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
ACTH cell adenomas a secrete ACTH leading to __________ syndrome.
Cushing
26
Multinodular goiter
* 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
27
nonenzymatic glycosylation of large and medium sized vessels leads to \_\_\_\_\_\_\_\_\_\_\_.
Artherosclerosis \*This can lead to cardiovascular disease and peripheral vascular disease, leading to nontraumatic amputations
28
How does riedel fibrosing thyroiditis present clinical?
Clinically mimics anaplastic carcinoma, but patients are younger (40s) and malignant cells are absent
29
Lab findings of secondary hyperparathyroidism
* elevated PTH, serum phosphate, and alkaline phosphatase * Decreased serum calcium
30
Hashimoto thyroiditis
Autoimmune destruction of the thyroid gland; associated with HLA-DR5
31
Graves disease
Autoantibody IgG that stimulates TSH receptor (type II hypersensitivity)
32
How does chronic adrenal insufficiency present?
Vague, progressive symptoms such as hypotension, weakness, fatigue, nausea, vomiting, and weight loss
33
Effect of 11-hydroxylase deficiency on steroidogenesis?
Androgen excess, but weak mineralocorticoids (DOC) are increased
34
potentially fatal complication of graves disease
Throid storm
35
Complications of anaplastic carcinoma
Often invades local structures, leading to dysphagia or respiratory compromise
36
What are the ACTH levels, high dose dexamethasone results, imaging results, and treatment for Cushing syndrome as a result on exogenous glucocorticoids?
ACTH: Low Highdose dexamethasone: N/A Imaging: N/A Treatment: Tapering of steroids, if possible
37
How do insulinomas present
Episodic hypoglycemia with mental status changes that are relived by administration of glucose
38
Characteristics of cretinism
* Mental retardation * Short stature with skeletal abnormalities * Coarse facial features * Enlarged tongue * Umbilical hernia
39
Associations of autosomal dominant form of pseudohypoparathyroidism
Short stature Short 4th and 5th digits
40
Syndrome of inappropriate ADH (SIADH)
* Excessive ADH * Most often due to ectopic production * CNS trauma, pulm infection and drugs are also causes
41
\_\_\_\_\_\_\_\_\_\_\_ is due to a congenital defect in thyroid hormone production. Most commonly involves thryoid peroxidase.
Dyshormonogenetic goiter
42
C cells are neuroendocrine cells that secrete \_\_\_\_\_\_\_\_\_\_\_\_.
Calcitonin
43
How does glucocorticoid-remediable aldosteronism present?
Clid wth HTN and hypokalemia; aldosterone is high and renin is low
44
Chronic inflammation with extensive fibrosis of the thyroid gland
Riedel fibrosisng thyroiditis
45
Major function of D2 receptors
Modulates transmitter release, especially in brain Inhibits indirect pathway of striaturm
46
Ortreotide
Somatostatin analog that suppresses GH release
47
Characteristics of nonfunctional pituitary adenoma
* Bitemporal hemianopsia * Hypopituitarism * Headache
48
VIPomas secrete excessive vasoactive intestinal peptide leading to \_\_\_\_\_\_\_\_\_, \_\_\_\_\_\_\_\_\_\_\_\_, and \_\_\_\_\_\_\_.
Watery diarrhea Hypokalemia Achlorhydria
49
Type 2 Diabetes mellitus
End-organ insulin resistance leading to a metabolic disorder charactrized by hyperglycemia
50
How does subacute granulomatous (dequervain) thyroiditis presnt
As a tender thryoid with transcient hyperthyroidism
51
How does hyperaldersteronism present?
HTN, hypokalemia, and metabolic alkalosis
52
Examples of dopamine agonists
Bromocriptine Cabergoline
53
Detection of __________ mutation warrants prophylactiv thyroidectomy.
RET
54
Sheehan syndrome
pregnancy releated infarction of the pituatary gland
55
Type 1 Diabetes mellitus
Insulin deficiency leading to a metabolic disorder characerized by hyperglycemia * Due to autoimmune destruction of beta cells by T lymphocytes
56
how is a growth hormone adenoma diagnosed?
Elevated GH and insulin growth factor-1 levels along with lack of GH suppression by oral glucose
57
Effect of 21-hydroxylase deficiency on steroidogenesis?
Aldosterone and cortisol are decreased; steroidogensis is shunted towards androgens
58
Secondary hyperparathyroidism
Excess production of PTH due to a disease process extrinsic to the parathyroid gland
59
Treatment for primary hyperparathyroidism
Surgical removal of the affected gland
60
Symptoms of hypoparathyroidism
* 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)
61
What drug can cause a myxedma?
Lithium
62
How do somatostatinomas present?
Achloryhydria (due to inhibition of gastrin) Cholelithiasis with steatorrhea (due to inhibition of cholecystokinin)
63
Cause of thyroid storm
Due to elevated catecholamines and massive hormone excess, usually in response to stress (like surgery or childbirth)
64
Liddle syndrome treatment
Potassium sparing diuretics (amiloride or triamterene), which block tubular sodium chanels **NOTE:** Spironolactone is not effective
65
Laboratory findings of primary hyperparathyroidism
* Increased serum PTH, calcium, urinary cAMP, and serum alkaline phosphatase * Decreased serum phospate
66
High dose dexamethasone suppresses _______ production by a pituitary adenoma.
ACTH (serum cortisol is lowered) **NOTE:** High does dexamethasone does not supress ectopic ACTH production (serum cortisol remains high)
67
Diabetic ketoacidosis often arises with \_\_\_\_\_\_\_\_\_\_.
Stress
68
is there a response to desmopressin with nephrogenic diabetes insipidus?
Naw son
69
Major long term consequences of diabetes
Nonenzymatic glycosylation of vascular basement membranes Osmotic damage
70
17-hydroxyprogestterone is increased in __________ deficiency and decreased in\_\_\_\_\_\_\_\_\_\_ deficiency.
21- and 11-hydroxylase deficiency; 17-hydroxylase deficiency.
71
Why does obesity lead to diabetes?
Obesity leads to decreased numbers on insulin receptors
72
What is the most common cuase of secondary hyperparathyroidism?
Chronic renal failure
73
Hypothyroidism in neonates and infants
Cretinism
74
Malignant proliferation of follicles surrounded by a fibrous capsule with invasion through the capsule
Follicular carcinoma
75
Which neoplasia result from MEN 2
Medullary carcinoma Pheochromocytoma Parathyroid adenoma Ganglioneuromas of the oral mucosa
76
Lab finds of pseudohypoparathyroidism
Hypocalcemia with increased PTH levels
77
Causes of cretinism
* Maternal hypothyroidism during early pregnancy * Thyroid agenesis * Dyshormonogenetic goiter * Iodine deficiency
78
Clinical presentation of Type 1 diabetes mellitus
* High serum glucose * Weight loss, low muscle mass, and polyphagia * Polyuria, polydipsia, and glycosuria
79
Treatment of thyroid storm. mechanism of action?
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
Waterhouse-Friderichsen syndrome
Hemorrhagic necrosis of the adrenal glands, clasically due to sepsis and DIC in young children with neisseria meningitidis infection
81
How does riedel fibrosing thyroiditis present?
Hypothyroidism with a "hard as wood" nontender thyroid gland
82
Clinical features of type ii diabetes mellitus
Polyuria, polydipsia, hyperglycemia
83
Risk factor for papillary carcinoma
Exposure to ionizing radiation in childhood
84
Why does cushing syndrome result in muscle weakness?
Cortisol breaks down muscle to produce amino acids for gluconeogenesis
85
Histo of hashimoto thyroiditis
Chronic inflammation with germinal centers and Hurthle cells (eosinophilic metaplasia of cells that line follicles)
86
How does stress cause diabetic ketoacidosis?
* 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
Medullary carcinoma biopsy
Sheets of malignant cells in an amyloid stroma
88
Hyperosmolar non-ketotic coma
* 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
Why does Cushing's syndrome cause immune suppression?
Cortisol inhibits phospholipase A2, IL-2, and histamine
90
Nonenzymatic glycosylation small vessels leads to \_\_\_\_\_\_\_\_\_\_\_\_\_\_.
Hyaline arteriolosclerosis
91
Central diabetes insipidus treatment
Desmopressin (ADH analog)
92
How does a thyroglossal duct cyst present?
As an anterior neck mass
93
Syndrome of apparaent mineralocorticoid excess (SAME)
11B-hydroxysteroid dehydrogenase 2 deficiency allows cortisol to activate renal aldosterone receptors; autosomal recessive
94
Causes of hypopiuitarism
Pituatary adenomas (adults) Craniopharyngioma (children) Sheehan syndrome Empty sella syndrome
95
ACTH response with _______ stimulation test suggests hypothalamic disease.
CRH
96
Histo Graves disease
Irregular follicles with scalloped colloid and chronic inflammation
97
How is a growth hormone adenoma treated?
Octretotide GH receptor antagonist Surgery
98
Secondary hyperaldosteronism arises with activation of the \_\_\_\_\_\_\_\_\_\_\_\_.
RAAS \*Renovascular hypertension or CHF
99
Hypothyroidism in older childrin or adults
Myxedema
100
Cause of exopthalmos and pretibial myxedema seen in graves disease
* 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
Lab findings of hypoparathyroidism
* Decreased PTH levels and decreased serum calcium
102
Treatment for cushing syndrome
Generally involves surgical resection Ketaconazole or metyrapone useful if surgery is not an option
103
NEG of hemoglobin produces \_\_\_\_\_\_\_\_\_\_\_\_\_\_, a marker of glycemic control.
Glycated hemoglobin (HbA1c)
104
How does 17-hydroxylase deficiency present?
* 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
Calcitonin often deposits within the tumor of medullary carcinoma as \_\_\_\_\_\_\_\_.
Amyloid
106
Glucocorticoid-remediable aldosteronis
Aberrant expression of aldosterone synthase in the fasciculata due to genetic mutation
107
Central diabetes insipidus
* ADH deficiency * Due to hypothalamic or posterior pituitary pathology (trauma, tumor, infection, or inflammation)
108
how do pituitary adeomas and craniopharyngiomas result in hypopituitarism?
Due to mass effect or pituitary apoplexy (bleeding into an adenoma)
109
myxedema
Accumulation of GAGs in the skin and soft tissue; results in a deeping of voice and large tongue
110
Symptoms of myxedema
* 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
papillary carcinoma often spreads to \_\_\_\_\_\_\_\_\_\_.
Cervical lymph nodes
112
Thyroglossal duct cyst
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
How is diabetes type II diagnosis made?
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
Glucococorticoid-remediable aldosteronism leads to a _________ hyperaldosteronism.
Familial
115
Lingual thyroud
Persistence of thyroid tissue at the base of the tongue
116
Genes associated with medullary carcinoma
MEN2A and 2B, which are associated with mutations in the RET oncogene
117
Drugs that can cause nephrogenic diabetes insipidus
lithium and demeclocycline
118
Treatment for bilateral adrenal hyperplasia
Spironolactone Epleronone
119
Diabetic ketoacidosis treatment
Fluids (corrects dehydration from polyuria) Insulin Replacement of electrolytes
120
Liddle syndrome
Decreased degradation of sodium channels in collecting tubules due to genetic mutation; autosomal dominant
121
Diagnosis for central diabetes insipidus
Water deprivation test fails to increase urine osmolality
122
How are primary and secondary hyperaldosteronism distinguished?
* By plasma renin and edema * Primary: low renin and no edema * Seconday: High renin and edema
123
Congenital aderenal hyperplasia cause
Due to enzymatic defects in cortisol production; autosomal recessive
124
CCK is important for contraction of the \_\_\_\_\_\_\_\_\_\_\_.
Gallbladder
125
TH is required for normal _______ and _______ development.
Brain;skeletal
126
Clinical features of Graves disease
Hyperthyroidism Diffuse goiter Exophthalmos and pretibial myxedema
127
G protein class for D1
S
128
Which conditions is a pheochromcytoma associated with?
MEN2A and 2B( RET) Von hippel-Lindau disease Neurofibromatosis Type I
129
How do you distinguish between follicular carcinoma and follicular adenoma?
Invasion through the capsule (carcinoma)
130
Clinical features of central diabetes insipidus
* Polyuria and polydispsia with risk of life-threatening dehydration * Hypernatremia and high serum osmolality * Low urine osmolality and specific gravity
131
How do gastrinomas present?
Treatment-resistant peptic ulcers (Zollinger-Ellison syndrome) Ulcers may be multiple and can extend into the jejunum
132
How is glucocorticoud-remediable aldosteronism treated?
Responds to dexamethasone
133
treatment for adrenal insufficiency
Glucocorticoids and mineralocorticoids
134
What are the ACTH levels, high dose dexamethasone results, imaging results, and treatment for Cushing syndrome as a result of ectopic ACTH secretion?
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
Causes of acute adrenal insufficiency
* Abrupt withdrawal of glucocorticoids * Treatment of Cushing syndrome * Waterhouse-Friderichsen syndrome
136
How does a thyroid storm present?
Arrhytmia, hyperthermia, and bomiting with hypovolemic shock
137
How does sheehan syndrome present?
Poor lactation Loss of pubic hair Fatique
138
hypopituitarism is insufficient production of hormones by the anterior pituatary gland. Symptoms arise when \> \_\_\_\_\_\_\_% of the pituatary parechyma is lost.
75
139
Prolatinoma treatment
Dopamine agonists to suppress prolatin production Surgery for larger lesions
140
Diagnosis of insulinoma
Decreased serum glucose (usually \<50) Increased insulin and C-peptide
141
How does growth hormone cell adenoma present?
* 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
Why is diabetes mellitus often present in patients with a growth hormone adenoma?
GH induces liver gluconeogenesis
143
Cause of the diffuse goiter seen in graves disease
Constant TSH stimulation leads to thyroid hyperplasia and hypertrophy
144
SAME may also arise with \_\_\_\_\_\_\_\_\_\_\_, which blocks 11B-HSD2.
licorice (glycyrrhetinic acid)
145
How does 11-hydroxylase deficiency present?
* Deoxycorticosterone (DOC) leads to HTN with mild hypokalemia; renin and aldosterone are low * Clitoral enlargement seen in females
146
Characteristics of Type 1 Diabetes
* Inflammation of islets * Associated with HLA-DR3 and HLA-DR4 * Autoantibodies against insulin are often present
147
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ is due to end-organ resistance to PTH.
Pseudohypoparathyroidism
148
Clincal features of Cushing syndrome
* Muscle weakness with thin extremities * Moon facies, buffalo hump, and truncal obesity * Abdominal striae * HTN with hypokalemia and metabolic alkalosis * Osteoporosis * Immune suppresion
149
Causes of myxedma
Iodine deficiency and hashimoto thyroiditis Drugs Surgical removal or radioablation of the thyroid
150
\_\_\_\_\_\_\_\_\_\_ uptake studies are useful to further characterize nodules in thyroid neoplasia.
131 I radioactive * Increased uptake: Graves disease or nodular goiter * Decreased uptake: Adenoma and carcnimona; often warrants biopsy
151
Causes hypoparathyroidism
Autoimmune damage to the parathyroids, surgical excision, and DiGeorge syndrome
152
Nephrocalcinosis
Metastatic calcification of renal tubules, potentially leading to renal insufficiency and polyuria
153
How does SAME present?
Child with HTN, hypokalemia, and metabolic alkalosis, but with low aldosterone and low renin
154
Clinical features of SIADH
* Hyponatremia and low serum osmolality * Mental status changes and seizures * Hyponatremia leads to neuronal swelling and cerebral edema
155
Major function of D1 receptors
Relaxes renal vascular smooth muscle Activates direct pathway of striatum
156
How does acute adrenal insufficiency present?
Weakness and shock
157
Anaplastic carcinoma
Undifferentiated malignant tumor of thyroid; usually seen in elderly
158
Clinical features of hyperthyroidism
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
Osteitis fibrosa cystica
Resoprtion of bone leading to fibrosis and cystic spaces
160
On what part of the kidneys does ADH act on?
Distal tubules Collecting ducts
161
How does sheehan syndrome result in hypopituitarism
Gland doubles in size during pregnancy, but blood suplt does not increase significantly; blood loss during parturition precipitates infarction
162
Drugs that case SIADH
Cyclophosphamide
163
How does 21-hydroxylase deficiency present?
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
Mechanism by which chronic renal failure leads to hyperparathyroidism
* 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
Primary causes of primary hyperaldosteronism
Bilateral adrenal hyperplasia Adrenal adenoma \*Adrenal carcinoma is rare
166
Laboratory findings of graves disease
* Increased total and free T4 * Decreased TSH * Hypocholesterolemia * Increased serum glucose
167
Why is there a decrease in TSH in graves disease
Free T3 downregulates TRH receptors in the anterior pituatary to decrease TSH release
168
What is the basis of the clinicl features of myxedema?
Decreased basal metabolic rate and decreased sympathetic nervous system activity
169
Cause of hypopituitarism seen in nonfunctional pituitary adenoma
Compression of normal pituitary tissue
170
Treatment for graves disease
b-blockers thioamide Radioiodine ablation
171
Cause of bitemporal hemianopsia seen in nonfunctional pituitary adenoma
Compression of the optic chiasm
172
How do chief cells regulate serum free calcium?
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
malignant proliferation of parafollicular C cells
Medullary carcinoma
174
histo of papillary carcinoma
Comprised of papillae lined by cells with clear, "orphan annie eye" nuclei and nuclear grooves; papillae are often associated with psammoma bodies
175
Clinical features of hashimoto thyroiditis
* 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
Clinical features of a pheochromocytoma
Episodic HTN, headaches, palpitations, tachycardia, and sweating
177
Granulomatous thyroiditis that follows a viral infection
Subacute hranulomatous (de quervain)thyroiditis)
178
Empty sella syndrome
* Conginetal defect of sella * Herniation of the arachnoid and CSF into the sella compresses and destroys the pituitary gland * Pituatary gland in "absent"
179
Treatment for Congenital adrenal hyperplasia
Glucocorticoids Mineralocorticoids (21-hydroxylase deficiency) Sex steroids (17-hydroxylase deficiency)
180
Newborn screening for confenital adrenal hyperplasia via serum ___________ is routine.
17-hydoxyprogesterone
181
High levels of calcitonin produced by tumor may lead to \_\_\_\_\_\_\_\_\_.
Hypocalcemia * Calcitonin lowers serum calcium by increasing renal calcium excretion but is inactive at normal physiologic levels
182
How does metastasis of follicular carcinoma typically occur?
Hematogenously
183
Why does cushing syndrome result in abdominal striae?
Impaired collagen synthesis results in thinning of skin
184
Effect of 17-hydroxylase deficiency on steroidogenesis?
Decreased cortisol and androgens
185
Nephrogenic diabetes insipidus
* Impaired renal response to ADH * Due to inherited mutations or drugs
186
Pheochromocytoma
Tumor of chromaffin cels
187
Treatment of pheochromocytoma
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
How does hyperthyroidism increase sympathetic nervous system activity?
Due to increased expression of B1-adrenergic receptors
189
How is cushing syndrome diagnosed?
* 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
Causes of cushing syndrome
Exogenous glucocorticoids ACTH-secreting pituitary adenoma Ectopic ACTH secretion Primary adrenal adenoma, hyperplasia, or carcinom
191
Possible consqequence of diabetes type 1
Diabetic ketoacidosis