Neonatal Conjunctivitis | Ophthalmia Neonatorum | Pediatrics | 5-Minute Review. Chemical Conjunctivitis, Neisseria gonorrhea, Chlamydia trachomatis, Herpes simplex virus (HSV) ophthalmitis. What is the cause of red eye? pink eye?
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High molecular weight kininogen is a plasma protein (alpha globulin) responsible for activating the intrinsic coagulation pathway as well as producing the inflammatory mediator known as bradykinin (via plasma kallikrein).
Plasma kallikrein, in addition to high molecular weight kininogen (HMWK), is responsible for activating factor XII into XIIa.
Kallikrein-Kinin system consists of a kallikrein (plasma kallikrein or tissure kallikrein) producing a kinin (bradykinin in the plasma and kallidin in the tissue).
Angiotensin-converting enzyme (ACE) degrades bradykinin into inactive metabolites.
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Don't forget, bradykinin is a pro-inflammatory mediator that causes vasodilation and increases vessel permeability (leading to angioedema). When you use ACE inhibitors, bradykinin increases. If you like my videos, please consider leaving a tip at https://www.paypal.me/perfectionalis/
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►???Antibiotics Lectures: https://www.medicosisperfectionalis.com/products/courses/antibiotics/ ... Check out my brand new "Electrolytes" course at https://www.medicosisperfectionalis.com/products/course/electrolytes/ and use the PROMO code: ELECTROLYTES50 to get a 50% discount. Platelet plug formation is also known as primary hemostasis.
Secondary hemostasis, on the other hand, deals with converting fibrinogen into fibrin via the coagulation cascade to form a strong plug to stop bleeding.
Too little coagulation and you'll bleed. Too much coagulation and you will thrombose. Both extremes are bad.
Primary hemostasis is balanced on the dynamic harmonious antagonism between the smooth endothelium (that prefers laminar blood flow) and thrombocytes (which favor clotting and thrombosis).
Platelets are called thrombocytes "cells of thrombus".
The smooth endothelium is squamous epithelium that lines the blood and lymphatic vessels from the inside.
When platelets roll over the smooth endothelium, nothing happens.
But, once there is an injured endothelium, platelets adhere, activate and aggregate to form a temporary platelet plug (primary hemostasis).
Then, the coagulation factors are stimulated "thanks to subendothelial collagen, tissue thromboplastin and platelet factor 3), coagulation cascade ensues until fibrinogen is converted into fibrin fibers trapping the RBCs and forming a stronger thrombus (secondary hemostasis).
After that, fibrinolysis occur (thanks to tissue plasminogen activator or tPA) to destroy the clot and restore function and flow.
Hemostasis is defined as “cessation of blood bleeding”.
There are 2 types of hemostasis:
1. Primary hemostasis: formation of weak, temporary platelet plug (by platelets).
2. Secondary hemostasis: formation of stronger fibrin meshwork (by coagulation factors).
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Rheumatoid arthritis (RA) is an autoimmune, systemic, chronic inflammatory, polyarticular arthritis that involves small, peripheral joints, and is more common in females than males.
Rheumatoid arthritis can have articular as well as extraarticular manifestations.
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