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Kirstys Flashcards > BMP: Steriodas > Flashcards

BMP: Steriodas Flashcards

1
Q

Facts about steriods

A
  1. Naturally occuring in both plants and animals
  2. Carried via the bloodstream, normally protein bound
  3. Easily passes thorugh membrane and can enter the nucleus
  4. Part of the lipid family
  5. Act as hormones (chemical messengers). Also give rigidy/integrity to the cell membrane. Also act as surfactants.
  6. Highly specific and selective
  7. Synthetic steriods have been developed, most are steriods, but some are non-steriod molecules can interact with steriod receptors because of similarity of shape
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2
Q

What are steriods derivaed from?

A

Steriods are derived from triterpenoids, which in turn is derived from their biosynthetic precursor squalene.

Squalene is made from 2 units of farnesyl pyrophosphate, which is made from 3x isoprene

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3
Q

Discuss the steps in forming cholseterol

A
  1. Squalene: 3x isoprene —> 2x farnesyl pyrophosphates — (NADH)–> Squalene –(O2, NADPH epoxidase) —> Squalene oxide —(backbone reaarnagement)–> to stable teritary carbocation
  2. Squalene to lanosterol: Teriary cation under goes steriod backbone reaarnagement: 4 consecutive 1,2-shifts and elimination
  3. Lanosterol to cholesterol: Introduction of an alkene and recuction of an alkene and removal of some methyl groups
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4
Q

Diagram of Squalene to lanosterol

A
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5
Q

Diagram of Latosterol to Cholesterol

A
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6
Q

Discuss stablility of different carbocations

A
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7
Q

What happens during anti-migration

A

(S to L)

Each group that migrates is onds are axial and os anti-periplanar to the one before

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8
Q

Describe the structure of cholesterol

A
  • 4 fused rings: very stable
    • 1x5-membered ring (cyclopentane)
    • 3x6-membered ring (cyclohexane)
  • All rings junctions trans exp A&B junction which may be cis or trans
    • If cis - axial OH
    • If trans - equitorial OH
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9
Q

Which bonds are a or B

A

Up is B (wedged). Down is a (dashed)

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10
Q

What types of steriods are there?

A
  • Sterol
  • Cardioactive glycosides
  • Saponins
  • Bile Acids
  • Hormones:
    • Sex hormones
    • Corticosteriods/ andrenocorticol
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11
Q

Discuss the properties of sterols

A
  • Steriod and alcohol
  • Carried in the blood by lipoprotiens
  • Ingested by also synthesised in the body
  • Found in cell membranes of all tissues
  • Biosynthetic precurosor of all steriod hormones
  • may cause gallstone disease and atherosclerosis (hardening of the arteieres)
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12
Q

Discuss the properties of saponins

A
  • Spiroketal at C-22
  • Of plant origins
  • Sugar residuses at 3B-OH
  • Acts as a surfactant/ soaps
  • May cause haemlysis - lysing of RBCs
  • Mostly harmless
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13
Q

Discuss cardioactive glycosides

A
  • Originates from plants
  • Cis fused A/B and C/D rings
  • 14B-OH
  • Unsaturated at C-17B
  • 1-4 sugar residuses on 3B-OH
  • Used as arrow posisioing and heart drugs
  • Treatment for arrythmias, espcially aterial fibrillation
  • Sugar units incr solubility and binding to heart muscle
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14
Q

Discuss properties of bile acids

A
  • •C24 cholane skeleton
  • •cis-fused A/B ring
  • •C5 carboxylic acid side chain
  • •3a & 7a OH’s
  • Occur in salt form in bile
  • Secreted into gut to emulsify fats
  • Act as detergents
  • Excreted as body’s main method for removing
  • excess cholesterol
  • Inability to do so causes atherosclerosis and gall
  • stones which contain 70% cholesterol
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15
Q

Where are hormones syntheised from and what are the main ones?

A

From specific glands. Control various body processed

sex and adrenocortical

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16
Q

Disscus properties of oestrogen

A
  • •C18 estrane skeleton
  • •Aromatic Ring A
  • •Absence of Me at C-10
  • •No side chain
  • •Ketone or hydroxyl at C-17
  • •Produced in ovaries
  • •Regulates ovulation and female characteristics
  • •Found in low levels in the testes
  • •Biosynthesised from testosterone
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17
Q

Discuss the properties of progesterone

A
  • C21 pregnane skeleton
  • D4 -3-keto group (conjugated)
  • Produced by the corpus luteum, and then by the placenta
  • Prepares uterus for pregnancy
  • Intermediate in biosynthesis of corticosteroids
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18
Q

Describe properties of tesosterone

A
  • •C19 androstane skeleton
  • •No side chain
  • • D4 -3-keto group (conjugated)
  • •17b-OH
  • •Secreted by the testes
  • •Responsible for male sex characteristics
  • •Secondary effect is anabolic activity:
    • –stimulates growth for bone & muscle
    • –promotes storage of protein
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19
Q

Where are alrenocorticoids/ corticosteriods synthesised?

What categories is therE?

A
  • Adrenal glands
  • Glucorticoids and mineralocorticoides
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20
Q

Give an example of a Glucocorticoid and its properties

Functions?

A
  • Hydrocortisone (cortisol)
  • C21 pregnane skeleton
  • •17b-C(O)CH2OH side chain
  • •11b-OH
  • • D4 -3-keto group (conjugated)
  • •17a-OH (usually)
  • Synthesis of carbohydrate from protein and lipids, therby controlling blood sugar levels
  • Deposisition of glycogen in the liver
  • Inflammatory response
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21
Q

Give an example of an mineralocorticoid and its properties and function

A

• Aldosterone

C21 pregnane skeleton

  • 17b-C(O)CH2OH side chain
  • D4 -3-keto group
  • Controls electrolyte balance in the kidney:

–Retention of Na+/Cl-

–Retention of water

–Excretion of K+

22
Q

Discuss the solubility of steriods

A
  • •Like dissolves like
  • •Steroids are hydrocarbons
  • •As such, they are fairly non-polar/lipophilic (hydrophobic)
  • •Freely soluble in most organic solvents
  • –E.g. light petroleum, diethyl ether, chloroform
  • •Almost insoluble in water
  • •Those carrying two or more hydroxyl groups, become more soluble in polar solvents (methanol, water)
  • •Steroids with ionized groups (salts of carboxylic acids, sulphates) are generally soluble in water
23
Q

What is the order of aqueous solubility of steriods

A
  • Most: Hydrocortisone
  • Testosterone
  • Progesterone
  • Estradiol
  • Cholesterol
24
Q

Due to the hydrophobicity of steriods, they need to be made more water-soluble in the body to allow them to be carried around. How can this be done?

A
  • Attaching to a largr water-compatible molecule e.g. protein
  • Attaching to a small compound e.g. suagr or salt such as sulphate
25
Q

Describe ADME of steriods

A
26
Q

What are transport mechanisms to cross cell membranes?

A
  • Active transport
  • Passive diffusion
  • Facilitated diffusion
  • Pinocytosis
27
Q

Which route of administration doesnt require the drug to pass through cell membranes to reach its target site?

A
  • IV
28
Q

How do steriods move in the blood?

How do they get into tissues?

A

Due to their hydrophobicity it is possible for them to be transported in the blood unless bound to a plasma carrier protein

When moving into tissues they must be in free steriod form

29
Q

Describe the mode of actino of steriods

A

Steriod passively diffuses into the cell nad binds ti the sreriod hormone recpepot. Steriod-receptor complex translocates into nucelus and binds to chrmoatin. This causes altered cell function

30
Q

Describe properties of specific carrier receptors

A
  1. High affinity and high specificity
  2. Sex hormone binding globulin:
    • Testosterone and Estradiol
    • Limits BA of these hormones
  3. Corticosteriod-binding globulin:
    • Hydrocortisone. Progesterone, aldosterone
    • Again, when bound is unaviavble to receptors
31
Q

How is cholesterol transported around the body?

A

By lipoproteins by:

  • Very low density lipoproteins (VLDL)
  • Low density LP (LDL)
  • Intermediate D LP (IDL)
  • High density LP (HDL)
32
Q

What is the purpose of metabolism and excretion?

A
  • To produce more polar products
  • To increase aqueous soluble
  • To make compound more readily excreted from the body
33
Q

What does metabolism involve?

A
  • Phase 1: oxidation, reduction, dealkylation
  • Phase 2: Addition of polar groups (e.g. glucuronic acid)
34
Q

Where does metabolism and excretion occur?

What happens to it?

A

In the liver to form bile salts.

The bile salts are either stored in the gall bladder or secreted into the small intestine to aid lipid digestion.

They bile salts are then excreted by the kidneys or intestine

35
Q

Describe the metabolism of cholesterol

A
  1. Cholesterol
    • ​​Undergoes oxidation, reduction and cleaving reactions
  2. Cholic acid​
  3. Sodium glycholate (glycine) or Sodium Taurochloate (taurline)
36
Q

Why are bile salts useful?

A
  • Efficent surfactants
  • Aid emulsification of dietry fats in small intestine
37
Q

What happens to bile salts?

A
  • 95% are recycled in the enterohepatic cycle. They can be recycled up to 20xs
  • Due to the pH in the small intestine, bile acids are actually bile salts
  • Enterohepatic recycling is important in controlling the stock of bile salts and is important factor in controlling cholesterol levels
38
Q

What happens during the metabolism of hydrocortisone?

A
  • Oxidatino, reduction, cleaving
  • It loses its biological acitvity
  • Usually undergo conjugation to form glucuronides or sulfates
39
Q
A
40
Q

What are therapeutic properties of glucocorticoids?

A
  • May be used in high doses for cancer treatments
  • Turn down inflammation
  • supresses heat, swelling, redness, tenderness
  • Used for conditions caused by an overactive immune system e.g. allergies, ahstma, autoimmune, sepsis
41
Q

How does Glucocoticoid transactivation occur?

A

GC binds to cytosololic GC receptor. This translocates to the nucleus and binds to the glucocorticoid response element and regulates gene expression

  • Anti-inflammatory
  • Increased glucogenesis - Glucose synthesis from fats and proteins
42
Q

Describe Transrepression

A

GR interacts with centre TFs and inhibits transcription of pro-inflammatory genes including interleukins, chemokines, cytokines

In GCs effect wanted immune genes and unwanted regulatory genes effecting other processes

43
Q

Describe Immunosupression

A
  • Supress cell mediated proliferation
  • By supressing gene for cytokines they reduce T cell proliferation
  • Can induce T cell apoptosis
44
Q

Describe the Anti-inflammatory effects of GC

A
  • Potent regardless of cause
  • Inhibit prostaglandins and leukotrienes
  • Supress COX 1 and 2 (similar to NSAID)
45
Q

What is the endogenous secretio of glucocorticoids controlled by?

A
  • Negative feed back loop.
  • If Hydrocortisone levels high HC inhibits corticosteriod releasing hormone (CRH) from the hypothalamus
  • This reduces secretion of Adrenocortiocotropic hormone from the pituitary
  • Less ACTH means less HC produced from the adrenal cortex
46
Q

What are side effects of glucocorticocoids?

A
  • Immune supression - more susceptible to infection
  • Adrenal supression
  • hyperglycemia - increased glucogenesis and insulin resistance
  • increased skin fragility
  • irregular menstrual periods
  • Steriod induced osteporosis
  • Growth failure, puberty delay
  • Weight gain - fat deposition and appite stimulation
  • Excitatory effect on the CNS
  • Cataroacts
  • Negative calcium balance
47
Q

Effects of mineralocorticosteriods?

A

Water and salt retion - hypertension

48
Q

SYNTHETIC CORTICOSTEROIDS-
QSAR

A
49
Q
  1. What route is not suitable for synthetic progestins?
  2. What modifications can be done to imporve this?
  3. Uses
A
  1. Though highly available, not absorbed well. Cant be taken orally due to metabolism by the liver
  2. Prevent ovulation and uterine contractions
  3. Feedback effect on hypothalamus
50
Q

What are synthetic estrogens used for?

A
  • Supress ovulation
  • Form basis of combine oral pill and hormone replacement therapy HRT
51
Q
A

Kirstys Flashcards (116 decks)

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