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RCPSC > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

In which directions do calcium and phosphate go in parathyroid mediated calcium problems?

A

Opposite directions

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2
Q

In which directions do calcium and phosphate go in Vitamin D related calcium problems?

A

Same direction

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3
Q

In which directions do calcium and phosphate go in teriary hyperpara?

A

Same direction

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4
Q

How does magnesium deficiency affect calcium levels

A
  1. Reduces PTH secretion and causes PTH resistance
  2. Appears like hypopara
    1.
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5
Q

Describe the calcium, phosphate, PTH and urine calcium patterns in the following disorders:

  • Primary hyperpara
  • Tertiary hyperpara
  • Pseudohypopara
  • FHH
  • Lithium
  • Thiazide
  • Vitamn D excess
  • PTHrP
  • Osteolysis
  • Vitamin D deficiency
A
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6
Q

What are the indications for surgery in primary hyperparathyroidism

A
  1. Symptomatic
  2. Asymptomatic (Stay The Fudge Away U Stupid Calcium)
    1. Serum calcium >0.25 above ULN
    2. T-score < -2.5 at L-spine, total hip, femoral neck or distal 1/3 of radius
    3. Fractures
    4. Age <50
    5. Urine calcium >10 mmol/day
    6. Stones or nephrocalcinosis by X-Ray, U/S, CT
    7. Creatinine clearance <60
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7
Q

What is the medical management for patients with primary hyperpara who are not candidates for surgery

A
  1. Correct vitamin D deficiency: Target serum 25OH vitD >50
  2. Amino-Bisphosphonates are effective at preventing BMD decrease and at reducing remodelling
  3. Consider cinecalcet if symptomatic and surgery is not an option
    1. Can be combined with bisphosphonates in select patients
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8
Q

What must always be ruled out before sending a patient for parathyroidectomy in primary hyperpara. How is it ruled out?

A
  1. R/O FHH
  2. Do 24hrs urine calcium
    1. Urine calcium:creatinine ration <0.01 think FHH
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9
Q

What is secondary hyperparathyroidism?

A

Appropriate increase in PTH secondary to hypocalcemia or vitamin D deficiency (most common)

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10
Q

How can calcium be supplemented following gastric surgery

A

Calcium citrate

*Calcium carbonate not absoorbed

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11
Q

How is secondary hyperparathyroidism treated in the context of CKD?

A
  1. Vitamin D
  2. Phosphate restriction
  3. Non-calcium phosphate binders
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12
Q

What is tertiary hyperparathyroidism?

A
  1. Parathyroid glands become autonomous in the setting of longstanding hypocalcemia
    1. Usually in the setting of ESRD
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13
Q

What are the indications for surgery in tertiary hyperpara

A
  1. Refractory hyperPTH despite Vitamin D analogues, calcimimetics
    1. No absolute cutoffs
  2. Severe or symptomatic hypercalcemia
  3. Calciphylaxis
  4. Progressive bone disease
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14
Q

Give a differential for Hypoparathyroidism

A
  1. Acquired
    1. Hypomagnesemia
    2. Post-surgical (common complication, post op thyroidectomy)
    3. Post-radiation
    4. Infiltrative disease
      1. Sarcoid
      2. Amyloid
      3. Cancer mets
    5. Autoimmune polyglandular syndrome type 1
  2. Congenital
    1. Pseudoohypoparathyroidism
    2. DiGeorge syndrome
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15
Q

What is Whitaker’s triad in the context of autoimmune polyglandular syndrome type 1

A
  1. Chronic mucocutaneous candidiasis
  2. Addison’s disease
  3. Hypoparathyrodism
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16
Q

List the 3 types of cancers associated with MEN-1

A
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17
Q

List the 3 types of cancers associated with MEN-2A

A
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18
Q

List the 3 types of cancers associated with MEN-2B

A
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19
Q

Explain how a radioactive iodine uptake scan is interpreted

A
  1. High uptake:
    1. Increased endogenous production:
      1. Graves
      2. Toxiic multinodular goiter
  2. Low uptake
    1. extra thyroid hormone without increased production
      1. Exogenous ingestion
      2. inflamatory leak
        1. Thyroiditis
          1. Acute, subacute
          2. post-partum
          3. amio induced
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20
Q

What is pathomnemonic for Graves (even if negative RAIU)

A

Ophtalmopathy

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21
Q

What can cause an RAIU to be falsely negative in graves disease?

A
  1. CT scan with iodinated contrast
  2. Amiodarone
  3. Iodine intake (kelp)
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22
Q

What causes a goiter

A
  1. Stimulation of the thyroid gland
    1. TSH (Hashimoto)
    2. Thyroid receptor antibodies (Graves)
    3. b-HCG (pregnancy)
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23
Q

What causes a tender thyroid gland

A
  1. Inflamation
    1. Thyroiditis
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24
Q

How are the symptoms of Hyperthyroidism treated in the acute setting. In whom should these meds be particularly considered?

A
  1. Beta blockers (non-cardio selective)
    1. Especially in the elderly, resting HR>90 or CVD
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25
Q

How long does it take before seing the full effect of MMZ ot PTU

A

4-6 weeks

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26
Q

What is the preferec anti-thyroid drug in most circumstances

A

MMZ

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27
Q

When should PTU be used instead of MMZ?

A
  1. Pregnancy
  2. Thyroid storm
  3. Minor MMZ reactions
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28
Q

How should a patient be prepped for RAI therapy

A
  1. Liberal use of b-blockers unless contrraindication
  2. Don’t give MMZ or PTU, reduce success rate
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29
Q

Compare the side effects of MMZ and PTU

A
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30
Q

What are the treatment options for graves disease

A
  1. Anti-thyroid
  2. RAI
  3. Surgery
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31
Q

How should anti-thyroid hepatotoxicity be managed

A
  1. Get LFTs if suspicion
    1. MMZ: cholestatic picture
    2. PTU: Fulminant hepatic necrosis and liver failure
  2. D/C offending med!
    1. D/C PTU id transaminases 3x ULN
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32
Q

How should anti-thyroid induced agranulocytosis be managed

A
  1. Usually within 1st 3 months on the medication
  2. Treat with G-CSF, steroids, ABx or supportive care
  3. Monitor for fever and sore throat, return to ED if they have it
  4. No routine monitoring but get BW if suspicious
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33
Q

How should anti-thyroid minor skin reactions be managed

A
  1. Antihistamines +/- prednisone (for allergi rcn)
  2. Rule out vasculitis
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34
Q

What is the only side effect of anti-thyroid medications for which it is OK to switch to another antithyroid med?

A
  1. Minor reactions
    1. Rash
    2. GI symptoms
    3. myalgias
    4. arthralgias
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35
Q

List contraindications to RAI therapy

A
  1. Pregnancy
  2. Breastfeeding
  3. Moderate to severe orbitopathy
  4. thyroid cancer
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36
Q

What are the side effects of RAI therapy

A
  1. Orbitopathy
  2. Thyroiditis
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37
Q

For how many months should pregnancy be avoided after RAI therapy

A

6 months

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38
Q

When giving RAI with orbitopathy, what should be given concurrently

A

steroids

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39
Q

How shoudl MMZ be managed if considering RAI

A

Stop at least 2-3 days before

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40
Q

What needs to be achieved before operating on a patient with graves for thyroidectomy

A

euthyroidism

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41
Q

How should graves disease with moderate to severe graves orbitopathy be treated when there are CI to surgery and ATDs

A

RAI with steroid prophylaxis

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42
Q

How is thyroid storm defined

A
  1. Very sick patient with signs of thyrotoxicosis
    1. Fever
    2. neurological Sx
    3. GI sx, hepatic dysfunction
    4. Tachycardia
    5. AF
    6. Heart failure
    7. Precipitant
      1. Infection
      2. Surgery
      3. Trauma
      4. iodine load
      5. pregnancy
      6. Rx non-adherence/discontinuation
  2. Burch Warftoski scale

*T4 excess not necessarily more than with other forms of hyper T4

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43
Q

How is thyroid storm managed

A
  1. Involve ICU early
  2. Supportive care
  3. Beta blockers
    1. Carefull with hemodynamic status
  4. PTU THEN
  5. Iodine
    1. Give 1hr after PTU loading dose
  6. Glucocorticoids
    1. Often AI coexists
    2. Helps reduce T4→T3 conversion
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44
Q

What is subclinical hypothyroidism

A
  1. TSH above ULN with normal free t4
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45
Q

When should subclinical hypothyroidism be treated in non-pregnant patients?

A
  1. TSH > 10
  2. Consider when
    1. Symptomatic
    2. Goiter
    3. Positive anti-TPO Ab
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46
Q

When should subclinical hypothyroidism be treated in in pregnant patients

A

First check TPO Ab

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47
Q

What is the TSH target for pregnant patients on thyroid replacement

A

<2.5

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48
Q

How should levothyroxine be adjusted when a patient becomes pregnant

A

Take 1 extra pill on saturday and sunday once patient becomes pregnant

Target TSH<2.5

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49
Q

How should graves disease be treated in pregnancy

A
  1. PTU in first trimester then swich to MMZ
    1. Discontinue all antithyroid meds if possible
  2. Use the lowest possible dose. Target T4 hign/normal range
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50
Q

What could be causing post-partum exacerbations of hyperT4 in graves disease

A

Could be from graves or from postpartum thyroiditis

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51
Q

Why do TSH-R Ab need to be monitored in the second trimester of pregnancy in graves patients

A
  1. They cross the placenta!
    1. If titers very high, (3x ULN) monitor for fetal graves
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52
Q

What are the adverse effects of long term beta blockade in pregnancy for graves patients

A
  1. IUGR
  2. fetal bradycardia
  3. Neonatal hypoglycemia
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53
Q

Describe gestational transient thyrotoxicosis and it’s pathophysiology

A
  1. hCG stimulates the TSH receptor on the thyroid gland causing increased thyroid hormones and reduced TSH
    1. In normal pregnancy, TBG and total T4 increase by week 7 and peak at week 16
  2. Generally self limited and improves by 14-18 weeks
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54
Q

In what contexts will the hCG effects on t4 be even more pronounced than regular pregnancy?

A
  1. Hyperemesis gravidarum
  2. Molar pregnancy
  3. Multiple gestation pregnancy
  4. Choriocarcinoma
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55
Q

how is gestationnal transient thyrotoxicosis treated?

A
  1. Treat hyperemesis if present
  2. Use BB if necessary for Sx
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56
Q

What clinical elements can help differentiate GTT from other causes of hyperthyroidism

A
  1. Ophtalmopathy and/or thyroid bruit: Graves
  2. Goitre: graves
  3. TRA + (graves)
  4. Nodules (toxic multinodular goitre or thyroid adenoma)
  5. Hyperemesis (GTT)
  6. Hx Thyroid disease (not GTT)
  7. Possibility of molar pregnancy (GTT but get pelvic US)
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57
Q

How is osteoporosis diagnosed?

A
  • Fragility Fx

OR

  • BMD 2.5 SD or more bellow peak BMD (T≤-2.5) on DEXA
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58
Q

Why do we risk-stratify patients with a diagnosis of osteoporosis

A
  1. To decide who gets treatment
  2. 3 categories: low, moderate, hiigh
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59
Q

How are patients risk-stratified in Osteoporosis?

A
  1. Look for signs of “automatic high risk”=makes patient high risk regardless of risk score
    1. Both of: prior fragility fracture and prolonged glucocorticoid use
      1. ≥7.5mg pred eq/day x 3 months
      2. Beware of AVN of hip
    2. hip or spine fracture
    3. >1 fragility fracture
  2. FRAX or CAROC score
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60
Q

How should patients with low risk osteoporosis be treated

A

No pharmacotherapy

Reassess risk in 5 years

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61
Q

How should patients with moderate risk osteoporosis be treated

A
  1. Consider pharmacotherapy
    1. Factors that CAN help in decision making:
      1. Additionnal vertebral Fx
      2. Previous wrist Fx in individuals >65 or t-score
      3. Lumbar T score << femoral neck T score
      4. Rapid bone loss
      5. Men undergoing ADT
      6. Women undergoing aromatase inhibitor Tx
      7. Long term or repeated use of corticosteroids not meeting criteria for recent prolonged use
      8. Recurrent falls (≥2 in 12 mo)
      9. Other disorders strongly associated with osteoporosis, rapid bone loss or fractures
  2. If treating, use bisphosphonates ideally
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62
Q

What factors can increase you CAROC risk without a change in BMD

A
  1. Fragility fracture after age 40
  2. Recent prolonged use of systemic glucocorticoids
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63
Q

How should patients with high risk osteoporosis be treated?

A
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64
Q

Which osteoporosis treatment options are effective for vertebral, hip and non-vertebral Fx

A
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65
Q

After how many years should treatment be reassessed in osteoporosis patients on pharmacotherapy? How should treatment be modified?

A
  1. Bosphosphonates: 3-5 years
  2. Denosumab: 5-10 years
  3. Teriparatide: 2 years
  4. Romosuzumab: 1 year

If risk low-moderate: Drug holliday

If risk remains high: Continue or switch to another therapy

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66
Q

What are the indications for teriparatide

A
  1. Severe osteoporosis with multiple vertebral fractures
    1. Look for CI to bisphosphonates and denosumab when considering
  2. Fractures despite prolonged bisphosphonate use
  3. High fracture risk and low bone formation
  4. Osteoporosis and prolonged steroid use
  5. Osteonecrosis of the jaw
  6. Atypical femoral Fx
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67
Q

list contraindications to teriparatide

A
  1. Renal insufficiency
  2. Renal stones
  3. Primary hyperpara/hypercalcemia
  4. Extensive skeletal radiation
  5. Paget’s disease
  6. don’t use in
    1. Children or young adults
    2. Pregnant or nursing women
    3. Gout or hyperuricemia
    4. Patients for >2 years
      1. Risk of osteosarcoma
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68
Q

What are the advantages of Romosuzumab

A
  1. Reduced vertebral, non-vertebral and hip Fx
  2. Very low risk of atypical Fx or osteonecrosis of the jaw
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69
Q

List side effects of romosuzumab

A
  1. Most worriesome: Increased risk of MACE
  2. Most common: Injection site and hypersensitivity reactions
  3. Very low risk of osteonecrosis of jaw and atypical femoral fracture, but still possible
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70
Q

Define treatment failure in osteopororsis

A
  1. Fx on therapy OR progressive decline in BMD despite being on therapy for 1 year with >80% adherence of osteoporosis medication. Specifically
    1. Major insufficiency Fx (spine, femoral neck, wrist, proximal humerus) OR
    2. Multiple minor insufficiency fractures OR
    3. BMD decrease > least significant after 5 years or earlier in patients with minor fractures
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71
Q

How is osteoporotic treatment failure managed?

A
  1. Assess compliance
  2. Ensure adequate calcium and vit D intake (25-OH-D should be >75)
  3. R/O secondary causes of osteoporosis
  4. R/O differences in T-Score assessment techniques
  5. Consider switching to another first line pharmacological agent
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72
Q

List side effects of bisphosphonates

A
  1. Flu-like Sx (esp zolendronic acid)
  2. Reflux Sx with PO
  3. Osteonecrosis of the jaw
  4. atypical femoral fractures
  5. Esophageal cancer (controversial)
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73
Q

List side effects of denosumab

A
  1. ? Increased risk of cellulitis
  2. Hypocalcemia
  3. Osteonecrosis of the jaw/ atypical femoral Fx
  4. Increased risk of vertebral fractures and BMD decline when therapy is stopped abruptly
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74
Q

What are the clinical characteristics of atypical femoral fracture

A
  1. Proximal femoral shaft fracture
  2. Atraumatic
  3. Chronic bisphosphonate use
  4. Asian women most likely
  5. May be associated with prodromal thigh pain
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75
Q

What are the radiographic characteristics of atypical femoral fracture

A
  1. Lateral cortical thickening
  2. Transverse fracture lines
  3. Beaking
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76
Q

How can you prevent atypical femoral fractures?

A

Drug holiday in low-risk patients on oral bisphosphonate therapy for 5 years (or IV bisphosphonates for 3 years)

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77
Q

How are atypical femoral fractures treated?

A
  1. Ortho consult
  2. Image controlateral femur
  3. Stop bisphosphonate
  4. Ensure adequate Ca and vitamin D
  5. Start teriparatide
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78
Q

How is vitamin D and calcium supplemented in osteoporosis

A
  1. Vitamin D
    1. Age >50: 800-2000 UI/day
    2. Age <50: 400-1000 UI/day
    3. Target 25-OH D ≥75
  2. Calcium
    1. Aim for intake of 1200 mg/day
    2. Supplement if not getting enough
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79
Q

List the non-pharmacological therapies for osteoporosis

A
  1. Appropriate resistance training, core training, balance training
  2. Hip protectors for older adults in LTC
  3. Smoking cessation
  4. Alcohol moderation
  5. Fall prevention strategies
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80
Q

What are the GFR cutoffs with:

  • Alendronate
  • Ibandronate
  • Risendronate
  • Adaloparatide
  • Teriparatide
  • Denosumab
  • Romosozumab
A
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81
Q

What are the A1C treatment targets?

A
  1. ≤6.5 in some T2DM if low risk hypos
  2. ≤7 in almost everyone
  3. 7.1-8 if functionally dependant
  4. 71.-8.5 if
    1. Recurrent severe hypoglycemia/hypo unawareness
    2. Decreased life expectancy (very elderly)
    3. Frail elderly with dementia
  5. Pregnancy planning
    1. ≤7, ≤6.5 ideally
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82
Q

List the factors that can affect A1C

A
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83
Q

How is T1DM treated

A

Basal-bolus, CSII

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84
Q

What are the benefits of switching to CSII

A
  1. Small improvement in A1C
  2. Increased treatment satisfaction, Dm related QOL
  3. Decreased rates of severe hypoglygemia
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85
Q

What are the benefits of adding CGM to BBI or CSII

A
  1. Decreased A1C with no increases in hypo
  2. Better QOL, reduced DM distress, fear of hypoglycemia and Tx satisfaction
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86
Q

What are the typical recommended targets in CGM

A
  1. Glucose management indicator ≤7%
  2. Glycemic variability ≤36%
  3. Time in range >70%
  4. Time bellow range: Total <4%
    1. Level 1 (3-3.8) <3%
    2. Level 2 (<3) <1%
  5. Time above range: Total <25%
    1. Level 1 (10-13.9) <20%
    2. Level 2 (>13.9) <5%
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87
Q

What are the recomended CGM ranges in older/hgh risk patients

A
  1. Time in range >50%
  2. Time bellow range: Total <1%
  3. Time above range
    1. Level 1 (10-13.9) N/A
    2. Level 2 (>13.9) <10%
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88
Q

What are the CGM targets in pregnancy for type 1 DM

A
  1. Time in range >70%
  2. Time bellow range
    1. Level 1 (3-3.8) <3%
    2. Level 2 (<3) <1%
  3. Time above range: Total <25%
    1. Level 1 (10-13.9) <25%
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89
Q

When should CBG testing be instituted in patients with T2DM not on insulin

A
  1. When A1C targets not beaing reached
  2. If A1C targets reached, only measure during illness or risk of hypoglycemia
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90
Q

Once T2DM is diagnosed, what are the initial treatment steps?

A
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91
Q

If A1C isn’t at target in 3-6 months, what additional steps should be taken in patients with ASCVD, CKD, HF, Age >60 or with 2 CV risk factors?

A
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92
Q

If A1C isn’t at target in 3-6 months, what additional steps should be taken in patients without ASCVD, CKD, HF, Age >60 or with 2 CV risk factors?

A
93
Q

List CV risk factors

A
  1. Smoking
  2. HTN
    1. Untreated BP >140/95 or
    2. current antihypertension therapy
  3. DLP
    1. Untreated LDL>3.4 OR HDL<1 (men) <1.3 (women) OR Triglycerides >2.3 ORR current lipid-lowering therapy
  4. Central Obesity
94
Q

What are the recommendations for treating T2DM in comorbid patients by comorbidity

A
95
Q

What does “symptomatic hyperglycemia with metabolic decompensation” mean? What are the symptoms?

A
  1. Polyuria
  2. Polydipsia
  3. Blurry vision
  4. Unintentional weight loss
  5. Volume depletion
  6. Ketosis
  7. DKA/HHS
96
Q

How should symptomatic T2DM or T2DM with metabolic decompensation be managed once they are on metformin and insulin

A
97
Q

How should the following antihypoglycemics be managed in CKD:

  • Metformin
  • SGLT2
  • GLP1
  • DPP4i
  • Insulins
  • Glyburide
    • Non-glyburide secretagogues
A
98
Q

What are the side effects of SGLT2i?

A
  1. Euglycemic DKA
  2. GU infections
    1. Inc. Fournier’s gangrene
  3. Stop on “sick days”
99
Q

What is the side effect presumably only attributed to Canagliflozin

A
  1. Increased risk of toe amputation
    1. Seen in CANVAS but not CREEDENCE
  2. Can possibly worsten osteoporosis
100
Q

What is a contraindication for Dapagliflozin specifically

A

Bladder Ca

101
Q

Which SGLT2 was note shown to improve MACE?

A

Ertugliflozin

102
Q

What is the Beneficial side effecto of GLP1

A

Weight los

103
Q

What are the non-beneficial side effects of GLP1

A
  1. GI side effects
    1. Dyspepsia
    2. Anorexia
    3. N/V/D
    4. Abdo pain
104
Q

What are contraindications to GLP1

A
  1. Personal or family historry of medullary Thyroid cancer or MEN2
  2. Caution in Hx of pancreatitis or pancreatic Ca (not formally CI)
105
Q

What is a side effect of Semaglutide specifically

A
  1. Worsening retinopathy
106
Q

Which GLP1 has no proven cardiorenal benefit

A

Exenatide

107
Q

Which GLP1 is approved for weight loss in non-diabetics

A

Liraglutide

108
Q

What are the guidelines for vascular protection in T2DM?

A
  1. A1C ≤7
  2. BP <130/80
  3. Cholesterol LDL<2 or >50% reduction
  4. Drugs with cardioprotective effects when indicated:
    1. Statin
    2. ACE/ARB
    3. ASA
    4. GLP-1, SGLT2
  5. Exercise/healthy eating
  6. Smoking cessation
109
Q

What are the indications for statins in DMT2?

A
  1. Clinical CVD
  2. Age≥40
  3. Age >30 and DM for >15 years
  4. Microvascular disease
  5. Other CV risk factors
110
Q

What are the indications for ACE/ARB in T2DM

A
  1. Clinical CVD
  2. Age≥55 with an additional CV risk factor or end-organ damage (albuminuria, retinopathy, LVH)
  3. Microvascular disease
111
Q

What are the indications for ASA in T2DM

A
  1. Established CV disease
112
Q

What is the clinical presentation of primary adrenal insufficiency

A
  1. Weakness, lethargy, GI Sx
  2. Hyponatremia, Hyperkalemia
  3. Orthostatic hypotension, hypoglycemia, uremia
113
Q

How is adrenal insufficiency diagnosed?

A
  1. First do AM cortisol
    1. <83 AI very likely
    2. >500 AI unlikely
  2. When in between, need to confirm with ACTH stim test
    1. If no rise in cortisol to >500 at either 30min or 60in AI is diagnosed
114
Q

Once a diagnosis of AI is made, how can you differentiate primary from secondary AI?

A
  1. Measure ACTH
    1. If elevated, primary AI
    2. If low or appropriately normal, central AI
115
Q

Once AI is diagnosed, what workup should be sent to determine the cause

A
116
Q

What is the difference between cushing syndrome and cushing disease

A

Cushing syndrome- hypercortisolemia

Cushing disease- Pituitary tumor secreting ACTH

117
Q

How is Cushing syndrome diagnosed

A
  1. 2/3 positive screening tests
    1. midnight salivary cortisol
    2. 1mg dex suppression test
    3. 24hrs urine free cortisol
118
Q

How is a 1mg dexamethasone suppression test interpreted?

A
  1. Cortisol ≤50 = normal
  2. Cortisol 50-140 possible cushing
  3. cortisol >140 positive test
119
Q

How is the etiology of cushing syndrome determined?

A
120
Q

What are the indications to screen for hyperaldosteronism in hypertensive patients?

A
  1. Refractory hypertension (despite 3 drugs)
  2. Spontaneous hypokalemia (<3.5) or severe diuretic induced hypokalemia (<3)
  3. Adrenal incidentaloma
121
Q

What is the screening test for hyperaldosteronism

A
  1. Plasma aldosterone to renin ratio
122
Q

What antihypertensives should be held for a plasma aldosterone to renin ratio? which ones can you continue

A
  1. Off
    1. MRA
    2. ACEi
    3. BB
    4. Clonidine
    5. Methyldopa
    6. DHP-CCB
  2. Can be on
    1. Hydralazine
    2. Verapamil
    3. Doxazocin
123
Q

What are the confirmatory tests for hyperaldo

A
  1. Saline suppression
  2. Oral salt load
  3. Captopril suppression test
124
Q

Who should be screened for Pheo?

A
  1. Paroxismal, unexplained, labile and/or severe (≥180/110) sustained HTN refractory to usual Tx
  2. HTN + Sx of pheo
    1. Palpitations
    2. Head aches
    3. sweating
    4. Panic attacks
  3. HTN triggered by BB, MAO-Is, Changes in abdo pressure, surgery, anesthesia, micturition
  4. Adrenal incidentaloma
  5. Genetic condition
    1. VHL
    2. Men2
    3. NFM-1
125
Q

How is screening for pheo performed?

A
  1. Start with biochemical test
    1. 24hrs urine metanephrines and cathecolamines
    2. Can consider plasma free metanephrines and free normetanephrines but not urinary VMA
  2. Once biochem screen confirmed
    1. MR abdomen or CT abdomen with delayed contrast washout
126
Q

How is pheochromocytoma managed clinically?

A
  1. Alpha blockade: phenoxybenzamine or Doxazocin
  2. Beta blockade only after high dose beta blockade
  3. Surgery after 2 weeks adequate alpha blockade with liberal salt and fluid intake
127
Q

What can be considered in the perioperative setting for Pheo?

A
  1. Phentolamine IV if necessary
  2. Vasopressors ready to go once adrenal gland manipulated
    1. Anesthesia consult pre-op
128
Q

What should be considered in the post-op setting in pheo

A
  1. ICU post-op
  2. Watch for hypotension, hypoglyceoma
  3. Conside familial syndromes (MEN)
129
Q

What is the definition of adrenal incidentaloma

A

Clinically unapparent mass greater than 1cm detected during imaging performed for reasons other than suspected adrenal disease

130
Q

What are indications that an adrenal incidentaloma might be malignant?

A
  1. Size>4cm
  2. >10 HU
  3. < 50% delayed contrast washout
  4. Calcifications, extension, adenopathy
  5. Hx of malignancy
131
Q

What should be done with adrenal incidentalomas to ensure they are not functionnal

A
  1. Screen for hypercortisolism (1mg dex supression test) and pheo in all
  2. Screen for hyperaldo only if HTN +/- hypoK
132
Q

What are the referral indications for bariatric surgery

A
  1. BMI 35-40 AND 1 serious comorbidity (DM, CAD, HTN)
  2. BMI≥ 40 without comorbidities
133
Q

What are the complications of bariatric surgery

A
  1. General surgical risks
  2. Stomal obstruction, Gastric perforation, GI Bleed, biliary stone disease, hernia, dumping syndrome, postprandial hypoglycemia
  3. Malabsorption: iron, B12, folate, calcium, vitamin ADEK, thiamine
134
Q

How should patients be managed after bariatric surgery

A
  1. Multidisciplinary in specialized centre
  2. Monitor and titrate Tx – DM/HTN may be cured
  3. Nutritional deficiencies and BMD screening annually
135
Q

What is the 5A framework in obesity

A
  1. ASK: Would it be allright if we discuss your weight today
  2. ASSESS:
    1. Goals that matter to the patient
    2. Obesity Hx
    3. Obesity classification
    4. functional assessment
  3. ADVISE:
    1. Refer to dietitian
    2. exercise 30-60 min most days
    3. obesity therapies inc. psychotherapy
    4. weight loss medications
  4. AGREE: on goals and on sustainable action plan
  5. ASSIST: with drivers and barriers
136
Q

What cancers does obesity increase the risk for?

A
  1. Colon
  2. Kidney
  3. Esophagus
  4. Endometrium
  5. Post-menopausal breast
137
Q

What can be used as pharmacotherapy for weight loss?

A
  1. Liraglutide
  2. naltrexone/bupropion
  3. Orlistat
138
Q

How should one medication be chosen over the other in obesity?

A
139
Q

List medications associated with weight gain and their alternatives

A
140
Q

Who should be screened for DLP

A
  1. Women ≥ 40 (or postmenopausal)
  2. Men≥40
  3. *Consider earlier in ethnic groups at increased risk such as south asian or indigenous
  4. In women with pregnancy related complications (GDM, HTN, pre-term birth, LowBW) Screen with full lipid profile in late post-partum period
  5. Council all women with pregnancy related complications of increased lifetime risk of ASCVD and reinforce lifestyle behaviors
  6. In this population use CV age>10 yr risk calculagor
  7. All patients with following conditions
    1. Clinical ASCVD
    2. Evidence of preclinical ASCVD (CACS or abnormal carotid US)
    3. AAA
    4. DM
    5. HTN
    6. Current smoker
    7. Stigmata of DLP
    8. Family Hx of CVD in 1st degree relative
    9. Family Hx of DLP
    10. CKD (GFR<60, ACR>3)
    11. Obesity (BMI>30)
    12. Inflammatory diseases (RA, SLE, PsA, AS, IBD)
    13. HIV
    14. erectile dysfunction
    15. COPD
    16. Pregnancy related complications
141
Q

How should screening for DLP be conducted

A
  1. For all
    1. H/P
    2. Standard lipid profile
    3. FPG or A1C
    4. eGFR
    5. lipoproteins– once in a lifetime
      1. if >100 earlier and more intensive behavior modification +/- statin
  2. Optional
    1. ApoB
    2. Urine ACR (if GFR <60, HTN, DM)
142
Q

What are the statin indicated conditions?

A
143
Q

How is familial hyperlipidemia diagnosed

A
144
Q

What are the LDL targets on statin therapy and what should be added on if they are not achieved on max statin therapy

A
145
Q

How should Patients with a AAA or ASCVD be treated if their LDL is not at target on max statin doses?

A
146
Q

Which patients have been shown to benefit the most from PCSK9i therapy

A
  1. Recent ACS
  2. Clinically evident ASCVD and any of the following:
    1. DM or metabolic syndrome
    2. Polyvascular disease
    3. Symptomatic PAD
    4. Recurrent MI
    5. MI in the last 2 years
    6. Previous CABG
    7. LDL≥2.6 or heterozygous FH
    8. lipoprotein ≥60
147
Q

How should DLP be managed when there are no statin indicated conditions present?

A

IF INTERMEDIATE OR HIGH RISK

148
Q

What is the pathophysiology of Paget’s disease

A
  1. Focal increase in bone resorption by very large osteoclasts, followed by increased osteoblastic activity
  2. High rate of bone formation and turnover
149
Q

What are the initial lab findings in Paget’s disease

A
  1. Elevated ALP +/- bone specific ALP
  2. No other abnormalities
150
Q

What imaging should be seeked when suspecting Paget’s disease. What will be found?

A
  1. Plain XR of suspicious area
  2. If asymptomatic, do squeletal survey/series
    1. Will show thickened cortices with tunneling and accentuated trabeculae
  3. If Dx is confirmed or already known, get bone scan to quantify extent of disease
151
Q

What illnesses are associated with Paget’s disease

A
  1. Hearing loss
  2. Compressive neuropathy
  3. OA
  4. Osteosarcoma
152
Q

What are the indications to treat Paget’s disease

A
  1. Symptoms:
    1. Pain
    2. Compression fracture
  2. Evidence of active disease with impending symptoms
    1. High risk for Fx
  3. Hypercalcemia
    1. Usually should only happen if imobile
  4. ALP > 2x ULN
  5. Pre-ortho surgery at or near site
153
Q

How is Paget disease treated?

A
  1. IV Zolendronic acid is 1st line
  2. Oral bisphosphonates can be used:
154
Q

What is primary amenoorrhea

A
  1. Absent menses at age 16
  2. Absent sexual characteristics at age 13
155
Q

What is the most common cause of primary amenorrhea

A

Chromosomal abnormality

156
Q

How would you work-up primary amenorrhea

A
157
Q

What is secondary amenorrhea

A
  1. No cycle >3 months in those with regular periods or > 6 months in those with irregular cycles
158
Q

What is the DDx for secondary amenorrhea

A
  1. Hypothalamic
    1. functional hypothalamic amenorrhea
  2. Pituitary
    1. Pituitary adenoma (Prl mediated)
    2. Other sellar masses
    3. Infiltration (HH)
    4. Sheehan
  3. Ovarian
    1. PCOS
  4. Pregnancy
  5. Other structural considerations
    1. Bicornate uterus
    2. Endometrioosis
    3. Asheman’s
159
Q

What are the FSH, LH and estradiol levels in hypothalamic amenorrhea

A

FSH, LH low

Estradiol Low

160
Q

What phenotype is associated with hypothalamic amenorrhea

A

When the body cant support a pregnancy

  1. High performance female athlete
  2. Eating disorder
  3. High stress environment
  4. Chronic illness
161
Q

What are the diagnostic criteria for PCOS

A
  1. 2/3:
    1. Menstrual irregularities
    2. Biochemical or clinical hyperandrogenism
    3. U/S finding of polycystic ovaries
162
Q

What are the physical exam findings in PCOS

A
  1. Elevated BMI
  2. Hyperandrogenism
    1. Ferriman gallway, alopecia, acne
  3. acanthosis nigricans
163
Q

What investigations should be sent when working up PCOS

A
  1. Prl
  2. TSH
  3. DHEAS
  4. LH, FSH
  5. Estradiol
  6. US pelvis
  7. fasting BG
  8. 2hr OGTT
  9. lipid profile
  10. sleep study
164
Q

What is the age cutoff for primary ovarian insufficiency

A

40

165
Q

What are the FSH, LH, estradiol level in primary ovarian insufficiency?

A

FSH, LH elevated

Estradiol low

166
Q

What are the etiologies of primary ovarian insufficiency

A
  1. Autoimmune
  2. Radiation
  3. chemotherapy
  4. Fragile X syndrome
167
Q

What investigations should be sent in primary ovarian insufficiency

A
  1. Clarify etiology
    1. Karyotype
    2. Fragile X
    3. Anti-adrenal antibodies
  2. Screening tests
    1. BMD
168
Q

How do you treat primary ovarian insufficiency?

A
  1. Hormone replacement until age of menopause
169
Q

How is PCOS managed

A
170
Q

What are the symptoms of hyperandrogenism in women

A
  1. Acne
  2. Voice changes
  3. Mood changes
  4. hirsutism
  5. Clitoromegaly
  6. Menstrual abnormalities
171
Q

What non sexual organs can be affected by hyperandrogenism in women

A
  1. Hypothyroidism
  2. Liver disease
172
Q

What illegal substance can cause hyperandrogenism in women

A

anabolic steroids

173
Q

What investigations should be sent if suspecting hyperandrogenism in women

A
  1. Total testosterone/free testosterone
  2. DHEA-S (if normal not an adrenal problem)
  3. 17-OH progesterone
    1. Increases in CAH. non-classic CAH
  4. Prl, TSH
  5. FSH, LH
    1. In PCOS LH>FSH
  6. Image ovaries and adrenals if testosterone ++ high (>5)
  7. Cushing screening if clinical suspicion
174
Q

What are red flags suggesting that hyperandrogenism is not from PCOS

A
  1. Increased muscle bulk
  2. voice
  3. clitoromegaly

*look for tumor

175
Q

What is the endocrinological DDx ofr hyperandrogenism

A
  1. PCOS
  2. NCCAH
  3. Virilizing tumor
  4. Cushing
  5. Acromegaly
  6. HypoT4
  7. Hyperprolactinemia (rarely)
  8. Also exogenous androgens/anabolic steroids, valproic acid
176
Q

What investigations should be sent in premenopausal hirsutism

A
  1. Random total testosterone (only if abnormal hirsutism score)
  2. Morning 17-hydroxyprogesterone assess for non-classic CAH (NCCAH)in women with high testosterone or high risk for CAH
177
Q

What is the treatment for hirsutism

A
  1. Cosmetic mesures
  2. Lifestyle changes if PCOS or obese
  3. First line pharmacotherapy: OCP
  4. Second line pharmacotherapy: anti-androgen (spirornolactone) + OCP if no improvement after 6 months OCP monotherapy
  5. Antiandrogens not recommended alone due to teratogenic potential
    1. unless not sexually active, permanent sterilization, or on ocntraception
178
Q

Describe Ferriman-Gallwey score

A
179
Q

Give a approach to male hypogonadism

A
180
Q

What are the causes of male hypogonadism

A
  1. Primary (High FSH/LH)
    1. Klinefelterr (XXY)
    2. Chemo
    3. testicular trauma
    4. mumps
    5. AI
    6. systemic illness
  2. Secondary (low FSH/LH)
    1. Pituitary adenoma
    2. hyperprolactinemia
    3. HH
    4. anabolic steroids
    5. Obesity
    6. opioiids
    7. DM2
181
Q

What are the clinical findings in Klinefelter syndrome

A
  1. Small firm testes
  2. Long arm and leg span
182
Q

What are the comorbidities associated with kleinfelter syndrome

A
  1. NHL
  2. Bronchectasis
  3. SLE
  4. DM
  5. osteopenia
  6. breast Ca
183
Q

How is Kleinfelter syndrome diagnosed

A

Karyotype

184
Q

What conditions increase and decrease SHBG and should be kept in mind when measuring free vs total testosterone

A
  1. Decrease
    1. Obesity
    2. DM
    3. Steroid use
    4. Nephrotic syndrome
    5. HypoT4
    6. acromegaly
    7. Polymorphisms in SHBG gene
  2. Conditions that increase SHBG
    1. Aging
    2. HIV
    3. cirrhosis
    4. hepatitis
    5. HyperT4
    6. use of estrogen
    7. use of anticonvulsivants
    8. polymorphisms in SHBG gene
185
Q

What are the indications and contraindications to testosterone replacement therapy in men?

A
  1. Recomended to maintain secondary sex characteristics and to correct symptoms of testosterone deficiency
  2. Not recommended if planning fertility in the near term, breast or prostate Ca, prostate nodule/induration, high PSA, High hematocrit, untreated OSA, severe LUTS, uncontrolled CHF, MI/Stroke in the last 6 months, thrombophilia
    1. Caution in older men
186
Q

HOw should patients on testosterone replacement therapy be monitored?

A
  1. Several times in the first year then annually
    1. Symptoms
    2. Testosterone level
    3. hematocrit
    4. PSA
187
Q

What is the differential for hyperprolactinemia

for each ddx, around what level of PRL would you expect

A
  1. Disruption of the stalk
    1. PRL <100
  2. lactotroph adenoma:
    1. if 1cm RPL ˜100
  3. Antidopaminergic drugs
    1. Antipsychotics particularily
  4. Hypothyroidism
  5. Renal failure
  6. Physiologic stimuli:
    1. nipple, chest wall, trauma, sex
188
Q

What are the symptoms of hyperprolactinemia

A
  1. Amenorrhea
  2. galactorrhea
  3. Hypogonadism
  4. Mass effect
189
Q

What should you suspect in a patient with ++ symptoms of hyperprolactinemia but PRL only mildly elevated

A
  1. Hook effect
    1. Lab peculiarity where very high PRL levels are read as low levels, if you dilute the sample, you can get a more accurate reading
190
Q

What should you suspect if a patient has a ++ elevated prolactin but mild Sx

A
  1. Macroprolactin
    1. Prolactin multimer that is biologically inactive
    2. Usually stick around because clearance is slow
191
Q

What should be ruled out in elevated prolactin

A

Stalk effect

other pit. dysfunctions

192
Q

How should a drug induced/hypothyroid hyperPRL be treated

A

Stop drug or give T4

193
Q

How should hyperprolactinemia from stalk effect be managed

A

Manage the primary tumor

194
Q

How should a prolactinoma be managed

A
  1. Treat with dopamine agonist even if mass effect
    1. Cabergoline: more effective, better tolerated, not well studied in pregnancy
    2. Bromocriptine: older, cheaper, more side effects
    3. Side effects: nausea, nasal stuffiness, headache
195
Q

What are the indications for surgery in non-PRL pituitary tumors

A
  1. Hormonal hypersecretion syndromes
  2. Hormonal hypofunction
  3. Mass effect (Visual field, cranial nerves, headache)
  4. Hemorrhage
196
Q

How should non-PRL pituitary tumors be treated if there are no indications for surgery?

A
  1. Follow clinically for development of surgical indication
197
Q

What is the clinical presentation of DI

A
  1. Polydypsia
  2. Polyuria
  3. Usually post-neurosurgery
198
Q

How is DI diagnosed

A
  1. Suspect based on
    1. Hypernatremia
    2. Elevated plasma OSm
    3. Inappropriately dilute urine
  2. Diagnosis on water deprivation test
199
Q

How does DI usually present post-sellar surgery

A
  1. Triphasic
    1. Transient DI from pit. stunning
    2. SIADH from release of stored ADH
    3. Permanent DI from loss of posterior pituitary function
200
Q

What are the symptoms of acromegaly

A
  1. Macrognathia
  2. macroglossia
  3. Increased ring, glove, shoe, collar size
  4. OSA
  5. Coarsened facial features
  6. gap between incisors
  7. Carpal tunnel
  8. OA
  9. T2DM
  10. Visual field defects
  11. Cranial neuropathies
201
Q

What is the screening test for acromegaly

A

IGF1 level

202
Q

What is the diagnostic test for acromegaly

A

75g glucose supression

203
Q

What is the treatment for acromegaly

A

Surgical

204
Q

What is the differential for a thyroid nodule

A
  1. Multinodular goiter, Toxic nodule, Benign non-functional nodule, cyst
  2. Thyroid Ca (papillary 90%, follicular, medullary, anaplastic)
  3. Lymphoma
205
Q

How should a thyroid nodule be worked-up?

A
  1. H/P
  2. TSH
    1. If TSH<0.5 do uptake scan
  3. U/S
  4. Bx if indicated
206
Q

Who needs a biopsy for a thyroid nodule

A
  1. High/int risk: >1cm
  2. Low risk: >1.5 cm
  3. Consider very low risk >2cm
  4. Purely cystic: Don’t Bx

*If multiple nodules, treat each individually

207
Q

List high risk sonographic features for thyroid nodules?

A
  1. Hypoechoic
  2. irregular margins
  3. microcalcifications
  4. Taller than wide
  5. Extrathyroidal extension
  6. Interrupted rim calcifications
  7. LADP
  8. >20% increase in 2 directions
208
Q

What are the post-thyroidectomy features of high risk disease in thyroid cancer?

A
  1. +LN
  2. +margins
  3. Extrathyroidal extension
  4. distant mets
  5. Needing RAI (High risk!)
209
Q

What are the TSH targets post thyroidectomy for thyroid cancer?

A
  1. Low-risk: 0.5-2
  2. Medium risk: 0.1-0.5
  3. Hiigh risk: <0.1
210
Q

What are the main management steps for graves orbitopathy

A
  1. Quit smoking
  2. Refer to specialized GO eye centre
  3. Artificial tears
  4. Restore euthyroidism
211
Q

What is the mainstay of treatment for graves orbitopathy

A

Steroids if no CI

second line: Radiotherapy, cyclosporine, ritux if partial or no response to steroids

Surgery only for stable inactive GO

212
Q

How is DM and pre-diabetes diagnosed

A
213
Q

What are the screening recommendations for DM retinopathy

A
  1. T1DM
    1. Start screening 5 years after Dx after age 15
    2. Screening done by dilated fundoscopy and fundus photography
    3. If present further monitoring and treatment as determined by ophtalmology
    4. If absent screen q1year
  2. T2DM
    1. Screen at diagnosis
    2. Screening done by dilated fundoscopy and fundus photography
    3. If present further monitoring and treatment as determined by ophtalmology
    4. If absent screen q1-2 years
214
Q

What are the screening recommendations for DM neuropathy

A
  1. Type1
    1. Start 5 years after poost-pubertal T1DM
  2. Type 2
    1. Start at Dx
  3. Screen with 10g monofilament or 128 Hz vibration
215
Q

How is DM neuropathy treated

A

Intensification of glycemic control

Anticonvulsivants>antidepressants>opioids>topical

216
Q

What are the screening recommendations for DM nephropathy

A
  1. Type 1
    1. Start 5 years after Dx
  2. Type 2
    1. Start immediately
  3. Screen with urine ACR
    1. Positive if >20 or 2 of 3 >2 mg/mmol and/or GFR <60
217
Q

How is DM nephropathy managed?

A
  1. ACE ARB
  2. Refer to neph of:
    1. Progressive loss of renal function
    2. ACR persistently above 60
    3. Inability to continue ACE/ARB
    4. Inability to achieve target BP
    5. eGFR <30
218
Q

What medications should be offered to all patients with T2DM above 60 with 2 CV risk factors

A
  1. GLP1 agonist or SGLT2
    1. in THIS population, evidence stronger for GLP1
219
Q

What other autoimmune diseases are associated with T2DM. What should be done to screen for them?

A
  1. autoimmune anti-thyroid disease (10%… 30% of females)
    1. Check TSH, anti-TPO ab at Dx then q2-5 years
  2. AI adrenal insufficiency is rare
  3. Celiac (5%)
    1. Screen if Sx
220
Q

How should you coucil your DM patients regarding driving

A
  1. Patients on insulin or secretagogues
    1. They must have a medical exam q2 years to assess fitness to drive
    2. Measure BG immediately before driving and at least q4hrs (q2 if history. of recurrent severe hypoglycemia or hypoglycemic unawareness) while driving. Or wear cgm
    3. No driving if BG<4
    4. No driving for at least 40 min after successful treatment of hypoglycemia, BG at least 5
  2. Patients should not drive if:
    1. Any episode of severe hypo while driving in past 12 months
    2. More than one episode of severe hypo while awake in past 6 months for private drivers or past 12 months for commercial drivers
221
Q

How should diabetics undergoing CABG be managed?

A
  1. Continuous IV infusion intraop
  2. BG 5.5-11.1 post op for infection prevention
222
Q

When and how should patients be screened for post-transplant DM?

A
  1. Patients undergoing solid organ transplant
    1. A1C at 3 and 12 months then yearly
    2. 2h OGTT or post lunch CBG within 3 months of transplant
223
Q

What are treatment considerations when treating post transplant DM

A
  1. Avoid agents that cause weight gain
  2. Avoid secretagogues in renal failure or in patients with poorly functioning pancreas transplant
  3. If metabolic decompensation or symptomatic/severe hyperglycemia, give insulin
224
Q

How are hypoglycemia episodes managed in DM

A
  1. Mild-moderate: 15g oral glucose or sucrose tabs
  2. Severe (i.e requiring 3rrd party assistance): 20g oral glucose tabs
  3. Unconcious: 1mg glucagon IM (not as effective if ≥2 EtOH drinks or advanced liver disease) or 10-25g dextrose IV if access
  4. Have a snack with protein after treating a low to ensure glucose stay up (or meal within 1 hr)

*Acarbose: Need to give dextrose or in unavailable milk or honey

225
Q

What is whipples triad

A
  1. Symptoms of hypoglycemia
  2. Low plasma glucose when Sx present
  3. Relief of Sx with Tx
226
Q

How should hypoglycemia be worked up in non-DM patients?

A
  1. 72hr fast with cap glucose monitoring until glucs drop (<3.3), increase to q1hr BW
  2. If venous glucose confirmed <2.5 send full Dx workup (image bellow)
227
Q

What are the non-pharmacological treatments for DLP?

A
  1. >150 min/week exercise
  2. Smoking cessation
  3. Healthy diet
    1. Mediterranian
    2. DASH
    3. Portfolio
228
Q

What P/E tests have the highest LR+ for osteoporosis

A
229
Q

What is the Edmonton obesity staging system

A

RCPSC (14 decks)

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