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ENDO > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are the two types of chromophils in histological staining?

A

Basophil (blue stain): corticotrophs, thyrotrophs, gonadotrophs) and acidophils . (:red/orange stain) somatotrophs and lactotrophes)

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2
Q

List the hormones secreted from anterior pituitary cellsand state the target glands for these hormones.

A

Thyrotropes –> TSH –> thyroid

Corticotropes –> ACTH –> Adrenyl cortex

Soatotropes –> GH –> liver

Gonadotropes –> FSH & LH –> Gonads

Lactotropes –> Prolactin (PRL) –> Mammary glands

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3
Q

ACTH is a peptide that is synthesised as a part of a larger prohormone. What is this prohormone called? This prohormone contains the peptide sequence for ATCH and 3 others. What are they?

A

The prohormone for ACTH is POMC (proopiomelanocortin).

POMC contains the peptide sequence for ACTH, a- and b-MSH, endorphins (endogenous opioids), and enkephalins.

ACTH is the sole active hormone secreted from these cells (in humans).

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4
Q

Is b-lipotropic hormone (b-LPH) cleaved out POMC cell when ACTH is synthesised?

A

Yes… lol I think can someone double check

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5
Q

What receptor does ACTH bind to in the adrenal cortex and what is the signaling pathway?

A

ACTH bind to MC2R on cells in the adrenal cortex.

MC2R is a GPCR coupled to Gs-cAMP-PKA signaling pathway

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6
Q

What do corticotropes secrete?

A

ACTH, which stimulates two zones of the adrenal cortex.

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7
Q

The parivicellular neurons that express CRH also coexpress ADH. How does it effect CRH?

A

ADH potentiates the action of CRH on corticotropes.

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8
Q

What sort of pattern does the secretion of ACTH usually have?

A

Secretion of ACTH shows a pronounced diurnal pattern, with a peak early in morning and a valley in late afternoon.

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9
Q

What can stimulate ACTH secretion?

A

Many types of stress, both neurogennic (e.g. fear) and systemic (e.g.infection) stimulate ACTH secetion

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10
Q

Cortisol exerts a negative feedback. How does this work?

A

On the pituitary - supresses POMC gene expression and ACTH secretion

On the hypothalamus - decreases pro-CRHgene expression and CRH release

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11
Q

What happens in long-term administration of exogenous corticosteroids?

A

Long term administration of exogenous corticosteroids will cause the adrenal cortex to atrophy (waste away) because of negative feedback

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12
Q

What are some reasons for excessive ACTH production?

A

Excessive ACTH production can rise from a corticotroph adenoma (benign tumour) or from a extrapituitary ectopic (abnormal) tumour source.

Small cell lung carcinomas, bronchial carcinoids, and neuroendocrine tumours are common causes of ectopic ACTH production.

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13
Q

What are the three pituitary glycoprotein hormones? (glycoproteins have a carbohydrate attached)

A

TSH, FSH, LH

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14
Q

What does it mean that TSH is a heterodimer?

A

Composed of an a-subunit (a-glycoprotein subunit) (a -GSU) and a B-subunit (B-TSH)

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15
Q

Briefly explain the heterodimer structures of TSH, FSH and LH

A

The a-GSU is common to TSH, FSH, and LH, wheras the B-subunit is specific to the hormone (b-TSH, B-FSH, and B-LH are all unique).

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16
Q

TSH binds to the TSH receptor on thyroid epithelial cells. What is the TSH signal transduction pathway?

A

TSH receptor is a GPCR linked to a Gs-cAMP-PKA

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17
Q

TSH stimulates essentially every aspect of thyroid function. What does it mean that TSH has a strong tropic effect?

A

TSH stimulates hypertrophy, hyperplasia and survival of thyroid epithelial cells.

Bit of a crappy worded question, feel free to change, just didnt know how to ask it.

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18
Q

What can elevated TSH levels lead to?

A

Elevated TSH can produce noticeable grwoth of the thyroid - goiter

19
Q

How does negative feedback work in the hypothalaus-pituitary-thyroid axis?

A

The active form of thyroid hormone T3 negatively feeds back on both pituitary thyrotropes and TRH-producing neurons.

T3 represses both b-TSH expression and the sensitivity of thrytropes to TRH

T3 also inhibits TRH production and secretion.

20
Q

Gonadotropes is a dual hormone produce (FSH and LH). FSH and LH bind to their respective receptors. What sort of receptors are they and what are their signaling pathways?

A

FSH and LH both have GPCRs primarily coupled to Gs-cAMP-PKA signalling pathways.

21
Q

FSH and LH (Gonadotropins) increase sex steroid synthesis. Lets talk about them, and how there feedback systems work.

A

In men, testorerone and estrogen negatively feed back to pituitary and hypothalamus.

Inhibin negatively feed backs ONLY FSH secretion in both men and women

In women, progesterone and testosterone negatively feed back to pituitary and hypothalamus.

At low doses, estrogen has negative feedback on FSH and LH.

HOWEVER, high estrogen levels cause a surge of LH (this positive feedback loops back to hypothalamus and pituitary)

22
Q

A major target of GH is the liver. What does it stimulate?

A

It stimulates the production of IGF-1

23
Q

How does the hypothalamus inhibit pituitary GH and TSH release?

A

Somatostatin

24
Q

Chemically, is prolactin related to growth hormone?

A

Yes, they have 199 amino acids in a single-chain polypetide

25
Q

Does prolactin circulate bound or unbound?

A

Circulates unbounded to proteins and thus has a relatively short half-life of about 20 minutes.

26
Q

What is the signaling pathway of PRL?

A

JAK-STAT Signaling pathway. Binding of PRL to its receptors in the mamary glands (tyrosine kinase activation, transcriptional regulation, and ultimately, synthesis of milk proteins?

27
Q

What are the effects of prolactin?

A
  • During puberty - prolactin stimulates breat development (stimulating growth of the alveolar component of breast tissue)
  • In pregnancy - the final alveolar and ductal development of breasts
  • After parturition (giving birth) - suckling promotes prolactin synthesis and release
  • Inhibition of gonadotropin-releasing hormone and therefore suppression of the femal reproductive cycle.
28
Q

What inhibits PRL release? What stimulates release of PRL?

A

PRL release usually inhibited by hyptohalamus via dopamine (which binds to D2 receptor, which is linked to a Gi signalling pathway.

Drugs that interfere with dopamine synthesis/ action increase PRL secretion. This can lead to hyperprolactinemia.

PRL-secreting tumours (prolactinomas) account for around 70% of all anterior pituitary tumours.

Somatostation also inhibits PRL

29
Q

What happens to the gonads and ultimately the reproductive cycle in hyperprolactinemia?

A

In hyperprolactemia, the GnRH release, the gonadotrope response to GnRH, and the ovarian response to LH all decrease. The preovulatory estrogen peak is lost, thereby lengthening the cycle and leading to oligomenorrhea (infrequent menstrual cycles) and anovulatory cycles (no ovulation).

In men, hyperprolactinemia produces infertility.

30
Q

How are lactotropes different to other endocrine cell types of the adenohypophisis?

A
  • Lactotropes are not part of an endocrne axis. PRL acts directly on non-endocrine cells to induce physiologic changes.
  • Production and secretion of PRL is predominatly under inhibitory control by the hypothalamus through dopamine.
31
Q

What happens when pituitary stalk and hypothalamohypophyseal portal vessels are disrupted (e.g. due to surgery or physical trauma)

A

Results in increase in PRL levels (because PRL is usally inhibited), but a decrease in ACT, FSH, LH and GH

32
Q

What are the sorts of things that happen due to hypothalamic-pituitary lesions?

A
  • Pituitary hormone hypersecretion (gland hyperactivity) and hyposecretion (gland hypoactivity)
  • Sellar enlargement
  • Visual loss (tumour pressing on optic chiasm)
33
Q

Who’s going to absolutely bloody NAIL Endo?

A

YOU ARE!

34
Q

What usually happens in Hypopituitarism? What order of pituitary hormones do you usally loose? What are some of the symptoms?

A

The onset of pituitary insuffieciency is usually gradual.

Classic course of progressive hypopituitarism is an initial loss of GH and gonadotropin secretion. Followed by deficiencies of TSH, then ACTH, and finally PRL.

Symptoms may include:

  • impairment of GH (decreased growth in children; decreased sense of well-being; lower health-related quality of life)
  • Hypothyroidism caused by TSH deficiency (cold intolerance, dry skin, mental dullness, bradycardia, constipation, hoarseness, and anemia)
  • ACTH deficiency, adrenocortical insufficiency (weakness, nausea, vomiting, anorexia, weight loss, fever, and hypotension; hypoglycemia aggravated by GH deficiency)
35
Q

What is a pituitary microadenoma?

A
  • An intrasellar adenoma less than 1cm in diameter
  • Present with manifestations of hormonal excess without extrasellar extension
  • No panhypopituitarism (panhypopituitarism is inadequate production of anterior pituitary hormone)
36
Q

What is Pituitary macroadenoma?

A
  • Larger than 1cm in diameter
  • Cause generalised sellar enlargement
  • Tumours confined to sella turcica can usually be treated
  • Larger tumours )especially those with suprasellar, or lateral extensions) more difficult ot manage
  • Panhypopituitarism and visual loss increase in frequency with tumour size and suprasella extension
37
Q

Name a placental hormone that has structure similar to ituitary glycoprotein hormones?

A

hCG

38
Q

A 61 year old man with a diagnosis of Addison’s disease (primary adrenal insuffciency) was admitted to hospital for further investigation of high ACTH levels and hyperpigmentation. His baseline cortisol was low and level of plasma ACTH was very high. Following administration of 25mg of cortisone, the ACTH level significantly decreased. The general pigmentation also showed improvement with cortisone administration.

Explain the physiological basis of hyperpigmentation in this patient and explain why his ACTH level decreased after cortisone administration.

A

Since Adison’s disease is a primary disorder, no cortisol is being produced. Since the negative feedback is telling the hypothalamus and the pituitary that there is no cortisol, more CRH and ACTH are being synthesised and secreted. Hence, high ACTH levels. ACTH is made from the POMC prohormone which also contains the peptide sequence for b-MSH. This means that in really high concentrations, ACTH will not only bind to MC2R receptors (which no cell response is happening), it is binding to MC1R which causes melanocyte stimulation. This causes the hyperpigentation.

After the cortisone administration, negative feedback could occur. This negative feedback was then like whoa hold up, we don’t need to secrete all this ACTH. Hence, MC1R wouldn’t be as saturated which would lead to normal pigmentation. Yay.

39
Q

Name a couple physiological factors that increase prolactin secretion in females.

A
  • pregnancy
  • puberty
  • child birth
  • breast feeding
  • excercise
  • sleep
  • stress
40
Q

In females, there is inhibition of ovulation and decreased fertility during breast-feeding. Explain.

A

After birth, suckling promotes prolactin synthesis and release. This in turn inhibits gonadotropin release hormone (FSH &LH) which supress female reproductive cylce. Hence, decreasing fertility and ihibition of ovulation.

41
Q

Adenoma is one type of pituitary gland tumour that can affect the production of one or more pituitary hormones. What would be the effect of a prolactin adenoma in a man?

A

Prolactin inhibit gonadotrophs. This would lead to less FSH and LH, which would lead to less testosterence which would lead to decreased libido, erectile dysfunction and infertility.

42
Q

If an upward growth of a pituitary tumour is detected by MRI, the patient should be referred urgently to an endocrinologist. Explain why.

A

The tumour may press on optic chiams which may cause vision loss. More importantly, a pituitary tumour may lead to a pituitary hormone hypersecretion or a hyposecretion. This will in turn affect the whole endocrine system, and your endocronoligst needs to sort that out.

43
Q

A 46 year old female patient has been diagnosed with acromeagaly and referred to an endocrinologist. Visual field assessment reveals bitemporal heminaopia. MRI demonstrates a large pituitary mass extending to and compressing the optic chiasm. Serum prolactin was 300ng/mL (57ng/mL), ACTH and TSH was undectectable; free thyroid hormone (T4) was 0.2ng/dl (0.4ng/dL0 and an ACTH stimulation test gave a serum cortisol value of 9ug/dL/L (9-11 ug/dL).

The pat

A

ENDO (10 decks)

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