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NUNP 547 - Older Adult > Endocrine > Flashcards

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

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2
Q

What is most important risk factor for insulin resistance and DM

A

Obesity

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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

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4
Q

Somogyi effect

A

Decreased BG level at night that may lead to increase in morning BG

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5
Q

Dawn phenomenon

A

Early morning rise in BG d/t GH, cortisol and catecholamines NOT preceded by hypoglycemia

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6
Q

Causes of blurred vision in DM

A

Macular edema
Hyperglycemia

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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

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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

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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

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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

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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

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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

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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

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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”

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15
Q

A1C target for functionally independent

A

= 7.0%

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16
Q

A1C target for functionally dependent frailty index 4-5)

A

<8.0%

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17
Q

A1C target for frail and/or dementia

A

<8.5%

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18
Q

BP target for functionally independent and life expectancy > 10 years

A

<130/80 mm Hg

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19
Q

Target LDL

A

<2.0 mmol/L or 50% reduction from baseline

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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
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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

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22
Q

True/False

Diabetes screening is beneficial in asymptomatic individuals over the age of 80

A

False

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23
Q

True/False

A1C is less reliable in older adults due to the effect of comorbid conditions

A

True

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24
Q

General screening for DM, average risk adults

A

Q3 years starting at age 40

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25
Q

General screening for DM, with risk factors or high CANRISK score

A

Q6-12 months at any age

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26
Q

Risk factors for DM

A
  • 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,
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27
Q

Diagnosis of DM

A
  • 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
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28
Q

True/False

A1C can be used in isolation to diagnose DM in older adults

A

False

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29
Q

Prediabetes diagnosis

A
  • FBG: 6.1 - 6.9
    • A1C: 6.0 - 6.5
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30
Q

Treatment: A1C < 1.5% above target

A

Lifestyle x 3 months, then if not at target start/increase metformin

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31
Q

Treatment A1C >/= 1.5% above target

A

Start metformin immediately, consider 2nd agent

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32
Q

Treatment if symptomatic hyperglycaemia with DM

A

Initiate insulin +/- metformin

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33
Q

A1C target for end of life

A

Do not measure, avoid symptomatic highs/lows

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34
Q

Low risk medications to prevent hypoglycemia

A

metformin, GLP1s, DDP4s, SGLT2s, TZD, alpha-glucosidase inhibitors

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35
Q

High risk medications for hypoglycemia

A

insulins, sulfonylureas, meglitinides (less risk than sulfonylureas)

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36
Q

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

A

E

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37
Q

What test can be used to predict cognitive and physical capability to inject insulin?

A

Clock drawing test

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38
Q

Geriatric monitoring (4 M’s)

A

Mentation - memory and mood

Mobility - fall, visual problems, neuropathy, weakness, BP

Medication - polypharm

Matters most - goals, MOST

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39
Q

Microvascular complications

A

Nephropathy

Retinopathy

Peripheral neuropathy

ANS dysfunction

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40
Q

Macrovascular complications

A

Coronary, carotid, PVD

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41
Q

SADMANs Medications

A

S - sulphonylureas

A - ACE-I

D - diuretics

M - metformin

A - ARBs

N - NSAID

S - SGLT-2 inhibitors

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42
Q

Antihyperglycemic drugs for CVD if GFR > 30

A

Empagliflozin (Grade A)

Liraglutide (Grade A)

Canagliflozin (Grade C)

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43
Q

ABCDESSS of Diabetes

A

A1C targets

BP targets

Cholesterol targets

Drugs for CVD

Exercise goals and healthy eating

Screening for complications

Smoking cessation

Self-management/Stress

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44
Q

Screening ECG for DM

A

Q3-5 years

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45
Q

Screening feet in DM

A

Monofilament yearly or > if abN

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46
Q

Screening for kidney dysfunction

A

eGFR and ACR yearly

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47
Q

Screening for retinopathy

A

Q 1-2 years with optometrist/opthamologist

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48
Q

4 A’s of smoking cessation

A
  1. Ask - Identify and document tobacco use
  2. Advise - to quit.
  3. Assess - readiness to quit
  4. Assist - counselling/pharmacotherapy
  5. Arrange - follow up
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49
Q

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

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)

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50
Q

What sensations are commonly lost in peripheral neuropathy

A

Loss of pain, temperature, and vibration sensation is more common than motor involvement

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51
Q

Describe autonomic neuropathy S&S

A
  • delayed gastric emptying, diabetic diarrhea, altered bladder fx, impotence, orthostatic hypoTN
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52
Q

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

A

C

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53
Q

True/False

T3 is 5 x more active than T4

A

False. T3 is 10 x more active

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54
Q

Thyroid hormone effect on body (CVS, metabolism)

A

Increase CO, HR, RR

Increase 02 demand

Increase glucose absorption, gluconeogenesis, glycogenolysis, lipolysis, and protein synthesis

Increase BMR

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55
Q
A

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.

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56
Q

Wolff Chaikoff effect

A

++ iodine = low levels thyroid hormone - hypothyroidism

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57
Q

Jod Basedow effect

A

If exposed to large/ normal amounts of iodine- results in ++ thyroid hormone secretion / hyperthyroidism

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58
Q

True/False

Elevated lipids OR depression are indications for checking TSH in elderly

A

True

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59
Q

What happens with T4 production and clearance in the older adult? How is T3 affected in this population?

A

T4 - reduced production, reduced clearance = unchanged

T3 - unchanged

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60
Q

Most common cause of hypothyroidism?

A

Hashimotos disease/ Chronic autoimmune thyroiditis

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61
Q

Less common causes of hypothyroidism

A

Radiation, surgical removal, idiopathic, excess iodine, meds - amiodarone, lithium, radio contrast

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62
Q

True/False

Hyper/hypothyroidism can be diagnosed in states of acute illness

A

False

Diagnosis in presence of acute illness should only be made if thyroid lab abnormalities continue 2 weeks after sickness resolution

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63
Q

Euthyroid sick syndrome

A

Changes in thyroid secondary to acute medical/psych illness. Treat underlying cause.

64
Q

Starting dose of synthroid in older adult

A

12.5-25mcg

65
Q

Repeat BW duration following medication adjustments for thyroid dysfunction

A

6 weeks

66
Q

When is stress test indicated before treating hypothyroidism?

A

In presence of high CAD risk and long-standing hypothyroidism

67
Q

Target TSH older adult

A

Upper limit of normal, T4 to normal

68
Q

Overtreatment of hypothyroidism can cause _____ in women

A

Osteoporosis

69
Q

Most common cause of hyperthyroidism

A

Graves’ disease

70
Q

Less common causes of hyperthyroidism

A

Iatrogenic - overtreatment, iodine induced via amiodarone

Nodular thyroid disease - Granulomatous (painful and tender thyroid) or lymphocytic thyroiditis (painless)

71
Q

Clinical manifestations of hyperthyroidism in older adults

A

Tachycardia/a.fib

SOBOE

Edema

Wt loss

72
Q

Apathetic thyrotoxicosis

A

Asymptomatic hyperthyroidism except weakness in older adult population

73
Q

Treatment for hyperthyroidism

A
  • 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
Q

TSH low

fT4 normal

fT3 normal

A

Repeat TSH in 6-12 months or sooner PRN

75
Q

What is your next step if BW completed and TSH normal

A

Review clinical diagnosis, no further testing indicated

76
Q

TSH low

fT4 high

A

Hyperthyroidism

  • Excessive thyroid hormone replacement (levothyroxine)
  • Graves’ disease
  • Subacute thyroiditis (viral)
  • Painless/postpartum thyroiditis (autoimmune)
  • Toxic (multinodular) goitre
77
Q

TSH low

fT4 normal

fT3 high

A

Hyperthyroidism

  • T3 thyrotoxicosis (e.g., autonomous nodule)
  • Excessive thyroid hormone replacement (liothyronine or desiccated thyroid)
78
Q

TSH high

fT4 low

A

Hypothyroidism

79
Q

TSH high

fT4 normal

A

Repeat TSH in 6-12 months or PRN

80
Q

The following are all risk factors for thyroid disease EXCEPT: (choose one)

  • men: age ≥ 55 years<u>2</u>
  • women: age ≥ 50 years<u>2</u>
  • 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<u>3</u>, Down syndrome<u>4</u> and mitochondrial disease<u>5</u>)
A
81
Q

True/False

Proximal muscle weakness is a sign of hyperthyroidism

A

True

82
Q

True/False

SBP and DBP HTN is a sign of hyperthyroidism

A

False. Isolated SBP HTN is a sign of hyperthyroidism

83
Q

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

A

C

84
Q

When to order anti-thyroid peroxidase (TPO) and when to repeat testing.

A

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
Q

TSH high

fT4 high

A

Very rare causes Consult with a specialist (lab physician, internist or endocrinologist)

  • Pituitary disease
  • Resistance to thyroid hormone
86
Q

TSH normal

fT4 low

A

Very rare causes Consult with a specialist (lab physician, internist or endocrinologist)

  • Central hypothyroidism (hypopituitarism)
87
Q

When to treat subclinical hypo/hyperthyroidism

A
  • 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
Q

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

A

True

89
Q

True/False

Patients with atrial fibrillation or osteoporosis should be screened for hyperthyroidism

A

True

90
Q

Treatment of subclinical hyperthyroidism should be considered in the ______

A

Elderly

91
Q

In patients over age 60 with TSH 0.1 mU/L but with a normal fT4, the relative risk for atrial fibrillation increases _____

A

3 x

92
Q

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 _______

A

Lithium - 6 month

Amiodarone - 3-6 months

93
Q

Statin indications with DM

A

age ≥40

age ≥30 and diabetes >15 years

94
Q

Hypoglycemia symptoms (He IS TIRED)

A

Headache

Irritability

Sweating

Tachycardia

Restless

Excessive hunger

Dizziness

95
Q

Hyperglycemia symptoms (“hot and dry, sugar is high”)

A

SAND WELT

Sweet breath

Altered LOC

Nausea/vomiting

Dry skin/mouth

Weakness

Excessive urination

Low BP

Tachycardia

96
Q

Clinical features of myxedema coma

A

Decreased LOC

Hypothermia

Bradycardia

Hyponatremia

Hypoglycemia

Hypotension

Preciptiating illness

97
Q

Possible causes of hypercalcemia

A

RHINOS

  • R: renal insufficiency
  • H: hyperparathyroidism
  • I: immobilization and iatrogenic
  • N: neoplasms
  • O: other endocrinopathies (multiple endocrine neoplasia 1 and 2)
  • S: sarcoidosis
98
Q

S&S of hyperparathyroidism

bones, stones, thrones, moans & groans, and psychiatric overtones

A
  • “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
Q

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

A

Primary hyperparathyroidism

100
Q

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

A

Secondary hyperparathyroidism

101
Q

Chronic secondary hyperparathyroidism can not cause primary hyperparathyroidism

A

False. It can!

102
Q

Name that condition →

both a metabolic disorder of purine metabolism, and a musculoskeletal disorder of monosodium urate crystal deposition in and around joints

A

Gout

103
Q

Risk factors for gout

A
  • 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
Q

Name that condition → Precipitation of crystals of calcium pyrophosphate dihydrate in connective tissues may be associated with several clinical syndromes, but is sometimes asymptomatic.

A

CPPD disease or pseudogout AKA sarah’s foot

105
Q

What diagnostic test should be considered BEFORE initiating thyroid treatment for elderly patient that has CAD risk factors and potential for longstanding hypothyroidism?

A

Cardiac stress test

106
Q

What 3 cardiac presentations would increase your suspicion for underlying thyroid dysfunction?

A
  1. Atrial fibrillation
  2. Angina
  3. HF
107
Q

True/False

Anemia can be a sign of hypothyroidism in the adult population

A

True

108
Q

Tachycardia, goitre and eye symptomatology are all symptoms of ____ in the older population

A

Hyperthyroidism

109
Q

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?

A

Order TSH and thyroid US

110
Q

True/False

Nuclear medicine thyroid scanning conclusively determines whether thyroid nodules are benign or malignant

A

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
Q

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?

A

Radionuclide thyroid scan and measure fT4 and fT3. Note: if nodule is non-functional it may meet sonographic criteria for fine needle aspiration

112
Q

True/False

Radionuclide thyroid scans can be ordered for suspected hypothyroidism in the presence of elevated or normal TSH

A

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
Q

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
A

It is extremely uncommon for a pre-menopausal female to have gout.

114
Q

What foods are high in purines?

A

meats, seafoods, and some vegetables (E.g. asparagus, cauliflower, spinach, beans, peas, mushrooms, etc.)

115
Q

True/False

A purine free diet is indicated for people with gout

A

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
Q

How is gout diagnosed?

A

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
Q

Name that condition →

A

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
Q

True/False

Don’t request uric acid as part of the routine evaluation of cardiovascular risk, obesity or diabetes.

A

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
Q

Oral colchicine is particularly efficacious for acute treatment of gout when started within the first ____ hours of the attack

A

36 hours

120
Q

Patient presents with acute gout attack. What do you prescribe and what is the starting dose?

A

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
Q

Colchicine SE

CI

When will it start working?

A

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
Q

In absence of significant clinical improvement with NSAID’s +/- colchicine (or polyarticular involvement) for gout, what treatment should be considered?

A

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
Q

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)

A

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
Q

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

A

Southeast Asian descent (e.g., Han Chinese, Korean, Thai) and for African American patients

125
Q

What is your next step if a patient develops a rash with allopurinol?

A

Can usually be switched to febuxostat 80mg daily

126
Q

With uric acid lowering treatment therapy, what blood work would you order and how often?

A

monthly uric acid, creatinine, and liver enzymes to ensure that the target uric acid (below 360 umol/l) is being reached

127
Q

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?

A

Refer to rheumatology

128
Q

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

A, B, C, D

129
Q

True/False

In patients already receiving urate-lowering pharmacotherapy at the time of a gout flare (eg, allopurinol, febuxostat, probenecid, lesinurad, benzbromarone, or pegloticase), the urate-lowering medication should NOT be continued without interruption.

A

False. There is no benefit to temporary discontinuation, and subsequent reintroduction after a period off the agent may predispose to another flare.

130
Q

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

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
Q

What needs to be considered before starting a patient on oral/injected corticosteroid therapy for gout?

A

R/O infection

132
Q

Causes of Gout

A

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
Q

Sequelae of gout

A
  1. Joint damage
  2. Kidney stones
    1. Urate nephropathy
134
Q

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

A

G

135
Q

CPPD joint(s) commonly affected

A

Knee, elbow, shoulder, wrist

136
Q

Can CPPD and gout coexist

A

Yes

137
Q

Diagnosis of CPPD

A
  1. Joint aspirate
  2. X-ray
    1. Screening for hyperparathyroidism, hypothyroidism, hypmagnesemia, hypophosphatesemia and hemachromatosis
138
Q

What medication is used for long-term treatment or prevention of CPPD?

A

There is none, its a trick

139
Q

Primary hyperparathyroidism is most commonly caused by a parathyroid ______ which is a ____ tumor

A

Ademona, benign

140
Q

Symptoms of primary hyperparathyroidism

A

Stones (kidney/gall), thrones (polyuria), bones (bone pain), groans (constipation/muscle weakness) and psychiatric overtones (depression/confusion)

141
Q

Diagnosis of hyperparathyroidism

A

Parathyroid

Ca

P04

Vitamin D

142
Q

Name that condition →

high calcium

low phosphate

A

Primary hyperparathyroidism (producing high amounts of parathyroid hormone NOT in response to/independent of circulating calcium levels

143
Q

Name that condition →

low calcium

high phosphate

low vitamin d

A

Secondary hyperparathyroidism (low calcium levels and high parathyroid hormone levels in response, most often due to kidney disease)

144
Q

Treatment of primary and tertiary hyperparathyroidism

A

surgical removal of abnormal gland

OR

calcimimetics

145
Q

Treatment of secondary hyperparathyroidism

A

Surgery

Supplements

146
Q

Cause of tertiary hyperparathyroidism

A

Chronic secondary hyperparathyroidism from CKD (high calcium, high or low phosphate depending on renal function)

147
Q

Name this condition → (pathognomonic for primary hyperparathyroidism)

A

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
Q

Parathyroid hormone concentration of ____ or higher in a hypercalcaemic setting is inappropriate and is consistent with a diagnosis of primary hyperparathyroidism

A

20 ng/L

149
Q

What do you suspect if very high parathyroid hormone and very high calcium levels in 40-50 year old?

A

Parathyroid cancer

150
Q

Diagnostics for suspected hyperparathyroidism

A

Serum Ca+, P04, PTH, 1,25-dihyroxyvitamin D, 24 hour urine for calcium and creatinine

DEXA scan

Consider renal CT/US

151
Q

True/False

Conservative treatment of hyperparathyroidism includes restricting calcium intake and supplementing vitamin D

A

False

Adequate vitamin D and calcium intake are necessary as abnormalities in these levels can further increase PTH levels

152
Q

Name this condition and its most COMMON cause

A

Pituitary adenoma (benign)

153
Q

Ectopic ACTH-producing tumors are found 50% of time in the ____

A

Lungs

154
Q

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

A

D

155
Q

True/False

Serum cortisol should be used as initial screening for Cushing’s disease

A

FALSE

Serum cortisol levels do not provide high-end diagnostic accuracy or sensitivity when used as an initial diagnostic test.

156
Q

What tests are commonly used to diagnose cushing’s disease

A

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
Q

Name that condition →

TSH low

fT4 high

fT3 normal

A

Euthyroid sick syndrome

NUNP 547 - Older Adult (19 decks)

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