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Pathophys > Pituitary Patho > Flashcards

Pituitary Patho Flashcards

1
Q

Why are steroid hormones able to cross cell membranes

A

They contain cholesterol making them fat soluable

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2
Q

What are the three classes of hormones

A

Peptide and protein, steriod, and Amine

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3
Q

what are the secondary messenger systems of protein hormones

A

Adenylate Cyclase Mechanism,Phospholipid Mechanism, Guanylate Cyclase Mechanism, Tyrosine Kinase Mechanism

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4
Q

What type of steriod hormones do the following produce

Adrenal Cortex

Testes

Ovaries

Corpus Luteum

Placenta

Kidney

A

Adrenal Cortex= Cortisol, Aldosterone, Androgens

Testes=Testosterone

Ovaries= Estrogens, Progesterone

Corpus Luteum= Estrogens, Progesterone

Placenta= Estrogens, Progesterone

Kidney= 1,25-Dihydroxycholecalciferol

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5
Q

what are the 2 pathways of the synythesis of Amine hormones from tyrosine

A

1) Tyrosine to Dopamine to NE to Epi
2) Tyrosine to Thyroid hormone

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6
Q

Why does the SNS release NE instead of Epi

A

the SNS lacks the enzymes(phenylethanolamine-N-methyltransferase) to make epi from NE

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7
Q

What type of amine hormones do the following tissues produce

Hypothalamus

Thyroid

Adrenal medulla

A

Hypothalamus= Dopaine

Thyroid= T3, T4

Adrenal medulla= NE, epi

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8
Q

how does dopamine act as a hormone

A

it inhibits Prolactin

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9
Q

what 3 things may occur to Free hormone after it is released from endocrine cells? when does it have biological effects?

A

1) Carrier-bound hormone
2) hormone receptor (bio effects)
3) Hormone degradation

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10
Q

what factor has the largest effect on hormone half-life

A

Those that are protein bound have longer half lives (days compared to min)

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11
Q

what is the formula for metabolic clearance rate of hormones

A

MCR = (mg/minute removed) / (mg/ml of plasma) = ml cleared/minute

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12
Q

what are the 6 hormones produced in the anterior pituitary

A

GHRH:

GIH (Somatostatin)

CRH:

TRH:

GnRH:

PIF (dopamine)

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13
Q

why does inc ACTH cause inc pigmentation

A

inc ACTH= inc MSH(melanocyte stimulating hormone)

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14
Q

what hormones would be affected by a clot in the pituitary? Why?

A

All of those released by the Ant pit because the ant pit is stimulated by vascular connections whereas the post pit only has neuro connections

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15
Q

what is the adenohypophysis

A

ant lobe of the pituitary

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16
Q

how does the post pituitary maintain BP

A

PVN responds to inc osmolarity by inc action potentials= inc ADH release

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17
Q

what local mass effects can result from hyperpit

A

Optic chiasm-
ICP
Hemorrhage into an adenoma resulting in rapid enlargement of lesion-pituitary apoplexy

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18
Q

what type of vision loss will occur from pituitary compression of the optic chiasm

A

bitemporal hemiopsia

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19
Q

what can cause hypopit

A

Result of various destructive processes including ischemia, radiation, inflammation and non-functioning neoplasms.

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20
Q

what is the most common cause of hyperpit

A

pituitary adenoma

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21
Q

which type of pit tumors of often more progressed when found(secretory or non-secretory)

A

secretory are often found earlier because they produce Sx from excess of hormone

22
Q

what the sizes of micro and macroadenomas of pituitary

A

micro=<1cm

macro =>1cm

23
Q

how are genetic abnormalities in G-protein(alpha, beta, gamma) associated with pituitary adenomas

A

activation of G-protein increases cAMP which is a mitogenic stimuli promoting cellular proliferation and hormone synthesis

24
Q

what is a GNAS gene mutation

A

It incodes for the Alpha subunit of the G protein

40% of somatotroph cell adenomas have GNAS mutations

25
Q

what is a inherited mutation leading to hyperpit tumors

A

mutation in tumor suppressor gene

26
Q

what is the most common functional pituitary tumor

A

prolactinoma (lactotroph adenoma)

27
Q

how large of a prolactinoma is required before Sx are produced

A

Prolactin secretion is extremely efficient; a microscopic adenoma can produce enough prolactin to produce symptoms.

28
Q

what occurs after prolactinomas undergo dystrophic calcification

A

pituitary stone formation

29
Q

what determines the amount of prolactin production from a prolactinoma

A

Prolactin production is proportional to tumor size.

30
Q

what inhibits prolactin production. When may this occur?

A

dopamine

1-interruption of dopamine due to head injury
2-drugs (psychotropics)

31
Q

what are the hormone effects of hyperprolactinemia. What population is it easiest to detect in?

A

Amenorrhea

Galactorrhea
Loss of libido
Infertility
Becasue of the Sx it is easier to detect in females 20-40yo

32
Q

what mass effects may prolactinomas produce

A

Headache
Fatigue
Neck pain
Seizures
Visual field effects

33
Q

what is the Tx for prolactinomas

A

Medications Bromocriptine: Dopamine agonist
Surgery
Radiation

34
Q

what other hormone effects are likely to occur with prolactinomas

A

dec TSH= hypothyroidism

dec cortisol= addisons

dec FSH= dec fertility

35
Q

what is the pathophys mechanism from somatotroph adenomas

A

Hypersecretion of GH stimulates hepatic secretion of insulin-like growth factors (IGF-1)which cause the clinical manifestations of this disorder.

36
Q

what occurs if excess GH prior to bone maturity

A

excess GH results in gigantism: generalized increase in body size & long limbs

37
Q

what occurs if excess GH post bone maturity

A

Acromegaly: Enlargement of the head, hands, feet, jaw (prognathism), tongue and soft tissues

38
Q

what other effects does GH cause besides musculoskeletal

A

Excess GH results in diabetes and accelerated atherosclerotic cardiovascular disease as well as other end organ effects from HTN.

39
Q

what is the pathophys mechanism of corticotroph adenomas

A

Excess production of corticotrophin ((ACTH) = Increased cortisol production hypercortisolism (Cushing syndrome)

40
Q

what s/sx are common with cushings

A
  1. fat/ water retention causing moon face, buffalo hump, trunkal obesity, striae
  2. DM2 (cortisol causes insulin resistance)
  3. infertility(dec FSH/LH)
  4. dec growth (dec GH)
  5. hypothyroid (dec TSH
41
Q

how much parenchyma is usually lost before hypopit s/sx occur

A

75%

42
Q

what is Sheehan syndrome

A

inc blood during preg so vessles become accustomed to lareg volume. Rapid hemorrhage causes vasospasm and death of ant pit. Usually dont see s/sx until months later

43
Q

what is panhypopituitarism

A

all hormones are deficient

44
Q

what is primary empty sellas syndrome

A

due to a defect in the diaphragma sellae or increased ICP allowing the encroachment of arachnoid and CSF into the sella and compressing the gland.

45
Q

what is secondary empty sella syndrome

A

due to intervention for a pituitary process usually adenoma which results in the destruction/removal

46
Q

what results from posterior hypopit

A

dec oxytocin

dec adh= diabetes insipidis

47
Q

what results from ADH excess? What can cause this?

A

SIADH

1-Ectopic production

2-Infection of the pituitary

3-Medications

4-inc ICP

48
Q

what Sx result from 130-140 Na

A

Anorexia, fatigue and dyspnea

49
Q

what Sx result from 120-130 Na

A

Nausea
Vomiting
Abdominal cramping

50
Q

what Sx result from 110-115 Na

A

Confusion
Lethargy
Muscle twitching
Convulsions

51
Q
A

Pathophys (15 decks)

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