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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the gene associated with Hashimoto thyroiditis

A

HLA-DR5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Hashimoto thyroiditis increases risk of what cancer?

A

B-cell lymphoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is de Quervain?

A

Subacute (granulomatous) thyroiditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

When would you expect a patient to get subacute thyroiditis

A

Following a flu-like viral illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

1 - Papillary carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe histology of papillary carcinoma of thyroid

A
  • Orphan Annie eye nuclei
  • Nuclear grooves
  • Psammoma bodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the prognosis of papillary carcinoma

A

Excellent prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe metastasis of follicular carcinoma of thyroid

A

Hematogenous (vs. lymphatic spread)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

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
Describe the pathogenesis, symptoms, labs, and treatment of hyperosmolar hyperglycemic nonketotic syndrome
* 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
What is the cause/presentation of pseudohypoparathyroidism?
* Due to end organ resistance to PTH due to defect in the PTH receptor * Present with: * Hypocalcemia * Hyperphosphatemia * Elevated PTH
27
What is Albright hereditary osteodystrophy?
* 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
What is pseudopseudohypoparathyroidism?
* 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
Cause and presentation of primary hyperparathyroidism
* 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
Pathogenesis and presentation of familial hypocalciuric hypercalcemia
* 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
What nerve is at risk for damage during a thyroidectomy
* Damage to external laryngeal nerve (branch of superior laryngeal) * Innervates the cricothyrid muscle
32
What is the cause of infertility in men with cystic fibrosis
Absent vas deferens
33
What are neurophysins and what might a mutation cause?
* 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
What is pituitary apoplexy (cause, treatment)
* 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
36
Funciton of the rough ER
§ 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
Function of the smooth ER
§ Contains enzymes for steroid and phospholipid biosynthesis § Well-developed in steroid-producing cells (e.g. adrenal, gonads, liver)
38
What is the effect of steroid abuse on RBCs?
Testosterone stimulates RBC production, leading to increased hematocrit
39
What does hematocrit measure?
(volume of RBC) / (total blood volume)