Brainscape's Knowledge GenomeTM

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


See full index

Pathology Exam 6 (FINAL :)) > Endocrine Disease > Flashcards

Endocrine Disease Flashcards

1
Q

Identify this concept

  • Secretion of a stimulating hormone inhibited by increased activity of target organ/tissue
  • Examples
    • Decreased secretion of pituitary hormones with increased levels of target hormone
    • Decreased secretion of parathyroid hormone (PTH) with increased calcium levels
  • The opposite is also true-decreased activity of target organ causes increased secretion of stimulating hormone.
A

Feedback Inhibition

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

What is the morphology of neuroendocrine tumors?

A
  • “Salt and Pepper” nuclear chromatin
  • Immunohistochemical markers
    • Neuron-specific enolase (NSE)
    • Chromogranin
    • Synaptophysin
      • ​if we find these markers we know there is a neuroendocrine tumor
    • CD56
  • Ultrastructure
    • Neurosecretory granules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What kind of neuroendocrine tumors are these an example of: Benign, Low grade malignant or High grade malignant?

  • Paraganglioma, pheochromocytoma, some islet

cell tumors

A

Benign

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

What kind of neuroendocrine tumors are these an example of: Benign, Low grade malignant or High grade malignant?

• Carcinoid tumor

A

Low grade malignant

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

What kind of neuroendocrine tumors are these an example of: Benign, Low grade malignant or High grade malignant?

  • Large cell neuroendocrine carcinoma
  • Small cell carcinoma
A

High grade malignant

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

What type of endocrine gland malfunction is this?

  • Diffuse or nodular; usually involves entire gland(s)
    • localized overgrowth
    • multinodular–more than one node!
  • May be primary or secondary (driven by stimulating hormone)
A

Endocrine Hyperplasia

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

What type of endocrine gland malfunction is this?

• Usually solitary; often nonfunctional

A

Endocrine Adenoma

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

What type of endocrine gland malfunction is this?

  • Less common than corresponding adenoma
  • Often well differentiated
    • Demonstration of tumor invasion or metastasis required for diagnosis
A

Carcinoma

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

What are some hormones produced by anterior pituitary?

A
  • Thyroid Stimulating Hormone (TSH)
  • Adrenocorticotrophic Hormone (ACTH)
    • Melanocyte Stimulating Hormone (MSH)
  • Follicle Stimulating Hormone (FSH)
  • Luteinizing Hormone (LH)
  • Prolactin, Growth Hormone
    • these two have direct physical effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Identify:

  • The most common cause of pituitary hyperfunction; usually in anterior lobe
  • 25% are nonfunctional
  • Most functional ones produce one hormone
  • Peak age-middle age adults (30-60)
  • Mass effects
    • Imaging-expansion of sella
    • Visual disturbances (pressure on optic chiasm)
    • Increased intracranial pressure (headache, nausea)
  • Hormonal effects
A

Pituitary Adenoma

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

What is this type of functioning pituitary adenoma?

  • MOST COMMON
  • Symptoms: Galactorrhea, amenorrhea, infertility
  • Symptoms most prominent in childbearing age women
A

Prolactinoma

Excess prolactin

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

What is this type of functioning pituitary adenoma?

  • SECOND most common
  • Growth disturbances (gigantism, acromegaly)
  • Diabetes-like metabolic effects
A

Growth Hormone (somatotroph) adenoma

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

What is this symptom of excess growth hormone?

  • Growth hormone excess onset before closure of epiphyses
  • General increase in body size with increased limb length
A

Gigantism

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

What is this symptom of excess growth hormone?

  • Growth hormone excess onset or continuance after closure of epiphysis
  • Coarsening of facial features and hands
  • Soft tissue/visceral effects
A

Acromegaly

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

Identify this functioning pituitary adeonma:

  • Cushing’s Disease
  • Hyperpigmentation (concomitant increase of MSH)
A

Corticotroph Adenoma

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

What are hormones produced by posterior pituitary?

A
  • Antidiuretic hormone (ADH)
    • Promotes retention of water by renal tubules
  • Oxytocin (vasopressin)
    • Uterine and breast smooth muscle stimulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the causes of diabetes insipidus?

A
  • Decreased or absent ADH secretion
    • Increase in urine output because lack of ADH
    • Other causes of hypopituitarism
    • Idiopathic
    • May be caused by renal tubular dysfunction (nephrogenic DI)
  • Clinical
    • Polyuria, polydipsia
    • Dilute urine (low specific gravity)
    • Life-threatening dehydration if water not replaced
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Identify:

  • Increased ADH usually due to ectopic production by malignant tumor
    • Most common is small cell carcinoma of lung
  • Kidneys retain too much water
    • Hyponatremia
    • Cerebral edema
A

Syndrome of Inappropriate ADH Secretion (SIADH)

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

What are these indications of?

  • Deficiency of all anterior pituitary hormones
  • These are the potential causes this:
    • Neoplasms (mass effect; usually nonfunctioning adenoma)
    • Ischemic necrosis
      • Postpartum (Sheehan’s syndrome)
    • Iatrogenic (surgery, radiation)
  • Clinical effects
    • Most important ones due to TSH and ACTH deficiency
A

Panhypopituitarism

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

What are the hormones produced by the adrenal CORTEX?

A

Hormones

  • Glucocorticoids
  • Mineralocorticoids
  • Sex steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is produced by the adrenal medulla?

A

Catecholamines

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

What type of adrneal hormone is this:

  • Metabolic effects
    • Catabolic hormone, principally carbohydrates
    • break down of carbs and proteins!
  • Other effects
    • Anti-inflammatory/immunosuppressive
      • use this for drug therapy!
    • Inhibit bone formation and calcium absorption
A

Glucocorticoids

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

What type of adrneal hormone is this:

Effects: sodium (and water) retention, potassium excretion

A

Mineralocorticoids

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

What type of adrneal hormone is this:

• Major source of androgens in females and in males with nonfunctional testes

A

Sex steroids

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

What type of adrneal hormone is this:

Modulates “fight or flight” response, including increase in blood pressure

A

Catecholamines

  • Epinephrine, norepinephrine
26
Q

Identify illness:

  • Excess in glucocorticoids
    • when ACTH is specifically causing hyperplasia
  • Causes
    • Iatrogenic (steroid therapy)-MOST COMMON
    • Primary adrenal disease
      • Hyperplasia or functioning adenoma
    • Hypersecretion of ACTH
      • Pituitary adenoma (_______)
      • Ectopic ACTH secretion (usually lung cancer)
A

Cushing’s Syndrome

Clinical:

  • Impaired glucose tolerance/diabetes
  • Weight gain/hypertension
  • Axial redistribution of fat
    • Moon facies
    • “Buffalo hump”
    • Truncal obesity
  • Bone resorption
    • brittle bones
  • Skin fragility (striae)
  • Susceptibility to infection
  • Virilization (hirsutism, menstrual abnormalities)
  • Mental disturbances
  • Skin pigmentation (ACTH hypersecretion causes only)
27
Q

Identify:

  • Excess in mineralocorticoids
    • Excess sodium/hypertension
    • Hypokalemia
  • Causes
    • Primary adrenal
      • Aldosterone-secreting adenoma (Conn’s syndrome)
      • Adrenal hyperplasia
    • Secondary (activation of renin-angiotensin system)
A

Hyperaldosteronism

28
Q

Identify:

  • Excessive secretion of adrenal androgens
  • Effects
    • Virilization (hirsutism, menstrual abnormalities,etc., primarily in females)
  • Causes
    • ACTH hypersecretion–> pituitary gland
    • Adrenal cortical adenoma/carcinoma
    • Congenital adrenal hyperplasia
      • Primarily 21-hydroxylase deficiency
A

Adrenogenital Syndromes

  • When we have a block in 21-hydroxylase we have a decrease in minealcorticoids and glucocorticoids, BUT sex steroids are still good
29
Q

Identify adrenal problem:

  • Usually solitary–not multiple nodes
  • Size usually 1.5-6 cm
  • Usually nonfunctional
  • Well-circumscribed; may not have capsule
  • can be benign or malignant
A

Adrenal Cortical Adenoma

30
Q
  • Malignant, very large, locally invasive
  • Uncommon (incidence 1 per 1 million)
  • Metastasis in 70-90%
    • Liver, lung, retroperitoneum, regional nodes
  • Criteria for malignancy
    • Vascular invasion or local spread
    • Size/weight
    • Marked pleomorphism
    • Tumor necrosis
    • Weight loss
A

Adrenal Cortical Carcinoma

31
Q

Identify this adrenal disease:

  • Progressive destruction of adrenal cortex
  • Causes
    • Autoimmune
      • Most common
      • May be isolated or associated with other autoimmune disease
    • Infections
      • Mycobacterial/fungal
      • May be associated with HIV, immunodeficiency states
    • Metastatic malignancy
A

Chronic Primary Adrenal Insufficiency (Addison’s Disease)

Clinical Features of Addisons:

  • Fatigue, weakness
  • Gastrointestinal symptoms
    • Nausea, vomiting, weight loss, diarrhea
  • Hyponatremia, hyperkalemia, volume depletion
  • Hyperpigmentation
    • decrease in glucocorticoids = increase in ACTH
      • because of the feedback inhibition loop
      • so result is hyperpigmentation
32
Q

Identify this adrenal problem:

  • Clinical EMERGENCY
  • Intractable vomiting, abdominal pain
  • Hypotension, vascular collapse, coma
  • Causes
    • Sudden withdrawal of long-term steroid therapy
      • you need to take people off steroids gradually
    • Adrenal hemorrhage
      • Coagulopathy
      • Sepsis (Waterhouse-Friedrichsen syndrome)
    • Acute stress in chronic adrenal insufficiency (Addisonian crisis)
A

Acute Adrenocortical Insufficiency

33
Q
  • Neoplastic hypersecretion
  • Neuroendocrine tumor, nodular
  • Arises from chromaffin cells of adrenal medulla
  • Usually secrete catecholamines; hypertension is usual symptom
  • “The 10 percent tumor”
    • 10 percent bilateral
    • 10 percent malignant
    • 10 percent extra-adrenal
    • 10 percent in children
A

Pheochromocytoma

34
Q

Identify this hormone:

  • Polypeptide hormone; 84 amino acids
  • Effects: Increase serum calcium, decrease serum phosphate
    • Increase in osteoclast activity
    • Promotes renal tubule retention of calcium and GI absorption of calcium
    • Promotes renal phosphate excretion
    • Promotes renal activation of vitamin D
  • Secretion of this is stimulated by low ionized calcium and inhibited by increased ionized calcium
A

Parathyroid Hormone (PTH)

35
Q

Identify:

  • Increase in PTH
  • Primary– actual problem in the parathyroid gland
    • Parathyroid hyperplasia or neoplasia
    • Hypercalcemia, hypophosphatemia
    • Clinical effects:
      • Skeletal abnormalities (“painful bones”)
      • “Renal stones”
      • Gastrointestinal problems (“abdominal groans”)
      • Depression, lethargy (“psychic moans”)
      • Neuromuscular (weakness, hypotonia)
  • Secondary
    • Increased PTH due to hypocalcemia; most common cause is chronic renal failure
A

Hyperparathyroidism

36
Q

What is this second most common cause of primary hyperparathyroidism?

  • 15-20% of primary hyperparathyroidism cases
  • Usually all four glands similarly enlarged-symetrical
  • Occasionally asymmetrical (pseudoadenomatous) gland enlargement
  • Functional parathyroid
A

Parathyroid Hyperplasia/neoplasia

37
Q

What is this most common cause of hyperparathyroidism?

  • About 80% of cases of primary hyperparathyroidism
  • One gland enlarged, the other three normal to atrophic
    • Limited to one gland
  • Surgeon can just remove the one gland and the pt is cured
  • functional parathyroid
A

Parathyroid Adenoma

38
Q

What is this least common cause of hyperparathyrodism?

  • Rare (less than 5% of cases of primary hyperparathyroidism)
  • PTH levels may be massively elevated
    • ​over 10,000
  • Diagnostic criteria:
    • Invasion of adjacent tissue
      • Difficult surgical dissection
        • because it is invading surrounding tissues
    • Fibrosis
    • Mitotic activity
  • Functional parathyroid
A

Parathyroid Carcinoma

39
Q

What are some causes decreased PTH?

A
  • Feedback inhibition by non-PTH causes of hypercalcemia
    • Most common is malignancy-associated hypercalcemia
  • Hypoparathyroidism
    • Hypocalcemia and hyperphosphatemia due to decreased PTH
    • Cause: usually surgical removal of parathyroid glands-iatrogenic
      • Treatment of parathyroid hyperplasia
      • Complication of thyroidectomy
    • Effects
      • Muscle hypertonia (spasms, tetany, tingling)
      • Cardiac arrythmias
40
Q

What are the thyroid gland hormones?

A
  • Thyroid Hormones
    • Thyroxine (T4)
      • Main thyroid hormone in blood
    • Triiodothyronine (T3)
      • Lesser amounts inblood than T4
      • More active than T4
  • Calcitonin
    • Synthesized by parafollicular cells (C cells)
    • Regulates calcium metabolism
      • Inhibits osteoclast activity
      • Promotes calcium uptake by bone
41
Q

What are the thyroid-associated proteins?

A
  • Thyroid binding globulin (TBG)
    • Protein transport; most serum T4 and T3 bound to TBG
    • Only unbound (free) hormone (FT4 or FT3) is biologically active
  • Thyroglobulin
    • Storage form of thyroid hormone in thyroid gland
    • Main component of colloid
42
Q

What are thyroid hormone effects?

A
  • Speeds everything up!!
  • Increase of basal metabolic rate
    • Increase of carbohydrate and lipid catabolism
    • Stimulation of protein synthesis
    • Stimulation of glucose absorption
  • Increase in cardiac output
  • Growth effects
43
Q

What are these clinical effects of?

  • General
    • Heat intolerance
    • Weight loss/increased appetite
  • Cardiac
    • Palpitations/tachycardia
    • Arrythmias
  • Gastrointestinal
    • Hypermotility
    • Malabsorption, diarrhea
  • Skin
    • Warm, moist skin
    • Sweating
  • Neuromuscular
    • Nervousness, irritability
    • Tremor
    • Muscle weakness
A

Hyperthyroidism –things are going to fast

44
Q

How do you diagnosis Hyperthyroidism?

A
  • Decreased TSH (primary)
    • because its not enough to inhibit the TH
  • Increased FT4
    • T3 toxicosis-decreased FT4, increased T3

These tests tell us what type

  • Radioactive iodine uptake (RAIU)
    • Diffuse increase-Graves disease
    • Focal/nodular uptake-toxic goiter/adenoma (“hot nodule”)–locally
    • Decreased uptake-thyroiditis (early stage), factitious (pt taking TH medication and its too much)
45
Q

What is this most common cause of hyperthyroidism?

  • Typically young to middle aged women
  • Etiology: autoimmune
  • Clinical features:
    • Hyperthyroidism–>increase in TH secretion
    • Opthalmapathy
      • proptosis–due to increased retrorbital tissue
    • Dermopathy
      • skin manifestation which are least common
A

Graves Disease

46
Q

How do you treat Grave’s Disease?

A
  • Surgery-thyroidectomy
  • Life long thyroid replacement therapy
  • Radioactive iodine treatment
  • Drugs
    • Beta blockers (propranolol, etc)
    • Antithyroid drugs
    • Propylthiouracil (PTU)
    • Methimazole (tapazole)
47
Q

Identify:

  • Acute, severe hyperthyroidism
  • Most commonly a complication of Graves disease
  • MEDICAL EMERGENCY!
    • Death from cardiac arrythmia or cardiac failure
  • Usually markedly elevated T4
A

Thyroid Storm

48
Q

What are some clinical effects of hypothyroidism?

A
  • General
    • Cold intolerance
    • Listlessness
    • Weight gain
  • Cardiac
    • Bradycardia
    • Pericardial effusion
  • Skin
    • Dry skin/decreased sweating
    • Brittle hair
    • Mucopolysaccharide accumulation (myxedema)
  • Neuromuscular
    • Slow reflexes
  • Gastrointestinal
    • Decreased motility/constipation
49
Q

What are these causes of?

  • Primary
    • Therapeutic ablation (thyroidectomy, radioactive iodine)–iatrogenic
    • Hashimoto’s thyroiditis
    • Dietary iodine deficiency–then we cant make TH
      • Cretinism-development of hypothyroidism in utero or infancy/childhood
    • Dyshormonogenetic goiter
    • Drugs (lithium, p-aminosalicylic acid)
  • Secondary (hypopituitarism)
A

Hypothyroidism

50
Q

How do you diagnosis and treat Hypothyroidism?

A
  • Diagnosis
    • Increased TSH-most sensitive test!!!
    • Decreased T4
  • Treatment-thyroxine
  • We will see increase in TSH before we see decrease in T4
51
Q

What is thyroid problem?

  • Autoimmune destruction of gland
    • inflammation of thyroid gland that eventually takes over the gland
  • Common cause of hypothyroidism
    • May have transient hyperthyroidism initially
  • Typically middle aged to elderly women
  • Morphology
    • Diffuse (occasionally nodular) enlargement of gland
    • Marked lymphocytic infiltration with hurthle cells
  • Diagnosis: antithyroid antibodies–specific Igs we measue when we suspect this disease
  • Complications
    • Lymphoma
    • Papillary carcinoma
A

Chronic Lymphocytic Thyroiditis (Hashimoto’s)

52
Q

What is this type of Thyroiditis?

  • Probably viral infection
  • Symptoms: pain, ENLARGED AND PAINFUL
  • self-resolving
  • Euthyroid; usually resolves in several weeks
A

Subacute–DeQuervain’s

53
Q

What is this type of thyroiditis?

  • Destruction of gland by cellular fibrous tissue
  • Clinically, hard mass; often mimics tumor
  • Autoimmune etiology; rare
A

Fibrosing (Riedel’s)

–he didnt really talk about this

54
Q

What is the MOST COMMON ENLARGEMENT of the thyroid gland?

  • Endemic—in areas of iodine deficiency
  • Sporadic—most common cause of thyroid enlargement
    • `3-5% incidence
    • Euthyroid-normal
    • `Multiple nodules, varying sizes
      • “Dominant” nodule
        • one that is significantly bigger than other ones
  • Marked variation in follicle size
  • Nodules without fibrous capsule
  • Secondary changes
    • Hemorrhage
    • Fibrosis
    • Calcification
    • Cystic degeneration
A

Nodular Hyperplasia (“Goiter”)

55
Q

What is the MOST COMMON THYROID TUMOR?

  • Usually nonfunctional
    • “cold” or “warm” on iodine scan
      • cold on iodine scan because not functional
    • “Hot” nodules rarely malignant
  • Usually solitary nodule with thin fibrous capsule
    • Entirely bounded by fibrous capsule
A

Follicular Adenoma

56
Q

What is this cancer of the thyroid?

  • Incidence—5-15% of all thyroid malignancies
  • More common in iodine- deficient areas
  • Minimally invasive or widely invasive
  • Metastases—usually bloodborne (lung, bones)
  • Ras point mutation in about 50%
  • Histology-same as adenoma, with capsular/vascular invasion–>inorder to diagnosis this you have to be able to see the vascular invasion because it looks so simalr to an adenoma
A

Follicular Carcinoma

57
Q

What is this tumor of the thyroid?

  • “Follicular tumor with oncocytic features”
  • >75% oncocytes
    • large cell with a lot of cytoplasma, and cytoplasm is granular = lots of mitochondria
  • Gross-brown color
  • Adenoma/carcinoma differential diagnosis same as for follicular tumors
  • if this is malignant than it is considered 20% of all follicular carcinomas
A

Hurthle Cell Tumors

58
Q

What is the most common malignant tumor of the thyroid?

  • 65-80% of all thyroid cancers in U.S.
    • >90% in children
  • Gross-usually ill-defined, unencapsulated
  • Spread and metastasis
    • Extrathyroid local spread
    • Cervical lymph nodes
      • spread via lymphatics!
    • Distant metastasis very uncommon
  • Nuclear abnormalities
    • Optically clear (“Orphan Annie”) nuclei
    • Nuclear grooves
    • Intranuclear cytoplasmic inclusions (INCIs)
  • Psammoma bodies
  • Oncogenes
    • RET/PTC (chromosome 10)
    • BRAF (chromosome 7)
A

Papillary Carcinoma

Can be a Cystic Papillary Carcinoma

  • About 10% of all PCT have marked cystic change
  • Node metastases may be cystic
  • Differential diagnosis is cystic goiter
59
Q

What is this Highly malignant tumor of they thyroid?

  • rapid growth and wide invasion
  • Elderly patients (>50 yrs)
  • May have squamous, sarcomatoid, or giant cell appearance
  • Often coexist with (arise from) better differentiated thyroid tumors
  • Very poor prognosis
    • most thyroid tumors have good prognosis except this one
A

Undifferentiated (Anaplastic) Carcinoma

60
Q

What is this tumor of the thyroid?

  • Tumor of parafollicular cells (C cells-secrete calcitonin)
  • Two types
    • Sporadic—70-80% of cases, usually >45 yrs
      • nodes are solitary
    • Familial—younger age group, better prognosis, associated with C cell hyperplasia
      • nodes are multiple or solitary
      • Associated with:
        • MEN IIA or IIB
        • Germline mutations of RET oncogene
  • Overall 5 year survival 70-80%
  • See Amyloid
  • To diagnosis look for calcitonin, CEA, neuroendocrine markers
  • frequently mets to cervical nodes and may show distant mets
A

Medullary Carcinoma (MCT)

61
Q

What is this thyroid tumor?

  • Highly associated with lymphocytic thyroiditis (80%)
  • Most are large B-cell lymphomas
    • Other common types—low grade follicular, marginal zone
  • Clinical—rapid enlargement of thyroid, often in patient with history of thyroiditis
A

Thyroid Lymphoma

62
Q

What is this thyroid tumor?

  • A group of familial syndromes characterized by tumors or hyperplasia in multiple endocrine organs
  • Autosomal dominant
  • Associated with described chromosomal abnormality
  • _____ compared to non-______ tumors:
    • Younger age
    • Multifocal
    • Tumors often preceded by hyperplasia
A

Multiple Endocrine Neoplasia (MEN)

Pathology Exam 6 (FINAL :)) (4 decks)

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