Acute Coronary Syndrome (ACS) Definitions - Stable Angina, Unstable Angina, NSTEMI, STEMI
1 STABLE ANGINA - Angina pain develops when there is increased demand in the setting of a stable atherosclerotic
plaque. The vessel is unable to dilate enough to allow adequate blood flow to meet the myocardial
2 UNSTABLE ANGINA
- The plaque ruptures and a thrombus forms around the ruptured plaque, causing partial occlusion of the
vessel. Angina pain occurs at rest or progresses rapidly over a short period of time.
3 NSTEMI
- During an NSTEMI, the plaque rupture and thrombus formation causes partial occlusion to the vessel
that results in injury and infarct to the subendocardial myocardium.
4 STEMI
- A STEMI is characterized by complete occlusion the blood vessel lumen, resulting in transmural injury and infarct to the myocardium, which is reflected by ECG changes and a rise in troponins.
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Allergic Rhinitis: Pathogenesis and clinical findings
1. Allergy Sensitization -> Antigen Exposure -> APC (macrophages, HLA class II) process antigen into peptides -> APC present peptides to Helper T cells -> Helper T cells release Interleukins (IL-4 and IL-3) -> IL-4 and IL-3 stimulate B-cell transformation to lgE producing Plasma Cells -> lgE Abs coat mast cells within nasal mucosa and basophils in the plasma
2. Primary Reaction Phase -> (initiated within 5 minutes of antigen exposure and maximum effect by 15 minutes) Antigen Exposure -> Antigen binds to lgE on mast cells and basophils -> Mast cells & basophils release mediators: preformed (histamine, serotonin, protease) & newly-generated (leukotrienes, prostaglandins, TNF-a)
3. Secondary Reaction Phase (occurs 4-6 hours after the primary reaction phase) Presence of mediators -> Recruitment of inflammatory cells (neutrophils, eosinophils, macrophages, lymphocytes), bone marrow proliferation of eosinophils -> Second phase of mediators released
• Rhinorrhea
• Sneezing and itching
• Congestion and pressure
• Tissue edema
#Allergic #Rhinitis #Rhinorrhea #pathophysiology