Материал: 2016_Kaplan_USMLE_Step_1_Lecture_Notes_Pharmacology

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Chapter 4 λ Blood Disorder Drug List and Practice Questions

Answers

1.Answer: A. Platelet aggregation is stimulated by many compounds, including

ADP, thromboxane A2, fibrin, and serotonin. Clopidogrel, along with ticlopidine, blocks ADP receptors and prevent platelet activation. Prostacyclin (PGI2) from endothelial cells is a naturally occurring compound that inhibits platelet

aggregation by stimulating PGI2 receptors. Aspiring inhibits the synthesis of thromboxane A2. Abciximab is a monoclonal antibody targeted to the glycoprotein IIb/IIIa receptor which inhibits aggregation. Montelukast blocks leukotriene receptors and is used in asthma.

2.Answer: D. Discontinuing warfarin is appropriate during pregnancy because it is a known teratogen that causes bone dysmorphogenesis. The patient will need continued protection against thrombus formation, and heparin (or a related low molecular weight compound) is usually advised, despite the fact that the drug will require parenteral administration and can cause thrombocytopenia.

3.Answer: E. Enoxaparin is a low-molecular weight heparin. As such, it is smaller and will have a longer half-life compared to heparin. It still has a risk of causing bleeding and thrombocytopenia, but is not more rapid in onset. Heparins do not affect the synthesis of clotting factors, but rather rapidly inactivate existing factors.

4.Answer: C. Warfarin inhibits the hepatic synthesis of factors II (prothrombin), VII, IX, and X. Its onset of anticoagulation activity is slow, and its impact on individual coagulation factors depends on their half-lives. Factor VII and protein C have much shorter half-lives than prothrombin, and so the extrinsic pathway and protein C system are the first to be affected by warfarin. The intrinsic pathway continues to function for 2 to 3 days, causing a state of hypercoagulability and possible vascular thrombosis.

5.Answer: D. Alteplase is thrombolytic (or “fibrinolytic”) because it activates plasminogen, resulting in the increased formation of plasmin. Its efficacy is equivalent to that of streptokinase, but alteplase has the advantage of only activating plasminogen bound to fibrin (clot specific) but not free plasminogen. All thrombolytics can cause bleeding, which may be counteracted to some extent by administration of antifibrinolysins, such as aminocaproic acid.

6.Answer: C. Warfarin binds extensively (98%) but weakly to plasma proteins and can be displaced by other drugs (e.g., ASA, chloral hydrate, phenytoin, sulfinpyrazone, and sulfonamides), resulting in an increase in its anticoagulant

effects. Bile acid sequestrants bind acidic drugs such as warfarin, preventing their gastrointestinal absorption (↓ prothrombin time [PT]), and cimetidine, which inhibits the metabolism of warfarin, causing an increase in PT. Vitamin K restores levels of prothrombin and several other coagulation factors, but the action is slow (24 to 48 hours). Due to antiplatelet effects, even low doses of ASA may enhance bleeding in patients on warfarin.

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SECTION VIII

Endocrine

Pharmacology

Drugs Used in Diabetes

1

Learning Objectives

Use knowledge of insulins to select appropriate dosage forms in clinical situations

Describe the mechanism of action and side effects of sulfonylureas, metformin, acarbose, pioglitazone and rosiglitazone

Answer questions about agents affecting glucagon-like peptide-1

Demonstrate understanding of sodium-glucose cotransporter-2 inhibitor

INSULINS

Diabetes Mellitus

λType 1 (IDDM):

–Early onset

–Loss of pancreatic B cells → absolute dependence on insulin (diet + insulin ± oral agents)

–Ketoacidosis-prone

λType 2 (NIDDM)

–Usually adult onset

–↓ response to insulin → (diet → oral hypoglycemics ± insulin)

–Not ketoacidosis-prone

In A Nutshell

Insulin Release

Increased by: Glucose Sulfonylureas M-agonists β2-agonists

Decreased by: α2-agonists

Insulin Forms

Table VIII-1-1. Kinetics (in Hours) of Insulin Forms with

Subcutaneous Injection

Form

 

Onset

 

Peak Effect

 

Duration

Lispro*

0.3–0.5

 

1–2

 

3–4

Regular*

0.5–1

 

2–4

 

5–7

Glargine

1

 

no peak

 

≥24

*Only forms that can be used intravenously; peak action in 2 to 4 min.

Clinical Correlate

Diabetic Ketoacidosis

λSymptoms: polyuria, polydipsia, nausea, fatigue, dehydration, Kussmaul breathing, “fruity” breath

λTreatment: regular insulin IV, fluid and electrolyte replacement

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Источник: https://studfile.net/preview/16445239/