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s2 - Embryo, Cardio, Endo, GI, Neuro, Pharm > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Where would a paracrine hormone act?

A

in local ECF to neighbouring cells

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2
Q

What controls neuroendocrine cells?

A

synaptic transmission

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3
Q

Where embryologically do the
- ant pituitary
- post pituitary
develop from?

A

ant - from oralpharynx ectoderm - rathke’s pouch
post - from neural ectoderm, extension of infundibulum

In floor of 3rd ventricle

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4
Q

Where do the hypothalamic parvocellular neurosecretatory cells release hormones?

A

into the capillaries of the median eminence to ant pituitary

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5
Q

Where do the hypothalamic magnocellular nuclei project to?

A

post pituitary

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6
Q

Name 3 parameters that cause increased release of GH.

A
  • Hypoglycaemia, starvation
  • low FA
  • excercise
  • sleep
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7
Q

Name 2 parameters that cause decreased release of GH.

A
  • hyperglycemia

- high FA

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8
Q

Outline GH action.

A
  • stimulates liver IGF1 production
  • increases lipolysis so increases FA
  • increases gluconeogenesis
  • stimulates chondrogenesis (more linear growth) up to 20yrs
  • stimulates somatic/organ growth
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9
Q

Acromegaly symptoms in adults may include…

A

…insulin resistance, diabetes and hyperglycemia

-increased mass/thickness of bones

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10
Q

Name whats made in these adrenal cortex layers:
zona glomerulosa -
zona fasiculata -
zona reticularis -

A

z glomerulosa - mineralocorticoids
z fasiculata - cortisol
z reticularis - testosterone

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11
Q

Explain 2 steps in screening for Cushing’s?

A
  • cortisol levels at night (loss of dinural rhythm)

- dexamethasone 11pm, measure cortisol in morning (los s of negative feedback)

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12
Q

What patient groups might be suspected to have Cushing’s, (but have pseudocushing’s)?

A

-depressed, alcoholics, anaorexics

baseline higher cortisol level individuals

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13
Q

How do you confirm a diagnosis of Cushing’s/rule out pseudocushings?

A

Low dose 48hr Dexamethasone Supression Test

should be <50 at end, if not it is true Cushings

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14
Q

How can you determine if Cushing’s is caused by excess ACTH from the pituitary/adrenal or an ectopic site?

A

High Dose 48hr Dexamethasone Supression Test

if pituitary/adrenal, ACTH should fall to 50% baseline-neg feedback, if ectopic will stay high

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15
Q

What metabolic results may you see in Cushing’s regarding:

  • K+ levels
  • Glucose
  • pH
A
  • hypokalemia
  • hyperglycemia
  • metabolic alkalosis
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16
Q

Why may you have the following in Cushing’s?
-hypokalemia
-metabolic alkalosis
The mineralocortidoid receptors in kidney respond normally to aldosterone, how does cortisol (usually inactivated as cortisone) have action here?

A

The enzyme 11BHSD2 which turns cortisol to cortisone can become saturated in cushings so cortisol can act in the same way as aldosterone…

  • by retaining Na+ (and lose K+ in return)
  • if K+ is depleted, when bringing in Na+ we lose H+ in return (–>low K+, high pH)
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17
Q

Which enzyme turns cortisol to cortisone?

A

11BHSD2 - 11 B Hydroxysteroid Dehydrogenase 2

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18
Q

Why can you have skin hyperpigmentation in Cushing’s?

A

-ACTH is a precursor of a-MSH which forms melanin.

Some of the ACTH forms this

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19
Q

How does the CRH test differentiate between all types of Cushing’s Syndrome?
(Results measure ACTH levels…)

A
  • an exaggerated ACTH response will be die to a pituitary tumour. It is sensitive to CRH levels.
  • an adrenal adenoma will be low. As its system is sensitive to ACTH levels, not CRH, so v low (no ACTH)
  • ectopic will be high, no neg feedback
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20
Q

Give 5 symptoms of Addison’s disease?

A
  • weight loss, hypoglycemia
  • postural hypotension
  • hyponatremia, salt craving
  • hyperkalemia, acidosis
  • nausea (steroids close pores that allow BBB to detect toxins, low steroids -> open pores -> more nausea)
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21
Q

Name 3 causes of Addison’s disease.

A
  • autoimmune condition (e.g. from TB)
  • steroid withdrawal (adrenal cortex had shrunk/reduced production)
  • enzyme defect e.g. congenital adrenal hyperplasia
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22
Q

One way to test for Addison’s is to illicit a huge stress response and measure the cortisol response. What is used to illicit this?

A

-Insulin

insulin tolerance test

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23
Q

2 Treatments for Addison’s disease

A
  • Hydrocortisone

- Fludrocortisone (also increases aldosterone)

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24
Q

What is the common enzyme deficiency in CAH-congenital adrenal hyperplasia? What is the result?

A

21-Hydroxylase

  • so cant convert progesterone-deoxycorticosterone-corticosterone to aldosterone
  • cant convert 17OH progesterone to 11-deoxycortisol-cortisol
  • so only pathway that can be maintained is testosterone production
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25
Q

What does excess sex steroids in 21OH deficiency of CAH lead to?

A
  • virilisation
  • hirsuitism
  • infertility
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26
Q

Without aldosterone in CAH Addison’s what happens to:

  • Na
  • K
  • BP
A
  • you lose salt (Na)
  • hyperkalemia
  • hypotension
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27
Q

The less common enzyme deficiency of CAH is 11BOH so deoxycorticosterone rises and has partial aldosterone action. How do these children present?
What is the synacthen test result?

A
  • Present with hypertension and hypokalaemia

- no cortisol rise with synacthen but 17OH progesterone rises (cholesterol precursor)

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28
Q

Which layer of the adrenal cortex makes aldosterone?

A

zona glomerulosa

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29
Q

What stimulates aldosterone release?

Where is this sensed?

A

-low BP
-low Na+
Macula densa of kidney

30
Q

What is Conn’s syndrome?

Give 2 symptoms

A

1ry aldosterone excess due to adrenal adenoma producing it.

  • hypertension
  • hypocalcemia
31
Q

What may be the cause of 2ndry Aldosterone Excess (driven by kidney) with hypertension?

A
  • renal disease/renin releasing tumour

- renal artery stenosis (low BP sensed)

32
Q

What may be the cause of 2ndry Aldosterone Excess (driven by kidney) with normal BP?

A

May be due to oedema in the tissues (kidney only senses low intravasular volume) caused by e.g. cirrhosis, dehydration, nephrotic syndrome…

33
Q

What is phaechromocytoma a “yellow” tumour of?

What does the tumour produce?

A

Tumour of the enterochromaffin cells of adrenal medulla

Produces catecholamines e.g. A, NA, DA

34
Q

How does a phaechromocytoma patient present?

A

-sweaty, paroxysmal HT (shoots up/down), palpitations, constipation, headache…

35
Q

How do we test for phaechromocytoma?

A

Look for metanephrines in urine (breakdown of catechols)

36
Q

A phaechromocytoma is a medical emergency how is it treated?

A
  • First a-adrenergic blockade, e.g. phentolamine
  • then B-adrenergic blockade
  • fluid resusitation and surgery
37
Q

Why is it contraindicated/dangerous to give B-blocker before a-blocker in treatment of a phaechromocytoma?

A
  • If B-blocker is given first, you cancel out the vasodilatory effect of peripheral B2 adrenoceptors
  • leading to unopposed alpha-adrenoceptor stimulation, causing vasoconstriction and ultimately hypertensive crisis
38
Q

What does lipoprotien lipase (LPL) hydrolise triglycerides from the blood into?
Which hormone favours this action?

A

Free fatty acids (in the adipocyte)

Insulin

39
Q

What does hormone sensitive lipase’s (HSL) hydrolise?

Which hormone favours this action?

A

Fat stored as triacylglycerol

Adrenaline

40
Q

Name 2 ways fat acts as an endocrine gland.

A
  • Amomatase enzymes in adipose act on androgens and oestrogens
  • leptin (secreted in response to adipose mass)
41
Q

What does the hormone adiponectin released from adipocytes do?
(this hormone is lower in obesity)

A

Increased insulin sensitivity

42
Q

Explain why you get cytokines, chemokines and macrophages raised in obesity.

A

As adipose cells increase and grow, they become further from capillaries so become hypoxic.
This triggers the inflammatory mediators.

43
Q

Give 3 effects of cholecystokinin’s (CCK).

A
  • supress appetite
  • stimulate secretion of pancreatic enzymes
  • empty gall bladder
44
Q

What type of hormones are gastric inhibitory peptide (GIP) and GLP-1?
What are their actions?

A

Incretin hormones
GIP-potentiates insulin release, inhibits gastrin release
GLP-1-potentiates insulin release, reduces appetite

45
Q

The lateral hypothalamus is the feeding centre. What 2 neurones are stimulated from here?

A

AGRP & NPY

46
Q

The ventromedial hypothalamus is the satiety centre. What neurones 2 are stimulated from here?

A

POMC & CART

47
Q

When is erythropoetin secreted by the kidney?

Where does it act?

A

In response to low partial pressure of O2 in circulation

Acts on bone marrow

48
Q

The SCN acts via the pineal gland to mediate release of….

When darkness falls, this hormone’s level..

A

MELATONIN

increases…promoting sleep

49
Q

Which thyroid hormone is responsible for the negative feedback? How?

A

T4
Intravascular T4 is de-iodinated into T3 which enters cells, so T4 is what decreases/runs out hence gives the negative feedback

50
Q

When a cell needs active T3, how does it get the intravascularly stored inactive T4 to enter and be active?

A
  • it expresses a de-iodinase on its cell surface
  • so passing T4–>T3
  • T3 enters cell
51
Q

The following are problems where?
Primary hyperthyroidism…
Secondary hyperthyroidism…
Sick Euthyroid…

A

Primary hyperthyroidism - thyroid gland (organ)
Secondary hyperthyroidism - ant pituitary
Sick Euthyroid - stress response (decreased TRH)

52
Q

What happens to LH/FSH with tumours of the ant pituitary?

A

They stop secretion as the secretion is so complex

53
Q

When/at what time does GH release peak?

A

during REM sleep

54
Q

Give 3 signs of acromegaly

A
  • acral enlargement (bigger fingers, feet, tongue, arthritis)
  • greasy sweat
  • diabetes and increased nitrogen retention (protein)
  • cardiomyopathy, bowel cancer (as fast turnover)
55
Q

Why is acromegaly described as “insiduous”

A

It takes 5yrs to notice symptoms such as coarsening of facial features

56
Q

Give 4 features of a Cushing’s Syndrome appearence

A
  • lemon on stick body shape (central obesity)
  • moon face
  • buffalo hump (temporal fat pad)
  • thin skin, bruises easily, sub-dermal cracks as purple striae
  • diabetes..osteoporosis
57
Q

What sex hormone changes occur in Cushing’s syndrome?

A
  • excess hair growth or hirtuism (as high testosterone)
  • irregular periods
  • problems conceiving (virulised)
  • impotence
58
Q

How does the hypothalamus inhibit prolactin (PRL) release?

A

Releases dopamine

59
Q

Name 3 things that may occur with a prolactinoma.

A
  • infertility as PRL inhibits LH&FSH (like contraception)
  • irregular periods, decreased sex drive
  • production of breast-milk even without a baby
60
Q

How can you treat prolactinomas pharmalogically?

A

Dopamine agonists

e.g. bromocriptine, cabergoline

61
Q

As LH and FSH pituitary tumours are “non-functioning” (dont cause a massive excess) how are they picked up?

A

Symptoms arise due to the space occupying lesion.

E.g. headache, visual field defect, nerve palsys

62
Q

The optic chiasm sits on top of the pituitary.

A pituitary tumour affects the nasal retina fibres that cross at the chiasm. Describe the visual defect?

A

Start as bitemporal upper quadrantopia as the bottom of the retina looks at the top of your visual field, and the tumour is growing from under the chiasm
-then bitemporal hemianopia

63
Q

In what order are the pituitary hormones lost with an expanding tumour?

A

In order of biological importance

  • LH/FSH (remember PRL increases as DA cant inhibit)
  • GH
  • TSH
  • ACTH last as important for survival
64
Q

What can treat GH excess pharmacologically?

A

Octreotide (biologically active somatostatin)

65
Q

Name a pharm. agent to correct deficiencies of:

  • thyroid hormones
  • sex steroids
  • cortisol
  • GH
A

thyroxine
testosterone/oestrogen
hydrocortisone
GH

66
Q

What is Vasopressin’s action and when is it released?

A
  • retains water, causes vasoconstriction

- released in response to increased plasma osmolality or decreased PaO2, or low BP

67
Q

How does Vasopressin retain water?

A

Increases CD permeability for H20

Vasoconstriction

68
Q

Name 3 causes of Syndrome of Inappropriate ADH (SIADH)

A
  • brain injury
  • infection esp pneumonia
  • lung cancer
  • asthma
69
Q

How is SIADH diagnosed?

A
  • low plasma Na+, dilute plasma

- urine Na+ high, and concentrated urine

70
Q

What are the 2 causes of underproduction of ADH also known as Diabetes Insipidus?

A
  • Cranial (lack of production)

- Nephrogenic (receptor resistance)

71
Q

Diabetes Insipidus is characterised by:
Plasma-
Urine-

A

Plasma-high Na+, high osmolality

Urine-low Na+, low osmolality (dilute)

72
Q

Diabetes insipidus categorisation as cranial/nephrogenic is via the water deprivation test. Explain this.

A
  • measure blood and urine concentration upon water deprivation
  • at end of dehydration phase give a shot of ADH
  • if body responds its cranial, if no change-nephrogenic

s2 - Embryo, Cardio, Endo, GI, Neuro, Pharm (6 decks)

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