Week 1 Flashcards

1
Q

Match the following hormones with the organ in which they are made and their type (lipid, peptide, amine).

  1. Parathyroid hormone
  2. Aldosterone
  3. Follicle stimulating hormone
  4. Norepinephrine
  5. Antidiuretic hormone
  6. Leptin
  7. Adrenocorticotropic hormone
  8. Thyroid stimulating hormone
  9. Glucagon
  10. Oxytocin
  11. Thyroxine (T4 thyroid hormone)
A
  1. Parathyroid hormone – parathyroid glands – peptide
  2. Aldosterone – adrenal cortex – lipid
  3. Follicle stimulating hormone (FSH) – anterior pituitary – peptide
  4. Norepinephrine – adrenal medulla – amine
  5. Antidiuretic hormone (ADH), also known as vasopressin, – posterior pituitary - peptide
  6. Leptin – adipose tissue – peptide
  7. Adrenocorticotropic hormone (ACTH) – anterior pituitary – peptide
  8. Thyroid stimulating hormone (TSH) – anterior pituitary – peptide
  9. Glucagon – pancreas - peptide
  10. Oxytocin – posterior pituitary – peptide
  11. Thyroxine (T4 thyroid hormone) – thyroid – amine

Other hormones you should know:

Anterior pituitary hormones are: prolatin (PRL), growth hormone (GH), luteinizing hormone (LH), all peptides

Adrenal cortex: cortisol, androgens (all lipids)

Adrenal medulla: epinephrine (amine)

Thyroid: triiodothyronine (T3) (amine), calcitonin (peptide)

Adipose tissue: adiponectin (peptide)

Pancreas: insulin (peptide)

SM_167b Introduction to the Endocrine System: Physiology/Pathophysiology

Objectives: 2. List the 3 classes of hormones

  1. Describe the role of the various organ systems involved in the Endocrine System, including the pituitary, adrenals, thyroid, parathyroids, pancreatic islets.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

A 15 year-old male does not demonstrate any signs of puberty. He is short for his age, his testicles show no evidence of enlargement, his testosterone levels are low, and he has a reduced ability to smell. Which of the following hormonal imbalances would you expect?

  1. Increased GnRH, increased FSH and LH
  2. Increased GnRH, decreased FSH and LH
  3. Decreased GnRH, decreased FSH and LH
  4. Decreased GnRH, increased FSH and LH
A

Answer: C

This patient has Kallmann’s Syndrome, a type of hypogonadotropic hypogonadism. This syndrome is characterized by a mutation in gene for protein that facilitates migration of GnRH and olfactory neurons from olfactory placode to anterior septal region of hypothalamus (GnRH neurons) and olfactory bulbs (olfactory neurons), and thus reduced ability to smell. This leads to the patient having decreased GnRH and associated decreased FSH and LH leading to delayed puberty.

SM_168b Hypothalamus-Pituitary Basic (MOLITCH)

SM_171b Hypothalamus-Pituitary Pathophysiology (MOLITCH)

Objectives

  1. Describe the biological actions and the hypothalamic regulation of the 6 anterior pituitary hormones
  2. List the types of hypothalamic disease and how they manifest.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

A 35-year-old woman presents with a complaint of missing her last two menstrual cycles after having regular menstrual cycles for the last 5 years. She denies having headaches, double vision, or facial numbness. For the last 3 months, she is treating her gastroesophageal reflux disease by taking a prokinetic medicine, which acts by being a dopaminergic antagonist. Human chorionic gonadotropin is not detected in her blood. Serum TSH levels are normal. Which of the following is the most likely cause of her developing amenorrhea?

(A) high prolactin levels

(B) low prolactin levels

(C) menopause

(D) pregnancy

(E) subclinical hypothyroidism

A

Answer: A) Dopamine is the major prolactin-inhibiting factor that tonically suppresses prolactin secretion from the pituitary. Hence, a dopamineblocking medication can lead to high prolactin levels. Besides stimulating milk production, prolactin also inhibits ovulation by inhibiting gonadotropin-releasing hormone (GnRH) so that hyperprolactinemia can lead to amenorrhea.

Low prolactin levels (choice B) would support the possibility that the pituitary may have been invaded by a tumor that inhibits prolactin release and has also destroyed the gonadotropes. Such tumors increase pressures on the dura, the optic chiasm, and the cranial nerve III, causing headaches, visual defects, and facial numbness, all of which are absent in the patient.

Menopause (choice C) is not the best answer due to the young age of the woman. Additionally, with the approach of menopause, menstrual cycles gradually become longer instead of being suddenly absent.

Pregnancy (choice D) is excluded due to the absence of human chorionic gonadotropin (hCG). Blood hCG increases progressively after implantation and is detectable after 11 days in the virtually all pregnant women.

Subclinical hypothyroidism (choice E) is diagnosed by elevated TSH levels, which are already elevated at an early stage when free thyroxine levels are still normal and symptoms are absent. TSH has a small FSH- and LH-like effect so that altered TSH levels can lead to disturbances of menstruation. The relationship between TSH, thyroid hormones, and sexual hormones is complex and excess or deficiency of TSH is known to cause either diminished or excessive menstrual blood flow.

SM_171b Hypothalamus-Pituitary Pathophysiology

Objectives

  1. Explain how the deficiencies of the pituitary hormones manifest, are diagnosed and treated

From: Lange USMLE Step 1 Q&A

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

A 32-year-old woman comes to the physician because of amenorrhea for the past 15 months after delivering a baby. She says that she has also had fatigue, facial swelling, cold intolerance and has gained an additional 4.5 kg (10 pounds) since her baby was born. Laboratory studies of serum show decreased LH, estradiol, and TSH. Injection with TRH fails to increase serum TSH or prolactin.

Biopsy of the pituitary is done and can be seen below. What condition does this patient most likely have?

  1. Lymphocytic hypophysitis
  2. Sheehan’s syndrome
  3. Pituitary “apoplexy”
  4. Sarcoidosis
  5. Nonfunctioning pituitary adenomas
A

Answer: (A) Lymphocytic hypophysitis: autoimmune disorder characterized by infiltration of lymphocytes in the pituitary characterized by anterior pituitary insufficiency. The small blue cells seen in the pathology slide are the infiltrating lymphocytes that can cause this condition.

(B) Sheehan’s syndrome occurs as a result of ischemic necrosis postpartum. However, the pathology slide shows lymphocyte infiltration, not ischemia.

(C) Pituitary “apoplexy” is a sudden hemorrhage into the pituitary gland, often occurring into a pituitary adenoma which can lead to pituitary insufficiency, but does not necessary have lymphocytic infiltration.

(D) Sarcoidosis can lead to pituitary insufficiency, but has characteristic Langerhans’ giant cells (multinucleated cells).

(E) Non-functioning adenomas can cause pituitary insufficiency, but is not characterized by lymphocytic infiltration on pathology.

Lecture SM_169b Hypothalamus-Pituitary Histology/Pathology (MAO)

Objective 3. List and compare the common etiologies of hypopituitarism. (MKS1b)

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

Which of the following is true about nuclear receptors?

  1. Nuclear receptors interact with peptide hormones
  2. Ligand binding activates nuclear receptors
  3. Androgen insensitivity syndrome is due to a mutation in the nuclear receptor and can be reversed by increasing the amount of ligand
  4. Nuclear receptors can directly bind to DNA leading to changes in gene expression
A

Answer: D) Nuclear receptors can directly bind to DNA leading to changes in gene expression

Nuclear receptor interact with lipid or other small molecule ligands (A). They can be activated or inactivated by ligand binding (B). Mutations that make the receptor insensitive to its ligand such as androgen insensitivity syndrome often cannot be reserved by increased ligand, since at no concentration will the receptor bind to the ligand.

Lecture: SM_170b Mechanisms of Hormone Action (El Muayed)

Objective: 4. Describe how nuclear receptors mediate their action by directly regulating gene expression

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

Assign the following characteristic as either being related to adrenal cortical adenoma or cortical carcinoma.

  1. Color yellow
  2. Larger size (>5 cm, >100 grams)
  3. Presence of necrosis
  4. No invasion of the surrounding tissue
  5. More likely to be function (can produce hormones)
  6. Homogenous surface
  7. Most common type of adrenal cortical neoplasm
A
  1. Color yellow: adenoma, color tan-grey: carcinoma
  2. Larger size (>5 cm, >100 grams): carcinoma, smaller (<5 cm, <100 grams): adenoma
  3. Presence of necrosis: carcinoma, no necrosis: adenoma
  4. No invasion of the surrounding tissue: adenoma, invasion of the surrounding issue: carcinoma
  5. More likely to be function (can produce hormones): adenoma
  6. Homogenous surface: adenoma, heterogenous surface: carcinoma
  7. Most common type of adrenal cortical neoplasm: adenoma

Lecture: SM_172b Adrenal Pathology: Cortex/Medulla (Yang)

Objective: 5. Identify fundamental histological difference between adrenal adenoma and carcinoma based on the established pathologic criteria

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

Which of the following is true with respect to the actions of the mineralocorticoids?

A) decrease carbohydrate metabolism

(B) increase appearance of the secondary sex characteristics

(C) increase synthesis of androgens

(D) regulate aldosterone secretion

(E) regulate sodium retention by the kidneys

A

(E) The principal mineralocorticod, produced by the zona glomerulosa cells of the adrenals, is aldosterone. Synthesis of aldosterone is primarily controlled by the rennin-angiotensin system and is thus involved in control of blood pressure. Aldosterone causes sodium reabsorption by the kidneys, which in turn regulate water balance, which leads to increases in blood pressure by increasing fluid volume.

Aldosterone action does not directly lead to decreased carbohydrate metabolism (choice A),

is not a sex characteristic determining steroid hormone (choice B), does not result in increased

synthesis of androgens (choice C), and does not regulate its own secretion (choice D).

Lecture: SM_173b Adrenal Cortex Physiology & Pathophysiology (Kravarusic)

Objective: Describe the physiologic activity of the adrenal cortical hormones.

From: Lange USMLE Step 1 Q&A

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

A 39-year-old woman reports headaches, weakness and fatigue, and frequent urination over

the past several weeks. Physical examination reveals diastolic hypertension. Laboratory findings include hypokalemia and reduced renin levels. Which of the following is the most likely cause of these various findings?

(A) Primary aldosteronism (Conn syndrome)

(B) diabetes insipidus

(C) diabetes mellitus

(D) pheochromocytoma

(E) polycystic renal disease

A

Answer: (A) Primary aldosteronism caused by an aldosterone-secreting adrenal neoplasm is

known as Conn syndrome. Excess aldosterone production leads to increased sodium retention and reciprocal potassium depletion in the renal distal tubule; polyuria results from

impairment in urinary concentrating ability. Increased sodium reabsorption and associated extracellular fluid expansion lead to diastolic hypertension and suppression of the reninangiotensin pathway. Muscle weakness and fatigue are a consequence of hypokalemia,

which may be severe in some cases.

Diabetes insipidus (choice B) is marked by the fairly sudden onset of extreme polyuria and (for the central type) is due to decreased activity of antidiuretic hormone typically associated with an intracranial lesion or trauma.

In diabetes mellitus (choice C), glucose levels exceed renal reabsorption capacity, leading to glycosuria and a consequent osmotic diuresis, hypovolemia, and pseudohyponatremia.

Pheochromocytomas (choice D) are unilateral, solitary neoplasms most commonly arising from chromaffin cells in the adrenal medulla. Although biologically benign, excessive secretion of catecholamines causes paroxysmal systolic and diastolic hypertension that may reach life-threatening pressures.

The adult form of polycystic renal disease (choice E) is an autosomal-dominant condition characterized by grossly enlarged bilateral kidneys containing numerous, and variably-sized expansile cysts. Hematuria, pyelonephritis, hypertension, and polyuria are common symptoms.

Lecture SM_173b Adrenal Cortex Physiology & Pathophysiology (Kravarusic)

Objective: Describe the types of adrenal cortex disorders and their manifestation

From: Lange USMLE Step 1 Q&A

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

Which of the following follows the most common route of iodine to become the active thyroid hormone?

  1. Iodine -> thyroglobulin -> diiodotyrosine/monoiodotyrosine -> triiodothyronine -> thyroxine
  2. Iodine -> diiodotyrosine/monoiodotyrosine -> thyroglobulin -> triiodothyronine -> thyroxine
  3. Iodine -> thyroglobulin -> diiodotyrosine/monoiodotyrosine -> thyroxine -> reverse triiodothyronine
  4. Iodine -> diiodotyrosine/monoiodotyrosine -> thyroglobulin -> reverse triiodothyronine -> thyroxine
  5. Iodine -> thyroglobulin -> diiodotyrosine/monoiodotyrosine -> thyroxine -> triiodothyronine
  6. Iodine -> diiodotyrosine/monoiodotyrosine -> thyroglobulin -> thyroxine -> triiodothyronine
A

Answer: E) Iodine -> thyroglobulin -> diiodotyrosine/monoiodotyrosine -> thyroxine -> triiodothyronine

Thyroglobulin is part of the organification step in which iodine gets attached to an organic molecule.

Diiodotyrosine/monoiodotyrosine (DIT/MIT) are part of the coupling step.

Since 80% of the produced thyroid hormone is T4 (thyroxine), this compound is the most common next step. T4 then exists the thyroid and enters the blood stream and reaches cells across the body. There T4 gets converted to T3 (triiodothyronine), which is the active form of the thyroid hormone. T4 can alternatively be catalyzed into reverse triiodothyronine (reverse T3), an inactive form of T3.

SM_174b Thyroid Basic Physiology (Soundarrajan)

Objectives: 2. Explain the principles of thyroid hormone synthesis.

  1. Explain the principles of thyroid hormone transport.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Match each of the following thyroid diagnosis with its common histological presentation:

  1. Follicular cell adenoma
  2. Follicular cell carcinoma
  3. Papillary carcinoma
  4. Medullary carcinoma
  5. Anaplastic carcinoma
  6. adjacently lined cells with atypical nuclei
  7. differentiated and undifferentiated clusters of cells
  8. repeated follicles of cells with capsular or vascular invasion
  9. polygonal and spindle shaped cells with acellular amyloid deposits
  10. repeated follicles of cells surrounded by fibrous capsule
A
  1. Follicular cell adenoma – repeated follicles of cells surrounded by fibrous capsule
  2. Follicular cell carcinoma – repeated follicles of cells with capsular or vascular invasion
  3. Papillary carcinoma – adjacently lined cells with atypical nuclei, Orphan Annie eyes
  4. Medullary carcinoma – polygonal and spindle shaped cells with acellular amyloid deposits (originate from neuroendocrine cells)
  5. Anaplastic carcinoma – differentiated (both follicular and papillary seen) and undifferentiated clusters of cells

SM_175b Thyroid Histology/Pathology (Nayar)

Objective: 4. Describe the pathologic changes seen in the major non neoplastic and neoplastic entities affecting the thyroid gland.

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

A 38-year-old woman has experienced the gradual onset of a goiter. Serum T4 and T3 are within the reference range and thyroid-stimulating hormone (TSH) is slightly increased. Serum

antithyroid peroxidase (antimicrosomal) antibodies are detected but there are no TSH receptor antibodies. Which of the following is the most likely diagnosis?

(A) chronic autoimmune thyroiditis

(B) Graves disease

(C) primary atrophy of the thyroid

(D) riedel struma

(E) subacute thyroiditis

A

(A) Patients with chronic autoimmune thyroiditis or Hashimoto disease may demonstrate

several different serum thyroid autoantibodies, but these vary from patient to patient. Thyroid peroxidase antibodies are found in roughly 85% of patients with Hashimoto disease, about 40% of patients with Graves disease, and in <15% of patients with other thyroid disorders. The absence of TSH receptor antibodies rules out Graves disease (choice B), making Hashimoto disease the most likely diagnosis.

Primary atrophy of the thyroid (choice C) and Riedel struma (choice D) are not usually associated with the formation of thyroid autoantibodies. Thyroid autoantibodies are only found transiently in a few patients with subacute thyroiditis (choice E) making this choice unlikely.

SM_176b Thyroid Pathophysiology & Nodules/Cancer (Bloomgarden)

Objectives: 1. Compare and contrast the signs and symptoms of hyperthyroidism and hypothyroidism.

  1. Identify the biochemical alterations associated with hyperthyroidism and hypothyroidism.

From: Lange USMLE Step 1 Q&A

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