Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine First Aid > LECTURE NOT FIRST AID: Endocrine I > Flashcards

LECTURE NOT FIRST AID: Endocrine I Flashcards

1
Q

What leads to a craniopharyngioma? Who gets them?

A

These slow growing benign intracranial tumors derive from Rathke’s pouch. They present with headache, visual disturbances, pituitary ischemia, and death due to mass effect.

It presents in both ages, children aged 5 - 15, and in adults 65+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Adamantinomatous craniopharyngioma?

A

This is the most common variant of craniopharyngioma, and can be cystic or solid in form (the cystic form contains a thick-yellow brown fluid).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Histology of Adamantinomatous Craniopharyngioma

A

Stratified Squamos epithelium with peripheral palisading.

Compact lamellar keratin known as “wet keratin” surrounds it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is papillary craniopharyngioma?

A

These account for 10% of craniopharyngiomas and are seen more often in adults than children.

Both this and the adamantinomatous version both have low recurrence values.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What hormones are released from the posterior pituitary and what do they do?

A

ADH - Increases free water reabsorption on the kidney collecting duct. Also increases smooth muscle tone around arterioles throughout the body

Oxytocin - Increases uterine smooth muscle contraction during labor. Stimulates contraction of around the lactiferous duct for milk production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where are posterior pituitary hormones synthesized and stored?

A

Posterior pituitary hormones are synthesized in the hypothalamus and stored in axon terminals within Herring Bodies, stored eosinophilic secretory material.

Hormones are released into secondary capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

DI vs SIADH

Discuss clinical features and lab values comparing them

A

DI - There is hypothalamic undersecretion (in central) or normal levels with unresponsive kidneys (Nephrogenic)

We see low ADH activity and low urine osmolality

SIADH - Total body water increased without edema due to either drugs increasing ADH or other CNS diseases. These patients have cerebral edema and neurologic dysfunction due to hyponatremia.

We see high ADH activity and high urine osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Anterior pituitary hormones are released from:

A

Acidophils and basophils, directly into hypophyseal veins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do acidophils release

A

Somatotrophe - Growth Hormone

Lactotrope - Prolactin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What do basophils release?

A

Corticotrope - ACTH

Gonadotrope - FSH/LS

Thyrotrope - TSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Histology of acidophils and basophils?

A

They all have purple centers under microscope.
Acidophil - Red cytoplasm
Basophil - Blue cytoplasm
Chromophobe - Clear cytoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Histology of pituitary adenoma

A

Bland monomorphic densely packed cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does lactotrophic adenoma present? In who?

A

Most commonly detected in women ages 20 - 40

Clinically, we see amenorrhea, galactorrhea, infertility, loss of libido

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What drug can we use for lactorophic adenoma and why does it work?

A

All pituitary adenomas can result in hyperprolactinemia by blocking dopamine release (Prolactin inhibiting factor).

Bromocriptine, a dopamine agonist, may be used for nonsurgical management

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Somatotrophic adenoma releases what?

A

Growth hormone causes production of Insulin-like growth factor (IGF-I) from the liver.

Stimulation of progenitor cells throughout the body, most conspicuous at growth plates and skeletal muscles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What do somatotrophic adenomas lead to?

A

Gigantism - Increase GH before epiphyses have closed. We see prominent musculoskeletal enlargement. INFANTS

Acromegaly - Increase GH after epiphyses have closed. Skin and soft tissue growth with enlarged jaw, broadened face, and elongation/thickening of the hands and feet. ADULTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Discuss corticotropic adenomas and what they lead to

A

These guys release ACTH, leading to Cushing Syndrome due to cortisol production in the adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Discuss Thyrotropic Adenomas and what they lead to

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where does Calcitonin come from and what does it do?

A

Comes from C cells of the thyroid and decreases blood Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

5 signs of hypothyroidism

A
  • Cold intolerance
  • bradycardia
  • heart failure
  • high lipids
  • lethargic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

5 causes of hypothyroidism

A
  • Los of thyroid tissue
  • Hypothalamic failure
  • Cretinism
  • Hashimoto Thyroiditis
  • Granulomatous Thyroiditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Discuss the pathway that causes cretinism and what it leads to

A

Iodine deficiency causes a decrease in T4 which leads to poor brain and growth development, leading to mental retardation and dwarfism in infants.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Discuss the histology of hashimoto thyroiditis

A

Dense lymphocytic infiltrate with germinal centers +/- Hurthle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Discuss the course of Hashimoto thyroiditis in the clinic

A

Painless, but on testing, we see radioactive iodine uptake diminished. Females get this 20x more often than males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Lab test for Hashimoto Thyroiditis

A

Anti-Thyroglobulin and Anti-thyroid peroxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What causes granulomatous thyroiditis, also known as DeQuervain Thyroiditis?

A

Upper respiratory infection/cytotoxic T-cell mediated condition.

Again, more common in females like Hashimoto’s, but only 4x as much instead of 20x as much

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Clinical course of granulomatous thyroiditis?

A

Unlike hashimotos, this is painful.

Thyroid enlargement is seen, and as before radioactive iodine uptake is diminished.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Histology of Granulomatous Thyroiditis

A

Early: Patchy, microabscesses

Later: Damaged follicles, lymphocyte aggregates, macrophages transforming into multinucleated giant cells, all of this leading to fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

5 Signs and symptoms of hyperthyroidism

A
  • Heat intolerance
  • Tachycardia and arrhythmias
  • Increased sympathetic tone
  • Tremor
  • Ocular changes/lid lag
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

5 causes of hyperthyroidism

A
  • Grave’s Disease
  • Toxic multinodular goiter
  • Hyperfunctioning (Toxic) Adenoma
  • Iodine induced thyrotoxicosis
  • Thyrotropic pituitary adenoma (secondary hyperthyroidism)
31
Q

Lab findings for hyperthyroidism

A

Decreased TSH (although in secondary we see increased)

Increased Free T4

Increased T3

32
Q

In Graves Disease we see ____ radioactive iodine uptake

A

Increased

33
Q

Key clinical feature of Graves Disease

A

Exopthalmos (TSH receptors in extraocular muscles)

34
Q

What causes the hyperthyroidism we see in Grave’s Disease

A

Autoantibodies to the TSH receptor cause activation (Thyroid Stimulating Immunoglobulin)

35
Q

Histology for Graves Disease

A

Crowded Tall columnar follicular cells with papillary infolding +/- scalloping

36
Q

What histology do we see with multinodular goiter?

A

Irregular nodules, colloid-rich follicles, +/- hemorrhage, Ca++, and some cystic changes

37
Q

Discuss the histology of the thyroid gland

A

Thyroid follicles surrounded by C-Cells. The lumen of the thyroid follicle is lined by follicular cells.

The interior of the thyroid follicle contains colloid, where we see T3 and T4

38
Q

What neoplasms do we see in the thyroid gland based on location?

A

Follicular cells - Follicular adenoma, Follicular carcinoma, papillary carcinoma

C-Cells - Medullary carcinoma

39
Q

What do we see under histology for papillary carcinoma?

A
  • Intranuclear pseudoinclusions
  • Nuclear grooves

We see cleared out nuclei referred to as Orphan Annie Eyes

40
Q

How do we differentiate between follicular adenoma and follicular carcinoma?

A

In follicular adenoma, we see well-differentiated follicles.

In follicular carcinoma, we see follicles with loss of colloid

41
Q

Four C’s of Medullary carcinoma?

A
  • C-cells derived neoplasm
  • Calcitonin producing
  • Congo Red (amyloid) positive
  • CEA (Carcinoembryonia Antigen) is elevated
42
Q

Neoplastic C-Cells secrete what?

A

A dense eosinophilic matrix (amyloid)

43
Q

Discuss the releasing pathway of parathyroid hormone

A

Low concentration of calcium in the blood causes the release of PTH, which causes a decrease in the loss of calcium in the urine and efflux of calcium from bone.

It causes an increased concentration of calcium in the blood, which inhibits further production of PTH

44
Q

Clinical manifestations of hyperparathyroidism

A

Painful bones, renal stones, abdominal groans, psychic groans (depression)

45
Q

Histology of Adenoma and how often we see it

A

Bland monomorphic chief cells with small, round, central nuclei. We will also see decreased adipocytes

These account for 85-90% of primary hyperparathyroidisms

46
Q

Histology of Primary hyperplasia and how often we see it

A

Similar to Adenoma, but may be diffuse or multinodular

These account for 5-10% of primary hyperparathyroidisms and involves multiple PT glands

47
Q

Histology of parathyroid Ca and how often we see it

A

Cytology unreliable, requires invasion or mets.

These account for

48
Q

What are MEN-1 and MEN-2

A

Mutation to calcium-sensing receptor gene causing familial hypocalciuric hypercalcemia

49
Q

What is secondary hyperparathyroidism?

A

Any condition that gives rise to chronic hypocalcemia. The primary cause is renal failure

50
Q

Chemical causes of secondary hyperparathyroidism

A
  • Increase phosphate causes decreased serum calcium.
  • Decreased a-1-hydroxylase causes decreased active vitamin D
  • Both stimulate the PTH production

Other causes include low dietary Calcium or a Vitamin D deficiency

51
Q

Histology of secondary hyperparathyroidism and organ sequelae that we may also see

A

Parathyroid glands are hyperplastic (increased chief cells and decreased adipocytes)

Metastatic calcification may be present in the lungs, heart, stomach, and blood vessels.

52
Q

Treating Secondary hyperparathyroidism

A

Patients often respond to Vitamin D and phosphate binding agents

53
Q

What clinical complications do we see with hypoparathyroidism

A
  • Hypocalcemia
  • Seizures
  • Tetany
  • Mental Status changes
  • Cardiac Arrhythmias
  • Prolonged QT syndrome on EKG
54
Q

Autoimmune polyendocrine syndrome Type I vs. Type II

A

APS1

  • Autosomal Recessive
  • AIRE Gene (21 q22.3)
  • Adrenalitis
  • Hypoparathyroidism
  • Hypogonadism
  • Candidiasis

APS2

  • HLA Types: DQ or DRB
  • Adrenal insufficiency
  • Hypothyroidism or Type I Diabetes
55
Q

Discuss how the hypothalamus leads to hormone release in the adrenal cortex

A

Hypothalamus releases corticotropin-releasing hormone. This hormone reaches the anterior pituitary gland and causes release of ACTH. ACTH causes the Adrenal cortex to release 3 different hormones:

  • Aldosterone from the Z.G.
  • Cortisol from the Z.F.
  • DHEA from the Z.R.
56
Q

What are the functions of the three hormones released from the adrenal cortex

A
  • Aldosterone - Regulates salt and water balance in the body
  • Cortisol - Regulates carbohydrate metabolism, immune system and maintains blood pressure
  • DHEA - Regulates the biosynthesis of androgen and estrogen sex steroids
57
Q

Based on what hormones we know are coming from what portions of the adrenal cortex, what diseases are associated with what areas of the adrenal cortex?

A
  • Z.G. - Hyperaldosteronism
  • Z.F. - Cushing Syndrome
  • Z.R. - Adrenogenital/Virilizing Syndromes
58
Q

What is Conn Syndrome?

A

Primary Hyperaldosteronism

Increase production of aldosterone that causes hypertension due to retention of Na+ and decreased renin activity (usually idiopathic, can be a neoplasm)

We also note a loss of K+ from the urine.

59
Q

Signs and symptoms of cushing syndrome

A
  • Weight gain
  • Moon face
  • Central obesity
  • HTN
  • Buffalo hump
  • Striae, typically on belly
60
Q

What leads to Adrenogenital/Virilizing Syndroms?

A

21-Hydroxylase deficiency

61
Q

Contrast Waterhouse-Friderichsen syndrome and Addison Disease

A

WFS - An acute condition of adrenocortical insufficiency (hypoadrenalism) where sepsis is caused by encapsulated bacteria (usually N.Meningiditis) leading to hemorrhagic/ischemic loss of adrenal glands.

AD - A chronic condition that presents with hyperpigmentation, weight loss and hypotension

62
Q

Deciding between an adrenal adenoma and an adrenal carcinoma can be difficult. Under histology, what can guide our decision making?

A

If we see a wel ldefined, bright yellow tumor that is eosinophilic with vacuolated cytoplasm, we think adrenal adenoma.

A large hemorrhagic/necrotic tumor with variable anaplastic cells under histology is indicative of adrenal carcinoma.

63
Q

Discuss pheochromocytoma and where we find it?

A

The chromaffin cells of the medulla produce epinephrine and norepinephrine. A tumor of these cells is termed a pheochromocytoma.

These patients will have episodic hypertension and headaches.

64
Q

What gene mutations will we see with pheochromocytoma and what lab tests will we get?

A

Genes: MEN-2A, MEN-2B, NF1, VHL

Lab: Metanephrine and Vanillomendelic Acid (VMA)

65
Q

Function of the pineal gland

A

Pinealocytes produce melatonin, a hormone that helps to regulate the wake/sleep cycle and menstral cycle.

66
Q

Endocrine vs. exocrine pancreas

A

Endocrine is going to secrete into the blood, so insulin, glucagon and somatostatin are gonna come from this part.

The exocrine pancreas is going to release outside of the body (remember your GI tract? Technically outside of the body!). Zymogens and digestive enzymes for the GI tract are released by this part.

67
Q

What three cells do we find in the pancreas and what do they release.

A

Alpha cells - Glucagon - Stimulates an increase in blood sugar levels, thus opposing the action of insulin

Beta cells - Insulin - Regulates metabolism of carbs/fat, esp. the conversion of glucose to glycogen, which lowers the blood glucose level

Delta Cells - Somatostatin - Inhibits the secretion of other hormones such as glucagon, insulin, and gastrin.

68
Q

What is ketoacidosis?

A

Insulin deficiency or resistance causes glucose utilization to not function in adipose and muscle, leading to the fat lysing itself and releasing fatty acids and muscle lysing proteins off of itself. This causes a mixture of hyperglycemia (amino acids stimulate gluconeogenesis) and DKA (fatty acids increase ketogenesis).

Plasma glucose (since it isn’t being used by the organs, it stays here) exceeds renal capacity, leading to osmotic diuresis.

69
Q

What renal complications do we worry about with diabetes?

A
  • Amyloidosis of islet cells
  • Diffuse and nodular glomerulosclerosis
  • Nephrosclerosis
  • Renal Hyaline arteriolosclerosis
70
Q

What is an insulinoma?

A

Tumor of Beta cells, this is the most common islet cell tumor. These are monotonous cells with a low mitotic rate and lots of amyloid.

Symptoms arise due to hypoglycemia - Confusion, stupor, coma

71
Q

What is a glucagonoma (struggle bus here)

A

Alpha cell tumor

Causes mild skin rash and DM

72
Q

What is a VIPoma?

A

Delta cell tumor

Patient has severe watery diarrhea, hypokalemia, and achlorhydria

73
Q

Discuss the tumors that fall into the category of MEN I - Wermer Syndrome

A

Pituitary Adenoma, Pancreatic Islet Cell Adenoma, and parathyroid adenoma fall into this category.

74
Q

Compare MEN IIA and MEN II B

A

MEN IIA and MEN IIB both involve medullary thyroid carcinomas and pheochromocytomas.

IIA, like I, involves the parathyroid Adenoma, as well as a primary hyperparathyroidism

IIB has ganglioneuromas and neurofibromas.

Endocrine First Aid (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions