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Module 6: Endocrine > Hypothalamo-pituitary axes > Flashcards

Hypothalamo-pituitary axes Flashcards

1
Q

Describe the function of the hypothalamus and its role in homeostasis

A
  • Acts to secrete endocrine hormones
  • Autonomic and motor function control
  • Regulates food and water intake
  • Sleep-wake cycle regulation
  • Circadian rhythm
  • Temperature regulation
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2
Q

Anterior pituitary gland: Adenomas - effect on function

A
  • Do NOT metastasise
  • Still produce hormones (well differentitated) and respond to feedback loops
    • Some do not produce hormones

HOWEVER:

  • Due to their location pressure symptoms are see produced and the optic chiasm may be compressed
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3
Q

Posterior pituitary gland: ADH - Function, pathology

A

Acts within the kidney tubules. Promotes the reabsorption of Na+ and H2O. Increases blood pressure.

Stimulus: Increased osmotic pressure and volume depletion

Pathology:

  • ↓ ADH can causes diabetes insipidus: Polyuria, polydipsia
  • ↑ ADH leads to haemodilution (too much water) e.g. SIADH
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4
Q

Posterior pituitary gland: Oxytocin - Function, pathology

A

Function:

  • Positive feedback mechanism
  • Milk ejection and uterine contraction

Pathology:

↓ oxytocin leads to inabilty to progress through labour and difficulty breast feeding

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5
Q

HPA: Outline the HPA axis and assoicated negative feedback loops

A
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6
Q

Describe the regulatory factors that can modulate or fine control hormone secretion (5 possible)

A
  • Negative/positive feedback
  • Receptor down regulation
  • Generating a precursor/prohormone
  • Circulating hormone is bound by a protein, renders it inactive
  • Regulation of intracellular mechanisms
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7
Q

Describe disorders of the HPA axis

A
  • Disorder of the anterior pituitary gland: Cushing’s disease
    • Leads to overproduction of ACTH and subsequent overproduction of cortisol
    • Symptoms: Centripetal obesity, buffalo hump, moon face, red straie, hyperpigmentation, recurrent infection, thinned skin
  • Disorder of the adrenal gland: Addison’s disease
    • Causes decreased synthesis of cortisol
    • Symptoms: Fatigue, weight loss, nausea hyperpigmentation (buccal surfaces)
  • Ectopic tumour
    • May produce ACTH, stimulating cortisol release
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8
Q

Describe, with examples, the basis of endocrine dynamic testing

A

Suspected deficiency - stimulation test

Suspected overproduction - suppression test

Stimulation test:

  • Use synthetic ACTH - synacthen
  • Should stimulate production of cortisol
  • If no increase in cortisol seen then indicates a problem at the adrenal gland
  • Repeated for CRH
  • Insulin stress test: Evoke hypoglycaemia. Should increase cortisol levels
  • Image glands

Suppression test:

  • Rule out exogenous steroid use!
  • Use cortisol e.g. dexamethasone
  • Use low dose (1 mg), should see suppression in normal axis
  • Use higher dose (2 mg) if no suppression. Should see some suppression for overproduction (acts via negative feedback loop)
    • If ACTH source outside of the pituitary gland then suppression will be < 50 %
  • Use 24 hr urine monitoring
  • Cortisol levels highest in the morning and lowest at night
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9
Q

Describe the structure and function of thryoid hormones

A
  • Phenylalanine derivative hormones
    • via Tyrosine on TGB
  • Hydrophobic so circulate bound TBG
  • Functions:
    • Increase BMR
    • Increase HR
    • Increase heat production
    • Increase production of energy producing enzymes
    • Released in response to stress, cold
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10
Q

Describe the anatomy and function of the thyroid gland

A
  • Found between vertebral levels C1-C5 (lobes)
  • Isthmus seen between the 2nd and 4th tracheal rings
  • Superior thyroid artery from external carotid artery
  • Inferior thyroid artery from the thryocervical trunk fo the subclavian artery

Functions:

  • Sequesters iodide from the blood
  • Synthesis of T3, T4, calcitonin and reverse T3
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11
Q

Describe the synthesis of thyroid hormone synthesis

A
  1. Na+/K+ ATPase linked Na+/I- symporter transports Iodide into follicular cells
  2. Pendrin channels allow passage of iodide into the colloid lumen
  3. TGB is packaged and released in the colloid
  4. TPO converts 2I- → I2
  5. TPO places iodine molecules on tyrosine residues of T1 and T2
  6. TPO then performs coupling and conjugation reactions of T1 and T2 to generate T3 and T3
  7. TGB is transported back into the follicular cell and undergoes degradation to release T4 and T3
  8. T3 and T4 circulate bound to TBG

T4 → T3 occurs in the thyroid, brain and peripheral tissues

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12
Q

Outline the HPT axis and any associated negative feedback pathways

A

Beta-blockers can act to prevent conversion of T4 to T3

Glucocorticoids may also inhibit TSH

Lithium and carbimazole can be used to decrease synthesis of T4 and T3 (TPO inhibition)

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13
Q

Describe the consequences of thyroid hormone dysregulation (hypo and hyper thyroidism)

A

Hypothyroidism: Hashimoto’s

  • A type IV hypersensitivity/autoimmune reaction which sees destruction of the thyroid gland
  • Symptoms: Cold intolerance, weight gain, decreased appetite, dry hair and skin, bradycardia, exopthalamus (inflammtion, accumulation of GAGs and oedema), goitre
    • In children causes dwarfism and retardation

Hyperthryroidism: Grave’s

  • An autoimmune condition which sees the production of TSI (thyroid stimulating IGs) which bind the TSH receptor, stimulating thyroid hormone production
  • Symptoms: Tremor, tachycardia, heat intolerance, polyphagia, weight loss, goitre
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14
Q

Outline the mechanism of action of thyroid hormone

A

Thyroid hormone binds RXR. The complex then acts at the TRE to induce changes in gene expression.

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15
Q

Outline the 3 types of thyroid disease

A

Secretory: Hypo or hyper

Swelling of the entire gland: Diffuse goitre

Nodules: Normal, hypo or hyper secretory

  • May be single, multiple, benign or malignant
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16
Q

Outline the treatment of hypo and hyperthyroidism

A

Hypothyroidism: Administer T4

Hyperthyroidism:

TPO inhibitor: Carbimazole.

Corticosteroids: Decreased T4 to T3 conversion

Beta-blockers: Decrease T4 to T3 conversion and decrease bradycardia.

☆ Results are delayed due to large stores of thyroid hormone in the thyroid gland (via TGB). Use beta-blockers to elicit immediate effects

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17
Q

HPS: Outline the HPS axis and associated negative feedback pathways

A

Positive regulation: Thyroid hormone, hypoglycaemia, dopamine, nicotinic acid, histamine

Negative regulation: Glucocorticoids, hyperglycaemia

18
Q

Describe IGF-1

A
  • Insulin-like growth factor-1
  • A peptide hormone
  • Circulates bind to IGF-BPs (mainly BP3)
  • MOA: Via 2 receptors IGFR and insulin receptor
  • Antagonises insulin - increases blood glucose levels
  • Increased IGF-1 levels are associated with neoplasm
19
Q

Describe the normal diurnal pattern of GH secretion

A
  • GH peaks every 4 hours
  • Largest peak is seen 1 hour after the onset of deep sleep
  • Lowest levels seen in the morning
  • Levels are very variable (a single measurement is inhelpful)
20
Q

Describe the changes in GH secretion throughout life and relate to normal growth patterns and auxologic criteria

A
  • High levels in utero and in early childhood
  • Decrease gradually
  • Peak seen following the onset of puberty
  • Decrease in later life
  • Growth is dependent upon the fusion of epiphyses - determined by levels of sex hormones
  • GH secretion is greater in females
21
Q

Describe the causes of abnormal GH production

A
  • Defect in the axis
  • Hypersecretion of GH
  • Nutrition
  • General health
22
Q

Describe the effects of GH deficiency in adults and children. How is this diagnosed?

A

Adults: Increased body fat, decreased muscle mass, reduced exercise tolerance

Children: Stunted growth

Diagnosis

Stimulation tests - insulin stress test: Fasting state. Induce hypoglycaemia, via insulin, or use arginine. Should cause GH levels to rise, and subsequent rise in IGF-1.

23
Q

Describe the effects of GH hypersecretion in adults and children. How is this diagnosed?

A

Adults: Acromegaly

  • Signs/symptoms: Prominent supraorbital ridges, blunting of features, bony growth of extremities, headaches

Children: Gigantism

Diagnosis

Suppression test- Glucose tolerance test: Induce hyperglycaemia. Should see a reduction in GH levels

24
Q

Describe the HPG axis in males and any associated negative feedback pathways

A

DESMOLASE

25
Q

Describe the HPG axis in females and any associated negative feedback pathways

A

ARATOMASE

26
Q

From which hypothalamic nuclei is GnRH released?

A

Pre-optic and arcuate nuclei

27
Q

Describe the function of GnRH and levels throughout life

A

Function: Determines primary sexual characteristics and secondary sexual characteristics

Levels:

  • Infrequent small release of GnRH, LH and FSH
  • Peak in amplitude and frequency in puberty
  • Levels decrease in later life
28
Q

Outline the factors influencing pulsatile release of GnRH

A
  • Adequate body fat levels must be reached (22%)
  • Kisspeptin
  • Maturation of hypothalamic nuclei
  • Inhibited by melatonin
29
Q

Outline the structure of FSH, LH and HCG

A

Glyoprotein hormones

All have identical α-chains but varied β-chains, allowing for specificity

30
Q

Outline the synthesis of mineralocorticoids, glucocorticoids and androgens

A
31
Q

Outline the basis for motivational interviewing

A
32
Q

Outline the empowerment model

A
33
Q

Outline treatments available for Type II DM

A

Sulphonureas: Act to inhibit the K+ATPase, causes hyperpolarisation, calcium influx and release of insulin.

Metformin: Reduces hepatic glucose production

SGLT-2 inhibitors: Decrease renal glucose absorption

Thiazolidinediones: PPAR-γ agonist. Increases the transcription of insulin sensitive genes

GLP-1 like molecules: Incretins which increase the first phase insulin response

  • May also use DPP-4 inhibitors
34
Q

Outline how the thyroid gland descends to its normal position.

A
  • The thyroid gland descends via the thyroglossal duct
  • Remnants of tissue may occur in this duct, leading to the formation of cysts
  • Typically located in the midline
  • Foramen caecum - linguinal node
35
Q

How could the cause of a midline cyst be determined?

A

Skin cyst, thyroid lump, thyroglossal cyst

36
Q

Name the deep fascial layers of the neck

A
37
Q

Outline the common routes of infection of the deep fascia of the neck: Retropharyngeal space and between investing and pre-tracheal fascia

A

Retropharyngeal space (posterior to the pre-vertebral fascia): Infection may spread to the superior mediastinum, carotid sheath, vertebrae and may cause inflammation of fascia (fasciitis)

Between investing and pre-tracheal fascia: Infection may spread to the anterior mediastinum

38
Q

Name the branches of the external carotid artery

A

Superior thyroid artery

Ascending pharyngeal artery

Linginal

Facial

Occipital

Posterior auricular

Maxillary

Supraclavicular

39
Q

Outline the venous drainage of the head and neck

A
40
Q

State the structures which pass through the parotid gland

A

Facial nerve

Retromandibular vein

External carotid artery

41
Q
A

Module 6: Endocrine (5 decks)

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