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BLOCK 2 Flashcards

1
Q

Eicosanoids include

A
  • prostaglandins
  • thromboxanes
  • leukotrienes
  • lipoxins
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2
Q

Range of responses by Eicosanoids and what are they mediated by

A

Inflammatory response & hypersensitivity

Mediated by G protein coupled receptors

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3
Q

Arachidonic acid is derived from?
Incorporated into?
Released by?

A

Arachidonic acid is derived by elongation & desaturation of LINOLEIC ACID

  • incorporated into phosphatidylinositol
  • released by phospholipase A2
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4
Q

Most prostaglandins referred to as:

A

Series 2 - due to 2 C-C double bonds

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5
Q

Synthesized by all mammalian cells — EXCEPT erythrocytes

A

Eicosanoids

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6
Q

When do Eicosanoids cause profound physiologic effects?

A

Only at very dilute concentrations

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7
Q

First step of cyclooxygenase pathway

A

Free arachidonic acid ———> PGH2 —> Eicosanoids

By prostaglandin -endoperoxide synthase
-two activities: COX and peroxidase

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8
Q

COX 1 expressed where? Constitutive or inducible

A

Gastric mucosa, kidney, platelets, and vascular endothelial cells

Constitutive - produced in constant amounts without regard to demand

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9
Q

COX 2 expressed where? Trigger induction of what?

A

Expressed in macrophages and monocytes —> inflammation

Trigger -> platelet activating factor (PAF) and interleukin-1 (IL-1)

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10
Q

Overexpression of COX 2 can lead to?

A

Colorectal cancer

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11
Q

Cyclooxygenase pathway

A

PLA2 hydrolyzes arachidonic acid

- COX 1 and 2 (PGH synthase) converts arachidonic acid to PGH2

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12
Q

What synthesizes PGH2 to PGI2

A

Prostacyclin synthase

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13
Q

What synthesizes PGH2 to TXA2

A

Thromboxane A synthase I

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14
Q

Cyclooxygenase pathway occurs where

A

ER

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15
Q

Mechanism of aspirin

A

Irreversibly inhibits cyclooxygenase by acetylation

—> decreases synthesis of TXA2 (thromboxanes) —> decrease clotting

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16
Q

Where should aspirin be avoided and why?

Exception?

A

Avoid in children - risk of Reye syndrome

Except those with Kawasaki disease

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17
Q

Toxic doses of aspirin leads to

A

Respiratory alkalosis, transitioning to mixed with metabolic acidosis

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18
Q

Mechanism of celecoxib

A

Reversibly and selectively inhibits COX 2 (“Selecoxib”)

- spares COX 1 and platelet function

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19
Q

Mechanism of acetaminophen (paracetamol)

A

Reversibly inhibits COX

  • NOT anti-inflammatory
  • used to avoid Reye syndrome
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20
Q

PGE2 significance

A

Labor induction, bronchodilator

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21
Q

PGF2 alpha significance

A

Medical termination of pregnancy

Stimulate uterine contractions

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22
Q

PGI2 significance

A

Inhibits platelet aggregation and promotes vasodilation

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23
Q

TXA2 significance

A

Vasoconstriction and aggregation of platelets

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24
Q

Which two prostanoids are antagonists

A

PGI2 and TXA2

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25
Lipooxygenase pathway
Bradykinin rec. (BDKR2) coupled to BOTH Gi and Gq —> Gq - PIP2 cleaves PLC to DAG and IP3 -DAG binds PKC —> increased calcium leads to activation of PKC - PKC will activate PLA2 PLA2 will hydrolyze arachidonic acid Arachidonic acid converts to 5-HPETE by 5LOX, then to LTA4 (leukotrienes) - inflammatory response
26
15-LOX leads to production of?
Lipoxins (ain’t-inflammatory)
27
What kind of relationship do lipoxins and leukotrienes have?
Antagonists | -inflammatory vs anti-inflammatory
28
12 LOX leads to production of?
Platelets
29
How is synthesis of leukotrienes affected by NSAIDs
LOL ITS NOT .. JOKES ON YOU AHAHA!
30
Clinical significance of LTC,D, and E4s
-anaphylaxis —> increased asthmatic response - functions: - smooth muscle contraction - bronchoconstriction - vasoconstriction
31
Clinical significance of LTB4
Chemotactic factor and activator of leukocytes | -release lysosomal enzymes
32
Significance of LXA4 & LXB4
Aortic and pulmonary relaxation
33
Significance of lipoxins and epi-LXs
Inhibit polymorphonuclear leukocyte chemotaxis
34
Significance of LXs (lipoxins)
Stimulate phagocytosis
35
Significance of blocking expression of IL-8 gene
Stimulates neutrophil migration
36
Significance of TNF alpha
Inhibit release of tumor necrosis
37
Significance of TGF beta
Stimulation of transforming growth factor beta
38
Significance of regulation of the actions of histamine
Reduction in swelling due to edema
39
LXA4 significance alone
Production of prostacyclin (PGI2) and nitric oxide (NO)
40
What quantities is cholesterol synthesized and by what tissues? From what?
Cholesterol is synthesized in larger quantities by almost all tissues from acetyl CoA
41
What form is cholesterol present in
Esterified form (hydrophobic)
42
Sterol poorly absorbed by humans
Beta-sitosterol
43
Cholesterol enters liver through...
1. Diet 2. Extra hepatic cholesterol synthesis 3. De novo synthesis by liver
44
Cholesterol leaves liver through...
1. Unmodified cholesterol in bile 2. As bile salts 3. Plasma lipoproteins
45
Where does synthesis of cholesterol happen?
Cytoplasm
46
Carbon for cholesterol synthesis provided by? | Reducing equivalents provided by?
Acetyl CoA | NADPH
47
Cholesterol synthesis driven by?
High energy thioester
48
Main steps of cholesterol synthesis
1. Synthesis of HMG-CoA and mevalonate from acetyl CoA 2. Synthesis of active isoprenoid units 3. Synthesis of squalene from isoprenoid units 4. Synthesis of lanosterol from squalene 5. Synthesis of cholesterol from lanosterol
49
Rate limiting step of cholesterol synthesis What is required?
Synthesis of HMG-CoA and mevalonate from acetyl -CoA - NADPH is required
50
Which step in cholesterol synthesis requires ATP
Synthesis of active isoprenoid units
51
Example this step of cholesterol synthesis: Synthesis of squalene from isoprenoid units
Isoprene —> geranyl —> farnesyl —> squalene Isoprenyl group added to cysteine residue - NADPH is used
52
What does the synthesis of lanosterol from squalene require?
NADPH and oxygen
53
Regiulation of HMG CoA reductase
1. Cholesterol content - cholesterol usually binds a transcription factor that normally stimulates transcription of HMG CoA reductase 2. Insulin stimulates 3. Cholesterol regulates degradation 4. Covalent modification
54
Explain covalent modification of HMG CoA reductase
High levels of AMP —> activation of AMP-dependent protein kinase —> inhibits HMG CoA reductase by phosphorylation NOT cAMP
55
When does hepatic cholesterol synthesis peak?
6 hours after dark
56
Statin drugs role in inhibition of cholesterol synthesis Used to treat?
Structural analog of HMG CoA -reversible, competitive inhibition Block formation of mevalonate Treatment for hypercholesterolemia patients
57
Bile acid resins role in inhibition of cholesterol synthesis Examples?
Decrease LDLs, prevent reabsorption of bile acids Cholestryramine, colestipol, colesevelam
58
Ezetimibe role in inhibition of cholesterol synthesis
Prevents cholesterol absorption
59
Phytosterols role in inhibition of cholesterol synthesis
Blockage of cholesterol incorporation into mixed micelles
60
Synthesis of bile acids
1. Introduction of hydroxyl group to cholesterol by 7 alpha hydroxylase - occurs on cyto P450 - uses NADPH 2. Conjugation of bile acids to glycine or taurine
61
Primary bile acids made...
Cholic acid 50% & Chenodeoxycholic acid (30%)
62
Effect of conjugation of bile acids to glycine or taurine
Lowers pKa, making more soluble
63
Secondary bile acids made... And where?
Deoxycholic acid (15%) & lithocholic acid (5%) In gut by bacterial action
64
Degradation of cholesterol... intact sterol ring eliminated by:
1. Bile acids —> feces 2. Secretion of cholesterol in bile —> intestines for elimination 3. Bacteria modifies cholesterol to coprostanol and cholestanol
65
Active form of vitamin D
1, 25- dihydroxycholecalciferol (calcitriol)
66
Sources of vitamin D
Fatty fish and fortified milk Dietary only necessary if sunlight exposure is limited
67
Significance of ergocalciferol
Found in diet contains extra methyl and double bond that do NOT affect vitamin D
68
Formation of vitamin D requires...
Requires participation of skin, liver, and kidney
69
Regulation of vitamin D
PTH stimulates 1-hydroxylase (in kidney)
70
Acts upon cell that synthesizes it
Autocrine
71
Diffuses to neighboring cells / NO transport via blood
Paracrine
72
Transport via blood plasma
Endocrine
73
Characteristics of steroid hormones
- lipophilic (high affinity for lipids) - hydrophobic - from cholesterol
74
Which steroid hormone classes are from cholesterol
1. Glucocorticoids 2. Mineralocorticoids 3. Sex hormones
75
Name a hormone that is NOT a steroid hormone but has the same cellular mechanism
Thyroid hormone
76
Synthesis of which steroid hormones happens in the adrenal cortex
Cortisol, aldosterone, and androgens
77
Synthesis of which steroid hormones occurs in ovaries and placenta
Estrogens and progesterone
78
Synthesis of which steroid hormone occurs in the testes
Testosterone
79
Side chain cleavage in steroid synthesis RLS
Translocation of cholesterol via StAR (steroidogenic acute regulator
80
Cytochrome P450 acts as an electron carrier, requires which proteins help?
Adrenodoxin and adrenodoxin reductase
81
Precursor for all other steroid hormones
Pregnenolone
82
Cells that secrete testosterone in presence of LH Effect of temperature?
Leydig cells -unaffected by temperature
83
Cells that secrete estrogen in presence of FSH
Theca interna cells
84
17 alpha hydroxylase leads to production of
Cortisol and testosterone
85
5 alpha reductase leads to production of?
Dihydrotestosterone (DHT)
86
Aromatase leads to production of
Estradiol
87
21 hydroxylase leads to production of
Cortisol and aldosterone
88
11 beta hydroxylase leads to production of
Aldosterone and cortisol
89
Which two enzyme deficiencies lead to increase in BP
17 alpha hydroxylase & 11 beta hydroxylase
90
Which enzyme deficiency leads to increase in K+ levels
21 hydroxylase
91
Starts with 1 —>
Hypertension
92
Ends with 1 —>
Virilization
93
Presentation of 17 alpha hydroxylase
XY: ambiguous genitalia, undescended testes XX: lacks secondary sexual development
94
Virilization occurs in which enzyme deficiencies
21 and 11 beta hydroxylase
95
Skin hyperpigmentation is due to?
Increase in MSH production
96
Cause of bilateral adrenal gland enlargement
Increase ACTH stimulation because decrease cortisol
97
Both ovarian and testicular tissue is present
Hermaphroditism
98
Gonadal tissue of only one sex, but external genitalia of opposite sex
Pseudohermaphroditism

MCB 2 (1 decks)

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