Endocrine Flashcards
1
Q
Criteria for metabolic syndrome (5)
A
3 of the following:
1) Waist circumference (>/= 102 male, female 88)
2) Triglycerides >/= 1.7 mmol/L
3) HDL < 1.0 men or <1.3 women
4) BP >/= 130/85 mm Hg
5) FBG >/= 5.6 mmol/L
2
Q
What is most important risk factor for insulin resistance and DM
A
Obesity
3
Q
Hormones involved in insulin resistance
A
1) Amylin - Decreased in DM I & II.
Fx - delay gastric emptying, decrease postprandial glucagon, and increases satiety
2) Ghrenlin - Decreased
Fx - produced by stomach and pancreas to regulate food intake and insulin levels
3) Incretins (GLP-1) - Decreased activity
Fx - released by GI tract in response to food. Stimulate pancreas to produce more insulin, slow emptying, promote satiety. Normally broken down by DPP-4.
4) Glucagon - increased
Fx - glycogenolysis and gluconeogenesis
4
Q
Somogyi effect
A
Decreased BG level at night that may lead to increase in morning BG
5
Q
Dawn phenomenon
A
Early morning rise in BG d/t GH, cortisol and catecholamines NOT preceded by hypoglycemia
6
Q
Causes of blurred vision in DM
A
Macular edema
Hyperglycemia
7
Q
Biguanide
A
Ex. Metformin
MOA - increase hepatic glucoses production, increase glucose uptake in muscles Pros - no weight gain, minimal hypoglyemia
+ cheap, first line treatment DM II
Negatives - GI SE, LACTIC ACIDOSIS, CI in liver and renal insufficiency and cardiac failure
8
Q
Sulfonylurea
A
MOA - Increase insulin secretion from pancreatic beta cells
Ex. glipizide, glimepiride, glyburide (highest risk of hypoglycemia)
+ cheap
Negative - hypoglycemia, weight gain, skin rash
9
Q
Meglinitides
A
MOA - Increased insulin secretion from beta cells
Ex. repaglinide, nateglinide
+ dosing before meals, decrease postprandial glucose
Negative - HYPOGLYCEMIA, wt gain, frequent dosing
10
Q
TZD
A
MOA - Increase insulin sensitivity
Ex. pioglitazone, rosiglitazone
+ increased HDL, decrease triglycerides
Negative - weight gain, edema/HF, bone fractures, increased LDL, ?MI
11
Q
DPP-4 inhibitors
A
MOA - Increased insulin secretion, decreased glucagon secretion
Ex. “gliptin”, saxagliptin (increased risk of HF)
+ once daily dosing, well tolerated
Negative - urticaria/angioedema, cost, increased risk of hypoglycemia, pancreatitis and ? HF hospitalizations
12
Q
GLP-1 agonist
A
Increased insulin secretion, decrease glucagon secretion, slow gastric emptying, increased satiety
Ex. “glutide”/”tide”
+ decreased postprandial glucose, well tolerated, liraglutide and semaglutide improve CV outcomes in older people with diabetes
Negative - GI upset, increased HR, pancreatitis, avoid in CKD, CI - DKA, cirrhosis and intestinal diseases
13
Q
Glucosidase inhibitors
A
Ex. acarbose, miglitol
MOA - Slows intestinal carbohydrate digestion and absorption
+ decrease postprandial glucose, minimal hypoglycemia
Negative - SE abd pain and flatulance, CI in cirrhosis, frequent dosing schedule
14
Q
SGLT-2 Inhibitors
A
Decreased glucose reabsorption in proximal tubule, increased urinary glucose excretion
+ once daily dosing, decrease BP. empagliflozin/canagliflozin has CV benefit
Caution renal insufficiency, GU infections, hyperkalemia, orthostatic hypotension, pancreatitis
Ex. “gliflozin”
15
Q
A1C target for functionally independent
A
= 7.0%
16
Q
A1C target for functionally dependent frailty index 4-5)
A
<8.0%
17
Q
A1C target for frail and/or dementia
A
<8.5%
18
Q
BP target for functionally independent and life expectancy > 10 years
A
<130/80 mm Hg
19
Q
Target LDL
A
<2.0 mmol/L or 50% reduction from baseline
20
Q
Frailty definition
A
3 or more of the following criteria are present:
- unintentional weight loss (>4.5 kg in the past year)
- self-reported exhaustion
- weakness (diminished grip strength)
- slow walking speed
- low physical activity
21
Q
True/False
In older people with obesity and type 2 diabetes, the principal metabolic defect is resistance to insulin-mediated glucose disposal, with insulin secretion being relatively preserved
A
True
22
Q
True/False
Diabetes screening is beneficial in asymptomatic individuals over the age of 80
A
False
23
Q
True/False
A1C is less reliable in older adults due to the effect of comorbid conditions
A
True
24
Q
General screening for DM, average risk adults
A
Q3 years starting at age 40
25
General screening for DM, with risk factors or high CANRISK score
Q6-12 months at any age
26
Risk factors for DM
* 1st degree Fmhx, high-risk ethnic group,
* Hx of prediabetes, hx of GDM, hx of macrosomic infant
* DM associated end organ damage (retino, nephropathy etc)
* Vascular RF: dyslipids, HTN, inc wt, abdo obesity, smoking
* Associated conditions: hx of pancreatitis, PCOS, acanthosis nigricans, gout, NAFLD, psych d/o, HIV, OSA, CF
* Meds: glucocorticoids, atypical antipsychotics, HIV meds, statins, anti-rejection meds,
27
Diagnosis of DM
* A1C _\>_ 6.5
* FBG _\>_ 7.0
* GTT _\>_ 11.1
* If asymptomatic 2 tests in diabetic range necessary for dx
* If symptomatic only 1 test required
28
True/False
A1C can be used in isolation to diagnose DM in older adults
False
29
Prediabetes diagnosis
* FBG: 6.1 - 6.9
* A1C: 6.0 - 6.5
30
Treatment: A1C \< 1.5% above target
Lifestyle x 3 months, then if not at target start/increase metformin
31
Treatment A1C \>/= 1.5% above target
Start metformin immediately, consider 2nd agent
32
Treatment if symptomatic hyperglycaemia with DM
Initiate insulin +/- metformin
33
A1C target for end of life
Do not measure, avoid symptomatic highs/lows
34
Low risk medications to prevent hypoglycemia
metformin, GLP1s, DDP4s, SGLT2s, TZD, alpha-glucosidase inhibitors
35
High risk medications for hypoglycemia
insulins, sulfonylureas, meglitinides (less risk than sulfonylureas)
36
When treating older adult which of the following should be considered:
a) use DPP-4 instead of sulfonylureas
b) treat with ½ of normal dose of sulfonylurea
c) use gliclazide or glimepiride instead of glyburide
d) opt for meglitinides instead of glyburide to prevent hypoglycemia
e) all of the above
E
37
What test can be used to predict cognitive and physical capability to inject insulin?
Clock drawing test
38
Geriatric monitoring (4 M's)
Mentation - memory and mood
Mobility - fall, visual problems, neuropathy, weakness, BP
Medication - polypharm
Matters most - goals, MOST
39
Microvascular complications
Nephropathy
Retinopathy
Peripheral neuropathy
ANS dysfunction
40
Macrovascular complications
Coronary, carotid, PVD
41
SADMANs Medications
S - sulphonylureas
A - ACE-I
D - diuretics
M - metformin
A - ARBs
N - NSAID
S - SGLT-2 inhibitors
42
Antihyperglycemic drugs for CVD if GFR \> 30
Empagliflozin (Grade A)
Liraglutide (Grade A)
Canagliflozin (Grade C)
43
ABCDESSS of Diabetes
A1C targets
BP targets
Cholesterol targets
Drugs for CVD
Exercise goals and healthy eating
Screening for complications
Smoking cessation
Self-management/Stress
44
Screening ECG for DM
Q3-5 years
45
Screening feet in DM
Monofilament yearly or \> if abN
46
Screening for kidney dysfunction
eGFR and ACR yearly
47
Screening for retinopathy
Q 1-2 years with optometrist/opthamologist
48
4 A's of smoking cessation
1. **Ask** - Identify and document tobacco use
2. **Advise** - to quit.
3. **Assess** - readiness to quit
4. **Assist** - counselling/pharmacotherapy
5. **Arrange** - follow up
49
Which of the following are presenting symptoms of DM **specific** to older adults:
a) dehydration, dry mouth
b) thin body habitus
c) P, P, P's
d) neuropathy
e) incontinence
f) hyperosmolar nonketotic coma
g) all of the above
A, D, E, F
Thin body habitus is not specific to older adult population and is seen in younger to middle adults. Dehdration (d/t decreased thirst sensation and delayed fluid intake). Less glycosuria (d/t inc renal threshold for glucose with age). Exacerbation of common age-associated syndromes (pain, incontinence, cognitive impairment depression, falls)
50
What sensations are commonly lost in peripheral neuropathy
Loss of pain, temperature, and vibration sensation is more common than motor involvement
51
Describe autonomic neuropathy S&S
* delayed gastric emptying, diabetic diarrhea, altered bladder fx, impotence, orthostatic hypoTN
52
Monofilament testing requires testing area 2 times with monofilament and one mock test (no contact). Which of the following indicate impaired sensation?
a) ⅔ right
b) ⅓ wrong
c) ⅔ wrong
d) none of the above
C
53
True/False
T3 is 5 x more active than T4
False. T3 is 10 x more active
54
Thyroid hormone effect on body (CVS, metabolism)
Increase CO, HR, RR
Increase 02 demand
Increase glucose absorption, gluconeogenesis, glycogenolysis, lipolysis, and protein synthesis
Increase BMR
55
![]()
Charcot arthropathy. characterized by collapse of the arch of the midfoot, which is replaced by a bony prominence (arrow). Several factors contribute to this painless condition, including small muscle wasting, decreased sensation, and maldistribution of weightbearing.
56
Wolff Chaikoff effect
++ iodine = low levels thyroid hormone - hypothyroidism
57
Jod Basedow effect
If exposed to large/ normal amounts of iodine- results in ++ thyroid hormone secretion / hyperthyroidism
58
True/False
Elevated lipids OR depression are indications for checking TSH in elderly
True
59
What happens with T4 production and clearance in the older adult? How is T3 affected in this population?
T4 - reduced production, reduced clearance = unchanged
T3 - unchanged
60
Most common cause of hypothyroidism?
Hashimotos disease/ Chronic autoimmune thyroiditis
61
Less common causes of hypothyroidism
Radiation, surgical removal, idiopathic, excess iodine, meds - **amiodarone, lithium**, radio contrast
62
True/False
Hyper/hypothyroidism can be diagnosed in states of acute illness
False
Diagnosis in presence of acute illness should only be made if thyroid lab abnormalities continue _2 weeks after_ sickness resolution
63
Euthyroid sick syndrome
Changes in thyroid secondary to acute medical/psych illness. Treat underlying cause.
64
Starting dose of synthroid in older adult
12.5-25mcg
65
Repeat BW duration following medication adjustments for thyroid dysfunction
6 weeks
66
When is stress test indicated before treating hypothyroidism?
In presence of high CAD risk and long-standing hypothyroidism
67
Target TSH older adult
Upper limit of normal, T4 to normal
68
Overtreatment of hypothyroidism can cause _____ in women
Osteoporosis
69
Most common cause of hyperthyroidism
Graves' disease
70
Less common causes of hyperthyroidism
Iatrogenic - overtreatment, iodine induced via amiodarone
Nodular thyroid disease - Granulomatous (painful and tender thyroid) or lymphocytic thyroiditis (painless)
71
Clinical manifestations of hyperthyroidism in older adults
Tachycardia/a.fib
SOBOE
Edema
Wt loss
72
Apathetic thyrotoxicosis
Asymptomatic hyperthyroidism except weakness in older adult population
73
Treatment for hyperthyroidism
* Diffuse overactive thyroid or hyper functioning nodules= Anti-thyroid medication‘s
* Propylthiouracil or methimazole
* Beta blockers may be used for symptomatic treatment during stabilization
* Once stabilized, radioactive iodine = definitive treatment
* Underlying malignancy = surgical treatment
74
TSH low
fT4 normal
fT3 normal
Repeat TSH in 6-12 months or sooner PRN
75
What is your next step if BW completed and TSH normal
Review clinical diagnosis, no further testing indicated
76
TSH low
fT4 high
Hyperthyroidism
* Excessive thyroid hormone replacement (levothyroxine)
* Graves’ disease
* Subacute thyroiditis (viral)
* Painless/postpartum thyroiditis (autoimmune)
* Toxic (multinodular) goitre
77
TSH low
fT4 normal
fT3 high
Hyperthyroidism
* T3 thyrotoxicosis (e.g., autonomous nodule)
* Excessive thyroid hormone replacement (liothyronine or desiccated thyroid)
78
TSH high
fT4 low
Hypothyroidism
79
TSH high
fT4 normal
Repeat TSH in 6-12 months or PRN
80
The following are all risk factors for thyroid disease EXCEPT: (choose one)
* men: age ≥ 55 years[2](https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/thyroid-testing#two)
* women: age ≥ 50 years[2](https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/thyroid-testing#two)
* personal history or strong family history of thyroid disease
* diagnosis of other autoimmune diseases
* past history of neck irradiation
* previous thyroidectomy or radioactive iodine ablation
* drug therapies such as lithium and amiodarone
* dietary factors (iodine excess and iodine deficiency in patients from developing countries); or
* certain chromosomal or genetic disorders (e.g., Turner syndrome[3](https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/thyroid-testing#three), Down syndrome[4](https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/thyroid-testing#four) and mitochondrial disease[5](https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/thyroid-testing#five))
* men: age ≥ 60 years[2](https://www2.gov.bc.ca/gov/content/health/practitioner-professional-resources/bc-guidelines/thyroid-testing#two)
81
True/False
Proximal muscle weakness is a sign of hyperthyroidism
True
82
True/False
SBP and DBP HTN is a sign of hyperthyroidism
False. Isolated SBP HTN is a sign of hyperthyroidism
83
Which of the following are signs of hypothyroidism?
a) Blurred or double vision
b) Dry eyes, conjunctivitis, proptosis or dysconjugate gaze
c) Menorrhagia
d) all of the above
C
84
When to order anti-thyroid peroxidase (TPO) and when to repeat testing.
In patients with a goitre or mildly elevated TSH, anti-TPO measurement is used to evaluate whether the cause is autoimmune thyroiditis. No repeat testing is indicated.
85
TSH high
fT4 high
**Very rare causes** Consult with a specialist (lab physician, internist or endocrinologist)
* Pituitary disease
* Resistance to thyroid hormone
86
TSH normal
fT4 low
**Very rare causes** Consult with a specialist (lab physician, internist or endocrinologist)
* Central hypothyroidism (hypopituitarism)
87
When to treat subclinical hypo/hyperthyroidism
* Treatment is considered when TSH is above 10 mU/L or below 0.1 mU/L
* Treatment can be considered when TSH is between the upper limit of the reference interval but ≤10 mU/L AND any of the following are present:
* symptoms suggestive of hypothyroidism
* elevated TPO antibodies
* evidence of atherosclerotic cardiovascular disease, heart failure, or CV RF
* pregnancy
88
True/False
TSH levels in the same individual can vary by 50% when measured at different times of day, with lowest values in the late afternoon and highest values at midnight
True
89
True/False
Patients with atrial fibrillation or osteoporosis should be screened for hyperthyroidism
True
90
Treatment of subclinical hyperthyroidism should be considered in the \_\_\_\_\_\_
Elderly
91
In patients over age 60 with TSH 0.1 mU/L but with a normal fT4, the relative risk for atrial fibrillation increases \_\_\_\_\_
3 x
92
Patients taking lithium are at increased risk for hypothyroidism and monitoring of TSH is recommended every \_\_\_\_\_
Amiodarone treatment may also lead to amiodarone-induced thyrotoxicosis and monitoring is recommended every \_\_\_\_\_\_\_
Lithium - 6 month
Amiodarone - 3-6 months
93
Statin indications with DM
age ≥40
age ≥30 and diabetes \>15 years
94
Hypoglycemia symptoms (He IS TIRED)
Headache
Irritability
Sweating
Tachycardia
Restless
Excessive hunger
Dizziness
95
Hyperglycemia symptoms ("hot and dry, sugar is high")
SAND WELT
Sweet breath
Altered LOC
Nausea/vomiting
Dry skin/mouth
Weakness
Excessive urination
Low BP
Tachycardia
96
Clinical features of myxedema coma
Decreased LOC
Hypothermia
Bradycardia
Hyponatremia
Hypoglycemia
Hypotension
Preciptiating illness
97
Possible causes of hypercalcemia
RHINOS
* **R**: renal insufficiency
* **H**: hyperparathyroidism
* **I**: immobilization and iatrogenic
* **N**: neoplasms
* **O**: other endocrinopathies (multiple endocrine neoplasia 1 and 2)
* **S**: sarcoidosis
98
S&S of hyperparathyroidism
## Footnote
**bones, stones, thrones, moans & groans, and psychiatric overtones**
* **“Groans”** - constipation and muscle weakness from decreased contractility
* **“Stones”** - calcium based kidney/gallbladder stones
* **“Thrones”** - (refers to a toilet) polyuria due to impaired sodium, water absorption
* **“Bones”** - pain from chronic demineralization
* **“Psychiatric Overtones”** - depressed mood, confusion
99
Name that condition →
the parathyroid gland makes PTH regardless of the calcium levels. The cause is usually a benign adenoma of the parathyroid gland, but may also be hyperplasia or a carcinoma of the parathyroid gland
Primary hyperparathyroidism
100
Name that condition →
chronic hypocalcemia causes excess PTH to be released to try to correct the low calcium levels. It is usually due to renal failure induced hyperphosphatemia (extra phosphate binds to any available calcium). Less frequently it can be due to lack of calcitriol, from lack of exposure to sunlight, or poor intake of Vitamin D
Secondary hyperparathyroidism
101
Chronic secondary hyperparathyroidism can not cause primary hyperparathyroidism
False. It can!
102
Name that condition →
both a metabolic disorder of purine metabolism, and a musculoskeletal disorder of monosodium urate crystal deposition in and around joints
Gout
103
Risk factors for gout
* Positive Family History
* Older Age
* Male
* Overweight
* Other chronic conditions (**CKD,** **Hypothyroidism**, Infections)
* Post-surgery
* Some Medications (E.g. Diuretics, low dose ASA)
* Alcohol
104
Name that condition → Precipitation of crystals of calcium pyrophosphate dihydrate in connective tissues may be associated with several clinical syndromes, but is sometimes asymptomatic.
CPPD disease or pseudogout AKA sarah's foot
105
What diagnostic test should be considered BEFORE initiating thyroid treatment for elderly patient that has CAD risk factors and potential for longstanding hypothyroidism?
Cardiac stress test
106
What 3 cardiac presentations would increase your suspicion for underlying thyroid dysfunction?
1. Atrial fibrillation
2. Angina
3. HF
107
True/False
Anemia can be a sign of hypothyroidism in the adult population
True
108
Tachycardia, goitre and eye symptomatology are all symptoms of ____ in the older population
Hyperthyroidism
109
A 75 year old female presents with constipation, weight loss, apathy and fatigue as primary symptoms. On exam you palpate her thyroid and notice a nodule. What are your next steps?
Order TSH and thyroid US
110
True/False
Nuclear medicine thyroid scanning conclusively determines whether thyroid nodules are benign or malignant
False
Cold nodules on thyroid scans will still require biopsy. Nuclear medicine thyroid scans are useful to evaluate the functional status of thyroid nodules in patients who are hyperthyroid ie. “hot nodules” (choosing wisely)
111
You suspect hyperthyroidism in a patient and after palpating a nodule on their thyroid you test their TSH and send for US. The results of the ultrasound identify a nodule and their TSH is subnormal. What is your next step in the diagnostic process?
Radionuclide thyroid scan and measure fT4 and fT3. Note: if nodule is non-functional it may meet sonographic criteria for fine needle aspiration
112
True/False
Radionuclide thyroid scans can be ordered for suspected hypothyroidism in the presence of elevated or normal TSH
False
Radioactive thyroid scans rule out “hot nodules” present in some cases of hyperthyroidism. If nodule is identified on US it may meet criteria for fine needle aspiration.
113
All of the following are risk factors for gout EXCEPT:
* Family history
* Premenopausal
* Male Gender
* Excessive weight
* Other chronic conditions (E.g. Kidney disease, hypothyroidism, infections, etc)
* Post-surgery
* Certain medications (E.g. diuretics, low dose aspirin)
* Alcohol
It is extremely uncommon for a pre-menopausal female to have gout.
114
What foods are high in purines?
meats, seafoods, and some vegetables (E.g. asparagus, cauliflower, spinach, beans, peas, mushrooms, etc.)
115
True/False
A purine free diet is indicated for people with gout
False
* It is not advisable to follow a purine free diet for the sole purpose of trying to prevent gout. If you did, it would likely not lower your uric acid levels enough to significantly improve your gout.
116
How is gout diagnosed?
Hx/PE
Uric acid level - Note: uric acid levels can decrease during a gout flare, meaning if it was tested, it could appear normal and you might make the mistake of dismissing the diagnosis.
Joint aspiration (definitive)
X-ray - in advanced cases
117
Name that condition →
Tophaceous gout.
Several of the lesions ruptured spontaneously over the next three days, exuding a pasty material composed of urate crystals and inflammatory cells but no organisms. The inflammation largely subsided over one week after the administration of a nonsteroidal antiinflammatory drug.
118
True/False
Don’t request uric acid as part of the routine evaluation of cardiovascular risk, obesity or diabetes.
Although evidence of a causative link between hyperuricemia and cardiometabolic risk is mounting, it still does not support the use of pharmacotherapy and its concentration is not used in equations for estimating vascular risk. Asymptomatic hyperuricemia is a frequent, coincidental, biochemical finding that does not require any treatment.
Not routinely measured but should be considered in the following: (choosing wisely)
* Investigation of acute joint pain
* Follow-up of hypouricemic treatment
* Follow-up of patients with kidney disease and kidney stone disease
* Preeclampsia
* Tumor lysis syndrome
119
Oral colchicine is particularly efficacious for acute treatment of gout when started within the first ____ hours of the attack
36 hours
120
Patient presents with acute gout attack. What do you prescribe and what is the starting dose?
Mono-therapy with NSAIDs or combination therapy with NSAIDs see the following:
Day 1: Colchicine 1.2mg at sign of flare, followed by 0.6 mg after 1 hour OR 0.6 mg 3 times daily on the first day of flare; maximum total dose: 1.8 mg/day on day 1
Day 2: oral 0.6 mg once or twice daily until flare resolves
**\*Dose adjustments may need to be made if CrCL \< 30**
121
Colchicine SE
CI
When will it start working?
Most commonly: Nausea, vomiting, diarrhea
CI: serious GI, hepatic, renal, and cardiac disease; existing blood dyscrasias.
Onset of action: Oral: Pain relief: ~18 to 24 hours
122
In absence of significant clinical improvement with NSAID's +/- colchicine (or polyarticular involvement) for gout, what treatment should be considered?
Inject the active joints with methylprednisolone or start the patient on prednisone 0.5 mg/kg for 5-10 days. Note: Rebound flares are relatively common once glucocorticoids are withdrawn, especially in patients who have previously suffered a number of prior flares. Consider slow taper over 14-21 days.
123
What treatment is **strongly recommended** for gout patients with any of the following:
a) history of renal stones; b) tophi (on exam or imaging); c) more than 2 attacks per year; d) CKD stage 2 or worse (eGFR \<90).
Note: may also be considered for patients who have previously experienced \>1 flare but have infrequent flares (\<2/year). (American College of Rheumatology, 2020)
Uric acid lowering treatment
Allopurinol at 100 mg PO daily and titrated by 100 mg every 2-4 weeks (max 800mg) until the serum uric acid goes below 360 umol/L. If the patient has CKD stage 4 (eGFR \<30) or worse, I start at 50 mg PO daily, and increase slowly.
124
True/False
Consider HLA-B\*5801 allele testing in patients who are of ___________ descent, given the increased risk of Allopurinol hypersensitivity syndrome in those with this HLA subtype
Southeast Asian descent (e.g., Han Chinese, Korean, Thai) and for African American patients
125
What is your next step if a patient develops a rash with allopurinol?
Can usually be switched to febuxostat 80mg daily
126
With uric acid lowering treatment therapy, what blood work would you order and how often?
monthly uric acid, creatinine, and liver enzymes to ensure that the target uric acid (below 360 umol/l) is being reached
127
In patients who have an unclear etiology of hyperuricemia, have difficulty reaching their target uric acid levels (especially in the setting of renal impairment) or have adverse events with uric acid lowering therapy, what is your next step?
Refer to rheumatology
128
Which of the following are lifestyle modifications indicated for gout:
a) limiting alcohol intake \< 1-2 units/day
b) limiting purine intake
c) limiting high-fructose corn syrup intake
d) weight loss
e) vitamin C supplementation
f) all of the above
A, B, C, D
129
True/False
In patients already receiving urate-lowering pharmacotherapy at the time of a gout flare (eg, [_allopurinol_](https://www.uptodate.com/contents/allopurinol-drug-information?search=gout&topicRef=1666&source=see_link), [_febuxostat_](https://www.uptodate.com/contents/febuxostat-drug-information?search=gout&topicRef=1666&source=see_link), [_probenecid_](https://www.uptodate.com/contents/probenecid-drug-information?search=gout&topicRef=1666&source=see_link), [_lesinurad_](https://www.uptodate.com/contents/lesinurad-drug-information?search=gout&topicRef=1666&source=see_link), benzbromarone, or [_pegloticase_](https://www.uptodate.com/contents/pegloticase-drug-information?search=gout&topicRef=1666&source=see_link)), the urate-lowering medication should NOT be continued without interruption.
False. There is no benefit to temporary discontinuation, and subsequent reintroduction after a period off the agent may predispose to another flare.
130
Which of the following are recommended when managing a patient with gout?
a) switching HCTZ to alternative antihypertensive when feasible
b) choosing losartan preferentially as a hypertensive agent when feasible
c) stopping low doses ASA (for patients taking this medication for appropriate indications)
d) Adding or switching cholesterol-lowering agents to fenofibrate
A, B
Note: low-dose aspirin that is being used for cardiovascular prophylaxis generally does not need to be discontinued during the treatment of a gout flare, although these very low doses can increase serum urate levels modestly in some patients. Insufficient evidence for D, fenofibrate despite its urate-lowering effects as the risks, including side effects of the medication, were felt to outweigh potential benefits.
131
What needs to be considered before starting a patient on oral/injected corticosteroid therapy for gout?
R/O infection
132
Causes of Gout
Underexcretion of uric acid by the kidneys - medications (TZD, ASA), idiopathic, renal dysfunction
Increased purines - diet high in purines, high fructose cornsyrup (increased purine production
Genetic
Chemotherapy - tumor lysis syndrome
133
Sequelae of gout
1. Joint damage
2. Kidney stones
1. Urate nephropathy
134
Pseudogout/CPPD can be associated with the following (choose the correct answer(s)):
a) trauma to joint
b) hyperparathyroidism
c) hypomagnesemia
d) hypothyroidism
e) hypophosphatemia
f) hemachromatosis
g) all of the above
G
135
CPPD joint(s) commonly affected
Knee, elbow, shoulder, wrist
136
Can CPPD and gout coexist
Yes
137
Diagnosis of CPPD
1. Joint aspirate
2. X-ray
1. Screening for hyperparathyroidism, hypothyroidism, hypmagnesemia, hypophosphatesemia and hemachromatosis
138
What medication is used for long-term treatment or prevention of CPPD?
There is none, its a trick
139
Primary hyperparathyroidism is most commonly caused by a parathyroid ______ which is a ____ tumor
Ademona, benign
140
Symptoms of primary hyperparathyroidism
Stones (kidney/gall), thrones (polyuria), bones (bone pain), groans (constipation/muscle weakness) and psychiatric overtones (depression/confusion)
141
Diagnosis of hyperparathyroidism
Parathyroid
Ca
P04
Vitamin D
142
Name that condition →
high calcium
low phosphate
Primary hyperparathyroidism (producing high amounts of parathyroid hormone NOT in response to/independent of circulating calcium levels
143
Name that condition →
low calcium
high phosphate
low vitamin d
Secondary hyperparathyroidism (low calcium levels and high parathyroid hormone levels in response, most often due to kidney disease)
144
Treatment of primary and tertiary hyperparathyroidism
surgical removal of abnormal gland
OR
calcimimetics
145
Treatment of secondary hyperparathyroidism
Surgery
Supplements
146
Cause of tertiary hyperparathyroidism
Chronic secondary hyperparathyroidism from CKD (high calcium, high or low phosphate depending on renal function)
147
Name this condition → (pathognomonic for primary hyperparathyroidism)
**Osteitis fibrosa cystica**
salt-and-pepper degranulation of the skull, tapering of the distal clavicle, subperiosteal resorption of the distal phalanges, bone cysts, and brown tumours
148
Parathyroid hormone concentration of ____ or higher in a hypercalcaemic setting is inappropriate and is consistent with a diagnosis of primary hyperparathyroidism
20 ng/L
149
What do you suspect if very high parathyroid hormone and very high calcium levels in 40-50 year old?
Parathyroid cancer
150
Diagnostics for suspected hyperparathyroidism
Serum Ca+, P04, PTH, **1,25-dihyroxyvitamin D**, 24 hour urine for calcium and creatinine
DEXA scan
Consider renal CT/US
151
True/False
Conservative treatment of hyperparathyroidism includes restricting calcium intake and supplementing vitamin D
False
Adequate vitamin D and calcium intake are necessary as abnormalities in these levels can further increase PTH levels
152
Name this condition and its most COMMON cause
Pituitary adenoma (benign)
153
Ectopic ACTH-producing tumors are found 50% of time in the \_\_\_\_
Lungs
154
All of the following are causes of Cushing's disease EXCEPT:
a) glucocorticoid hormone use
b) pituitary adenoma
c) benign of malignant cancers from outside the pituitary
d) anabolic steroids
e) adrenal tumors
f) Genetic - MEN I
D
155
True/False
Serum cortisol should be used as initial screening for Cushing's disease
FALSE
Serum cortisol levels do not provide high-end diagnostic accuracy or sensitivity when used as an initial diagnostic test.
156
What tests are commonly used to diagnose cushing's disease
Late night salivary cortisol samples employing an approved collection device
24-hour urine free cortisol [UFC]
1 mg overnight dexamethasone suppression test [DST]
x-ray of adrenal and/or pituitary glands
157
Name that condition →
TSH low
fT4 high
fT3 normal
Euthyroid sick syndrome
