Sapna Gupta, Associate Professor
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CH 251, Respiratory DrugsSkeletal Muscle Relaxants, Antihypertensive Drugs, Angina Pectoris, Cardiac Arrhythmias, Congestive Heart Failure, Coagulation Disorders and Hyperlipidia, Endocrine Pharmacology, Male and Female Hormones, Thyroid and Parathyroid, Diabetes

Final Exam Objectives


COAGULATION DISORDERS AND HYPERLIPIDIA

Coagulation prevents excess blood loss or hemorrhage.

Excessive clotting, thrombogenesis, would lead to arterial blockage.

Hyperlipidia: chronic and excessive increase in plasma lipids.  Causes cholesterol deposition in arterial walls (arteriosclerosis)

COAGULATION DISORDERS

Clot formation:

            Intrinsic Factors                                                 Extrinsic Factors

(factors XII and XI)                                    tissue factor VII and thromboplastin 

     needs vit K                                

                                            form factor Xa

with Ca2+ and platelets Xa converts Prothrombin to Thrombin.

Thrombin converts Fribrinogen to Fibrin which results in clot formation.

 Clot Breakdown:

Tissue Plasminogen causes Profibrinolysin to form Fibrinolysin which breaks the clot.

 Overclotting: usually originates in the leg because of sluggish blood transport.  Also can occur in patients who have been bedridden for a while (post surgery etc.) 

Treatment Mechanism Used for Adverse effects (for all drugs)
Anticoagulants

Heparin

Warfarin

Inhibit synthesis and function of clotting factors Given to patients who have been inactive for a long time.

Heparin is given IV (it’s a large sugar molecule)

Warfarin can be given orally hence may take longer

Hemorrhage

Blood work should be done constantly

Antithrombotics

Aspirin

Inhibit function of platelets.  Usually given for arterial occulation.(eg aspirin inhibits synthesis of thromboxanes which prevents platelets from working)  
Thrombolytics

Streptokinase

Urokinase

Facilitate clot breakdown by making more fibrinolysin    

Clotting deficiencies

Disease Cause Treatment Adverse effects
Hemophilia Hereditary disease

Lack of clotting factors:

Hemophilia A: factor VIII and

Hemophilia B: factor IX

Replacing factors from human blood Infections from blood
Deficiency of Vit K Deficiency from diet or lack of intestinal bacteria Administration of vit K  
Antifibrinolytics Excessive bleeding after surgery because of overactive fibrinolytic activity Antifibrinolytics eg aminocaproic acid  

Rehabilitation Concerns:          

  1. watch for open wounds

  2. avoid rigorous exercises

  3. keep aspirin handy

HYPERLIPIDIA

High concentration of lipids in blood.

Cause is usually poor diet and lifestyle.  Sometimes can be genetic.

HDL: high density lipoproteins (good)

LDL: low density lipoproteins  (bad)

Treatment Mechanism Adverse effects for all
HMG-CoA inhibitors eg Zocor, Mevacor (3-hydroxy-3-methylglutarylcoenzymeA) reductase catalyzes cholesterol formation.  The HMG-CoA inhibitors prevent this enzyme from working Nausea, diarrhea are common but usually well tolerated.
Fibric acids eg Lopid These lower triglyceride levels by increasing breakdown of LDL  
Others eg Niacin decreases LDL synthesis  

 Rehabilitation Concerns:          

Help out with a diet plan for hyperlipidia

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