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ENDOCRINE Flashcards

1
Q

What is the origin and consequence of a craniopharyngioma?

A

Origin: Above sella turcica from remnants of Rathke Puoch

Consequence: cystic mass with compression of adjacent tissues causing destruction of the posterior lobe of the pituitary

Imaging: mass replaces midline structure sin the region of the hypothalamus

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2
Q

SIADH is associated with what carcinomas?

A 
small cell carcinoma of lung
prostate carcinoma
GI carcinoma
pancreatic carcinoma
thymoma
lymphoma
Hodgkin disease
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3
Q

What are the major clinical manifestations of Sheehan syndrome?

A 
PALLOR (decreased MSH)
HYPOTHYROIDISM (decreased TSH)
OVARIAN FAILURE (decreased FSH and LH)
 FAILURE OF LACTATION (decreased Prolactin)
ADRENAL INSUFFICIENCY
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4
Q

Acromegaly symptoms

A 
thickened skin
Facial Changes
Goiter
Barrel Chest
abnormal glucose tolerance
male sexual dysfunction
menstrual disorders in women
degenerative arthritis
peripheral neuropathy
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5
Q

What are the symptoms of functional lactotrope adenoma?

A

Amenorrhea
Galactorrhea
Infertility

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6
Q

What is most commonly used goitotrogenic drug?

A

Lithium (used in the management of manic-depressive states)

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7
Q

What is Endemic goiter?

A

Goitrous hypothyroidism of dietary iodine deficiency in locales with a high prevalence of the disease

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8
Q

somatotrope adenoma

A

growht hormone-secreting tumor of the pituitary

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9
Q

What are some pathological processes that result from a somatotrope adenoma?

A 
Acromegaly (many with neurological and msk symptoms/ some with HTN)
Gigantism (in children)
Menstrual irregularities in women
Diabetes Mellitus
Headache
Optic Chiasm compression
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10
Q

What is used to treat lactotroph microadenomas

A

Dopamine agonists

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11
Q

What is Adrenogenital syndrome? what is it’s cause?

A

Virilization of external genitalia in female infants (pseudohermaphroditism)
Appearance: hypertrophic clitoris and parital fusion of labioscrotal folds in a genetic female

caused by congenital deficiency of 21-hydroxylase

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12
Q

What hormones increase in 21 Hydroxylase deficiency?

A

Adrenal androgens and progesterone

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13
Q

What congenital anomalies are seen in DiGeorge Syndrome?

A

Failure to develop 3rd and 4th Branchial pouches result int he following

Parathyroid Agenesis/Hypoplasia
Thymus Agenesis/Hypoplasia
Congenital Heart Defects
Dysmorphic faces

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14
Q

What is characteristic phenotype of Albright hereditary Osteodystrophy?

A 
Short stature 
obesity
mental retardation
subcutaneous calcification
congenital anomalies of the bone
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15
Q

What genetic abnormality and consequent pathology is seen in Albright Hereditary Osteodystophy?

A

Mutations in a gene (GNAS1) whose product, the protein, Gs, couples hormone receptors on the stimulation of adenylyl cyclase.

Consequently, in the renal tubular epithelium, the production of cAMP in response to PTH is impaired, and inadequate resorption of calcium from the glomerular filtrate. This causes Psuedohypoparathyroidism

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16
Q

What mental changes are often observed in cases of hyperparathyroidism?

A

Depression
Emotional Liability
Poor Mentation
Memory Defects

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17
Q

Describe a parathyroid adenoma microscopically and macroscopically/on gross exam.

A

Micro: Sheets of neoplastic CHIEF CELLS in a rich capillary network. A rim of normal parathyroid tissue is usually evident outside the tumor capsule and distinguises adenoma from parathyroid hyperplasia

Macro: Circumscribed, reddish brown, solitary mass, measuring 1 to 3 cm in diameter

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18
Q

What are common causes of secondary hyperparathyroidism?

A

Most common cause: Renal failure
- Diabetic glomerulosclerosis is a major cause of renal Insufficiency

Other causes: Vitamin D Deficiency
Intestinal malabsorption
Fanconi Syndrome
Renal Tubular Acidosis

19
Q

What diseases are seen with MEN-2A affected patients? What is cause?

A

C-cell derived medullary thyroid carcinoma
Chromaffin cell-derived pheochromocytoma
Hirschspring Dieases (Congenital Megacolon)
Nueroal Crest Tumors (eg. glioma)

Cause: Mutations of the RET protooncogene, a transmembrane receptor of the tyrosine kinase family

20
Q

What diseases are seen with MEN-1 affected patients? What is cause?

A

Pituitary Adenoma
Parathyroid Hyperplasia or Adenoma
Islet Cell Tumors of the Pancreas (Insulinoma and gastrinoma)

Cause: Mutation of the MEN 1 tumor suppressor gene

21
Q

What is the most common cause of neonatal hypothroidism today?

A

Thyroid Agenesis

22
Q

What are symptoms of cretinism in a newborn?

A 
Early Weeks: 
Umbilical Herniation and Large Abdomen
Sluggish
Low body temperature
Refractory Anemia

Later Weeks:
Mental Retardation Stunted Growth
Charactersitic facies

23
Q

Describe Osteitis Fibrosa Cystica. What are the symptoms?

A

Severe bone deformities
“Brown Tumor” Formation(of Hyperparathyroidism)

Symptoms:  
Bone Pain 
Bone Cysts
Pathologic Fractures
Localized Bone Sewllings (brown tumors)
24
Q

What are dominant clinical manifestations of hypothyroidism?

A 
In both sexes:
Muscular Weakness
Peripheral Edema
"Myxedema Madness"
Pallor
Enlarged Tongue

In females:
Ovulatory Failure
Progesterone Deficiency
Irregular and Excessive Menstrual Bleeding

In males:
Erectile Dysfunction
Oligospermia

25
Nongoitrous Hypothyroidsm amy result from what pathology?
Antibodies that block TSH itself or the TSH receptor without activating the thyroid
26
What are the complications seen in Toxic Goiter
Usually cardiac complications, including atrial fibrillation and CHF in older patients (usually over 50 years of age)
27
What is HASHIMOTO Thyroiditis?
Chronic Autoimmune Thyroiditis characterized by circulating antibodies to thyroid antigens and features of cell-mediated immunity to thyroid tissue commonly arising in the 40s/50s - mostly women
28
Describe a Thryoid gland of a patient suffering from Hashimoto Thyroiditis
An enlarged, firm gland weighing from 60-200 g The cut surface is pale tan and fleshy and exhibits a vaugely nodular pattern Micro: .1. a conspicuous infiltrate of lymphocytes and plasma cells 2. destruction and atrophy of the follicles 3. oxyphilic metaplasia of the follicular epithelial cells (Hurthle or Askanazy cells) inflammatory infiltraes are cocallyarranged in lymphoid follicles, often with germinal centers
29
Reidel thyroiditis features
Fibrosis (retroperitoneum, mediastinum, orbit) Involves soft tissues of the neck "Woody" stony hard thyroid
30
Dequervain thyroidits features
Hyperplastic and vascular thyroid
31
Multinodular Goiter features
a nodular gland without inflammation
32
A nontoxic goiter microscopically features
Hypertophy and Hyperplasia Variation in the size of follicles Fibrosis Evidence of Old Hemorrhage
33
Graves Disease features what thyroid pathology?
Hyperplastic and Vascular Thyroid
34
Most common thyroid tumor in young women is..
Papillary carcinoma | tends to metastasize to regional lymph nodes but only rarely distantly
35
What characterized papillary carcinoma
Branching papillae lined by epithelial cells with clear (ground glass or Orphan Annie_ nuclei and fibrovascular cores. Sometimes calcospherites (psammoma body) is evident
36
What characterizes Subacute Thyroiditis?
Subacute Thyroiditis (deQuervain, granulomatous, or giant-cell thyroidits) is caused by a viral infection (ex. Influenza virus, adenovirus, echovirus, coxsackievirus) It is self-limiting Characterized by GRANULOMATOUS INFLAMMATION. Acute inflammation often with microabscesses Thyroid is enlarged to 40-60g and th e cut surface is firm and pale
37
What is the cause of Graves Disease? What is the microscopic appearance?
IgG antibodies bind the TSH receptor expressed on the plasma membrane of thyrocytes Follicles are lined by hyperplastic, tall columnar cells. Colloid is pink and scalloped at the periphery adjacent to the follicular cells
38
What pathology and clinical symptoms are seen in Medullary Thyroid Carcinoma?
MTC has polygonal, granular cells, spearated by a distincly vascular stroma. MTC extends by direct invasion into soft tissues and metastasizes to the regional lymph nodes and distant organs. Patients with MTC often suffer a number of symptoms related to endocrine secretion, including carcinoid syndrome (serotonin) and Cushing Syndrome (ACTH)
39
How does a Neuroblastoma appear on histologic examination?
Pseudorosettesfeaturing tumor cells clustered radially around small vessels Tumor cells may secrete catecholamines (simlar to mature descendants sin the adrenal medulla). These compounds are metabolized and excreted as urinary vanillylmandelic acid in the urine
40
What does Dexamethasone accomplish in a Dexamethasone suppression test?
Dexamethasone suppresses pituitary secretion of corticotropin and hense, hypercotisolism whereas it is without effect in cases of adarenal hyperplasia or functional adrenal tumors. Thus, the demamethasone suppression test distinguishesACTH-dependent and ACTH-independent forms o fCushing Syndrome.
41
What are clinical manifestations of untreated Addison Disease
``` Weakness Weight Loss GI symptoms Hypotension Electrolyte Disturbances Hyperpigmentation ``` (90% of the adrenal gland must be destroyed for these symptoms to appear)
42
What are common causes of Addison Disease?
Most Common: Autoimmune destruction of adrenal gland Other Causes: TB, Metastatic Carcinoma, Amyloidosis, Sarcoidosis, Adrenoleukodystrophy, and Congenital Adrenal Hypoplasia
43
What findings often are seen in CONN syndrome?
Muscle weakness and fatigue are produced by the effect of potassium depletion oon skeletal muscle. Most patients with primary aldosteronism are diagnnoesd after the detection of asymptomatic DIASTOLIC HTN. Syndrome can be associated with low or nomral renin levels
44
What are key clinical manifestations of Pheochormocytoma?
1. Asymptomatic HTN discovered on a routine PE 2. symptomatic HTN resitnat to antiHTNtherapy 2. Malignant HTN (encephalopathy, papilledema, proteinuria) 4. MI or Aortic Dissection 5. Convulsions

Pathology (30 decks)

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