Endocrinology Flashcards
Pituitary
Normal feedback
- Hypothalamic hormones excite or inhibit the pituitary
- Pituitary hormone has negative feedback to the hypothalamus and stimulates the target endocrine organ
- Target organ produces hormones which affect the target tissue and have a negative feedback to the hypothalamus
- Thyroid action:
- Thyrotropin releasing hormone(TRH) produced by hypothalamus stimulates the secretion of pituitary hormones
- Pituitary produces thyroid stimulating hormone(TSH)
- TSH stimulates the target endocrine organ (thyroid gland) and that will result in the hormonal production of the thyroid hormone to affect target tissues like the heart, bone and skin
- The thyroid hormone provides a negative feedback on the hypothalamic production of TRH,(turning the loop off)
Primary vs secondary endocrine disorder
Primary disorder - The target organ is non functional - It is an actual disorder or abnormality of the gland; the organ itself is malfunctioning Target endocrine organ does not produce hormones
Secondary disorder - The organ functions normally but it receives an erroneous message to the gland from somewhere higher up (the defect is further up, and the gland is not stimulated properly) - Hypothalamic or pituitary dysfunction are secondary disorders Hypothalamic signaling issues are a tertiary issue
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Hypothalamus on the top - sits right above the pituitary , releases hormones to the pituitary stalk
Anterior pituitary gland - releases PRL, GH, TSH, LH/FSH, ACTH - then go to their target organs and release hormones from the target organs to where they need to go
Anterior pituitary -communicates with hypothalamus with GHRH, TRH, GNRH , CRH
Posterior pituitary - makes Oxytocin, ADH – does not release any hormone
PRL - is the only hormone that is always released, the way it regulates by hypothalamus , is that dopamine releases from the stalk to shut it off. (so dopamine from the stalk inhibits PRL )
Growth hormone - if you have an excess or deficiency - you measure IGF-1 not GH in the blood. GH and ACTH are counter regulatory hormones. - what they do they OPPOSE insulin- their job is to see that you have low blood sugar and release it
- Causes the body to release more glucose into the blood.
Adrenal gland - ACTH as it releases stimulates the adrenal glands which releases aldosterone, epinephrine/norepinephrine, adrenal androgens, cortisol.
COUNTER- REGULATORY HORMONES:
GH -> Liver-> IGF-1
ACTH-> (Adrenal Gland)-> Cortisol
GH and ACTH oppose HYPOglycemia / insulin
Which means you help to release blood sugar into the bloodstream
- When you have low blood sugar, these hormones help increase sugar in the bloodstream
Excess regulatory hormones= HYPERglycemia and can cause diabetes
Renin- Angiotensin- Aldosterone regulation of Blood Pressure and Volume
Renin- angiotensin system - basically means you have low serum NA+ and low renal perfusion pressure- blood volume is low , not
enough water so blood volume is low. You go through the renin angiotensin system to release angiotensin II – vasoconstriction artery and BP increases.
Talks to the adrenal glands which releases aldosterone which helps increase blood volume and increase BP - goal is to get BP up
Angiotensin II is a major contributor to release of aldosterone
Anterior pituitary releases ACTH and stimulates adrenal glands to release more aldosterone.
Aldosterone - causes you to hang on to salt, water follows salt increases blood volume and increases blood pressure
Renin- Angiotensin- Aldosterone regulation of Blood Pressure and Volume
GOAL : To regulate blood pressure and volume
Activation:
HYPOtension
LOW serum sodium (Na+)
LOW perfusion through kidney
LOW blood volume
Aldosterone secreted by adrenal glands
Sodium (Na+) retention (water follows salt) = water retention= higher blood volume = HIGHER blood pressure
Remember:
Sodium (Na+) retention = potassium (K+) and proton (H+) excretion
EXCESS aldosterone= HYPOkalemia (too little K+)
DEFICIENCY in aldosterone = HYPERkalemia (too much K+)
Your goal - activate the system if you have low blood pressure – means you have low salt.
Low blood volume
When the system is activated your system secretes aldosterone - which causes you to hang onto salt and hang onto blood volume
– when you hang onto NA+ you excrete K+ and H+
So you can have HYPOkalemia (too little K+) - with excess aldosterone
- If you have a deficiency in aldosterone - you’ll have too much K+ hyperkalemia
Anterior Pituitary Hormones * know these
Posterior Pituitary Hormones * know these
Signs/ Sx of hormonal excess and deficiency * know these
Specific Disease Entities Associated with Endocrine Dysfunction *know this list
- Pituitary
- Acromegaly, gigantism
- Polycystic ovarian disease
- Syndrome of inappropriate antidiuretic hormone (SIADH)
- Diabetes insipidus
- Adrenal
- Cushing’s syndrome and disease
- Addison’s disease
- Congenital adrenal hyperplasia (CAH)
- Pheochromocytoma
- MEN 1/ MENII
- Neurofibromatosis
- Von Hippel-Lindau syndrome
- Thyroid
- Grave’s disease
- Thyroid storm (thyrotoxicosis)
- Apathetic hyperthyroidism
- Transient thyroiditis
- De Quervain’s syndrome (subacute painful thyroiditis/ granulomatous thyroiditis)
- Lymphocytic (painless) thyroiditis
- Hashimoto’s thyroiditis (chronic lymphocytic thyroiditis
- Parathyroid
- Osteoporosis
- Hypercalcemia (primary hyperparathyroidism)
45 y.o women presents with lethargy, fatigue, weight gain, constipation, and dry skin. Menstrual cycles have been decreasing in frequency.
She has otherwise been healthy.
Meds: daily calcium (No Rx)
Social History: No tobacco , 2 alcohol beverages per week
- These are symptoms of hypothyroidism
Which of the following scenarios is consistent with this clinical picture?
A)increase TSH, free T4 decreases
B)decrease TSH, free T4 Increase
C) decrease TSH, Free T4 Decrease
D)TSH normal, Free T4 decreases
A)increase TSH, free T4 decreases
C) decrease TSH, Free T4 Decrease
D)TSH normal, Free T4 decreases
Explanations:
Increase T4 = hyper hypothyroidism - so we look at A, C, or D , is this a primary dysfunction or secondary
Primary- it means you have a problem with the thyroid gland itself
secondary - means you have a problem with pituitary affecting thyroid
A) Hashimoto’s thyroiditis
B) a lot of T4 released so this should tell TSH to stop releasing which it does
- Primary dysfunction, thyroid gland is oversecreting T4
C) low T4- the pituitary needs to release more TSH to bring it up but TSH is not releasing
- This is secondary - the pituitary gland itself is the problem
D) low T4 , and thyroid gland is releasing TSH and hasn’t responded to the low t4 release–
- Can be possible that the pituitary gland has not had time to respond - can be the thyroid gland itself that is the problem
Clinical Signs in Thyroid Eye Disease
Lid retraction - upper & lower (“scleral show”)
- You get the stare , note to self - you should never see the upper sclera
- Conjunctival hyperemia
- Proptosis
- EOM limitation
- Optic neuropathy
Thyroid eye disease - belly of EOM and fat tissues will swell and pushes the eyeball forward causing eye retraction and proptosis
- You can also get pressure in the back of the nerve and optic neuropathy can occur
- *Thyroid Eye Disease
- Most common order of rectus muscle involvement in TED:
- Inferior> Medial> Superior> Lateral (IMSLO)
- Other orbital inflammatory disorders can mimic TED (lymphoma, pseudo tumor) -TED spares the muscle tendons on neuroimaging**
You should be most concerned about optic neuropathy in thyroid eye disease when which EOM is involved? Medial or lateral rectus?
Medial rectus- because it runs closest alongside the optic nerve, especially towards the orbital apex
*Order or most common EOM involvement:
Inferior rectus > Medial rectus > Superior rectus > Lateral rectus (rare) > Obliques (rare)
IMSLO
1. Inferior rectus
2. Medial rectus
3. Superior rectus
4. Lateral
5. Superior oblique
Is the ON towards the nose or temporally –its always oriented towards the nose, inserts nasally
The MEDIAL RECTUS - if the medial rectus is large - it can make contact with the ON and cause the compression of optic neuropathy
If they have trouble ADDUCTION , eye can’t look in – look hard for optic neuropathy because there can be compression
In TED involving the eye muscles, the muscle bellies are swollen and the tendons are spared- this can help you in your diff dx.
- Lymphoma and orbital pseudotumor are the 2nd and 3rd most common orbital inflammatory disorders and can mimic TED
In other orbital problems - what you’ll see is that everything is swollen
Thyroid eye disease is the muscle belly not the tendons !
Lab testing reveals Low TSH and low free T4. which of the following would be an appropriate next step?
A) Diagnose Thyroiditis- usually results in hyperthyroidism
B) Obtain pituitary MRI
C) Begin treatment with T3 (triiodothyronine) – usually start treatment with T4 which is more likely to circulate and easier to
regulate and treat with, most people respond well with T4
D) Begin glucocorticoids– patient has hypothyroidism - and secondary hypothyroidism, there is no thyroid eye disease - which is then you would use glucocorticoids
B) Obtain pituitary MRI
Low free T4 - HYPOTHYROIDism - so pituitary should be signaled to increase TSH , but it’s not, so the problem is with pituitary
(secondary)