HPA + Thyroidal axis Flashcards

1
Q

Where does the thyroid gland develop from?

A

Pharyngeal pouches before migrating into the neck to its adult position

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2
Q

Describe the thyroidal axis?

A

TRH - Hypothalamus
TSH - Anterior pituitary
T3/T4 - Thyroid gland

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3
Q

How are T3 + T4 hormones produced?

A

Iodine is absorbed from the diet and converted to I-
I- is added to the tyrosine units of thyroglobin to form T3 or T4
T3= mostly and is more potent

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4
Q

What is hypothyroidism, what are the types and what hormones are affected?

A
hypothyroidism = low levels of thyroid home 
Primary = defect in thyroid -> normal TSH + low T3/4
central = defect in pituitary/hypothalamus -> LOW EVERYTHING
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5
Q

What are some symptoms of hypothyrodism?

How do we treat hypothyroidism?

A
dry skin
brittle nails 
menorhagia - heavy periods 
weight gain 
cold and fatigue 

Treated using levothyroxine = block and replace or dose titration

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6
Q

What is thyrotoxicosis?

What are typical features?

A

Clinical syndrome when the tissues are exposed to very high levels of thyroid hormone

  • weight loss but appetite
  • missed/irregular periods
  • lack of energy
  • mood changes
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7
Q

What is graves disease?

A

Auto immune disorder which is characterised by hyperthyroidism

Autoantibodies are produced which mimic thyroid stimulating hormone = TSH receptor antibodies

The autoantibodies can bind to thyroid stimulating receptors on the thyroid gland which causes the thyroid gland to synthesis more T3 + T4

This provides negative feedback on the hypothalamus and pituitary gland but the thyroid stimulating receptor is still active

There are other antibodies e.g thyroglobulin antibodies and thyroid peroxidase antibodies

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8
Q

What are some typical features associated with hyper thyroidism and graves?

A

Thyroid eye disease: Swelling of extra occular muscles and lymphocytic infiltration
dermopathy : skin thickening due to accumulation of amino glycans and lymphocyte infiltration

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9
Q

What can cause hyperthyroidism?

A

Toxic multi nodular goitre : Independent of the pituitary
Graves disease
Toxic adenoma : Only one area of thyroid produces XS hormones
TSHoma ( pituitary tumour)

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10
Q

How do we investigate thyroid problems?

A

TSH auto antibodies - Graves
TPO antibodies = hasimotos
Ultrasounds indicate nodules

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11
Q

How do we treat hyper thyroidism?

A

Propanolol - stop symptoms
Carbimazole
Radio active iodine: Iodine tagged with radioactive tracer and kills the thyroid follicular cells
Surgery

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12
Q

What is a thyroid storm?

What are some signs + symptoms?

A

Major complication of hyper thyroidism
Life threatening event which is caused by an XS of thyroid hormones

Tachycardia, pyrexia, vomiting, cardiac failure, congestive hepatomegaly, respiratory distress

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13
Q

What is thyroiditis?

What normally triggers it?

A
  • Inflammation of the thyroid gland -> thyrotoxicosis -> hypothyroidism
    Triggered by auto immune diseases such De Quervain’s or Ridels
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14
Q

What is the effect of amiodarone?

A

Drug that can cause severe hypo or hyperthyroidism

1: Increased thyroid hormones
2: Direct toxic effect causing leakage of contents out of the cell

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15
Q

Describe the adrenal axis?

A

CRH: Hypothalamus
ACTH: Pituitary
Cortisol: Adrenal cortex ( zona fasiculata)

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16
Q

What are the types of adrenal insufficiencies?

A
Primary = fault in adrenal gland 
Secondary = HPA axis fault. No mineralocorticoid receptor
17
Q

What is Addisons disease?

A

Addison’s disease = auto immune disease causing primary adrenal insufficiency - cortisol and aldosterone deficiencies
Symptoms = lack of energy or motivation,muscle weakness,low mood, loss of appetite and unintentional weight loss, increased thirst

18
Q

How do we diagnose and treat adrenal deficiencies?

A

9am cortisol measurements as dirunal variation
ACTH measurements - secondary adrenal insufficiencies

steroids : produces negative feedback on the pituitary to supress CRH + ACTH. Long term use may cause atrophy of the adrenal gland

19
Q

What are some of the functions of the hypothalamus ?

A
Homeostasis
Sleep
Weight and appetite 
Hormone synthesis 
HPA axis control
20
Q

Where does the APG develop from?

Where does the PPG develop from?

A

Rathkes pouch = protrouding ectodermal tissue from the roof of the mouth
Neuroectodermal tissue from the diencephalon

21
Q

What is Cushings disease + symptoms?

What is Cushings syndrome?

A
XS cortisol due to increased ACTH release from the pituitary 
Plethora
Hump back fat
thinning of the limbs 
hair loss 
abdominal obesity 
lethary 
low libido and erectile dysfunction 

Cushing syndrome = XS cortisol it may not be due to increased ACTH

22
Q

How do we diagnose Cushings?

How do we treat Cushings?

A

9am Cortisol - dirunal variation
ACTH measurements - cushings disease
Dexomethosone supression test: Dexomethosone would cause ACTH + cortisol to decrease, this would not happen in Cushings

  • Drugs that inhibit steroidgenesis
  • Removing the effector organs of cortisol e.g adrenakl glands
23
Q

What type of secretion is GnRH?
Describe the gonadol axis ?
How do we treat faults of this axis?

A

Pulsatile, is at low frequency before puberty and then will increase

  • LH = increased frequency pulses
  • FSH = low frequency pulses
  • e.g increased frequency at ovulation

GnRH
LH/FSH
Oestrogen/progesterone/tesosterone
Hormonal replacement therapy will restore these faults. But exogenous testosterone in males will not restore their fertility.

24
Q

How is prolactin regulated?

What does high levels of pro lactin cause?

A

prolactin - lactation + enlargement of mammary glands

Regulated by inhibition via dopamine
Release of dopamine -> no prolactin
Less dopamine -> more prolactin
Dopamine inhibits pro lactin release

Inhibits GnRH release -> hypogonadism

25
Q

What are prolactinomas?

What are the 2 types of prolactinomas?

A

They are pituitary tumours which disrupt the inhibitor signals of dopamine leading to hyper prolactinaemia

Micro prolactinoma < 1CM (<2000 micrograms)
Macro prolactinoma> 1CM (>400 micrograms)

26
Q

What regulates HGH ?

How does HGH exhibit its effects?

A

Human growth hormone releasing hormone
Human growth hormone inhibiting hormone ( somatostatin)

IGF-1 - affects glucose metabolism
When glucose = high less growth hormone is released
High IGF-1 = less HGH

27
Q

What is acromegaly?
What are some common symptoms?
How do we diagnose acromegaly?

A

Disorder that occurs in adult hood when there is an XS of human growth hormone

  • enlargement of bones in face, hands and feet
  • sweating
  • change in ring/shoe size
  • lethargy

Diagnosis

  • Measure IGF-1 + HGH
  • Oral glucose tolerance test: High glucose will not cause HGH to decrease
28
Q

What is diabetes insipidus?

A
  • Insufficient ADH
  • Large volumes of dilute urine
  • ## Use desmopressin to treat ( analogue of vasopressin/ADH)
29
Q

What is SIADH?

A

Syndrome of inappropriate ADH

  • XS ADH produced
  • Na+ loss in the urine
  • Conc urine is produced
30
Q

What is pituitary apoplexy?

What is Sheehans syndrome?

A

Stalk compressed causing infarction

PPH causes infarction of the pituitary gland and it enlarges after birth