Lecture 9.2 Highlights Flashcards
* = also MJ slide
List the 2 types of anterior pituitary tumors and their symptoms
1) Hormone secreting = “functional”
-Hormone excess Sx; likely small
2) Non-hormone secreting = “hypofunctioning”
-No hormone Sx, likely large
-Structural Sx: bitemporal hemianopsia
What type of anterior pituitary tumor is more likely to have bitemporal hemianopsia?
Non-hormone secreting
1) Normal function of prolactin axis: Because prolactin is typically released during pregnancy, the desired effect is to ________ ovulation and _________ lactation
2) Therefore, symptoms of prolactinoma are _________ and _____________.
1) inhibit; stimulate
2) amenorrhea; galactorrhea
*List the three cases that increase prolactin levels and their respective pathways (abbreviated version)
1) Pregnancy: disinhibits lactotrophs [inhibits dopamine release]
2) Schizophrenia: disinhibits lactotrophs [and mimics prolactinoma Sx]
3) Hypothyroidism: TRH also stimulates lactotrophs
*Prolactinoma pathology of Dx in women :
1) What are the 2 primary Sx?
2) What does the med list NOT include?
3) What is normal?
4) What is elevated?
1) Amenorrhea and galactorrhea
2) Antipsychotics
3) TSH is normal
4) Prolactin is elevated
*Prolactinoma
1) Men may present with ___________ Sx.
2) What do men’s labs look like?
3) What are both men and women often treated with?
1) structural
2) Labs should be the same, sans the beta HCG test
3) Dopamine agonists first, resection later
Under normal function, hypothalamus stimulates somatotrophs w. the release of GHRH and ___________ them with release of somatostatin
inhibits
True or false: IGF-1 normally is like insulin, and most importantly, causes growth
True
Pathological IGF-1 levels; describe how they affect the:
1) Heart
2) Bones
3) Liver + spleen
4) Metabolic
1) Diastolic heart failure
2) Hypertrophy and linear growth (if growth plates are not fused)
3) Hepatosplenomegaly
4) HTN, DM, HLD, obesity
1) If hypersecreting tumor occurs __________ puberty, pt will be tall, and proportionally developed; this is called “______________”
2) If hypersecreting tumor occurs ___________ puberty, the epiphysial plates will be closed and pt will have bone growth without elongation; this is called “_______________”
3) Both patients will risk what and develop what?
1) before; “gigantism”
2) after; “acromegaly”
3) obesity and develop DM, HTN, hyperlipidemia
GH Tumor pathology of Dx:
1) What should you test for?
2) What should you do if this is elevated? Why?
3) What supports Dx?
1) IGF-1
2) “Glucose suppression” f/u test
-Because GH is counter to insulin in its effects, it works as a regulatory hormone
3) Failure to suppress GH with glucose challenge supports diagnosis
Describe the Pathology of treatment of a GH tumor
1) Surgery is usually performed first
2) If ineffective, medicinal treatment with octreotide
-Why? This is synthetic somatostatin
-Why? Review axis slide
GH Pathology: If there is too little GH, is this achondroplasia?
No
1) Adaptation to injury is one cause of what kind of hypopituitarism?
2) Why?
1) Chronic
2) Pituitary will priorities which hormones to secrete
Acute Hypopituitarism: List 2 causes and give examples
1) Sheehan’s
2) Adaptation: Hypotension, lethargy, coma, or death
SIADH causes __________ urine and _________ blood
concentrated; dilute
SIADH pts will have what:
1) Blood concentration?
2) Blood volume?
3) Sodium level?
1) Dilute
2) Normal
3) Low
True or false: aldosterone primary impacts volume
True
*When patient has low sodium, low serum osmolality, and normal blood volume, they have “euvolemic hypoosmolar hyponatremia”, you should think of what?
SIADH
1) Give 2 examples of what causes SIADH
2) What doesn’t cause SIADH? Why?
1) Meds and lung cancer
2) Adenomas; this is neural tissue
*In a DI Patient:
1) What will the urine osm. be?
2) What will the serum sodium be?
3) Volume will be ________________.
1) low (i think)
2) elevated (I think)
3) normal
*What can help treat DI?
Water depravation
What are the 2 main causes of DI? Give examples
highlighted 37
1) Give an example of a mineralocorticoid
2) What does it increase?
1) Aldosterone
2) Blood volume
1) Give an example of a glucocorticoid
1) List 5 of its effects
1) Cortisol
2) Anti-inflammatory
Increase in blood glucose
Increase in blood glucose
42
Reticularis
DHEA is a sex hormone precursor that transforms external genitalia
Regulated by ACTH along with cortisol
Adrenal medulla
43
CAH (congenital adrenal hyperplasia) most common subtype is what?
The enzyme 21-hydroxylase.
Adrenogenital syndromes: androgen excess
The adrenal cortex can secrete excess androgens in either of two settings
Adrenocortical neoplasms (usuallyvirilizingcarcinomas)
Congenital adrenal hyperplasia (CAH)
Under Normal Function:
1) Hypothalamus causes a bunch of steps that ultimately cause the fasciculata to release _____________
2) Cortisol inhibits ACTH and CRH
cortisol
49
Normal ACTH synthesis
Pro-opio-melanocortin (POMC) is turned into ACTH in the corticotropes
*Note that keratinocytes also
*List 3 effects of hypercortisolism
1) HTN
2) DM
3) Obesity
1) Patients with ___________ symptoms of HTN, DM, Central obesity should have their ______-night cortisol checked
2) Alternative testing is ______________ collection
refractory; late-night
2) 24-hour urine
*1) So, the cortisol is high? Now what do you give?
2) What 2 effects should this suppress?
3) What are the 2 potential outcomes?
1)
2) Hypothalamus and the anterior pituitary
3)) 52 highlight
If there is not suppression of cortisol, they have an illness of hypercortisolism
If there is suppression of cortisol, they have no illness, and you need to look elsewhere to explain s/s
*1) So, the low-dose test didn’t suppress cortisol. Now what?
2) What do you check? What do you know if the result of this is low?
-Give an example of a potential cause
3) What if the result is still high?
-Give 2 examples of potential causes
1) They have hypercortisolism
2) ACTH; if low, then the axis is responding to suppression, and you know the cortisol is coming from somewhere outside the axis; Adrenal adenoma!
3) If ACTH is still high, then the illness is ACTH dependent
Pituitary adenoma
Paraneoplastic disease
-
So, the ACTH remains high after dexamethasone suppression, now what?
1) The endocrine axis __________ respond to a high enough dose of counterregulatory hormone.
2) This means that a _________-dose dexamethasone suppression test will cause a drop in ACTH if the source is a _______________.
3) When will the ACTH will high no matter what?
1) will
2) high-dose; pituitary adenoma
3) If the source is a small-cell lung cancer, the ACTH will be high no matter what
Primary hypercortisolism:
55 HL
This is the patient with adrenal tumor
Because the cortisol is always high, there is consistent negative feedback decreasing CRH and ACTH
Because ACTH is therefore low, the remaining adrenal tissue atrophies due to lack of stimulation
55 HL
Secondary Hypercortisolism:
ACTH dependent illness
Whether from pituitary adenoma or malignancy, this patient will have very high levels of ACTH
Because ACTH is always high, the adrenal glands will hypertrophy
Because ACTH is always high, melanocytes will be stimulated and will demonstrate hyperpigmentation
What are the 2 main types of hypercortisolism?
Primary and secondary
What causes you to look tan?
need to know
High ACTH
(has nothing to do w cortisol)
56 HL
Exogenous use of steroid:
These patients have high levels of cortisol
This will decrease the hormones produced upstream
They will have atrophy of the adrenal glands
This is why patients on long term steroids need to be taperedq
Primary adrenal insufficiency
1) Primary adrenal insufficiency means what?
2) How does it cause hyperpigmentation?
3) What 2 things does it cause to be low?
1) Adrenal glands not working
2) ACTH rises
3) aldosterone
List and name the 2 kinds of hypocortisolism
1) Chronic = Addison’s disease
2) Acute = almost dead
Pituitary hypocortisolism:
1) What does it do to ACTH?
2) What abt cortisol?
1) Low ACTH
2) Low cortisol
Hypo-functioning adrenal treatment
1) What do you do for low cortisol ?
2) What abt low aldosterone?
Give them what they lack:
1) Low cortisol = hydrocortisone
2) Low aldosterone = fludrocortisone
Review:
After low GFR or sodium triggers the RAAS, eventually, angiotensin II triggers thirst response, release of ADH, and stimulates the glomerulosa to release the mineralocorticoid called _______________
aldosterone
Review: What does aldosterone do?
Through the use of these [ENAC] channels, sodium is absorbed, which increases blood volume, and potassium is excreted
Review: Formula?
CO2 + H2O <> H2CO3 <> HCO3- + H+
(carbonic anhydrase helps w. first rxn)
Review: Give the short version of what aldosterone does
It increases blood volume with sodium, and “dumps” potassium into the urine
It raises the blood pH (more basic)
68
This will never be a kidney disorder
Why? Look at the mechanisms described above – there is no pathway for decreasing aldosterone production in renal pathology
Therefore, the issue will be due to the adrenal gland and its production of mineral corticoid
Hypo-functioning of the adrenal gland usually means a deficiency of both cortisol and aldo, which we have already discussed
69
This would be a “salt wasting” syndrome
Hyponatremia
Remember, that ENAC channels also discard potassium
Therefore, pts with low aldo will have
Hyperkalemia
70
*
What will happen to the blood pressure?
What will happen to the electrolytes, based on what you know?
71
*List and give examples of the 2 main kinds of hyperaldosteronism causes
1) Primary: adenoma; adrenal hyperplasia
2) Secondary: a problem with the kidney
1) Which is active, T3 or T4?
2) Which is inactive?
1) T3 = active
2) T4 = inactive
Thyroid peroxidase (TPO) and thyroglobulin (TG) work together to oxidize iodide and turn it into ________________
thyroid hormone
What 2 things work together to oxidize iodide and turn it into thyroid hormone?
“need to know”
Thyroid peroxidase (TPO) and thyroglobulin (TG)
Thyroid Hormone Release
1) T___ > T___ in the target cells, where it becomes more potent.
2)
3) These hormones increase cellular metabolism protein synthesis and catabolism as well as triglyceride mobilization
1) T4 > T3
2) These hormones increase cellular respiration thus increasing ATP consumption and heat
HYPERthyroid vs. hypOthyroid
77
*
HYPERthyroid vs. hypOthyroid
77
*
The opposite of what I just said. . .
*Grave’s disease (hyperthyroid):
1) A TSH receptor ___________ (Type II Hypersensitivity)
2) _____________, secondary to antibody causing increased fibroblast activity in the eye
1) antibody
2) Exophthalmos
1) In what condition will the pt develop a singular nodule?2) What happens to the remainder of the organ?
1) Toxic adenoma
2) Remaining thyroid will become less active
Toxic Multinodular Goiter: ________ nodules formed by receptor or second messenger mutations in several cells
many
Give examples of hyperthyroid causes
1) Grave’s disease
2) Toxic adenoma
3) Toxic Multinodular Goiter
4) Factitious
5) Stroma Ovarii
81
Give 2 other hyperthyroid causes
1) Factitious
2) Stroma Ovarii
Other thyroid disorders:
1) Subacute thyroiditis, also called “granulomatous,” also called ______________
2) Is this condition painful?
1) De Quervain’s
2) Thyroid hurts the whole time
*Thyroid Cancer: List 4 different kinds in order of freq
Calcium and Vit D:
1) Which is the Vit D you eat?
2) UV light creates D3 - Vit D precursor in your skin
Liver takes both forms and makes 25 Vit D, which is still an intermediate form
Kidney turns 25 Vit D into 1, 25 Vit D in the proximal convoluted tubule
1) D2
UV light creates D3 - Vit D precursor in your skin
Liver takes both forms and makes 25 Vit D, which is still an intermediate form
Kidney turns 25 Vit D into 1, 25 Vit D in the proximal convoluted tubule
1) In a healthy parathyroid, what does PTH do?
2) List the 3 target organs of PTH
1) Raises Ca+ when it’s low
2) Bone
GI tract
Kidney
Normal PTH activitiy
1) Kidney PTH Signals the release of 1, 25 Vit D
and tells kidney to resorb Ca and ELIMINATE Phosphate
1) eliminate
2) Serum Ca++ is HIGH and Phosphate is LOW
3) Increase in URINE Calcium
*HYPERparathyroid:
1) Bones: Osteoclast activity increased watch for _________ and _________________
2) Stones:
3) Abdominal groans
Increased Ca constipation and pain
4) Psychic moans
Ca encephalopathy
1) osteopenia and bone pain
2) Urine Calcium UP, urine phosphate UP calcium phosphate and calcium oxalate kidney stones
Hypoparathyroid:
1) The ________ tried to resect some of the thyroid and cut out parathyroid glands or cut their vascular supply. . .
_________ calcium
1) surgeon; LOW
Hyperactive nerves
Calcium is not available to block sodium channels on neuron, increasing total activity
In the _____________ of glucose, the pancreas releases insulin
presence
The chief trigger for pancreas to release insulin is what?
Glucose
Differentiate between fasting and non-fasting states
1) Fasting state: Low insulin and high glucagon > hepatic gluconeogenesis and glycogenolysis (glycogen breakdown) > we prevent hypoglycemia
2) Non-fasting state: pancreas releases insulin
Islets of Langerhans: ___________ cells (70%) release Insulin
Beta (B)
*Type I diabetes:
1) A __________ disease that’s a failure of self of tolerance in __________ specific for ______________.
2) Progressive destruction of islet beta cells → leading to absolute insulin deficiency.
1) Autoimmune disease; T cells; beta cell antigens
2)
*Type 2 diabetes 94
94
1. Peripheral Insulin resistance
2. Inadequate insulin section (beta cells) even with insulin resistance and ↑ blood glucose
95
Pancreatogenic diabetes
Gestational diabetes
What are 2 kinds of Multiple Endocrine Neoplasia?
1) MEN 1
2) MEN 2
MEN 1: List the 3 Ps
1) Parathyroid
2) Pancreas
3) Pituitary
MEN 2:
1) List 3 examples of type 2A
3) List 3 examples of type 2B
1) Pheochromocytoma
Medullary Thyroid Cancer
Parathyroid tumor
2) Pheochromocytoma
Medullary Thyroid Cancer
Neuronal Tumors
Differentiate between the inheritance of MEN 1 and MEN 2
MEN 1 is germline, MEN 2 is inherited autosomal dominant
