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Pathology And Medicine > Endocrine disorders I > Flashcards

Endocrine disorders I Flashcards

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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
Thyrotropin-releasing hormone (TRH)
stimulates production of TSH stimulating thyroid hormone production
26
Growth Hormone Releasing Hormone (GHRH)
stimulates GH production
27
Antidiuretic hormone/Vasopressin (ADH)
increases how much water is absorbed into the blood by the kidneys
28
Oxytocin
release of a mother’s breast milk, moderating body temperature, and regulating sleep cycles
29
Two parts of Pituitary
anterior and posterior
30
Anterior Pituitary Hormones
 Thyroid Stimulating Hormone (TSH)  Adrenocorticotropic Hormone (ACTH)  Growth Hormone (GH)  Follicle Stimulating Hormone (FSH)  Luteinizing Hormone (LH)  Prolactin (Prl)
31
Posterior Pituitary
 Antidiuretic hormone - Vasopressin (AVP)  Oxytocin
32
Prolactin
major function of prolactin is milk production – oxytocin stimulates ejection release is tonically inhibited by dopamine from hypothalamus Inhibits gonadal function (nature’s contraceptive!)
33
Posterior Pituitary - where are hormones synthesised?
Hormones synthesized in the hypothalamus (neurons) are transported down the axons to the endings in the posterior pituitary
34
Where are posterior pituitary hormones stored?
Hormones are stored in vesicles in the posterior pituitary until release into the circulation
35
What are the principal hormones in posterior pituitary?
Antidiuretic hormone & Oxytocin
36
Antidiuretic Hormone (ADH)- Antidiuretic actions
V2 receptors - increases permeability of the collecting ducts to water – retaining water
37
Antidiuretic Hormone (ADH) - Vasopressor actions
V1 receptors - constricts vascular smooth muscle cells
38
Oxytocin
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
Thyroid gland
- Small gland in the neck
40
What hormones does thyroid release?
- Release thyroid hormones: * Thyroxine (T4) - Triiodothyronine (T3)
41
What are Tyrosine based hormones comprised of?
Partially composed of iodine - Increases Basal Metabolic Rate and thermogenesis - Increases sympathetic nerve activity
42
LH - men
acts on Leydig cells to stimulate Testosterone production
43
FSH -men
with Testosterone act on Sertoli cells to stimulate spermatogenesis
44
Testosterone
produced in Testes (Leydig Cells) and adrenal glands (zona reticularis)
45
LH - women
Stimulates androgen and progesterone production Stimulates ovulation
46
FSH - women
stimulates oestrogen production
47
Oestrogen
Endometrial Proliferation Breast Development
48
Progesterone
Increases Body temperature Secretory endometrium
49
Where is insulin produced?
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
What do alpha cells produce?
Alpha cells produce glucagon in response to lowering glucose
51
What do beta cells produce?
insulin
52
Hypopituitarism
Progressive loss of Anterior Pituitary function: FSH/LH and GH; TSH; ACTH.
53
What disease does cortisol excess in central lead to?
Cushing’s Disease
54
Cushing’s Disease
Excess cortisol in the blood due to an ACTH secreting pituitary tumour High cortisol, high ACTH
55
What disease does cortisol excess in adrenal lead to?
Cushing’s Syndrome
56
Cushing’s Syndrome
Excess cortisol in the blood due to overproduction of cortisol in the adrenals High Cortisol, low ACTH
57
Principles of endocrine investigation
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
Overnight Low Dose Dexamethasone Suppression Test
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
Posterior Pituitary - Diabetes Insipidus
Excretion of a “large” volume (usually >4 L/d) of hypotonic urine in absence of glycosuria.
60
Test for Posterior Pituitary - Diabetes Insipidus
water deprivation test
61
Hypothyroidism
Low thyroid hormones T4/T3 and high TSH (periphery cause)
62
Hypothyroidism - Clinical Features
Insidious onset, tiredness, lethargy, cold intolerance, constipation, weight gain, bradycardia, loss of hair/eyebrow, slow relaxing reflex
63
Hypothyroidism - Treatment
Thyroxine replacement
64
Hyperthyroidism
High thyroid hormones T3/T4, Low TSH, Thyroid antibodies positive
65
Hyperthyroidism - Clinical features
Excess sweating, weight loss, diarrhoea, heat intolerance, palpitations, atrial fibrillation (irregular Heart rate), heart failure, anxiety, eye signs, goitre
66
Hyperthyroidism - Treatment
surgery, radioactive iodine, Carbimazole – prevents iodinating tyrosine by thryroid peroxidase reducing levels of hormones
67
Addisons Disease
Autoimmune destruction of adrenal cortex Low cortisol, aldosterone, high ACTH
68
Addisons Disease - Clinical Features
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
Female infertility - amenorrhea - Central
Pituitary Destruction – tumour, trauma Hyperprolactinaemia – high prolactin inhibits LH/FSH Genetic syndromes - Kallman’s Syndrome Anorexia Nervosa
70
Female infertility - amenorrhea - Ovarian
Polycystic Ovarian Syndrome Ovarian Failure – tumour, trauma Ovarian dysgenesis – genetic syndromes
71
Male infertility - Central
Pituitary Destruction – tumour, trauma Hyperprolactinaemia – high prolactin inhibits LH/FSH Genetic syndromes - Kallman’s Syndrome Anorexia Nervosa
72
Male infertility - Testicular
Tumour, torsion, varicele, orchitis, trauma Testicular dysgenesis due to genetic disorders
73
Diabetes Mellitus
Chronic diseases characterised by abnormalities of metabolism (carbohydrate, fat and protein) resulting from either
74
What is one of the common diseases in the world and one of the major health burdens on the NHS?
Diabetes Mellitus
75
type 1
Deficiency of insulin
76
type 2
Resistance to the actions of insulin
77
type 2
Damage to pancreas
78
Diagnosis of diabetes
HbA1c (glycolated haemoglobin) cut point of ≥6.5% (48mmol/mol)
79
Type 1 diabetes
- 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
Type 2 treatment focus
Metformin GLP-1 analogues SGLT2 inhibitors Insulin at later stages
81
Diabetes is dangerous due to two complications
Microvascular complication - Retinopathy - Neuropathy - Nephropathy Macrovascular Complication - stroke - myocardial infarction - peripheral vascular disease
82
Type 2 diabetes
- 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

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