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MBM 421 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are hormones

A

small regulatory molecules that act through receptors to bring about changes in cellular activity of specific tissues

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2
Q

Functions of hormones

A

Regulates all body processes

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3
Q

Factors that affect the concentration of a hormone at the target cell

A

Rate of synthesis and secretion
Dilution effect
Affinity for and availability of transport proteins if applicable
Rate of clearance from the body
The conversion of inactive or suboptimally active forms into fully functional ones

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4
Q

Two techniques for detecting, and quantifying hormones

A

ELISA and radioimmunoassay

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5
Q

Major characteristic of hormones

A

Specificity

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6
Q

5 methods for classification of hormones in

A

Solubility
Nature of signal of hormonal action
Chemical composition
Location of receptors
Mode of transport to target tissue

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7
Q

Two classification of hormones based on chemical structure and mode of action

A

Group 1
Group 2

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8
Q

Group 1 hormones

A

Steroid hormones, vitamin D(Calcitriol) , Retinoid and thyroid hormones

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9
Q

Group II hormones

A

Peptide, catecholamines, eicosanoids

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10
Q

Mode of action of group I hormones

A

Use of intracellular receptors (nuclear)

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11
Q

Mode of action of group II hormones

A

Use extracellular receptors/ use of second messengers

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12
Q

Nitric oxide

A

Gas that enters the cell to activate cytosolic enzyme guanylyl cyclase

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13
Q

Hormone classification based on mode of transport to target tissue

A

Autocrine, Paracrine and endocrine

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14
Q

Autocrine

A

Affects the same cell that releases them by binding to the cell’s surface receptors. Usually somatostatin and some eicosanoids

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15
Q

Paracrine hormones

A

Released into the ECF and diffuse to neighboring target cells. Usually employed by eicosanoid hormones

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16
Q

Endocrine

A

Released into the blood and are carried to target cells throughout the body(e.g insulin and glucagon)

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17
Q

Synthetic path of the 8 hormone groups

A

Peptide- proteolytic cleavage of pro hormones
Catecholamines- Tyrosine
Eicosanoids- Arachidonate

Steroids- cholesterol
Vitamin D- Cholesterol
Retinoids- vitamin A
Thyroid hormones- Tyr in thyroglobulin
Nitric oxide- Argunine + O2

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18
Q

Differences between group 1 and 2 hormones

A

Based on solubility
Use of transport proteins
Plasma Half life
Mediator

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19
Q

Three classes of hormones based on chemical composition

A

Amines
Peptides
Steroids

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20
Q

Examples of peptide hormones

A

All hormones of hypothalamus and pituitary
Parathyroid hormone(calcitonin)
Pancreatic hormones (Insulin, somatostatin and glucagon)

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20
Q

5 properties of hormones

A

Synthesised in the body
Work in very small concentrations
Relatively short half lives
Utilize feedback regulation
Exert multipoint control

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21
Q

Two facts about peptide hormones

A

They are produced and stored as prohormones, then cleaved into active form when needed
They are made from 20 - 300 amino acid residues

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22
Q

Pituitary and hypothalamic hormones

A

Hypothalamic- GnRh, Trh, Somatostatin, GHRH, ADH, PRH, CRH, produces Aldosterone

Anterior pituitary- Growth hormone(Somatotropin), TSG, Prolactin, ACTH, LH and FSH

Posterior pituitary- Oxytocin, secretes aldosterone

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23
Q

Function of LH and FSH

A

LH stimulates testosterone, oestrogen and progesterone secretion
FSH stimulates maturation of ovarian follicles and sperm cells production

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24
Q

Female gonad hormones

A

estrogen and progesterone

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25
Q

Estrogen

A

Estrogens are responsible for maturation and growth of the vagina and uterus, widening of pelvis, breast and the uterus changes during the menstrual cycle, and increasing growth of hairs on the body.

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26
Q

Progesterone

A

Makes the body ready for a baby. Ovulation, prepares the uterus for implantation and regulates uterine changes, stimulates gland development for milk during pregnancy

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27
Q

Male Gonad Hormones

A

Testosterone
Androstenedione
Inhibin

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28
Q

Testosterone function

A

Testosteroneis responsible and essential for increased growth of bone and muscle, growth of body hair, developing broader shoulder, voice deepening and growth of the penis.

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29
Q

Androstenedione

A

Androstenedione– These are the hormones that act as a precursor to estrogens and testosterone.

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30
Q

Inhibin

A

Inhibin– These hormones inhibit the release of FSH and thought to be involved in sperm cell regulation and development.

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31
Q

Steroid hormones are divided into 2 classes, name them

A

Adrenocorticoids and
Sex hormones

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32
Q

Classification of corticosteroids based on their actions

A

Glucocorticoids
Mineralocorticoids

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33
Q

Glucocorticoids

A

Glucocorticoids (such as cortisol) primarily affect the metabolism of carbohydrates

34
Q

Mineralocorticoids

A

Mineralocorticoids (such as aldosterone) regulate the concentrations of electrolytes (K, Na, Ca2, Cl–) in the blood.

35
Q

Synthesis of steroid hormones

A

Produced by reactions that remove the side chain from the D ring of cholesterol and introduce oxygen to form keto and hydroxyl groups.
Many of these reactions involve cytochrome P-450 enzymes

36
Q

Properties of steroid hormones

A

Have nuclear receptors (some have cytoplasmic receptors)
Require transport proteins
Made from cholesterol

37
Q

Catecholamines are synthesized from

A

dopamine, norepinephrine, and epinephrine-are synthesized from tyrosine in the chromaffin cells of the adrenal medulla.

38
Q

Group II hormones generally affect ____ and group I hormones generally affect ______

A

Group II lead to a change in the activity of one or more preexisting enzymes in the cell, by allosteric mechanisms or covalent modification.

Group I alter gene expression, resulting in the synthesis of more (upregulation) or less (downregulation) of the regulated protein(s).

39
Q

Five types of hormonal interaction

A

a second messenger (such as cAMP, cGMP, or inositol trisphosphate) generated inside the cell acts as an allosteric regulator of one or more enzymes,

a receptor tyrosine kinase is activated by the extracellular hormone,

a change in membrane potential results from the opening or closing of a hormone-gated ion channel,

an adhesion receptor on the cell surface conveys information from the extracellular matrix to the cytoskeleton,

a steroid or steroidlike molecule causes a change in the level of expression of one or more genes, mediated by a nuclear hormone receptor protein

40
Q

Thyroid hormones

A

T4 Thyroxine
T3 Triiodothyronine

41
Q

Synthesis of thyroid hormones

A

Both are synthesized from the precursor protein thyroglobulin. Tyrosine residues in thyroglobulin are enzymatically iodinated in the thyroid gland, then two iodotyrosine residues condense to form the precursor to thyroxine.
When needed, thyroxine is released by proteolysis.
Condensation of monoiodotyrosine with diiodothyronine
produces T3, which is also an active hormone
released by proteolysis

42
Q

Function of thyroid hormones

A

stimulate energy-yielding metabolism, especially in liver
and muscle, by increasing the expression of genes
encoding key catabolic enzymes.

43
Q

Steps involved in biosynthesis of the three catecholamines

A

ring hydroxylation;
decarboxylation;
side-chain hydroxylation to form norepinephrine;
N-methylation to form epinephrine

44
Q

Biosynthesis of catecholamines

A

ring hydroxylation of tyrosine by tyrosine hydroxylase to give DOPA.
decarboxylation of DOPA by DOPA decarboxylase to give dopamine.
Beta chain hydroxylation of dopamine by dopamine beta-hydroxylase to give norepinephrine
N-methylation of norepinephrine by PNMT to give epinephrine

45
Q

rate-limiting enzyme in catecholamine biosynthesis

A

Tyrosine hydroxylase

46
Q

Adrenal glands and their hormones

A

Adrenal cortex- corticosteroids (mineralocorticoids e.g aldosterone and glucocorticoids e.g cortisol) and sex hormones

Adrenal medulla - catecholamines (Dopamine, epinephrine and norepinephrine)

47
Q

10 hormones of the gi tract

A

Gastrin
Secretin
Grhelin
GIP
Motilin
Somatostatin
Enteroglucagon
Pancreatic Polyeptide
Peptide YY
Cholecystokinin (CCK)

48
Q

Sources and functions of the 10 GI tract hormones

A

Gastrin - Gastric antrum mucosa. Increases stomach acid
Ghrelin- A cells of gastric fundus. hunger hormone, increases food intake
CCK- I cells of duodenum and Jejunum. Decreases hunger, stimulates pancreatic enzyme release.
Secretin- S cells of upper portion of small intestine. Augments action of CCK and decreases acid secretion. Secretes bicarb.
Polypeptide YY - L cells of distal part of small intestine and large intestine. Inhibits food intake.
Somatostatin- D cells of GI tract and Pancreas. Inhibits secretion of GI tract hormones and growth hormone.
Motilin - Increases intestinal motility
Enteroglucagon- Increases enterocyte proliferation
GIP- decreases gastric acid
Pancreatic polypeptide - decreases bicarbonate secretion`

49
Q

Hormones of the pancreas (5)

A

Gastrin
Somatostatin
Insulin
Glucagon
VIP

50
Q

Diseases of the pancreas

A

Type 1& 2 diabetes
Hyperglycemia and Hypoglycemia

51
Q

Hormones regulating calcium metab

A

Parathyroid hormone, calcitriol and
calcitonin

52
Q

How is calcium regulated- PTH

A

High levels causes reduced muscle responsiveness
Low levels causes convulsion/muscle spasms
PTH acts on kidneys, intestines and bone to increase blood calcium levels. It is triggered by low calcium levels and has a -ve feedback relationship with calcium.
PTH causes kidneys to reabsorb more calcium, increases osteoclase activity, reduces osteoblase activity and indirectly stimulates more absorption of dietary calcium by the intestines by stimulating the production of calcitriol(active vit d) which then goes and acts on them

53
Q

How is calcium regulated- Calcitonin

A

Calcitonin is produced by the parafollicular cells of the thyroid. Has opposite effect of PTH. Particularly important in starvation, children and pregnant women. Role in normal adults in unclear

54
Q

Hyper and hypo parathyroidism significance

A

Hyper leads to bone loss and excess blood calcium
Hypo leads to tetany and convulsions
both causes problems in conduction of nerve impulses

55
Q

Low synthesis of calcitriol causes

A

Rickets

56
Q

4 examples of second messengers

A

cAMP, DAG, 1P3 &Ca2+.

57
Q

What is the hormone response element (HRE)

A

a short DNA sequence within a gene that is capable of binding to specific hormone receptor complexes and regulating transcription.

58
Q

7 cardinal elements of the signalling mechanism in plasma membrane control

A

External Signal i.e. The First Messenger (Hormones & Neurotransmitters)
Plasma Membrane Receptor
Transducer (e.g. G-Proteins)
Amplifier (e.g. Adenylate Cyclase)
Second Messenger (e.g. cAMP, DAG etc)
Effectors (e.g. Protein Kinase)
Response (e.g. Glycogen Mobilization)

59
Q

The G-protein that controls Adenylate Cyclase is called

A

Stimulatory G-protein or Gs.

60
Q

Structure of Gs

A

Trimeric. It consists of 3 Subunits: α, β and γ

61
Q

Active and inactive forms of Gs

A

Gαβγ - GDP Inactive
Gα - GTP Active

62
Q

How does Gs get activated

A

When the receptor is activated, the G-protein undergoes a conformational change that causes it to associate with the cytoplasmic part of the receptor, while exchanging GDP for GTP.

Displacement of GDP by GTP causes the α-subunit to dissociate from the trimeric complex & to associate with other intracellular signalling proteins (like adenylate cyclase).

63
Q

3 types of second messenger system

A

Adenylate Cyclase - cAMP System

Phospholipase C System

Calcium - Calmodulin System

64
Q

Adenylase cyclase activation process

A

First, the hormone (e.g. Epinephrine) binds to the receptor, leading to the activation of Gs (Gα - GTP) .

Gα - GTP diffuses & binds to Adenylate Cyclase, leading to its activation.

Adenylate Cyclase then converts ATP to cAMP.
After Adenylate Cyclase has been activated, Gα - GTP is converted into Gα - GDP, which then diffuses from away from the enzyme and binds to Gβγ.

cAMP activates Protein Kinase A/PKA, which stimulates the phosphorylation of many target proteins in order to alter their activity e.g. Glycogen metabolism.

65
Q

Phospholipase C & Calcium - Calmodulin System– Phospholipase c/ 1st stage

A

Work hand in hand
A hormone (e.g Vasopressin) binds to a cell surface receptor, leading to the activation of the enzyme Phospholipase C/PLC.

PLC then catalyses the breakdown of Phosphoinositol 4,5-Bisphospahte/PIP2 into 1,2-Diacylgycerol/DAG & Inositol 1,4,5-Trisphosphate/IP3.

IP3 binds to receptors on the membrane of the Endoplasmic Reticulum ( one of the Intracellular stores of Ca2+), leading to to an increase in the concentration of cytosolic Ca2+.

Increase in Cytosolic Ca2+ stimulates DAG to activate Protein Kinase C, thus leading to the Phosphorylation of Target Proteins.

66
Q

Phospholipase C & Calcium - Calmodulin System – Second stage

A

As stated previoulsy, IP3 binding leads to the opening of Ca2+ channels, which in turn leads to an increase in the concentration of cytosolic Ca2+.

Ca2+ then either acts solitarily or binds to Calmodulin, which activates protein kinases I, II & III, causing phosphorylation of specific proteins, which leads to responses in target cells like smooth cell contraction, metabolism & transport of molecules, neurotransmitter release etc.

67
Q

Agonists

A

An Agonist is a drug/substance that mimic the activities of normal hormones/neurotransmitters & emulate a similar response from the receptors they bind to.

68
Q

Antagonists

A

An Antagonist is a substance that binds to the receptor either at the primary site or at another allosteric site, which serve to block or dampen the normal biological response. They can also be called Blockers.

69
Q

7 Types of agonists

A

Physiological Agonists: Compounds that ellicit the same response but doesn’t bind to the same receptor.

Endogenous Agonists: Compounds naturally produced by the body that bind to & activate a specific receptor. E.g. the endogenous receptor for serotonin receptors is serotonin.

Full Agonists: Bind to & activate a given receptor with the maximum response that an agonist can ellicit at the receptor. E.g. Isoproterenol, a drug that mimics the action of adrenaline at β adrenoreceptors.

Partial Agonists: Bind to & activate a given receptor, but only have partial efficacy at the receptor, even at maximal receptor occupancy.
Co-Agonists: Compounds that work with other co-agonists to produce the desired effect togther. E.g. Ca2+ and IP3 act as co-agonists at the IP3 receptor.

Inverse Agonists: Compounds that bind to the same binding site as an agonist for a specific receptor, but produce an opposing response instead of a normal one.

Irreversible Agonists: Bind permanently to a receptor through he formation of covalent bonds.

70
Q

3 types of antagonists

A

Competitive
Non competitive
Uncompetitive

71
Q

Competitive antagonists

A

Bind to receptors at the same binding site as the normal hormone/neurotransmitter/agonist, but don’t activate the receptor.
They are used to prevent the activity of drugs and to reverse the effects of drugs that have already been consumed. E.g. Naloxone is used to reverse opiod overdose caused by heroin or morphine.

72
Q

Two types of competitive antagonists

A

Reversible
Irreversible

73
Q

Reversible Competitive Antagonists

A

They bind via Non-covalent Intermolecular Forces
Will eventually dissociate from the receptor, leaving it free to be bound again.

74
Q

Irreversible Competitive Antagonists

A

Bind via Covalent Intermolecular Forces
Because there is not enough free energy to break covalent bonds in the local environment, the Receptor - Antagonist Complex will never dissociate. The receptor will remain ‘‘permanently’’ antagonized until it is destroyed.

75
Q

Non-Competitive Antagonists

A

These antagonists bind to an allosteric site of the receptor.

76
Q

Difference between competitive and non- competitive besides their binding site

A

Unlike Competitive Antagonists (which affect the amount of agonists necessary to achieve a maximumresponse, but DON’T affect the magnitude of that response), Non-Competitive Antagonists REDUCE THE MAGNITUDE of the maximum response that can be attained by any amount of agonists.

77
Q

Uncompetitive Antagonists

A

These compounds require that the receptor should be activated by an agonist 1st before they can bind to a separate allosteric binding site on the receptor.
Once these antagonists bind, they fully prevent the activation of the receptor i.e. no response is produced.

78
Q

Radioimmunoassay procedure

A

First an antibody, highly specific for the target hormone is engineered.
Then, this antibody is mixed in with a fluid containing the target hormone(gotten from an animal)
After that, an engineered standard hormone that has isotopic markers is mixed in as well
NB: The antibody conc should be lower than the two hormones to ensure competition for its binding site
After binding reaches equilibrum, the antibody-hormone complex is separated from the rest and the standard hormone is measured by radioisotope counting techniques. If it’s quantity is small, its conc is higher than the standard hormone. And vice versa

79
Q

Drawback of radioimmunoassay

A

It is not clinically feasible

80
Q

ELISA process

A

3 antibodies AB1, AB2 and AB3. AB3 has an enzyme attached that facilitates the production of a specific substrate. Uses a plate with 96 wells.
First, each well is coated with AB1.
Then a fluid containing the target hormone is poured in.
After that, Ab2 is added in. AB2 and AB1 are specific to the hormone but at different sites.
Then AB3 is added in. AB3 is specific to AB2. Its enzyme then creates products that can be detected using colorimetric techniques.
The conc of this product is equal to the conc of target hormone.

81
Q

Difference in theory between Elisa and radioimmunoassay

A

ELISA use EXCESS ANTIBODIES so that all hormone molecules are captured in Antibody-Hormone Complexes
Radioimmunoassay uses conc of antibodies smaller than the target hormone

82
Q

Parahormones/hormonoids

A

Hormone-like substances.
properties & actions resemble those of hormones.
Usually uses autocrine or paracrine signalling
E.g Eicosanoids

MBM 421 (10 decks)

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