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ENRP Exam 2 > Ednocrine Pathology Dr. Singh > Flashcards

Ednocrine Pathology Dr. Singh Flashcards

1
Q

Neoplasia is the most common cause of primary H. Secretions except what organ

A

Thyroid

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2
Q

PP and AP made of what

A

PP : neuro (scattered nuclei, wispy)

AP : adeno (glandular, acidophils red, basophils blue, chromophobes pale)

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3
Q

Mass effect on pituitary means what and can cause

A

= neoplasm growing in size causing Intracrainial P

  1. Bilateral temporal hemianopsia
  2. Pituitary apoplexy = hemorrhage in adenoma
  3. Low hormones
  4. Hyperprolactinemia
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4
Q

Intracranial Edema SX

A
  1. Papilledema
    2 Bradycardia + shallow breathing
  2. HTN
  3. HA,N,V
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5
Q

Pituitary lesion growing big can compress what

A

The optic chiasm = bilateral temporal hemianopsia (loss of temporal vision due to nasoretinal nerves)

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6
Q

Pituitary tumor that hemorrhages in itself

A

Pituitary adenoma

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7
Q

Mass effect has what effect on hormones

A
  1. If it cuts communication between Hypo and P = decrease in all H except PROLACTIN and others where the hypo has negative effect on P
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8
Q

How to look at biopsy and know what type of cells and if there is a tumor

A

Colonal uniform sheet of cells, stain with that hormone immunostain (turns brown )

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9
Q

Lactotroph Adenoma (prolactemia)
1. Male vs female
2. How females present
3 . How males present

A
  1. Males dx at larger tumor, females dx at smaller tumor due to effect on mentruation and other visual sx
  2. Menstruated irregularity, galactorrhea, low libido, infertility,
  3. Mass effect (ICP), low sperm count, low libido
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10
Q

Lactotroph Adenoma

    • stain for
  2. Biopsy findings
  3. TX
A
  1. Prolactin
  2. Stromal Hyalinization + Psammoma bodies (calcifications) ——> Dense calcifications causing pituitary stone = usually not functional anymore (involuted Adenoma)
  3. Give Dopamine or Somatostatin——I Prolactin, then go to surgery
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11
Q

Surgery for

A

Transsphenoidal approach = through sella Tursica

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12
Q

Hyperprolactemia not in adenoma 5 ways

A
  1. Preg, lactation
  2. Loss of dopamine due to head trauma damaging hypothalamus,
  3. Antidepressants + Antipsychotics —-I Dopamine
  4. Hypothyroidism (increased TRH can cause increase in Prolactin)
  5. Renal failure (lower clearance of prolactin)
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13
Q

Lactational Amenorrhea Method

A

Not ovulating sue to high prolactin during breastfeeding = serving as birth control if you dont want a baby soon agian

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14
Q

Somatotroph Adenoma

  1. Secretes what H
  2. Can cause what
A
  1. GH
  2. Gigantism (before epiphyseal plates close) and Acromegaly (after epiphyseal plates close = big hands, thicken bones like face, hands are spadelike
    + can cause higher chance of optic chiasm compression + hemorrhage in itself in the Pituitary
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15
Q

Acromegaly signs

A
  1. Spade like hands : thick tissue big and fat
  2. Big thick face , protruding jaw, big lips
  3. A lot of joint pain
  4. Enlarged organs
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16
Q

How to see if someone has increased GH

A

High GH causing high secretion of IGF (Insulin-like Growth Factor) from liver= test for this level in blood
1. If elevated do oral glucose tolerance test and look for IGF response (normal = should decrease, if somatotropic adenoma it will stay high)

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17
Q

Glucose does what to GH

A

Inhibits GHRH in hypothalamus

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18
Q

How to treat Somatotropic adenoma

A

Give ALOT of Somatostatin to decrease GH, or GH antagonist, or DA agonist, or surgery

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19
Q

Somatotropic adenoma

1. Biopsy findings

A
  1. Diffuse growth, GH +stain, can be mixed with prolactin cells
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20
Q

Corticotroph Adenoma

  1. Causes what
  2. Thing about identifying this
A
  1. High ACTH causing high cortisol = Cushing Disease

2. Small tiny tumor can cause this

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21
Q

Cushing Syndrome vs Cushing disease

A

1 .Cushing syndrome = hypercortisolism and all its sx

2. Cushing disease = high pituitary ACTH (Corticotroph Adenoma)

22
Q

Cushing symptoms

A
  1. Centropetal obesity + moon face + hump between shoulder blades
  2. Striae thick,
  3. Hirsutism (facial that is soft),
  4. Thin skin
23
Q

4 things that can cause Cushing’s syndrome, and which is most common

A
  1. Corticotroph Adenoma (tumor of AP secretion of high ACTH)
  2. Adrenal gland tumor (secreting high cortisol)
  3. Ectopic ACTH (Small Cell Carcinoma of lung, Pancreatic carcinoma, neural tumor)
  4. Iatrogenic Cushings from Glucocorticoid administrations
24
Q

When I give someone glucocorticoids (steroids ) what can happen as a side effect

A

Cushing syndrome

25
Q

ACTH Dependent Hypercortisolism how to know where it is coming from

A

ACTH is high + cortisol high

  1. Dexamethasone suppresses ACTH = normal
  2. HIGH DOSE Dexamethasone suppress ACTH = Corticotroph Adenoma
  3. HIGH DOSE Dexamethasone does NOT suppress ACTH = ectopic SMALL CELL Carcinoma**, or adrenal hyperplasia
26
Q

Inferior Petrosal Sinus Sampling

A

How to know if high ACTH is from AP ( thread catheter up jugular vein to pterosal sinus of AP and sample cells there (adenoma seen)

27
Q

TX Corticotroph Adenoma

A
  1. Surgery is ideal

2. Get rid of adrenal glands (Nelson Syndrome)

28
Q

Nelsons Syndrome

A
  1. After removing adrenal glands

2. AP keeps secreating more and more ACTH (increasing MSH, melanocyte stimulating H = increased pigmentation)

29
Q

Thyrotrophs adenoma

1. Is what

A
  1. High TSH from AP = excess TH secreted
30
Q

Gonadotroph Adenoma

1. Is what

A
  1. FSH/LH high secreting

2. Mass effect*, or after malignant, rare and silent adenoma, usual no effect symptomatically

31
Q

Transcription Factors for all Pituitary adenoma except one is what

A

PIT-1 **
(Corticotroph adenoma = TPIT)**

(Thyrotrophs adenoma = GATA2 + PIT1)
(Gonadotroph Adenoma = SF1, ERa, GATA2)

32
Q

Genetic mutations for Pituitary adenomas (somatic + Familial)

A 
Somatic :
1. GNAS
2. USP8 (Corticotroph adenoma due to EGFR upregulation 
Familial : 
1 AIP (somatotroph adenoma)
33
Q

GNAS mutation what happens

A

Makes a subunit mutation = G receptor remain active

= all pituitary adenomas, most common in somatotroph and corticotroph adenoma

34
Q

AIP gene is associated with

A

Familial Somatotroph adenoma (gigantism, acromegaly)

AIP (FIPA)

35
Q

Aggressive adenomas and Pituitary carcinomas

A
  1. Aggressive adenomas = invades into brain

2. Pituitary carcinoma = metastasize all over brain

36
Q

Rathke’s Cleft Cyst from what and a consequence

A

PP tumor retained from Embryonic formation

= can rupture

37
Q

Rathke’s Cleft Cyst histology seen

A

From oral ectoderm = epithelial lined, respiratory epithelium (from larynx part of body)

38
Q

Craniopharyngioma

2 types

A

PP from Rathkes cyst epithelium tumor

  1. Kids 5yo-15yo: :adamantinomatous (Anamle type tissue tough calcified and hard*) = growth retardation from hypopituitarism
  2. Adults over 65yo : Papillary Craniopharyngioma = increases ICP (gets very large), or hypopituitarism
39
Q

Craniopharyngioma histology you see

A

Also from rathkes pouch only more squamous* in nature

  1. Wet keratin (almost like a keratin pearl)
  2. Calcified cyst
40
Q

Hypopituitarism can happen how

A
  1. Tumor mass or something that squashed the communication between hypo and AP+PP
  2. Ischemia or inflammation or surgery
  3. Bled into AP + PP
41
Q

Empty Sella Syndrome

  1. Is what
  2. Primary
  3. Secondary
A
  1. Infarction causing loss of communication between hypo and AP + PP = ANTERIOR hypopituitarism
  2. CSF leaks into sella and compresses Pituitary
  3. Pituitary expands and infarcts inside the sella = causing empty space to form
    (Diaphragm Sella = keeps CSF away from pituitary gland)
42
Q

Anterior Hypopituitarism happens from what and means what

A
  1. Empty Sella syndrome

2. Low GH, Gonadotrophs, TSH, ACTH, PRL

43
Q

Sheehan Syndrome is what and happens from what

A
  1. From Postpartum Necrosis
  2. Physiologic swelling of pituitary gland = expanded too much and when you deliver it rapidly expands to you infarct the AP = causing empty sella)
44
Q

Sheehan Syndrome first SX you usually see

A

They can lactate after birthing child, then other hormones being low becomes more obvious

45
Q

ADH : no enough causing and too much causes

A
  1. ADH low : Diabetes Insipidus

2. ADH high : SIADH (Syndrome of inappropriate ADH secreation)

46
Q

Diabetes Insipidus what happens and causing

A
  1. Low ADH : low water being reabsorbed = excess urination (tasteless urine, not sweet like in DM)
  2. Low ADH : more water loss = hypernatriemia
47
Q

What can cause low ADH (central vs nephrogenic) + how to know which one someone has

A
  1. Central = PP is not making enough ADH
  2. Nephrogenic = KIDNEY is not responding to ADH when it binds to receptors
  3. Give DDAVP (which is ADH) = if it treats them it is CENTRAL
48
Q

Too much ADH causes what to happen

A
  1. Fluid retention that is put in serum (urine is concentrated)
  2. Hyponatremia = mental status changes, muscle weakness, seizures)
49
Q

SIADH most common cause

A
  1. Small cell carcinoma
  2. Traumatic Brian injury , Subarachnoid Hemorrhage
  3. SSRIs
50
Q

Diabetes Insipidus and SIADH similar sx

A

THIRST : in SIADH (inappropriate thirst due to mental alternations), in DI (dehydration)

ENRP Exam 2 (8 decks)

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