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Endrocrine Exam 2 > Clinical: Directed Study > Flashcards

Clinical: Directed Study Flashcards

1
Q

On the TSH to FT4 diagram, where is the bubble for patients with TSH-secreting tumors?

A

In the middle of the X-axis towards the top of the Y-axis

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2
Q

On the TSH to FT4 diagram, where is the bubble for patients with thyroid hormone resistance?

A

A big blob that is in the center area underneath the one for TSH-secreting tumors

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3
Q

On the TSH to FT4 diagram, where is the bubble for overt non-pituitary hyperthyroidism?

A

On the very bottom right

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4
Q

What is the clinical ulitility for radionuclide imagins?

A

Determine functional activity and morphology of the thyroid

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5
Q

123I, how given, when take picture?

A

Orally, 8-24 hours

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6
Q

99mTcO4, how given, when take picture?

A

IV, 30-60 minutes

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7
Q

What features are seen on radionuclide imaging?

A

Size and shape of the thyroid and distribution of tracer activity within the gland

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8
Q

In Grave’s disease, what is seen on radionuclide imaging?

A

Enlarged gland, intense and homogenous concentration of tracer

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9
Q

What is seen in radionuclide imaging for toxic nodular goiter?

A

1 or more discrete regions of tracer activity (suppression of extranodular tissue), correlate with palpable nodule/nodules

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10
Q

What is a hot thyroid nodule?

A

Functioning, suppression of extranodular tissue, benign

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11
Q

What is a cold thyroid nodule?

A

Hypofunctioning, benign or malignant

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12
Q

When do you do whole body scanning with radionuclide imaging?

A

Follow up for thyroid cancer, identify ectopic thyroid tissue

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13
Q

What is US for thyroid good for?

A

Best imaging for size and characteristics of nodular lesions (solid, cystic, complex)

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14
Q

Malignant lesions on US?

A

Irregular nodule capsule, microcalcifications

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15
Q

Benign lesions on US?

A

Spongiform appearance, cystic change

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16
Q

What is the use of US for thyroid?

A

Monitor size of nodules serially, guide fine-needle aspiration, assess regional lymph nodes

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17
Q

What is a thyroid biopsy (fine-needle aspiration biopsy) good for?

A

Differentiating benign from malignant and diffuse goiters

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18
Q

What is the role of detection of thyroid autoantibodies?

A

Establishing diagnosis of autoimmune thyroid disease

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19
Q

How are thyroid autoantibodies assessed?

A

ELISA or RIA

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20
Q

What autoantibodies are seen in Hashimoto thyroiditis?

A

Serum anti-TPO (diffuse goiter or hypothyroidism…doesn’t rule out presence of 2nd thyroid disorder)

21
Q

True or False: Anti-TPO may be present in Graves Disease?

A

TRUE

22
Q

What autoantibody is seen in 90% of Grave’s disease cases?

A

Thyroid-Stimulating Immunoglobulin (TSI)

23
Q

What is myxedema coma?

A

Rare condition in end stage of untreated hypoparathyroidism

24
Q

Who is myxedema coma seen in?

A

Older females with underlying pulmonary or vascular disease, winter

25
Q

What is the pathology of myxedema coma?

A

CO2 retention and hypoxia (depression of ventilation); fluid and electrolyte imbalance; hypothermia

26
Q

What are precipitating conditions for myxedema coma?

A

Heart failure, pneumonia, sedative/narcotic drugs

27
Q

What is the clinical presentation of myedema coma?

A

Progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia–> Ultimately results in shock and death

28
Q

What is the prognosis of myedema coma?

A

Over 50% mortality

29
Q

What are the labs seen in myxedema coma?

A 
High serum carotene
Elevated serum cholesterol
Increased CSF protein
Low FT4
Markedly elevated TSH
30
Q

What is seen on ECG for myxedema coma?

A

Sinus bradycardia

31
Q

What is the treatment for myxedema coma?

A

Intubation with mechanical ventilation

IV T4*****

32
Q

What is the dosing for IV T4 in myxedema coma?

A

300-400ug followed by 80% of calculated full replacement dose

33
Q

What is given if there is suboptimal response to IVT4 in myxedema coma?

A

Add IV T3 (5ug every 6 hours)

34
Q

What can a large dose of T4 precipitate in older patients with CAD?

A

Angina, heart failure, arrhythmias

35
Q

What is a positive Pemberton sign?

A

Facial dilatation of cervical veins (facial plethora) on lifting arms over head

36
Q

What does a positive Pemberton sign indicate?

A

Obstruction of jugular venous flow

37
Q

When are ketone bodies formed and how are they excreted?

A

Formed in absence of adequate insulin, excreted in urine

38
Q

What are 3 ketone bodies?

A
  1. B-hydroxybutyrate (most prevalent in DKA)
  2. Acetoacetate
  3. Acetone
39
Q

What reacts with sodium nitroprusside in the presence of alkali to produce purple-colored complex?

A

Acetone and aceoacetate

40
Q

What measures capillary blood B-hydroxybutyrate?

A

Paper strip (Precision Xtra)

41
Q

What is an advantage of continuous subcutaneous insulin infusion?

A

Allows for establishment of basal profile tailored to patient–> Able to eat with less regard to timing*, ability to adjust basal level allows easier management of glycemic excursions

42
Q

Who are appropriate patients for a continuous subcutaneous insulin infusion pump?

A

Motivated, mechanically adept, educated about diabetes, willing to monitor blood glucose 4-6 times a day

43
Q

What are 2 complications with continuous subcutaneous insulin infusion pumps?

A

Ketoacidosis, skin infection

44
Q

What is diabetic ketoacidosis a common complication of?

A

Insulin pump therapy, type 2 DM under severe stress (like sepsis, trauma, or major surgery)

45
Q

What are precipitating factors to DKA?

A

Infection, trauma, MI, surgery

46
Q

What is the pathology of DKA (this one is long…sorry)?

A
  1. Rapid mobilization of energy stores in muscle and fat deposits
  2. Increased flux of AA to liver for conversion to glucose and FA conversion to ketones (acetoacetate; acetone; β-hydroxybutyrate)
  3. Elevation of insulin-antagonist hormones (corticosteroids; catecholamines; glucagon; GH) and decreased utilization of glucose and ketones (insulin deficiency)
  4. Accumulation of substances in blood (plasma glucose reaching > 500 mg/dL
  5. Osmotic diuresis (depletion of intravascular volume)
  6. Severe hyperosmolarity (CNS depression; coma).
47
Q

What are the clinical features of DKA?

A
  • Preceded by day or more of polyuria and polydipsia
  • Marked fatigue
  • N/V
  • Mental stupor (progresses to coma)
  • Dehydration
  • Fruity breath (acetone)
  • Postural hypotension with tachycardia
  • Abdominal pain/tenderness
  • Mild hypothermia
48
Q

What are the labs associated with DKA?

A
  1. Plasma glucose 350-900 mg/dL
  2. Serum ketones (positive dilution of 1:8 or greater)
  3. Hyperkalemia (5-8 mEg/L)
  4. Hyponatremia (130 mEq/L)
  5. Hyperphosphatemia (6-7 mg/dL)
  6. Elevated BUN and creatinine
  7. Acidosis (pH 6.9-7.2)
  8. Elevated serum amylase (salivary and pancreatic).
49
Q

What is done for the treatment of DKA?

A
  1. Fluid replacement
  2. Insulin
  3. K
  4. Sodium bicarb
  5. Phosphate (rarely required)

Endrocrine Exam 2 (7 decks)

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