Pituitary and Adrenals Flashcards

1
Q

list homones secreted by the

adrenal cortex

adrenal medulla

A

Cortext

  • glucocorticoids - cortisol
  • Mineralocorticoids - Aldosterone
  • Androgens - testosterone

Medulla

  • Epinephrine (80%)
  • Norepinephrine (20%),
  • Dopamine catecholamines = Chromaffin cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

fucntions of cortisol

A

•released at diurnal basal rate with bursts d/t stress response regulated by Anterior pituitary & ACTH via negative feedback loop (hydrocortisone is rx of cortisol)

  • Mobilize sugar
  • Suppress immune system
  • Stimulate Gluconeogenesis = Increase in glucose metabolism and glycogen formation, especially in the liver
  • anti-inflammtory effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mineralocorticoids (aldosterone)- Production in the Zona ______

Androgens - Production in the Zona_____

A

Mineralocorticoids (aldosterone)- Production in the Zona Glomerulosa

Androgens - Production in the Zona Reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Adrenal medulla tumor - produce, store, secrete catecholamines

Extra-adrenal originating in ANS

MEN2a/2B

A

Pheochromocytoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

si/sx of phenochromocytoma

A

Recurrent episodes that occur suddenly:

  • HTN(most common) +/- tachycardia
  • HA
  • Diaphoresis
  • Palpitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

dx phenochromocytoma

A

24-hour urine metanephrine,

  • VMA (vanillylmandelic acid),
  • total catecholamines, creatinine

Abnormal THEN image

Abdominal CT/MRI – mRI preferred

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

dx phenochromocytoma

A

Surgical resection – Laparoscopic if <8mm preferred

Alpha-adrenergic blockade– 10-14 days

Beta adrenergic blockade 2 days prior to surgical resection to prevent intra-operative HTN crisis to prevent intra-operative HTN crisis

  • Phenoxybenzamine HCl (Dibenzyline)
  • Propranalol or Nadolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2 etiologys of Hyperaldosteronism

A

Primary (Conn’s syndrome)

  • Adrenal adenoma
  • Bilat cortical nodular hyperplasia - Idiopathic hyperaldosteronism
  • Hypersecretion Aldosterone = Renal distal tubular exchange of Na+ K+ and H+ secretion

Secondary: appropriate ↑ aldosterone production d/t RAAS –> low flow through JGA

  • Edema (nephrotic syndrome, cirrhosis, CHF)
  • Assoc w/ HTN –> Renin overproduction –> ↓ in renal blood flow (ie RAS Renin producing tumor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

si/sx of Hyperaldosteronism

A
  • Diastolic HTN so HIGH - HA
  • Hypokalemia == muscle weakness/fatigue
  • Hypernatremia
  • Metabolic alkalosis –> Excess H+ secretion = ↑HCO3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

dx of primary vs secondary Hyperaldosteronism

A

Primary - DEC plasma renin

Secondary - INC plasma Renin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

dx Hyperaldosteronism

A

Renin hyposecretion w/ volume depletion – STILL ↓renin

  • SHOULD - ↑ w/ vol depletion

Failed aldosterone suppression w/ volume expansion – STILL ↑aldosterone

  • SHOULD ↓ renin and aldosterone

ECG (flat T-waves, ST depression, U waves)

Hypokalemia / Hypernatremia

CXR

Metabolic alkalosis (­↑ HCO3) – Loss of H+ in urine and Shift H+ into cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

tx hyperaldosteronisms

A

Adenoma – Surgical excision

Hyperplasia

  • Diet Na+ restriction
  • Spironolactone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

criteria for dx of Hyperaldosteronism

A

Diastolic HTN without edema

↓Secretion of renin when stimulated - Stimulate w/ volume depletion

↑Secretion of aldosterone that cannot suppress - Try to suppress w/ volume expansion

No diuretic use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cushings endogogenous vs exogenous causes

A

Endogenous - ­ ↑ cortisol from adrenal cortex

  • Pituitary overproduction ACTH (80%) - Cushing’s
  • ↓ TSH, FSH, LH, GH, prolactin, and if lrg ?vasopressin(ADH)
  • Adrenal adenoma
  • Small cell lung ca.
  • Thyroid neoplasm
  • Pancreatic neoplasm

Exogenous (most common)

  • Chronic steroid use —> HPA suppression
  • prednisone, decadron, hydrocortisone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

si/sx of cushings

A
  • Weight gain – central adiposity
  • Skin Δ (purple striae, buffalo hump, moon face)
  • Proximal muscle weakness
  • Neuropsych (depression, cognitive dysfunction)
  • DM (­ infections, poor wound healing)
  • Sexual dysfunction
  • Hyperpigmented “healthy glow”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

dx cushings

A

Stepwise Approach

24-hour urine cortisol >300 diagnostic

1mg Dexamethasone suppression test

  • Nl < 5 mcg/dL

CRH/Dex suppression test – >50 is diagnostic

ACTH (independent vs. dependent)

  • ACTH level (should be low normally in early afternoon 4p)
  • ACTH high? = cranial MRI & high dose dex-suppression test
  • ACTH nl or low? = Abd CT/MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

tx cushings

A

Surgical resection (transphenoidal resection) +/- radiation

  • Adrenalectomy w/ failed pituitary resection

Medical Mgt:if surgery fails

Ketoconazole: ↓ cortisol production

  • Side effects Headache, sedation, nausea, decreased libido, impotence, gynecomastia, elevated LFT’s, irregular menses

Metyrapone: Blocks final step of cortisol synthesis

  • Used w/ ketoconazole should it fail to be fully effective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Adrenal insufficency (Addisons) shows an overall decrease of ???

A

↓aldosterone

↓cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

list primary and secondary addisons (adrenal insufficency)

A

Primary – destruction of adrenal cortex

  • Anatomic destruction or metabolic failure of the adrenal cortex INCREASE ACTH

Secondary

  • Suppression or disease of the HPA axis DECREASE ACTH
  • exogenous steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

si/sx of primary addisons (adrenal insuff)

A
  • Weakness/fatigue (initially asthenia)
  • Dehydration–> hypotension/orthostasis
  • Weight loss/anorexia

• Hyperpigmentation

  • N/V/D
  • Abd pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

si/sx of secondary addisons (adrenal insuff)

A
  • Weakness/fatigue (initially asthenia)
  • Dehydration –> hypotension/orthostasis
  • Weight loss/anorexia
  • N/V/D
  • Abd pain

(NO hyperpigmentation)

Panhypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

dx of addisons (adrenal insuff)

A

Cortosyn stimulation test (Cosyntropin)

  • ACTH stimulation test
  • Tests functional ability of adrenal cortex to synthesize cortisol

Hyponatremia / Hyperkalemia

↑urine Na, BUN/Cr

ECG (hyperkalemia - TWiFP)

Abd CT

  • Calcified adrenals- Tb, histoplasmosis
  • Atrophic adrenals- Idiopathic autoimmune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tx of addisons (adrenal insuff)

A

Glucocorticoid - Hydrocortisone +

Mineralocorticoid - Fludrocortisone

Ample sodium intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

define adrenal crisis

A

complciation od addisons

Rapid/Severe adrenal collapse

exacerbation of chronic adrenal insufficiency –> Stress precipitant OR Sudden withdrawal/ noncompliance of chronic steroid

Acute hemorrhagic destruction of bilateral adrenal glands

  • Waterhouse-Friderichsen syndrome –> Pseudomonas, Meningococcemia septicemia

Anticoagulation

Pregnancy complication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

dx of adrenal criss

A

Hypoglycemia

Hyponatremia

Hyperkalemia

metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

tx adrenal criss

A

Treat underlying cause

IVF resuscitation - 2L NS followed by D51/2NS

Stress dose hydrocortisone or Dexamethasone

Sx management (ex. vasopressors)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Stressors for adrenal crisis Infection

A

need to ↑ steroid doses, usually do not

  • Trauma
  • Surgery
  • Vomiting/Diarrhea
  • Emotional turmoil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

adrenal carcinoma classifications of MEN1

A

3Ps

Hyperparathyroid (most common)

  • Hyperplasia or adenoma
  • Symptom’s hypercalcemia
  • Elevated ionized serum Ca++ and PTH normal

Pancreatic islets

  • Occurs in parallel w/ hyperparathyroid
  • Hyperplasia, adenoma, or carcinoma
  • Increase production pancreatic islet cell hormones

Pituitary

  • Prolactin = prolactinoma (most common)
  • Growth hormone = acromegaly
  • ACTH = Cushing’s disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

most common P from MEN 1

most common pituitary presentation

A

Hyperparathyroid (most common P)

Pituitary: Prolactin = prolactinoma (most common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

tx of MEN 1 & MEN 2a

A

Surgical resection (often multiple required)

  • Transphenoidal approach w/ pituitary tumors (often difficult b/c multicentric)
  • Parathyroidectomy + thyroidectomy
  • Subtotal or total pancreatectomy

Medical management

  • Dopamine agonists (bromocriptine) for prolactinoma
  • H2 receptor antagonist, PPI for ZES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Dx of MEN 1 and MEN 2a

A

Hormone/electrolyte assays

  • Gastrin level & Glucagon level
  • Ca++ and PTH levels
  • Hypokalemia, hypochloremia, metabolic acidosis
  • Growth hormone
  • Prolactin level
  • ACTH level

Provocative testing

  • Secretin stimulation test w/ gastrin levels
  • Short or 72hr fast w/ serum insulin & C-peptide levels
  • Dexamethasone suppression test

Radiologic testing –> CT/MRI

  • Annual screening basal and post-prandial pancreatic polypeptides
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

etiology of MEN 2a

most common manifestation?

A

MTC, Pheo (50%)

Hyperparathyroidism (15-20%) –> Most common manifestation

MTC typically develops in childhood

and >1cm tumor assoc w/ local and distant metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

etiology MEN 2b

A
  • MTC, Pheo (>50%), mucosal neuromas, marfanoid body habitus
  • Childhood marfanoid morphology and mucosal neuromas most distinctive

•MTC develops earlier and is more aggressive than 2a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

si/sx of MEN 2b

A

Angiofibroma skin findings – on nares

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

dx MEN 2b

A
  • Genetic testing
  • Annual 24-hour urine - metanephrine/VMA
  • Serum Ca++ - PTH q 2-3yrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Tx MEN 2b

A

Thyroidectomy w/ central LN dissection -> mortality prevented

Pheo = unilateral vs bilateral resection?

Hyperparathyroidism

  • Excise 3 ½ w/ remnant in neck
  • Full excision w/ remnant implanted back in forearm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

location of pituitary

A

Pea sized gland at base of brain

  • below hypothalamus within the sella turcica
  • inferior to optic chiasm
  • Laterally by c_avernous sinu_s
    • Receives blood from ophthalmic veins and cerebral veins
    • Cranial nerves travel through (III, IV, V1, V2, VI)
    • Internal carotid arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

function of anterior vs posterior pituitrayr

A

Anterior Pituitary Gland/Lobe (adenohypophysis)

  • Synthesizes and secretes hormones (6)
  • Controlled by hormones from the hypothalamus

Posterior Pituitary Gland/Lobe (neurohypophysis)

  • Does NOT make hormones
  • Stores and secretes hormones (2) synthesized in the hypothalamus
  • Controlled by nerve impulses from the hypothalamus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

ant pit hormines

post pit hormones

A

Anterior: GH (FSH, LH, prolactin, TSH, ACTH)

Posterior: ADH (oxytocin, vasopressin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ADH — ____ hydration

A

ADH - ADDS hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Anterior pit dz

Posterior pit dz

A

Ant : Dwarfism

Posterior: DI, Psychogenic polydypsia, SIADH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

define dwarfism and 2 types

A

Adult ≤ 4’10”

Disproportionate Dwarfism

  • Some average-sized parts of the body and some shorter than average parts of the body
  • Achondroplasia (70% of all dwarfism)à Disproportionately short limbs, average sized torso, disproportionately large head

Proportionate Dwarfism

  • Short stature condition with arms, legs, trunk and head being in same proportion (relative size to one another) as in an average-sized person
  • Pituitary Dwarfism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

dx dwarfism

A

Provocative GH Testing-

  • GH is low even with provocation of pituitary gland

↓ IGF-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

tx dwarfism

A

Recombinant Human Growth Hormone à Somatotropin injections daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Dwarfism

DI
PP
Sheehan synd

SIADH

For conditions idtentify if they are due to

Posterior / anterior pit

hypo / hyperactivity of pit ??

hormones involved

A
46
Q

defien diabetes insipidus

A

DEC ADH

Condition of decreased release of ADH causing large volumes of dilute urine

47
Q

2 types of DI

most common causes of each

A

Central (neurogenic): Absent or ↓ synthesis or secretion of ADH

  • Idiopathic – most common cause
  • Hypothalamus-pituitary head trauma, neurosurgery, tumors
  • Vascular (Sheehan Syndrome)
  • Infection (meningitis, encephalitis, TB)
  • Congenital structural malformations or genetic

Nephrogenic : Kidneys are unresponsive to ADH secreted

  • Lithium toxicity- most common cause
  • Hypercalcemia
  • Acute or CKD- Polycystic kidney disease, pyelonephritis, renal amyloidosis
  • Genetic
48
Q

Si/sx of DI

A

Polyuria (No/little ADH or Kidneys unresponsive to ADH)

  • Neurogenic- varies based on degree of ADH production/secretion
  • Nephrogenic: Adults (>3L/day), Children (>2L/m2)

Nocturia (Enuresis in children)

Fatigue/sleepiness, irritability

Polydipsia (Intense thirst from hyperNa and hyperosmolality)

49
Q

dx difference b/w central and nephrogenic DI

A

Central - Primary issue with ADH –> ↓ADH

Nephrogenic - No issue with ADH –> ↑ADH

50
Q

dx DI

A

Cranial MRI – central (Hyperintensities, pituitary stalk thickening)

BMP (­ INC serum osm)

Hypernatremia / Hypercalcemia / Hypokalemia

DEC urine osm, urine Na

INC ser osms

Water deprivation/ADH stimulation test - Used to differentiate Central DI from Nephrogenic DI from psychogenic polydipsia

51
Q

tx DI

central

nephrogenic

Lithium toxicity

A

Central :

  • Desmopressin - first line
  • Alt Chlorpropamide

Nephrogenic

  • HCTZ –Blocks Na reabsorption in kidneys
  • Indomethacin - Inhibits prostaglandin synthesis (prostaglandins are ADH antagonists)

Lithium Toxicity - Amiloride

  • Blocks lithium from entering cells
52
Q

define Psychogenic polydipsia

A

INC ADH

Excess intake of fluids not associated with thirst

Polydipsia > 5 L/day

53
Q

who gets Psychogenic polydipsia

A

most commonly seen w/ schizophrenia

other psych disorders

54
Q

si/sx of Psychogenic polydipsia

A
  • Polyuria
  • Polydipsia
  • Xerostomia
  • Hyponatremia (ex. HA, muscle weakness, twitching, AMS, vomiting)

Severe hyponatremia –> cardiac arrest, coma, cerebral edema

55
Q

Dx Psychogenic polydipsia

A

Dx of exclusion

DEC serum osm

DEC urine osm

DEC ADH

56
Q

dx Psychogenic polydipsia

A

Water deprivation/ADH stimulation test

NORMAL ADH and kidneys –> depriving

  • sosm and uosm to be normal
57
Q

Tx Psychogenic polydipsia

A

Asymptomatic

  • Fluid restriction
  • High protein, high salt diet

Symptomatic

  • IV hypertonic saline (3% NaCl)
58
Q

High Serum Osms suggest volume ____

Low Serum Osms suggest volume ____ , dilution of solutes

A

High Serum Osms suggest volume depletion

Low Serum Osms suggest v_olume overload_, dilution of solutes

59
Q

DI - blood is (conc / dilute)

PP - blood is (conc / dilute)

A

DI - blood is conc

PP - blood is (dilute)

60
Q

hyper/hyponaturemia

DI -

PP

SIADH

A

DI - hyperNA

PP - Hypo Na

SIADH - Hypo Na

61
Q

INC/DEC ADH

DI

PP

SIADH

A

DI

  • central - DEC ADH
  • nephrogenic - INC ADH

PP - DEC ADH

SIADH - INC ADH

62
Q

DEC serum osm

DEC urine osm

dx?

A

PP

63
Q

INC serosm

DEC urosm

dx?

A

DI

64
Q

DEC serosms

INC urosms

Dx

A

SIADH

65
Q

define SIADH

A

Secretion of ADH (vasopressin) in excess of what is appropriate for hyperosmolality or intravascular volume depletion –> Retain fluid

  • Something causes pituitary to secrete to excess ADH (infection, drugs)
  • Something else is secreting ADH (small cell lung Ca)
  • Something is causing ADH to be stimulated more in the kidneys (genetic)
66
Q

etiology SIADH

A

Tumors: Lung carcinoma (particularly small-cell type)

CNS disorders

  • Masses: Tumor, abscess, hematoma, congenital malformation
  • Infections: Encephalitis, meningitis, AIDs related CNS opportunistic infection
  • Cerebrovascular occlusions, hemorrhage, cavernous sinus thrombosis
  • Hydrocephalus, Head trauma, MS, ALS, GB

Pulmonary disorders

  • Infections: PNA (bacterial or viral), abscess, cavitation

Drugs

  • Vasopressin (DDAVP), chlorpromide, clofibrate, carbamazepine, narcotics
  • Antidepressants: TCAs, MOAIs, SSRIs
67
Q

si/sx of SIADH

A

DEC urine output

Hyponatremia w/o edema –> Symptoms depend on how acute and severe hypoNa is

  • Mild: Weakness, nausea
  • Mod: Headache, vomiting, confusion
  • Severe: Lethargy, myoclonus, tremors, asterixis, generalized seizures, comasi/sx DIASH
68
Q

dx SIADH

A

Euvolemic hypotonic, hyponatremic

  • DEC serum osm
  • INC urine osm

Blood

  • ↓Sodium
  • ↓Osmolality

Urine

  • ↑Sodium
  • ↑Osmolality

CXR

Heat CT/MRI

Abdominopelvic CT

Addt. labs

69
Q

tx SIADH

A

Asymptomatic/mild Sx

  • Fluid restriction <500-1000
  • High protein, high salt diet

Symptomatic (mod-severe)

  • IV hypertonic saline
  • Furosemide
  • Salt tablets
  • ADH receptor antagonists - Tolvaptan , Conivaptan
  • Demecycline
  • Urea - ↑urine output
70
Q

Severe post-partum hemorrhage ® ischemic necrosis

Pituitary increases in size during gestation but blood supply does not

dx?

A

Sheehan syndrome (panhypopituitarism)

71
Q

si/sx of Sheehan synd

A

Mild : Variable, insidious onset

Mod

  • Failure of postpartum lactation & menses
  • Hair loss
  • Anorexia/weight loss
  • Fatigue

Severe

  • Lethargy
  • Anorexia/weight loss
  • Inability to lactate after delivery
72
Q

dx sheeham synd

A

MRI

  • Early- Enlarged pituitary, Ring enhancement
  • Late – Small pituitary in normal sella or Empty sella

Pituitary hormones (ACTH)

Adrenal insufficiency must be evaluated immediately

  • Anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, fever, confusion, or coma => death
73
Q

tx sheehan synd

ACTH deficiency

TSH deficiency

LH and FSH deficiency

GH deficiency

Prolactin deficiency

A

ACTH deficiency –> hydrocortisone (immediately)

TSH deficiency –> levothyroxine

LH and FSH deficiency

  • Interested in fertility: Gonadotropins (LH & FSH)
  • Not interested in fertility: Estradiol & progesterone

GH deficiency –> Recombinant GH (not routine in adults)

Prolactin deficiency –> No available treatment

74
Q

name if value is high or low in central vs nephrogenic DI

Serosms

ur osms

serum Na

urine Na

Urine volume

ADH

A
75
Q

name if value is high or low in PP vs SIADH

Serosms

ur osms

serum Na

urine Na

Urine volume

ADH

A
76
Q

Most common cause of sellar masses in 3rd decade and above

name types

A

Pituitary adenoma

  • Functional -=- Produce hormones, MOST common
  • Non-functional –== Don’t produce hormones
77
Q

size and cell types (w/ hormones) of pit adenomas

most common?

A

Size

  • Macroadenoma >1cm
  • Microadenoma <1 cm

Cell type

  • Gonadotroph – LH & FSH
  • Thyrotroph – TSH
  • Corticotroph - ACTH
  • Lactrotroph – prolactin (most common)
  • Somatotroph – growth hormone
  • Lactrotroph/somatotroph – GH+prolactin
78
Q

si/sx of pit adenomas

A

Asymptomatic

Neurologic symptoms

  • Visual changes *
  • Headache
  • CSF rhinorrhea (rare)
  • Hormonal abnormality sx’s

Blurry vision

Diplopia

Bitemporal hemianopia (#3 ) tunnel vision

Visual field defect

Diminished visual acuity

79
Q

dx pit adenomas

A

Hormonal evaluation

  • Serum prolactin (lactotroph adenomas)
  • Insulin-like growth factor 1 : IGF-1 (somatotroph adenomas)
  • 24 hour urinary free cortisol & elevated ACTH (corticotroph adenomas)

thyrotroph adenoma suspected

  • Alpha subunit
  • Total or free thyroxine (T4)
  • (TSH)

Gonadotroph adenoma - LH / FSH

80
Q

tx pit adenomas

A

Surgical excision + hypercortisolism

Relieve visual/neurologic Sx

Management of hormonal deficiencies

+/- adjuvant radiation

81
Q

Incidentaloma pit adenomas Evaluation :

A

> 10 mm typical hormone evaluation

< 10 mm without clinical findings of pituitary dysfunction

  • Only measure serum prolactin concentration
  • Could consider MRI at 6 months and 12 months
  • No evaluation for hormone hyposecretion
  • No evaluation for visual abnormalities
82
Q

common complication of pit adenomas

A

Pituitary Apoplexy infarct or hemorrhage into the adenoma

83
Q

si/sx of Pituitary Apoplexy

A

•Severe acute onset headache(89%)

  • Vomiting (57%)
  • Visual field deficits (51%) – diplopia/BTH ]
  • Other (III, IV, V, VI) cranial nerve dysfunction (46%)
  • Fever (16%), neck stiffness (25%)
  • Impaired consciousness/AMS (14%)
84
Q

Hyperprolactinemia causes

A

Physiological Causes

  • Sleep, Physical exertion, Food, Stress/trauma, Coitus , Pregnancy / Postpartum state / Nursing/nipple stimulation , Surgery

Hypothalamic-pituitary disease

  • Lactotroph adenomas (prolactinomas)
  • Decreased dopaminergic inhibition of prolactin secretion(drugs or damage)
  • Disease in or near hypothalamus/pituitary(tum or,infiltrative dz)

Drug induced – dec dopamine

  • Ranitidine
  • Cocaine/Amphetamines
  • Metoclopramide , Opioids
  • Risperidone , SSRI’s
  • Verapamil , Hydroxyzine
85
Q

Hyperprolactinemia is seen w/ MEN 1 or MEN 2a or b

A

(MEN1) syndrome

Parathyroid, Pancreatic islets, Pituitary

86
Q

si/sx of Hyperprolactinemia

A
  • Galactorrhea
  • Infertility
  • Osteopenia

DEC libido nonresponsive to hormonal therapy

+/- visual Δ

  • •Dysmenorrhea
  • •Estrogen deficiency
  • •Dyspareunia
  • •Acne/hirsutism
  • •Anxiety/depression
  • •ED
  • •Gynecomastia
  • •Hypogonadism
87
Q

dx Hyperprolactinemia

A

Diluted fasting prolactin >200

Hormonal evaluation

MRI with and without gadolinium–> pituitary lesion/adenoma

Formal visual field eval

INC serum prolactin

88
Q

tx Hyperprolactinemia

A

Dopamine agonists – first choice

  • Cabergoline: First choice
  • Bromocriptine: First choice for women wanting pregnancy

Surgery

Radiation

89
Q

Hyperprolactinemia Indications for Surgery

A
  1. Visual field defects unresponsive to medical therapy
  2. Macroadenomas unresponsive to medical therapy
  3. Tumor growth while on medical therapy
  4. Intolerance to dopamine agonist therapy
  5. Pituitary apoplexy (rare)
  6. Cerebrospinal rhinorrhea due to prolactinoma erosion into sphenoid sinus (rare)
90
Q

define Acromegaly/ gigantism & co-morbidities

A

INC GH & IGF-1

Acromegaly Co-morbidities

  • Hypertension and heart disease
  • Sleep apnea
  • Insulin-resistant diabetes
  • Cerebrovascular events and headache
  • Arthritis
91
Q

si/sx of Acromegaly/ gigantism

A

•Prognathism (protruding jaw)

  • HA
  • Visual Δ
  • Skin tags
  • Macroglossia

•Frontal bossing – flat nose

•Coarse features

•Enlarged hands/feet & tongue

92
Q

dx Acromegaly/ gigantism

A

Hormonal eval

­INC IGF-1

OGTT ->> GH suppression

Formal visual field eval

Glucose

LFTs

BUN/Cr

93
Q

tx Acromegaly/ gigantism

A

Surgical debunking - Transphenoidal pituitary microsurgery (70% fail surgery only)

Medical:

  • Dopamine agonists - Bromocriptine, Cabergoline (mixed)
  • Somatostatin analogs (Octreotide, Lanreotide)
  • Pegvisomant - GH receptor antagonists

Radiation - Stereotactic radiosurgery

94
Q

Acromegaly/ gigantism goals of therapy

A

Control tumor size

IGF-I normal

and OGTT suppression of GH <1

95
Q

list Dopamine agonists used in Acromegaly/ gigantism

A

Bromocriptine

Cabergoline

96
Q

list somastostatin analogs used in Acromegaly/ gigantism

A

Octreotide

Lanreotide

97
Q

list GH R antagonists used in Acromegaly/ gigantism

A

Pegvisomant

98
Q

Stereotactic radiosurgery is used to tx??

A

Acromegaly/ gigantism

99
Q

list malignant Pituitary carcinoma

A

Pituicytoma

Germ cell tumor

Chordomas

Primary lymphomas

Mets from breast ca (F) & lung ca (M)

100
Q
  • Arises from posterior pituitary
  • Presents as sellar mass; usually mistaken for pituitary adenoma
A

Pituicytoma

101
Q

•Parinaud’s syndrome (paralysis of upward gaze) is assoc w/ what type of pit tumor?

A

Germ cell tumor

102
Q

Germ cell tumor dx?

Tx?

A

Imaging shows mass in third ventricle

↑Serum concentrations of B-hCG or AFP

Tx:

  • Radiation - Highly radiosensitive
  • Highly malignant and metastasize readily
103
Q

pit tumor w/ si/sx

  • HA
  • Visual impairment
  • Ant. pituitary hormonal deficiencies
A

Chordomas

104
Q

MRI - sellar mass with variable extrasellar extension

dx of what pit tumor??

A

Primary lymphomas

105
Q

dx of what pit tumor?

  • Retroorbital pain and ophthalmoplegia
  • Diabetes insipidus
  • Visual field defects
A

Mets from breast ca (F) & lung ca (M)

106
Q

•Visual & oculomotor deficits assoc w/ what pit tumor

A

Primary lymphomas

107
Q

↑Serum concentrations of B-hCG or AFP

what pit tumor?

A

Germ cell tumor

108
Q

Presents as sellar mass; usually mistaken for pituitary adenoma

what pit tumor??

A

Pituicytoma

109
Q

Arises from posterior pituitary

pit tumor??

A

Pituicytoma

110
Q

most common cancers assoc w/ metastesiszes of pit tumor?

men??

women??

A

breast cancer in women

lung cancer in men