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PATHOLOGY 2 > Endocrine system > Flashcards

Endocrine system Flashcards

1
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    ADENOHYPOPHYSIS hormones
A
  • CRH ⇒ ACTH and MSH
  • GHRH ⇒ GH
  • GnRH ⇒ FSH and LH
  • Dopamine ⇒ PRL
  • TRH ⇒ TSH
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2
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    HYPOPITUITARISM etiology
A
  • Congenital
  • Acquired
    • nonfunctioning pituitary adenomas compressing the whole gland
    • ischemic injury ⇒ Sheehan syndrome
    • surgery
    • radiation
    • inflammatory reactions
    • trauma
    • metastatic neoplasms
    • hypothalamic disorders
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3
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    HYPOPITUITARISM clinical features
A
  • GH ⇒ pituitary dwarfism
  • GnRH ⇒ amenorrhea, infertility, decreased libido, impotence, loss pf pubic + axillary hair
  • TSH ⇒ hypothyroidism
  • ACTH ⇒ hypoadrenalism
  • Prolactin ⇒ failure of postpartum lactation
  • MSH ⇒ pallor from loss of stimulatory effects on melanocytes
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4
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    HYPERPITUITARISM causes
A
  • adenoma in anterior lobe
  • hyperplasia
  • carcinoma
  • extra pituitary tumors
  • hypothalamic disorders
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5
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    HYPERPITUITARISM classification based on hormones produced
A
  • Corticotroph ⇒ ACTH
    • tumor type: densely granulated + sparsely granulated
    • cushing + nelson syndrome
  • Somatotroph ⇒ GH
    • densely + sparsely granulated
    • Gigantism + acromegaly
  • Lactotroph ⇒ Prolactin
    • densely + sparsely granulated
    • galactorrhea, amenorrhea, sexual dysfunction, infertility
  • Mammosomatotroph ⇒ Prolactin, GH
    • mammosomatotroph
    • combined GH and prolactin excess
  • Thyrotroph ⇒ TSH
    • thyrotroph
    • hyperthyroidism
  • Gonadotroph ⇒ FSH, LH
    • gonadotrophy, “null cell” oncocytic adenomas
    • hypogonadism, hypopituitarism
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6
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    HYPERPITUITARISM pathogenesis
A
  • Gs encoded by GNAS1
  • G-protein mutations ⇒ alpha-subunit mutated ⇒ constitutive activation of Gsalpha ⇒ persistent generation of cAMP ⇒ unchecked cell proliferation
  • Familial MEN-1 syndrome ⇒ mutation in MEN-1 gene
  • activating mutation of RAS oncogene, overexpression of CMYC, inactivation of NM23
  • p53 mutations
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7
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    HYPERPITUITARISM morphology
A
  • well-circumscribed, soft lesions
  • if small ⇒ constrained to sella turcica
  • larger lesion ⇒ compress optic chiasma ⇒ extend into cavernous and sphenoidal sinuses
  • nonencapsulated, infiltrate bone, dura and brain
  • Histo: uniform, polygonal cells, arranged in cheers, cords or papillae
    • nuclei pleiomorphic
    • mitotic acitvity rare
    • cellular monomorphism + absence of reticulin
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8
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    PROLACTINOMA
A
  • range: microadenoma ⇒ large expandable tumors
  • hyperprolactinemia causes:
    • amenorrhea
    • galactorrhea
    • loss of libido
    • infertility
  • symptoms more subtle in men + older women
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9
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    GH-PRODUCING ADENOMAS
A
  • large before diagnosed ⇒ clinical symptoms increased GH may be subtle
  • stimulates hepatic secretion of insulin-like GF 1
    GIGANTISM
    • prepubertal children
    • increased body size
      ACROMEGALY:
    • after closure of epiphysis
    • gowth in soft tissues, skin, viscera + bones in face, hands and feet
      OTHER DISTURBANCES:
    • abnormal glucose tolerance
    • DM
    • muscle weakness
    • HT
    • arthritis
    • osteoporosis
    • congestive HF
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10
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    CORTICOTROPHIN CELL ADENOMA
A
  • microadenomas
  • stain positive with PAS ⇒ accumulation of glycosylated ACTH protein
  • clinically silent
  • cause Hypercortisolism (Cushing syndrome)
    NELSON SYNDROME:
    • develops after surgical removal of adrenal glands
    • occurs bc loss of inhibitory effect of adrenal corticosteroids on preexisting corticotrophin micro adenoma
    • hypercortisolism doesn’t develop
      CUSHING DISEASE:
    • hypercorticosolism is due to excessive production of ACTH
      ⇒ hyperpigmentation
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11
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    GONADOTROPH ADENOMA
A
  • difficult to recognize ⇒ secrete hormones inefficiently and variably
  • found in middle-aged men and women
  • cause neurologic symptoms
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12
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    THYROTROPH ADENOMA
A
  • rare cause of hyperthyroidism
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13
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    NONFUNCTIONING PITUITARY ADENOMA
A
  • clinically silent forms of functioning adenomas and true hormone-negative adenomas
  • typical presentation is mass effect
  • compromise remaining adenohypophysis ⇒ hypopituitarism
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14
Q
  1. Hypo- and hyper function of the hypothalamic-hypophyseal system:
    NEUROHYPOPHYSIS diseases
A
  1. SIADH:
    - increased ADH
    - hyponatremia
    - cerebral edema
    - neurologic dysfunction
  2. Diabetes insipidus:
    - brain trauma
    - neoplasm
    - idiopathic
    - increased diluted urine
    - hypernatremia
    - thirst
    - polydipsia
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15
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

THYROIDITIS

A

CLINICAL TYPES:
1. acute illness with severe thyroid pain
2. little inflammation + thyroid dysfunction
TYPES:
1. Hashimoto thyroiditis
2. De Quervain thyroiditis
3. Subacute lymphocytic thyroiditis

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16
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

HASHIMOTO THYROIDITIS general + pathogenesis

A
  • chronic lymphocytic thyroiditis
  • gradual thyroid failure due to autoimmune destruction
  • age: 45-65 yrs
  • predominance: women 10:1
  • cause of goiter in small children
    PATHOGENESIS:
    • progressive depletion of thyroid epithelial cells ⇒ replaced by fibrosis
    • CD8+ T cell mediated cell death
    • cytokine mediated cell death- excessive T cell activation ⇒ cytokines ⇒ activate macrophages ⇒ damage follicles
    • binding of antithyroid AB ⇒ AB-dependent cell-mediated cytotoxicity
    • HLA-DR3 and HLA-DR5 alleles
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17
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

HASHIMOTO THYROIDITIS morphology + clinical features

A 
MORPHOLOGY:
  - painless enlargement, symmetric + diffuse
  - pale, grey-tan, firm tissue, friable
  - follicles atrophied + lined by oxyphil cells
  - increased interstitial CT
CLINICAL FEATURES:
  - hypothyroidism develops gradually
  - transient thyrotoxicosis
  - increased risk for B cell NHL
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18
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

DE QUERVAIN THYROIDITIS general + morphology

A
  • age: 30-50yrs
  • female predominance
  • caused by viral infection or postviral inflammatory process
  • inflammatory process is limited
    MORPHOLOGY:
    • firm gland, intact capsule, uni-or bilaterally enlarged
    • infiltrate: lymphocytes, plasma cells, macrophages
    • granulomatous reaction with giant cells
    • healing ⇒ resolution of inflammation + fibrosis
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19
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

DE QUERVAIN THYROIDITIS clinical features

A
  • acute onset
  • pain in neck, fever, malaise
  • enlargement of thyroid
  • transient hyperthyroidism
  • increased leukocyte count + ESR
  • transient hypothyroidism
  • self-limited ⇒ recovery in 6-8 weeks
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20
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

SUBACUTE LYMPHOCYTIC THYROIDITIS

A
  • silent + painless thyroiditis
  • disease follows pregnancy ⇒ postpartum thyroiditis
  • autoimmune disease ⇒ antithyroid ABs
  • affects middle aged women
    CLINICAL FEATURES:
    • initial phase thyrotoxicosis
    • return to normal after few months
    • increased risk for reoccurrence
    • leads to hypothyroidism
    • mild enlargement
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21
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

RIEDEL THYROIDITIS

A
  • extensive fibrosis involving thyroid + neck structures
  • hard + fixed thyroid mass
  • associated with idiopathic fibrosis in other body sites
  • antithyroid ABs ⇒ autoimmune disease
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22
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

PALPATION THYROIDITIS

A
  • cause: vigorous clinical palpation of gland ⇒ multifocal follicular disruption
  • incidental finding
  • no abnormalities in function
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23
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

HYPOTHYROIDISM etiology

A 
PRIMARY:
 - surgery, radioiodine therapy, external radiation
 - Hashimoto thyroiditis
 - Iodine deficiency
 - drugs
 - developmental abnormalities of thyroid
 - congenital biosynthetic defect
SECONDARY:
 - pituitary of hypothalamic failure
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24
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

CRETINISM

A
  • severly shunted physical and mental growth
  • due to congenital deficiency of thyroid hormones due to maternal nutritional deficiency of iodine
  • sporadic cretinism= inborn errors in metabolism ⇒ interfere with synthesis of thyroid hormone
    CLINICAL FEATURES:
    • skeletal system: short stature, coarse facial features, protruding tongue, umbilical herniation
    • CNS: mental retardation
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25
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

MYXEDEMA

A
  • in older children + adults
  • generalized apathy + mental sluggishness ⇒ listless, cold intolerant, obese
  • mucopolysaccharide rish edema accumulated in skin, subcutaneous tissue and visceral sites
    ⇒ coarse facial features, enlarged tongue, deep voice
    ⇒ decreased bowel motility ⇒ constipation
    ⇒ HF
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26
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

HYPOTHYROIDISM diagnosis

A
  • laboratory evaluation
  • measure serum TSH (increased in primary hypothyroidism)
  • serum T4 decreased
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27
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

HYPERTHYROIDISM etiology

A 
PRIMARY:
 - diffuse toxic hyperplasia ⇒ graves disease
 - hyperfunctioning multinodular goiter
 - hyperfunctioning adenoma
SECONDARY:
 - TSH secreting pituitary adenoma
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28
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

HYPERTHYROIDISM clinical features

A
  1. Constitutional symptoms:
    - skin: soft, warm, flushed, heat intolerance, excessive sweating
    - weight loss even though increased appetite
  2. GI:
    - hypermotility, malabsorption, diarrhea
  3. Cardiac:
    - palpitations, tachycardia, congestive HF
  4. Neuromuscular:
    - nervousness, tremor, irritability, proximal muscle weakness
  5. Ocular:
    - wide, staring gaze, lid lag
    - ophthalmopathy + exophthalmos in Graves
  6. Thyroid storm:
    - abrupt onset of hyperthyroidism
    - medical emergency
  7. Apathetic:
    - thyrotoxicosis in elderly ⇒ unexplained weight loss + worsening cardiovascular disease
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29
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

GRAVES DISEASE/ BASEDOW DISEASE epidemiology

A
  • peak incidence: 20-40 yrs
  • female predominance 7:1
  • genetic factors:
    • family members in risk
    • HLA-DR3
    • CTLA4 and PTPN22 polymorphism
30
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

GRAVES DISEASE/ BASEDOW DISEASE pathogenesis

A
  • autoimmune disease
  • Autoantobodies:
    1. Thyroid-stimulating Ig
    • IgG ⇒ bind TSH receptor ⇒ stimulate adenylyl cyclase ⇒ increased release of hormone
    • specific for Graves disease
      2. Thyroid growth- stimulating Ig:
    • directed against TSH receptor
    • proliferation of thyroid follicular epithelium
      3. TSH-binding inhibitor Ig:
    • prevent TSH from binding ⇒ stimulate/ inhibit
31
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

GRAVES DISEASE/ BASEDOW DISEASE morphology

A
  • diffuse enlargement of thyroid - smooth and symmetric ⇒ diffuse hypertrophy + hyperplasia of thyroid follicular cells
  • Histo: follicular epithelial cells are tall, columnar + crowded ⇒ form papillae
  • extrathyroid tissues:
    • lymphoid hyperplasia
    • ophthalmopathy ⇒ retro-orbital CT and extraocular muscles is increased + edematous
32
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

GRAVES DISEASE/ BASEDOW DISEASE clinical features

A
  • diffuse hyperplasia of thyroid
  • ophthalmopathy ⇒ exophthalmos
  • dermopathy ⇒ pretibial myxedema
  • elevated serum free T3 and T4
  • decreased serum TSH
33
Q
  1. Thyreoiditis, hypo- and hyper function of thyroid gland:

GOITER

A 
= enlargement of thyroid gland
TYPES:
1. Diffuse 
2. Multinodular
PATHOGENESIS:
 - iron deficiency ⇒ impaired hormone synthesis ⇒ rise in serum TSH ⇒ hypertrophy + hyperplasia of follicular cells ⇒ enlargement
CLINICAL FEATURES:
  - enlarged gland
  - airway obstruction, dysphagia, compression of neck vessels
34
Q
  1. Tumors of thyroid gland:

CLINICAL CRITERIA FOR THYROID NODULES

A

More likely to be neoplastic:

  1. solitary nodules
  2. nodules in younger patients
  3. nodules in males
  4. history of radiation treatment to head and neck region
  5. nodules don’t take up radioactive iodine in imaging studies
35
Q
  1. Tumors of thyroid gland:

ADENOMAS general + pathogenesis

A
  • benign neoplasm ⇒ derive from follicular epithelium
  • usually solitary
  • non-functional or toxic adenomas ⇒ secrete thyroid hormone
    PATHOGENESIS:
    • Toxic adenomas ⇒ TSH receptor signaling pathway:
    • activating somatic mutation (in receptor or Gsalpha)⇒ chronic overproduction of cAMP ⇒ cells produce that gave growth advantage ⇒ clonal expansion of epithelial cells ⇒ produce thyroid hormone
    • Point mutation in RAS family (⇒ might progress to carcinoma)
36
Q
  1. Tumors of thyroid gland:

ADENOMAS morphology + clinical features

A 
MORPHOLOGY:
  - solitary, spherical lesion
  - well-demarcated by intact capsule
  - cells arranged in uniform follicles, contain colloid
CLINICAL FEATURES:
  - painless nodules
  - large mass ⇒ local symptoms
  - toxic adenoma ⇒ thyrotoxicosis
  - excellent prognosis, do not recur or metastasize
DIAGNOSIS:
  - Radionuclide scanning:
    * adenoma ⇒ cold nodules
    * toxic adenoma ⇒ warm nodules
  - ultrasonography
  - fine-needle aspiration biopsy
37
Q
  1. Tumors of thyroid gland:

CARCINOMA general + pathogenesis

A
  • female predominance ⇒ early-middle adult years
  • equal predominance ⇒ childhood, late adult years
  • derived from follicular epithelium (medullary cc ⇒ parafollicular cells)
    PATHOGENESIS:
    1. Genetic factors:
    • in both familial and non familial forms
      2. Environmental factors:
    • exposure to ionizing radiation during first 20yrs
38
Q
  1. Tumors of thyroid gland:

PAPILLARY CARCINOMA pathogenesis

A
  • previous exposure to ionizing radiation
    1. Chromosomal rearrangement of RET or NTRK1 genes
    • rearrangement ⇒ fusion gene RET/PTC ⇒ activate RET and MAP kinase
      2. Activating point mutation in BRAF
    • produces intermediate products in MAP kinase pathway
39
Q
  1. Tumors of thyroid gland:

PAPILLARY CARCINOMA morphology + clinical features

A 
MORPHOLOGY:
 - solitary/ multifocal
 - well-circumscribed + encapsulated / infiltrative
 - cystic with fibrosis + calcification
 - Nuclear features:
  * nuclei finely dispersed chromatin ⇒ Ground glass
  * invagination in cytoplasm
  * papillary architecture + psammon bodies
CLINICAL FEATURES:
  - nonfunctional tumors
  - painless mass in neck
  - metastasis: cervical LN, lung
  - 10yr survival ⇒ 95%
40
Q
  1. Tumors of thyroid gland:

FOLLICULAR CARCINOMA general + pathogenesis

A
  • female predominance
  • peak age 40-60yrs
  • increased in areas of dietary iodine deficiency
    PATHOGENESIS:
    • mutation in PI3/AKT oncogenic signaling pathway ⇒ induces RAS, PIK3CA, PTEN
    • translocation between PAX8 and PPARG ⇒ fusion
41
Q
  1. Tumors of thyroid gland:

FOLLICULAR CARCINOMA morphology + clinical features

A 
MORPHOLOGY:
  - uniform cells ⇒ small follicles
  - widely invasive or minimally invasive
CLINICAL FEATURES:
  - solitary cold thyroid nodules
  - may be hyper functional
  - metastasize hematogenously ⇒ lungs, bone, liver
  - treatment: surgical excision
42
Q
  1. Tumors of thyroid gland:

MEDULLARY CARCINOMA general + pathogenesis

A
  • neuroendocrine neoplasms derived from parafollicular cells
  • peak incidence 40-50yrs
  • secrete calcitonin
    PATHOGENESIS:
    • sporadically
    • familial ⇒ MEN-2
    • RET proto-oncogene mutations
43
Q
  1. Tumors of thyroid gland:

MEDULLARY CARCINOMA morphology + clinical features

A

MORPHOLOGY:
- solitary or multiple
- large lesions ⇒ hemorrhage + necrosis areas
- polygonal- spindle shaped cells ⇒ form nests or follicles
- amyloid deposits in stroma
- calcitonin
- multicentric C cell hyperplasia in familial form
CLINICAL FEATURES:
- mass in neck ⇒ compression effect
- secretion of peptide hormone

44
Q
  1. Tumors of thyroid gland:

ANAPLASTIC CARCINOMA general + pathogenesis

A
  • among most aggressive human neoplasms
  • mean age 65yrs
    PATHOGENESIS:
    • arise de novo or dedifferentiation of well-differentiated papillary or follicular carcinoma
    • mutations in RAS or PIK3CA
    • point mutation in p53
45
Q
  1. Tumors of thyroid gland:

ANAPLASTIC CARCINOMA morphology + clinical features

A

MORPHOLOGY:
- bulky masses, grow fast
- highly anaplastic cells:
* large, pleomorphic giant cells
* spindle cells with sarcomatous appearance
* mixed spindle and giant cell lesions
CLINICAL FEATURES:
- grow with wild abandon despite therapy
- metastasis common
- death within <1yrs ⇒ aggressive local growth + compression of vital structures

46
Q
  1. Pathology of parathyroid gland:

PATHOLOGY OF PARATHYROIDS

A
  1. Hyperparathyroidism
  2. Hypoparathyroidism
  3. Adenoma
  4. Carcinoma
  5. Hyperplasia
    ⇒ hypercalcemia:
    ⇒ Recklinghausens disease
    ⇒ Metastatic calcification
    ⇒ Nephrolithiasis
47
Q
  1. Pathology of parathyroid gland:

PRIMARY HYPERPARATHYROIDISM general + pathogenesis

A 
CAUSES:
  - adenoma
  - primary hyperplasia
  - parathyroid carcinoma
  - familial: MEN-1, MEN2A
PATHOGENESIS:
1. Cyclin D1 gene inversions
  - chromosomal inversion of chr11 ⇒ relocation of cyclin D1 ⇒ next to PTH gene ⇒ abnormal expression ⇒ increased proliferation
2. MEN1 gene mutation
48
Q
  1. Pathology of parathyroid gland:

PRIMARY HYPERPARATHYROIDISM morphology

A
  1. Solitary adenoma:
    - well-circumscribed, soft, tan nodule + capsule
    - single gland
    - chief cells
    - endocrine atypia
  2. Parathyroid hyperplasia:
    - multi gland process
    - chief cell hyperplasia
    - glycogen accumulation in cytoplasm
  3. Parathyroid carcinoma:
    - circumscribed or invasive
    - enlarge gland + grey-white irregular masses
    - uniform cells + dense fibrinous capsule surrounding
    - invasion of surroundings + metastasis
  4. Skeleton:
    - increased osteoclastic activity ⇒ erosion of bone matrix ⇒ osteotitis fibrosa cystica
  5. Kidney:
    - kidney stones, calcification
49
Q
  1. Pathology of parathyroid gland:

PRIMARY HYPERPARATHYROIDISM clinical features

A
  • female predominance 3:1
  • adults
  • increased serum ionized calcium
  • paraneoplastic syndrome
  • parathyroid hyper function ⇒ serum PTH elevated
  • painful bones, renal stones, abdominal groans, psychic moans
  • osteoporosis
  • GI: constipation, nausea, peptic ulcer, pancreatitis, gallstones
  • CNS: depression, lethargy, seizures
  • Neuromuscular: weakness, hypotonia
  • Polyuria, polydipsia
50
Q
  1. Pathology of parathyroid gland:

SECONDARY HYPERPARATHYROIDISM renal failure

A
  • chronic renal insufficiency ⇒ decreased phosphate excretion ⇒ hyperphosphatemia ⇒ depress Ca2+ levels ⇒ stimulate parathyroid gland activity
  • loss of renal substance ⇒ reduce alpha1-hydroxylase ⇒ reduces intestinal absorption of Ca2+
51
Q
  1. Pathology of parathyroid gland:

SECONDARY HYPERPARATHYROIDISM morphology + clinical features

A 
MORPHOLOGY:
  - glands hyperplastic
   * chief cells or water clear cells  
   * less fat cells
  - bone changes similar to primary hyperparathyroidism
  - metastatic calcifications
CLINICAL FEATURES:
  - bone abnormalities
  - serum Ca normal 
  - metastatic calcification of blood vessels ⇒ ischemic damage to skin + organs (calciphylaxis)
52
Q
  1. Pathology of parathyroid gland:

HYPOPARATHYROIDISM

A

CAUSES:
- surgically induced ⇒ inadvertent removal of parathyroids during thyroidectomy
- congenital absence (Di George syndrome)
- autoimmune hypoparathyroidism
CLINICAL FEATURES:
- secondary to hypocalcemia
- increased neuromuscular irritability: tingling, muscle spasm, facial grimacing, carpopedal spasm
- cardiac arrhytmias
- increased ICP + seizures

53
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

HYPERCORTICOLISM (CUSHING SYNDROME) general

A

= caused by condition that elevates glucocorticoid levels
CAUSES:
1. exogenous administration of glucocorticoids
2. endogenous
* primary hypothalamic-pituitary disease + hyper secretion of ACTH ⇒ Cushing disease
- pituitary adenoma / hyperplasia
* primary adrenal neoplasms + primary cortical hyperplasia ⇒ Cushing syndrome
* ectopic ACTH secretion by non-endocrine neoplasm ⇒ Cushing syndrome
- small cell cc in lung

54
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

HYPERCORTICOLISM (CUSHING SYNDROME) morphology + clinical features

A 
MORPHOLOGY:
- pituitary:
  - crooke hyaline change ⇒ keratin filament accumulated in cytoplasm
- adrenal gland:
  - cortical atrophy
  - diffuse hyperplasia
  - nodular hyperplasia
  - adrenocortical adenoma
CLINICAL FEATURES:
  - HT
  - weight gain
  - buffalo hymp + moon face
  - hyperglycemia- glucosuria- polydispia
  - cutaneous striae
  - osteoporosis
  - menstrual abnormalities
  - mental distrubance
55
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

HYPERALDOSTERONISM

A
  • excessive aldosterone secretion ⇒ sodium retention + potassium excretion
  • Primary: aldosterone producing adrenocortical neoplasm or hyperplasia
  • Secondary: RAA due to:
    • decreased renal perfusion
    • arterial hypovolemia + edema
    • pregnancy
      MORPHOLOGY:
  • adenoma ⇒ Conn syndrome
    • solitary+ encapsulated
    • spironolactone bodies
  • hyperplasia ⇒ bilateral, nodular
    TREATMENT: surgery + aldesterone antagonist
56
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

ADRENOGENITAL SYNDROME

A 
CAUSE:
 - adrenogenital neoplasm 
 - congenital adrenal hyperplasia 
   * AR 
   * 21-OHase deficiency
   * 11B-OHase deficiency
CLINICAL FEATURES:
 - 21OHase deficiency:
  * female: masculinization, oligomenorrhea, hirsutism, acne
  * male: enlarged external genitalia, oligospermia
 - 11BOHase deficiency:
  * HT
57
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

PRIMARY ACUTE ADRENOCORTICAL INSUFFICIENCY

A
  • Waterhouse-Friderichsen syndrome: N. meningitis sepsis
  • Sudden withdrawal of long term corticosteroid therapy
  • Stress in patients with underlying chronic adrenal insufficiency
58
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

PRIMARY CHRONIC ADRENAL INSUFFICIENCY - ADDISON DISEASE

A
  • result of progressive destruction of adrenal cortex
  • Associated with:
    • autoimmune adrenilitis
    • TB
    • metastatic disease
    • amyloidosis
    • survivor of W-F syndrome
  • Symptoms:
    • hyper pigmented skin, hypotonia, hyponatremia, hyperkalemia
59
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

SECONDARY ADRENOCORTICAL INSUFFICIENCY

A
  • caused by disorder of hypothalamus and pituitary that reduces output of ACTH
    PRIMARY:
    • TB-granuloma, autoimmune- shrunken, metastasis-enlarged
    • increased ACTH precursor hormone-hyperpigmentation
    • decreased mineralocorticoid activity ⇒ hyperkalemia, hyponatremia, hypotension
      SECONDARY:
    • atrophy of cortex
    • no hyperpigmentation
    • deficient cortisol and androgen output ⇒ hypoglycemia
60
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

ADENOMAS

A

FUNCTIONAL:

  • glucocorticoid production ⇒ Cushing syndrome
  • mineralocorticoid production ⇒ Conn syndrome
  • yellow, small
  • non-functional
  • surgical removal
61
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

CARCINOMA

A
  • rare, large, invasive
  • necrosis, hemorrhage + cystic changes
  • invade surrounding vessels
  • give distant metastasis
  • poor prognosis
62
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

METASTASIS

A
  • from lung small cell cc ⇒ bilateral tumor

- other: stomach, breast

63
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

PHEOCHROMOCYTOMA

A
  • benign neoplasm composed of chromaffin cells ⇒ catecholamines ⇒ HT
  • 10%: malignant, extra-adrenal, bilateral, part of familial syndrome
    MORPHOLOGY:
    • well-circumscribed
    • yellow-brown color
    • hemorrhagic, necrosis, cystic
    • metastasis: regional LN, liver, lung, bone
      CLINICAL FEATURES:
    • HT + headache, sweating, tremor
    • pain in abdomen, chest, nausea, vomiting
    • urinary excretion of free catecholamines + metabolites
    • chromogranin A
64
Q
  1. Hypo- and hyper function and tumors of adrenal medulla:

NEUROBLASTOMA

A
  • childhood malignant tumor
  • age: 0-5 yrs
  • arise from neural crest cells in sympathetic ganglia + adrenal medulla
  • features: spontaneous regression + therapy induced maturation
    MORPHOLOGY:
    • varies in size, soft
    • dystrophic calcification, hemorrhage, necrosis
    • small round cells, undifferentiated, scant cytoplasm
    • Homer-Wright pseudo-rosettes
    • metastasis: liver, lung, bone
    • neuroblastoma ⇒ neuroganglioblastoma ⇒ ganglioneuroma
65
Q
  1. Multiple endocrine neoplasia (MEN) and carcinoid syndrome:
    MEN FEATURES
A
  • young age
  • arise in multiple endocrine organs
  • multifocal
  • preceeded by hyperplasia
  • aggressive and high recurrent
66
Q
  1. Multiple endocrine neoplasia (MEN) and carcinoid syndrome:
    MEN TYPE 1 (WERMER SYNDROME)
A
  • AD ⇒ mutation in chr 11q13
  • MEN1 gene is tumor suppressor gene ⇒ codes for menin protein
  • Organs involved: Parathyroid, Pancreas, Pituitary gland
    1. Parathyroid:
    • primary hyperparathyroidism ⇒ from hyperplasia
    • age 40-50yrs
      2. Pancreas:
    • pancreatic islet cell carcinoma
    • endocrine tumor ⇒ aggressive + metastatic disease or multifocal
    • often functional tumors
    • Zollinger-Ellison syndrome ⇒ gastrinoma, hypoglycemia ⇒ insulinoma
67
Q
  1. Multiple endocrine neoplasia (MEN) and carcinoid syndrome:
    MEN TYPE 2 general
A
  • activating mutations of the RET protooncogene
  • strong genotype-phenotype correlation
  • AD pattern
  • MEN2 gene located at 10q1.2
68
Q
  1. Multiple endocrine neoplasia (MEN) and carcinoid syndrome:
    MULTIPLE ENDOCRINE NEOPLASIA, TYPE 2A
A

= SIPPLE SYNDROME

  • organs involved: thyroid, adrenal medulla, parathyroid
    1. Thyroid:
    • medullary carcinoma
    • age 20yrs
    • multifocal, foci of C-cell hyperplasia
      2. Adrenal medulla:
    • pheochromocytoma
      3. Parathyroid:
    • parathyroid gland hyperplasia + primary hyperparathyroidism
69
Q
  1. Multiple endocrine neoplasia (MEN) and carcinoid syndrome:
    MULTIPLE ENDOCRINE NEOPLASIA, TYPE 2B
A

= MUCOSAL NEUROMA SYNDROME

  • organs involved: thyroid, adrenal medulla
    1. Thyroid:
    • thyroid medullary carcinoma
      2. adrenal medulla:
    • pheochromocytoma
      3. Extraendocrine:
    • ganglioneuromas of mucosal sites
    • marfanoid habitus
  • no hyperparathyroidism!!
70
Q
  1. Multiple endocrine neoplasia (MEN) and carcinoid syndrome:
    CARCINOID SYNDROME
A
  • slow-growing endocrine tumor, can metastasize.
  • location: ileum, appendix, lungs, resp tract
    PATHOPHYSIOLOGY:
    • endogenous secretion of serotonin + kallikrein ⇒ carcinoid syndrome
      PRECIPITATING EVENTS:
    • emotion
    • ingestion of specific foods
    • hot water
    • alcohol
    • surgery, induction of anesthesia
      CLINICAL FEATURES:
    • flusching, diarrhea, RS HF, bronchoconstriction, pellagra, malabsorption
    • treatment: surgery
      CRITERIA: size, angioinvasivity, infiltration, proliferative index (Ki67)

PATHOLOGY 2 (11 decks)

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