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467 Cards in this Set
- Front
- Back
What are the two basic types of hormonal activity?
|
Interact with cell surface receptors producing 2nd messengers--cAMP, increased Ca2+
Interact with intracellular receptors |
|
If there is a decrease in the amount of hormone produced, what does this usually mean?
|
Autoimmune
|
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If there is an increase in the amount of hormone produced, what does this usually mean?
|
Adenoma
|
|
What are the ways the endocrine system can be disturbed?
|
Impaired Synthesis
Impaired release Abnormal interaction between hormones and target tissues Abnormal target organ response |
|
What is the master gland involved in the endocrine system?
|
The pituitary gland
|
|
What are the two portions in the pituitary gland?
|
The anterior portion and the posterior portion
|
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Where is the anterior pituitary gland derived from?
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Rathke's pouch--oral ectoderm
|
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Where is the posterior pituitary gland derived from?
|
Diencephalon
|
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What portion of the pituitary is the adenohypophysis?
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The anterior pituitary
|
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What portion of the pituitary is the neurohypophysis?
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The posterior pituitary
|
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Where does the pituitary gland sit?
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In the sella turcica
|
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What do the somatotrophs produce?
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Growth hormone
|
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What do the lactotrophs produce?
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Prolactin
|
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What do the corticotrophs produce?
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ACTH, MSH, POMC
|
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What do the thyrotrophs produce?
|
TSH
|
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What do gonadotrophs produce?
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FSH and LH
|
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How does the hypothalamus control the anterior pituitary?
|
By the portal venous system that links the hypothalamus and the anterior lobe
|
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Why does the posterior pituitary not need a portal venous system?
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Because it is directly connected to the brain
|
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What does the hypothalamus contain?
|
Releasing hormones that act on the anterior pituitary
|
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What happens during pregnancy to the anterior pituitary?
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It doubles in size because of the increase need in hormones
|
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What inhibits prolactin?
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Dopamine
|
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What is the only anterior pituitary hormone that has an inhibitory effect?
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Prolactin
|
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What are the two hormones released from the posterior pituitary?
|
Oxytocin and Vasopressin (ADH)
|
|
What do gonadotrophs produce?
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FSH and LH
|
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How does the hypothalamus control the anterior pituitary?
|
By the portal venous system that links the hypothalamus and the anterior lobe
|
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Why does the posterior pituitary not need a portal venous system?
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Because it is directly connected to the brain
|
|
What does the hypothalamus contain?
|
Releasing hormones that act on the anterior pituitary
|
|
What happens during pregnancy to the anterior pituitary?
|
It doubles in size because of the increase need in hormones
|
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What inhibits prolactin?
|
Dopamine
|
|
What is the only anterior pituitary hormone that has an inhibitory effect?
|
Prolactin
|
|
What are the two hormones released from the posterior pituitary?
|
Oxytocin and Vasopressin (ADH)
|
|
Where are oxytocin and ADH made?
|
In the hypothalamus and released by the posterior pituitary
|
|
What is hyperpituitarism?
|
Excess secretion of trohpic hormones
|
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What things can cause hyperpituitarism?
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Adenooma (most common)
Hyperplasia Carcinoma (VERY RARE!) |
|
What is hypopituitarism?
|
Deficiency of trophic hormones--usually caused by destructive processes
|
|
What do pituitary local mass effects produce?
|
Visual disturbances and also exert effects on the sella turcica
|
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What are diseases of the posterior pituitary?
|
Diabetes Insipdis
Inappropriate ADH secretion |
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Are pituitary adenomas usually benign or malignant?
|
Usually benign
|
|
In what ways do pituitary adenomas cause problems?
|
By mass effects (visual disturbances) or by production of hormones (prolactin or ACTH)
|
|
The larger a tumor is......
|
The less likely it is to be producing hormones
|
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What is the most common cause of hyperpituitarism?
|
Adenoma arising in the anterior lobe
|
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What is a functional pituitary adenoma?
|
Secrete active hormones
|
|
What is a silent pituitary adenoma?
|
Cells are producing hormones but they don't have clinical effects
|
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What is a nonfunctional adenoma?
|
No evidence of hormonal production; usually gets recognized by mass effects
|
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Who usually gets pituitary adenomas?
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4th to 6th decade
|
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What are the most common hormones secreted in pituitary adenomas?
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Prolactin
ACTH Growth Hormone |
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What percentage of clinically detected pituitary adenomas are responsible for intracranial neoplasms?
|
10%
|
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What do 25% of routine autopsies find?
|
Microadenomas (<1cm)--rarely have a hormonal output
|
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What type of pituitary adenomas have the GNAS1 mutation?
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Somatotroph cell adenomas
|
|
What MEN commonly has pitutiary adenomas?
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MEN-1 (Wermer Syndrome)
|
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What oncogenes are seen in aggressive tumors?
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RAS and c-MYC
|
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What is the most common somatotroph tumor?
|
GHRH-40%
|
|
What is a large pituitary adenoma usually producing?
|
NOTHING
|
|
What type of cells are usually seen in a pituitary adenoma?
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Monomorphic cells
|
|
What is the most common type of pituitary adenoma?
|
Prolactinoma (20-30%)
|
|
What is the classic triad of symptoms seen in a prolactinoma?
|
Amenorrhea
Galactorrhea Infertility |
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Do proalactinomas usually cause symptoms in men?
|
Not usually--but can--impotence, ha, visual loss
|
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Who are the prolactinomas the most prevalent in?
|
Women with adult onset amenorrhea
|
|
What level of prolactin is diagnostic of a prolactinoma?
|
No absolute level--levels >1000 are usually suggestive of a macroadenoma
|
|
How is a prolactinoma usually treated?
|
With Dopamine agonists and surgical removal if necessary
|
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What is the 2nd most common pituitary adenoma?
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Growth Hormone (Somatotroph)
|
|
What are the two subtypes of growth hormone adenomas?
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Densely granulated (acidophilic)
Sparsely granulated (chromophobe) |
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What is the densely granulated growth hormone adenoma?
|
Reacts with GH antibody and has cytokeratin; tumors with both growth hormone and prolactin
|
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What is the sparsely granulated growth hornome adenoma?
|
Weak reaction with GH antibody
|
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What happens if there is persistent secretion of growth hormone?
|
Stimulates hepatic secretion of IGF-1
|
|
If the growth hormone adenoma occurs before puberty, what is the result?
|
Gigantism--occurs before the epiphyseal plate closes
|
|
If the growth hormone adenoma occurs after puberty, what is the result?
|
Acromegaly--after ephysieal plate closed
|
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What is the most common etiology of acromegaly?
|
Growth hormone secreting adenoma--95%
|
|
What causes acromegaly besides a growth hormone adenoma?
|
Small cell carcinoma of the lung
|
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What are the major characteristics of acromegaly?
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Organomegaly
Spade like hands Frontal bossing Big nose |
|
How is acromegaly diagnosed?
|
Elevated serum GH and IGF-1
|
|
How do we test for acromegaly?
|
Give a glucose load
|
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If the patient does have acromegaly, what will be the result of the glucose load test?
|
GH will not fall rapidly as it normally does with administration of glucose
|
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What are the classic complaints of patient's who have acromegaly?
|
"My wedding ring won't go on"....."My hat doesn't fit anymore"
|
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What is another common type of somatotroph adenoma that is nearly as common as growth hormone adenoma?
|
Corticotroph cell adenoma
|
|
What are corticotroph adenomas usually at the time of diagnosis?
|
Microadenomas
|
|
What type of tumors are usually seen in corticotroph adenomas?
|
Densely granulated
|
|
What does the excess ACTH production in a corticotroph adenoma lead to?
|
Cushing's disease
|
|
What is Cushing's disease?
|
Increase in ACTH and an increase in cortisol
|
|
What is Cushing's syndrome?
|
Just an increase in cortisol
|
|
What is Nelson's syndrome?
|
A large adenoma that develops after an adrenalectomy--loss of negative feedback
|
|
What is hypopituitarism?
|
Reduction in normal hormonal output
|
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How much of the pituitary is required to be lost before symptoms are present?
|
About 75%
|
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What are some clinical findings that are seen with hypopituitarism?
|
Hypothyroid
Amenorrhea Infertility Pallor Lactation failure Hypoadrenalism |
|
What are some causes of hypopituitarism?
|
Tumors/lesions including Rathke's pouch
Pituitary surgery Pituitary apoplexy Ischemic Necrosis Empty sella syndrome |
|
What is Sheehan syndrome?
|
Post-partum necrosis of the pituitary--changes in blood volume after delivery
|
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Who is most commonly affected by empty sella syndrome?
|
Obese multips
|
|
What are some presenting signs of Sheehan's syndrome?
|
Fatigue
Not bonding well (resembles pp depression) |
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What is empty sella syndrome?
|
No tissue seen in the sella turcica
|
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What are the two types of posterior pituitary syndrome?
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Diabetes Insipidus and SIADH
|
|
What is the ADH level in Diabetes Insipidus?
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Low--excess water being excreted
|
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What is the ADH level in SIADH?
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High--not enough water is urine
|
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What are the subclasses of Diabetes Insipidus?
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Neurogenic (Central)
Nephrogenic Primary Polydipsia Gestational diabetes insipidus |
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What is nerogenic or central diabetes insipidus?
|
The posterior pituitary fails to secrete ADH due to injury
|
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What is nephrogenic diabetes insipidus?
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The kidney fails to respond to ADH
|
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What is primary polydipsia diabetes insipidus?
|
Abnormal thirst causes patient to consume excessive amounts of water
|
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What is gestational diabetes insipidus?
|
Increased metabolism of ADH which causes deficiency
|
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What is a good way to tell if the patient has neurogenic (central) or nephrogenic diabetes insipidus?
|
Give the patient ADH
|
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What is a usual cause of nephrogenic diabetes insipidus?
|
Drugs
|
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What are the clinical findings in patients with diabetes insipidus?
|
Polyuria--dilute urine with low specific gravity
Polydipsia HYPERNATREMIA |
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In SIADH, do patient's have dilute or concentrated urine?
|
Concentrated urine--unable to make dilute urine
|
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What are the clinical findings in SIADH?
|
HYPONATREMIA
Fluid overload Weakness Confusion Irritability and hostility |
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What is the most common cause of hospital acquired hyponatremia?
|
SIADH
|
|
What are the two causes of SIADH?
|
Abnormal regulation of post pituitary secretion of ADH--high levels of ADH
Ectopic secretion of ADH by a malignant tumor |
|
What is the most common cause of ectopic secretion of ADH?
|
Small cell carcinoma
|
|
Hyponatremia occurs how often in hospitalized patients over the age of 65?
|
25% of the time with half of those having evident SIADH
|
|
What are the two types of suprasellar tumors?
|
Gliomas
Craniopharyngioma |
|
What is a craniopharyngioma?
|
Derived from remnants of Rathke's pouch
|
|
Is a craniopharyngioma slow or fast growing?
|
Slow growing
|
|
Where do craniopharyngiomas occur?
|
In the hypothalamic region above the sella turcica
|
|
What are common symptoms seen in craniopharyngiomas?
|
Diabetes Insipidus and visual disturbances
|
|
What is unique about the epidemiology of craniopharyngiomas?
|
It has a bimodal age distribution---Children 5-15 years and adults 50 and up
|
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What type of tumors do craniopharyngiomas typically form?
|
Cystic tumors
|
|
What do craniopharyngiomas arrise from?
|
Epithelial neoplasm dervied from Rathke's pouch
|
|
What does a non palpable thryoid mean?
|
Normal size
|
|
Where is the most common place for ectopic thyroid tissue?
|
Lingual
|
|
What are C cells and what do they secrete?
|
C cells are parafollicular cells and they secrete calcitonin
|
|
What is the most abundant thyroid hormone produced?
|
T4
|
|
What is the most metabolically active hormone produced?
|
T3
|
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Which of the thyroid hormones has a much shorter half life?
|
T3
|
|
What is a goiter?
|
Enlargement of the thyroid gland
|
|
What is a diffuse nontoxic goiter?
|
A goiter that involves the entire thyroid gland and is not functional
|
|
What is the most common cause of a diffuse goiter?
|
Iodine deficiency
|
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What is the thyroid state in patients with a diffuse goiter?
|
Usually euthyroid
|
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What is a multinodular goiter?
|
A diffuse goiter that has recurrent episodes of hyperplasia and involution resulting in a mulitnodular goiter
|
|
What is thyroiditis?
|
Inflammation of the thyroid gland
|
|
What is the problem with a asymptomatic, nontoxic goiter?
|
Nothing--purely cosmetic
|
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What does the epithelium look like in multinodular goiters?
|
"Flattened" epithelium
|
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What is thyrotoxicosis?
|
Hypermetabolic state caused by high levels of circulating T3 and T4
|
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What is subclinical hyperthyroid?
|
An asympotmatic patient with a low TSH but normal T3 and T4
|
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What is exophthalmos?
|
Accumulation of loose connective tissue in the soft tissue of the posterior orbit
|
|
What is thryoid storm?
|
ABRUPT onset of thyrotoxicosis
|
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What are the clinical findings in thyrotoxicosis?
|
Increased BMR
Tachycardia Tremor Weight loss Intolerance to heat Nervousness |
|
What are three signs found in 50% of older patients?
|
Tachycardia
Fatigue Weight loss |
|
Who normally presents with thyrotoxicosis?
|
Women
|
|
What are the four causes of Sustained thryotoxicosis?
|
Primary
Secondary Tertiary Exogenous |
|
What is primary sustained thyrotoxicosis?
|
Overactivity of the thyroid gland--the most common
|
|
What is secondary sustained thyrotoxicosis?
|
Excessive TSH
|
|
What is tertiary sustained thyrotoxicosis?
|
Caused by hypothalamic disorders
|
|
What is exogenous sustained thyrotoxicosis?
|
Caused by taking thyroid hormones when you don't really need them
|
|
What is the cause of transient or temporary thyrotoxicosis?
|
Thyroiditis
|
|
How do you distinguish between thyrotoxicosis and thyroiditis?
|
Thyroiditis won't light up on a thryoid scan
|
|
What is the main cause of Primary Hyperthyroidism?
|
Graves Disease--85% (Diffuse Hyperplasia)
|
|
Besides Graves Disease, what are other causes of primary hyperthyroidism?
|
Toxic Multinodular Goiter
Toxic Adenoma/Carcinoma Drug-Induced Goiter |
|
What is critical to obtain when taking a patient's history who is presenting with hyperthyroidism?
|
The medication history--Amiodarone, Iodides, and Lithium can all cause hyperthyroidism
|
|
Thyroiditis, Struma ovarii, and exogenous hyperthryoidism are all causes of what?
|
Thyrotoxicosis
|
|
What are two examples of Exogenous Hyperthyroidism?
|
Iatrogenic and Factitious Thyroidism
|
|
What is Iatrogenic Hyperthryoidism?
|
Excessive administration of thyroxine by physicians
|
|
What is Factitious Thyrotoxicosis?
|
Result of patient self administering excessive doses of thryoxine--for weight loss or malingering
|
|
What is the typical age of onset and who is mostly affected by hyperthyroidism?
|
Women between 40-60 years of age
|
|
What is the classic triad of symptoms seen in Graves Disease?
|
Hyperthyroidism
Exophthalmos Pretibial Myxedema |
|
What is the typical age of onset for Graves Disease?
|
Ages 20-40
|
|
Is there a genetic component associated with Graves Disease?
|
Yes
|
|
What type of disorder is Graves Disease?
|
Autoimmune disorder
|
|
What antibodies are produced in Graves Disease?
|
TSI--binds to the TSH receptor and triggers release of T3 and T4
|
|
What is the vast majority of thyroiditis caused be?
|
Autoimmune disorder
|
|
What is the most common cause of hypothyroidism?
|
Hashimoto Thyroiditis
|
|
What type of thyroiditis is believed to be caused by a viral infection?
|
Subacute Granulomatous Thyroiditis (DeQuervain)
|
|
What do most patients with DeQuervain present with?
|
An antecedent respiratory infection
|
|
What are the symptoms of DeQuervain?
|
PAINFUL, enlarged thyroid that resolves
Difficutly swallowing Symptoms of hyperthyroidism |
|
What is the recovery like in DeQuervain?
|
Almost always complete and rarely progresses to chronic thyroiditis and hypothyroidism
|
|
What type of thryoiditis is associated with post partum?
|
Subacute Lymphocytic Thyroiditis
|
|
What type of goiter is associated with subactue lymphocyctic thyroiditis?
|
Painless goiter
|
|
What symptoms are associated with subacute lymphocytic thyroiditis?
|
Typical thyrotoxicosis symptoms--tremor, palpitations, tachycardia, weakness, and fatigue
|
|
Are the symptoms mild or severe in subactue lymphocyctic thyroiditis?
|
Usually mild and transient--develop over 1-2 weeks and last for 2-8 weeks
|
|
What is the difference between subacute lymphocyctic and DeQuervian thyroiditis?
|
A minority of patients may progress to hypothyroidism in subacute lymphocyctic thyroiditis
|
|
What is the rare variant of subacute lymphocyctic thyroiditis?
|
Reidel Struma
|
|
What happens in Reidel Struma?
|
Complete replacement of the thyroid gland by fibrous tissue
|
|
What is subclinical hypothryoidism?
|
An asymptomatic patient with a high measured sensitive TSH and a normal T3 and T4
|
|
What is cretinism?
|
Hypothyroidism developing in infancy or early childhood--severe mental retardation--short stature, coarse facies, and protruding tongue
|
|
What are the two main causes of hypothyroidism?
|
Autoimmune disorder and postablative surgery
|
|
What is the most common cause of hypothyroidism?
|
Hashimoto's Thyroiditis
|
|
Who is normally affected by Hashimoto's?
|
Usually older women
|
|
How does a patient with Hashimoto's present?
|
Initially with hyperthyroidism but progresses to hypothyroidism
|
|
What type of antibodies are produced in Hashimoto's?
|
Anti-TPO or anti-thyroglobulin
|
|
What is a classic cell seen in Hashimoto's?
|
Hurthle cells--eosinophilic and stain pink
|
|
What are the preferred tests for the functional state of the thyroid?
|
TSH and FT4
|
|
If your TSH test is elevated, what does this suggest?
|
Hypothyroid
|
|
If you TSH test is decreased, what does this suggest?
|
Hyperthyroid
|
|
If the FT4 test is high, what does this suggest?
|
Hyperthyroid
|
|
If the FT4 test is low, what does this suggest?
|
Hypothyroid
|
|
What is the preferred test for autoimmune thyroiditis?
|
Anti-TPO antibody
|
|
What is the preferred test for Graves disease?
|
Thyrotropin receptor anitbodies (TRA)
|
|
To confirm a diagnosis of hyperthryoidism, what test would you order?
|
Anti-TPO and/or Anti-TRA )TSI, TGI)
|
|
If the TSH is low but the FT4 is normal, what test would you order next?
|
Free T3
|
|
To confirm hypothyroidism, what test would you order?
|
Anti-TPO antibody
|
|
What is a solitary thyroid nodule?
|
Palpable discrete mass within an otherwise normal thyroid
|
|
What accounts for 90% of solitary nodules?
|
Non-neoplastic disorders--Nodular hyperplasia, Colloid cysts, and Foci of thryoiditis
|
|
What percentage of solitary nodules are cacinoma?
|
Less than 1%
|
|
What are the risk factors for a solitary nodule containing carcinoma?
|
Solitary nodule vs. mulitple
Nodules in younger patients Nodules in males History of radiation tx to neck |
|
What type of nodules are more likely to contain carcinoma?
|
Non-functioning or "cold" nodules
|
|
What type of nodules are almost always benign?
|
Functioning or "warm" nodules
|
|
What does a radionuclide thyroid scan tell us?
|
The functionality of the thyroid
|
|
What other tests can be done to evaluate solitary nodules?
|
Thryoid function tests
U/S Fine Needle Aspiration Biopsy |
|
Does a thryoid that is hypoactive or hyperactive take up a lot of iodine?
|
Hyperactive thyorid takes up a lot of iodine
|
|
Does a thyroid that is hypoactive or hyperactive take up a only a small amount of iodine?
|
Hypoactive thyroid takes up a small amount of iodine
|
|
What is a normal amount of iodine uptake seen in a euthryoid patient?
|
6-7%
|
|
Is a "cold" nodule non-functioning or functioning?
|
Non-functioning--meaning it is not secreting hormone
|
|
Is a "warm" nodule non-functioning or functioning?
|
Functioning--releasing hormone--takes up dye because it doesn't suppress the entire gland
|
|
What does a "hot" nodule do to the thyroid gland?
|
Turns the gland off so you won't see any iodine uptake
|
|
Is a multinodular goiter a good or a bad sign?
|
Usually a good sign
|
|
What test remarkably reduces the amount of thryoid nodules that need to be removed?
|
Fine Needle Aspiration Biospy
|
|
What does the term adenoma refer to?
|
A single thryoid nodule or mass--can also be called uninodular
|
|
Are the vast majority of adenomas functional or non-functional?
|
Non-functional--designated non-toxic
|
|
What do follicular adenomas look like?
|
Well-circumscribed, solid, gray-white to red-brown
|
|
Do follicular adenomas have a capsule?
|
Yes
|
|
What does the term "toxic" mean in reference to a follicular adenoma?
|
Inidicates that the adenoma is producing thyroid hormone independent of TSH
|
|
What is papillary carcinoma of the thyroid?
|
Malignant neoplasm with numerous, irregular, finger like projections of fibrous stroma that is covered with surface layer of neoplastic epithelia cells
|
|
What is the most common type of thyroid carcinoma?
|
Papillary carcinoma
|
|
Are papillary carcinomas small or large and are they usually unifocal or multifocal?
|
They vary in size and are most often multifocal
|
|
What size are the neoplasms that are designated as carcinomas?
|
1-3 cm
|
|
What are the neoplasms that are <1.0 cm in size termed?
|
Microcarcinomas--rarely assoicated with metastisis
|
|
!/3 of patients with papillary carcinoma of the thyroid present with what?
|
Clinically evident enlarged lymph nodes
|
|
Where is the primary diesease of papillary carcinoma confined to in 90% of the patients?
|
Confined to the neck
|
|
What is the 5-year and 10-year survival rate of papillary carcinoma of the thyroid?
|
5 year-105%
10 year-95% |
|
What type of cell is typically seen in papillary carcinoma of the thyroid?
|
Orphan Annie cells
|
|
What should all papillary neoplasms of the thryoid be considered as?
|
Malignant--papillary adenomas do not exist
|
|
Besides Orphan Annie Cells, what is another characteristic thing seen in Papillary carcinoma?
|
Psammoma bodies--areas of calcification
|
|
If you collect a cervical sample from a patient and there are lymph nodes present, what must you rule out?
|
Papillary carcinoma of the thryoid
|
|
Does papillary carcinoma have a variant form assoiciated with it?
|
Yes--Follicular variant of papillary carcinoma
|
|
What is the median age of diagnosis of Follicular Carcinoma of the Thyroid?
|
6th decade of life
|
|
What is a risk factor assoiciated with follicular carcinoma?
|
Radiation exposure and also increased frequency with iodine deficiency
|
|
Does follicular carcinoma usually present with lymph node involvement?
|
No--occurs in less than 10% at presentation
|
|
How does follicular carcinoma tend to spread?
|
Hematogenously
|
|
What percentage of patients with follicular carcinoma present with distant metastisis?
|
15% overall
|
|
What percentage of patients with follicular carcinoma develop metastisis and where?
|
5-40% develop metastisis to the lung and bone
|
|
What is the 10-year survival rate of patients with follicular carcinoma?
|
90%
|
|
Why has the prevalence of follicular carcinoma changed over the years?
|
Decreasing incidence
Increased recognition of the follicular variant of papillary carcinoma 15% of normal thryoid glands have thryoid follicles in the thyroid capsule (less diagnosis of follicular carc.) |
|
What two settings does medullary carcinoma of the thyroid occur in?
|
Familial and sporadic
|
|
What are the familial medullary carcinoma (MEN) characteristics?
|
Typically bilateral
Associated with other benign or malignant endocrine tumors More common in children Much earlier age of onset |
|
What are the sporadic form of medullary carcinoma charactersitics?
|
Unilateral
Presents age 40 to 60 |
|
How is the medullary carcinoma tumor idenitifed histologically?
|
By the presence of amyloid
|
|
What do all medullary tumors produce?
|
Calcitonin
|
|
What is the 10-year survival rate associated with medullary carcinoma?
|
65%--worse prognosis than papillary or follicular cancer
|
|
What are the characteristics of anaplastic carcinoma of the thyroid?
|
Rapidly progressive, lethal rare cancer that occurs in older individuals (mean age of onset is 65)
|
|
What is the mean survial for a diagnosis of anaplastic carcinoma of the thryoid?
|
6 months
|
|
What do patients diagnosed with anaplastic carcinoma frequently have a history of?
|
Long standing goiter
Prior papillary thryoid carcinoma Concurrent papillary carcinoma |
|
Out of the 10 cases of thryoid cancer/100,000, how many of them are anaplastic carcinoma?
|
<10%
|
|
How does anaplastic carcinoma appear histologically?
|
Wildly undifferentiated
|
|
What is the best way to tell if the parathyroid glands have increased in size?
|
Weight
|
|
What does the relative size neoplasia clue tell us?
|
4 Big glands--Hyperplasia
1 Big gland + 3 Average--Adenoma |
|
How is the parathyroid gland regulated?
|
By the free calcium level
|
|
What are the metabolic effects of the parathyroid?
|
Stimulates osteoclasts
Increases calcium resorption in the GI and kidney Converts Vit D to an active form in the kidney Increases phophate excretion |
|
What is the most common cause of hypercalcemia?
|
Primary hyperparathyroidism
|
|
What is the most common cause of symptomatic hypercalcemia?
|
Malignancy
|
|
What is primary hyperparathyroidism known as?
|
The disease of bones, stones, groans, and moans
|
|
What are the causes of hyperparathyroidism?
|
Parathyroid adenoma (80%)
Parathyroid Hyperplasia Parathyroid Carcinoma |
|
What is the most common symptom of hyperparathyroidism?
|
Kidney stones
|
|
What is osteitis fibrosa cystica?
|
"Brown tumor"; Osteoclast burrowing themselves in bone--seen in hyperparathryoidism
|
|
Where is a common location for brown tumors to occur?
|
The jaw
|
|
What is osteitis fibrosis cytica sometimes referred to?
|
von Recklinghausen disease of bone
|
|
What is the age associated with the greatest incidence of hyperparathyroidism?
|
age 40-65
|
|
What are some diseases associated with hyperparathyroidism?
|
Diabetes mellitus type 2
Thyroid Disease |
|
What are parathyroid adenomas?
|
Solid neoplams that are almost always solitary nodules
|
|
Where do parathyroid adenomas typically occur?
|
Superior parathryoid glands
|
|
What is the normal weight of a prathyroid gland?
|
30 mg
|
|
What is the weight of a parathyroid adenoma?
|
Anywhere from 300-3000 mg
|
|
How do pituitary adenomas typically appear?
|
Reddish-brown appearance and measure from 1-4 cm in dimension
|
|
What are the most common cell type seen in PTH adenoma?
|
Cheif cells
|
|
What is the 2nd most common form of primary hyperparathyroidism?
|
Parathyroid hyperplasia
|
|
How is the diagnosis of parathyroid carcinoma made?
|
By properties seen in the gland--Necrosis, hemorrhage, and attachment
|
|
How do the cells in parathyroid carcinoma typically appear?
|
Uniform
|
|
What is secondary hyperparathyroidism caused by?
|
Renal failure
|
|
Is the calcium low or high in secondary hyperparathyroidism?
|
Low--hypocalcemia
|
|
What does the low calcium level in secondary hyperparathyroidism stimulate?
|
Secretion of PTH--causing hyperplasia of the parathyroid glands
|
|
What are the symptoms of hyperparathyroidism?
|
Fatigue, muscle weakness, nausea, bone pain, and fractures
|
|
What do patients with a CCr of less than 40 have histological evidence of?
|
Hyperparathyroid bone disease
|
|
What is the most common cause of hypoparathyroidism?
|
Surgical removal
|
|
What is the most important thing to do following thyroid surgery?
|
Must monitor the calcium levels after surgery
|
|
What are other causes of hypoparathyroidism?
|
Familial
Idiopathic Hypomagnesemia Replacement of destruction of normal PTH tissue |
|
In who are the adrenal glands abnormally large compared to the rest of the body?
|
Fetal/Newborns
|
|
What is Cushing syndrome?
|
High cortisol levels
|
|
What are most causes of Cushing's syndrome the result of?
|
Administration of exogenous glucocorticoids
|
|
What is the most common cause of endogenous Cushing syndrome?
|
Primary hypothalamic-pituitary disease associated with hypersecretion of ACTH
|
|
What is it called when there is high levels of cortisol and ACTH?
|
Cushing disease
|
|
What is the cause of primary aldosteronism/hyperaldosteronism?
|
Excess production of aldosterone
|
|
What are the symptoms of hyperaldosteronism?
|
Hypertension
Hypokalemia Decreased renin activity |
|
What is the most common cause of hyperaldosteronism?
|
Adenoma--Conn syndrome
|
|
What is primary acute adrenocortical insufficiency?
|
Acute failure of the adrenal cortex
|
|
What can cause acute adrenocorticol insuffiency?
|
Stress
Too rapid withdrawal from exogenous corticosteroids Massive Adrenal Hemorrhage |
|
What is Waterhouse-Friderichsen Syndrome?
|
Massive adrenal hemorrhage
|
|
What are the causes of Waterhouse-Friderischsen Syndrome?
|
Bacterial infection
Septicemia--usually Nisseria meningiditis Shock DIC |
|
What are the causes of Primary Chronic Adrenocorticol Insufficiency--Addison's Disease?
|
Autoimmue adrenalitis
AIDS Tuberculosis Metastatic cancer |
|
What are the symptoms of Addison's Disease?
|
Fatigue/Weakness
GI symptoms Hyperpigmentation Hypotension Hyperkalemia Hypoglycemia |
|
Which is more common, to get a primary tumor of the adrenal gland or to get metastatic cancer of the adrenal gland?
|
Metastatic cancer of the adrenal gland
|
|
What causes secondary chronic adrenocorticol insuffiency?
|
Any disorder of the hypothalamus or pituitary which reduces the output of ACTH
|
|
What symptom is different in secondary chronic adrenocorticol insuffiency from primary?
|
Hypopigmentation
|
|
What is the "PEARL" of secondary adrenocortical insuffiency?
|
Hypopigmentation
|
|
What is the one constant finding in secondary insufficiency?
|
Moderate to marked reduction in adrenal size
|
|
What is an adrenocortical adenoma?
|
Benign neoplasm of adrenal cortical cells
|
|
What is the most common adrenocortical adenoma?
|
Aldosterone producing adenomas
|
|
Who is most likely to have adrenocortical adenoma?
|
Females in their 3rd to 5th decade
|
|
Are adrenocortical carcinomas common or rare?
|
Rare--between 0.05% and 0.2% of all cancers
|
|
What can adrenocortical carcinomas be confused with?
|
Renal tumors--ususally large when discovered
|
|
Who does adrenocortical carcinoma affect and what is the prognosis?
|
Affects any age----Poor prognosis (mean survival 2 years)--may be functional (secreting hormones)
|
|
What is the most common type of cancer causing metastisis to the adrenal glands?
|
Lung cancer
|
|
What is a pheochromocytoma?
|
Adrenal medulla neoplasm
|
|
What is the most common symptom of a pheochromocytoma?
|
Hypertension
|
|
What is characteristic about the "attacks" seen in pheochromocytoma?
|
They are sudden severe attacks assoiciated with release of cathecholamines
|
|
What is the "Pluin triad" seen in pheochromocytoma?
|
Headache
Sweating Palpitations |
|
What are the laboratory findings of a pheochromocytoma?
|
Increased urinary free catecholamines and metabolites (VMA, metanephrines)
|
|
What are Robbins Rule of 10's for pheochromocytoma?
|
10% arise in association with familial syndromes
10% are extra-adrenal 10% of non-familial are bilateral 10% are biologically malignant 10% arise in childhood |
|
Where do 10% of pheochromocytomas occur?
|
In the aortosympathetic system
|
|
What is characteristic of a pheochromocytoma seen histologically?
|
"Zellballen" nests of cells
|
|
What is MEN-1?
|
Werner Syndrome
|
|
What organs are affected in Werner Syndrome?
|
Parathyroid, Pancreas, Pituitary
|
|
What is MEN-2?
|
Sipple Syndrome
|
|
What is assoicated with Sipple Syndrome/MEN-2?
|
Meduallry carcinoma of the thyroid, Pheochromocytoma, and Hyperplasia of the PTH
|
|
What gene locus is mutant in MEN-2?
|
RET
|
|
What gene locus is mutant in MEN-1?
|
MEN
|
|
What is associated with MEN-2B?
|
Mucosal veroma and medullary carcinoma and pheochromocytoma
|
|
What do alpha cells of the pancreas secrete?
|
Glucagon
|
|
What do beta cells of the pancreas secrete?
|
Insulin
|
|
What do gamma cells of the pancreas secrete?
|
Somatostatin
|
|
What is the most important stimulus that triggers insulin synthesis?
|
Glucose
|
|
What is insulin's principle function?
|
To increase the rate of glucose transport into the cells of the body
|
|
What is the anabolic effect of insulin?
|
To increase synthesis and reduce degradation of glycogen, lipids, and proteins
|
|
What is Type 1 Diabetes Mellitus?
|
An absolute deficiency of insulin caused by an autoimmune destruction of beta cells (IDDM)
|
|
What is Type 2 Diabetes Mellitus?
|
Resistance to insulin and inadequate secretory response by the pancreatic beta cells
|
|
What is MODY?
|
A primary defect in beta cell function without beta cell destruction
|
|
What is gestational diabetes?
|
Any degree of glucose intolerance during pregnancy
|
|
What is the ADA criteria for the diagnosis of Diabetes Mellitus?
|
DM symptoms--polyuria, polydipsia, and unexplained weight loss PLUS a random plasma glucose greater than 200
OR Fasting plasma glucose >126 repeated on a different day OR OGTT 2-hr PG >200 |
|
What is the intial diagnostic testing done for Diabetes Mellitus?
|
Fasting plasma glucose
|
|
What is the confirmatory test for diabetes mellitus?
|
Repeat fasting glucose on a different day
|
|
What is a monitoring test that can be done for Diabetes Mellitus?
|
Hemoglobin A1c--done following intial diagnosis and quarterly until patient is well controlled--once patient is well controlled can be done 2x a year
Self monitoring BG Dipstick |
|
What numbers are diagnostic diabetes mellitus?
|
126 or greater--provisional diagnosis of diabetes until confirmed by a test on a different day
110-125--impaired fasting glucose--represents an intermediate group "at risk" |
|
What type of diabetes is insulinitis often associated with?
|
Type 1
|
|
What type of diabetes is amyloid often associated with?
|
Type 2
|
|
Who is typically affected by Type 1 Diabetes?
|
Children--usually less than 20 years old
|
|
Who is typically affected by Type 2 Diabetes?
|
Usually adults
|
|
What is the clincal presentation of a patient with Type 1 diabetes?
|
<20 years
Polyuria, polydipsia, polyphagia Skinny |
|
What is the clincal presentation of a patient with Type 2 diabetes?
|
>30 years
Common family history Obese Can be asymptomatic 3 P's Blurred vision Tingling in the feet |
|
Which type of diabetes mellitus has a definite genetic component?
|
MODY--usually autosomal dominant
|
|
What is gestational diabetes?
|
Normal pregnancy creates a condition of impaired target organ response to insulin or insulin resistance--similar to type 2
|
|
Are gestational diabetics affected for life?
|
Not usually--glucose returns to normal rapidly
|
|
What are the maternal clinical associations with GDM?
|
More likely to develop hypertension and preeclampsia
Increased risk for C/S Increased risk for PTL Increased UTI's Higher incidence of PP hemorrhage |
|
What are the fetal clinical associations with GDM?
|
Macrosomia
Higher incidence of birth trauma--shoulder dystocia |
|
What are the macrovascular complications seen in diabetes?
|
Atherosclerosis
MI Stroke Gangrene |
|
What are the microvascular complications seen in diabetes?
|
Capillary dysfunction
Retinopathy Nephropathy Neuropathy **Leading cause of blindness and renal failure** |
|
What is the #1 cause of limb amputation?
|
Diabetes Mellitus
|
|
What is the #1 cause of death in diabetics?
|
Myocardial infarction
|
|
What are the syndromes associated with pancreatic endocrine neoplasms?
|
Insulinoma (Hyperinsulinism)
Gastrinoma (Zollinger-Ellison) MEN syndrome |
|
What is the criteria used to diagnose pancreatic endocrine neoplasm malignancy?
|
Metastases to lymph nodes or distant site
Vascular invasion Gross invasion of adjacent tissues |
|
What are the two types of pancreatic endocrine neoplasms?
|
Functioning and Non-functioning
|
|
What percentage of non-functioning pancreatic tumors have clinical evidence of metastisis?
|
90%
|
|
What is the best predictor of metastasis in pancreatic tumors?
|
The polypeptide secreted by the tumor?
|
|
What is the most common pancreatic neoplasm?
|
Insulinoma--Hyperinsulinsim
|
|
Are insulinomas most often benign or malignant?
|
Benign--90%
|
|
What is the clinical triad associated with pancreatic neoplasms?
|
Attacks of hypoglycemia
Confusion, stupor, loss of consciousness Attacks precipitated by fasting or exercise--relieved by administering glucose |
|
What is a gastrinoma?
|
Islet cell carcinoma secreting gastrin
|
|
Where do gastrinomas usually arise?
|
Duodenum, pancreas, or near pancreas
|
|
About how many gastrinomas are malignant
|
About 50%
|
|
What are the symptoms assoiciated with a gastrinoma?
|
Peptic ulcer disease
Diarrhea |
|
What are the syndromes associated with pancreatic endocrine neoplasms?
|
Insulinoma (Hyperinsulinism)
Gastrinoma (Zollinger-Ellison) MEN syndrome |
|
What is the criteria used to diagnose pancreatic endocrine neoplasm malignancy?
|
Metastases to lymph nodes or distant site
Vascular invasion Gross invasion of adjacent tissues |
|
What are the two types of pancreatic endocrine neoplasms?
|
Functioning and Non-functioning
|
|
What percentage of non-functioning pancreatic tumors have clinical evidence of metastisis?
|
90%
|
|
What is the best predictor of metastasis in pancreatic tumors?
|
The polypeptide secreted by the tumor?
|
|
What is the most common pancreatic neoplasm?
|
Insulinoma--Hyperinsulinsim
|
|
Are insulinomas most often benign or malignant?
|
Benign--90%
|
|
What is the clinical triad associated with pancreatic neoplasms?
|
Attacks of hypoglycemia
Confusion, stupor, loss of consciousness Attacks precipitated by fasting or exercise--relieved by administering glucose |
|
What is a gastrinoma?
|
Islet cell carcinoma secreting gastrin
|
|
Where do gastrinomas usually arise?
|
Duodenum, pancreas, or near pancreas
|
|
About how many gastrinomas are malignant
|
About 50%
|
|
What are the symptoms assoiciated with a gastrinoma?
|
Peptic ulcer disease
Diarrhea |
|
What are the syndromes associated with pancreatic endocrine neoplasms?
|
Insulinoma (Hyperinsulinism)
Gastrinoma (Zollinger-Ellison) MEN syndrome |
|
What is the criteria used to diagnose pancreatic endocrine neoplasm malignancy?
|
Metastases to lymph nodes or distant site
Vascular invasion Gross invasion of adjacent tissues |
|
What are the two types of pancreatic endocrine neoplasms?
|
Functioning and Non-functioning
|
|
What percentage of non-functioning pancreatic tumors have clinical evidence of metastisis?
|
90%
|
|
What is the best predictor of metastasis in pancreatic tumors?
|
The polypeptide secreted by the tumor?
|
|
What is the most common pancreatic neoplasm?
|
Insulinoma--Hyperinsulinsim
|
|
Are insulinomas most often benign or malignant?
|
Benign--90%
|
|
What is the clinical triad associated with pancreatic neoplasms?
|
Attacks of hypoglycemia
Confusion, stupor, loss of consciousness Attacks precipitated by fasting or exercise--relieved by administering glucose |
|
What is a gastrinoma?
|
Islet cell carcinoma secreting gastrin
|
|
Where do gastrinomas usually arise?
|
Duodenum, pancreas, or near pancreas
|
|
About how many gastrinomas are malignant
|
About 50%
|
|
What are the symptoms assoiciated with a gastrinoma?
|
Peptic ulcer disease
Diarrhea |
|
What are the syndromes associated with pancreatic endocrine neoplasms?
|
Insulinoma (Hyperinsulinism)
Gastrinoma (Zollinger-Ellison) MEN syndrome |
|
What is the criteria used to diagnose pancreatic endocrine neoplasm malignancy?
|
Metastases to lymph nodes or distant site
Vascular invasion Gross invasion of adjacent tissues |
|
What are the two types of pancreatic endocrine neoplasms?
|
Functioning and Non-functioning
|
|
What percentage of non-functioning pancreatic tumors have clinical evidence of metastisis?
|
90%
|
|
What is the best predictor of metastasis in pancreatic tumors?
|
The polypeptide secreted by the tumor?
|
|
What is the most common pancreatic neoplasm?
|
Insulinoma--Hyperinsulinsim
|
|
Are insulinomas most often benign or malignant?
|
Benign--90%
|
|
What is the clinical triad associated with pancreatic neoplasms?
|
Attacks of hypoglycemia
Confusion, stupor, loss of consciousness Attacks precipitated by fasting or exercise--relieved by administering glucose |
|
What is a gastrinoma?
|
Islet cell carcinoma secreting gastrin
|
|
Where do gastrinomas usually arise?
|
Duodenum, pancreas, or near pancreas
|
|
About how many gastrinomas are malignant
|
About 50%
|
|
What are the symptoms assoiciated with a gastrinoma?
|
Peptic ulcer disease
Diarrhea |
|
What are the main causes of Adult Respiratory Distress Syndrome?
|
Pulmonary infection
Gastric aspiration Sepsis Trauma |
|
What happens to the lungs in ADRS?
|
Diffuse damage to alveolar capillary walls mediated by cytokines--IL-8, IL-1, and TNF--which lead to PMNs
|
|
Who usually gets ARDS?
|
Patients who are already sick
|
|
What is the clinical presentation of ARDS?
|
Rapid onset in already ill patients
Dyspnea and tachypnea Cyanosis and respiratory failure Diffuse bilateral infiltrates |
|
Is ARDS associated with a high or low mortality rate?
|
High--60%
|
|
How does ARDS typically stain?
|
Pink--staining proteins--hyaline membrane
|
|
What is idiopathic ARDS?
|
Acute Interstital Pneumonia (AIP)--Hamman-Rich Syndrome
|
|
What is the difference between AIP and ARDS?
|
AIP has no associated causative disorder
|
|
What are the two categories of Chronic Diffuse Lung Disease?
|
Obstructive and Restrictive
|
|
What are obstructive diseases?
|
Diseases that limit the rate of flow due to resistance
|
|
What is the FEV1 level in obstructive diseases?
|
Markedly reduced
|
|
What are examples of obstructive lung diease?
|
Emphysema
Chronic Bronchitis Bronchiectasis Asthma |
|
What are restrictive diseases?
|
Disease that limit the total lung capacity and residual volume with near normal flow rate
|
|
What is the FEV1 rate in restrictive diseases?
|
Mildly reduced
|
|
What are examples of restrictive diseases?
|
Chest wall disorders
Obesity ARDS Interstitial fibrosis Pneumoconioses |
|
What are the characteristics of obstructive lung diseases?
|
Air flow obstruction
Increased compliance Decreased elasticity Increased TLC Barrell chested Can't get air out Decreased FEV |
|
What are the characteristics of restrictive lung diseases?
|
Can't get air in
Decreased compliance Increased elasticity Decreased TLC Decreased FEV |
|
What are the two main types of emphysema?
|
Centriacinar/centrilobular (most common)
Panacinar/panlobular |
|
Which type of emphysema is caused by smoking?
|
Centriacinar
|
|
Where in the lung is centriacinar emphysema seen?
|
Upper lobes/apices
|
|
What the main cause of panacinar/panlobular emphysema?
|
Alpha-1 antitrypsin and smoking
|
|
Where in the lung is panacinar/panlobular emphysema mostly seen?
|
Lower lobes/anterior
|
|
What are the localized types of emphysema?
|
Irregular/paracicatrical
Distal acinar/paraseptal |
|
Which type of emphysema is associated with a damaged lung?
|
Distal acinar/paraseptal--spontaneous pneumothorax in young adults
|
|
What does emphysema destroy in the lungs?
|
The alveolar wall
|
|
What enzyme is deficient in emphysema?
|
Alpha-1 antitrypsin
|
|
What is the "primary villan" in emphysema?
|
Neutrophil secreted elastase
|
|
Do emphysema patients have adequate gas exchange?
|
Yes--Pink Puffers
|
|
Are emphysema patients acidotic or alkalotic?
|
Acidotic--can move CO2 outW
|
|
What is chronic bronchitis?
|
Defined as 3 months of productive cough/year for 2 consecutive years
|
|
What is the most common cause of chronic bronchitis?
|
SMOKING
|
|
Do chronic bronchitis patients have hyper or hypo secretion of mucus?
|
Hypersecretion of mucus
|
|
Is the Reid Index elevated or decreased in chronic bronchitis?
|
Elevated due to hypertrophy of submucosal glands
|
|
What is the most common finding of chronic bronchitis?
|
Destruction of the bronchus--small airways can also be involved
|
|
What often overshadows the lung problem in chronic bronchitis?
|
Cor pulmonale
|
|
Do chronic bronchitis patients have good or bad gas exchange?
|
Bad gas exchange--"Blue Bloaters"
|
|
What is the Reid Index?
|
Ratio of the thickness of mucous glands to wall from epithelium to cartilage
|
|
What is an abnormal Reid Index and with what disease is it usually seen in?
|
>0.4 in Chronic Bronchitis
|
|
What age group is typically affected by chronic bronchitis?
|
40-45
|
|
What age group is typically affected by emphysema?
|
50-75
|
|
Do chronic bronchitis patients have dyspnea?
|
Mild late in the disease
|
|
Do emphysema patients have dyspnea?
|
Severe early in the disease
|
|
What kind of cough is seen in chronic bronchitis?
|
Productive cough with copious sputum
|
|
What kind of cough is seen in emphysema?
|
Late cough with scant sputum
|
|
Are infections common in chronic bronchitis?
|
Yes
|
|
Are infections common in emphysema?
|
No--occasional
|
|
Is cor pulmonale more common in chronic bronchitis or emphysema?
|
Chronic bronchitis--rarely seen in emphysema
|
|
Is airway resistance increased in chronic bronchitis or empysema?
|
Chronic bronchitis
|
|
Is the elastic recoil low in emphysema or chronic brochitis?
|
Emphysema
|
|
What is seen on a chest x-ray of chronic bronchitis?
|
Prominent vessels and a large heart
|
|
What is seen on a chest x-ray of emphysema?
|
Hyperinflation and a small heart
|
|
Who are the blue bloaters?
|
Chronic Bronchitis
|
|
Who are the pink puffers?
|
Emphysema
|
|
What is asthma?
|
Chronic inflammatory disorder of airways--recurrent wheezing or breathlessness
|
|
When is asthma most often a problem?
|
At night and early morning
|
|
What are inducers of asthma?
|
Allergens
Exercise Cold Anxiety |
|
Is asthma associated with bronchoconstriction or bronchodilation?
|
Episodic bronchoconstriction
|
|
What is status asthmaticus?
|
Prolonged severe attacks
|
|
What is atopic asthma?
|
Genetic tendency to develop IgE antibodies to inhaled allergens--usually seen in childhood
|
|
What is the pathogenesis of atopic asthma?
|
Mucosal mast cells react releasing inflammatory meidators--Stimulation of vagal receptors causing bronchoconstriction
|
|
What is non-atopic asthma?
|
Associated with pulmonary infections that are usually viral--no allergic indicators
|
|
What is drug induced asthma?
|
Asthma usually caused by aspirin
|
|
What is the morphology associated with asthma?
|
Overinflated lungs
Over production of thick mucous Thickened bronchial basement membranes Eosinophils in bronchial wall Hypertrophy of submucosal glands and smooth muscle Goblet cell metaplasia |
|
What is pathognomonic for asthma?
|
Charcot Leyden Crystals--dead eosinophils
Curschmann spirals |
|
What is bronchiectasis?
|
Permanent dilation of bronchi and bronchioles
|
|
What causes bronchiectasis?
|
Tissue destruction secondary to infection
|
|
What are the characteristics of restrictive lung diseases?
|
Can't get air in
Decreased TLC Decreased residual volume Decreased FEV |
|
What is classic at the end stage of restrictive diseases?
|
Honeycomb lung
|
|
What is the pathogenesis of Idiopathic Pulmonary Fibrosis?
|
Unknown
|
|
What is another name for Idiopathic Pulmonary Fibrosis?
|
Cryptogenic Fibrosing Alveolitis
|
|
What happens to the pneumocytes in Idiopathic Pulmonary Fibrosis?
|
Type I pneumocytes die and Type II hyperplasia
|
|
What types of things are involved in Idiopathic Pulmonary Fibrosis?
|
Inflammation
Cytokines Macrophages Fibroblast proliferation Collagen deposition |
|
What are the symptoms of IPF?
|
Insidious, unpredictable
Dyspnea Dry cough Cyanosis **Mean survival 3 years** |
|
What leads to fibrosis in IFP?
|
Repeated healing and scarring
|
|
What is Cryptogenic Organizing Pneumonia?
|
COP/BOOP--Unknown etiology
Possibly an unusual reaction to known infection and inflammatory process |
|
Is the pneumonia organized or unorganized in COP/BOOP?
|
Organized pneumonia--all connective tissue is the same age ad no interstital fibrosis--NO HONEYCOMB LUNG
|
|
Is COP/BOOP treatable?
|
Yes--usually responds to steroid treatment
|
|
What type of cells are usually seen in COP/BOOP?
|
Masson's bodies
|