Endocrine Flashcards
Name the mealtime insulin analogs
Describe their onset/ offset
Glulisine, Aspart, Lispro
They have rapid onset and offset of action, mimicking physiologic postprandial insulin secretion
Describe the structure of the mealtime insulin analogs
AA substitution at the C terminal end of the B chain
Major SEs of Corticosteroids
- Immunosuppression (except with neutrophilia!!)
- Corticosteroid-induced psychosis
The 22q11.2 microdeletion associated with DiGeorge, causes what embryological component(s) not to develop?
3rd and 4th branchial pouches
Describe the Chvostek sign and the Trousseasu sign associated with DiGeorge Syndrome
The hypocalcemia assc. with DGS leads to increased neuromuscular excitability.
Chvostek sign- tapping on the facial nerve elicits twitching of the nose and lips
Trousseau sign- inflation of the BP cuff leads to carpal spasm
Tx of Acute Adrenal insufficiency
Hydrocortisone or dexamethasone
Lung mass + hyponatremia, is suggestive of what?
SIADH (secondary to Small cell lung carcinoma)
What is rT3 and what is it created from?
An inactive form of T3, that is generated almost entirely from peripheral conversion of T4
What effect does expgenous steroid abuse have on hematocrit?
Increases hematocrit
In Kallmann syndrome, there is an absence of GnRH secretory neurons in the _____________
hypothalamus
Finasteride MOA and indication
MOA: 5-alpha-reductase inhibitor that suppresses conversion of testosterone to DHT
Ind: BPH, Androgenetic alopecia
Hypoglycemia with an elevated insulin and low C-peptide level, suggests what?
High C-peptide level?
Low: exogenous insulin injection
High: insulin secretagogue or insulin-secreting tumor
Xanthomas are found where? What are they associated with?
These yellowish macules/papules are found on the medial eyelids. They are accumulations of macrophages + cholesterol/ TG and are assc. with hyperlipidemia/ dyslipidemia
Where is ADH synthesized? Is this the same location, or a different location from where it is stored?
In the hypothalamus. It is then transported, to the posterior pituitary for storage and later release into the circulation.
Only hypothalamic damage will be enough to cause central Diabetes insipidus
Leuprolide MOA
Continuous GnRH agonist
What is the most effective preventative intervention in almost all patients?
Smoking cessation
How do chronically elevated FFA levels contribute to insulin resistance?
By impairing insulin-dependent glucose uptake and increasing hepatic gluconeogenesis
How do OC treat hirsutism?
They suppress pituitary LH secretion and subsequently decrease ovarian androgen production
What are the key effects of uncontrolled gestational diabetes on the fetus?
- Beta cell hyperplasia due to increased trans-placental glucose delivery to the fetus (leads to hypoglycemia at birth)
- Fetal macrosomia (large size at birth!)
Familial Hypocalciuric Hypercalcemia (FHH)
What is it?
Describe the associated receptor?
A benign autosomal dominant disorder casued by a defective calcium-sensing receptor (G-protein coupled), which is suppose to regulate PTH secretion. Defect raises the Ca2+ threshold
Elevated prolactin levels (from a prolactinoma), directly suppress what?
GnRH
Following cleavage of pro-insulin, what is the fate of insulin and C-peptide?
They are both stored in islet cell secretory granules unti they are secreted in equimolar amounts
Phosphorylation of what residues (and via what?), leads to insulin resistance?
Phosph. of serine and threonine residues of insulin receptor and insulin receptor substrate by serine kinase, leads to insulin resistance
17a-hydroxylase def.
Presentation?
Boy appear phenotypically femaile at birth, but girls develop normally. (Result of dec. androgen, estrogen, and cortisol synthesis)
Patients present with hypogonadism, HTN, and hypokalemia
