Lesson 3, Topic 5

Angina – Chest Pain – Part 5

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A 69 year old male presents to the emergency room complaining of increasingly severe chest pain for the past 2 hours. He has a 45 pack year history of cigarette smoking. Medications include thiazide, captopril and atorvastatin.


    • Describe the patient.
    • What is the chief complaint and differential diagnosis?
    • Describe the blood supply of the heart.
      • Normal structure and local regulation
      • Adaptation
      • Ischemia (supply vs demand)
      • Atherosclerosis
        • Pathogenesis
    • Describe types of plaque
      • Stable plaque (& CPC)
      • Unstable plaque (& CPC)
    • Describe the clinical-pathologic correlation:
      • What next?
      • EKG results:
        • What is the interpretation and next action? (3)
    • Describe the natural history for an acute STEMI (CPC)
    • How should the patient be treated?


QU Angina.chest pain 8.17.20



- Acute inflammation

CPC: Local effects in acute inflammation

Clinical pathologic correlation: systemic effects

-          When an acute infection becomes severe enough, the local production of cytokines and hormones gets into the systemic circulation and causes generalized responses, typically called sepsis. Sepsis is a systemic inflammatory response syndrome (SIRS) due to infection.

-          IL-1 and fever:

·       Fever is an increase in core temperature due to the hypothalamus elevating the body’s set point. Endothelial cell overlying the hypothalamic temperature centers have an IL-1 receptor. When stimulated by a cytokine like IL-1, called a pyrogen, the endothelial cells release PGE2 that crosses the blood brain barrier and stimulates the hypothalamic temperature regulatory neurons.

·       The commonest therapy for fever is a NSAID. The Cox inhibition decreases PGEproduction.

-          IL-6 and the acute phase reactants (APRs):

·       Hepatocytes have an IL-6 receptor that triggers the production of over 30 proteins as part of a systemic response to inflammation. An APR is any protein or cell that increases or decreases more than 20% in inflammation. APRs are used in clinical medicine to assess the degree of inflammation. Examples include C reactive protein (CRP) and erythrocyte sedimentation rate (ESR) which is determined mostly by fibrinogen.

-          TNF-α and shock:

·       High levels of cytokines can cause dysregulation of endothelial cells. Endothelial cells are key regulators of peripheral resistance (TPR) and their dysfunction can lead to a loss of TPR and blood pressure. Shock is defined as blood pressure is < 90 mmHg systolic pressure and leads to ineffective perfusion. Septic shock is a type of distributive shock.

Bradykinin/histamine and anaphylaxis:


-          Massive mast cell degranulation, seen with IgE allergic reactions such as peanut or bee sting allergies can lead to shock from vasodilation and fluid extravasation. It is a type of distributive shock as it is due to vasomotor collapse.


Natural history of STEMI

General pathology: gross patterns of necrosis