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Cardiac Cascade, JR Assessment, Caused By, Pain Inhibitors, Angiotensin…
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JR Assessment
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Malaise and fatigue
Inhibits DHEA conversion: spironolactone, antifungles (azole), increased sugars, apegenin
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Swelling in limbs
Inflammation Cascade
Allergic Response
Stimulus releases from cells due to chronic illness or irritative trigger. Stems from cell damage or chronic disease
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Caused By
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Mechanical stretch
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A delta fibers (myelinated, localized sharp pain)
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Interleukins (IL-1,6,7,17)
Pain Inhibitors
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GABA, Gamma-aminobutyric acid
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Beta-blockers, effect blood pressure and heart rate (Beta I focuses on heart, Beta II more the lungs)
Lungs 
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Liver
Angiotensionogen
Angiotensin I
Angiotensin II
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Increases constriction
Arterial Vessels
Increases tubular excretion of potassium (K), and increased reabsorption of Sodium (Na), and Chloride (Cl)...and reabsorption of water.
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Amiodarone, blocks potassium channels and delays depolarization of myocytes
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Effects on Sleep
disruption of sleep due to pain can stop the bodies normal cyclic process of restoring and maintaining normal function.
Effects on Mood
Serotonin is thought to have a relationship to mood and depression SSRI may help over weeks to reduce reuptake. However, chronic pain can also be depressing and considered in similar diagnosis
gabapentin
Interacts with calcium channels on presynaptic neurons in the CNS to reduce action potential in post synaptic neuron.
NSAIDS
reduces COX-2 if selective or a mix of COX-1 and COX-2 this reduces formation of PGE which increase action potential of 1st order neuron.
NSAIDS
reduces COX-2 if selective or a mix of COX-1 and COX-2 this reduces formation of PGE which increase action potential of 1st order neuron.
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alpha 2 agonists
reduce release of Norepinephrine and epinephrine by interacting with catecholamine receptors blocking CNS neurotransmitter release in modulation phase and have rebound effects.
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Stroke Volume (SV) x Heart Rate (HR)= Cardiac Output (CO)
Cardiac Output (CO) x Peripheral Vascular Resistance (PVR) = Blood Pressure (BP)
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Patel, S., Rauf, A., Khan, H., & Abu-Izneid, T. (2017). Renin-angiotensin-aldosterone (RAAS): The ubiquitous system for homeostasis and pathologies. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 94, 317–325. https://doi.org/10.1016/j.biopha.2017.07.091
Fountain JH, Lappin SL. Physiology, Renin Angiotensin System. [Updated 2022 Jun 18]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470410/
Generally Angiotensin I attaches to AT1 receptor sites and Angiotensin II attaches to AT2 receptor sites
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ReferencesMegha, K. B., Joseph, X., Akhil, V., & Mohanan, P. V. (2021). Cascade of immune mechanism and consequences of inflammatory disorders. Phytomedicine : international journal of phytotherapy and phytopharmacology, 91, 153712. https://doi.org/10.1016/j.phymed.2021.153712Osmosis (2020). Inflammation- causes symptoms, diagnosis, treatment, and pathology. https://www.bing.com/videos/search?q=Inflammatory+Response+Cartoon&&view=detail&mid=B8CD83D3B9D1BA7CEF4FB8CD83D3B9D1BA7CEF4F&&FORM=VRDGAR&ru=%2Fvideos%2Fsearch%3Fq%3DInflammatory%2BResponse%2BCartoon%26FORM%3DHDRSC4McCance, K. L. & Huether, S. E., (2019). Pathophysiology: the biologic basis for disease in adults and children. (8th ED.) Elsevier. ISBN 978-0-323-58347-3
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