Clinical: Directed Study Flashcards by Gretchen Hackett

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

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

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

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

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

On the very bottom right

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What is the clinical ulitility for radionuclide imagins?

Determine functional activity and morphology of the thyroid

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123I, how given, when take picture?

Orally, 8-24 hours

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99mTcO4, how given, when take picture?

IV, 30-60 minutes

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What features are seen on radionuclide imaging?

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

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

Enlarged gland, intense and homogenous concentration of tracer

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What is seen in radionuclide imaging for toxic nodular goiter?

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

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What is a hot thyroid nodule?

Functioning, suppression of extranodular tissue, benign

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What is a cold thyroid nodule?

Hypofunctioning, benign or malignant

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When do you do whole body scanning with radionuclide imaging?

Follow up for thyroid cancer, identify ectopic thyroid tissue

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What is US for thyroid good for?

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

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Malignant lesions on US?

Irregular nodule capsule, microcalcifications

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Benign lesions on US?

Spongiform appearance, cystic change

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What is the use of US for thyroid?

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

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

Differentiating benign from malignant and diffuse goiters

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What is the role of detection of thyroid autoantibodies?

Establishing diagnosis of autoimmune thyroid disease

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How are thyroid autoantibodies assessed?

ELISA or RIA

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What autoantibodies are seen in Hashimoto thyroiditis?

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

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

TRUE

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

Thyroid-Stimulating Immunoglobulin (TSI)

What is myxedema coma?

Rare condition in end stage of untreated hypoparathyroidism

Who is myxedema coma seen in?

Older females with underlying pulmonary or vascular disease, winter

What is the pathology of myxedema coma?

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

What are precipitating conditions for myxedema coma?

Heart failure, pneumonia, sedative/narcotic drugs

What is the clinical presentation of myedema coma?

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

What is the prognosis of myedema coma?

Over 50% mortality

What are the labs seen in myxedema coma?

``` High serum carotene Elevated serum cholesterol Increased CSF protein Low FT4 Markedly elevated TSH ```

What is seen on ECG for myxedema coma?

Sinus bradycardia

What is the treatment for myxedema coma?

Intubation with mechanical ventilation | IV T4*****

What is the dosing for IV T4 in myxedema coma?

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

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

Add IV T3 (5ug every 6 hours)

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

Angina, heart failure, arrhythmias

What is a positive Pemberton sign?

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

What does a positive Pemberton sign indicate?

Obstruction of jugular venous flow

When are ketone bodies formed and how are they excreted?

Formed in absence of adequate insulin, excreted in urine

What are 3 ketone bodies?

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

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

Acetone and aceoacetate

What measures capillary blood B-hydroxybutyrate?

Paper strip (Precision Xtra)

What is an advantage of continuous subcutaneous insulin infusion?

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

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

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

What are 2 complications with continuous subcutaneous insulin infusion pumps?

Ketoacidosis, skin infection

What is diabetic ketoacidosis a common complication of?

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

What are precipitating factors to DKA?

Infection, trauma, MI, surgery

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

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).

What are the clinical features of DKA?

- 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

What are the labs associated with DKA?

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).

What is done for the treatment of DKA?

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