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Endocrine Axes: / Hypothalamus / Pituitary Gland / Target Organs…

- - - - SCN = Suprachiasmatic Nuclei
        
        "SUPRA CIRCADIAN Rhythm"
        
        Notes:
        
        SCN recieves info from the retinohypothalamic tract = RHypo tract
        --> is actually stimulated through the RHypo tract
        
        tells pineal gland to make melatonin
        --> spikes at night
        
        decreases body temperature and cortisol levels
        --> cortisol peaks in the morning
        
        Clinical Cases
        
        Clinical Case
        
        Clinical Case
        
        Notes:
        
        note that
- - - - *Adrenal Glands
        
        Adrenal Medulla = MIDDLE = "CAT in the MIDDLE of a BED curled up..."
        Adrenal Cortex = OUTER = "OUTER part of kidney = GFR... and SEX"
        --> In SEX, the DEEPER you go in GFR, the SWEETER IT GETS
        GFR = think the RAAS system from kidney (GFR) to the adrenals for aldosterone production
        G = glomerulus zona = salt = aldosterone
        --> stimulated by Angiotensin 2
        F = fascicularis zona = sugar = cortisol
        --> stimulated by ACTH and CRH
        R = reticularis zona = sex = androgens
        --> stimulated by ACTH and CRH
        CAT in bed = adrenal medulla cat = c =atecholamines
        --> Epi and norepi
        --> stimulated by ACh from SNS
        
        Adrenal Gland Pathology
        
        Pheochromocytoma
        
        adrenal medulla benign tumor
        
        chromaffin cells
        --> chromocytoma
        
        secretes atecholamines (Epi and NE)
        
        Paraganglioma
        
        Differential to Pheochromocytoma
        
        .
        
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        Case Presentation:
        
        Notes:
        
        Pheochromocytoma is a benign tumor of the adrenal medulla
        
        it is a catecholamine producing tumour
        --> tachycardia
        --> paroxysmal hypertensive episodes
        
        Adrenal Gland Hormones
        
        Catecholamine Release
        
        from the adrenal medulla --> cat in the bed
        
        stimulated by ACh release for Sympathetic NS
        
        Notes:
        
        solution = adrenal medulla stimmed by ACH from SNS
        
        note that the adrenal medulla makes catechols
        --> 80% mostly = epi, 20% norepi
        
        Clinical Case
        
        Catecholamine Synthesis
        
        Tyrosine --> DOPA --> dopamine --> NE --> Epi
        
        Tyrosine --> DOPA = rate limiting step
        
        TYRANTS are DOPE and they make PerMNT (permanent) Epi
        
        Catecholamine Synthesis example
        
        Case Presentation:
        
        Notes:
        
        note PNMT = phenyl .. - N methyl transferase = last step to make Epi in the Tyrosine --> DOPA line
        
        note that ACTH also leaks from the cortex into the medulla to increase the PNMT and Epi synthesis
  - - - Thyroid Glands
        
        T3 = diiodothyronine
        
        T4 = thyroxine
        
        Bound T4
        
        99% of thyroxine is bound
        to plasma carrier proteins
        
        large reservoir of binding proteins
        
        80% thyroid binding globulin
        
        10% prealbumin
        
        remain on albumin
        
        T3 = diiodothyronine
        
        at target cells, T4 converted to T3
        
        PARATHYROID GLANDS
        
        parathyroid Hormone (PTH)
        
        increases Ca2+ and PO4- levels
        --> by stimulating osteoclasts to break down bone
        
        - BONES
        
        PTH related conditions
        
        Pseudohypoparathyroidism
        
        Notes:
        
        recall the actions of PTH
        --> 3 main actions = liver (+ kidney through VD3), osteoblasts (bone)
        
        PTH acts on the liver where stored vit D = 1-OH-VD3 is, converts it into active 1,25-OH D3
        
        1,25-OH D3 then acts on the kidneys to increase reabsorption of Ca++ and increase excretion of PO4-3 (phosphate)
        
        PTH also activates the RANKL binding from osteoblasts onto RANK receptors of osteoclasts to start bone reabsorption for Ca++
        --> PTH also stops the OPG self inhibition from osteoclasts, thus also increasing their activity
        
        PTH acts on the gut to increase absorption of vit D
        
        Clinical Case:
        
        .
        
        calcitonin
        
        opposite to parathyroid hormone (PTH
        
        decreases blood Ca2+ and PO4- levels
        --> by stimulating osteoblasts to lay down more bone
        
        +
        
        calcitriol = active form of Vitamin D
        
        -
        
        GIT
        
        calcitonin increases the uptake of Ca2+ from the diet to increase bone growth
        
        .
        
        +
        
        *Thyroid Pathology
        
        Ectopic Thyroid
        
        failure of Thyroid Migration during development
        
        Notes:
        
        note that the thyroid gland actually migrates down to below he cricothyroid cartilage joint
        
        failure of this migration results in ectopic thyroid
        --> this can be sublingual, etc.
        
        Clinical Case
        
        Hyperthyroidism
        
        Hashimotos Disease
        
        autoimmune hypothyroidism
        
        present earlier in life
        
        .
        
        Notes:
        
        note the large germinal lymphoid centres in the histology that develop in Hashimotos
        
        Hashimotos usually present with a diffuse goiter that enlarges slowly over time
        
        Clinical Case
  - - - .
        
        GnRH
        low frequency
        high amplitude
        
        FSH
        Follicle Stimulating
        Hormone
        
        Gonads
        
        testosterone/estradiol
        
        .
        
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        .
        
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        inhibin
        
        upregulates the FSH beta subunit and
        
        also inibits Hypothalemus
        
        inhibin is actually an activator on cells in paracrine to it
        
        -
        
        activin
        
        upregulates the FSH beta subunit
        
        +
        
        GnRH
        low amplitude
        high frequency
        
        LH
        Leutinizing Hormone
        
        .
  - - - *GH Growth Hormone
        = somotatropin
        
        LIVER
        
        IGF-1
        Insulin-like Growth Factor 1
        
        .
        
        Bound IGF-1
        
        90% bound to IGF
        binding globulin/protein
        (=IGFBP)
        
        80% on specific IGFBP-3
        
        IGF- 2
        Insulin-like Growth Factor 2
        
        mainly fetus growth
        
        Indirect IGF1,2 Effect
        
        Indirect effect in body
        
        Mostly (not always)
        long term metabolic effects
        
        hours to days
        --> DNA, RNA synthesis,
        cartilage growth (
        main growth in vert and legs),
        increased cell hyperplasia
        & hypertrophy
        
        Muscle, Bone, Adipose Tissue
        
        Bound GH
        
        50% of GHis bound
        to GH binding globulin
        
        GH = somatotropin
        
        Direct effect in body
        
        Mostly (not always)
        short term metabolic effects
        
        min. to hours
        
        AA uptake
        
        lipolysis
        
        protein synthesis
        
        ..
      - *IGF-1
        
        Insulin like Growth Factor -1
        --> note that fetus has IGF-2 for growth and this switches to IGF-1 at birth?
        
        IGF-1 is the major growth factor that is released secondary to GH
        
        IGF-1 is made in the liver in response to GH release
  - - - TRH (+)
        
        TRH
        
        main activator of Prolactin
      - Dopamine (-)
        
        Dopamine
        
        main inhibitor of Prolactin
      - Prolactin inhibits GnRH
        
        thus lowers FSH and LH
        
        reason why breastfeeding prevents ovulation
        
        (-) GnRH
        
        *Pregnancy and prolactin control
        
        note that during pregnancy it is the high estrogen that increases the prolactin release
        
        note that prolactin actually inhibits estrogen though
        
        *Hyperprolactinemia Causes
        
        Prolactinomas
        --> benign tumors
        
        hypothyroidism (Hashimotos)
        --> since they have low t3/t4 and high TRH
        --> TRH increases BOTH TSH from the Anterior Pit for the thyroid and also prolactin from the Anterior Pit
        
        *Prolactinomas
        
        benign tumors that have a classic triad P/C
        --> galactorrhea, down bone density, ammenorrhea
        --> can have +/- headaches and also bitemporal hemianopia
        
        hypothyroidism (Hashimotos) amd high prolactinemia
        --> since they have low t3/t4 and high TRH
        --> TRH increases BOTH TSH from the Anterior Pit for the thyroid and also prolactin from the Anterior Pit
        
        *Tuberinfundibular Dopaminergic Pathway
        
        nucleus accumbans (hypothalamus) --> anterior pituitary gland
        
        dopamine inhibitory pathway from the hypothalamus on prolactin release from the anterior pit
        
        Antipsycotics --> prolactinemia
        
        since you are stopping the 1/4 dopamine pathways that is meant for inhibiting prolactin release
        --> hypothal control over the anterior PIT
        
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        Lesions (-)
        
        Supra sellar / Infundibular lesions
        
        Prolactin is the ONLY hormone in the pituitary glands that is negative inhibited by the hypothalamus
        
        so if you get something that stops the hypothalamus releasing dopamine
        --> antipsychotics
        
        also a lesion pushing on the pituitary stalk
        
        it will stop the inhibition and TRH will cause prolactin release
        --> headache is a key symptom then
        --> think of the classic triad for prolactinoma
        
        Clinical Cases
        
        Clinical Case
        
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- - - - *Neuorphysin 1
        
        carrier proteins for Oxytocin?
        
        *Neuorphysin 2
        
        carrier proteins for Vasopressin = ADH