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DEMS Unit 3 > Pituitary Dysfunction > Flashcards

Pituitary Dysfunction Flashcards

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

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

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

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

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

A
  1. ACTH dependent (70-75%)

2. ACTH Independent (25-30%)

23
Q

Specific Signs and sx of CUshings syndrome

5

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?

A

bound - to transcortin

cortisol binding globulin - CBG

25
Q

Screening test for Cushings syndrome

A
  1. midnight salivary or serum cortisol

for disrupted circadian rhythm

26
Q

Pseudo-Cushing’s disease

  • what is it?
  • what can cause it? (6)
A

overactivation of HPA axis without tumorous cortisol hypersecretion

  • severe depression,anxiety/OCD
  • Severe obesity
  • Obs. Sleep apnea
  • Alcoholism
  • Poorly controlled DM
  • physical stress
27
Q

Cushing’s disease work up

A

Plasma ACTh lvls are high-nl to mildly elevated –>
Pituitary MRI (microadenomas) –>
Inferior petrosal sinus sampling

28
Q

Secondary/Tertiary Adrenal Insufficiency (AI)

A

suppression of HPA axis
- Exogenous glucocorticoid use (most coommon)
> 5-7.5 mg predisone

29
Q

Central adrenal insufficiency test

A

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
Q

Hypogonadotropic hypogonadism is due to ______

A

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
Q

Clinical features of hypogonadism in females (6)

A
  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
Q

Clinical features of hypogonadism in males (6)

A
  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
Q

LH/FSH (gonadotropin) excess

A

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
Q

Apoplexy

A

Clinical syndrome of HA, vision changes, ophthalmoplegia,

altered mental status caused by the sudden hemorrhage or infarction of the pituitary gland

35
Q

Hypopituitarism

  • types
  • etiologies
A

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
Q

Clinical syndromes of posterior pituitary gland are primarily associated with ______

A

disorders of AVP
AVP = ADH

release is controlled by HIGH osmolar states or
HYPOvolemia

37
Q

Mechanism of ADH action

A

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
Q

SIADH

A

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
Q

SIADH dx

A

Hyponatremia (

40
Q

SIADH tx

A
  1. Identify and reverse underlying disorder
  2. If mild-mod hyponatremia (120-134):
    - water restriction (500-1000mL/24 hrs)
    - V2 receptor antagonish
41
Q

Risk of hyponatremia correction in chronic hyponatremia

A
42
Q

Diabetes Insipidus

A

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
Q

Classic triphasic response related DI

A
  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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