 30s and men in their 40s. 2x higher for women: 10x as many people are diagnosed with apah as with ipah or fpah, because the conditions that can lead to apah are relatively more common, cause. Increased blood pressure in the pulmonary arteries occurs when the small arteries of the lungs become abnormally narrow.

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Related Questions

Your company, DrugsRUs, has developed a generic angiotensin-converting-enzyme inhibitor, Vasotec, as a pharmaceutical drug used primarily for the treatment of hypertension and congestive heart failure. You are leading the regulatory strategy team and have been asked to describe the path to approval comparing introduction in the US versus Brasil.

Please discuss the following:

(1) Which agency or agencies will be responsible for approving/reviewing your Vastec drug: (a) before commercial introduction, and (b) after approval for commercialization/sale within the US., and

(2) Compare known issues your company will need to consider to market your generic drug is Brasil.


The lab you work in has discovered a previously unidentified extracellular signal molecule called QGF. You add purified QGF to different types of cells to determine its effect on these cells. When you add QGF to heart muscle cells, you observe an increase in cell contraction. When you add it to fibroblasts, they undergo cell division. When you add it to nerve cells, they die. When you add it to glial cells, you do not see any effect on cell division or survival.

A) How can the same signaling molecule cause such diverse affects? Why do the glial cells not respond at all?

B) Using effectors and second messengers discussed in class, devise a signaling pathway that QGF could use to increase contractions in in the heart. (Hint: Ca2+ is very important for muscle contraction)

C) Using effectors and second messengers discussed in class, devise a signaling pathway that QGF could use to lead to apoptosis of nerve cells. Give possible proteins or genes that need to be activated or inactivated.

D) Using effectors and second messengers discussed in class, devise a signaling pathway that QGF could use to induce cell division in the fibroblast cells? Give possible proteins or genes that need to be activated or inactivated.