Lecture 9.2 (Endocrine) MJ slides Flashcards
List the three cases that increase prolactin levels and describe their respective hormones and pathways
1) Pregnancy: Estrogen, which is elevated in pregnancy, inhibits hypothalamus
This inhibits dopamine release and disinhibits lactotrophs
2) Schizophrenia: Antipsychotic medications also block dopamine
This disinhibits lactotrophs and mimics the symptoms of prolactinoma
3) Hypothyroidism: Thyroid releasing hormone from the hypothalamus also stimulates lactotrophs, which increases prolactin release and mimics symptoms of prolactinoma
Prolactinoma in women:
1) How does it present?
2) What things are not present/ abnormal?
3) What is abnormal?
1) Women: “amenorrhea and galactorrhea”
2) Med list does not include antipsychotic medication
TSH is normal
And pregnancy test is negative
3) Prolactin is elevated
MRI confirms pituitary adenoma, and it’s probably small (<1cm)
1) What is the main Sx of prolactinoma in men?
2) What will labs look like in men w prolactinoma ?
3) Describe the Tx of prolactinomas in both men and women
1) Men: might have “low libido”
May present with structural symptoms
2) Labs should be the same, sans the beta HCG test
3) Both are often treated with dopamine agonists first, resection later
GH tumor:
1) What happens if it occurs before puberty?
2) What if after puberty?
3) What do both pre and post puberty groups have in common?
1) Pt will be tall, and proportionally developed
They will still develop the pathological states of internal organs; this is called “gigantism”
2) The epiphysial plates will be closed and pt will have bone growth without elongation
-Jaw, hands, feet, will all continue to thicken
-This is called “acromegaly”
3) Both patients will risk obesity and develop DM, HTN, hyperlipidemia
SIADH pt pathology:
1) Describe blood osmolarity
2) Describe blood volume
3) Describe other Sx
1) These patients will have dilute blood
Blood is dilute because of the excess ADH
-How can you tell their blood is dilute? They will have a low “serum osmolality” on lab
2) These patients will have a normal blood volume
Volume is normal (euvolemic) because aldosterone is functioning normally
3) They will not have increased JVP, crackles, edema or other signs of volume overload
SIADH: Explain why these pts will have low sodium
This has nothing to do with salt resorption; salt is low because the excess water resorption is diluting the salt.
When a patient has low serum osm and low sodium, this is called “hypoosmolar hyponatremia”
List the wide array of effects of hypercortisolism
1) HTN
Alpha-1 agonism
Production of vasopressors
2) DM
Hyperglycemia
Obesity
3) Central obesity
“Purple Striae, buffalo hump, moon facies”
So, the cortisol is high? Now what?
1) Give low-dose dexamethasone suppression test
-Giving this artificial glucocorticoid should suppress the hypothalamus and the anterior pituitary
2) This, in turn, should suppress the adrenal gland’s production of cortisol
Hypercortisolism: When you give low-dose dexamethasone suppression test:
1) If there is not suppression of cortisol, you know what?
2) If there is suppression of cortisol, then what?
1) It’s an illness of hypercortisolism
2) They have no illness, and you need to look elsewhere to explain s/s
Hypercortisolism:
So, the low-dose test didn’t suppress cortisol. Now what?
1) They have hypercortisolism, but you don’t know where in the axis it is coming from, so check ACTH
-If it is low, then the axis is responding to suppression, and you know the cortisol is coming from somewhere outside the axis
2) If ACTH is still high, then the illness is ACTH dependent
So, the ACTH remains high after dexamethasone suppression, now what?
1) The endocrine axis will respond to a high enough dose of counterregulatory hormone.
-This means that a high-dose dexamethasone suppression test will cause a drop in ACTH if the source is a pituitary adenoma
2) If the source is a small-cell lung cancer, the ACTH will be high no matter what
List and describe the 2 types of hypercortisolism
1) Primary hypercortisolism: This is the patient with adrenal tumor
-Bc the cortisol is always high, there is consistent negative feedback decreasing CRH and ACTH
-Bc ACTH is therefore low, the remaining adrenal tissue atrophies due to lack of stimulation
2) Secondary Hypercortisolism: ACTH dependent illness
-Whether from pituitary adenoma or malignancy, this patient will have very high levels of ACTH
-Bc ACTH is always high, the adrenal glands will hypertrophy
-Bc ACTH is always high, melanocytes will be stimulated and will demonstrate hyperpigmentation
What are 2 causes of primary hyperaldosteronism?
1) Renin independent adenoma on the adrenal gland: “Conn’s Syndrome”
2) Adrenal hyperplasia
1) Describe causes of Secondary Hyperaldosteronism
2) Describe why it happens
1) A problem with the kidney
a) Obstructed renal artery, b) end stage renal disease
a) Kidney thinks the blood pressure is too low, b) everything else
2) The way that a dying kidney tries to save itself is through the renin/angio/aldo system
-Deeper explanation: sick kidney = low GFR = renin/angio/aldo system activated
-There is no known disorder of excess angiotensinogen, excess ACE, etc. . .
Hyperthyroid: List the Sx associated with each and what you should look out for
1) Heart
2) Gut
3) Brain
4) Bone
5) Temp
6) Metabolism
7) Nerves
1) Increased HR and contractility; afib
2) Increased motility; diarrhea
3) Increased activity; insomnia, poor concentration, emotional lability
4) Increased osteoclast activity; osteopenia and hypercalcemia
5) Increased temp; heat intolerance
6) Increased activity; increased appetite AND weight loss
7) Increased sensitivity; increased DTRs
Hypothyroid:
1) What are the Sx the opposite of?
2) Give examples of Sx
3) Which Sx is called cretinism?
4) What should you look for?
5) You can fix the poor growth, but you can’t correct what?
1) Hyperthyroid
2) Bradyarrhythmia
Constipation
Lethargy > coma
Cold intolerance
Weight gain
Decreased DTR (with some exceptions)
3) Mental retardation and poor growth (in children)
4) Macroglossia
5) Mental retardation
Grave’s Disease:
1) What causes it?
2) Why does a diffuse goiter occur?
3) What will be “hot” throughout?
1) TSH receptor antibody (Type II Hypersensitivity)
2) Thyroid is being stimulated throughout - there is uniform hyperplasia
3) Iodide uptake scan of the thyroid
Grave’s disease:
1) What is an important Sx? What causes it?
2) What helps it?
1) Exophthalmos, secondary to antibody causing increased fibroblast activity in the eye
2) NOT improved with treatment of hyperthyroidism
Improved with glucocorticoid
Pretibial myxedema
Thyroid cancer:
1) Which kind is the most common and is treated with reseaction?
2) Which is second most common? Describe its spread and how it’s treated?
3) Name + describe the third most common and what it’s assoc. with
4) What abt the 4th?
1) Papillary
2) Follicular; spreads readily + Tx with radioactive iodine ablation
3) Medullary; associated with MEN syndromes
4) Anaplastic
-Virulent
-Rapidly fatal
HYPERparathyroid: Describe how it effects each of the following and what you should watch for:
1) Bones
2) Stones
3) Abd. groans
4) Psychic moans (what is noteworthy abt this one?)
1) Osteoclast activity increased; osteopenia and bone pain
2) Urine Calcium UP, urine phosphate UP; calcium phosphate and calcium oxalate kidney stones
3) Increased Ca; constipation and pain
4) Ca; encephalopathy
Note: most of the time, a Ca high enough to cause encephalopathy is likely caused by malignancy (not parathyroid hormone)
Causes
MEN 1 syndrome
Chromosome 11 inversion
hypOparathyroid:
1) Why may it happen?
2) What is low? What does this cause and why?
3) Sx?
1) The surgeon tried to resect some of the thyroid and cut out parathyroid glands or cut their vascular supply. . .
2) LOW calcium; Calcium is not available to block sodium channels on neuron, increasing total activity
3) Perioral tingling
Digital paresthesia
Trousseau and Chvostek’s sign
T1 diabetes:
1) What type of condition is it?
2) What are involved?
3) Why does it occur?
4) Describe why there’s insulin deficiency
1) Autoimmune disease
2) Both autoreactive T cells and autoantibodies are involved.
3) Failure of self of tolerance in T cells specific for beta cell antigens
4) Progressive destruction of islet beta cells → leading to absolute insulin deficiency.
T2 DM: Describe the 2 main effects
NO Autoimmune Component
1. Peripheral Insulin resistance
2. Inadequate insulin section (beta cells) even with insulin resistance and ↑ blood glucose
