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Pharma 1 > Endocrinology: > Flashcards

Endocrinology: Flashcards

1
Q

Define hormones:

A

Hormones: are the natural secretions of endocrine glands
= A hormone is a chemical substance produced in one part of the body (restricted area) that diffuses or transported to another area (circulating hormones), where it influences activity and tends to integrate component parts of the organ. Definition is extended to “local hormones” (any hormones acting in aparacrine,
autocrine, and/or intracrine i.e.
inside acell manner).

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2
Q

Role of hormones are:

A

Role: integration and control body functions in close co-operation with nervous system.

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3
Q

How are hormones released:

A
  1. An action potential in a neuron innervating an endoctine cell, stimulates secretion of a stimulatory neurotransmitter.
  2. The endocrine cell secretes its hormones into the blood where it will be transported to its target
  3. An action potential in the neuron stimulates secretion of an inhibitory neurotranmitter
  4. Then endoctine cell is inhibited and stops producing the hormone
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4
Q

Chemical classes of hormones:

A
  1. Amine, peptide, protein, glycoprotein
    (hypothalamus, adeno-, neurohypophysis, thyroid, parathyroid, islets of Langerhans)
  2. Steroids
    (e. g. gonadal and adrenocortical hormones)
  3. Unsaturated fatty acids
    (prostaglandins – local h.)
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5
Q

Hormone-Receptors and their localisation

  1. what are the receptors made of?
  2. Where are they localised?
A
  1. All known hormone receptors are proteins.
  2. They may be localised:
    - Membrane-active hormones
    *on the surface of the cells
    (peptide and releasing hormones)
  • Gene-active hormones
    * in the cytoplasm (steroids)
    * on the cell nuclear chromatin (thyroid hormones)
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6
Q

Mode of application:

A

PO (steroid yes, peptide not)

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7
Q

Size of dose

  • What happens if high dose is given?
  • what happens if low dose is given?
  • Physiological level?
A

opposite effect:
low oestrogen dose: milk production increases
large dose: milk production decrease

Physiological level: substitution therapy, well tolerated

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8
Q

Side effects of hormones:

A
  • Over dose, permanent large doses: increase number and intensity of side effects
  • Corticosteroides - iatrogenic Cushing-disease, obesitas
  • oestrogen, progestogens – pyometra,
  • insulin – hypoglycaemia
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9
Q

Overlapping effect of hormones found in:

A
  • gluco – mineralo-corticoids
  • oxytocin-vasopressin
  • FSH – LH
  • eCG/PMSG – hCG
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10
Q

For increased hormone efficacy (augmentation) you can use:

A
  • Synthetic analogues (glucocorticoids progesterone, etc.)
  • Esterification (steroids)
  • complex formation (e.g. insulin zinc complex)
  • Enhanced synthesis (sulfonylurea type p.o. antidiabetics)
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11
Q

To decrease hormone efficacy, you can use:

A
  • Antagonists (spironolacton, cabergolin)
  • Anti-hormone (antibody against peptides)
  • Inhibitors of hormone synthesis (thiouracil-T4, T3)
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12
Q

Which groups of hormones can be found in the body?

A
  1. Releasing and inhilbitory hormones
  2. Hormones in the pituitary gland
  3. Hormones of the thyroid gland
  4. Hormones of the endrocrine pancreas
  5. Sex steroid hormones and anabolic agents
  6. Corticosteroids
  7. Hormones of the pineal gland
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13
Q

Releasing and inhilbitory hormones:

Which hormones are most important?

A 
- Gonadotrophin-releasing hormone (GnRH)
	 Anterior Pituitary (AP) ---> releases LH and FSH --->
 ovary, testis
  • Corticotrophin-releasing hormone (CRH)
    AP —> releases ACTH —-> adrenal cortex —>
    Diagnostic agent to asses ACTH secretory capacity 1 µg/kg iv.
  • Thyrotrophin-releasing hormone (TRH)
  • Somatotrophin-releasing hormone (GRH)
  • Somatotrophin-inhibitory hormone (GIH)
  • Prolactin-releasing hormone (PRH)
  • Prolactin-inhibitory hormone (PIH)
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14
Q

Releasing and inhilbitory hormones:

- production site and transport

A

Produced by hypothalamus and transported via the hypophyseal portal system into the adenohypophysis.

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15
Q

Hormones in the pituitary gland

- production site?

A

Adenohypophysis (anterior pituitary - oral ectoderm)

Neurohypophysis (posterior pituitary - neural ectoderm)

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16
Q

Hormones in the pituitary gland

- which hormones are produced in adenohypophysis?

A
  • Somatotrophin
  • Adrenocorticotropic hormone (corticotrophin, ACTH)
  • Thyrotrophic hormone (TSH, thyrotropin)
  • Prolactin (lactotrophin)
  • Gonadotrophins
  • Follicle-stimulating hormone (FSH)
  • Luteinizing hormone (LH)
  • (Non-hypophyseal gonadotrophins)
    - Human chorionic gonadotrophin (hCG)
    - Pregnant mare’s serum gonadotrophin (PMSG, eCG)
    mainly FSH-like activity, but LH-like activity is significant
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17
Q

HORMONES OF THE PITUITARY GLAND

Hormones produced in neurohypophysis are?

A
  • Antidiuretic hormone (ADH, vasopressin)
     renal tubules
  • Oxytocin
     uterine myometrium and mammary myoepithelium
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18
Q

SEX STEROID HORMONES and ANABOLIC AGENTS

  • What are they?
  • which exists?
A

= Endogenous steroids and synthetic compounds with steroid activity

  • Oestrogens
  • Progesteron and progestagens
  • Androgens
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19
Q

CORTICOSTEROIDS

- which types?

A

Mineralocorticoids

Glucocorticoids

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20
Q

hormones of the pineal gland:

A
  • Melatonin (sc. implant 18 mg preseason mating in ewe, doe, goat)
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21
Q

Somatotropin:

  • what kid of substance is it?
  • How to give it?
A
  • growth hormone/ insulin-like growth factor production in liver
  • orally it is ineffective
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22
Q

Somatotropin:

- release is controlled by:

A
  • Release of GH is controlled by Growth Hormone Releasing Hormone and Growth Hormone-inhibitori Hormone
  • Ghrelin: primarily from GI and hypothalamus (+kidney, placenta, pituitary gland)
  • Plansma levels of GH
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23
Q

SOMATOTROPIN:
Plasma level of GH (STH, ST,GH)
increase, decrease during?

A
  • Increasing: during sleep and by hypoglycaemia, exercise, stress, alpha-adrenoceptor agonists, dopamine (but receptor agonists can be controversial)
  • Decreasing: hyperglycaemia, glucocorticoids, beta-adrenoceptor agonists
24
Q

Somatotropin:

- GH effects:

A
  • basically anabolic action
  • it stimulates growth (praepubertal function)
  • controls the metabolism of carbohydrates, proteins and fats
  • promotes N retention, increasing transport of AAs into tissues, accelerates their incorporation into protein (lactation)
25
Q

Disordered GH production:

A
  • giant (praepubertal)
  • acromegaly (adult)
  • dwarfism, deficiency
26
Q

Diagnosis of disorders in GH production:

A

Diagnosis by stimulation test:

  • Clonidin 10 µg/kg b.w.,
  • Xylazine 100 µg/kg b.w. IV
  • Sermirelin; synthetic GHRH
27
Q

GH is used for:

A
  • to increase milk production, meat quality (meat:fat ↑)
  • replacement therapy
  • growth-hormone responsive alopecia in dog
  • Recombinant biosynthetic human
28
Q

Somatotropin/GH drugs:

GH inhibitory drugs:

A

Somatrem - slow release inj

inhibitory:
- Synthetic somatostatin analogues: Octreotide, Lanreotide
- Dopaminergic agents (e.g. Cabergoline) - feedback, praesynaptic!
- Pegvisomant (Somavert®)
GH receptor antagonist, inhibition of IGF-1 synthesis.

29
Q

Corticotropin (ACTH):

- Effects:

A

Effect:
- Increased synthesis of enzymes involved in steroid biosynthesis
(incr. conversion of cholesterol to pregnenolone)
level of cortisol and corticosterone is increased (sexual steroids and slightly aldosterone)

30
Q

Corticotropin (ACTH):

- Uses:

A
  1. To increase glucocorticoid level in such conditions where its level is relatively or absolutely low (e.g. secondary adrenal insufficiency - adrenal hypofunction due to a lack of ACTH -)
  2. Cow-ketosis
  3. To restore (recall) the function of adrenal cortex (after prolonged use of glucocorticoids)
  4. Stimulation test /differential diagnosis of adrenocortical hypo- and/or hyperplasia/:
31
Q

How do you give corticotropin:

- disadvantages?

A
  • depot preparations are available for IM injection
  • DISADVANTAGES:
    short half-life (15 min.)
    immunogenicity
    orally ineffective
32
Q

THYROTROPIN (TSH):

products available

A
  • No approved vet. thyrotropin product on the market today.

- Recombinant human TSH in humans (earlier: bovine thyrotropin)

33
Q

THYROTROPIN (TSH):

- effects?

A

EFFECT: it increases iodine uptake by the thyroid gland and the production and secretion of thyroid hormones.

34
Q

THYROTROPIN (TSH):

- Uses:

A

USE:

  • in research
  • treatment of acanthosis nigricans (?)
  • Diagnose primary hypothyroidism TSH or biosynthetic
35
Q

HORMONES OF ADENOHYPOPHYSIS:

- Name them:

A
  1. SOMATOTROPIN
  2. CORTICOTROPIN (ACTH)
  3. THYROTROPIN (TSH)
  4. GONADOTROPINS FSH & LH
36
Q

HORMONES OF NEUROHYPOPHYSIS :

A
  • ANTIDIURETIC HORMONE (ADH)
  • VASOPRESSIN
  • Oxytocin
37
Q 
ANTIDIURETIC HORMONE (ADH), VASOPRESSIN
- function:
A
  • control the water water balance
  • ADH: –> Smooth m. :) vasoconstriction
    - -> kidney: increase water permeability and reabsorption in the collecting ducts
38
Q

Uses of ADH:

A

USE:

  • Diagnosis and treatment of total and partial central diabetes insipidus (DI)
  • Separation from diabetes melitus (DM) (differential diagnosis)
39
Q

ADH preparations:

A

Preparations:
- Natural Vasopressin nasal spray (short duration of action, local irritation, low PO bioavailability)

  • Synthetic analogue Desmopressin (with longer duration of action) injectable (SC), oral and nasal spray dosage forms are available
  • Other possibility: Chlorpropamide (see under oral sulfonylurea antidiabetics): PO
  • In DI thiazide diuretics may be used, paradoxical action
40
Q

Preparations for overproduction of ADH:

A
  • Conivaptan: only for iv. use (less seletive also V1),
  • Tolvaptan and Lixivaptan V2 receptor selective antagonists, p.o. application is also available

Non-specific drugs:

  • demeclocycline
  • teracyclines
  • lithium
41
Q
  • In which animals does Diabetes Mellitus most commonly observed?
  • And which type?
A

dog and cats (mostly insulin deficient type)

42
Q

Where is insulin produced:

A

produced by the beta-cells of the islets of Langerhans in the endocrine pancreas

43
Q

Biosynthesis of insulin:

A
  1. preproinsulin in the endoplasmic reticulum
  2. proinsulin
  3. transportation to the Golgi complex
  4. insulin
  5. storage in secretory granules in a complex form with zinc.
44
Q

Actions of insulin are related to:

- How does it work?

A
  • The storage and use of fuels (glucose, amino acids, fatty acids)
    —> intracellular uptake of glucose, AAs, FA, K+
    in the cells  glucose metabolism
     protein synthesis
     deposition of fat and glycogen

These anabolic actions are increased by actions to glycogenolysis, gluconeogenesis and lipolysis which are reduced.

45
Q

Lack of insulin results in: (Signs of DM)

A
  • glucose intolerance
  • hyperglycaemia
  • glucosuria
  • polyuria/polydipsia (PU/PD)
  • saluresis (Na, K)
  • weight loss
  • incomplete fat metabolism —> increased plasma free fatty acids –> ketoacidosis —> coma = complicated form of diabetes mellitus
46
Q

Insulin uses:

A

Use:

  • to treat diabetes mellitus (dog and cat)
  • ketosis and fatty liver in cattle which are non-responsive to glucose or glucocorticoid therapy alone (protamine zinc insulin)
47
Q

Formulation of insulin:

A
  • Regular (crystalline zinc, soluble) insulin
    *rapid onset
    * duration of action generally short (depends on
    route of admin.) —> 4-8 h
    *IV (only this type), SC (IM)
  • Insulin Zinc Suspension (Lente insulin)
    *Caninsulin
    * amorphous intermediate duration, crystalline more
    prolonged (12-24 h)
  • Protamine Zinc Insulin (PZI)
    *protamine sulphate and zinc chloride in buffered
    water - duration 24-36 h
  • Isophane insulin
    *suspension of zinc insulin crystals and protamine
    zinc in buffered water
    *duration 12-30 h

-(Surfen insulin, long activity– aminoquinuride surfactant)

48
Q

Side effects of insulin:

A
  1. acute hypoglycaemia - excessive insulin dose or inadequate food intake
  2. Somogyi rebound effect - hypoglycaemia induced
  3. hyperglycaemia due to compensatory release of insulin-antagonistic hormones (glucagon, catecholamines, glucocorticoids, growth hormone)
  4. Allergic reaction, antibody formation
49
Q

Insulin interactions with:

- examples of drugs from these groups:

A
  • drugs which reduce hypoglycaemic activity: glucocorticoids, dobutamin, oestrogen/progesterone, xylazine, thiazide diuretics
  • drugs which increase hypoglycaemic activity: anabolic steroids, beta-adrenerg blockers (propranolol), MAO inhibitors, phenylbutazone, salicylates, (alcohol)
50
Q

ORALLY ACTIVE HYPOGLYCEAMIC DRUGS /
oral antidiabetics:
1. General warnings:
2. Groups of drugs:

A
  1. hypoglycaemia, serious liver or kidney insufficiency
    • Sulphonylurea substances
    • Biguanides
    • Thiazolidine diones
    • Acarbos
51
Q

Sulphonylurea substances:

- Drugs:

A
  • Tolbutamide - short action, cardiovascular side effect
  • Chlorpropamide - long acting (see ADH - D. insipidus too)
  • Metahexamide
  • Glibenclamide
  • Glipizide - 5 mg/cat
52
Q

Sulphonylurea substances:

- Action?

A
  • release of insulin increase
  • sensitivity of the cells to insulin increase
  • number of receptors increase
  • the binding of isulin to plasma proteins decrease
  • glucagon releases decrease
53
Q

Biguanides:
Drugs?
Action?

A
  • Fenformine - pheny-ethyl biguanide
  • Buformine - butyl biguanide (ADEBIT°)
  • Methformine – dimethyl biguanide

Action: simulation of the action of insulin (increased
utilisation in cells), decreased oral absorption of glucose.

54
Q

Thiazolidine diones

- drugs

A
  • glitazones, troglitazone, draglitazone

- veterinary experiences are not available; modulation of insulin dependent genes, reduction of blood sugar level

55
Q

Acarbos

- function

A

in GI inhibition of the alpha-glycosidase (e.g. amylase) activity, less rapid elevation of blood sugar level after food consumption

56
Q

HORMONES OF THYROID GLAND

A
  1. Calcitonin

2. Thyroid hormones

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