The Endocrine System - Chapter 24 Flashcards

1
Q

What are the two lobes of the pituitary gland called? What is the function of the pituitary?

A

Anterior lobe (adenohypophysis)
Posterior lobe (neurohypophysis) Hormone Secretion

google: Your pituitary gland (also known as hypophysis) is a small, pea-sized gland located at the base of your brain below your hypothalamus. It sits in its own little chamber under your brain known as the sella turcica. It’s a part of your endocrine system and is in charge of making several essential hormones.

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2
Q

What structure regulates the functional activity of the anterior pituitary?

A

Hypothalamus

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3
Q

What are the five cell types of the anterior pituitary?

A

Somatotrophs, lactotrophs, corticotrophs, thyrotrophs, gonadotrophs

nmenonic : lac-som- cortisol-thryroid-gonads

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4
Q

What anatomical structure does the pituitary gland rest upon?

A

Sella turcica

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5
Q

How is hormone secretion of the pituitary gland inhibited? Give a brief example.

A

Most pituitary hormones are controlled predominantly by positive-acting releasing factors from the hypothalamus, which are carried to the anterior pituitary by a portal vascular system. Prolactin is the major exception, since its primary hypothalamic control is inhibitory through the action of dopamine

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6
Q

What hormones are released by the neurohypophysis?

A

Oxytocin and antidiuretic hormone (ADH)

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7
Q

What hormones are released by the neurohypophysis?

A

Oxytocin and antidiuretic hormone (ADH)

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8
Q

What two clinical syndromes are associated with a pituitary adenoma?

A

Hyperpituitarism – caused by a functional adenoma arising in the anterior lobe.
Large pituitary adenomas may cause hypopituitarism as they encroach on and destroy adjacent anterior pituitary parenchyma.

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9
Q

Name some causes of hypopituitarism.

A

Tumors and other mass lesions, traumatic brain injury and subarachnoid hemorrhage, surgery or radiation, pituitary apoplexy, Sheehan syndrome (are condition involving injury to your pituitary gland following extreme blood loss during childbirth.)and ischemic necrosis of the pituitary gland, Rathke cleft cyst, empty sella syndrome, genetic defects, hypothalamic lesion, inflammatory disorders and infections

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10
Q

What is the only true criterion of a malignant pituitary gland tumor

A

The demonstration of systemic metastases

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11
Q

simmonds disease is an insufficiency of 3 organs due to lack of secretion of pitutary hormone. What are these 3 organs ?

A

thyroid, adrenals, gonads

acronym TAG

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12
Q

The patients who have Froehlich syndrome show what physical characteristics?

A

Obesity, sexual infantilism (lack of sexual development), atrophy or hypoplasia of the gonads, and altered secondary sex characteristics

google:
Froehlich syndrome, also known as adiposogenital dystrophy, is a constellation of endocrine abnormalities believed to result from damage to the hypothalamus, a part of the brain that links the nervous system to the endocrine system via the pituitary gland.

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12
Q

The patients who have Froehlich syndrome show what physical characteristics?

A

Obesity, sexual infantilism (lack of sexual development), atrophy or hypoplasia of the gonads, and altered secondary sex characteristics

google:
Froehlich syndrome, also known as adiposogenital dystrophy, is a constellation of endocrine abnormalities believed to result from damage to the hypothalamus, a part of the brain that links the nervous system to the endocrine system via the pituitary gland.

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13
Q

Diabetes insipidus is induced by anti-diuretic hormone (ADH) deficiency. What are some of the causes of ADH deficiency?

A

Head trauma, tumors, inflammatory disorders of the hypothalamus and pituitary and surgical procedures involving these organs.
google:
Diabetes insipidus is a rare disorder that causes the body to make too much urine. While most people make 1 to 3 quarts of urine a day, people with diabetes insipidus can make up to 20 quarts of urine a day. People with this disorder need to urinate frequently, called polyuria.

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14
Q

Describe and differentiate between primary and secondary empty sella syndrome. What is the major clinical symptom that these patients will present with?

A

In a primary empty sella there is a defect in the diaphragma sella that allows the arachnoid mater and CSF to herniate into the sella, resulting in expansion of the sella and compression of the pituitary.

In a secondary empty sella, a mass, such as a pituitary adenoma enlarges the sella and is either surgically removed or undergoes spontaneous necrosis leading to loss of pituitary function. Hypopituitarism is the major clinical symptom.

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15
Q

Which tumors are most likely to metastasize to the pituitary?

A

Breast and lung

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16
Q

The thyroid gland develops as a tubular evagination from what structure? What does a normal adult thyroid weigh? Occasionally the thyroid gland has 3 lobes instead of 2. What is this third lobe called?

A

Pharyngeal epithelium
10 g-30 g
Pyramidal lobe (Not in Robbins)

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17
Q

What are cretinism and myxedema and what are the clinical features of each?

A

Cretinism refers to hypothyroidism developing in infancy or early childhood. Clinical features include impaired development of the skeletal system and CNS, manifested by severe mental retardation, short stature, coarse facial features, a protruding tongue, and umbilical hernia. Severity of mental impairment is related to the time at which thyroid deficiency occurs in utero.

Myxedema is applied to hypothyroidism developing in the older child or adult. Clinical features of myxedema are characterized by a slowing of physical and mental activity. The initial symptoms include generalized fatigue, apathy, and mental sluggishness, which may mimic depression. Speech and intellectual functions become slowed. Patients with myxedema are listless, cold intolerant, and frequently overweight.

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18
Q

What does a thyroid with Hashimoto thyroiditis look like?

A

The thyroid is often diffusely enlarged with an intact capsule. The gland is well demarcated from the surrounding tissues. The cut surface is pale, yellow-tan, firm and somewhat nodular. There is an extensive infiltration of the parenchyma by mononuclear cell infiltrate.

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18
Q

What does a thyroid with Hashimoto thyroiditis look like?

A

The thyroid is often diffusely enlarged with an intact capsule. The gland is well demarcated from the surrounding tissues. The cut surface is pale, yellow-tan, firm and somewhat nodular. There is an extensive infiltration of the parenchyma by mononuclear cell infiltrate.

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19
Q

What are Hürthle cells?

A

In Hashimoto thyroiditis, the thyroid follicles are atrophic and are lined in many areas by epithelial cells with abundant eosinophilic granular cytoplasm, termed Hürthle cells.

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19
Q

What are Hürthle cells?

A

In Hashimoto thyroiditis, the thyroid follicles are atrophic and are lined in many areas by epithelial cells with abundant eosinophilic granular cytoplasm, termed Hürthle cells.

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20
Q

DeQuervain’s (granulomatous) thyroiditis has a suspected viral etiology. Why?

A

The majority of patients have a history of an upper respiratory infection just before the onset of thyroiditis. The disease has a seasonal incidence with occurrences peaking in the summer, and clusters of cases have been reported in association with coxsackievirus, mumps, measles, adenovirus, and other viral illnesses.

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21
Q

What is the triad of clinical findings in Graves disease?

A

Hyperthyroidism do to diffuse enlargement of the thyroid
Infiltrative ophthalmopathy with resultant exophthalmos
Localized, infiltrative dermopathy sometimes called pretibial myxedema

google:
exopthalmos protrusion of one or both eyes anteriorly out of the orbit due to an increase in orbital contents within the rigid bony orbi

Pretibial myxedema is a skin condition that causes plaques of thick, scaly skin and swelling of your lower legs.

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22
Q

What is endemic goiter? What is the major cause of endemic goiter?

A

Endemic goiter occurs in geographical areas where the soil, water, and food supply contain low levels of iodine. The term endemic is used when goiters are present in more than 10% of the population in a given region.

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23
Q

On a radioactive iodine uptake scan, a “hot” nodule is likely to be

A

Benign

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24
Q

How high is the risk of malignant transformation of a follicular adenoma?

A

Low risk

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25
Q

What is the most common form of thyroid carcinoma?

A

Papillary

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26
Q

What are some of the histological hallmarks of papillary carcinoma of the thyroid?

A

Branching papillae, ground glass or Orphan Annie nuclei, pseudo-inclusions or intranuclear grooves, psammoma bodies

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27
Q

Papillary carcinoma has a peak incidence in ages 25 to 50 years. When is the peak incidence of follicular carcinoma?

A

Ages 40-60

28
Q

What are the common metastasis sites for follicular carcinoma?

A

Bone, lungs, and liver

29
Q

From what cells do medullary thyroid carcinomas originate?

A

Parafollicular cells or C cells

29
Q

From what cells do medullary thyroid carcinomas originate?

A

Parafollicular cells or C cells

30
Q

Where is a thyroglossal duct cyst usually located?

A

Midline of the neck anterior to the trachea

30
Q

Where is a thyroglossal duct cyst usually located?

A

Midline of the neck anterior to the trachea

31
Q

what is the normal weight of normal adult parathyroid gland?

A

25-40 mg, each gland

31
Q

what is the normal weight of normal adult parathyroid gland?

A

25-40 mg, each gland

32
Q

What are the three cell types of a parathyroid gland?

A

Chief cells, oxyphil cells, transitional oxyphils

33
Q

What are the major functions of parathyroid hormone (PTH)?

A

It increases the renal tubular resorption of calcium, thereby conserving free calcium, increases the conversion of vitamin D to its active dihydroxy form in the kidneys, increases urinary phosphate excretion, thereby lowering serum phosphate level, augments gastrointestinal calcium absorption

34
Q

what is the most important cause of primary hyperparathyroidism?

A

Parathyroid adenoma resulting in hypercalcemia

35
Q

What are some of the major clinical manifestations of PHPT, primary hyperparathyroidism

A

Bone disease, nephrolithiasis (kidney stones, also known as renal calculi), GI disturbances, CNS alterations (depression, lethargy, seizures), neuromuscular abnormalities, aortic and mitral valve calcifications

36
Q

What is the most common manifestation of PHPT?

A

Hypercalcemia

37
Q

What is the most common cause of secondary hyperparathyroidism?

A

Renal failure

38
Q

List some of the causes and clinical manifestations of hypoparathyroidism.

A

Surgically induced, congenital absence of all glands, familial isolated hypoparathyroidism, autosomal dominant hypoparathyroidism, autoimmune hypoparathyroidism
Clinical manifestations – tetany, Chvostek sign (tapping facial nerve tapping leading to muscle contraction around eye, mouth nose) and Trousseau sign (carpal spasms produced by occlusion of fore arm and hand vessels), mental status changes, ocular disease, cardiac conduction defects, dental abnormalities, basal ganglia calcifications

39
Q

What are the major diseases associated with diabetes mellitus in the United States?

A

End-stage renal disease, adult-onset blindness, non-traumatic lower extremity amputations (due to atherosclerosis of the arteries)

40
Q

Within which cells of what structure of the pancreas is insulin produced?

A

B cells within the islets of Langerhans

41
Q

What is the underlying cause of diabetes mellitus type I? What are the overt diagnostic symptoms and what do they indicate?

A

Autoimmune reactivity to the β- cells in the endocrine pancreas. Clinically, patients present with hyperglycemia and ketosis, after 90% of the β cells have been destroyed.

42
Q

What is the most important risk factor for type II diabetes mellitus?

A

Obesity, specifically central or visceral

43
Q

What is the most important risk factor for type II diabetes mellitus?

A

Obesity, specifically central or visceral

44
Q

What is the classic triad of diabetes? What do these symptoms result from?

A

Polyuria, polydipsia (intense thirst), polyphagia(increased appetite) and, when severe, diabetic ketoacidosis
These symptoms result from metabolic derangements

44
Q

What is the classic triad of diabetes? What do these symptoms result from?

A

Polyuria, polydipsia (intense thirst), polyphagia(increased appetite) and, when severe, diabetic ketoacidosis
These symptoms result from metabolic derangements

45
Q

Name the complications of diabetes mellitus

A

Macrovascular disease – accelerated atherosclerosis, myocardial infarction, stroke and lower extremity gangrene
Microvascular disease – diabetic retinopathy, nephropathy, and neuropathy

46
Q

Microvascular disease is one complication of diabetes. This is most commonly believed to be related to __________.

A

Hyperglycemia

47
Q

What are the histologic pancreatic manifestations of diabetes?

A

Reduction in the size and number of islets
Leukocytic infiltrates in the islets
Subtle reduction in the islet cell mass - specific to type 2 and requires special studies Amyloid deposition within islets (type 2)
Increase in size and number of islets (in nondiabetic newborns of diabetic mothers)

48
Q

The pathognomic lesions of diabetes found in the kidney are known as?

A

Kimmelstiel-Wilson lesions (nodular glomerulosclerosis)

49
Q

What are Kimmelstiel-Wilson lesions?

A

Nodular glomerulosclerosis – glomerular lesions take the form of ovoid or spheroid, often laminated, hyaline masses situated in the periphery of the glomerulus

50
Q

What are the main morphologic changes of diabetic glomerulosclerosis and diabetic nephropathy?

A

Diabetic glomerulosclerosis - Capillary basement membrane thickening, diffuse mesangial sclerosis, nodular glomerulosclerosis
Diabetic nephropathy - includes glomerular lesions, renal vascular lesions, and pyelonephritis

google:
Glomerulosclerosis in diabetic nephropathy is caused by accumulation of extracellular matrix (ECM) proteins in the mesangial interstitial space, resulting in fibrosis manifested by either diffuse or nodular changes (1). The most common matrix proteins detected are collagen types I, III, and IV and fibronectin

sorry only way to add 2 pictures is to add it to the question and answer

51
Q

The most common causes of death in patients with diabetes are

A

Macrovascular complications such as myocardial infarction caused by atherosclerosis of the coronary arteries, renal vascular insufficiency, and cerebrovascular accidents.

52
Q

Name two clinical syndromes associated with pancreatic endocrine neoplasms.

A

Hyperinsulinism (insulinoma)
Zollinger-Ellison syndrome (gastrinoma)

google:
Zollinger-Ellison syndrome is a rare condition in which one or more tumors grow in the pancreas or in the upper part of the small intestine. The tumors are called gastrinomas. These gastrinomas produce large amounts of the hormone gastrin. Gastrin causes the stomach to produce too much acid, which leads to peptic ulcers. High gastrin levels also can cause diarrhea, belly pain and other symptoms.

53
Q

What is Cushing syndrome and what are some of its major clinical features?

A

Cushing syndrome is hypercortisolism caused by any condition that produces an elevation in glucocorticoid levels. Major clinical features – central obesity, facial plethora, rounded face, decreased libido, thin skin, decrease in linear growth in children, menstrual irregularity, hypertension, hirsuitism, depression

54
Q

What ACTH secreting tumor accounts for approximately 70% of endogenous hypercortisolism?

A

pituitary adenoma

55
Q

what is primary hyperaldosteronism (PHA) characterized by?

A

An autonomous overproduction of aldosterone with resultant suppression of the renin-angiotensin system and decreased plasma renin activity; hypertension is the most common manifestation.

56
Q

what is conn syndrome

A

Primary hyperaldosteronism caused by a solitary aldosterone-secreting adenoma in the adrenal gland.

57
Q

Briefly list some of the causes of acute adrenocortical insufficiency.

A

Any form of stress that requires an immediate increase in steroid output from glands incapable of responding
Rapid withdrawal of steroids in patients dependent on exogenous corticosteroids
Massive adrenal hemorrhage

google: Adrenal crisis occurs if the adrenal gland is deteriorating (Addison’s disease, primary adrenal insufficiency), if there is pituitary gland injury (secondary adrenal insufficiency), or if adrenal insufficiency is not adequately treated.

remember this is acute not chronic, chronic is Addison’s

58
Q

What are the characteristics of Waterhouse-Friderichsen Syndrome? What do the adrenal glands of these patients look like grossly?

A

An overwhelming bacterial infection (Neisseria meningitides)

Rapidly progressive hypotension leading to shock
DIC with widespread purpura
Rapidly developing adrenocortical insufficiency associated with massive bilateral adrenal hemorrhage

59
Q

What is Addison disease? What are the major clinical manifestations?

A

Addison disease, or chronic adrenocortical insufficiency, is an uncommon disorder resulting from progressive destruction of the adrenal cortex.
Clinical manifestations – progressive weakness and easy fatigability, GI disturbances, hyperpigmentation of the skin, hyperkalemia, hyponatremia, volume depletion, hypotension

60
Q

What are some of the causes of secondary adrenocortical insufficiency?

A

Any disorder of the hypothalamus and pituitary, such as metastatic cancer, infection, infarction, or irradiation, which reduces the output of ACTH

google: Adrenal insufficiency is a condition that develops when most of the adrenal gland is not functioning normally. Primary adrenal insufficiency arises due to the damage of the glands or because of using drugs that halt synthesis of cortisol. On the other hand, secondary adrenal insufficiency stems from processes that inhibit the secretion of the adrenocorticotropic hormone (ACTH) by the hypophysis as a result of a hypothalamic or pituitary pathology

61
Q

What catecholamines are secreted by the adrenal medulla?

A

Epinephrine and norepinephrine

62
Q

Name the rule of 10s associated with pheochromocytoma.

A

10% of pheochromocytomas are extra-adrenal
10% of sporadic adrenal pheochromocytomas are bilateral
10% of adrenal pheochromocytomas are biologically malignant
10% of adrenal pheochromocytomas are not associated with hypertension
25% (traditionally 10%) of individuals with pheochromocytomas and paragangliomas harbor a germline mutation in one of at least six known genes.

63
Q

what is the dominant complication of a pheochromocytoma?

A

hypertension

google:
Pheochromocytoma is a rare tumor that usually starts in the cells of one of your adrenal glands. Although they are usually benign, pheochromocytomas often cause the adrenal gland to make too many hormones

64
Q

MEN I (Wermer syndrome) primarily affects what organs?

A

Parathyroid, pancreas, pituitary gland, duodenum and pancreas
An increase in carcinoid tumors, thyroid and adrenocortical adenomas are also more frequent

google:
Multiple endocrine neoplasia, type 1 (MEN 1), sometimes called Wermer’s syndrome, is a rare disorder that causes tumors in the endocrine glands and parts of the small intestine and stomach. In MEN 1, the endocrine glands — usually the parathyroids, pancreas and pituitary — grow tumors and release excessive amounts of hormones that can lead to disease. However, the tumors are usually noncancerous (benign).

65
Q

What is Sipple syndrome?

A

MEN 2A or Sipple syndrome is characterized by pheochromocytoma, medullary thyroid carcinoma, and parathyroid hyperplasia

google:
Familial medullary carcinoma of the thyroid gland is often associated with phaeochromocytoma; this condition is known as Sipple syndrome.

66
Q

What is another name for the “brain sand” seen microscopically in the pineal gland?

A

Acervulus cerebri

google: The pineal organ (pineal gland, epiphysis cerebri) contains several calcified concretions called “brain sand” or acervuli (corpora arenacea). These concretions are conspicuous with imaging techniques and provide a useful landmark for orientation in the diagnosis of intracranial diseases.