Endocrine Flashcards

1
Q

Name the mealtime insulin analogs

Describe their onset/ offset

A

Glulisine, Aspart, Lispro

They have rapid onset and offset of action, mimicking physiologic postprandial insulin secretion

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2
Q

Describe the structure of the mealtime insulin analogs

A

AA substitution at the C terminal end of the B chain

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3
Q

Major SEs of Corticosteroids

A
  1. Immunosuppression (except with neutrophilia!!)
  2. Corticosteroid-induced psychosis
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4
Q

The 22q11.2 microdeletion associated with DiGeorge, causes what embryological component(s) not to develop?

A

3rd and 4th branchial pouches

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5
Q

Describe the Chvostek sign and the Trousseasu sign associated with DiGeorge Syndrome

A

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

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6
Q

Tx of Acute Adrenal insufficiency

A

Hydrocortisone or dexamethasone

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7
Q

Lung mass + hyponatremia, is suggestive of what?

A

SIADH (secondary to Small cell lung carcinoma)

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8
Q

What is rT3 and what is it created from?

A

An inactive form of T3, that is generated almost entirely from peripheral conversion of T4

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9
Q

What effect does expgenous steroid abuse have on hematocrit?

A

Increases hematocrit

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10
Q

In Kallmann syndrome, there is an absence of GnRH secretory neurons in the _____________

A

hypothalamus

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11
Q

Finasteride MOA and indication

A

MOA: 5-alpha-reductase inhibitor that suppresses conversion of testosterone to DHT

Ind: BPH, Androgenetic alopecia

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12
Q

Hypoglycemia with an elevated insulin and low C-peptide level, suggests what?

High C-peptide level?

A

Low: exogenous insulin injection

High: insulin secretagogue or insulin-secreting tumor

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13
Q

Xanthomas are found where? What are they associated with?

A

These yellowish macules/papules are found on the medial eyelids. They are accumulations of macrophages + cholesterol/ TG and are assc. with hyperlipidemia/ dyslipidemia

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14
Q

Where is ADH synthesized? Is this the same location, or a different location from where it is stored?

A

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

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15
Q

Leuprolide MOA

A

Continuous GnRH agonist

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16
Q

What is the most effective preventative intervention in almost all patients?

A

Smoking cessation

17
Q

How do chronically elevated FFA levels contribute to insulin resistance?

A

By impairing insulin-dependent glucose uptake and increasing hepatic gluconeogenesis

18
Q

How do OC treat hirsutism?

A

They suppress pituitary LH secretion and subsequently decrease ovarian androgen production

19
Q

What are the key effects of uncontrolled gestational diabetes on the fetus?

A
  1. Beta cell hyperplasia due to increased trans-placental glucose delivery to the fetus (leads to hypoglycemia at birth)
  2. Fetal macrosomia (large size at birth!)
20
Q

Familial Hypocalciuric Hypercalcemia (FHH)

What is it?

Describe the associated receptor?

A

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

21
Q

Elevated prolactin levels (from a prolactinoma), directly suppress what?

A

GnRH

22
Q

Following cleavage of pro-insulin, what is the fate of insulin and C-peptide?

A

They are both stored in islet cell secretory granules unti they are secreted in equimolar amounts

23
Q

Phosphorylation of what residues (and via what?), leads to insulin resistance?

A

Phosph. of serine and threonine residues of insulin receptor and insulin receptor substrate by serine kinase, leads to insulin resistance

24
Q

17a-hydroxylase def.

Presentation?

A

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