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DEMS Unit 3 > Pituitary Dysfunction > Flashcards

Pituitary Dysfunction Flashcards

(43 cards)

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1
Q

Anterior pituitary secretes which H?

A

6 hormones

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2
Q

Posterior pituitary secretes which H?

A

ADH (vasopressin)

Oxytocin

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3
Q

Higher CNS centers in pituitary gland regulation

A

Thalamus
Limbic system
RAS
Retina

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4
Q

Growth Hormone stimulatory factors

A

Sleep
Stress
Ghrelin
Protein/Arginine

HYPOglycemia

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5
Q

Growth H Inhibitory factors

A

Obesity/FFA
Glucocorticoids
Leptin

HYPERglycemia (OGTT to test for GH excess prod)

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6
Q

Excess H results in what?

  1. GH
  2. PRL
  3. ACTH
  4. TSH
  5. ADH
A
  1. GH - Acromegaly
  2. PRL - hypogonadism
  3. ACTH - Cushing’s disease
  4. TSH - Hyperthyroidism
  5. ADH - SIADH
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7
Q

Deficiency in H results in what?

  1. PRL
  2. FSH/LH
  3. ACTH
  4. ADH
A
  1. PRL - Failed lactation
  2. FSH/LH - Hypogonadism
  3. ACTH - Adrenal insufficiency
  4. ADH- Diabetes Insipidus
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8
Q

Hypothalamic-Pituitary - Target organ defect

A

Peripheral:
Primary disorder
- Target organ

Central:
Secondary Disorder
- Pituitary gland

Tertiary Disorder
- Hypothalamus

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9
Q

Hormone excess is assessed by _______ test.

Hormone deficiency is assessed by ______ test

A

Suppression test
- OGTT for GH suppression to confirm acromegaly
(give them glucose, hyperglycemia should inhibit GH)

Stimulation test
- Insulin tolerance test to eval ACTH and GH reserves

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10
Q

GH regulation

A

GHRH +
Somatostatin -

GH is pulsatile and acts at level of liver (Insulin-like growth factor: IGF-1)

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11
Q

Actions of GH

A

Acts on IGF-1 hormone

  1. Increase blood glucose
  2. Increase bone and cartilage mass/growth
  3. Increase protein synth/muscle mass
  4. Increase fat breakdown, TGA levels
  5. Increase Salt/H2O
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12
Q

Problems of GH excess

A

Gigantism:
- GH excess b4 puberty
(b4 closure of growth plates)

Acromegaly:
- GH excess after puberty
(after completion of linear growth)

*Elevated IGF-1 found, then do pituitary MRI (detected in >80% acromegaly)

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13
Q

Clinical presentation of Acromegaly (6)

A
  1. Acral/gacial changes
  2. HA
  3. Hyperhidrosis
  4. Oligo/Amenorrhea
  5. Obstructive sleep apnea
  6. HTN
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14
Q

Tx for acromegaly

A
  1. surgery
  2. medical
    - somatostatin analog
    - GH receptor antagonist
  3. radiation therapies
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15
Q

Manifestations of adult growth hormone deficiency (GHD)

A
  1. Body composition
    - Increased Fat deposition
    - Decreased muscle mass, strength, exercise capacity
  2. Bone strength
    - increased bone loss and fracture risk
  3. MEtabolic and cardiovascular effects
    - Increased cholesterol levels
    - increased inflamm and prothrombotic markers (CRP)
  4. Psycological well being
    - Impaired E and mood
    - Quality of life
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16
Q

Dx of adult onset GHD (AoGHD)

A

Gold standard:
Insulin induced hypoglycemia
*Central adrenal insufficiency dx too

contraindications: elderly, h/o seizure disorder, CAD, or cerebrovascular disease

IGF-1 lvls are low

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17
Q

Stimulants of Lactotropes (and ultimately producing prolactin)

A

E2, TRH, Suckling,

DA is inhibitory

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18
Q

Causes of hyperprolactinemia

Study These Flashcards
A
  1. Physiological
    - Pregnancy, suckling, sleep, stress
  2. Pharmacological
    - Estrogens
    - Antipsychotics, antidepressants, anti-emetics, opiates
  3. Pathological
    - Pituitary stalk interruption
    - Hypothyroidism, chronic renal failure/liver failure, seizure
    - prolactinoma
19
Q

Prolactinoma common findins

at least 5 each

Study These Flashcards
A

females 10: males 1

women:

  1. galactorrhoea
  2. menstrual irregularity
  3. infertility
  4. Impairs GnRH pulse generator
  5. MICROadenomas

men:

  1. galactorrhoea
  2. visal field abnormalities
  3. HA
  4. Impotence
  5. EOM paralysis
  6. anterior pit. malfxn
  7. MACROadenomas
20
Q

Primary fxn of cortisol

Study These Flashcards
A
  1. gluconeogenesis
  2. breakdown of fat and protein for glucose prod.
  3. control inflammatory rxns

*BIGFIB (319)

21
Q

Complications in chronic cortisol excess

Study These Flashcards
A
  1. changes in carb, prot, and fat metab
    - peripheral wasting of fat/muscle
    - central obesity, moon facies, fat pads
    - osteoporosis
    - diabetes
    - hypertriglyceridemia
  2. Changes in sex hormones
    - amenorrhea/infertility
    - excess hair growth
    - impotence
  3. salt and water retention
    - HTN + edema
  4. Impaired immunity
  5. Neuro cognitive changes

*BIGFIB (319)

22
Q

Two types of cortisol excess

Study These Flashcards
A
  1. ACTH dependent (70-75%)

2. ACTH Independent (25-30%)

23
Q

Specific Signs and sx of CUshings syndrome

5

Study These Flashcards
A
  1. Plethoric/moon facies
  2. Wide violaceous striae
    (Abdominal, axillary)
  3. Spontaneous ecchymoses
  4. Proximal muscle weakness
  5. early/atypical osteoporosis
    (atraumatic rib fracture)
24
Q

Is most cortisol bound or unbound?

Study These Flashcards
A

bound - to transcortin

cortisol binding globulin - CBG

25
Screening test for Cushings syndrome
1. midnight salivary or serum cortisol | for disrupted circadian rhythm
26
Pseudo-Cushing's disease - what is it? - what can cause it? (6)
overactivation of HPA axis without tumorous cortisol hypersecretion - severe depression,anxiety/OCD - Severe obesity - Obs. Sleep apnea - Alcoholism - Poorly controlled DM - physical stress
27
Cushing's disease work up
Plasma ACTh lvls are high-nl to mildly elevated --> Pituitary MRI (microadenomas) --> Inferior petrosal sinus sampling
28
Secondary/Tertiary Adrenal Insufficiency (AI)
suppression of HPA axis - Exogenous glucocorticoid use (most coommon) > 5-7.5 mg predisone
29
Central adrenal insufficiency test
Basal test - random am cortisol level 18 then exclude dx) Stimulation tests: - GOLD std: Insulin-induced hypoglycemia (assesses entire hypothalamic-pituitary-adrenal axis) *Dx of adult onset GHD (AoGHD)
30
Hypogonadotropic hypogonadism is due to ______
Low FSH/LH 1. Hypothalamic/pituitary diseases - macroadenomas, prolactinomas, XRT - Isolated GnRH deficiency - Hemochromatosis 2. Fxnal deficiency - critical illness - OSA - Starvation - Meds-opiates - glucocorticoids
31
Clinical features of hypogonadism in females (6)
1. Anovulatory cycles - oligo/amenorrhea, infertility 2. vagina dryness, dyspareunia 3. Hot flashes 4. Decreased libido 5. Breast atrophy 6. Reduced bone mineral density BMD
32
Clinical features of hypogonadism in males (6)
1. Reduced libido 2. Erectile dysfxn 3. Oligospermia or azoospermia 4. Infertility 5. Decreased muscle mass, testicular atrophy, decreased BMD 6. Hot flashes with acute and severe onset of hypogonadism
33
LH/FSH (gonadotropin) excess
Gonadotrope adenomas (FSH/LH) tumors are clinically silent Middle aged pts with macroadenomas and related mass effects (HA, vision loss, cranial nerve palsies, pituitary hormone deficiency)
34
Apoplexy
Clinical syndrome of HA, vision changes, ophthalmoplegia, | altered mental status caused by the sudden hemorrhage or infarction of the pituitary gland
35
Hypopituitarism - types - etiologies
Deficiency of 1 or more pituitary hormones Panhypopituitarism = loss of all pituitary hormones Etiologies: 1. congenital genetic diseases 2. Acquired pituitary lesions and/or treatments (75%)
36
Clinical syndromes of posterior pituitary gland are primarily associated with ______
disorders of AVP AVP = ADH release is controlled by HIGH osmolar states or HYPOvolemia
37
Mechanism of ADH action
AVP binds to V1: vascular vasoconstriction + platelet aggregation AVP binds to V2: antidiuretic effects in kidney Adenylate cyclase activation --> movement of aquaporin water channels to the cell membrane --> water reabsoprtion
38
SIADH
syndrome of inappropriate AVP release/action in the absence of physiologic osmotic or hypovolemic stimulus Most frequent cause of HYPOnatremia Hallmark: excretion of inappropriately [urine] in the setting of hypo-osmolality and hyponatremia
39
SIADH dx
Hyponatremia (
40
SIADH tx
1. Identify and reverse underlying disorder 2. If mild-mod hyponatremia (120-134): - water restriction (500-1000mL/24 hrs) - V2 receptor antagonish
41
Risk of hyponatremia correction in chronic hyponatremia
42
Diabetes Insipidus
A syndrome of hypotonic polyuria as a result of: - inadequate ADH secretion or - Inadequate renal response to ADH Hallmark: voluminous dilute urine (getting up at night) Confirm polyuria with 24 hr urine volume collection
43
Classic triphasic response related DI
1. DI-polyuric phase due to axonal shock/decreased AVP release (days 1-5) 2. SIADH from degenerating neurons/excessive AVP release (days 6-11) 3. Permanent DI after depleted ADH stores and if >80% AVP neuronal cell death

DEMS Unit 3 (26 decks)

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