Endocrinology Flashcards
(229 cards)
1
Q
In which directions do calcium and phosphate go in parathyroid mediated calcium problems?
A
Opposite directions
2
Q
In which directions do calcium and phosphate go in Vitamin D related calcium problems?
A
Same direction
3
Q
In which directions do calcium and phosphate go in teriary hyperpara?
A
Same direction
4
Q
How does magnesium deficiency affect calcium levels
A
- Reduces PTH secretion and causes PTH resistance
- Appears like hypopara
1.
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
6
Q
What are the indications for surgery in primary hyperparathyroidism
A
- Symptomatic
- Asymptomatic (Stay The Fudge Away U Stupid Calcium)
- Serum calcium >0.25 above ULN
- T-score < -2.5 at L-spine, total hip, femoral neck or distal 1/3 of radius
- Fractures
- Age <50
- Urine calcium >10 mmol/day
- Stones or nephrocalcinosis by X-Ray, U/S, CT
- Creatinine clearance <60
7
Q
What is the medical management for patients with primary hyperpara who are not candidates for surgery
A
- Correct vitamin D deficiency: Target serum 25OH vitD >50
- Amino-Bisphosphonates are effective at preventing BMD decrease and at reducing remodelling
- Consider cinecalcet if symptomatic and surgery is not an option
- Can be combined with bisphosphonates in select patients
8
Q
What must always be ruled out before sending a patient for parathyroidectomy in primary hyperpara. How is it ruled out?
A
- R/O FHH
- Do 24hrs urine calcium
- Urine calcium:creatinine ration <0.01 think FHH
9
Q
What is secondary hyperparathyroidism?
A
Appropriate increase in PTH secondary to hypocalcemia or vitamin D deficiency (most common)
10
Q
How can calcium be supplemented following gastric surgery
A
Calcium citrate
*Calcium carbonate not absoorbed
11
Q
How is secondary hyperparathyroidism treated in the context of CKD?
A
- Vitamin D
- Phosphate restriction
- Non-calcium phosphate binders
12
Q
What is tertiary hyperparathyroidism?
A
- Parathyroid glands become autonomous in the setting of longstanding hypocalcemia
- Usually in the setting of ESRD
13
Q
What are the indications for surgery in tertiary hyperpara
A
- Refractory hyperPTH despite Vitamin D analogues, calcimimetics
- No absolute cutoffs
- Severe or symptomatic hypercalcemia
- Calciphylaxis
- Progressive bone disease
14
Q
Give a differential for Hypoparathyroidism
A
- Acquired
- Hypomagnesemia
- Post-surgical (common complication, post op thyroidectomy)
- Post-radiation
- Infiltrative disease
- Sarcoid
- Amyloid
- Cancer mets
- Autoimmune polyglandular syndrome type 1
- Congenital
- Pseudoohypoparathyroidism
- DiGeorge syndrome
15
Q
What is Whitaker’s triad in the context of autoimmune polyglandular syndrome type 1
A
- Chronic mucocutaneous candidiasis
- Addison’s disease
- Hypoparathyrodism
16
Q
List the 3 types of cancers associated with MEN-1
A
17
Q
List the 3 types of cancers associated with MEN-2A
A
18
Q
List the 3 types of cancers associated with MEN-2B
A
19
Q
Explain how a radioactive iodine uptake scan is interpreted
A
- High uptake:
- Increased endogenous production:
- Graves
- Toxiic multinodular goiter
- Increased endogenous production:
- Low uptake
- extra thyroid hormone without increased production
- Exogenous ingestion
- inflamatory leak
- Thyroiditis
- Acute, subacute
- post-partum
- amio induced
- Thyroiditis
- extra thyroid hormone without increased production
20
Q
What is pathomnemonic for Graves (even if negative RAIU)
A
Ophtalmopathy
21
Q
What can cause an RAIU to be falsely negative in graves disease?
A
- CT scan with iodinated contrast
- Amiodarone
- Iodine intake (kelp)
22
Q
What causes a goiter
A
- Stimulation of the thyroid gland
- TSH (Hashimoto)
- Thyroid receptor antibodies (Graves)
- b-HCG (pregnancy)
23
Q
What causes a tender thyroid gland
A
- Inflamation
- Thyroiditis
24
Q
How are the symptoms of Hyperthyroidism treated in the acute setting. In whom should these meds be particularly considered?
A
- Beta blockers (non-cardio selective)
- Especially in the elderly, resting HR>90 or CVD
25
How long does it take before seing the full effect of MMZ ot PTU
4-6 weeks
26
What is the preferec anti-thyroid drug in most circumstances
MMZ
27
When should PTU be used instead of MMZ?
1. Pregnancy
2. Thyroid storm
3. **Minor** MMZ reactions
28
How should a patient be prepped for RAI therapy
1. Liberal use of b-blockers unless contrraindication
2. Don't give MMZ or PTU, reduce success rate
29
Compare the side effects of MMZ and PTU
30
What are the treatment options for graves disease
1. Anti-thyroid
2. RAI
3. Surgery
31
How should anti-thyroid hepatotoxicity be managed
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
32
How should anti-thyroid induced agranulocytosis be managed
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
33
How should anti-thyroid minor skin reactions be managed
1. Antihistamines +/- prednisone (for allergi rcn)
2. Rule out vasculitis
34
What is the only side effect of anti-thyroid medications for which it is OK to switch to another antithyroid med?
1. Minor reactions
1. Rash
2. GI symptoms
3. myalgias
4. arthralgias
35
List contraindications to RAI therapy
1. Pregnancy
2. Breastfeeding
3. Moderate to severe orbitopathy
4. thyroid cancer
36
What are the side effects of RAI therapy
1. Orbitopathy
2. Thyroiditis
37
For how many months should pregnancy be avoided after RAI therapy
6 months
38
When giving RAI with orbitopathy, what should be given concurrently
steroids
39
How shoudl MMZ be managed if considering RAI
Stop at least 2-3 days before
40
What needs to be achieved before operating on a patient with graves for thyroidectomy
euthyroidism
41
How should graves disease with moderate to severe graves orbitopathy be treated when there are CI to surgery and ATDs
RAI with steroid prophylaxis
42
How is thyroid storm defined
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
43
How is thyroid storm managed
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
44
What is subclinical hypothyroidism
1. TSH above ULN with normal free t4
45
When should subclinical hypothyroidism be treated in non-pregnant patients?
1. TSH \> 10
2. Consider when
1. Symptomatic
2. Goiter
3. Positive anti-TPO Ab
46
When should subclinical hypothyroidism be treated in in pregnant patients
First check TPO Ab
47
What is the TSH target for pregnant patients on thyroid replacement
\<2.5
48
How should levothyroxine be adjusted when a patient becomes pregnant
Take 1 extra pill on saturday and sunday once patient becomes pregnant
Target TSH\<2.5
49
How should graves disease be treated in pregnancy
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
50
What could be causing post-partum exacerbations of hyperT4 in graves disease
Could be from graves or from postpartum thyroiditis
51
Why do TSH-R Ab need to be monitored in the second trimester of pregnancy in graves patients
1. They cross the placenta!
1. If titers very high, (3x ULN) monitor for fetal graves
52
What are the adverse effects of long term beta blockade in pregnancy for graves patients
1. IUGR
2. fetal bradycardia
3. Neonatal hypoglycemia
53
Describe gestational transient thyrotoxicosis and it's pathophysiology
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
54
In what contexts will the hCG effects on t4 be even more pronounced than regular pregnancy?
1. Hyperemesis gravidarum
2. Molar pregnancy
3. Multiple gestation pregnancy
4. Choriocarcinoma
55
how is gestationnal transient thyrotoxicosis treated?
1. Treat hyperemesis if present
2. Use BB if necessary for Sx
56
What clinical elements can help differentiate GTT from other causes of hyperthyroidism
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)
57
How is osteoporosis diagnosed?
* Fragility Fx
OR
* BMD 2.5 SD or more bellow peak BMD (T≤-2.5) on DEXA
58
Why do we risk-stratify patients with a diagnosis of osteoporosis
1. To decide who gets treatment
2. 3 categories: low, moderate, hiigh
59
How are patients risk-stratified in Osteoporosis?
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
60
How should patients with low risk osteoporosis be treated
No pharmacotherapy
Reassess risk in 5 years
61
How should patients with moderate risk osteoporosis be treated
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
62
What factors can increase you CAROC risk without a change in BMD
1. Fragility fracture after age 40
2. Recent prolonged use of systemic glucocorticoids
63
How should patients with high risk osteoporosis be treated?
64
Which osteoporosis treatment options are effective for vertebral, hip and non-vertebral Fx
65
After how many years should treatment be reassessed in osteoporosis patients on pharmacotherapy? How should treatment be modified?
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
66
What are the indications for teriparatide
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**
67
list contraindications to teriparatide
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
68
What are the advantages of Romosuzumab
1. Reduced vertebral, non-vertebral and hip Fx
2. Very low risk of atypical Fx or osteonecrosis of the jaw
69
List side effects of romosuzumab
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
70
Define treatment failure in osteopororsis
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
71
How is osteoporotic treatment failure managed?
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
72
List side effects of bisphosphonates
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)
73
List side effects of denosumab
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**
74
What are the clinical characteristics of atypical femoral fracture
1. Proximal femoral shaft fracture
2. Atraumatic
3. Chronic bisphosphonate use
4. Asian women most likely
5. May be associated with prodromal thigh pain
75
What are the radiographic characteristics of atypical femoral fracture
1. Lateral cortical thickening
2. Transverse fracture lines
3. Beaking
76
How can you prevent atypical femoral fractures?
Drug holiday in low-risk patients on oral bisphosphonate therapy for 5 years (or IV bisphosphonates for 3 years)
77
How are atypical femoral fractures treated?
1. Ortho consult
2. **Image controlateral femur**
3. Stop bisphosphonate
4. Ensure adequate Ca and vitamin D
5. **Start teriparatide**
78
How is vitamin D and calcium supplemented in osteoporosis
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
79
List the non-pharmacological therapies for osteoporosis
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
80
What are the GFR cutoffs with:
* Alendronate
* Ibandronate
* Risendronate
* Adaloparatide
* Teriparatide
* Denosumab
* Romosozumab
81
What are the A1C treatment targets?
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
82
List the factors that can affect A1C
83
How is T1DM treated
Basal-bolus, CSII
84
What are the benefits of switching to CSII
1. Small improvement in A1C
2. Increased treatment satisfaction, Dm related QOL
3. Decreased rates of severe hypoglygemia
85
What are the benefits of adding CGM to BBI or CSII
1. Decreased A1C with no increases in hypo
2. Better QOL, reduced DM distress, fear of hypoglycemia and Tx satisfaction
86
What are the typical recommended targets in CGM
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%
87
What are the recomended CGM ranges in older/hgh risk patients
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%
88
What are the CGM targets in pregnancy for type 1 DM
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%
89
When should CBG testing be instituted in patients with T2DM not on insulin
1. When A1C targets not beaing reached
2. If A1C targets reached, only measure during illness or risk of hypoglycemia
90
Once T2DM is diagnosed, what are the initial treatment steps?
91
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?
92
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?
93
List CV risk factors
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
What are the recommendations for treating T2DM in comorbid patients by comorbidity
95
What does "symptomatic hyperglycemia with metabolic decompensation" mean? What are the symptoms?
1. Polyuria
2. Polydipsia
3. Blurry vision
4. Unintentional weight loss
5. Volume depletion
6. Ketosis
7. DKA/HHS
96
How should symptomatic T2DM or T2DM with metabolic decompensation be managed once they are on metformin and insulin
97
How should the following antihypoglycemics be managed in CKD:
* Metformin
* SGLT2
* GLP1
* DPP4i
* Insulins
* Glyburide
* Non-glyburide secretagogues
98
What are the side effects of SGLT2i?
1. Euglycemic DKA
2. GU infections
1. Inc. Fournier's gangrene
3. Stop on "sick days"
99
What is the side effect presumably only attributed to Canagliflozin
1. Increased risk of toe amputation
1. Seen in CANVAS but not CREEDENCE
2. Can possibly worsten osteoporosis
100
What is a contraindication for Dapagliflozin specifically
Bladder Ca
101
Which SGLT2 was note shown to improve MACE?
Ertugliflozin
102
What is the **Beneficial** side effecto of GLP1
Weight los
103
What are the non-beneficial side effects of GLP1
1. GI side effects
1. Dyspepsia
2. Anorexia
3. N/V/D
4. Abdo pain
104
What are contraindications to GLP1
1. Personal or family historry of medullary Thyroid cancer or MEN2
2. _Caution_ in Hx of pancreatitis or pancreatic Ca (not formally CI)
105
What is a side effect of Semaglutide specifically
1. Worsening retinopathy
106
Which GLP1 has no proven cardiorenal benefit
Exenatide
107
Which GLP1 is approved for weight loss in non-diabetics
Liraglutide
108
What are the guidelines for vascular protection in T2DM?
1. **A**1C ≤7
2. **B**P \<130/80
3. **C**holesterol LDL\<2 or \>50% reduction
4. **D**rugs with cardioprotective effects when indicated:
1. Statin
2. ACE/ARB
3. ASA
4. GLP-1, SGLT2
5. **E**xercise/healthy eating
6. **S**moking cessation
109
What are the indications for statins in DMT2?
1. Clinical CVD
2. Age≥40
3. Age \>30 and DM for \>15 years
4. Microvascular disease
5. Other CV risk factors
110
What are the indications for ACE/ARB in T2DM
1. Clinical CVD
2. Age≥55 with an additional CV risk factor or end-organ damage (albuminuria, retinopathy, LVH)
3. Microvascular disease
111
What are the indications for ASA in T2DM
1. Established CV disease
112
What is the clinical presentation of primary adrenal insufficiency
1. Weakness, lethargy, GI Sx
2. Hyponatremia, Hyperkalemia
3. Orthostatic hypotension, hypoglycemia, uremia
113
How is adrenal insufficiency diagnosed?
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
Once a diagnosis of AI is made, how can you differentiate primary from secondary AI?
1. Measure ACTH
1. If elevated, primary AI
2. If low or appropriately normal, central AI
115
Once AI is diagnosed, what workup should be sent to determine the cause
116
What is the difference between cushing syndrome and cushing disease
Cushing syndrome- hypercortisolemia
Cushing disease- Pituitary tumor secreting ACTH
117
How is Cushing syndrome diagnosed
1. 2/3 positive screening tests
1. midnight salivary cortisol
2. 1mg dex suppression test
3. 24hrs urine free cortisol
118
How is a 1mg dexamethasone suppression test interpreted?
1. Cortisol ≤50 = normal
2. Cortisol 50-140 possible cushing
3. cortisol \>140 positive test
119
How is the etiology of cushing syndrome determined?
120
What are the indications to screen for hyperaldosteronism in hypertensive patients?
1. Refractory hypertension (despite 3 drugs)
2. Spontaneous hypokalemia (\<3.5) or severe diuretic induced hypokalemia (\<3)
3. Adrenal incidentaloma
121
What is the screening test for hyperaldosteronism
1. Plasma aldosterone to renin ratio
122
What antihypertensives should be held for a plasma aldosterone to renin ratio? which ones can you continue
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
What are the confirmatory tests for hyperaldo
1. Saline suppression
2. Oral salt load
3. Captopril suppression test
124
Who should be screened for Pheo?
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
How is screening for pheo performed?
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
How is pheochromocytoma managed clinically?
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
What can be considered in the perioperative setting for Pheo?
1. Phentolamine IV if necessary
2. Vasopressors ready to go once adrenal gland manipulated
1. Anesthesia consult pre-op
128
What should be considered in the post-op setting in pheo
1. ICU post-op
2. Watch for hypotension, hypoglyceoma
3. Conside familial syndromes (MEN)
129
What is the definition of adrenal incidentaloma
Clinically unapparent mass greater than 1cm detected during imaging performed for reasons other than suspected adrenal disease
130
What are indications that an adrenal incidentaloma might be malignant?
1. **Size\>4cm**
2. **\>10 HU**
3. **\< 50% delayed contrast washout**
4. Calcifications, extension, adenopathy
5. Hx of malignancy
131
What should be done with adrenal incidentalomas to ensure they are not functionnal
1. Screen for hypercortisolism (1mg dex supression test) and pheo in all
2. Screen for hyperaldo only if HTN +/- hypoK
132
What are the referral indications for bariatric surgery
1. BMI 35-40 AND 1 serious comorbidity (DM, CAD, HTN)
2. BMI≥ 40 without comorbidities
133
What are the complications of bariatric surgery
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
How should patients be managed after bariatric surgery
1. Multidisciplinary in specialized centre
2. Monitor and titrate Tx -- DM/HTN may be cured
3. Nutritional deficiencies and BMD screening annually
135
What is the 5A framework in obesity
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
What cancers does obesity increase the risk for?
1. Colon
2. Kidney
3. Esophagus
4. Endometrium
5. Post-menopausal breast
137
What can be used as pharmacotherapy for weight loss?
1. Liraglutide
2. naltrexone/bupropion
3. Orlistat
138
How should one medication be chosen over the other in obesity?
139
List medications associated with weight gain and their alternatives
140
Who should be screened for DLP
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, I**BD)
13. HIV
14. erectile dysfunction
15. COPD
16. **Pregnancy related complications**
141
How should screening for DLP be conducted
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
What are the statin indicated conditions?
143
How is familial hyperlipidemia diagnosed
144
What are the LDL targets on statin therapy and what should be added on if they are not achieved on max statin therapy
145
How should Patients with a AAA or ASCVD be treated if their LDL is not at target on max statin doses?
146
Which patients have been shown to benefit the most from PCSK9i therapy
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
How should DLP be managed when there are no statin indicated conditions present?
IF INTERMEDIATE OR HIGH RISK
148
What is the pathophysiology of Paget's disease
1. Focal increase in bone resorption by very large osteoclasts, followed by increased osteoblastic activity
2. High rate of bone formation and turnover
149
What are the initial lab findings in Paget's disease
1. Elevated ALP +/- bone specific ALP
2. No other abnormalities
150
What imaging should be seeked when suspecting Paget's disease. What will be found?
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
What illnesses are associated with Paget's disease
1. Hearing loss
2. Compressive neuropathy
3. OA
4. Osteosarcoma
152
What are the indications to treat Paget's disease
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
How is Paget disease treated?
1. IV Zolendronic acid is 1st line
2. Oral bisphosphonates can be used:
154
What is primary amenoorrhea
1. Absent menses at age 16
2. Absent sexual characteristics at age 13
155
What is the most common cause of primary amenorrhea
Chromosomal abnormality
156
How would you work-up primary amenorrhea
157
What is secondary amenorrhea
1. No cycle \>3 months in those with regular periods or \> 6 months in those with irregular cycles
158
What is the DDx for secondary amenorrhea
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
What are the FSH, LH and estradiol levels in hypothalamic amenorrhea
FSH, LH low
Estradiol Low
160
What phenotype is associated with hypothalamic amenorrhea
When the body cant support a pregnancy
1. High performance female athlete
2. Eating disorder
3. High stress environment
4. Chronic illness
161
What are the diagnostic criteria for PCOS
1. 2/3:
1. Menstrual irregularities
2. Biochemical or clinical hyperandrogenism
3. U/S finding of polycystic ovaries
162
What are the physical exam findings in PCOS
1. Elevated BMI
2. Hyperandrogenism
1. Ferriman gallway, alopecia, acne
3. acanthosis nigricans
163
What investigations should be sent when working up PCOS
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
What is the age cutoff for primary ovarian insufficiency
40
165
What are the FSH, LH, estradiol level in primary ovarian insufficiency?
FSH, LH elevated
Estradiol low
166
What are the etiologies of primary ovarian insufficiency
1. Autoimmune
2. Radiation
3. chemotherapy
4. Fragile X syndrome
167
What investigations should be sent in primary ovarian insufficiency
1. Clarify etiology
1. Karyotype
2. Fragile X
3. **Anti-adrenal antibodies**
2. Screening tests
1. BMD
168
How do you treat primary ovarian insufficiency?
1. Hormone replacement until age of menopause
169
How is PCOS managed
170
What are the symptoms of hyperandrogenism in women
1. Acne
2. Voice changes
3. Mood changes
4. hirsutism
5. Clitoromegaly
6. Menstrual abnormalities
171
What non sexual organs can be affected by hyperandrogenism in women
1. Hypothyroidism
2. Liver disease
172
What illegal substance can cause hyperandrogenism in women
anabolic steroids
173
What investigations should be sent if suspecting hyperandrogenism in women
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
What are red flags suggesting that hyperandrogenism is not from PCOS
1. Increased muscle bulk
2. voice
3. clitoromegaly
\*look for tumor
175
What is the endocrinological DDx ofr hyperandrogenism
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
What investigations should be sent in premenopausal hirsutism
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
What is the treatment for hirsutism
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
Describe Ferriman-Gallwey score
179
Give a approach to male hypogonadism
180
What are the causes of male hypogonadism
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
What are the clinical findings in Klinefelter syndrome
1. Small firm testes
2. Long arm and leg span
182
What are the comorbidities associated with kleinfelter syndrome
1. NHL
2. Bronchectasis
3. SLE
4. DM
5. osteopenia
6. breast Ca
183
How is Kleinfelter syndrome diagnosed
Karyotype
184
What conditions increase and decrease SHBG and should be kept in mind when measuring free vs total testosterone
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
What are the indications and contraindications to testosterone replacement therapy in men?
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
HOw should patients on testosterone replacement therapy be monitored?
1. Several times in the first year then annually
1. Symptoms
2. Testosterone level
3. hematocrit
4. PSA
187
What is the differential for hyperprolactinemia
for each ddx, around what level of PRL would you expect
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
What are the symptoms of hyperprolactinemia
1. Amenorrhea
2. galactorrhea
3. Hypogonadism
4. Mass effect
189
What should you suspect in a patient with ++ symptoms of hyperprolactinemia but PRL only mildly elevated
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
What should you suspect if a patient has a ++ elevated prolactin but mild Sx
1. Macroprolactin
1. Prolactin multimer that is biologically inactive
2. Usually stick around because clearance is slow
191
What should be ruled out in elevated prolactin
Stalk effect
other pit. dysfunctions
192
How should a drug induced/hypothyroid hyperPRL be treated
Stop drug or give T4
193
How should hyperprolactinemia from stalk effect be managed
Manage the primary tumor
194
How should a prolactinoma be managed
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
What are the indications for surgery in non-PRL pituitary tumors
1. Hormonal hypersecretion syndromes
2. Hormonal hypofunction
3. Mass effect (Visual field, cranial nerves, headache)
4. Hemorrhage
196
How should non-PRL pituitary tumors be treated if there are no indications for surgery?
1. Follow clinically for development of surgical indication
197
What is the clinical presentation of DI
1. Polydypsia
2. Polyuria
3. Usually post-neurosurgery
198
How is DI diagnosed
1. Suspect based on
1. Hypernatremia
2. Elevated plasma OSm
3. Inappropriately dilute urine
2. Diagnosis on water deprivation test
199
How does DI usually present post-sellar surgery
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
What are the symptoms of acromegaly
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
What is the screening test for acromegaly
IGF1 level
202
What is the diagnostic test for acromegaly
75g glucose supression
203
What is the treatment for acromegaly
Surgical
204
What is the differential for a thyroid nodule
1. Multinodular goiter, Toxic nodule, Benign non-functional nodule, cyst
2. Thyroid Ca (papillary 90%, follicular, medullary, anaplastic)
3. Lymphoma
205
How should a thyroid nodule be worked-up?
1. H/P
2. TSH
1. If TSH\<0.5 do uptake scan
3. U/S
4. Bx if indicated
206
Who needs a biopsy for a thyroid nodule
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
List high risk sonographic features for thyroid nodules?
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
What are the **post-thyroidectomy** features of high risk disease in thyroid cancer?
1. +LN
2. +margins
3. Extrathyroidal extension
4. distant mets
5. **Needing RAI (High risk!)**
209
What are the TSH targets post thyroidectomy for thyroid cancer?
1. Low-risk: 0.5-2
2. Medium risk: 0.1-0.5
3. Hiigh risk: \<0.1
210
What are the main management steps for graves orbitopathy
1. Quit smoking
2. Refer to specialized GO eye centre
3. Artificial tears
4. Restore euthyroidism
211
What is the mainstay of treatment for graves orbitopathy
Steroids if no CI
second line: Radiotherapy, cyclosporine, ritux if partial or no response to steroids
Surgery only for stable inactive GO
212
How is DM and pre-diabetes diagnosed
213
What are the screening recommendations for DM retinopathy
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
What are the screening recommendations for DM neuropathy
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
How is DM neuropathy treated
Intensification of glycemic control
Anticonvulsivants\>antidepressants\>opioids\>topical
216
What are the screening recommendations for DM nephropathy
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
How is DM nephropathy managed?
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
What medications should be offered to all patients with T2DM above 60 with 2 CV risk factors
1. GLP1 agonist or SGLT2
1. in THIS population, evidence stronger for GLP1
219
What other autoimmune diseases are associated with T2DM. What should be done to screen for them?
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
How should you coucil your DM patients regarding driving
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
How should diabetics undergoing CABG be managed?
1. Continuous IV infusion intraop
2. BG 5.5-11.1 post op for infection prevention
222
When and how should patients be screened for post-transplant DM?
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
What are treatment considerations when treating post transplant DM
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
How are hypoglycemia episodes managed in DM
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
What is whipples triad
1. Symptoms of hypoglycemia
2. Low plasma glucose when Sx present
3. Relief of Sx with Tx
226
How should hypoglycemia be worked up in non-DM patients?
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
What are the non-pharmacological treatments for DLP?
1. \>150 min/week exercise
2. Smoking cessation
3. Healthy diet
1. Mediterranian
2. DASH
3. Portfolio
228
What P/E tests have the highest LR+ for osteoporosis
229
What is the Edmonton obesity staging system
