Week 6 Ecosinoids- Skildum Flashcards Preview

Foundations of Medicine > Week 6 Ecosinoids- Skildum > Flashcards

Flashcards in Week 6 Ecosinoids- Skildum Deck (22):
1

Why do we need Arachidonic acid or linoleate from out diet?

We can't unsaturate bonds so close to the omega carbon

2

How is A.A. stored?

As a membrane phospholipid (PIP2)

3

How is A.A. released from membrane phospholipid PIP2?

Phospholipase A2 can cleave it directly from PIP2

Phospholipase C cleaves into diacylglycerol and inisitol head group, diacylglycerol lipase cleaves into A.A. and monoacylglycerol

4

What do hydroxycortisone, prednisone and dexamethasone (cortiocsteroids) inhbit?

phospholipase A2
and cyclooygenases

5

What does A.A. produce using the cyclic pathway? What enzymes are involved?

cyclooxygenase and peroxidase makes PGH2,

PGI synthase makes prostaglandins from PGH2

TXA synthase makes throboxanes from PGH2

6

What does A.A. produce using the linear pathway? What enzymes are involved?

lipoxygenase makes 5-HPETE to 5-HETE which is converted to epoxide and reduced to make Leukotrienes (released by mast cells, and causes bronchoconstriction)

7

What is a sign of oxidative stress?

isoprostanes produced from membrane lipids under oxidative stress

8

what do monetlukast and zafirlukast do?

block leukotriene receptor, long term treatment of asthma

9

What does PGI2 do?

secreted by vascular endothelium
stops clotting, prevents platelet aggregation, promotes relaxation of smooth muscle and vasodialation (normal physiology)

10

What does TXA2 do?

promotes clotting
secreted by platelets
paracrine/ autocrine
supports platelet aggregation

11

Normal physiology ecosinoids?

PGI2, PGE2, PGD2

12

How do you make an anandamide?

add A.A. to ethanolamine head group

13

Where does Anadamides bind and what do they do?

Binds to CBI, CB2, TRPVI
They stop overporduction of cytokines, reduce inflammatory response

14

Where does PLC and PLD cleave in respect to the phosphate?

PLD - phosphate stays with glycerol

PLC- phosphate stays with head group

15

COX1 and COX2

COX1 makes prostaglandins involved in normal physiology (always on) (like stimulating stomach to secrete mucin to protect it from acidity)

COX2 on in response to cell damage and infection. Stimulates inflammatory prostaglandins (inflammation, pain, fever)

16

Aspirin, Naproxen, Acetaminopen, ibuprofen

non-specific inhibitors of COX1 and COX2

Aspirin- suicide inhibitory, covalently bonds COX1 and COX2, decreases Vmax

Others are competitive inhibitors

17

alpha-lactalbumin

upregulated after giving birth, changes specificity of galactosyltransferase to attach galactose to glucose to make lactose

18

Jaundice

RBC broken down, need to get rid of heme

heme -> biliverdin(green) --> bilirubin (yellow)

bilirubin is not very soluble so transported in blood by albumin

in liver, bilirubin is glycosylated with glucuronates

it is then more soluble and can be excreted in bile or urine

*if heme degredation exceeds capacity to excrete it, bilirubin will diffuse out to blood and into tissues making you yellow

19

Mannose 6- phosphate

tag put on hydrolytic proteins in golgi to be sent to lysosome, in lysosome lower pH dissociates enzyme from its receptor

20

lysosomal storage disease

defects in enzymes that degrade glycolipids (can only be digested in lysosome)

21

Tay-Sachs disease

early onset
retardation
defective gene in alphas subunit of hexosaminidase (only A defective)
autosomal recessive
most die by age three

22

Sandhoff disease

similar to tay-sachs, earlier onset, defect in B subunit of hexosaminidase (both A and B defective)