Endocrine Flashcards

1
Q

Which of the following statements is correct regarding the pituitary gland?

A Prolactin - posterior - acidophil
B Luteinizing hormone (LH) - anterior - basophil
C Growth hormone - posterior- acidophil
D Vasopressin (VP) - posterior - basophil

A

B

Explanation
Prolactin and growth hormone are produced in the anterior pituitary. Vasopressin is produced by modified glial cells and stored in the posterior pituitary

Note: a nice way to remember it

Post - Vasopressin (ADH) and Oxytocin Ant - FLAT PiG (pig=acid) F-FSH L-LH A-ACTH T-TSH all basophil Prolactin GH both acidophil

An even better way to remember this is: B-FLAT: basophils = FSH, LH, ACTH and TSH, and GPA (as in grade-point average): growth hormone and prolacting = acidophils

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2
Q

The pathogenesis of Type 1 diabetes includes which of the following?

A Auto immune insulitis
B Decreased insulin sensitivity
C No anti-islet cell antibodies found at diagnosis
D Abnormal glucokinase activity

A

A

Explanation
A summary of the pathogenesis of type 1 diabetes mellitus (DM) includes: decreased blood insulin, anti-islet cell antibodies, HLA-D linked autoimmune immunopathologic mechanisms, severe insulin deficiency, early insulitis, beta cell depletion and marked atrophy and fibrosis of the islet cells. There is a 50% concordance in twins.

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3
Q

Cushings disease is associated with all of the following except?

A Truncal obesity
B Osteoporosis
C Hypotension
D Glucose intolerance

A

C

Explanation
Osteoporosis occurs in 75% of patients with Cushing’s disease. There is no hair loss. Central obesity occurs around the trunk and upper back in 85-90% of patients. Hypertension occurs in 75% of cases. Other clinical features include: moon facies, weakness and fatigability, plethora, glucose intolerance, skin striae, menstrual abnormalities and neuropsychiatric abnormalities.

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4
Q

Which of the following is not typical of Type II DM?

A Insulitis early
B Relative insulin defeciency
C 60-80% concordance in monozygotic twins
D Mild B cell depletion

A

A

Explanation
Type 2 DM- Clinical: onset >30yr, obese, normal or increased blood insulin, no anti-islet cell antibodies and ketoacidosis rare.

Genetics: 60-80% concordance in monozygotic twins, no HLA association. (Note in the table it says 90-100%)

Pathogenesis: insulin resistance, relative insulin deficiency. Islet cells: no insulitis, focal atrophy and amyloid deposits. Mild B cell depletion. The association of type II DM with obesity is greater than 80% in patients.

The two metabolic defects that are characteristic of type 2 DM: a decreased response of peripheral tissue to insulin (insulin resistance) and B cell dysfunction that is manifested as inadequate insulin secretion the presence of insulin resistance and hyperglycaemia

Note: current textbook says greater than 90% concordance. However, I have left the question in the old format

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5
Q

Which of the following is characteristic of type 2 diabetes?

A Less than 30% concordance in monozygotic twins
B Early insulitis
C The association of type II DM with obesity is greater than 90%
D Decreased peripheral receptor sensitivity

A

D

Explanation
A summary of the characteristics of type II diabetes mellitus (DM) include: normal or increased blood insulin, no anti-islet cell antibodies, no HLA association, insulin resistance, relative insulin deficiency, no insulitis, focal atrophy and amyloid deposits along with mild Beta cell depletion. There is 60-80% concordance in monozygotic twins compared with nearly half that in dizygotic twins. In first degree relatives with type II DM (and in non-identical twins) the risk of developing disease is 20-40% versus 5-7% in the population at large. The association of type II DM with obesity is greater than 80% in patients.

The two metabolic defects that are characteristic of type II DM: a decreased response of peripheral tissue to insulin (insulin resistance) and Beta cell dysfunction that is manifested as inadequate insulin secretion the presence of insulin resistance and hyperglycaemia

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6
Q

Which of the following is not typical of type 1 diabetes mellitus

A Insulitis early
B Anti-islet cell antibodies
C HLA-D linked
D Focal atrophy and amyloid deposits

A

D

Explanation
Type 1 DM- Clinical: onset <20yr, normal weight, anti islet cell antibodies, ketoacidosis common. Genetics: 50% concordance in twins, HLA-D linked.Pathogenesis: Autoimmunity, immunopathologic mechanisms. Severe insulin defeciency. Islet cells: Insulitis early, marked fibrosis and atrophy. B cell depletion

Type 11 DM- focal atrophy and amyloid deposits

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7
Q

Hypothyroidism is associated with all of the following, with the exception of?

A Weight gain
B Cretinism
C Cold intolerance
D Decreased hair growth

A

D

Explanation
Coarse hair is found in hypothyroidism rather than a decrease in hair growth. Hair loss seems to be an uncommon finding in hypothyroidism. Many sources say that coarse brittle hair is more common. Cretinism hypothyroidism that develops in infancy or early childhood has a higher prevalence (due to endemic dietary iodine deficiency) in populations of mountainous areas. It has become less frequent in recent years due to the widespread supplementation of foods with iodine. Cretinism on rare occasions results from inborn errors of metabolism that interfere with biosynthesis of thyroid hormone

Clinical picture - impaired skeletal system and CNS development; manifested by severe mental retardation, short stature, coarse facial features, protruding tongue, and umbilical hernia

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8
Q

Type I Diabetes is which if the following hypersensitivity reactions?

A Hypersensitivity reaction 2
B Hypersensitivity reaction 4
C Hypersensitivity reaction 1
D Hypersensitivity reaction 3

A

B

Explanation
IDDM is a type IV hypersensitivity reaction

It is thought that during early life, damage to islet cells leads to exposure of islet cell antigens to CD4+ Th1 cells in peri pancreatic lymph. Activated T cells are then trafficked to the pancreas and cause B cell injury. There is thus a failure of self-tolerance in T cells which may be due to defective clonal deletion or regulatory processes. A role for antibodies has been suspected as most patients have autoantibodies against islet antigens, however it is unclear if the antibodies are involved in causing injury or are produced as a consequence of islet cell damage. Therefore, it is classed as a Type IV hypersensitivity reaction

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9
Q

50-year-old woman is referred to the ED with a critically elevated Calcium level. She is asymptomatic. What is the most likely cause of her clinical picture?

A MEN-1
B Primary parathyroid hyperplasia
C Metastatic bone malignancy
D Solitary parathyroid adenoma

A

D

Explanation
Primary hyperparathyroidism (associated with raised PTH) is the most common cause of hypercalcaemia overall. Malignancy (associated with low PTH) is the most common cause of symptomatic hypercalcaemia. Primary hyperparathyroidism and malignancy account for 90% of cases of hypercalcaemia.

Causes of primary hyperparathyroidism include:

Adenoma: 85-95% (most are monoclonal)
Primary hyperplasia: 5-10% (most are monoclonal, as well)
Parathyroid carcinoma: 1%

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10
Q

32-year-old woman presents with tremor, exophthalmos and localized dermopathy. She reports a 10kg history of unintentional weight loss. Which of the following laboratory results best explains her clinical picture?

A Low TSH, elevated T3, elevated T4
B Elevated TSH, elevated T3, elevated T4
C Low TSH, low T3, elevated T4
D Elevated TSH, low T3, elevated T4

A

A

Explanation
Her clinical presentation is consistent with Graves’ disease.

Graves’ disease presents with a clinical triad of:

1) Hyperthyroidism due to hyperfunctional, diffuse thyroid enlargement

2) Infiltrative ophthalmopathy with resultant exophthalmos

3) Localised, infiltrative dermopathy present in a minority of patients

It is an autoimmune disorder caused by TSH-receptor antibodies, which mimic actions of TSH causing T4 and T3 release. Some patients though have TSH-receptor blocking antibodies that can potentially cause hypothyroidism. Normally, T4 and T3 levels are elevated and TSH is suppressed.

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11
Q

Sick euthyroid state is best characterized by

A Low TSH, low T4
B Normal TSH, low T4
C Low TSH, normal T4
D Normal TSH, normal T4

A

D

Explanation
Sick euthyroid syndrome is a biochemical pattern of decreased circulating T3 levels, without a strong compensatory TSH response. It is due to a dysregulation of normal hormonal feedback in critical illness.

Extra:

Typical TFT abnormalities in sick euthyroid syndrome

T3: low
rT3: high
T3/rT3 ratio: low
T4: high or normal
TSH: high or normal
The above reflects the fact that normal hormonal feedback is dysregulated in critical illness. The “sick euthyroid” syndrome is part of the generalised response to critical illness, and reflects a sort of “hormonal economy”

Source: www.derangedphysiology.com

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12
Q

A somatotrope adenoma of the pituitary gland is likely to cause:

A Estrogen deficiency
B Diabetes insipidus
C Thyroid adenoma
D Growth hormone excess

A

D

Explanation
Somatotroph adenomas are growth hormone secreting tumours and are the second most common functioning pituitary adenoma, behind lactotroph adenomas (prolactinomas).

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13
Q

The Wolf-Chaikoff effect is caused by which substance acting on the thyroid gland?

A Potassium
B Iodide
C Calcium
D Sodium

A

B

Explanation
The Wolff-chaikoff effect refers to the fact that in normal people, large doses of iodide act directly on the thyroid to produce mild/transient inhibition of iodide and hence hormone synthesis.

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