General Flashcards
DiGeorge Syndrome is ______ deletion
22q11.2
In DiGeorge syndrome, there is an absence of ______ (organs) due to failure of development of ______.
Thymus and parathyroid glands; failure in development of 3rd and 4th pharyngeal pouch
Immunity in DiGeorge Syndrome
Absence of thymus, no T cells, absence of Type IV hypersensitivity
Appearance in DiGeorge Syndrome
Low set ears, hypertelorism (far apart eyes), micrognathia (small/absent jaw), cleft palate, smooth philtrum
Arachidonic acid comes from ______ and is cleaved using ______ enzyme
The phospholipid membrane; phospholipase A2
______ enzyme cleaves ______ to make leukotrienes, which are important in ______ (disease)
Lipooxygenase (LOX); arachidonic acid; asthma
______ enzyme acts on ______ to make prostaglandins
Cyclooxygenase 1 & 2; arachidonic acid
Prostacyclins (PGI2) are made in ______ cells from ______ with ______ (enzyme). They function to ______ and ______
Endothelial; arachidonic acid; COX-2; vasodilation and platelet gathering inhibitors (PGI)
Thromboxane (TXA) is made in ______ from ______ with enzyme ______. They function to ______.
Platelets; arachidonic acid; COX-1; increase platelet aggregation
Prostaglandins in the gut are made from ______ with enzyme ______. They function to ______ and ______
Arachidonic acid; COX-1; promote bicarb and mucous secretion and inhibit acid secretion
The COX-1 enzyme can convert arachidonic acid to ______ or ______
Prostaglandins in the gut; thromboxane in platelets
How do NSAIDS function? Side effects and why?
NSAIDS inhibit COX (non-selectively) and decrease synthesis of prostaglandins from arachidonic acid. Consequently, COX-1 in the gut gets inhibited which makes prostaglandins to regulate the acidity in the stomach. Increase risk of ulcers.
Celecoxib functionality and adverse effects
Selective COX-2 inhibitor (prostaglandins that produce pain) and doesn’t affect COX-1 (gut prostaglandins). But COX-2 also makes prostacyclins in endothelial cells which are responsible for decreasing platelet aggregation. The non-inhibited COX-1 in platelets can make Thromboxane. This will promote thrombosis.
Function of Prostaglandin E
Pain, fEver
Also kEEps ductus arteriosis open in congenital heart malformations
Function of aspirin
NSAID. Inhibits COX (non-selectively) and decreases production of thromboxane which is necessary for platelet aggregation
Arachidonic acid uses COX-1 to make TXA