Endocrinology Flashcards

1
Q

how to initially diagnose primary adrenal insufficiency (Addison disease)?

A
  1. Early morning (8 am) cortisol levels; if low or low-normal then
  2. Confirm it with ACTH (cosyntropin) stimulation test
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2
Q

what effect does cortisol has on insulin and aldosterone?

A

Anti-insulin (diabetic like) and Pro-Aldosterone (hyperaldosteronism)

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3
Q

Metabolic syndrome is defined by what factors?

A

Abdominal obesity; Fasting glucose; Blood pressure; Triglycerides; HDL cholesterol

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4
Q

Zona glomerulosa?

A

Stimulated by Angiotensin 2 and production of Aldosterone

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5
Q

Zona fasciculata?

A

stimulated by ACTH and production of cortisol

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6
Q

Zona reticularis?

A

stimulated by ACTH and production of Androgens

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7
Q

Glucagon like peptides 1 (GLP-1) agonists?

A

“-glutide”; increase glucose dependent insulin secretion; slows gastric emptying; suppress release of glucagon; decease apetite; assist in weight loss; decrease mortality in patients with CVD; Adverse effects are nausea, bloating, abdominal pain and rarely pancreatitis

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8
Q

Sodium glucose co-transporter (SGLT) 2 inhibitors?

A

“-gliflozin”; increase renal excretion of sodium and glucose; lower BP, decease risk of heart failure; minor weight loss; Adverse effects are euglycemia ketoacidosis and UTIs

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9
Q

What are the recommended options for add on therapy for glycemic control in patients with established CVD?

A

GLP 1 agonists or SGLT-1 inhibitors

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10
Q

what are contraindications for SGLT 2 inhibitors?

A

Type 1 DM; History of DKA; Impaired renal function (eGFR <30ml/min/1.73 m2)

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11
Q

What are the symptoms of aldosterone deficiency?

A

hyperkalemia, salt wasting, volume contraction, hypotension

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12
Q

What happens to sodium levels in primary adrenal insufficiency vs central adrenal insufficiency?

A

Hyperkalemia in Primary AI whereas it is normal in Central AI

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13
Q

When there is Hypertension and Hypokalemia in a patient? What is the next thing to do?

A

Plasma Aldosterone to Renin ratio

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14
Q

What is the initial evaluation to confirm hypercortisolism?

A

24 hr urine free cortisol measurements (4 times normal);
Late night salivary cortisol levels;
Low dose dexamethasone suppression test

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15
Q

What is the most common and most adverse effect of anti-thyroid drugs?

A

Most common is allergic reaction;

Most adverse is agranulocytosis (Patient suffering from sore throat and fever should stop meds and see doctor)

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16
Q

Which anti thyroid drug can be used during 1st trimester?

A

PTU

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17
Q

What is subacute thyroiditis?

A

tender/painful goiter with elevated T3/T4 and ESR/CRP and low TSH and low RAIU. Treatment is symptomatic with beta blockers and NSAIDs.

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18
Q

What is euthyroid sick syndrome?

A

low t3 levels with normal t4 and tsh in the presence acute illness. it is due to decreased peripheral conversion of t4 to t3

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19
Q

how to differentiate between Graves disease and painless thyroiditis in patient with hyperthyroidism and suppressed TSH?

A

perform radioactive iodine uptake test

20
Q

Which anti-thyroid treatment can worsen Graves disease ophthalmopathy?

A

Radioiodine ablation; give glucocorticoids with RAI

21
Q

What causes Ophthalmopathy i.e proptosis or periorbital tissue swelling?

A

Thyrotropin receptor antibodies (TRAB) on the TSH receptor of retro-orbital fibroblasts and adipocytes

22
Q

Adjustment of the dose of antithyroid medication should be based on what?

A

Free (thyroxine) T4 levels

23
Q

What is the LDL level goal in diabetic patients?

A

less than 2.0 mmol/L

24
Q

What are the high intensity statins?

A

Atorvastatin 40mg-80mg

Rosuvastatin 20mg-40mg

25
Q

What are the two major controllers of aldosterone secretion?

A

Renin-angiotensin system and Potassium level; high K level stimulates and low K level inhibits the release of aldosterone

26
Q

What is the most appropriate initial test to rule out adrenal insufficiency?

A

early morning serum cortisol level >359mmol/L

27
Q

What are the appropriate bolus insulins with short onset?

A

Aspart and Lispro have onset of 15 min and peak in about 1 hr

28
Q

What is the best initial treatment for Sjogren’s syndrome?

A
Dry eyes (xerophthalmia) Tx with cyclosporin;
Dry mouth (xerostomia) Tx with pilocarpine/cevimeline
29
Q

What is the most common cause of hypoglycemia in the well controlled and stable diabetic patient who has not changed his diet and insulin dosage?

A

Renal disease. Insulin is normally metabolized by kidneys.

30
Q

Which of the oral diabetic agents most likely to produce hypoglycemia in older patients with renal insufficiency?

A

Sulfonylureas with longer duration of action like Glyburide and chlorpropamide

31
Q

What is the first line management for severe hypercalcemia?

A

Saline infusion

32
Q

What is considered the most sensitive and specific test for pheochromocytoma?

A

urine or plasma metanephrines and catecholamines

33
Q

What are the clinical markers of insulin resistance?

A

central obesity, acanthosis nigricans and skin tags.

34
Q

What is the laboratory features of pheochromocytoma?

A

Hypercalcemia; Hyperglycemia; Erythrocytosis

35
Q

What is the screening test of choice for pituitary adenomas?

A

Head MRI

36
Q

What is the usual starting dose of insulin in a diabetic patient?

A

0.3 units/kg - 0.5 units/kg; Most physiologic insulin therapy closest to the natural insulin release in a normal person is BASAL-BOLUS insulin consisting of long acting and short acting. 70-30 ratio.

37
Q

What is the theory behind statin induced myopathy?

A

Firstly, genetic predisposition i.e single nucleotide polymorphism SLCO1B1; Secondly, decrease in mevalonate pathway product such as coenzyme Q10.

38
Q

What are the second most effective class of drugs for lowering LDL cholesterol levels and tolerated well with Statins?

A

Bile acid sequestrants such as cholestryamine, colestipol, colesevelam

39
Q

Which class of drugs should be avoided in the patient with pheochromocytoma?

A

Diuretics and salt restriction; pheochromocytoma is associated with volume depletion and diuretics will further worsen the volume depletion and will precipitate severe attacks of orthostatic hypotension

40
Q

Patient with thiazide diuretic has hypercalcemia with normal PTH levels?

A

Hyperparathyroidism; Most patients have mild hyperparathryroidism which becomes evident after adding calcium load. Usually with increased calcium level there is suppression of PTH but inappropriately “normal” PTH is diagnostic for HPTH.

41
Q

How to diagnose acromegaly?

A

First test in evaluation is measurement of IGF-1 and clinical signs and sxs.
The most specific test is oral glucose tolerance test. Oral glucose will not suppress the GH level.

42
Q

What is the effect of insulin on K+?

A

Insulin stimulates Na/H antiporter increasing intracellular Na level which will stimulate Na/K atpase resulting in intracellular shift of K.

43
Q

How to treat patients with SIADH?

A

Asymptomatic patients with Na <109mmol/L and osmolality <238 can be treated with strict water retention.
Symptomatic patients such as those with neurologic issues need to be treated immediately with IV 3% saline at 100ml/Hr. Make sure not correct hyponatremia at a fast rate as keep it < or = 10 mmol/L in 24 hr

44
Q

When is use of metformin contraindicated?

A

Hepatic dysfunction, Heart failure, Renal failure (eGFR <30ml/min)

45
Q

How to calculate plasma osmolality?

A

Calculate plasma osm = 2[Na] + [Glucose] + [Urea]

46
Q

What is osmolar gap?

A

Osmolar gap is difference between measured and calculated plasma osmolality; The difference of >10mmol/kg is considered high.

47
Q

What factors cause hypokalemia?

A

Diuretic therapy, vomiting/diarrhea, Hypomagnesemia, Hyperaldosteronism, increased beta agonist activity