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MS2 Endocrine > 10/5- Disease of the Hypothalamus and Posterior Pituitary > Flashcards

10/5- Disease of the Hypothalamus and Posterior Pituitary Flashcards

1
Q

Basics of hypothalamic-pituitary circuit?

A

Hypothalamus stimulates pituitary, which stimulates endocrine glands to secrete substances to work on distal target organs

  • Endocrine glands have negative inhibition back to pituitary and hypothalamus
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2
Q

Important!

A

Know this

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3
Q

What does GH stimulate downstream?

A

IGF-1

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4
Q

What hormones are secreted by the anterior pituitary?

A
  • GH
  • TSH
  • PRL
  • LH, FSH
  • ACTH
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5
Q

What hormones are inhibited by SS?

A
  • GH
  • TSH
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6
Q

What promotes/inhibits prolactin secretion?

A

Promotes: TRH

Inhibits: DA

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7
Q

What hormones are promoted by TRH?

A
  • TSH
  • PRL
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8
Q

Where is the hypothalamus in the brain?

A

Forms the floor of the 3rd ventricle

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9
Q

Where is the pituitary?

A

Housed in the base of the skull in the sphenoid bone “sella turcica”

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10
Q

Describe the development/embryological origin of the:

  • Hypothalamus
  • Posterior pituitary
  • Anterior pituitary
  • Intermediate lob or “pars intermedia”
A

Hypothalamus

  • derived from the diencephalon (part of the forebrain)
  • forms the floor of the third ventricle

Posterior pituitary or ”neurohypophysis”

  • arises as an evagination of the ventral hypothalamus and third ventricle

Anterior pituitary or “adenohypophysis” or “pars anterior”

  • develops from an evagination of ectoderm from the oropharynx called Rathke’s pouch

Intermediate lobe or “pars intermedia”

  • cells eventually integrate into the anterior pituitary in humans
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11
Q

Describe the neurohypophysis of the HT and posterior pituitary

A
  • Neurons organized as paraventricular and supraoptic “nuclei” in the hypothalamus
  • Axons travel down stalk to the posterior pituitary
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12
Q

Describe the vascular connection of the hypothalamic-pituitary axis

A

Rich vascularization (0.8 ml/g/min)

Internal carotid arteries

  • Superior hypophyseal artery
  • capillary network in hypothalamus
  • forms portal veins draining to the anterior pituitary
  • second capillary network in anterior pituitary
  • Middle and inferior hypophyseal arteries
  • posterior pituitary
  • pituitary stalk (infundibulum)

Venous channels:

  • Cavernous sinus
  • Petrosal sinuses
  • Jugular vein
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13
Q

What are some input signals received by the hypothalamus?

A
  • Light (circadian rhythms)
  • Olfactory
  • Neural stimuli
  • autonomic
  • Molecular stimuli: cytokines, hormones, adipokines and GI peptides, glucose, osmoles
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14
Q

How do the input molecules get through the BBB to the hypothalamus?

A
  • Fenestrated capillaries
  • Circumventricular organs
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15
Q

The hypothalamus integrates the signals and sends outgoing messages (neural and hormonal) to regulate what?

A
  • Appetite
  • Circadian rhythms (sleep-wake cycles)
  • Energy expenditure
  • Temperature (fever)
  • Endocrine systems (pituitary)
  • Sodium and water balance
  • Glucose disposal
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16
Q

Describe the basics in the hypothalamic regulation of appetite?

A
  • Leptin (produced by fat cells) stimulates arcuate nucleus, and medial hypothalamus to promote satiety (anorexigenic)
  • Ghrelin (produced by stomach) stimulates lateral hypothalamus (feeding center) to promote hunger (orexigenic)
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17
Q

If almost everyone has leptin, why is there an obesity epidemic?

A

The fatter we get, the more resistant our hypothalamus is to the signal to stop eating

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18
Q

What is the acronym for coming up with a thorough differential diagnosis?

A

VINDICATE

V- vascular

I- infection/infiltrative/immune

N- neoplastic

D- drugs

I- idiopathic/iatrogenic

C- congenital

A- autoimmune

T- trauma/surgery

E- endocrine & metabolism/electrolytes

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19
Q

What cranial nerves lie in the cavernous sinus that may be impinged upon by large masses in the pituitary (or hypothalamus?)

A

CNs 3, 4, V1, V2

20
Q

Dysregulation of hypothalamic function can cause what diseases in relation to its normal functions:

  • Appetite
  • Energy expenditure
  • Circadian rhythms
  • Temperature
  • Endocrine systems
  • Sodium/water balance
  • Limbic system
A
  • Appetite: hypothalamic obesity/anorexia
  • Energy expenditure
  • Circadian rhythms: disturbed sleep-wake signals
  • Temperature: fever/hypothermia
  • Endocrine systems: panhypopituitarism
  • Sodium/water balance: diabetes isnpidus
  • Limbic system: emotional liability, apathy, memory loss
21
Q

Dysfunctional levels of anterior pituitary hormones include what?

A
  • Decreases in: GH, TSH, LH/FSH, ACTH
  • Increases in prolactin
22
Q

What are the posterior pituitary hormones?

A
  • Anti-diuretic hormone (ADH or vasopressin)
  • Oxytocin
23
Q

What is Kallmann’s syndrome?

A

Isolated hypogonadotropic hypogonadism with anosmia (decreased sense of smell)

  • X-linked KAL gene mutation (adhesion molecule) causes abnormal migration of GnRH and olfactory neurons during development
  • Hypoplasia of the olfactory lobes
  • No GnRH pulsatile secretion; no gonadotropins (LH/FSH)
24
Q

What is hypothalamic amenorrhea?

A

Disordered GnRH pulsatility

  • Decreased LH surge during menstrual cycle
  • Lack of follicle development and anovulation
  • Decreased estrogen production (loss of bone mass)
  • ?Leptin
25
Q

What is anorexia nervosa?

A

“A disordered hypothalamus without an identifiable analotomical hypothalamic defect”

  • Weight loss
  • Loss of fat decreases leptin levels and there is dysregulation of neuropeptides involved in appetite
  • Endocrine dysfunction
  • Hypothalamic Amenorrhea due to low gonadotropins (LH and FSH)
  • Low TSH, T3, and T4
  • Normal to high GH but low IGF-1
26
Q

What is stored in the posterior pituitary?

  • Where are these substances made?
A
  • The posterior pituitary stores and secretes oxytocin and arginine vasopressin (AVP) or anti-diuretic hormone (ADH)
  • Both hormones are synthesized in cell bodies located in the paraventricular neucleus (PVN) and the supraoptic nucleus (SON) as precursors pro-pressophysin and pro-oxyphysin
27
Q

Describe the production of posterior pituitary hormones and their modification as they travel

A
  • Precursor molecules are cleaved
  • They travel with their respective neurophysins in granules down long axons through the infundibular stalk to the posterior pituitary
  • When neurons fire, the granules fuse with the axonal plasmalemma and ADH and oxytocin are released separately from the neurophysins
28
Q

How is the posterior pituitary visualized on CT? (CT or x-ray?)

A

Posterior pituitary shines brighter (without contrast) because of high numbers of granules

29
Q

What functions is oxytocin involved in?

A

“Labor, love, and lactation”

Parturation

  • Initiation and completion of labor
  • Fergusson reflex (cervical dilation)
  • Contraction of uterine myometrium: delivery, and clamping down on vessels to prevent blood loss

Lactation

  • Mechanoreceptors/touch receptors enhance milk flow by widening ducts and promoting emptying of milk from the alveoli
30
Q

What functions is Vasopressin (ADH) involved in (based on receptor subtypes)?

A

V1- vasoconstriction

  • Vascular sm
  • Liver
  • Platelets
  • CNS

V2- increased production and action of aquaporin2 water channels in principal cells of renal tubule

  • Basolateral membrane of distal nephron

V3- enhanced ACTH release

31
Q

What is the mechanism of AVP (ADH) action?

A
  • G-protein coupled V2 receptors in the collecting duct of the nephron
  • Acts via cyclic AMP to increase permeability of the tubular cell to water
  • Increase in water-conduction channels (aquaporins)
  • Glomerular filtrate becomes highly concentrated (water resorbed; anti-diuresis)
  • Lack of ADH -> impermeability and marked diuresis
32
Q

How is vasopressin release regulated?

What stimulates it?

A
  • Osmoreceptors in anterior hypothalamus stimulate vasopressin release when serum osmolality is high
  • Low pressure detected by baroreceptors in heart/major vessels can override the osmoreceptors to trigger release of vasopressin when BP is low
33
Q

ADH deficiency causes what disorder?

A

Diabetes insipidus

34
Q

What are the signs/symptoms of diabetes insipidus?

A
  • Polydipsia
  • Polyuria (nocturia)
  • Large volume urine (> 3 L/d)
  • Concentrated plasma (Na and Osm but normal if thirst intact)
  • Inappropriately dilute urine (max concentrating ability is 800-1200)
  • Complete DI: under 100 mOsm/kg
  • Partial DI: 100-800 (or 600ish)
35
Q

How is primary polydypsia distinct from diabetes insipidus?

A

Primary polydipsia (psychogenic) can look similar but plasma sodium or Osmoles are lower because of excess fluid intake (drinking drives urine output rather than urine output drives drinking)

36
Q

What are some causes of central DI?

A

Anything that threatens hypothalamus or posterior pituitary

37
Q

What is the “triphasic response”?

A

Classic changes in water balance following pituitary stalk damage

  • Posterior pituitary “shocked” and not releasing Vasopressin (0-4 days)
  • Urine output increases greatly
  • Interphase has release of ADH from damaged neurons (or from recovering)
  • In recovering, may swing back too far the other direction
  • If permanent damage to the pituitary, pt will have permanent problems
38
Q

What is the basis of nephrogenic DI/what is the problem?

A

Renal resistance to ADH

39
Q

How is Diabetes Insipidus diagnosed?

  • For what suspected conditions is it done
  • Process
A

Goal is to see if pt concentrates urine

  • Central DI (complete or partial)
  • Nephrogenic DI
  • Primary polydypsia

Deprive pt of water over hours

  • Measure every 1-2 hrs (ADH level, serum Na, serum Osm, urine Osm, urine output)
  • Monitor BP and weight (stop when orthostatic or 2-3% weigh tloss)

Give DDAVP (desmopressin) to see if they can respond by concentrating urine (urine Osm rise)

40
Q

What is desmopressin?

A

Desamino D-8 arginine vasopressin

  • Decreased vasopressor activity (D-arg change)
  • Increased half life ins erum Oral, nasal, subcutaneous (100 mcg: 10mcg: 1 mcg)
41
Q

What is the normal response to water deprivation test?

A
  • Maximally concentrated urine, so no additional response to DDAVP
  • ADH will come back high at the end of the test
42
Q

What is the response to water deprivation in central DI?

  • Distinguishing central from partial
A
  • Excellent response to DDAVP
  • ADH will come back low at the end of the test

Complete central Di:

  • Urine Osm under 100 mOsm/kg (less than serum Osm)
  • DDAVP causes > 50% increase in urine Osm
  • Undetectable or very low AVP (ADH) levels

Partial Di:

  • Urine Osm 300-400 (greater than serum Osm)
  • DDAVP causes 10-50% increase in serum osm
  • Low AVP (ADH) levels
43
Q

What is the response to water deprivation in nephrogenic DI?

A
  • May concentrate urine somewhat (300 – 500 mOsm/kg)
  • DDAVP < 10% increase in urine Osm because resistant - High AVP (ADH)
44
Q

What is the response to water deprivation in primary polydypsia?

A
  • Concentrate urine (300-800 mOsm/kg)
  • Increase in AVP levels with water deprivation
  • Doesn’t respond further to DDAVP because endogenous AVP (ADH) already high
45
Q

How to treat Central DI?

A
  • DDAVP
  • (Chlorthalidone, clofibrate, carbamazepine)
46
Q

How to treat nephrogenic DI?

A

Treat underlying cause

Thiazide diuretics

  • Hydrochlorothiazide 25 mg once to twice per day
  • Mild volume depletion increases proximal tubule resorption of water and decreases the water delivered to the collecting tubules
  • Can combine with amiloride to decrease hypokalemia and enhance the effect

NSAIDs

  • Prostaglandins inhibit ADH
  • Use of NSAIDs may increase the ability of endogenous ADH to work
  • Indomethacin
  • Lithium induced dysfunction

MS2 Endocrine (25 decks)

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