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CAS 3 > Hypothalamic & pituitary disorders > Flashcards

Hypothalamic & pituitary disorders Flashcards

1
Q

Master Gland of the endocrine system
- secretes hormones that stimulate other endocrine organs

A

Pituitary Gland

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2
Q

Hormones in the anterior lobe (adenohypophysis)

A
  • somatotrophs - GH
  • lactotrophs (mammotrophs)- Prolactin
  • corticotrophs- ACTH, POMC, Endorphins, Lipotropin
  • thyrotrophs- TSH
  • gonadotrophs- FSH & LDH
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3
Q

Hormones in the Posterior lobe (nuerohypophysis)

A
  • oxytocin
  • ADH
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4
Q

which hormones are Acidophilic cells

A

A-SP

  • somatotrophs - GH
  • lactotrophs (mammotrophs)- Prolactin
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5
Q

which hormones are Basophilic cells

A

B-FLAT

  • corticotrophs- ACTH, POMC, Endorphins, Lipotropin
  • thyrotrophs- TSH
  • gonadotrophs- FSH & LDH
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6
Q

Posterior lobe is made up of what cells ?

A

Consists of modified glial cells and axonal processes

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7
Q

embryological origin of the anterior lobe?

A

makes up 80 % of the gland and by epithelial cells
- ectodermal derivative formed from Rathke’s pouch ( which is an upward diverticulum from the primitive buccal cavity)
- no direct neural connection but has indirect connection through capillary portal circulation by which it receives the blood

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8
Q

embryological origin of the posterior lobe?

A

downgrowth from the primitive neural tissue
- has direct neural connection superiorly with hypothalamus

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9
Q

what separates the posterior and anterior lobes?

A

VESTIGIAL INTERMEDIATE LOBE
-containing a few cyst cavities lined by cuboidal/columnar epithelium (considered part of the anterior pituitary)

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10
Q

where does the pituitary drain into?

A

venous drainage from pituitary follows the cavernous sinus both inferior petrosal sinuses
-IPSS is an infrequently used invasive procedure confirming the presence of a hormonally active pituitary microadenoma

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11
Q

why can pituitary enlargement alter vision or cause palsies?

A

By impinging near the optic chiasm and cranial nerves 3, 4, 5, 6

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12
Q

increase in dopamine will cause?

A

inhibition of prolactin secretion

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13
Q

what is the most powerful stimuli for prolactin release

A
  1. SUCKLING
  • TRH
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14
Q

______ increases sensitivity of lactotrophs to TRH

A

estrogen

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15
Q

what is the MOA of Kallmann Syndrome

A

due to failure in the differentiation or migration of neurons that arise embryologically in the olfactory mucosa to take up residence in the hypothalamus, as GnRH neurons.

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16
Q

what are the 3 manifestations of Kallmann Syndrome

A
  • congenital hypogonadotropic hypogonadism
  • hypo- or anosmia and dec.in gonadal function
  • de.c in GnRH hormone = dec. levels of sex steriods ( FSH &LH) —> sexual imaturity and asbsence of secondary characteristics
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17
Q

OXYTOCIN:
site of synthesis
Target organ
physiological effects

A

paraventricular nuclei
- uterus
- mammary glands

  • urterine contractions
  • milk-let down and excretion
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18
Q

ADH:
site of synthesis
Target organ
physiological effects

A

Supraoptic nuclei
CD- renal tubules
inc. water retention (concentrates the urine)

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19
Q

clinical manifestations of pituitary disease:

A

-Hyperpituitarism
- hypopituitarism
- local mass effects:
- visual field defects:
- Inc. intracranial pressure

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20
Q

Hyperpituitarism

A

pituitary adenoma, hyperplasia, carcinoma

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21
Q

Hypopituitarism

A

ischemic injury, surgery or radiation, inflammatory rxns, and nonfunctiona; pituitary adenomas (1/3; dec. secretions)

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22
Q

local mass effects :

A

sellar expansion , Bony erosion & disruption

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23
Q

visual field defects

A

bitemporal heminaopsia

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24
Q

ALWAYS : hypothalamic etiology

A

hypopituitarism + posterior pituitary dysfunction

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25
Q

HYPOpituitarism etiology

A

-pituitary adenomas and metastatic tumors ( compressing anterior pituitary or stalk (2/3 adenomas are functional))

-hemorrhage; pituitary apoplexy —-> undergoing ischemic necrosis

-infarction; ischemic necrosis of pituitary (sheehan syndrome)

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26
Q

hypothalamic lesions

A

mass lesions: craniopharyngioma and metastatic tumors
infiltration (sarcoidosis)/ infections (TB)

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27
Q

hypopituitarism: Iatrogenic hypopituitarism

A

Radiation damage to the hypothalamic- pituitary axis or neurosurgical procedures

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28
Q

hypopituitarism: infiiltrative diseases

A
  • bacterial and viral infections
  • langerhans cell histiocytosis
    -hemochromatosis
  • Lymphocytic Hypophysitis
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29
Q

langerhans cell histiocytosis:

A

involvement of hypothalamic - pituitary axis causes endocrine abnormalities ( panhypopituitarism in 5-20%)

  • increased prolactin and galactorrhea (central diabetes insipidus)
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30
Q
  • Lymphocytic Hypophysitis:
A

rare autoimmune condition in Women, infiltrate by T/ B cells

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31
Q

Hypopituitarism patholgy;

A
  • hormone deficiencies
  • panhypopituitarism ; all 6 anterior pituitary hormones deficient
  • increased mortality esp. due to cardiorespiratory effects
  • ADH loss => Diabetes insipidus
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32
Q

what is the correct order of hormone deficiencies for hypopituitarism:

A

GH, LH/FSH, TSH, ACTH, PR

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33
Q

most common adenoma

A

prolactinoma

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34
Q

most common deficiency in hyperpituitarism?

A

GH defeciency

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35
Q

hypo-pituitary effects of ACTH

A

ex. addison disease
dec. ACTH -> dec. Corstisol
- orthostatic hypotension
- tachycardia
- weakness & lethargy
- adrenal crisis
- mental status changes
- nausea
- vomitting
- abdominal pain
-shock

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36
Q

hypo-pituitary effects of TSH

A

dec. TSH –> dec. thyroxine
- fatigure
- cold intolerance
- depression
-bradycardia
-constipation
- dry skin
- puffy face
- slow reflexes

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37
Q

hypo-pituitary effects of LH / FSH

A

dec. LH/FSH –> dec. sex steroids
premenopausal women
- irregular/absent periods
- hot flashes
- vaginal atrophy
- infertility
Men
- erectile dysfn / infertility
- dec. libido
- weight gain

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38
Q

hypo-pituitary effects of GnRH

A

GnRH–> dec. GH
children
-short
-failure to thrive

adults
- dec. muscle mass / bone density
- inc. fat

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39
Q

hypo-pituitary effects of prolactin

A

-agalactorrhea
- amenorrhea
- cold intolerance

40
Q

hypo-pituitary effects of ADH

A

polyuria
polydipsia
-lethargy
-hypernatremia
-dehydration

41
Q

what is a Pituitary Apoplexy

A

Is sudden hemorrhage into the pituitary gland usually associated with a preexisting adenoma.

42
Q

Pituitary Apoplexy side effects

A
  • Neurosurgical emergency
  • Sudden onset excruciating headache, diplopia due to pressure on the oculomotor nerves or ophthalmoplegia
    due to involvement of the third (oculomotor), fourth (trochlear), or sixth (abducens)
  • hypopituitarism.
  • In severe cases, it can cause cardiovascular collapse, loss of consciousness, and sudden death ( cortisol
    deficiency)
43
Q

Sheehan’s syndrome sequence of events

A

pregnancy–> inc . pituitary growth –> hyperplasia (inc . LDH) –> eosinophilic pink stain–> Hypotension in Peripartal period & Low pressure hypophyseal portal system – No increase in blood flow—-> Pituitary ischemic necrosis

*Postpartum necrosis of Anterior pituitary - Panhypopituitarism *

44
Q

why is the post. pituitary much less susceptible to ischemic injury?

A

Posterior pituitary receives blood directly from arterial branches

45
Q

Sheehan’s syndrome pregnant patient will mostly have normal levels of what hormones?

A

oxytocin and ADH (post pituitary, less likely for ischemic injury)

46
Q

Sheehan’s syndrome RX?

A

hormone replacement therapy.

47
Q

MOA of Empty Sella syndrome

A

Congenital defect of Sella
* Herniation of arachnoid and CSF
compresses and destroys pituitary
* Pituitary shrinks
* Sella turcica fills up with CSF

48
Q

Symptoms of empty sella syndrome?

A

CSH rhinorrhea, headache,
hypopituitarism
* Pituitary absent - empty sella on
imaging

49
Q

which is the 1º ite in the body where ADH is stored & released?

A

post. pit. lobe

50
Q

Hypofunction of hypothalamus and posterior pituitary – Reduced ADH ( Vasopressin secretion) leads to?

A

diabetes insipidus

51
Q

different stimuli where ADH is released from axon terminals in the neurohypophysis include:

A
  • increased plasma osmotic pressure (Dehydration)
  • left atrial distention
  • exercise
52
Q

pathology of Central Diabetes Insipidus:

A

ADH deficiency
reduced aquaporins
reduced water moving from tubules to blood

53
Q

pathology of Nephrogenic Diabetes Insipidus:

A

kidney not responding to ADH

54
Q

Etiology of Central Diabetes Insipidus:

A

➢Pituitary disorders
- Transection of pituitary stalk (post-traumatic) or suprasellar tumors compressing
pituitary stalk .
- Infiltrative disease to posterior pituitary (ex: metastasis, sarcoidosis)
➢Hypothalamic disease (eg. Histiocytosis X)

55
Q

Etiology of Nephrogenic Diabetes Insipidus:

A

-Drugs - Lithium, demeclocycline)
- PKD
- Genetic disease – ADH receptor / Aquaporin

56
Q

effects of Central Diabetes Insipidus:

A

inc. serum osmo- thirsty (polydipsia)
lots of urine excreted - polyuria , reduced urine osmo.

57
Q

effects of psychogenic Diabetes Insipidus:

A
  • inc. water intake
  • reduced ADH secretion
  • inc. urine output (polyuria)
58
Q

after 2-3hrs of water deprivation give ADH what will happen to urine osmolality for Central diabetes insipidus?

A

inc. urine osmo.

59
Q

Central diabetes insipidus RX?

A

DDAVP

60
Q

after 2-3hrs of water deprivation give ADH what will happen to urine osmolality for Nephrogenic diabetes insipidus?

A

NO CHANGE in urine osmo

61
Q

Nephrogenic diabetes insipidus treatment?

A

Thiazide

62
Q

what is SYNDROME OF INAPPROPRIATE SECRETION (SIADH)

A

Excessive production of ADH → oliguria, resorption of excessive amounts of free water, hyponatremia and cerebral edema

63
Q

What are some causes of SIADH

A

-Paraneoplastic syndrome- ectopic ADH by malignant neoplasms (particularly small cell carcinomas of the lung)/ Pneumonia
- Head trauma- local injury to the hypothalamus or neurohypophysis ,stroke, hemorrhage
- Drugs = Carbamazepine, SSRI, NSAID

64
Q

MOA for SIADH

A

Increased ADH–> Increased Aquaporins–> (Increased water retained in blood) Reduced plasma osmolality –> Oliguria & Increased urine osmolality –> inc. Na+ excretion in urine >40mEq/L –>Hyponatremia
induced neuronal swelling and cerebral edema

65
Q

Summary of electrolyte abnormalities in SIADH:

A

-Urine Osm is greater than Plasma Osm
-Dilutional hyponatremia
-Increased urinary sodium excretion(>40mEq/L)

66
Q

Clinical Feautures of electrolyte abnormalities in SIADH:

A
  • Hyponatremia:
    Mild- nausea and forgetfulness
    Severe - Seizures and coma
  • Euvolemia
    Moist mucous membranes, No edema, No JVD
67
Q

what is the diagnosis:
Head trauma + dec. serum Na+, + inc. urinary osmolality

A

SIADH

68
Q

what is the diagnosis:
frequent urination
thirst
hypernatremia
sig. inc. in urine conc. w/ desmopressin

A

Diabetes insipidus (central)

69
Q

MEN- 1 are the 3P’s:

A

Pituitary
PTH
pancreas

70
Q

Non Functional tumors – mass effect:

A
  1. Optic chiasm compression – bitemporal hemianopsia
  2. Headache
  3. Hypopituitarism- compression of anterior pituitary or stalk (>75% causes Panhypopituitarism)
71
Q

Pituitary Adenoma causes ?

A

Benign tumor of anterior pituitary cells
* May be associated with MEN syndrome
* Majority are hyperfunctioning (2/3rds)
✓ Functional tumors present with features based on hormone produced

72
Q

Classification- based on size:
(<1cm)

A

Microadenoma– incidentaloma, 14% prevalence at autopsy

73
Q

Classification- based on size:
(>1cm)

A

Macroadenoma– cause visual defects

74
Q

Classification – Based on cell type:

A

PRL/GH/ACTH/TSH/ FSH LH

75
Q

what distinguishes Adenomas from non-neoplastic tissue

A

Cellular monomorphism (all eosinophilic) and absence of reticulin network

76
Q

Prolactinoma (Lactotroph adenoma) Hormonal symptoms:

A
  • Gonadotrophin inhibition
    ✓Females- infertility & menstrual disorders ( amenorrhea) diagnosed early
    ✓Males-decreased libido & Gynaecomastia, headache ( late diagnosis - macroadenoma)
  • Induction of lactation ( galactorrhea-milky nipple discharge)
  • Osteoporosis & fractures – low estrogen
77
Q

Prolactinoma Treatment:

A

Inhibited by Dopamine agonists – Bromocriptine, cabergoline

78
Q

what is stalk effect

A

mass in the suprasellar compartment may disturb the normal
inhibitory influence of hypothalamus on prolactin secretion

79
Q

Somatotroph Adenomas ( Growth hormone secreting adenoma)

A
  • 2nd most common functional adenoma
  • elevated growth hormone (GH) and elevated somatomedin C (insulin-like growth
    factor 1[IGF-1]).
80
Q

what is GH – direct tissue effect

A

Increased insulin resistance
Increased fat utilization
increased protein synthesis

81
Q

IGF-1 – growth & proliferation is for

A

Bone, cartilage, soft tissue

82
Q

what is Gigantism (children)

A
  • rare!
    – increased linear bone growth (epiphyses not fused)
    Tall stature with long extremities, large hands & feet, thickened calvarium, prognathism, excess sweating and oily skin
83
Q

what is Acromegaly (adults)

A

-(Acro- extremity)
- enlarged bones of hands, feet and jaw
fingers thickened- sausage shaped
- Growth of visceral organs - Thyroid, heart, liver, adrenals
enlarged tongue
- Organ dysfunction – cardiac failure

84
Q

GH adenomas Lab Dx for GH

A

➢GH increased
GH secretion pulsatile + short half life ( 20 min)
- Increases muscle mass
- Anti-insulin effect – Gluconeogenesis, resistance
(Diabetogenic)

85
Q

GH adenomas Lab Dx for IGF-1

A
  • IGF-1(Somatomedin C) increased
  • enhances chondrogenesis + soft tissue and linear growth
    of bones.
  • half life 20 hrs, secreted by liver in response to GH
  • Levels of IGF-1 correlate with adenoma size
86
Q

What is the test for acromegaly?

A
  1. Serum IGF-1:-Raised
  2. If raised, perform OGTT:-
    * Healthy person: Glucose will provide negative feedback and decrease GH
    * Acromegaly: Glucose does NOT suppress the GH
87
Q

Lack of suppression of GH levels with IV bolus of
glucose confirms __________

A

GH hyper secretion

88
Q

Diagnose the following:
“hat does not fit”
more common
mean age= 4th decade
delay onset
M=W affected

A

Acromegaly

89
Q

describe Laron syndrome

A
  • defect in growth hormone receptor (GHR).
    -GROWTH HORMONE INSENSITIVITY
90
Q

Laron Syndrome occurs in what ppl?

A

occurs mainly in people of Mediterranean origin and is responsible for dwarfism in African pygmies.

91
Q

describe physical characteristics for growth hormone insensitivity (laron syndrome)

A
  • short stature due to extreme resistance to GH
  • Tend to be obese
92
Q

why does growth hormone insensitivity (Laron syndrome) have high serum GH levels, but low concentrations of IGF-I.

A

bcuz there is no GH receptor on hepatocytes , which secretes IGF-1

93
Q

__________________ indirectly reflects GH receptor status

A

Low GH binding protein

94
Q

what is Corticotroph adenomas MOA?

A
  • Produce ACTH, causing hypercortisolism (Cushing disease) + hyperpigmentation (MSH- same precursor as ACTH)
95
Q

what is Nelson Syndrome

A

mostly microadenomas ( may grow into large aggressive tumors if both adrenals are removed for treating Cushing syndrome in a patient with pre-existing pituitary adenoma

96
Q

what is the DX:
* benign tumour commonly in suprasellar region
* arising from remnants of Rathke’s pouch.
* more common in children and young adults.
* Though benign, compresses as well as invades the adjacent structures extensively
- Caudally into sella turcica to destroy the pituitary gland
- Anteriorly optic chiasm (causing visual field defects)
- Superiorly into hypothalamus (increasing intracranial pressure)

A

craniopharyngioma

97
Q

describe the GROSS morphology of craniopharyngioma

A

cystic, reddish-grey mass with dark “motor oil” fluid composed of cholesterol and hemorrhage

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