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OS4 > Endocrine Pathology > Flashcards

Endocrine Pathology Flashcards

1
Q

Causes of addision disease

A

Autoimmune destruction

TB

Metastatic carcinoma

Pituitary or hypothalamic disease

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2
Q

Symptoms of parathyroid adenoma

A
  • Most often results in asymptomatic hypercalcemia; however may present with consequences of increased PTH and hypercalcemia such as:
    • Nephrolithiasis
    • Nephrocalcinosis
    • CNS disbances
    • Constipation, peptic ulcer disease, and acute pancreatitis
    • Osteitis fibrosa cystica
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3
Q

Treatment for SIADH

A

Free water restriction

Demeclocycline

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4
Q

Neoplasms of MEN1

A

parathyroid hyperplasia

Pituitary adenoma

Tumors of islet cells

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5
Q

treatment for diabetes 2

A

Weight loss

Sulfonylureas or metformin

Exogenous insulin

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6
Q

How does hyperthyroidism increase basal metabolic rate?

A

Increased synthesis of Na+-K+ ATPase

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7
Q

3 layers of the adrenal cortex

A

Glomerulosa

Fasciculata

Reticularis

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8
Q

Diagnosis of pheochromocytoma

A

Increased metanephrines and catecholamines in serum and in urine

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9
Q

hashimoto increases risk for which neoplasmia?

A

B-cell (marginal zone) lymphoma; presents as an enlarging thyroid gland late in disease course

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10
Q

How does diabetes result in osmotic damage?

A
  • Glucose freely enters into Schwann cells, pericytes of retinal blood vessels, and the lens
  • Aldose reductase converts glucose to sorbitol, resulting in osmotic damge
  • Leads to peripheral neuropathy, impotence, blindness, and cataracts
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11
Q

Histo of type 2 diabetes mellitus

A

Amyloid deposition in the islets

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12
Q

How does prolactinoma present?

A

Galactorrhea and amenorrhea (females)

Decreased libido and headche (males)

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13
Q

Patients with type II diabetes mellitus have a risk for _____________

A

Hyperosmolar non-ketotic coma

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14
Q

benign proliferation of follicles surrounded by a fibrous capsule

A

Follicular adenoma

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15
Q

What are the ACTH levels, high dose dexamethasone results, imaging results, and treatment for Cushing syndrome as a result of ACTH-secreting pituitary adenoma?

A

ACTH: High; androgen excess may be present

High-dose dexamethasone: Suppresion

Imaging: Pituitary adenoma

Treatment: Transsphenoidal resection of pituitary adenoma; bilateral adrenalectomy in refractory cases can lead to enlargement of pituitary adenoma, resulting in hyperpigmentation, heaches, and bitemporal hemianopsia

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16
Q

Clinical presentation of diabetic ketoacidosis

A

Kussmaul respirations

Dehydration

Nausea

Vomiting

Mental status changes

Fruity smelling breath

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17
Q

hyperpigmentation (high ACTH) and hyperkalemia (low aldosterone) suggest __________ adrenal insufficiency.

A

Primary

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18
Q

How is SAME diagnosed?

A

By low urinary free cortisone and genetic testinf

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19
Q

Primary hyperparathyroidism

A

Excess PTH due to a disorder of the parathyroid gland itself

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20
Q

What are the ACTH levels, high dose dexamethasone results, imaging results, and treatment for Cushing syndrome as a result of primary adrenal adenoma, hyperplasia, or carcinoma?

A

ACTH: Low

High-dose decamethosone: N/A

Imaging: Adrenal carcinoma with contralateral atrophy or bilateral nodular hyperplasia

Treatment: Resectopm of adenoma/carcinoma or bilateral resection of hyperplasia with hormone replacement

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21
Q

__________ mediates uterine contraction during labor and release of breast milk in lactating mothers.

A

oxytocin

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22
Q

Lack of ACTH response with ___________ stimulation test supports a secondary or tertiary cause of adrenal insufficiency.

A

Metyrapone

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23
Q

How does liddle syndrome present?

A

Child with HTN, hypokalemia, and metabolic alkalosis, but with low aldoserone and low renin

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24
Q

Result on nonenzymatic glycosylation of efferent arterioles of kidneys

A
  • Gromerular hyperfiltration injury with microalbuminuria that eventually progresses to nephrotic syndrome; characterized by Kimmelstiel-Wilson nodules in glomeruli
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25
Q

ACTH cell adenomas a secrete ACTH leading to __________ syndrome.

A

Cushing

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26
Q

Multinodular goiter

A
  • Enlarged thyroid gland with multiple nodules
  • Usually due to relative iodine deficiency
  • usually nontoxic
  • Rarely, regions become TSH-independent leading to T4 release and hyperthyroidism
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27
Q

nonenzymatic glycosylation of large and medium sized vessels leads to ___________.

A

Artherosclerosis

*This can lead to cardiovascular disease and peripheral vascular disease, leading to nontraumatic amputations

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28
Q

How does riedel fibrosing thyroiditis present clinical?

A

Clinically mimics anaplastic carcinoma, but patients are younger (40s) and malignant cells are absent

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29
Q

Lab findings of secondary hyperparathyroidism

A
  • elevated PTH, serum phosphate, and alkaline phosphatase
  • Decreased serum calcium
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30
Q

Hashimoto thyroiditis

A

Autoimmune destruction of the thyroid gland; associated with HLA-DR5

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31
Q

Graves disease

A

Autoantibody IgG that stimulates TSH receptor (type II hypersensitivity)

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32
Q

How does chronic adrenal insufficiency present?

A

Vague, progressive symptoms such as hypotension, weakness, fatigue, nausea, vomiting, and weight loss

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33
Q

Effect of 11-hydroxylase deficiency on steroidogenesis?

A

Androgen excess, but weak mineralocorticoids (DOC) are increased

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34
Q

potentially fatal complication of graves disease

A

Throid storm

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35
Q

Complications of anaplastic carcinoma

A

Often invades local structures, leading to dysphagia or respiratory compromise

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36
Q

What are the ACTH levels, high dose dexamethasone results, imaging results, and treatment for Cushing syndrome as a result on exogenous glucocorticoids?

A

ACTH: Low

Highdose dexamethasone: N/A

Imaging: N/A

Treatment: Tapering of steroids, if possible

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37
Q

How do insulinomas present

A

Episodic hypoglycemia with mental status changes that are relived by administration of glucose

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38
Q

Characteristics of cretinism

A
  • Mental retardation
  • Short stature with skeletal abnormalities
  • Coarse facial features
  • Enlarged tongue
  • Umbilical hernia
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39
Q

Associations of autosomal dominant form of pseudohypoparathyroidism

A

Short stature

Short 4th and 5th digits

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40
Q

Syndrome of inappropriate ADH (SIADH)

A
  • Excessive ADH
  • Most often due to ectopic production
  • CNS trauma, pulm infection and drugs are also causes
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41
Q

___________ is due to a congenital defect in thyroid hormone production. Most commonly involves thryoid peroxidase.

A

Dyshormonogenetic goiter

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42
Q

C cells are neuroendocrine cells that secrete ____________.

A

Calcitonin

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43
Q

How does glucocorticoid-remediable aldosteronism present?

A

Clid wth HTN and hypokalemia; aldosterone is high and renin is low

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44
Q

Chronic inflammation with extensive fibrosis of the thyroid gland

A

Riedel fibrosisng thyroiditis

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45
Q

Major function of D2 receptors

A

Modulates transmitter release, especially in brain

Inhibits indirect pathway of striaturm

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46
Q

Ortreotide

A

Somatostatin analog that suppresses GH release

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47
Q

Characteristics of nonfunctional pituitary adenoma

A
  • Bitemporal hemianopsia
  • Hypopituitarism
  • Headache
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48
Q

VIPomas secrete excessive vasoactive intestinal peptide leading to _________, ____________, and _______.

A

Watery diarrhea

Hypokalemia

Achlorhydria

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49
Q

Type 2 Diabetes mellitus

A

End-organ insulin resistance leading to a metabolic disorder charactrized by hyperglycemia

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50
Q

How does subacute granulomatous (dequervain) thyroiditis presnt

A

As a tender thryoid with transcient hyperthyroidism

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51
Q

How does hyperaldersteronism present?

A

HTN, hypokalemia, and metabolic alkalosis

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52
Q

Examples of dopamine agonists

A

Bromocriptine

Cabergoline

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53
Q

Detection of __________ mutation warrants prophylactiv thyroidectomy.

A

RET

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54
Q

Sheehan syndrome

A

pregnancy releated infarction of the pituatary gland

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55
Q

Type 1 Diabetes mellitus

A

Insulin deficiency leading to a metabolic disorder characerized by hyperglycemia

  • Due to autoimmune destruction of beta cells by T lymphocytes
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56
Q

how is a growth hormone adenoma diagnosed?

A

Elevated GH and insulin growth factor-1 levels along with lack of GH suppression by oral glucose

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57
Q

Effect of 21-hydroxylase deficiency on steroidogenesis?

A

Aldosterone and cortisol are decreased; steroidogensis is shunted towards androgens

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58
Q

Secondary hyperparathyroidism

A

Excess production of PTH due to a disease process extrinsic to the parathyroid gland

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59
Q

Treatment for primary hyperparathyroidism

A

Surgical removal of the affected gland

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60
Q

Symptoms of hypoparathyroidism

A
  • Numbness and tingling (particularly circumoral)
  • Muscle spasms
    • May be elicited with filling a blood pressure cuff (Trousseau sign) or tapping on the facial nerve (Chvostek sign)
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61
Q

What drug can cause a myxedma?

A

Lithium

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62
Q

How do somatostatinomas present?

A

Achloryhydria (due to inhibition of gastrin)

Cholelithiasis with steatorrhea (due to inhibition of cholecystokinin)

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63
Q

Cause of thyroid storm

A

Due to elevated catecholamines and massive hormone excess, usually in response to stress (like surgery or childbirth)

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64
Q

Liddle syndrome treatment

A

Potassium sparing diuretics (amiloride or triamterene), which block tubular sodium chanels

NOTE: Spironolactone is not effective

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65
Q

Laboratory findings of primary hyperparathyroidism

A
  • Increased serum PTH, calcium, urinary cAMP, and serum alkaline phosphatase
  • Decreased serum phospate
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66
Q

High dose dexamethasone suppresses _______ production by a pituitary adenoma.

A

ACTH (serum cortisol is lowered)

NOTE: High does dexamethasone does not supress ectopic ACTH production (serum cortisol remains high)

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67
Q

Diabetic ketoacidosis often arises with __________.

A

Stress

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68
Q

is there a response to desmopressin with nephrogenic diabetes insipidus?

A

Naw son

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69
Q

Major long term consequences of diabetes

A

Nonenzymatic glycosylation of vascular basement membranes

Osmotic damage

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70
Q

17-hydroxyprogestterone is increased in __________ deficiency and decreased in__________ deficiency.

A

21- and 11-hydroxylase deficiency; 17-hydroxylase deficiency.

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71
Q

Why does obesity lead to diabetes?

A

Obesity leads to decreased numbers on insulin receptors

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72
Q

What is the most common cuase of secondary hyperparathyroidism?

A

Chronic renal failure

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73
Q

Hypothyroidism in neonates and infants

A

Cretinism

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74
Q

Malignant proliferation of follicles surrounded by a fibrous capsule with invasion through the capsule

A

Follicular carcinoma

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75
Q

Which neoplasia result from MEN 2

A

Medullary carcinoma

Pheochromocytoma

Parathyroid adenoma

Ganglioneuromas of the oral mucosa

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76
Q

Lab finds of pseudohypoparathyroidism

A

Hypocalcemia with increased PTH levels

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77
Q

Causes of cretinism

A
  • Maternal hypothyroidism during early pregnancy
  • Thyroid agenesis
  • Dyshormonogenetic goiter
  • Iodine deficiency
78
Q

Clinical presentation of Type 1 diabetes mellitus

A
  • High serum glucose
  • Weight loss, low muscle mass, and polyphagia
  • Polyuria, polydipsia, and glycosuria
79
Q

Treatment of thyroid storm. mechanism of action?

A

Propylthiouracil(PTU), b-blockers, and steroids

  • PTU inhibits peroxidase-mediated oxidation, organification, and coupling steps of thyroid hormone synthesis, as well as peripheral conversion of T4 to T3
80
Q

Waterhouse-Friderichsen syndrome

A

Hemorrhagic necrosis of the adrenal glands, clasically due to sepsis and DIC in young children with neisseria meningitidis infection

81
Q

How does riedel fibrosing thyroiditis present?

A

Hypothyroidism with a “hard as wood” nontender thyroid gland

82
Q

Clinical features of type ii diabetes mellitus

A

Polyuria, polydipsia, hyperglycemia

83
Q

Risk factor for papillary carcinoma

A

Exposure to ionizing radiation in childhood

84
Q

Why does cushing syndrome result in muscle weakness?

A

Cortisol breaks down muscle to produce amino acids for gluconeogenesis

85
Q

Histo of hashimoto thyroiditis

A

Chronic inflammation with germinal centers and Hurthle cells (eosinophilic metaplasia of cells that line follicles)

86
Q

How does stress cause diabetic ketoacidosis?

A
  • Epinephrine stimulates glucagon secretion increasing lipolysis
  • Increased lipolysis leads to increased free fatty acids
  • Liver converts FFAs to ketone bodies
  • Results in hyperglycemia, anion gap metabolic acidosis, and hyperkalemia
87
Q

Medullary carcinoma biopsy

A

Sheets of malignant cells in an amyloid stroma

88
Q

Hyperosmolar non-ketotic coma

A
  • High glucose >500 mg/dL leads to life-threatening diuresis with hypotension and coma
  • Ketones are absent due to small amounts of circulating insulin
89
Q

Why does Cushing’s syndrome cause immune suppression?

A

Cortisol inhibits phospholipase A2, IL-2, and histamine

90
Q

Nonenzymatic glycosylation small vessels leads to ______________.

A

Hyaline arteriolosclerosis

91
Q

Central diabetes insipidus treatment

A

Desmopressin (ADH analog)

92
Q

How does a thyroglossal duct cyst present?

A

As an anterior neck mass

93
Q

Syndrome of apparaent mineralocorticoid excess (SAME)

A

11B-hydroxysteroid dehydrogenase 2 deficiency allows cortisol to activate renal aldosterone receptors; autosomal recessive

94
Q

Causes of hypopiuitarism

A

Pituatary adenomas (adults)

Craniopharyngioma (children)

Sheehan syndrome

Empty sella syndrome

95
Q

ACTH response with _______ stimulation test suggests hypothalamic disease.

A

CRH

96
Q

Histo Graves disease

A

Irregular follicles with scalloped colloid and chronic inflammation

97
Q

How is a growth hormone adenoma treated?

A

Octretotide

GH receptor antagonist

Surgery

98
Q

Secondary hyperaldosteronism arises with activation of the ____________.

A

RAAS

*Renovascular hypertension or CHF

99
Q

Hypothyroidism in older childrin or adults

A

Myxedema

100
Q

Cause of exopthalmos and pretibial myxedema seen in graves disease

A
  • Fibroblasts behind the orbit and overlying the shin express the TSH receptor
  • TSH activation results in GAG (chondroitin sulfate and hyaluronic acid) buildup, inflammation, fibrosis, and edema leading to exopthalmos and pretibial myxedema.
101
Q

Lab findings of hypoparathyroidism

A
  • Decreased PTH levels and decreased serum calcium
102
Q

Treatment for cushing syndrome

A

Generally involves surgical resection

Ketaconazole or metyrapone useful if surgery is not an option

103
Q

NEG of hemoglobin produces ______________, a marker of glycemic control.

A

Glycated hemoglobin (HbA1c)

104
Q

How does 17-hydroxylase deficiency present?

A
  • Weak mineralocorticoids (DOC) are increased leading to HTN with mild hypokalemia; renin and aldosterone are low
  • Decreased androgens lead to primary amenorrhea and lack of pubic hair (females) or ambiigous genitalia with undescended testes (males)
105
Q

Calcitonin often deposits within the tumor of medullary carcinoma as ________.

A

Amyloid

106
Q

Glucocorticoid-remediable aldosteronis

A

Aberrant expression of aldosterone synthase in the fasciculata due to genetic mutation

107
Q

Central diabetes insipidus

A
  • ADH deficiency
  • Due to hypothalamic or posterior pituitary pathology (trauma, tumor, infection, or inflammation)
108
Q

how do pituitary adeomas and craniopharyngiomas result in hypopituitarism?

A

Due to mass effect or pituitary apoplexy (bleeding into an adenoma)

109
Q

myxedema

A

Accumulation of GAGs in the skin and soft tissue; results in a deeping of voice and large tongue

110
Q

Symptoms of myxedema

A
  • Weight gain despite normal appetite
  • Slowing of mental activity
  • muscle weakness
  • cold intolerance with decreased sweating
  • bradycardia with decreased CO, leading to shortness of breath and fatigue
  • oligomenorrhea
  • hypercholesterolemia
  • constipation
111
Q

papillary carcinoma often spreads to __________.

A

Cervical lymph nodes

112
Q

Thyroglossal duct cyst

A

Cystic dilation of thyroglossal duct remnant

  • Thyroid develops at the base of tongue and then travels along the thyroglossal duct to the anterior neck
  • Thyroid duct normally involutes; a persistent duct, however, may undergo cystic dilation
113
Q

How is diabetes type II diagnosis made?

A

Random glucose >200 mg/dL

Fasting glucose >126 mg/dL

Glucose tolerance test with a serum glucose level >200 mg/dL two hrs after glucose loading

114
Q

Glucococorticoid-remediable aldosteronism leads to a _________ hyperaldosteronism.

A

Familial

115
Q

Lingual thyroud

A

Persistence of thyroid tissue at the base of the tongue

116
Q

Genes associated with medullary carcinoma

A

MEN2A and 2B, which are associated with mutations in the RET oncogene

117
Q

Drugs that can cause nephrogenic diabetes insipidus

A

lithium and demeclocycline

118
Q

Treatment for bilateral adrenal hyperplasia

A

Spironolactone

Epleronone

119
Q

Diabetic ketoacidosis treatment

A

Fluids (corrects dehydration from polyuria)

Insulin

Replacement of electrolytes

120
Q

Liddle syndrome

A

Decreased degradation of sodium channels in collecting tubules due to genetic mutation; autosomal dominant

121
Q

Diagnosis for central diabetes insipidus

A

Water deprivation test fails to increase urine osmolality

122
Q

How are primary and secondary hyperaldosteronism distinguished?

A
  • By plasma renin and edema
    • Primary: low renin and no edema
    • Seconday: High renin and edema
123
Q

Congenital aderenal hyperplasia cause

A

Due to enzymatic defects in cortisol production; autosomal recessive

124
Q

CCK is important for contraction of the ___________.

A

Gallbladder

125
Q

TH is required for normal _______ and _______ development.

A

Brain;skeletal

126
Q

Clinical features of Graves disease

A

Hyperthyroidism

Diffuse goiter

Exophthalmos and pretibial myxedema

127
Q

G protein class for D1

A

S

128
Q

Which conditions is a pheochromcytoma associated with?

A

MEN2A and 2B( RET)

Von hippel-Lindau disease

Neurofibromatosis Type I

129
Q

How do you distinguish between follicular carcinoma and follicular adenoma?

A

Invasion through the capsule (carcinoma)

130
Q

Clinical features of central diabetes insipidus

A
  • Polyuria and polydispsia with risk of life-threatening dehydration
  • Hypernatremia and high serum osmolality
  • Low urine osmolality and specific gravity
131
Q

How do gastrinomas present?

A

Treatment-resistant peptic ulcers (Zollinger-Ellison syndrome)

Ulcers may be multiple and can extend into the jejunum

132
Q

How is glucocorticoud-remediable aldosteronism treated?

A

Responds to dexamethasone

133
Q

treatment for adrenal insufficiency

A

Glucocorticoids and mineralocorticoids

134
Q

What are the ACTH levels, high dose dexamethasone results, imaging results, and treatment for Cushing syndrome as a result of ectopic ACTH secretion?

A

ACTH: High; androgen excess and hyperpigmentation may be present

High-dose dexamethasone: No supression

Imaging: Ectopic source of ACTH (small cell carcinoma or carcinoid)

Treatment: Resection of ectopic source

135
Q

Causes of acute adrenal insufficiency

A
  • Abrupt withdrawal of glucocorticoids
  • Treatment of Cushing syndrome
  • Waterhouse-Friderichsen syndrome
136
Q

How does a thyroid storm present?

A

Arrhytmia, hyperthermia, and bomiting with hypovolemic shock

137
Q

How does sheehan syndrome present?

A

Poor lactation

Loss of pubic hair

Fatique

138
Q

hypopituitarism is insufficient production of hormones by the anterior pituatary gland. Symptoms arise when > _______% of the pituatary parechyma is lost.

A

75

139
Q

Prolatinoma treatment

A

Dopamine agonists to suppress prolatin production

Surgery for larger lesions

140
Q

Diagnosis of insulinoma

A

Decreased serum glucose (usually <50)

Increased insulin and C-peptide

141
Q

How does growth hormone cell adenoma present?

A
  • Gigantism in children
    • Increased linear bone growth (epiphyses are not fused)
  • Acromegaly in adults
    • Enlarged bones of hands, feet, jaw
    • Growth of visceral organs leading to dysfunction
    • Enlarged tongue
  • Secondary diabetes mellitus is often present
142
Q

Why is diabetes mellitus often present in patients with a growth hormone adenoma?

A

GH induces liver gluconeogenesis

143
Q

Cause of the diffuse goiter seen in graves disease

A

Constant TSH stimulation leads to thyroid hyperplasia and hypertrophy

144
Q

SAME may also arise with ___________, which blocks 11B-HSD2.

A

licorice (glycyrrhetinic acid)

145
Q

How does 11-hydroxylase deficiency present?

A
  • Deoxycorticosterone (DOC) leads to HTN with mild hypokalemia; renin and aldosterone are low
  • Clitoral enlargement seen in females
146
Q

Characteristics of Type 1 Diabetes

A
  • Inflammation of islets
  • Associated with HLA-DR3 and HLA-DR4
  • Autoantibodies against insulin are often present
147
Q

_______________ is due to end-organ resistance to PTH.

A

Pseudohypoparathyroidism

148
Q

Clincal features of Cushing syndrome

A
  • Muscle weakness with thin extremities
  • Moon facies, buffalo hump, and truncal obesity
  • Abdominal striae
  • HTN with hypokalemia and metabolic alkalosis
  • Osteoporosis
  • Immune suppresion
149
Q

Causes of myxedma

A

Iodine deficiency and hashimoto thyroiditis

Drugs

Surgical removal or radioablation of the thyroid

150
Q

__________ uptake studies are useful to further characterize nodules in thyroid neoplasia.

A

131 I radioactive

  • Increased uptake: Graves disease or nodular goiter
  • Decreased uptake: Adenoma and carcnimona; often warrants biopsy
151
Q

Causes hypoparathyroidism

A

Autoimmune damage to the parathyroids, surgical excision, and DiGeorge syndrome

152
Q

Nephrocalcinosis

A

Metastatic calcification of renal tubules, potentially leading to renal insufficiency and polyuria

153
Q

How does SAME present?

A

Child with HTN, hypokalemia, and metabolic alkalosis, but with low aldosterone and low renin

154
Q

Clinical features of SIADH

A
  • Hyponatremia and low serum osmolality
  • Mental status changes and seizures
    • Hyponatremia leads to neuronal swelling and cerebral edema
155
Q

Major function of D1 receptors

A

Relaxes renal vascular smooth muscle

Activates direct pathway of striatum

156
Q

How does acute adrenal insufficiency present?

A

Weakness and shock

157
Q

Anaplastic carcinoma

A

Undifferentiated malignant tumor of thyroid; usually seen in elderly

158
Q

Clinical features of hyperthyroidism

A

Weight loss despite increased appetite

Heat intolerance and sweating

Tachycardia with increased CO

Arrhythmia

Tremor, anxiety, insomnia, and heightened emotions

Staring gaze with lid lag

Diarrhea with malabsorption

Oligomenorrhea

Bone resorption with hypercalcemia

Decreased muscle mass with weakness

Hypocholesterolemia

Hyperglycemia

159
Q

Osteitis fibrosa cystica

A

Resoprtion of bone leading to fibrosis and cystic spaces

160
Q

On what part of the kidneys does ADH act on?

A

Distal tubules

Collecting ducts

161
Q

How does sheehan syndrome result in hypopituitarism

A

Gland doubles in size during pregnancy, but blood suplt does not increase significantly; blood loss during parturition precipitates infarction

162
Q

Drugs that case SIADH

A

Cyclophosphamide

163
Q

How does 21-hydroxylase deficiency present?

A

In neonates (classic form)

  • Hyponatremia and hyperkalemia with life-threatening hypotension (salt-wasting type)
  • Females have clitoral enlargement

Non classic form (presents later in life)

  • Androgen excess leading to precocious puberty (males)
  • hirtuism with menstrual irregularities (females
164
Q

Mechanism by which chronic renal failure leads to hyperparathyroidism

A
  • Renal insufficiency leads to decreased phosphate excretion
  • Increased serum phosphate binds free calcium
  • Decreased free calcium stimulates all four parathyroid glands
  • Increased PTH leads to bone reabsorption, contributing to renal oseodystrophy
165
Q

Primary causes of primary hyperaldosteronism

A

Bilateral adrenal hyperplasia

Adrenal adenoma

*Adrenal carcinoma is rare

166
Q

Laboratory findings of graves disease

A
  • Increased total and free T4
  • Decreased TSH
  • Hypocholesterolemia
  • Increased serum glucose
167
Q

Why is there a decrease in TSH in graves disease

A

Free T3 downregulates TRH receptors in the anterior pituatary to decrease TSH release

168
Q

What is the basis of the clinicl features of myxedema?

A

Decreased basal metabolic rate and decreased sympathetic nervous system activity

169
Q

Cause of hypopituitarism seen in nonfunctional pituitary adenoma

A

Compression of normal pituitary tissue

170
Q

Treatment for graves disease

A

b-blockers

thioamide

Radioiodine ablation

171
Q

Cause of bitemporal hemianopsia seen in nonfunctional pituitary adenoma

A

Compression of the optic chiasm

172
Q

How do chief cells regulate serum free calcium?

A

Via PTH secretion which,

  • Increases bone osteoclast activity, releasing calcium and phosphate
  • Increases small bowel absorption of calcium and phosphate (indirectly by activating vitamin D)
  • Increases renal calcium reabsorption and decreases phosphate reabsorption
173
Q

malignant proliferation of parafollicular C cells

A

Medullary carcinoma

174
Q

histo of papillary carcinoma

A

Comprised of papillae lined by cells with clear, “orphan annie eye” nuclei and nuclear grooves; papillae are often associated with psammoma bodies

175
Q

Clinical features of hashimoto thyroiditis

A
  • Initialy may present as hyperthyroidism (due to follicle damage)
  • Progresses to hypothyroism; decreased T4 and increased TSH
  • Antithyroglobulin and antithyroid peroxidase antibodies are often present (sign of thyroid damage)
176
Q

Clinical features of a pheochromocytoma

A

Episodic HTN, headaches, palpitations, tachycardia, and sweating

177
Q

Granulomatous thyroiditis that follows a viral infection

A

Subacute hranulomatous (de quervain)thyroiditis)

178
Q

Empty sella syndrome

A
  • Conginetal defect of sella
  • Herniation of the arachnoid and CSF into the sella compresses and destroys the pituitary gland
  • Pituatary gland in “absent”
179
Q

Treatment for Congenital adrenal hyperplasia

A

Glucocorticoids

Mineralocorticoids (21-hydroxylase deficiency)

Sex steroids (17-hydroxylase deficiency)

180
Q

Newborn screening for confenital adrenal hyperplasia via serum ___________ is routine.

A

17-hydoxyprogesterone

181
Q

High levels of calcitonin produced by tumor may lead to _________.

A

Hypocalcemia

  • Calcitonin lowers serum calcium by increasing renal calcium excretion but is inactive at normal physiologic levels
182
Q

How does metastasis of follicular carcinoma typically occur?

A

Hematogenously

183
Q

Why does cushing syndrome result in abdominal striae?

A

Impaired collagen synthesis results in thinning of skin

184
Q

Effect of 17-hydroxylase deficiency on steroidogenesis?

A

Decreased cortisol and androgens

185
Q

Nephrogenic diabetes insipidus

A
  • Impaired renal response to ADH
  • Due to inherited mutations or drugs
186
Q

Pheochromocytoma

A

Tumor of chromaffin cels

187
Q

Treatment of pheochromocytoma

A

Adrenalectomy

  • Catecholamines may leak into the bloodstream upon manipulation of the tumor
  • Phenoxybenzamine followed by a B-blocker is administered preoperatively to prevent a hypertensive crisis
188
Q

How does hyperthyroidism increase sympathetic nervous system activity?

A

Due to increased expression of B1-adrenergic receptors

189
Q

How is cushing syndrome diagnosed?

A
  • 24-hr urine cortisol level
  • Late night salivary cortisol level
  • Low-dose dexamethasone suppresion test

*Low dose dexamethasone suppresses cortisol in normal individuals but fails to suppress cortisol in all causes of Cushing syndrome

190
Q

Causes of cushing syndrome

A

Exogenous glucocorticoids

ACTH-secreting pituitary adenoma

Ectopic ACTH secretion

Primary adrenal adenoma, hyperplasia, or carcinom

191
Q

Possible consqequence of diabetes type 1

A

Diabetic ketoacidosis

OS4 (4 decks)

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