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ABPN 2022 > Neuroendocrine > Flashcards

Neuroendocrine Flashcards

1
Q

Hypothalamus and posterior pituitary

A

Hypothalamic magnocellular neurons in supraoptic nucleus and paraventricular nucleus
-Vasopression released in response to changes in osmotic pressure, controls water balance
-Oxytocin promotes uterine contraction during birth and milk ejection after birth

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2
Q

Hypot

A

Hypothalamic parvocellular neurons produce releasing and inhibitory hormones
In preoptic: (GnRH- Gonadotropin releasing hormone)
In arcuate and ventromedial (GHRH-Growth hormone releasing hormone)
In periventricular (TRH-thyrotroph releasing hormone, CRH- corticotroph releasing hormone, somatostatin)
Im paraventricular (TRH, CRH, PRF-prolactin releasing factor)

SON = Supraoptic nucleus, PVN = Paraventricular

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3
Q

Hypothalamus and anterior pituitary

A

Hypothalamic parvocellular neurons produce releasing and inhibitory hormones:
- In preoptic: GnRH- Gonadotropin releasing hormone)
- In arcuate and ventromedial: GHRH-Growth hormone releasing hormone)
- In periventricular: TRH-thyrotroph releasing hormone, CRH- corticotroph releasing hormone, somatostatin)
- In paraventricular: TRH, CRH, PRF-prolactin releasing factor

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4
Q

Preoptic area

A

Regulatory function: Parasympathetic/Temp reg/male sex behavior
Pathology: Hyperthermia/men: low libido/parenting

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5
Q

Medial/preoptic

A

Regulatory function: Thirst/Drinking
Pathology: Polydipsia/Adipsia

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6
Q

Suprachiasmatic

A

Regulatory function: Circadian rhythm
Pathology: Sleep/wake disturbance

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7
Q

Anterior

A

Regulatory function: Cooling/Parasympath.
Pathology: Hyperthermia (B/L)

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8
Q

Dorsomedial

A

Regulatory function: ANS/Aggression/Satiety
Pathology: Hyperphagia

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9
Q

Ventromedial

A

Regulatory function: Satiety/ sex behavior
Pathology: Hyperphagia (B/L)

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10
Q

Posterior

A

Regulatory: Heating/Sympathetic
Pathology: Poikilothermia (B/L)

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11
Q

Lateral

A

Regulation: Hunger
Pathology: Aphagia

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12
Q

Sellar masses - etiology

A

Benign tumors:
- Pituitary adenoma (most common sellar mass in
adults, from 3rd decade on)
- Craniopharyngioma
- Meningioma
Malignant tumors (primary or metastases)
- Cysts
- Infections (rare - abscess, tuberculoma)
- Lymphocytic Hypophysitis
- Carotid Aneurysm

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13
Q

Hypothalmic damage

A

Severe memory loss, obesity, and personality changes (apathy, aggressive antisocial behavior, severe food cravings, inability to work or attend school, poor concentration)

2/2 extrasellar extension of pituitary tumors, hypothalamic radiation, or damage from surgical removal of parasellar tumors

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14
Q

Sellar masses clinical presentation

A

Neurologically: Visual loss, headache, diplopia, CSF rhinorrhea, pituitary apoplexy
Hormonally: Excessive hormone secretion (a pituitary adenoma, stalk compression), hypopituitarism (any sellar mass)
Incidentally, on a radiologic procedure

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15
Q

Pituitary apoplexy

A

Sudden hemorrhage into a pituitary adenoma
Acute, severe headache, impaired vision, meningeal irritation, nausea
Acute deficiency of pituitary hormones (most importantly of ACTH)
MRI: radiologic study of choice
Treatment: medical (glucocorticoid) ± surgical (early) if there are visual changes

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16
Q

Pituitary Adenomas

A

Benign, true neoplasms
Micro or macroadenomas (< 1 cm or > 1 cm)
Classification by cell type:
• Lactotroph -High prolactin, hypogonadism
• Corticotroph - Cushing’s syndrome
• Somatotroph - Acromegaly
• Gonadotroph - clinically nonfunctioning, OHS (ovarian hyperstimulation), premature puberty
• Thyrotroph - clinically nonfunctioning, hyperthyroidism

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17
Q

Lactotroph adenomas

A

40% of all pituitary adenomas
Majority are microadenomas, rarely grow
Clinical manifestations: Hyperprolactinemia: galactorrhea (women), impotence (men), hypogonadism (women and men)
Diagnosis: High prolactin parallels tumor size

Dopamine agonists- Act on D2 receptors on the lactotroph cell
- Goal: Normalization of PRL/ decrease tumor size
- Two approved for treatment of high PRL / lactotroph adenomas: Bromocriptine (Parlodel®) 1.25-2.5mg/d, Cabergoline(Dostinex®) 0.25 mg p.o. biw w/dinner
- Side effects: mostly GI (nausea, constipation), headache, postural hypotension, depression
- Decrease in prolactin occurs within 2-3 weeks after treatment begins, usually precedes a decrease in size of tumor

18
Q

Corticotroph Adenomas

A

Clinical: Cushing’s syndrome
Diagnosis: Elevated 24 hour urine free cortisol and a high-normal or high ACTH
Treatment: Transsphenoidal surgery (80% cure rate) ± pituitary irradiation (45-85% cured) ± total B/L adrenalectomy

19
Q

Somatotroph adenomas

A

Clinical syndrome: Acromegaly (in adults), gigantism (in children)
Diagnosis: Elevated IGF-1, high GH after an oral glucose load (OGTT)
Treatment: Transsphenoidal surgery (60% cure rate) ± medical treatment (dopamine agonists, somatostatin analogues, GH receptor antagonist) ± XRT

20
Q

Physiologic Enlargement of the Pituitary

A

Lactotroph Hyperplasia (most frequent)-during pregnancy
Thyrotroph Hyperplasia- due to long-standing untreated primary hypothyroidism
Gonadotroph Hyperplasia-due to long-standing untreated primary hypogonadism
Somatotroph and Corticotroph Hyperplasia -due to neuroendocrine tumors and gangliocytomas

Treatment: Treat the cause of the hyperplasia, e.g. treat the primary hypothyroidism or hypogonadism, clearly nothing has to be done to the pituitary itself

21
Q

Craniopharyngiomas

A

Benign tumors, solid or solid-cystic
Arise from remnants of Rathke’s pouch
Peak of incidence: 11-20 and 41-50 yrs
Clinically: Growth retardation (children), increased ICP, hypopituitarism and DI
Radiologically: Calcifications on CT (not pathognomonic)
Treatment: If symptomatic, surgical resection (if possible) followed by XRT for residual tumor

22
Q

Lymphocytic hypophysitis

A

Post-partum (most frequent), women not post-partum and men; autoimmune?
Clinically: Headache out of proportion to sellar mass, hypopituitarism (prominent ACTH deficiency), DI
MRI: enlarged pituitary, delayed or absent enhancement of the posterior pituitary
Rx: partial recovery is possible

23
Q

SIADH

A

Hypotonic hypoNa+, impaired urinary dilution
Congenital or acquired: trauma, stroke, drugs, infections, AML, Guillain-Barré, MS, hydrocephalus, delirium tremens, psychosis, cerebrovascular occlusion/hemorrhage, cavernous sinus thrombosis,
Treatment: cause, water restriction

24
Q

Central DI

A

Polyuria (>3L), usually nocturia, dilute urine
Destruction of >80% magnocellular neurons, congenital or acquired: tumors, granulomas, AI, vascular, idiopathic, trauma
Treatment: DDAVP (nasal spray, oral, injectable)

25
Q

Adipsic hypernatremia

A

Hypertonic dehydration, lack of thirst
Selective defect in hypothalamic osmoreceptors, congenital or acquired: ACOM aneurysms, tumors, granulomas, psychologic
Treatment: Water intake based on weight

26
Q

AEDs and endocrine issues

A

PCOS (more frequent with valproate) / Infertility/Anovulatory cycles
Low bone mineral density

27
Q

Bipolar disorders and some antipsychotics

A

Wt gain (Lithium, valproate), menstrual abnls., Li - hypothyroidism

28
Q

Atypical antipsychotics;

A

Wt gain, fasting hyperinsulinemia, diabetes mellitus, and DKA

29
Q

Na abnormalities/Medical situation/Symptoms

A

HypoNa/1. SIADH, adr insuff 2. diarrhea, diuretic, poor PO 3. CHF, cirrhosis/Lethargy, confusion, seizures, coma; osmotic demyelination if too rapid correction

HyperNa/DI, dehydration/Lethargy, confusion

30
Q

Hypokalemia/Medical situation/Symptoms

A

Hypokalemia/Vomiting, diuretic, diarrhea, RTA/Myopathy, profound weakness

31
Q

Ca, Mg abnormalities/Medical situation/Symptoms

A

Hypercalcemia/Inc PTH, malignancy, bone mets/Obtundation

Hypocalcemia, hypomagnesemia/Parathyroidectomy - Ca, Cisplatin - Mg/Increased DTRs, tetany, seizures

32
Q

Hypermanganese

A

2/2 TPN, cholestatic liver disease, resulting in Parkinsonism, with MRI hyper intensities in base ganglia

33
Q

Osmotic demyelination

A

-Previously referred to as central pontine myelinolysis but there is extrapontine myelinolysis
-Occurs following rapid correction of hyponatremia
-Clinical: dysarthria, dysphagia, abducens palsies, coma, flaccid quadriplegia

34
Q

Neuropsychiatric lupus

A
35
Q

Neurosarcoidosis epidemiology

A

15% of patients with sarcoidosis may have neurological complicsyiond f
Half of neurosarcoidosis cases are diagnosed before autopsy (1993)
More than half of patients with systemic sarcoidosis who develop neurologic symptoms do so within 2 years of systemic diagnosis (1995)
Protean manifestations affecting any part of nervous system

36
Q

Neurosarcoidosis presentation

A
37
Q

Neurosarcoidosis in imaging

A
38
Q

Leptomeningeal vs pachymeningeal

A

Lepto- involves pia mater and arachnoid mater
Pachy- involves dura and arachnoid mater

39
Q

Renal disease: neurological problems with dialysis/CKD

A

Headache (Triptans) 60% patients (r/o subdurals!)
Polyneuropathy (end stage creatinine clearance<5 ml/min)
cramps, restless legs improves with transplantation > dialysis
AV shunt “steal” neuropathy: carpal tunnel due to amyloid deposition after several years of dialysis, beta-2-microglobulin not well dialyzed
Dysequilibrium - H/A, vomitting, increased ICP; idiogenic osmoles create gradient shifting water into brain
Chronic uremia - cognitive symptoms very common
Seizures: beware heavily protein bound AEDs free level

40
Q

Nephrogenic systemic fibrosis

A
41
Q
A

Nephrogenic systemic fibrosis

42
Q

Neurologic complications of celiac disease

A

ABPN 2022 (26 decks)

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