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Review / Wrong Answers > DIT review - Endocrinology 2 > Flashcards

DIT review - Endocrinology 2 Flashcards

1
Q
  • Hyperthyroidism vs. Thyrotoxicosis
A
  • Hyperthyroid - thyroid gland producing too much hormone
  • Thyrotoxicosis - increased thyroid hormone from any source (exogenous hormone, inflammation leading to release of hormone
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2
Q

Describe toxic multinodular goiter

A
  • Focal patch of hyperfunctioning follicular cells working independently of TSH
    • Usually due to TSH receptor mutations
  • Will see multiple hot nodules on iodine uptake scan
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3
Q

What is Jod-basedow phenomenon

A
  • Iodine-induced hyperthyroidism
  • Due to a patient with iodine deficiency and partially autonomous thyroid nodule being repleted of iodine
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4
Q

Describe the cause/course of subacute thyroiditis

A
  • Aka de Quervain
  • Self-limited disease often following flu-like illness
  • Will present with hyperthyroid early on, followed by hypothyroidism
  • Present with very tender thyroid
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5
Q

Compare Hashimoto thyroiditis to subacute thyroiditis

A

Both present as hyperthyroid followed by hypothyroid

Hashimoto:

  • Painless goiter
  • Lymphocytic infiltration

Subacute thyroiditis

  • Very tender goiter
  • Granulomatous inflammation
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6
Q

What is the gene associated with Hashimoto thyroiditis

A

HLA-DR5

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7
Q

Hashimoto thyroiditis increases risk of what cancer?

A

B-cell lymphoma

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8
Q

What is de Quervain?

A

Subacute (granulomatous) thyroiditis

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9
Q

When would you expect a patient to get subacute thyroiditis

A

Following a flu-like viral illness

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10
Q

What is Riedel thyroiditis and its presentation

A
  • Thyroid replaced by fibrous tissue
  • Fibrosis may extend to local structures, mimicking anaplastic carcinoma
  • Presentation:
    • Euthyroid or hypothyroid
    • Fixed, hard (rock-like), painless goiter
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11
Q

What is #1 and #2 most common types of thyroid cancer

A

1 - Papillary carcinoma

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12
Q

Describe histology of papillary carcinoma of thyroid

A
  • Orphan Annie eye nuclei
  • Nuclear grooves
  • Psammoma bodies
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13
Q

What is the prognosis of papillary carcinoma

A

Excellent prognosis

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14
Q

How do you diagnose follicular carcinoma of the thyroid

A

Will see uniform follicles on histology

Must invade the capsule (vs. follicular adenoma)

  • Usually genetic testing to differentiate adenoma vs. carcinoma
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15
Q

Describe metastasis of follicular carcinoma of thyroid

A

Hematogenous (vs. lymphatic spread)

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16
Q

What electrolyte level might be off in medullary carcinoma of the thyroid

A

Hypocalcemia (medullary carcinoma produces calcitonin)

17
Q

Describe anaplastic carcinoma of the thyroid

A
  • Undifferentiated tumor of the thyroid
  • In the elderly
  • Invades local structures
  • Poor prognosis
18
Q

Describe complications of thyroidectomy

A
  • Parathyroid removal/damage
    • Hypocalcemia
  • Damage to recurrent laryngeal nerve
    • Hoarseness
19
Q

Describe the regulation of insulin release via glucose

A
  • Glucose enter beta cells of pancreas through GLUT-2 transporters
  • Glucose is metabolize by glucokinase to glucose-6-phosphate
  • Glucose-6-phosphate is further metabolized by glycolysis and the Krebs cycle to produce ATP
  • High ATP leads to closure of ATP-sensitive potassium channels
  • Closure of potassium channels leads to depolarization which results in opening of voltage-gated calcium channels (à inflow of calcium)
  • High intracellular calcium causes exocytosis of insulin vesicles
20
Q

What type of DM has a higher genetic predisposition?

A

Type 2

21
Q

What HLA are associated with Type 2 DM

A

HLA-DR3 and HLA-DR4

22
Q

What are the 2 main types of chronic complications in diabetes

A
  • Nonenzymatic glycosylation (leads to leaky vessels)
    • Small vessel disease
      • Retinopathy
      • Nephropathy
    • Large vessel disease
      • Atherosclerosis, CAD, MI
      • Gangrene
  • Osmotic damage
    • Recall:
      • Glucose à (aldose reductase) à sorbitol à (sorbitol dehydrogenase) à fructose
    • Sorbitol accumulation in organs with aldose reductase and decreased or absent sorbitol dehydrogenase
    • Sorbitol is an osmol that increases osmotic pressure causing:
      • Neuropathy (glove and stocking)
      • Cataracts
23
Q

What is HbA1c and what causes it?

A

Due to non-enzymatic glycosylation of hemoglobin

Measures the percent of Hb covered by glucose (> 6.5 = cutoff)

Reflects blood glucose over prior 3 months

24
Q

What is the major complication of T1DM vs. T2DM?

A

Type 1 - diabetic ketoacidosis

Type 2 - hyperosmolar hyperglycemic state (HHS)

25
Q

Describe the pathogenesis, symptoms, labs, and treatment of hyperosmolar hyperglycemic nonketotic syndrome

A
  • Hyperglycemia - excessive osmotic diuresis - dehydration - HHNS
  • Symptoms: thirst, polyuria, lethargy, focal neurological deficits (e.g. seizures), can progress to coma and death
  • Labs: hyperglycemia, increased serum osmolarity, no acidosis
    • Ketone production inhibited by presence of insulin
  • Treatment:
    • IV fluids, insulin
26
Q

What is the cause/presentation of pseudohypoparathyroidism?

A
  • Due to end organ resistance to PTH due to defect in the PTH receptor
  • Present with:
    • Hypocalcemia
    • Hyperphosphatemia
    • Elevated PTH
27
Q

What is Albright hereditary osteodystrophy?

A
  • Pseudohypoparathyroidism type 1a:
    • Unresponsiveness of kidney to PTH -> hypocalcemia despite elevated PTH
    • Characterized by short stature, short metacarpal, and short metatarsals
    • Autosomal dominant disorder
    • Due to defective Cs protein a-subunit, causing end-organ resistance to PTH
    • Defect must be inherited by mother due to imprinting
      *
28
Q

What is pseudopseudohypoparathyroidism?

A
  • Physical exam features of Albright hereditary osteodystrophy but without end-organ PTH resistance (PTH levels normal)
  • Occurs when defective Cs protein a-subunit is inherited from father
29
Q

Cause and presentation of primary hyperparathyroidism

A
  • Due to parathyroid adenoma or hyperplasia
  • Presentation:
    • THINK: Stones, thrones, bones, groans, psychiatric overtones
      • Hypercalcemia, increased PTH
      • Renal stones
      • Polyuria (thrones)
      • Osteitis fibrosa cystica (cystic bone spaces filled with brown fibrous tissue)
      • Weakness and constipation (gorans)
      • Depression (psychiatric overtones
30
Q

Pathogenesis and presentation of familial hypocalciuric hypercalcemia

A
  • Due to defective G-coupled Ca2+ sensing receptors
  • Higher levels of Ca2+ are needed in order to suppress PTH
  • Causes excessive renal Ca2+ reuptake, leading to mild hypercalcemia and hypocalciuria with normal to increased PTH levels
31
Q

What nerve is at risk for damage during a thyroidectomy

A
  • Damage to external laryngeal nerve (branch of superior laryngeal)
    • Innervates the cricothyrid muscle
32
Q

What is the cause of infertility in men with cystic fibrosis

A

Absent vas deferens

33
Q

What are neurophysins and what might a mutation cause?

A
  • Neurophysin = carrier protein for oxytocin and vasopressin from hypothalamus to posterior pituitary
    • Mutation in neurophysin can lead to defective transport of vasopressin = Central diabetes insipidus
34
Q

What is pituitary apoplexy (cause, treatment)

A
  • Acute hemorrhage into the pituitary gland
  • Occurs most often in patients with preexisting pituitary adenoma
  • Cardiac collapse caused by ACTH deficiency and subsequent adrenocortical insufficiency
  • Treatment – Medical emergency
    • Glucocorticoid replacement (to prevent life-threatening hypotension)
    • Surgical decompression
35
Q
A
36
Q

Funciton of the rough ER

A

§ Site of synthesis of secretory, lysosomal, and integral membrane proteins

§ Once synthesized, many proteins undergo post-translational modification inside the RER and are targeted for export to the Golgi apparatus

§ Golgi apparatus sorts and distributes proteins to the cell membrane, organelles and secretory granules

37
Q

Function of the smooth ER

A

§ Contains enzymes for steroid and phospholipid biosynthesis

§ Well-developed in steroid-producing cells (e.g. adrenal, gonads, liver)

38
Q

What is the effect of steroid abuse on RBCs?

A

Testosterone stimulates RBC production, leading to increased hematocrit

39
Q

What does hematocrit measure?

A

(volume of RBC) / (total blood volume)

Review / Wrong Answers (140 decks)

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