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Pathology And Medicine > Endocrine disorders I > Flashcards

Endocrine disorders I Flashcards

1
Q

hormone

A
  • a chemical messenger that travels from one cell to another.
  • biologically active substances released in one part of the body, travel in the blood stream and have an effect on other part (often remote) of the body.
  • helps different parts of the human body to communicate with each other and integrate body functions
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2
Q

Chemical structure of hormones

A

Amino Acid Derivatives
Peptides
Proteins
Steroid

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3
Q

amine hormone

A

derived from the modification of single amino acids such as tryptophan, tyrosine

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4
Q

Examples of Amine Hormones

A

Melatonin (pineal gland) regulates circadian rhythm (synthetic form taken as tablets)

Thyroid hormones (thyroid gland) -metabolism- regulating thyroid hormones

Catecholamines (adrenals) such as epinephrine, norepinephrine play a role in the fight-or-flight response,

Dopamine (hypothalamus) inhibits the release of certain anterior pituitary hormones

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5
Q

Peptide and Protein Hormones

A

consist of multiple amino acids linked to form an amino acid chain.

synthesized like other body proteins: DNA is transcribed into mRNA, which is translated into an amino acid chain

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6
Q

Peptide hormones

A

shortest chain of amino acids

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7
Q

Peptide hormones

A

Antidiuretic hormone (ADH) -pituitary -important in fluid balance

Atrial-natriuretic peptide (ANP)- heart - reduced blood pressure

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8
Q

Protein Hormones

A

Protein hormones - longer polypeptides

Growth hormone (pituitary gland)

Follicle-stimulating hormone (FSH) – pituitary - glycoprotein (attached carbohydrate group) - stimulate the maturation of eggs in the ovaries and sperm in testes

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9
Q

Steroid hormones

A

Derived from the lipid cholesterol

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10
Q

Examples of Steroid Hormones

A

Testosterone and the estrogens (testes and ovaries)

Aldosterone (adrenal) involved in osmoregulation

Cortisol (adrenals) - regulates metabolism

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11
Q

Steroid hormones characteristics

A

Not soluble in water - they are hydrophobic

Blood is water-based - steroid hormones require a
transport protein (eg Sex Hormone Binding Globulin)

This complex structure extends the half-life (time required for the half of the hormone to be degraded) of steroid hormones much longer than that of hormones derived from amino acids.

Cortisol has a half-life of approximately 60 to 90 minutes

Epinephrine has a half-life of one minute

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12
Q

Mode of action of Non-Steroid hormones

A

amino acid, peptides, protein hormones

water soluble & lipid insoluble - cannot pass through the cell membrane

act through second messengers – bind to receptors on cell membranes

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13
Q

Mode of action - Steroid hormones

A

lipid soluble and can pass through the cell membrane directly enter the cell.

Thyroid hormones that are amine derivatives but are lipid soluble

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14
Q

Non-steroid Hormone action

A

Effects target tissues by binding to the receptors - specific for a hormone

Receptors are extra cellular (surface) protein molecules in the cell membrane associated with G-proteins (GDP) and Adenyl cyclase

Hormones (First messenger) bind to the receptor and produces Second Messengers with the help of receptors

Hormone bind to receptor causing activation of G-protein which further activates Adenyl cyclase that converts ATP to Cyclic AMP (Adenosine monophosphate). This causes a signaling pathway.

The cAMP activates the Kinase enzyme which triggers specific intracellular biochemical changes like enzyme activation, secretion, ion channel changes etc.

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15
Q

Steroid Hormone Action

A

Diffuse through the cell membrane of the target cell

Bind to intracellular receptors in either the cytoplasm or within the nucleus creating hormone-receptor complex which moves to the cell nucleus and binds to a particular segment of the DNA

It triggers transcription of a target gene to mRNA, which moves to the cytosol and directs protein synthesis.

These proteins promote specific to hormones metabolic reactions in the cell.

Actions are slower but last longer

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16
Q

Regulation of hormone release

A

humoral

hormonal

neural

in a negative feedback loop

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17
Q

humoral

A

changes in ion/nutrient level in the blood

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18
Q

hormonal

A

changes in hormone levels that initiate or inhibit the secretion of another hormone

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19
Q

neural

A

a nerve impulse prompts the secretion or inhibition of a hormone

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20
Q

What are the man endocrine glands?

A

hypothalamus/pituitary axis

thyroid gland

adrenals

pancreas

gonads - ovaries and testes

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21
Q

Hypothalamus

A

Part of limbic system in the brain

Body homeostasis

Controls the release of hormones from the anterior and posterior pituitary

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22
Q

Hypothalamus – hormones

A

Corticotropin-releasing hormone (CRH)

Gonadotropin-releasing hormone (GnRH)

Thyrotropin-releasing hormone (TRH)

Growth Hormone Releasing Hormone (GHRH)

Antidiuretic hormone/Vasopressin (ADH)

Oxytocin

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23
Q

Corticotropin-releasing hormone (CRH)

A

stimulates production of ACTH activating cortisol axis

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24
Q

Gonadotropin-releasing hormone (GnRH)

A

stimulates production of LH/FSH stimulating further gonads – ovaries and testis

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25
Q

Thyrotropin-releasing hormone (TRH)

A

stimulates production of TSH stimulating thyroid hormone production

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26
Q

Growth Hormone Releasing Hormone (GHRH)

A

stimulates GH production

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27
Q

Antidiuretic hormone/Vasopressin (ADH)

A

increases how much water is absorbed into the blood by the kidneys

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28
Q

Oxytocin

A

release of a mother’s breast milk, moderating body temperature, and regulating sleep cycles

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29
Q

Two parts of Pituitary

A

anterior and posterior

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30
Q

Anterior Pituitary Hormones

A

 Thyroid Stimulating Hormone (TSH)

 Adrenocorticotropic Hormone (ACTH)

 Growth Hormone (GH)

 Follicle Stimulating Hormone (FSH)

 Luteinizing Hormone (LH)

 Prolactin (Prl)

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31
Q

Posterior Pituitary

A

 Antidiuretic hormone - Vasopressin (AVP)

 Oxytocin

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32
Q

Prolactin

A

major function of prolactin is milk production – oxytocin stimulates ejection

release is tonically inhibited by dopamine from hypothalamus

Inhibits gonadal function (nature’s contraceptive!)

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33
Q

Posterior Pituitary - where are hormones synthesised?

A

Hormones synthesized in the hypothalamus (neurons) are transported down the axons to the endings in the posterior pituitary

34
Q

Where are posterior pituitary hormones stored?

A

Hormones are stored in vesicles in the posterior pituitary until release into the circulation

35
Q

What are the principal hormones in posterior pituitary?

A

Antidiuretic hormone & Oxytocin

36
Q

Antidiuretic Hormone (ADH)- Antidiuretic actions

A

V2 receptors
- increases
permeability of the collecting ducts to water
– retaining water

37
Q

Antidiuretic Hormone (ADH) - Vasopressor actions

A

V1 receptors
- constricts vascular smooth muscle cells

38
Q

Oxytocin

A

Breast-feeding
- Promotes milk ejection as a reflex to baby cry

Childbirth (parturition)
- in late pregnancy, uterine smooth muscle (myometrium) becomes sensitive to oxytocin
- positive feedback

39
Q

Thyroid gland

A
  • Small gland in the neck
40
Q

What hormones does thyroid release?

A
  • Release thyroid hormones: * Thyroxine (T4)
  • Triiodothyronine (T3)
41
Q

What are Tyrosine based hormones comprised of?

A

Partially composed of iodine
- Increases Basal Metabolic Rate and thermogenesis
- Increases sympathetic nerve activity

42
Q

LH - men

A

acts on Leydig cells to stimulate Testosterone production

43
Q

FSH -men

A

with Testosterone act on Sertoli cells to stimulate spermatogenesis

44
Q

Testosterone

A

produced in Testes (Leydig Cells) and adrenal glands (zona reticularis)

45
Q

LH - women

A

Stimulates androgen and progesterone production

Stimulates ovulation

46
Q

FSH - women

A

stimulates oestrogen production

47
Q

Oestrogen

A

Endometrial Proliferation

Breast Development

48
Q

Progesterone

A

Increases Body temperature

Secretory endometrium

49
Q

Where is insulin produced?

A

Beta cells in the islets of Langerhans produce insulin in response to rising glucose/food.
Promote the storage of glucose in fat, muscle, liver and other body tissues

50
Q

What do alpha cells produce?

A

Alpha cells produce glucagon in response to lowering glucose

51
Q

What do beta cells produce?

A

insulin

52
Q

Hypopituitarism

A

Progressive loss of Anterior Pituitary function: FSH/LH and GH; TSH; ACTH.

53
Q

What disease does cortisol excess in central lead to?

A

Cushing’s Disease

54
Q

Cushing’s Disease

A

Excess cortisol in the blood due to an ACTH
secreting pituitary tumour

High cortisol, high ACTH

55
Q

What disease does cortisol excess in adrenal lead to?

A

Cushing’s Syndrome

56
Q

Cushing’s Syndrome

A

Excess cortisol in the blood due to
overproduction of cortisol in the adrenals

High Cortisol, low ACTH

57
Q

Principles of endocrine investigation

A

Based on negative feedback – the hormone suppresses its own production

Administer supra-physiologcal levels of hormones – eg 1mg Dexamethasone

Healthy response – endogenous cortisol low - suppressed

Abnormal response – cortisol not suppressed suggesting lack of physiological control

58
Q

Overnight Low Dose Dexamethasone Suppression Test

A

Dexamethasone 1mg is given at 11pm the night before

Cortisol is measured at 8am the next morning

Cortisol suppression to <50nmol/l is normal

Cortisol above 100nmol/l suggests autonomous cortisol production – likely Cushing’s

59
Q

Posterior Pituitary - Diabetes Insipidus

A

Excretion of a “large” volume (usually >4 L/d) of hypotonic urine in absence of glycosuria.

60
Q

Test for Posterior Pituitary - Diabetes Insipidus

A

water deprivation test

61
Q

Hypothyroidism

A

Low thyroid hormones T4/T3 and high TSH (periphery cause)

62
Q

Hypothyroidism - Clinical Features

A

Insidious onset, tiredness, lethargy, cold intolerance, constipation, weight gain, bradycardia, loss of hair/eyebrow, slow relaxing reflex

63
Q

Hypothyroidism - Treatment

A

Thyroxine replacement

64
Q

Hyperthyroidism

A

High thyroid hormones T3/T4, Low TSH, Thyroid antibodies positive

65
Q

Hyperthyroidism - Clinical features

A

Excess sweating, weight loss, diarrhoea, heat intolerance, palpitations, atrial fibrillation (irregular Heart rate), heart failure, anxiety, eye signs, goitre

66
Q

Hyperthyroidism - Treatment

A

surgery, radioactive iodine,

Carbimazole – prevents iodinating tyrosine by thryroid peroxidase reducing levels of hormones

67
Q

Addisons Disease

A

Autoimmune destruction of adrenal cortex

Low cortisol, aldosterone, high ACTH

68
Q

Addisons Disease - Clinical Features

A

Pigmentation – from ACTH excess

Lethargy, malaise, weight loss

“salt wasting” - hyponatraemia (low sodium),

hyperkalemia (high potassium which could be potentially
life-threatening)

Hypoglycaemia, vomiting, low blood pressure along
with

hyponatraemia and hyperkalemia = Addisonian Crisis – Medical emergency

69
Q

Female infertility - amenorrhea - Central

A

Pituitary Destruction – tumour, trauma

Hyperprolactinaemia – high prolactin inhibits LH/FSH

Genetic syndromes - Kallman’s Syndrome

Anorexia Nervosa

70
Q

Female infertility - amenorrhea - Ovarian

A

Polycystic Ovarian Syndrome

Ovarian Failure – tumour, trauma

Ovarian dysgenesis – genetic syndromes

71
Q

Male infertility - Central

A

Pituitary Destruction
– tumour, trauma

Hyperprolactinaemia
– high prolactin inhibits LH/FSH

Genetic syndromes
- Kallman’s Syndrome

Anorexia Nervosa

72
Q

Male infertility - Testicular

A

Tumour, torsion, varicele, orchitis, trauma

Testicular dysgenesis due to genetic disorders

73
Q

Diabetes Mellitus

A

Chronic diseases characterised by abnormalities of metabolism (carbohydrate, fat and protein) resulting from either

74
Q

What is one of the common diseases in the world and one of the major health burdens on the NHS?

A

Diabetes Mellitus

75
Q

type 1

A

Deficiency of insulin

76
Q

type 2

A

Resistance to the actions of insulin

77
Q

type 2

A

Damage to pancreas

78
Q

Diagnosis of diabetes

A

HbA1c (glycolated haemoglobin) cut point of ≥6.5% (48mmol/mol)

79
Q

Type 1 diabetes

A
  • requires insulin from the moment of diagnosis
  • no insulin production due to a combination of genetic, environmental and immunological factors leading to β-cells destruction
  • Onset “dramatic” and insulin required to sustain life
80
Q

Type 2 treatment focus

A

Metformin

GLP-1 analogues

SGLT2 inhibitors

Insulin at later stages

81
Q

Diabetes is dangerous due to two complications

A

Microvascular complication
- Retinopathy
- Neuropathy
- Nephropathy

Macrovascular Complication
- stroke
- myocardial infarction
- peripheral vascular disease

82
Q

Type 2 diabetes

A
  • Combination of cell secretary defect and insulin
    resistance
  • Late Onset, usually in adulthood
  • Insulin resistance
  • Risk factors include:
    Obesity especially central (abdominal) obesity
    Lack of exercise

Family history
Insulin resistance syndromes

Pathology And Medicine (15 decks)

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