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Step Up To Medicine > Endocrine And Metabolic Diseases > Flashcards

Endocrine And Metabolic Diseases Flashcards

1
Q

What is type 1 diabetes?

A

An autoimmune disease in which the immune system mediates the destruction of beta-cells.

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2
Q

Which HLA is associated with type 1 DM?

A

HLA-DQ
HLA-DR2 and DR4

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3
Q

What is the criteria to diagnose type 2 DM?

A
  1. Random: >200 (11.1) and patient is symptomatic
  2. Fasting: >126 (7) on 2 occasions
  3. 2 -hr postprandial: >200 (11.1) on 2 occasions
  4. HbA1c: >6.5
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4
Q

What is the criteria to diagnose pre-diabetes or Impaired Glucose Tolerance?

A
  1. Fasting BG: 110-126 (5.6-6.9)
  2. 2-hr postprandial: 140-200 (7.7-11.1)
  3. HbA1c: 5.7-6.4
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5
Q

What is the criteria for screening DM?

A
  1. Started from age of 35 and older, if results are normal repeat within 3 years or earlier depending on risk factors and lab result levels
  2. Started earlier than 35 year old if patient is overweight or obese with an additional risk factor for T2DM
  3. Pre-diabetes should be repeated yearly
  4. Women with gestational diabetes should repeat every 3 years
  5. HIV infection
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6
Q

What are the general principles of outpatient management and monitoring of all diabetic patients?

A
  1. Monitor HbA1c every 3-4 months, not recommended if patient has hemoglobinopathies
  2. Monitor daily glycemic levels especially if on insulin therapy: before meals, 90-120 minutes after meal and at bedtime
  3. Screen for microalbuminurea at least once per year, if positive give ACE inhibitor or ARB
  4. Check BUN, creatinine, urine albumin:creatinine ratio once per year
  5. Eye screening once per year
  6. Check the feet at every visit
  7. Check cholesterol level once per year, give statins if LDL is >100
  8. Check BP at every visit
  9. Daily aspirin
  10. Vaccine
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7
Q

What are the goal levels of microalbumin, BP and lipids?

A

Microalbumin: < 30 mg/g
BP: <140/90 mmHg
LDL: <70
HDL: >40 in males, >50 in females
Triglycerides: <150

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8
Q

What is the recommended pharmacological treatment for diabetic with high ASCVD risk or high risk individual?

A

SGLT2 (empagliflozin) or GLP-1 (liraglutide)

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9
Q

What is the recommended pharmacological treatment for diabetic with heart failure?

A

SGLT-2 (empagliflozin)

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10
Q

What is the recommended pharmacological treatment for patient with CKD?

A

SGLT-2 (empagliflozin), but if not tolerated or contraindicated GLP-1 can be used instead

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11
Q

What is preprandial and postprandial glycemic target?

A

Preprandial: <130 (7.2)
Postprandial: <180 (10)

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12
Q

What are the indications for insulin therapy in T2DM?

A
  1. If patient’s glycemic targets are not met despite sufficient anti-diabetic treatment
  2. If patient has contraindications for non-insulin anti-diabetic drugs
  3. Pregestational and gestational diabetes
  4. Hyperglycemia crisis
  5. Newly diagnosed patients with:
    • Initial glucose >300 mg/dL or HbA1c >10%
    • Symptoms of hyperglycemia
    • Signs of a continued catabolic state, e.g. weight loss
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13
Q

What is the amount of basal insulin given in T2DM?

A

0.2-0.3 units/kg

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14
Q

What is the amount of insulin required in T1DM to achieve glycemic control?

A

0.5-1 unit/kg per day, divided into 50% basal and 50% prandial insulin

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15
Q

What is the most common cause of death in diabetic patients?

A

CAD

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16
Q

What are the macrovascular complications of DM?

A
  1. Coronary artery disease
  2. Peripheral vascular disease
  3. Cerebrovascular disease
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17
Q

What are the microvascular complications of DM?

A
  1. Diabetic nephropathy
  2. Diabetic retinopathy
  3. Diabetic neuropathy
  4. Diabetic foot
  5. Increased susceptibility to infection
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18
Q

What are the key features of DKA?

A
  1. Hyperglycemia (>450 mg/dL and <850 mg/dL)
  2. Positive serum or urine ketones
  3. Metabolic acidosis (pH <7.3 and HCO3 <18 mEq/L)
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19
Q

How DKA managed?

A
  1. Insulin priming dose of 0.1 units/kg of regular insulin (IV) followed by infusion of 0.1 units/kg/hr. BUT withhold insulin if potassium is <3.3 mEq/L, give 20-30 mEq/hr of potassium and once it has reached 3.3-5.2 mEq/L then give insulin
  2. Fluid replacement of 1L/hr 0.9% saline infusion for the first 2 hours and then 0.5L/hr. Add 5% glucose once blood glucose reaches 200 mg/dL to prevent hypoglycemia.
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20
Q

How is Hyperosmolar Hyperglycemic Nonketotic Syndrome diagnosed?

A
  1. Hyperglycemia >900 mg/dL
  2. Hyperosmolarity >320 mOsm/L
  3. No acidosis
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21
Q

How is HHNS managed?

A
  1. Fluid replacement: 1L in the first hour and another liter in the next 2 hours
  2. Insulin: check potassium levels before initiating insulin, initial bolus of 0.1 units/kg as IV bolus and then continuous low-dose infusion 0.1 units/kg/hr
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22
Q

What is the most common cause of hyperprolactinemia?

A

Prolactinoma

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23
Q

What are the clinical features of hyperprolactinemia in men?

A
  1. Hypogonadism, decreased libido, infertility, impotence
  2. Galactorrhea or gynecomastia
  3. Parasellar signs and symptoms
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24
Q

What are the clinical features of hyperprolactinemia in women?

A

Premenopausal:
- Menstrual irregularities, oligomenorrhea or amenorrhea, anovulation and infertility, decreased libido, dyspareunia, vaginal dryness, risk of osteoporosis, galactorrhea

Postmenopausal:
- Parasellar signs and symptoms

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25
Q

How can hyperprolactinemia cause such clinical features relate to estrogen and testosterone?

A

High levels of prolactin inhibits secretion of GnRH which leads to decreased secretion of LH and FSH that in turn leads to decreased production of estrogen and testosterone.

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26
Q

How is hyperprolactinemia diagnosed?

A
  1. Elevated serum prolactin level (>200 NT/mL)
  2. Order pregnancy test and TSH level to r/o other causes of hyperprolactinemia
  3. CT scan or MRI to identify any mass lesions
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27
Q

How is Prolactinoma treated?

A
  1. Bromocriptine or cabergoline for 2 years
  2. Surgery if symptoms progress despite medical therapy
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28
Q

What is acromegaly?

A

Broadening of skeleton, which results from excess secretion of pituitary GH after epiphyseal closure.

29
Q

Which would happen if excess GH is secreted before epiphyseal closure?

A

Gigantism

30
Q

What tests are ordered to diagnose acromegaly?

A
  1. IGF-1
  2. Oral glucose suppression test
  3. MRI of the pituitary
31
Q

What are the 2 forms of diabetes insipidus?

A

Centra DI: low ADH secretion by posterior pituitary
Nephrogenic DI: ADH secretion is normal but tubules cannot respond to ADH

32
Q

What is the hallmark feature of diabetes insipidus?

A

Polyuria: 5-15 L daily

33
Q

How is DI diagnosed?

A
  1. Urine: low specific gravity and low osmolality
  2. Plasma osmolality: high 280-310 mOsm/kg
  3. Water deprivation test: REQUIRED to make the diagnosis
    • Central DI: urine osmolality after dehydration is <300 mOsm/kg, but after desmopressin administration osmolality rises
    • Nephrogenic DI: urine osmolality after dehydration is <300 mOsm/kg, and no response after desmopressin administration
34
Q

How is DI managed?

A
  1. Central DI: by desmopressin
  2. Nephrogenic DI: sodium restriction and thiazide diuretics
35
Q

What is the normal effect of parathyroid hormone?

A

Increases serum calcium and decreases serum phosphate

36
Q

What are the clinical features of hyperparathyroidism?

A
  1. Stones
  2. Bones
  3. Groans
  4. Psychiatric overtones
37
Q

Cushing syndrome vs Cushing disease

A

Syndrome: excessive levels of glucocorticoids due to any cause
Disease: ACTH-secreting pituitary adenoma

38
Q

What are the changes in appearance seen in Cushing syndrome?

A

Central obesity, hirsuitism, moon fancies, buffalo hump, purple striae on abdomen, lanugo hair, acne, easy bruising, skin thinning, plethora, thinning of scalp hair, supraclavicular fat pads.

39
Q

How is Cushing syndrome diagnosed?

A
  1. Initial screening: 2 out 3 must be positive
    • Overnight low dose dexamethasone suppression test
    • 24-hr urinary free cortisol level
    • Late night salivary cortisol
  2. ACTH level
  3. High dose dexamethasone suppression test
  4. CRH stimulation test
  5. MRI
  6. Inferior petrosal sinus sampling
40
Q

What will be the findings if Cushing disease is suspected?

A
  1. High cortisol
  2. High ACTH
  3. No suppression with low dose dexamethasone
  4. Suppression with high dose dexamethasone
  5. Great increase in cortisol after CRH test
41
Q

What will be the findings if adrenal tumor is suspected?

A
  1. High cortisol
  2. Low ACTH
  3. No suppression with low dose dexamethasone
  4. No suppression with high dose dexamethasone
  5. No change after CRH test
42
Q

What will be the findings if ectopic ACTH-producing tumor is suspected?

A
  1. High cortisol
  2. High ACTH
  3. No suppression with low dose dexamethasone
  4. No suppression with high dose dexamethasone
  5. No change after CRH test
43
Q

How is Cushing syndrome managed?

A
  1. If iatrogenic then taper glucocorticoid
  2. If pituitary then transsphenoidal ablation of pituitary adenoma
  3. If adrenal adenoma or carcinoma then adrenalectomy + cortisol replacement to secondary adrenal insufficiency of the other gland
  4. If unable to do surgical intervention, medical therapy includes ketoconazole
44
Q

What are the classic symptoms of pheochromocytoma?

A
  1. Headache
  2. Profuse sweating
  3. Palpitations
  4. Tachycardia
45
Q

How is pheochromocytoma managed?

A
  1. Alpha blockade to control BP for 14 days prior to surgery and beta blockade to decrease tachycardia for 2-3 days prior to surgery
  2. Surgical tumor resection with early ligation of venous drainage
46
Q

What should be suspected when a patient is hypertensive with hypokalemia and not on a diuretic?

A

Hyperaldosteronism

47
Q

What is the screening test for primary hyperaldosteronism?

A

Ratio of the plasma aldosterone level to plasma renin. If >30 evaluate further

48
Q

What tests are done to confirm primary hyperaldosteronism?

A
  1. Saline infusion test
  2. Oral sodium loading
49
Q

What is the treatment for primary hyperaldosteronism?

A
  1. If adenoma (conn syndrome) then adrenalectomy is often curative
  2. If bilateral hyperplasia then spironolactone is given to inhibit aldosterone action
50
Q

What is adrenal crisis?

A

It is an acute and severely symptomatic stage of adrenal insufficiency that can include severe hypotension and cardiovascular collapse, abdominal pain, acute renal failure, and death.

51
Q

How is adrenal crisis managed?

A
  1. IV hydrocortisone
  2. IV fluids (several liters of normal saline with 5% dextrose)
52
Q

What are the characteristic features of primary adrenal insufficiency?

A
  1. Hyperpigmentation
  2. Hyperkalemia
53
Q

How is adrenal insufficiency diagnosed?

A
  1. Decreased plasma cortisol level
  2. Plasma ACTH level (low in secondary adrenal insufficiency)
  3. Standard ACTH test:
    • In primary adrenal insufficiency, cortisol doesn’t increase sufficiently
    • In secondary adrenal insufficiency, cortisol fails to respond but if repeated for 4-5 days a response will be seen
  4. MRI if secondary cause is diagnosed
54
Q

How is adrenal insufficiency managed?

A
  1. Primary: daily oral glucocorticoid (dose should be doubled during illness and stress) and daily fludrocortisone
  2. Secondary: only oral glucocorticoid
55
Q

What is Graves disease?

A

An autoimmune disorder in which thyroid-stimulating immunoglobulin (IgG) antibody binds to the TSH receptors on the surface of the thyroid cells and triggers the synthesis of excess thyroid hormone. It shows diffuse uptake on radioiodide scan.

56
Q

What is Plummer disease?

A

Hyperfunctioning areas that produce high T4 and T3 levels, thereby decreasing TSH levels and the rest of the thyroid is not functioning. It shows patchy uptake on radioiodide scan.

57
Q

What are 3 signs of hyperthyroidism specific to Graves’ disease?

A
  1. Exophthalmos
  2. Pretibial myxedema
  3. Thyroid bruit
58
Q

What are the tests ordered for hyperthyroidism?

A
  1. Serum TSH level
  2. Thyroid hormone levels
59
Q

What are the autoantibodies associated with Graves’ disease?

A
  1. TSI (thyroid stimulating immunoglobulin)
  2. TPOAB (thyroperoxidase antibody)
  3. TRAb (thyrotropin receptor antibody)
60
Q

What are the autoantibodies associated with Hashimoto disease?

A
  1. TPOAb (thyroperoxidase antibody)
  2. TgAb (thyroglobulin antibody)
61
Q

What is subclinical hyperthyroidism?

A

TSH is suppressed and free T4 and T3 are normal. Treated when TSH is <0.1

62
Q

What are treatment options for hyperthyroidism?

A
  1. Pharmacological: methimazole and propylthiouracil. Beta blockers are given for acute managements of some symptoms
  2. Radioactive ablation: causes destruction of thyroid follicular cells. Contraindicated in pregnancy and breastfeeding. So women should avoid pregnancy for at least 6 months post-treatment. Steroids are given 1 week before and 2 weeks after ablation to reduce the effects of excess hormone released by destruction of follicular cells
  3. Surgical: subtotal thyroidectomy, often reserved for very large goiters, those who can’t tolerate medication and those who prefer surgery.
63
Q

For how long is methimazole used?

A

For 1-2 years, and thyroid-stimulating IgG antibody are measured at 12 months and if absent then therapy can be stopped. BUT if it relapse occurs then continue for 1 year.

64
Q

What is thyroid storm?

A

A life-threatening complication of thyrotoxicosis characterized by an acute exacerbation of the manifestations of hyperthyroidism.

65
Q

How is thyroid storm managed?

A
  1. IV fluids, cooling blankets, and glucose
  2. PTU every 2 hours, follow with iodine to inhibit thyroid hormone release
  3. Beta blockers for control of heart rate
  4. Dexamethasone to impair peripheral conversion of T3 to T4
66
Q

What is the most common cause of primary hypothyroidism?

A

Hashimoto disease

67
Q

What is myxedema coma and how is it managed?

A

Medical emergency, most feared complication of hypothyroidism, that presents with a depressed state of consciousness, profound hypothermia, and respiratory depression. Give IV thyroxine and hydrocortisone

68
Q

What is subclinical hypothyroidism?

A

Thyroid function is inadequate, but increased TSH production maintains T4 levels within normal reference range.

69
Q

How is hypothyroidism managed?

A

Levothyroxine lifelong

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