Brainscape's Knowledge GenomeTM

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


See full index

Path Fall > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are the 2 main kinds of hormones?

A
  1. Hormones that bind to cell surface receptors (use cAMP 2nd messengers)
  2. Hormones that bind to intracellular receptors (lipid soluble)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Identify 3 main causes of endocrine diseases

A
  1. Underproduction/overproduction of hormones
  2. End-organ resistance to hormone effect.
  3. Neoplasms (nonfunctional, hormone overproduction, hormone underproduction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What hormones are produced by the anterior pituitary?

A
  1. TSH
  2. ACTH
  3. PRL
  4. GH
  5. FSH
  6. LH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What hormones are produced by the posterior pituitary?

A
  1. Oxytocin

2. Vasopressin (ADH)

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

What hormones are produced by the hypothalamus?

A
  1. Thyroid releasing hormone (TRH)
  2. Corticotropin-releasing hormone (CRH)
  3. Growth hormone releasing hormone (GHRH)
  4. Gonadotropin releasing hormone (GnRH)
  5. Somatostatin (GIH)
  6. Dopamine (PIF)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the most common cause of hyperpituitarism?

A

Adenoma arising in anterior lobe

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

What is a functional vs. non-functional pituitary adenoma?

A
  1. functional= hormone excess

2. non-functional= no clinical manifestations of hormone excess

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

What are the risks of non-functional pituitary adenoma?

A
  1. Does not produce hormones and so is usually found late.
  2. Destroys adjacent parenchyma causing hypopituitarism
  3. compresses optic chiasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference between micro and macro pituitary adenomas?

A
  1. Micro= less than 1 cm

2. Macro= greater than 1 cm

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

What are the 3 most common types of pituitary adenomas?

A
  1. Lactotroph (secretes PL, causes amenorrhea, galactorrhea, infertility)
  2. Somatotroph (secretes GH, causes gigantism and acromegaly)
  3. Corticotroph (secretes ACTH, causes Cushing’s syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Nelson’s syndrome?

A

Adenoma that develops in pituitary gland after the removal of adrenal glands due to loss of inhibitory effect of adrenal corticosteroids.

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

What is hypopituitarism?

A

Loss or absence of +75% of anterior pituitary. Could be congenital (rare) or due to: tumors, ischemia, iatrogenic, trauma.

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

What are the two subtypes of diabetes insipidus?

A
  1. Central: ADH deficiency

2. Nephrogenic: Renal tubular unresponsiveness to circulating ADH

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

What are clinical manifestations of syndrome of inappropriate ADH (SIADH)?

A
  1. Hyponatremia
  2. Cerebral edema/neurological dysfunction
  3. Peripheral edema does NOT develop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is thyroid hormone made?

A
  1. TRH from hypothalamus stimulates TSH from pituitary.
  2. TSH binds to thyroid follicular epithelial cells.
  3. Thryoglobulin converted to thyroxine (T4) and triiodothyronine (T3)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is thyrotoxicosis/ hyperthyroidism?

A

Bother terms refer to elevated levels of free T3 and T4.

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

What are the 3 most common causes of thyrotoxicosis?

A
  1. Graves disease
  2. Multinodular goiter
  3. Adenoma of thyroid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are signs and symptoms of hyperthyroidism?

A
  1. Warm, flushed skin.
  2. Weight loss with increased appetite.
  3. Stimulation of gut, increased transit time, causes steatorrhea.
  4. Palpitation/ tachycardia.
  5. Nervousness/ tremor
  6. Wide, staring gaze (proptosis with Grave’s dz)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Distinguish between primary and secondary hypothyroidism

A
  1. Primary: intrinsic abnormality of the thyroid (iodine deficiency, genetic, autoimmune Hashimoto, iatrogenic).
  2. Secondary: caused by pituitary failure or hypothalamic failure.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is cretinism?

A

Hypothyroidism in infancy or early childhood. Leads to impaired skeletal and CNS, cognitive disability, short stature, coarse facial features, protruding tongue, umbilical hernia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is myxedema?

A

Hypothyroidism in older children and adults.
S/S:
1. Fatigue, apathy, mental sluggishness
2. Decreased sympathetic activity (constipation, decreased sweating)
3. Cold, pale skin.
4. Shortness of breath and decreased exercise capacity.
5. Non-pitting edema
6. Coarsening of facial features
7. Enlargement of tongue
8. Deepening of voice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is Hashimoto’s?

A

Circulating antibodies destroy thyroid epithelial cells.

Causes englarged thyroid and hypothyroidism.

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

What is Grave’s disease?

A

Autoantibodies bind to TSH receptor that stimulates thyroid follicular cells.
Causes hyperplasia of thyroid, exophthamos, scaly skin, elevated T3 and T4, decreased TSH.

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

What is deQuervain thyroiditis?

A

Viral infection or inflammatory process causes transient hyperthyroidism, thyroid enlargement, neck pain, fever, malaise.

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

What is a goiter?

A

Enlargement of thyroid.

  1. Endemic: geographic area with little iodine.
  2. Sporadic: excessive ingestion of substances that interfere with thyroid synthesis, inherited enzymatic defect, or idiopathic.
26
Q

What is the clinical criteria of a thyroid nodule that increases risk of malignancy?

A
  1. Solitary nodule
  2. Age: <20 or >70
  3. Males more than females.
  4. History of radiation
27
Q

What are the common anatomical characteristics of a thyroid adenoma?

A
  1. Solitary
  2. Spherical
  3. Intact, well-formed capsule encircling tumor
  4. Painless nodule
28
Q

What is a “cold” thyroid nodule?

A

Adenomas are described as “cold” when they pick up less radioactive iodine than normal thyroid tissue upon radionuclide imaging. 10% become malignant.

29
Q

What is a “hot” thyroid nodule?

A

Toxic adenomas that pick up more radioactive iodine in radionuclide imaging. Uncommon to become malignant.

30
Q

Resected thyroid adenoma risk of recurrence or metastasis?

A

Thyroid adenomas carry excellent prognosis and generally do not recur or metastasize.

31
Q

What is a thyroid papillary carcinoma?

A
  1. Most common thyroid carcinoma
  2. Well-differentiated epithelial cells
  3. Risk factors: History of ionizing radiation exposure
  4. Presents as painless mass in neck, nonfunctional
  5. Good prognosis, rare to metastasize.
32
Q

What is a thyroid follicular carcinoma?

A
  1. Well-differentiated follicular epithelial cells
  2. Risk factors: 40-60 yr woman, iodine deficiency
  3. Presents as solitary cold nodules
  4. Poor prognosis, metastasizes via blood stream
33
Q

What is a thyroid anaplastic (undifferentiated) carcinoma?

A
  1. Rare
  2. Undifferentiated thyroid follicular epithelium
  3. Risk factors: Mean age- 65 years old. History of well-differentiated thyroid carcinoma.
  4. Presents as multiple tumors, escapes thyroid capsule.
  5. Poor prognosis, near 100% mortality rate.
34
Q

What is a thyroid medullary carcinoma?

A
  1. Neuroendocrine tumors.
  2. Parafollicular C cells
  3. Risk factors: 30% Familial, 70% sporadic
  4. Features: Mass in neck, hoarseness/dysphagia, diarrhea
35
Q

What is the histology of the parathyroid glands?

A
  1. Mostly chief cells- secrete parathyroid hormone.

2. Oxyphil cells

36
Q

What is the physiology of the parathyroid gland?

A
  1. Activity of parathyroid gland regulated by Calcium blood levels
  2. Low calcium = secretion of PTH
  3. High calcium = inhibition of PTH
37
Q

What are the effects of PTH?

A
  1. Increase renal tubular reabsorption of calcium
  2. Increase urinary phosphate excretion, lower serum phosphate levels
  3. Increase vitamin D conversion in kidney, increase GI calcium absorption
  4. Enhance osteoclast activity
38
Q

What are the most common lesions of hyperparathyroidism?

A
  1. Adenoma- 85-95% single gland.
  2. Primary hyperplasia- 5-10% multi-glandular.
  3. Parathyroid carcinoma- 1% single gland.
39
Q

What are risk factors for primary hyperparathyroidism?

A
  1. Typically adults
  2. Women > men (4:1)
  3. Cyclin D1 and MEN1 genetic mutations
40
Q

What are common lab findings for hyperparathyroidism?

A
  1. Increased serum ionized calcium
  2. Inappropriately elevated serum PTH
  3. Hypophosphatemia
  4. Increased urine excretion with calcium and phosphate
41
Q

What are common symptoms of hyperparathyroidism?

A

Bones, Stones, Groans, Moans!

  1. “Painful bones”: osteoporosis or osteitis fibrosa cystica.
  2. “Renal stones”: due to hypercalcemia.
  3. “Abdominal groans”: constipation, nausea, peptic ulcers, pancreatitis, gallstones.
  4. “Psychic moans”: depression, lethargy, seizures

Also: weakness, hypotonia, polyuria and polydipsia

42
Q

What is the most common cause of secondary hyperparathyroidism?

A

Chronic hypocalcemia most often secondary to renal failure

43
Q

What are the causes of hypoparathyroidism?

A
  1. Surgical ablation
  2. Congenital absence (Di George syndrome)
  3. Autoimmune hypoparathyroidism
44
Q

What are the clinical manifestations of hypoparathyroidism?

A
  • Secondary to hypocalcemia:
    1. Acute- neuromuscular irritability (tingling, spasms, grimacing, tetany), cardiac arrhythmias, seizure, increased intracranial pressure.
    2. Chronic- cataracts, calcification of cerebral basal ganglia, dental abnormalities
45
Q

What are the 4 main cell types of the pancreas?

A
  1. Alpha: glucagon
  2. Beta: insulin
  3. Delta: somatostatin
  4. Pancreatic polypeptide (PP): secretes PP for stimulation of digestive enzymes and inhibition of intestinal motility
46
Q

What is the metabolic effects of insulin?

A

Increased synthesis and reduced degradation of glycogen, lipids, and proteins.
Increases rate of glucose transport into cells.

47
Q

What are the mitogenic effects of insulin?

A

Initiation of DNA synthesis in certain cells and stimulation of their growth and differentiation.

48
Q

Describe the opposing regulatory effects of glucagon and insulin.

A

During fasting, low insulin and high glucagon facilitate hepatic gluconeogenesis (glycogen breakdown) while decreasing glycogen synthesis.
After a meal, insulin rises and glucagon falls.

49
Q

Describe 2 classes of diabetes.

A
  1. Type 1: autoimmune, Beta cell destruction, insulin deficient. Failure of self-tolerance in T cells.
  2. Type 2: caused by combination of peripheral resistance to insulin and inadequate secretory response by beta cells. Obesity related.
50
Q

What are clinical features of long-term diabetes?

A
  1. Microangiopathy
  2. Cerebral vascular infarcts and hemorrhages.
  3. Hypertension
  4. Retinopathy
  5. Cataracts
  6. Glaucoma
  7. Myocardial infarct
  8. Atherosclerosis
  9. Nephrosclerosis
  10. Peripheral neuropathy
  11. Autonomic neuropathy
  12. Peripheral vascular atherosclerosis
51
Q

What is the anatomy of the adrenal cortex?

A
  1. Zona glmoerulosa: aldosterone and mineralocorticoids.
  2. Zona fasciculata: cortisol and glucocorticoids.
  3. Zona reticularis: sex steroids (estrogens and androgens)
52
Q

What is the anatomy of the adrenal medulla?

A

Composed of chromaffin cells, which synthesizes and secretes catecholamines, mainly epinephrine.

53
Q

List 4 main causes of hypercortisolism (Cushing’s syndrome)

A

Iatrogenic
1. Administration of exogenous glucocorticoids (Most common)
Endogenous
2. Primary hypothalamic-pituitary diseases associated with hypersecretion of ACTH
3. Secretion of ACTH by nonpituitary neoplasms
4. Primary adrenocortical neoplasms (adenoma or carcinoma), and rarely primary cortical hyperplasia

54
Q

What is the difference between Cushing’s disease and Cushing’s syndrome?

A
  1. Disease: caused by primary hypothalamic-pituitary disease associated with hypersecretion of ACTH
  2. Syndrome: Refers to signs and symptoms associated with excess cortisol in the body, regardless of the cause.
55
Q

What are the common clinical features of Cushing’s syndrome?

A 
EARLY:
1. Hypertension
2. Weight Gain
LATE:
3. Moon facies, buffalo hump
4. Decrease in muscle mass and proximal limb weakness
5. Secondary diabetes
6. Thin skin, fragile, easily bruised
7. Cutaneous striae
8. Osteoporosis
9. Immunosuppression
10. Hirsutism
11. Menstrual abnormalities
12. Psych: depression, mood swings, frank psychosis
56
Q

Distinguish between primary and secondary hyperaldosteronism

A

Both cause hypertension and hypokalemia
1. Primary: Adrenocortical neoplasm, glucocorticoid-remediable hyperaldosteronism (heritable), or idiopathic.
Secondary: Occurs through activation of the renin-angiotensin system due to congestive heart failure, decreased renal perfusion, pregnancy.

57
Q

What are the most common causes of chronic adrenocortical insufficiency (Addison disease)?

A
  1. Autoimmune adrenalitis
  2. Infections (TB, fungal infection, AIDS)
  3. Metastatic neoplasms of adrenals
58
Q

What are signs and symptoms of Addison’s disease?

A
  1. Progressive weakness and fatigue
  2. Anorexia and weight loss
  3. Vomiting and diarrhea
  4. Hyperpigmentation of skin and mucosa
  5. Hyperkalemia, hyponatremia, decreased aldosterone
59
Q

What is the “rule of 10s” for pheochromocytoma?

A

10% of pheochromocytomas are:

  1. extra adrenal (paragangliomas)
  2. bilateral
  3. malignant
  4. Not associated with hypertension
60
Q

What organs are most commonly affected by Multiple Endocrine Neoplasia (MEN) syndrome?

A 
MEN type 1:
1. Parathyroid
2. Pancras
3. Pituitary
MEN type 2:
1. Thyroid
2. Adrenal medulla
3. Parathyroid
MEN type 3:
1. Mucosal neuromas
2. Marfanoid body habitus
3. Medullary thyroid carcinoma
4. Pheochromocytoma

Path Fall (8 decks)

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