Pituitary Glands Flashcards

1
Q

According to FSH and LH

there are two types of disorder in releasing of these hormones.

A

1-Primary –> the deFect on testes

2. Secondary —> defect on anterior Pituitary that lead tp decrease of production pf LH&FSH

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2
Q

Whats considered as Posterior Feedback Mechanism

A

So body sends signals for hypothalmus to produce LHRH &FSRH

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3
Q

Negative Feedback Mechanism

Example + moa

A

Thyroxine
if its level is high in body —>body gives signal for pituitary to decrease corticatropin hormone production
But if there’s an tumor in pituitary this may lead to increase in production of thyroxine hormone, then increase both T4 and T3 level, then there’s a problem

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4
Q

Increase in production due to hypersensitivity to other hormones like

A

if there’s B hypersensitivity, to TSH —>The production f T4 will increase as we can see in Thyrotoxicosis disease.

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5
Q
Growth Hormone (Somatotropin)
prevalence
A

GH increase highly in the adolscence period and may be absent neonatal and adult period.

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6
Q

Note: Increase in GH may lead to DM - explain

A

One to increase the insulin resistance and hypoglycemic effect when patient taking carbohydrates

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7
Q

Growth hormone excess lead to

A

Acromegally –> insidious cosymptomatic disorder

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8
Q

What occurs during Benign pituitary Tumor

A

In Benign pituitary Tumor there is an increase in size of production cells of gonadtropins which are gonadotrophes cells which finally lead to increase in GH production

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9
Q

When does Acromegaly Occur?

A

Acromegaly usually occurs after fusion of epiphysis (growth plate) of the long bones

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10
Q

Whats the difference between Acromegaly and Gigantism?

A

Gigantism occurs before epiphysis (epiphysis closure) - then theres an increase in height, length of arms, legs to abnormal level.

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11
Q

IGF-I location and whats it stimulated by

A

IGF-I produced in the liver and t’s production is stimulated by the GIT

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12
Q

What’s IGF-I ?

A

IGF-I is the hormone that goes to body organs ( heart, bone, etc.) and act as a function of GIT.

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13
Q

GH can also be increased by stress

A

True

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14
Q

Diagnosis of Acromegaly

A

MRI and CT scan

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15
Q

Goal of Management for Acromegaly

A

1- Normalize biochemical marker ( blood sugar level which increases with GH increase, cholesterol, etc.)
2- Reduce tumor size ( as in edema)
3- keep normal pituitary function, improve clinical function
4-Decrease in mortality rate, morbidities

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16
Q

Acromegaly associated with high mortality , why?

A

This may be due to its enlargemnt of heart and other agents or vessels

17
Q

Treatment for Acromegaly

When surgery is impossible

A

1- Somatostatin–>hormone that go to the hypothalmus and prevent GHRH
2- Dopamine act inversely with GH- Dopamine Antagonists
*Surgery - removing a part of pituitary gland- patients may suffer from hypopituitarism.
3- Dopamin Agonists ( Cabergoline=dostinex)
4- GH receptor Antagonists
5-Radiation Therapy ( radiation=Hypothyroidism

18
Q

For patients with increase in both GH & Prolactin, the treatment is

A

by Bromocriptine or Carbegoline can be beneficial for Acromegaly.

19
Q

Laboratory test- according to MRI and CT scan

A

1) Patient older than 1 year (x-ray: left wrist and hand)

2) Patient younger than 1 year( x-ray: knee and ankle)

20
Q

If there’s an increase in prolactin level

A

Hyperprolactinemia

21
Q

Anti-dopamine

A

can increase prolactin like domperidone

22
Q

Pathophysiology of Hyperprolactinemia

A

High level of prolactin –> Inhibition of GnRh
During breast feeding, prolactin level will increase –>inhibition of of GnRh —>decrease both LH &FSH= No ovulation or spermatogenesis.

23
Q

Prolactin Treatment

A

1- Normalize prlactin level, because like we said prolactin is toxic for GnH, also it can cause skin problems, uscle and others.

24
Q

Primary vs Secondary

A

Primary- defect in primary target organ

Secondary- defect in pituitary gland

25
Q

Acromegaly

A

GH excess

26
Q

when do we give somatostatin analogues

A

when surgery and radiation failed

s/e: gallstone, biliary slude

27
Q

Example of GH receptor antagonist

A

peg visomant coinly genetic engineering GH antagonist

28
Q

why pegvisomant increase GH, while it block its receptor

A

by declining IGF-I levels

29
Q

Dopamine Agonist examples

A

Bromocriptine, gabergoline

indications- Mildly elevated IGF-1 level, GH - prolctin co secreted tumor

30
Q

problems with radiation therapy

A

Hypopituitarism

31
Q

GH deficiency

A

During childhood

32
Q

GH Deficiency may be due to

A

Methoxamine, Isoproterenol, Glucorticoids, cimidine, Methylphendate, Amphetamine

33
Q

Clinical Diagnosis of GH deficiency

A
1- Decrease in Growth Velocity
2- Short Stature also may be present
3- Abdominal obesity
4-Prominence for the forehead 
5- Immaturity of the face
34
Q

Lab Tests in child

A
  1. Gh stimulation test
  2. decrease IGF-1 and IGF3
  3. hypoglycemia, hypothyroidism
  4. CT,MRI
  5. x-RAY LEFT CHEST, hand for child younger than 1 year
    for knee , ankle for child older than 1 year
35
Q

Lab test for Adult

A
1- GH Stimulation
2- IGF-1 
3. Increase in lipid profile 
4. decrease in bonedensity 
5. Insulin resistance increase 
6Loss of other pituitary hormone