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Parathyroid Flashcards

1
Q

What are the effects of parathyroid hormone on the body?

A

PTH = Increase serum calcium, decrease serum phosphates

A. BONE:
- Increase osteoclasts

B. KIDNEY:
- Increase calcium reabsorption
- Decrease phosphate reabsorption
- Increase 1,25-dihydroxyvitamin-D (calcitriol or D3) synthesis (increases efficiency of calcium reabsorption)

C. GUT:
- Increase calcium absorption via stimulation by Vitamin D (from kidney)

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2
Q

What are the effects of calcitonin on the body?

A

CALCITONIN = Decrease serum calcium

A. BONE:
- Inhibits osteoclasts

B. KIDNEY:
- Increase excretion of calcium and phosphate

C. GUT:
- Inhibits calcium absorption

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3
Q

What is the blood supply to the superior and inferior parathyroid glands?

A

Superior and inferior parathyroid arteries
- Originate from inferior thyroid artery (86% of the time)
- Some contribution from superior thyroid artery (10-20%)

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4
Q

How much do each parathyroid weigh?

A

30-40g

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5
Q

What are the most common number of parathyroids? What percentage have a different number?

A
  • 85% have 4 parathyroids
  • 10% have < 4
  • 5% have >4
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6
Q

What are the different types of hyperthyroidism? What are their laboratory findings?

A

Normal kidney = excretes phosphate, absorbs calcium

A. PRIMARY HYPERPARATHYROIDISM
- Elevated calcium, decreased phosphate, high urine Calcium
- FHH: Urine Ca low
- Normocalcemic primary hyperpara: Normal Ca2+, high PTH
- Significantly elevated PTH
- If PTH is mildly elevated or normal but calcium is inappropriately high, most likely diagnosis is still primary hyperparathyroidism, but have to exclude familial hypocalciuric hypercalcemia

B. SECONDARY HYPERPARATHYROIDISM
- Due to malfunction of another organ system (makes serum calcium look low, so parathyroid glands compensating)
- Low or normal calcium, high phosphate, high PTH
- PO4 supresses calcitonin, decreases Ca2+ absorption, therefore elevating PTH
- PO4 high = renal problem (normal kidney excretes excess PO4 and absorbs calcium, but if problematic then they can’t excrete and absorb)
- Prevent with phosphate binders and Vitamin D replacement

C. TERTIARY HYPERPARATHYROIDISM
- Autonomous production (e.g. gland abnormal now) after the cause of secondary hyperpara has been corrected (like an “induced” primary hyperpara because of secondary issues) - parathyroid gland more commonly becomes hyperplastic rather than creates another adenoma (similarly in secondary hyperpara, starting to become hyperplastic)
- Normal or high Ca2+, elevated PTH, low vitamin D, variable PO4 (usually high if Ca2+ high, but dependent on kidney function)

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7
Q

List 4 causes of primary hyperparathyroidism

A
  1. Benign adenoma (most common)
  2. Parathyroid hyperplasia (syndromic MEN1/2a, or sporadic)
  3. Familial hypocalciuric hypercalcemia
  4. Normocalcemic primary hyperparathyroidism
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8
Q

List 7 causes of secondary hyperparathyroidism

A
  1. Chronic renal failure
  2. Vitamin D deficiency
  3. Multiple myeloma
  4. Osteogenesis imperfecta
  5. Paget’s disease
  6. Bone metastasis (PTBLK - prostate, thyroid, breast, kidney, lung)
  7. PItuitary basophilism
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9
Q

What are 4 different ways to differentiate between parathyroid adenoma vs. hyperplasia?

A
  1. 4-gland exploration (one gland enlarged, or all glands enlarged)
  2. Permanent section (frozen can’t tell)
    - Decreased or no fat in hyperplastic glands, vs. fat in adenoma
    - Adenoma will have a rim of normal tissue surrounding it whereas hyperplastic glands won’t
  3. Intraoperative PTH measurement
  4. Thyroid ultrasound (As part of work-up for hyperparathyroidism)
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10
Q

What is the incidence of the following parathyroid pathologies in primary hyperparathyroidism?
1. Adenoma
2. Hyperplasia
3. Multiple adenoma
4. Carcinoma

A
  1. Adenoma - 85%
  2. Hyperplasia - 10%
  3. Multiple adenoma - 5%
  4. Carcinoma - < 1%
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11
Q

Regarding familial hypocalciuric hypercalcemia, discuss:
1. Genetics and inheritence
2. Investigations and findings 4
3. Managememnt

A

GENETICS:
- CaSR (mutation in the calcium-sensing receptor gene, expressed in kidney and parathyroid) on chromosome 3q13
- Autosomal dominant

INVESTIGATIONS: Parathyroids can’t tell that calcium is elevated because of problem in the sensing-receptor gene so the PTH is normal/elevated; kidney’s can’t tell there is calcium, so they increase absorption

  1. Urine calcium < 100ng/24 hours
  2. Calcium-to-creatinine ratio < 0.01
  3. Mildly elevated to normal PTH
  4. High calcium, low phosphate

Management:
Not excreting appropriately –> not a surgical disease

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12
Q

Regarding primary normocalcemic hyperparathyroidism, discuss:
1. Hallmark laboratory findings
2. Diagnostic criteria
3. Management

A

pnHPT was discovered due to overzealous endocrinologists checking PTH in patients with low bone mineral density, despite having normal calcium

HALLMARK (labs look like secondary Hyperpara):
- Normal calcium
- Elevated PTH
- Usually in the setting of osteoporosis (tissue resistance to PTH; normally elevated PTH should have HIGH calcium)

DIAGNOSIS requires exclusion of secondary causes of elevated PTH:
1. Vitamin D deficiency (< 20µg/L)
2. Renal abnormalities - reduced creatinine clearance (< 60mL/min)
3. Medications (HCTZ, loop diuretics, lithium)
4. Hypercalciuria (CKD)
5. Gastrointestinal disorders associated with calcium malabsorption (e.g. Gluten enteropathy, IBD, gastric bypass surgery, CF, celiac)
6. PTHrp (“related protein” - to identify paraneoplastic secretion)

MANAGEMENT (controversial)
- Most follow guidelines for primary hyperparathyroidism
- Localization study - most will have a negative study
- Four gland exploration

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13
Q

What are the normal anatomic locations of the parathyroid glands?

A

SUPERIOR PAIR:
- Usually on deep surface of the thyroid, within 1cm of RLN entry at cricothyroid joint; OR 1cm above intersection of RLN and inferior thyroid artery (within 2cm of this point)

INFERIOR PAIR:
- Usually within 1-2cm of inferior thyroid artery entry into the thyroid gland

SUPERIOR PARATHYROID = deep to plane of the RLN and lateral to the nerve

INFERIOR PARATHYROID = Superficial to the plane of the RLN and medial to the nerve

Vancouver Pg 157

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14
Q

What are 4 non-invasive localization studies that can be used for a parathyroid adenoma diagnosis?

A

A. ULTRASOUND
- Poor if < 5mm

B. SESTAMIBI SCINTIGRAPHY (measurements at 10min & 2 hours)
- Tracer accumulates in mitochondria - adenomas have high oxyphilic cells, rich in mitochondria. Initial uptake of tracer in the parotids, submandibular glands and thyroid. However after 2 hours, tracer washes out of the thyroid except for the parathyroid adenoma
- 99mTc-sestamibi by itself: 89% sensitive for single adenomas, poor for multiple adenomas/hypertrophy
- SPECT - Sestamibi-single photon emission computer tomography - improved visualization but uses same transfer, sensitivity 98%
- SPECT-CT - SPECT fused with CT scanning
- Subtraction scans - Technetium-thallium. Technetium accumulates in parathyroid, thallium accumulates in thyroid and parathyroid. Final image = thallium - technetium (poor for multigland disease)

C. 4D-CT
- Images rapid contrast uptake and washout from parathyroid adenomas
- High dose of radiation (do not use in young people)
- Needs to be more than 1cm, poor for intrathyroidal

D. OTHERS:
- MRI
- Choline 11 - Methionine PET

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15
Q

What are 6 alternative sites for parathyroid gland location and their relative % incidences?

A
  1. Retroesophageal (most common location for ectopic superior glands) - 25%
  2. Superior mediastinal (most common location for ectopic inferior glands) - 25%
  3. Intrathymic (20%)
  4. Intrathyroidal (10%)
  5. Carotid sheath
  6. Tracheoesophageal
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16
Q

What are 5 invasive localization studies for parathyroid adenoma?

A

A. ARTERIOGRAPHY
- Thyrocervical trunk, internal mammary and carotids

B. DIGITAL SUBTRACTION ANGIOGRAPHY
- For multiple gland disease in revision cases
- 60-70% sensitive

C. SELECTIVE VENOUS CATHETERIZATION
- 80% sensitive
- Two-fold rise in PTH
- Expensive, high skill required
- 3-5 hours to complete
- Difficult if post-op with ligation of vessels

D. U/S GUIDED FNA

E. INTRAOPERATIVE LOCALIZATION METHODS
1. Intraoperative ultrasound
2. Injection of methylene or toluidine blue
3. Gamma probes (after Tc99m injection 2 hours pre-op, radiation > 20% than surgical bed is positive)
4. Intraop PTH & frozen section
5. Urinary adenosine monophosphate (historic)

17
Q

Why and how is intraoperative PTH monitoring done? 2 indications that surgery is complete

A
  • Mainly done for primary hyperparathyroidism
  • PTH intraop monitoring has replaced bilateral exploration
  • Bilateral exploration used to be routine for primary hyperparathyroidism (to exclude 4 gland hyperplasia - 10% risk; and multiple adenomas - 5% risk)

Several protocols for monitoring exist.

The most widely accepted protocol = “dual criteria”
1. PTH half life is 3-5 minutes
2. Two samples: (1) before skin incision, (2) 10 minutes post-gland excision

Surgery finished when:
1. Decrease PTH by 50%; AND
2. PTH level normalized

18
Q

What are the indications for surgery for primary hyperparathyroidism?

A

A. SYMPTOMATIC PATIENTS (Essentially all symptomatic patients)
1. Muscle weakness
2. Osteitis fibrosa cystica (Brown’s tumor - giant cell focal lesion arises in result of abnormal bone metabolism)
3. Renal calculi ± radiograph
4. Life threatening hypercalcemic crisis
5. Psychiatric problems
6. GI symptoms
7. Fibromyalgia symptoms

B. ASYMPTOMATIC PATIENTS, if:
1. Serum calcium > 1mg/dL (0.25mmol/L)
2. Skeletal scan:
- BMD by DEXA: T-score < -2.5 at the tested site (more negative)
- Vertebral fracture by radiograph (CT/MRI) or vertebral fracture assessment
3. Renal:
- Creatinine clearance/GFR < 60mL/min
- 24-hour urine for calciu, > 400mg/day and increased stone risk by biochemical analysis
- Nephrolithiasis or nephrocalcinosis by radiograph (US or CT)
4. Age < 50

C. CHRONIC RENAL FAILURE INDICATIONS (50% effective)
1. Calciphylaxis (tissue calcification) unresponsive to hemodialysis or meds
2. Refractory bone pain/pruritus
3. Renal osteodystrophy
4. Pathologic fractures
5. Anemia non-responsive to EPO

19
Q

What is one medication that can be used in patients with primary hyperparathyroidism that are poor surgical candidates, and for patients with secondary hyperparathyroidism?

A

CINACALCET
- Calcimimetic (activates the calcium-sensing receptor in the parathyroid gland)
- Decreases PTH
- Decreases calcium

Indications:
1. Secondary hyperparathyroidism
2. PTH carcinoma

20
Q

Regarding parathyroid carcinoma, discuss:
1. Lab findings
2. Management
3. Pathology findings

A

RARE

Lab findings:
1. Severe hypercalcemia
2. Elevated PTH

Pathology findings:
1. Angioinvasion seen on histology

Management:
1. Resection and neck dissection prophylactically
2. IMRT for palliative cases

21
Q

What are 3 surgical options for parathyroid hyperplasia?

A
  1. SUBTOTAL PARATHYROIDECTOMY
    - Preferred if patient doesn’t have MEN or renal failure (ie. use in sporadic 4-gland hyperplasia)
    - Involves removal of 3 glands and removal of 1/3 to 2/3 of the fourth gland
    - Can use PTH titration
  2. TOTAL PARATHYROIDECTOMY W/ AUTO-TRANSPLANTATION
    - For chronic renal failure, 50% effective
    - Implant into SCM, brachioradialis or infraclavicular
    - Can cryopreserve parathyroid up to 18 months
  3. TOTAL PARATHYROIDECTOMY W/ CRYOPRESERVATION OF 1 GLAND
    - Chronic renal failure or MEN
22
Q

What is the 6 differential diagnosis of persistent hypercalcemia post-surgical exploration and excision (>6 months post-op)?

A
  1. Supranumerary gland
  2. Second adenoma
  3. Residual gland
  4. Failure to recognize diseased gland
  5. 4-gland hyperplasia (wrong diagnosis)
  6. Malignancy
23
Q

Discuss the management of hypercalcemia crisis. Name 6 things

A
  1. Saline hydration and electrolyte correction
  2. Furosemide diuresis
  3. Glucocorticoids
  4. Calcitonin (inhibits osteoclasts) - 5 IU/Kg IM
  5. Bisphosphonates (inhibits osteoclasts) - Pamidronate 60mg IV over 4 hours
  6. Organic phosphates - 8mg IV, PO, or PR
  7. Mithramycin (MOA poorly understood but works well) - 25 mcg/kg IV over 4 hours
  8. Gallium nitrate (inhibits osteoclasts)
  9. Hemodialysis for life threatening situations
  10. Cinacalcet
24
Q

Describe the symptoms of hypercalcemia

A

BONES: Osteoporosis

STONES: Renal lithiasis

GROANS:
- N/V
- Constipation
- Cramps
- Gallstones
- Pancreatitis
- Peptic ulcers

MOANS:
- Depression
- Fatigue
- Confusion
- Stupor
- Coma

TONES:
- Shortened QT

25
Q

Describe the ECG findings of hypercalcemia

A
  1. Shortening QTc interval
  2. Osborn waves (J-waves)
  3. Ventricular irritability and VF arrest (if severe)

Vancouver pg 160

26
Q

Describe the ECG findings of Hypocalcemia

A

Q-Tc prolongation –> Torsade’s –> Ventricular arrhythmia

27
Q

What are the causes of hypercalcemia?

A

CHIMPANZEES

C: Calcium supplementation
H: Hyperparathyroidism
I: Iatrogenic (drugs such as thiazides, or immobility after surgery)
M: MIlk-alkali syndrome (caused by taking too much calcium, usually in the form of dietary supplements taken to prevent osteoporosis, and absorbable alkali (found in antacid drugs))
P: Paget’s disease of the bone, also osteogenesis imperfecta
A: Acromegaly and Addison’s disease
N: Neoplasia (common cause) - Multiple myeloma, bone metastasis
Z: Zollinger-Ellison Syndrome (MEN Type 1)
E: Excessive Vitamin D
E: Excessive Vitamin A
S: Sarcoidosis

28
Q

Describe hungry bone syndrome. What are the risk factors for this?

A
  • Rapid, profound, and prolonged hypocalcemia associated with hypophosphatemia and hypomagnesemia, and exacerbated by suppressed PTH levels
  • Follows parathyroidectomy in patients with severe primary hyperparathyroidism (pHPT) and pre-operative high bone turnover
  • Believed to be due to increase influx of calcium into bone, due to sudden removal of the effect of high circulating levels of PTH on osteoclastic reabsorption
  • Elevated alkaline phosphatase (high bone turover) pre-op suggests patient will need Ca2+/Mg+ post-op
29
Q

What enzyme stimulated by PTH activates Vitamin D?

A

1-alpha hydroxylase

30
Q

What investigations should be ordered (other than calcium and PTH) could be performed with diagnosis of hyperparathyroidism?

A
  1. Albumin
  2. Alkaline phosphatase (measure of bone turnover)
  3. Bone densitometry (DEXA)
  4. BUN and Creatinine
  5. Calcitonin (r/o MEN 2A)
  6. Thyroid function test (TSH)
  7. 24h urine calcium (r/o familial hypocalciuric hypercalcemia)
  8. Gastrin (r/o MEN 1)
  9. ACE (r/o sarcoid)
  10. Phosphorus
  11. Urine catecholamines (r/o MEN 2a)
  12. Prolactin (r/o MEN 1)
  13. Thyroid U/S - high rate of concurrent thyroid nodules (easiest to manage concurrently)
31
Q

Discuss the follow up management of hyperparathyroidism 3

A
  1. Labs: Ca2+, Cr/GFR, Urinalysis, PTH q6 months
  2. Bone density yearly
  3. Restrict oral calcium intake < 1g/day
32
Q

Discuss the management of hyperparathyroidism associated with renal failure 3

A

Renal failure - Phosphate high, calcium low/normal, PTH high

  1. Calcium salts (phosphate binder for hyperphosphatemia) - Sevelamer - binds to phosphate and prevents its absorption (increases excretion)
  2. Vitamin D (because hypovitamin D) - Calcitriol
  3. Cinecalcet
33
Q

What is the danger of primary hyperparathyroidism in pregnancy?

A
  1. Neonatal tetany (involuntary muscle contractions and peripheral nerve stimulation)
  • Calcium crosses placenta, PTH doesn’t
  • Newborn PTH is suppressed and serum Ca2+ drops soon after delivery –> leading to hypocalcemia (tetany)
34
Q

What are the causes of congenital hypoparathyroidism? 2

A

Due to agenesis of the parathyroids

  1. Deletion 22q11.2 spectrum (DiGeorge, Velocardiofacial syndrome)
  2. Mother hyperparathyroid - supresses fetal parathyroid function –> hypocalcemia after birth/withdrawal of PTH –> Possible neonatal tetany (due to hypocalcemia)
35
Q

What does primary hyperparathyroidism in infancy present with? 3

A
  1. Respiratory distress
  2. Hypotonia
  3. Skeletal Demineralization
36
Q

Regarding Hyperparathyroidism-Jaw tumor syndrome, discuss:
1. Genetics and inheritance
2. Clinical presentation -3

A

GENETICS/INHERITANCE:
1. Gene: CDC73 on chromosome 1q31
2. Inheritance: Autosomal dominant
3. Protein affected: Parafibromin (tumor suppressor gene)

CLINICAL PRESENTATION:
1. Hyperparathyroidism (solitary or multiple adenomas, 10% will present as parathyroid carcioma, severe hypercalcemia as a teenager)
2. Jaw: Cemento-ossifying fibromas
3. Renal: Cysts, hamartomas, Wilms’ tumor (nephroblastoma)

37
Q

What is a Brown’s tumor?
Pathophysiology?
What should be ruled out when you see a patient with a Brown’s tumor?

A

Brown’s tumor = A type of Osteitis fibrosa cystica

OFC = Combination of cystic brown tumors, peritrabecular fibrosis and increased bone activity

PATHOPHYSIOLOGY:
- Giant cell focal lesions that arise from abnormal bone metabolism due to hyperparathyroidism
- Areas of extensive bone resorption, replaced by fibrovascular tissue and giant cells with abundant deposits of hemorrhage and hemosiderin (brown color)

Clinical presentation:
- Most common present in mandible or maxilla

RULE OUT:
1. Primary hyperparathyroidism
2. Renal osteodystrophies (renal disease causing skeletal abnormalities) - much more secondary than primary hyperparathyroidism, so more commonly seen in secondary HPT
3. MEN 1/2a

38
Q

Regarding parathyroid cysts, discuss:
1. Presentation
2. Diagnosis 2
3. Differential 4
4. Management

A

PARATHYROID CYSTS:
- Rare presentation, most are non-functional
- Functional cysts are often secondary to degeneration of parathyroid adenomas

PRESENTATION:
- Majority located in neck (some in mediastinum)
- Can (rarely) present with parathyroid crisis

DIAGNOSIS:
1. Cystic mass with CLEAR fluid
2. Elevated PTH in the fluid

DIFFERENTIAL:
1. TGDC
2. Branchial cleft cyst
3. Thyroid cyst
4. Parathyroid carcinoma

MANAGEMENT:
1. Asymptomatic with normal calcium = observation
2. Symptomatic or increased Ca2+ = surgery

39
Q

Recurrent hyperparathyroidism, post-4-gland - what else can you do?

A

Thymectomy (in case of intra-thymic parathyroid)

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