General Flashcards

1
Q

DiGeorge Syndrome is ______ deletion

A

22q11.2

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2
Q

In DiGeorge syndrome, there is an absence of ______ (organs) due to failure of development of ______.

A

Thymus and parathyroid glands; failure in development of 3rd and 4th pharyngeal pouch

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3
Q

Immunity in DiGeorge Syndrome

A

Absence of thymus, no T cells, absence of Type IV hypersensitivity

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4
Q

Appearance in DiGeorge Syndrome

A

Low set ears, hypertelorism (far apart eyes), micrognathia (small/absent jaw), cleft palate, smooth philtrum

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5
Q

Arachidonic acid comes from ______ and is cleaved using ______ enzyme

A

The phospholipid membrane; phospholipase A2

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6
Q

______ enzyme cleaves ______ to make leukotrienes, which are important in ______ (disease)

A

Lipooxygenase (LOX); arachidonic acid; asthma

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7
Q

______ enzyme acts on ______ to make prostaglandins

A

Cyclooxygenase 1 & 2; arachidonic acid

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8
Q

Prostacyclins (PGI2) are made in ______ cells from ______ with ______ (enzyme). They function to ______ and ______

A

Endothelial; arachidonic acid; COX-2; vasodilation and platelet gathering inhibitors (PGI)

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9
Q

Thromboxane (TXA) is made in ______ from ______ with enzyme ______. They function to ______.

A

Platelets; arachidonic acid; COX-1; increase platelet aggregation

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10
Q

Prostaglandins in the gut are made from ______ with enzyme ______. They function to ______ and ______

A

Arachidonic acid; COX-1; promote bicarb and mucous secretion and inhibit acid secretion

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11
Q

The COX-1 enzyme can convert arachidonic acid to ______ or ______

A

Prostaglandins in the gut; thromboxane in platelets

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12
Q

How do NSAIDS function? Side effects and why?

A

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.

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13
Q

Celecoxib functionality and adverse effects

A

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.

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14
Q

Function of Prostaglandin E

A

Pain, fEver

Also kEEps ductus arteriosis open in congenital heart malformations

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15
Q

Function of aspirin

A

NSAID. Inhibits COX (non-selectively) and decreases production of thromboxane which is necessary for platelet aggregation

Arachidonic acid uses COX-1 to make TXA

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