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Pathoma - Endocrine Pathology Flashcards

1
Q

Nonfunctional pituiatry adenoma will exert its forces on what?

A

This will be a mass effect that will lead to bitemporal hemianopsia which occurs due to compression of the optic chiasm

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2
Q

What is a prolactinoma?

A

A benign tumor of the anterior pituitary that will secrete excessive amounts of prolactin

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3
Q

What are the characteristic symptoms in female with a prolactinoma and why do these occur?

A

Galactorrhea and amenorrhea - due to increased prolactin cause mammary stimulation

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4
Q

What are the characteristic symptoms of prolactinoma in males and what causes them?

A

Increased prolactin in males will lead to decreased GnRH which will lead to decreased libido and headaches

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5
Q

A growth hormone adenoma will cause what in children and why?

A

Gigantism in children due to increased linear bone growth (epiphyses are not fused)

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6
Q

How will a growth hormone adenoma present in adults?

A

Acromegaly

Enlarged bones in hands and feet

Growth of visceral organs

Enlarged tongue

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7
Q

What is the treatment of a prolactinoma?

A

Dopamine agonist to suppress prolactin production

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8
Q

What is a common symptom of growth hormona adenoma in regards to blood levels?

A

Secondary diabetes mellitus is often present - GH lowers glucose uptake in cells

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9
Q

Why is somatostatin used to treat GH adenoma?

A

It will suppress the formation of GHRH in the anterior pituitary

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10
Q

What is the common pituitary adenoma that presents with hypopituitarism in children?

A

Craniopharyngioma (Wet Keratin)

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11
Q

What is Sheehan syndrome?

A

Pregnancy related infaction of the pituitary gland - loss of blood from birthing leads to insufficient blood to the pituitary

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12
Q

How will Sheehan syndrome present?

A

Poor lactation, loss of pubic hair, and fatigue

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13
Q

What are the 2 hormones that are made in the hypothalamus and transported to the posterior pituitary?

A

ADH and oxytocin

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14
Q

What is the use of oxytocin?

A

Oxytocin mediates uterine contractions during labor and release of breast milk

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15
Q

What is syndrome of inappropriated ADH secretion (SIADH)?

A

Excessive ADH production usually cause by trauma or infection

Hyponatremia and low serum osmo

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16
Q

What is this an image of and what is important to note?

A

Follicular adenoma - benign proliferation of follicles surrounded by dense fibrous capsule

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17
Q

What is this an image of?

A

Papillary carcinoma - notice white clearing in the center of the nucleus - orphan annie eye

Line or groove within nucleus

Psamomma body - calcification

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18
Q

Why do patients with hyperthyroidism have an increased metabolic rate and increased sympathetic nervous system?

A

Increased basal metabolic rate is due to increased synthesis of Na/K ATPase

Increased sympathetic nervous system activity is due to increased expression of B1-adrenergic receptors

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19
Q

What would hyperthyroidism do to blood glucose levels?

A

Present with hyperglycemia due to increased gluconeogenesis and glycogenolysis

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20
Q

What is a clinical feature of graves disease?

A

Diffuse goiter - constant stimulation of the thyroid leads to hyperplasia and hypertrophy

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21
Q

Histologically, what would graves present with?

A

Irregular follicles with scalloped colloid and chronic inflammation

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22
Q

What is the process of creating T3/T4 and what are the important enzyme?

A

Tyrosine is converted into thyroglobulin and iodine is taken up from the blood and both are transported to the luminal side. Peroxidase catalyzed the reaction to create T3/T4

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23
Q

What are the important lab findings associated with Graves?

A

Increased total and free T4

Decreased TSH - due to Free T3 downreglates TRH receptors in the anterior pituitary

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24
Q

Cretenism is characterized by?

A

Infantile hypothyroidism leading to mental retardation, short stature and skeletal abnormalities

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25
What are some of the causes of Cretinism?
Maternal hypothyroidism during early pregnancy and iodine deficiency
26
What is Hashimoto's thyroiditis?
Autoimmune destruction of the thyroid gland.
27
What are the common findings histologically in Hashimotos?
chronic inflammatory cells with germinal centers and hurthle cell
28
What are the clinical features of hashimotos?
May present as initial hyperthyroidism - due to destruction of follicles leading to hyperthyroidism Progression to hypothyroidism - Low T4 and increased TSH
29
What are the features of Subacute Granulomatous (DeQuervain) Thyroiditis?
Granulomatous thyroiditis that follows a viral infection Presents as **tender thyroid gland** with transient hyperthyroidism
30
What are the key features of Riedel Fibrosing Thyroiditis?
Characterized as chronic inflammation that leads to fibrosis of the thyroid Hypothyroidism - hard as wood thyroid Fibrosing may extend into the local structures
31
How could you differentiate between Riedel fibrosing and anaplastic carcinoma?
The age of the patients Riedel fibrosing is younger \<40 Anaplastic - Older patient
32
How can radioactive iodine studies be used to differentiate between different thyroid diseases?
Increased uptake - will be seen in diseases like graves and nodular goiter Decreased uptake - seen in adenoma and carcinoma
33
Follicular adenoma is characterized by?
The presence of a fibrous capsule
34
What are the key characteristic findings of papillary carcinoma?
Papillary carcinoma - notice white clearing in the center of the nucleus - orphan annie eye Line or groove within nucleus Psamomma body - calcification
35
What are the characteristics of Follicular carcinoma?
Malignant proliferation of follicles surrounded by fibrous capsule, but there is invasion of the capsule
36
Medullary carcinoma is caused by proliferation of what cells?
C cells in the thyroid - neuroendocrine cells that secrete calcitonin
37
What is a key laboratory finding associated with medullary carcinoma?
Increased calcitonin - leading to decreased serum calcium by excretion of calcium through the kidney
38
Medullary carcinoma is associated with what familial condition?
Multiple endocrine neoplasia (MEN2A and B) - associated with a mutation in the RET oncogene
39
What are the important cells of the parathyroid that monitor Ca2+ levels?
Chief cells regulate free ionized calcium via parathyroid hormone (PTH)
40
What is the role of PTH on the bone?
Stimulation of osteoblast which will in turn stimulate osteoclast activity and increase bone reabsorption (increase Ca2+ and phosphate)
41
How will PTH act on the small bowel?
Increase reabsorption of calcium and phosphate reabsorption indirectly through Vitamin D
42
How will PTH act on the kidneys?
Increase renal calcium reabsorption and increase "dumping" of phosphate - this allows for increase of free calcium
43
What are the key lab findings associated with primary hyperparathyroidism?
Increase PTH and serum Calcium Decreased phosphate - due to kidney excretion
44
Chronic renal failure will lead to increased serum phosphate which can have what effect?
Serum phosphate will bind free calcium leading decreased stimulation of the parathyroid - leading to hyperparathyroidism
45
Insulin is secreted by what cells?
Beta cells that lie in the center of islets
46
What is the role of insulin in skeletal mucle and adipose tissue?
Up-regulates the synthesis of the GLUT-4 transporter which will increase glucose uptake and decrease serum glucose
47
What do alpha cells secrete and what is its role?
Glucagon which acts to oppose insulin in order to increase blood glucose levels in states of fasting Glycogenolysis and lipolysis
48
What is the cause of Type I diabetes mellitus?
Insulin deficiency caused by an autoimmune destruction of beta cells by T lymphocytes
49
How will T1 DM manifest itself?
High serum glucose as a result of insulin deficiency - decreased uptake by muscle and fat
50
What is diabetic ketoacidosis?
This is characterized by excessive serum ketones Often occurs with elevated epinephrine which will stimulate glucagon secretion increasing lipolysis to increased FFA FFA will be converted in the liver to ketone bodies
51
How will diabetic ketoacidosis present in clinic?
High glucose (\>300), anion gap metabolic acidosis, and hyperkalemia Treatment is insulin
52
What is Type II DM characterized by?
End-organ insulin resistance leading to metabolic disorder characterized by hyperglycemia
53
Who is the most common population affected by TII DM? Why?
Middle aged obese adults Obesity leads to decreased number of insulin receptors
54
Histology can reveal what on the islets?
Amyloid deposits
55
Diagnosis of TII DM can be made from which studies?
Random glucose \>200 Fasting glucose \>126 Glucose tolerance test with serum glucose level \> 200 after glucose loading
56
What is the acute risk in TII DM?
Hyperosmolar non-ketogenic coma Caused by high glucose leading to life-threatening diuresis and hypotension and coma
57
What are the long term consequences associated with large vessels?
Atherosclerosis
58
How can nonenzymatic glycosylation of small vessels become problematic?
This can lead to hyaline arteriolosclerosis Can injure the glomeruli and cause KW nodules
59
How can diabetes lead to osmotic damage and what can the result be?
Glucose freely enters into schwann cells and pericytes of retinal blood vessels Aldose reductase converts glucose into sorbitol which results in osmotic damage The will cause neuropathy, blindness, impotence, and cataracts
60
Glomerulosa produces what?
Mineralocorticoids - aldosterone
61
Fasciculata produces what?
Glucocorticoids - cortisol
62
Reticularis produces?
androgens
63
Hyperaldosteronism is clinically characterized by?
HTN, hypokalemia, and metabolic alkalosis Alkalosis due to alpha cells in collecting duct "dumping" hydrogen ions
64
Aldosterone has what effect in the distal tubule and collecting duct?
Absorption of sodium and secretion of potassium in the distal tubule and collecting duct
65
How does primary hyperaldosteronism differ from secondary?
Primary - high aldosterone and low renin Secondary - high aldosterone and high renin
66
How could you identify Liddle's syndrome?
Liddle's is a disease where there is little degradation of sodium channels in the collecting tubule. Classically presents as HTN, hypokalemia and metabolic alkalosis in a young patient. This will present with low aldosterone and renin levels.
67
How can hypercortisolism lead to muscle weakness?
Cortisol breaks down muscle to produce amino acids
68
How can hypercortisolism lead to moon facies and truncal obesity?
High insulin due to high glucose which will increase the storage and fat centrally
69
Why will hypercortisolism present with abdominal striae?
Impaired collagen synthesis
70
What causes HTN associated with hypercortisolism?
Increased sensitivity of peripheral vessels to catecholamines
71
21-H deficiency cause lead to what life-threatening complication?
Hypotension due to salt wasting
72
Waterhouse-Friderichsen syndrome is characterized by?
Acute renal insufficiency - hemorrhagic necrosis of the adrenal glands due to DIC in young children with N Meningitidis infection Lack of cortisol can lead to hypotension and death
73
Clinical features of adrenal insufficiency?
Hypotension, hyponatremia, hypovolemia, hyperkalemia, metabolic acidosis
74
Why can adrenal insufficiency lead to hyperpigmentation?
ACTH is linked to POMC which is a stimulator of melanocytes

Renal and Endocrine (46 decks)

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