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Week 2 Diabetes & endocrine Flashcards

1
Q

hypothyroidism on exam

A
  • Puffy or pale face
  • Dry hair, brittle nails
  • Weight gain
  • Delayed relaxation of deep tendon reflexes (DTRs)
  • Cerebellar ataxia
  • Bradycardia
  • Diastolic hypertension
  • Goiter may be present
    • Hashimoto’s thyroiditis
    • More common in younger pts
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2
Q

primary vs secondary hypothyroidism

A
  • Primary [TSH increased]
    • thyroid is the problem it self
    • autoimmune (most common)
    • drugs
  • Secondary aka centra hypothyroidism [TSH decreased]
    • damage to pituitary
    • associated with other signs of pituitary hormone insufficiency
    • pituitary disease or tumor
    • Less common
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3
Q

hypothyroidism risk factors

A
  • Amiodarone (contains iodine)
  • Female
  • Older age
  • Iodine deficiency
  • radiation for head and neck
  • cancer
  • Personal or family history of
  • autoimmune disease
  • Down syndrome
  • Turner syndrome
  • Postpartum thyroiditis
  • Goiter with positive thyroid antibodies
  • Thyroidectomy
    • Type 1 DM and vitiligo
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4
Q

hypothyroidism diagnostics

A
  • Order TSH with reflex (with T4 if abnormal)
  • Thyroid hormone will always be low but TSH level varies
    • primary cause: TSH will be high
    • secondary cause: TSH low or normal
  • If suspect secondary hypothyroidism: check both TSH and free T4
    • If have sx’s of irregular menses, galactorrhea, h/a
  • If abnormal TSH or high TSH, check thyroid peroxidase/TPO antibody
    • Will be elevated in chronic autoimmune thyroiditis
  • If have goiter, check anti-thyroglobulin antibodies
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5
Q

elevated TSH and normal TH levels:

5-10 TSH vs >10 TSH

A

check TPO antibody → can indicate autoimmune thyroiditis (increases risk of hypothyroidism in future)

if > 10 TSH, give levothyroxine!

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6
Q

primary hypothyroidism management /education

A
  • Levothyroxine 1.6 mcg/kg/day
  • Low dose in coronary artery disease or older age
  • Recheck TSH in 6–8 weeks to see if euthyroid
    • If euthyroid, check yearly
  • Educate: 1st thing in morning empty stomach
    • Wait ½ hr before anything to eat
    • Don’t take with vitamins
    • Space it 4 hrs so doesn’t interfere with thyroxine
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7
Q

1st, 2nd, and 3rd trimester TSH goals

A

if pt becomes positive during hypothyroid tx, need to increase dose by 30%

1st: < 0.5-2.5

2nd & 3rd: < 3

monitor TSH q 4 weeks until 30 weeks, then once in 3rd trimester

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8
Q

Referral hypothryoid pt to endocrinology

A
  • Infants and children
  • Unresponsive to therapy
  • Pregnancy
  • Cardiac patients
  • Nodule or structural problem of thyroid
  • Presence of other endocrine disease
  • Unusual constellation of thyroid test results
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9
Q

subacute thyroiditis

A

from recent viral illness

  • Concurrent fever, URI
  • Thyroid is painful and tender
  • starts out with hyperthyroid low TSH, high T4 then hypothyroid then euthyroid
  • tx
    • NSAIDs/aspirin for pain, or prednisone taper
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10
Q

postpartum thyroiditis

A
  • PAINLESS thyroiditis
  • Becomes thyrotoxic (becomes hyperthryoid briefly)
  • Then transitions to hypothyroidism lasting 5-6 months and recovers to euthyroid
  • 40% go on to develop overt hypothyroidism
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11
Q

graves disease

A
  • Autoimmune
  • Autoantibodies bind to the TSH receptors → stimulates TH into body
  • Risk factors: similar to thyroiditis and hypothyroidism
  • Cause:
    • Toxic multinodular goiter
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12
Q

Toxic multinodular goiter

A
  • chronic lack of dietary iodine (can’t make iodine = less TH) → pituitary releases TSH & causes thyroid to hypertrophy
  • Evaluated with radioactive/thyroid uptake scan
    • If confirmed dx, treat with surgery or medication
  • Referred to endocrine to manage
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13
Q

Graves disease diagnostics

A
  • Low TSH
  • Elevated T4, Free T3 or total T3
  • Thyrotropin receptor antibodies
    • Positive in 98% of patients with untreated Graves’
    • • Helps confirm diagnosis
  • Elevated: Erythrocyte sedimentation rate (ESR), and liver function tests (LFTs), Alk phos
  • CBC
  • If see nodule, do imaging study
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14
Q
  • graves disease management
A
  • Refer to endo
  • Refer to opthalm if ophthalmopathy
  • Tx
    • Antithyroid meds
      • Methimazole
        • Use in 2nd and 3rd trimester
      • Propylthiouracil/PTU
        • Use in 1st trimester
    • Radioactive iodine (131 therapy if more than 10 yrs old)
    • Thyroidectomy
    • Beta blockers
      For palpitations, tremors
  • Monitoring:
    • CBC, LFTs before med therapy
    • monitor q 2-8 weeks until stable if on meds
    • Meds taken for 1-2 years
    • Remission is 40%
  • Meds is preferred during pregnancy
  • Mild, older age, ophthalmopathy → medications
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15
Q

Hyperthyroidism complications

A
  • Thyroid storm
    • Med emergency
      • Fever, tachycardia, edema, arrhythmias, CNS sx’s, GI sx’s
  • Osteoporosis
    • If postmenopausal, do bone density scan
  • Atrial fib
  • Worsening HF
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16
Q

Thyroid nodules

A
  • during PE, note size, consistency, mobility, and presence/consistency of lymphadenopathy
  • solid vs cystic
  • If < 1 cm, don’t need FNA (rarely malignant)
  • 90% nodules are benign
  • High cure rate for malignancy
  • typically non painful, non tender
  • get thyroid function test and US, if sus on US → fine needle aspiration
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17
Q

clinical finding suggesting cancer in euthyroid pt with nodule (high vs mod suspicion)

A
  • thyroid US on all patients
  • high suspicion:
    • family hx of medullary thyroid carcinoma
    • rapid tumor growth esp during levo therapy
    • very firm/hard nodule
    • fixed nodule
    • paralysis of vocal cords
    • regional lympathadneoepathy
    • distant metastasis
  • moderate sus
    • < 20 or >70 yrs old
    • male
    • hx head /neck radiation
    • sx of compression (dysphagia, dystonia, hoarseness, dyspnea, cough)
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18
Q

sus for malignancy thyroid nodules

A
  • Repeat exam, US, and TSH in 12 months
    • If unchanged nodule, repeat at 24 months
    • Consider repeating fine needle aspiration (FNA) if increased more than 50%
  • • Surgery if large size (more than 4 cm) or symptomatic
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19
Q
A
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20
Q

benign growth on parathyroid gland

A
  • common cause
  • hyper more common than hypo (growth causes more PTH released and increase CA levels)
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21
Q

primary vs secondary vs tertiary hyperparathyroidism

A
  • Primary:
    • gland itself
    • growth/tumor on gland
    • neck/radiation or trauma
  • Secondary
    • compensatory response to hypOcalcemia
      • vit D deficiency
      • CKD/renal failure
  • Tertiary
    • long standing secondary hyperparathyroidism → permanently overactive
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22
Q

sx’s hypercalcemia/hyperparathryoidism

A

“bones, stones, thrones, abdominal groans, psychic moans”

  • stones: kidney stones, gall stones
  • thrones: polyuria
  • groans: constipation, muscle weakness
  • bones: osteoporosis
  • psychotic moans: mental status changes
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23
Q

HyperCa/HyperPara diagnostics

A
  • repeat serum Ca to confirm
    • 24 hour urine calcium
  • Phosphate
  • Vitamin D
  • Alkaline phosphatase
  • PTH assay (if PTH is dependent or independent)
    • independent: need calcitriol level, PTHrP level
  • if high levels of PTH, Ca, Alk Phos → consider malignancy
  • if high levels of PTH, Ca, low Phos → primary hyperparathyroidism
  • if high levels of PTH, high/N Phos, low/N Ca → secondary
  • if high levels of PTH, Ca, phos → tertiary
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24
Q

hyperCa/parathyroidism imaging

A
  • bone density scan (lumbar, hip, distal radius)
  • xray
  • abdominal ultrasound (renal stones)
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25
Q

hyperCa/parathyroidism management

A
  • Endocrine referral
  • Surgical referral
    • Criteria:
      • Need to be symptomatic
      • Recurrent neprholithaissi
      • Osteoporosis
        • Fractures
      • Ca > 1 mg per deciliter above normal limits
  • Medical management - if mild
    • Monitor labs and bone density
    • Ca, Vit D
    • Increase fluid intake
    • Weight bearing exercise
  • Ca Crisis
    • Sx’s: Ca increase 14 or higher
      • need aggressive IV NS restoration of volume status
    • Referral to ED
      • symptomatic hyperca with n/v
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26
Q

Pituitary adenomas

A
  • Benign 10-15% intracranial masses
  • < 1 cm = microadenoma
  • > 1 cm = macroadenoma
  • majority are prolactinomas (secrete prolactin) 40-57%
    • 11% Growth hormone tumors
    • 2% ACTH secreting (cushings)
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27
Q

Cushing syndrome

A
  • highest ACTH release when waking up, lowest at night
  • overproduction of cortisol from adrenal
    • Most common: high doses of steroids for long periods of time causes suppression of pituitary ACTH production
      • steroids used > 10-14 days for asthma management, derm, neoplasma = careful monitoring for suppression
    • Long term exogenous > 15 mg/day → suppresses HPA axis
    • < 3 weeks okay
    • Heavier steroid dose should be done in morning cus night suppresses the morning pulse significantly
    • take heavier steroid dose in morning
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28
Q

Cushing disease

A

pituitary caused symptoms

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29
Q

Cushing syndrome sx’s

A
  • Elevated cortisol levels
    • Central obesity, hirsutism, purple striae
  • psychological , skin , short term memory, menstrual irregularities, h/a
  • Buffalo hump dorsocervical fat pad
  • Increased supraclavicular fat pad
  • Muscle wasting/weakness
  • Acne
  • Emotional liability/depression
  • Senile purprua on the hands/bruses
  • Most common cause: exogenous steroids
  • Long term prednisone
  • Women >>
  • 50-60 yrs
  • Acanthosis nigricans
  • Galactorrhea, irregular menses (decreased LH/fsh)
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30
Q

cushing syndrome diagnostics

A
  • Testing needs to be done in ABSENCE of acute illness
  • Dx: > 100 mcg of cortisol in urine during 24 hr period
    • or single midnight (nadir) serum cortisol >7.5 (100% specificity/96 sensitivity)
  • Initial testing, 1 of the following:
    • 24-hour urine-free cortisol 2 times
    • Late-night salivary cortisol 2 times
    • Low-dose dexamethasone suppression test
      • Take low dose at 10pm then blood draw/cortisol taken next day
      • Healthy person: cortisol is suppressed
      • Cushing: don’t see cortisol suppression
  • Refer to endocrinology even if abnormal test or not :
    • If initial testing is positive
    • If high clinical suspicion and testing is negative
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31
Q

Cushing treatment

A
  • Cushing disease:
    • first line: Surgical resection via transsphenoidal surgery (pituitary tumor resection)
  • Daily ketoconazole admin (mitigates cortisol impact)
  • chemo, radiation
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32
Q

pituitary prolactinoma

A
  • Secreting excess prolactin hormone
  • Females 20-50 yrs
    • Oligomenorrhea
    • • Galactorrhea
    • • Vaginal dryness
    • • Hirsutism
  • Males
    • Erectile dysfunction
    • • Decreased body and facial
    • hair
    • • Gynecomastia
  • Both
    • Infertility
    • Loss of interest in sex
    • Low bone density
    • Headaches
    • Visual disturbance
    • Delayed puberty
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33
Q

Pituitary prolactinema on exam

A
  • Thorough ophthalmic exam
  • Neuro exam - visual field defects
  • Tumors can impinge on optic apparatus
  • Hirsutism
  • Acne
  • Hair growth
  • Thyroid exam - goiter
  • Children
    • Puberty changes
    • Look for hypogonadism
    • gynecomastia and galactorrhea
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34
Q

pituitary prolactinemia diagnostics

A
  • Prolactin hormone
    • If have sx’s, get level
    • If asx, consider repeating in morning
    • Prolactin levels correlate with size of adenoma
      • Bigger = higher prolactin
  • Blood urea nitrogen (BUN) and creatinine
  • HCG if child bearing age
    • r/o pregnancy
  • TSH/free T4
    • r/o hypothyroidism
  • ALT/AST - liver dz or hepatitis
  • Get MRI to search for prolactinoma
  • Refer to endo
  • Refer ophthalmology (neuro-opth exam)
  • If have microadenoma and asx, don’t need treatment
  • If microadenoma and sx, treat
  • All macroadenoma → treat
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35
Q

pituitary prolactinemia management

A
  • Cabergoline - dopamine agonist
    • Preferred; fewer SE; greater efficacy
  • Bromocriptine
  • Respond fast with meds
  • Monitor prolactin levels more freq in beginning and less freq ad time goes on
  • Repeat MRI to know it’s decreasing in size
  • After a few yrs, can get off meds if prolactin and MRI normal
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36
Q

hyperglycemia crisis: diabetic ketoacidosis

A
  • blood sugar 250-300
  • Ketones
  • Acidosis
  • Type 1 DM
  • juvenile/kids
  • pH < 7.3 (acidotic)
  • Bicarb < 15
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37
Q

Hyperglycmeic crisis: Hyperglycemic Hyperosmolar syndrome (HHS)

A
  • Blood sugar 600
  • Hyperglycemia
  • Hyperosmolality
  • Dehydration
    • Alt mental status (brain swelling, coma, death)
  • Type 2 DM
  • Adults
  • pH > 7.3
  • Bicarb > 15
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38
Q

4 different diagnostic criteria for diabetes in NON pregnant adults?

A

If 1 is positive, need REPEAT test on different day OR a 2nd different test to confirm diagnosis using same sample or 2 separate test samples. Can be used to screen too.

  • Fasting plasma glucose ≥ 126 mg/dL
    • No food for 8 hrs
  • Oral glucose tolerance test (75g) with plasma glucose ≥ 200 mg/dL 2 hours post glucose load
  • HgbA1c ≥ 6.5
    • POC A1c testing is NOT recommended to diagnose but can use it for screen
      • If elevated, f/u with primary care provider
  • Random glucose ≥ 200 mg/dL AND classic symptoms of hyperglycemia or hyperglycemic crisis (polyuria, polydipsia, or unexplained weight loss
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39
Q

which ONE test can diagnose diabetes right away?

A

having classic symptoms of hyperglycemia or hyperglycemic crisis AND a random glucose > 200 mg/dL

  • want PLASMA glucose to dx (serum glucose varies 10-20% while plasma varies 1-3% in testing)
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40
Q

what conditions make A1C less accurate?

A

anything with rapid blood cell turnover

  • anemia
  • hemoglobinopathies
  • recent blood loss/transfusion
  • erythropoietin therapy
  • hemolysis/hemodialysis
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41
Q

recommended criteria for testing for prediabetes or diabetes in asymptomatic adults?

A
  • All adults begin 45 yrs+ regardless of their weight or any other risk factors
  • test younger than 45 yrs old it overweight (BMI > 25) (Asian >23 BMI) + other risk factors:
    • 1st degree relative with diabetes
    • Black, Hispanic/Latino, Indian, Alaska Native, Asian, Pacific Islander
    • Hx of gestational diabetes or giving birth to a baby weighing > 9 lbs
    • Physical inactivity
    • BP ≥ 140/90 or on therapy for hypertension
    • HDL < 35 mg/dL
    • Fasting triglycerides > 250 mg/dL
    • PCOS
    • Previously A1c > 5.7%, impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) on previous testing
    • Sx’s of insulin resistance
      • acanthosis nigricans, non-alcoholic steatohepatitis, PCOS, and SGA
    • Hx CVD
    • on Atypical antipsychotics or glucocorticoids
42
Q

Recommended criteria for testing for prediabetes or diabetes in asymptomatic children?

A
  • Overweight (BMI > 85th percentile for age and sex, weight for height greater than 85th percentile, or weight > 120% for height)

AND who meet one or more of the following criteria

  • Maternal gestational DM
  • Family history of type 2 diabetes in first- or second-degree relatives
  • Native American, African America, Latino, American, Asian American, and Pacific Islander)
  • Signs of insulin resistance or conditions associated with insulin resistance (eg, acanthosis nigricans, hypertension, dyslipidemia, PCOS, or small-for-gestational-age birth weight)
43
Q

For a patient who develops GDM, what is the likelihood that she will develop type 2 diabetes mellitus in the next decade?

A
  • risk for developing DM2 is highest in the decade immediately following delivery.
  • 40-60% - decrease that risk by following diabetic diet / lifestyle changes, lose weight
  • The greatest risk of developing diabetes in the first decade after having gestational diabetes
44
Q

range for impaired fasting glucose

range for impaired oral glucose tolerance test

A

fasting: blood sugar 100-125
oral: 140-199

45
Q

what are the 3 types of oral glucose tolerance test?

A
  • For NON pregnant, use the 2 hour 75g
    • >200 is positive AND need symptoms of hyperglycemia (if no sx’s, need another diagnostic test to confirm)
  • For pregnant women:
    • 1 hr 50g, if >180, go to 3 hr
    • 3 hr 100g, if >140 = positive
46
Q

Name the four clinical classifications of diabetes mellitus

A
  • Type 1
    • autoimmune β-cell destruction, typically leading to absolute insulin deficiency.
  • Type 2
    • multifactorial process, insulin insufficiency (the pancreas does release enough insulin), insulin resistance, unregulated gluconeogenesis in the liver (producing glucose in the face of hyperglycemia)
  • Gestational diabetes
    • Diabetes diagnosed during the 2nd or 3rd trimester of pregnancy that was not clearly present prior to gestation
  • Other:
    • Monogenic diabetes syndromes (neonatal diabetes and maturity-onset diabetes of the young [MODY])
    • Diseases of the exocrine pancreas (cystic fibrosis)
    • Pancreatic insufficiency secondary to chronic/recurrent pancreatitis
    • Drug/chemical induced (use glucocorticoids and those treated for HIV/AIDS or after organ transplantation)
47
Q

tests to order if suspicious for type 1 DM

A
  • The presence of any of these support dx of type 1 DM:
    • islet cells autoantibodies (ICAs)
    • insulin autoantibodies (IAAs)
    • autoantibodies to glutamic acid decarboxylase 65 (GAD65)
    • tyrosine phosphatases IA-2 transmembrane proteins
    • zinc transporter (ZnT8)
  • 70% to 80% of patients with type 1 DM have anti-GAD antibodies
    • adding a check for ICA can increase the sensitivity of detection of type 1 DM to >90%.
  • Insulin Autoantibodies (IAA) in 100% of young patients but NOT in older patients.
  • Anti-GAD antibodies are more likely to be present in young adults with type 1 diabetes than they are in children.
48
Q

consider screening what other autoimmune diseases after diagnosis of DM 1?

A
  • Thyroid disease
  • Celiac disease
  • Hashimoto thyroiditis, Graves disease, Addison disease, autoimmune hepatitis, dermatomyositis, myasthenia gravis, vitiligo, and pernicious anemia.
49
Q

when is metformin safe to use?

A
  • Metformin is SAFE to use if > 30 GFR so DON”T use it if less than 30
50
Q

Are there recommended goals for weight loss and increasing physical activity that should be targeted for patients with impaired glucose tolerance or impaired fasting glucose?

A
  • Goal 10%, results with 5%
  • Start seeing effects with 5% body weight loss
    • Maintain at 7%
  • 30 mins day exercise
  • Unless contraindicated, children with prediabetes and diabetes should be encouraged to engage in physical activity at least an hour a day (play an hour a day)
51
Q

when is bariatric surgery considered?

A

if BMI > 35 AND with comorbidity or with BMI > 40

52
Q

what preventive care, tests, and recommended goals of DM 1 & 2?

A

think ABC’s!

  • A1c
    • Every 6 months if stable
    • Every 3 months if not at goal
    • A1c goal: < 7%.
    • A1c goal for children and adolescents with diabetes: < 7.5%
    • Point-of-care testing of the A1c may allow for more timely decision on adjustments of therapy, when available.
  • Aspirin/antiplatelet agents
    • Aspirin 75 to 162 mg/day
    • Secondary prevention in those with diabetes and a history of CVD
    • Primary prevention in men and women 50 years old and older with type 1 or 2 diabetes or who have additional CV risk factors
    • no benefit if under 30 yrs
    • NO Aspirin if < 21 years old (Reye syndrome)
    • Clopidogrel (75 mg/day) ok instead of aspirin
  • Blood pressure
    • Measured at every visit
    • Goals are:
    • Adults: SBP < 140 / < 90
    • Children and adolescents: < 130 / < 80 OR < 90th percentile for age, sex, and height
    • Start meds if lifestyle mods (DASH diet, weight loss, and exercise) don’t lower BP
    • ACE inhibitors, ARBs, CCB, or diuretics are recommended.
      • NO ACE, ARBs, and spironolactone in pregnancy.
    • It is also recommended that at least one antihypertensive agent be given at night.
  • Cholesterol
    • If LDL > 190 (doesn’t matter about ASCVD #), it’s very high → start on statin
    • Get lipid profile (total cholesterol, LDL, HDL, and triglycerides) at the time of diagnosis, and at least q 5 years thereafter in patients under the age of 40 years.
    • a calculated 10-year risk of atherosclerotic cardiovascular disease (ASCVD) of > 20% and the patient’s age is what primarily drives the decision to treat with statin therapy or not
  • Screening for neuropathy
    • Diabetic foot exam annually for DM 2, and w/in 5 years for DM 1
    • if have insensate feet, foot deformities, or ulcers = screen every visit
    • The foot examination: inspection, foot pulses, and testing for loss of protective sensation:
      • light-touch perception with 10-g monofilament and at least one of the following: temperature, vibration using 128 Hz tuning fork, pinprick sensation, and ankle reflexes.
    • Cardiovascular neuropathy
      • resting tachycardia and/or orthostatic hypotension. Electrophysiologic testing is rarely needed.
    • Screening for diabetic gastroparesis
      • get history history.
      • If suspicious, get a gastric emptying
  • Screening for retinopathy
    • Dilated retinal exam done at the time of diagnosis in all persons with type 2 diabetes and in those older than age 10 with type 1 diabetes for 5 or more years
    • If there is no retinopathy present after serial annual exams, the recommended screening intervals may increase to no longer than every 2 years.
  • Screening for nephropathy
    • Serum creatinine at least YEARLY to get GFR
    • Urine albumin excretion YEARLY in all persons with type 2 diabetes and in those with type 1 diabetes who have had the diagnosis for 5 or more years.
      • This is done via spot urine-to-creatinine ratio
      • Get UA, CMP
    • Persistent albuminuria is a marker for CVD.
  • Immunizations
    • Pneumoccocal
      • Age 2 to 64 years old with diabetes= get PPSV23 vaccine.
      • if < 65 yrs old when vaccine is given, repeat after age 65 with at least 5 years between doses.
      • If > 65, one vaccine is sufficient–unless there is also a history of nephrotic syndrome, chronic renal disease, or other immunocompromised states, such as post-transplantation.
      • if > 65 years or older and who have not previously received PCV13 should receive a dose of PCV13 first, followed 6 to 12 months later by a dose of PPSV23.
    • Flu vaccine yearly when > 6 months with diabetes
    • Hepatitis B vaccine 19 yrs and older
  • Tobacco use assessment
53
Q

what is used instead of micro and macroalbuminuria?

A

persistent albuminuria for >30 mg (abnormal)

54
Q

Additional screenings for children/adolescents with DM 1?

A
  • celiac disease and hypothyroidism.
  • don’t recommend screening for these because it’s ‘rare’: primary adrenal insufficiency, autoimmune hepatitis, autoimmune gastritis, dermatomyositis, and myasthenia gravis are more common in individuals with type 1 diabetes
55
Q

Which classes of diabetes medications are weight neutral or cause weight loss?

A
  • Biguanides – metformin (Glucophage and others)
  • Glucagon-like peptide-1 (GLP-1) receptor agonists – albiglutide (Tanzeum), dulaglutide (Trulicity), exenatide (Byetta, Bydureon), liraglutide (Victoza), lixisenatide (Lyxumia ), and semaglutide (Ozempic)
  • Amylin agonist - pramlintide (Symlin)
  • Dipeptidyl peptidase-4 (DPP-4) inhibitors – alogliptin (Nesina), linagliptin (Tradjenta), sitagliptin (Januvia), and saxagliptin (Onglyza)
  • Sodium/glucose cotransporter 2 (SGLT2) inhibitors (aka gliflozins) – canagliflozin (Invokana), dapagliflozin (Farxiga), empagliflozin (Jardiance), and ertugliflozin (Steglatro)
  • Pramlintide (Symlin)
56
Q

if A1C is <7.5%…

A

mono therapy

  • Metformin
  • GLP1-RA
  • SGLT-2
  • DPP4
  • thiazolidinediones TZD
  • alpha glucosidase inhibitors (AGIs)
  • sulfonylureas

if pt is “high risk” for ASCVD, have stage 3 CKD, HF use:

  • GLP1 or SGLT-2 inhibitor

if goal not at 3 months, try dual therapy

57
Q

metformin contraindications

A
  • Lactic acidosis
  • Decompensated congestive heart failure (CHF)
  • Severely impaired renal function (< 30 GFR)
  • Liver failure, heavy alcohol use, or in patients undergoing major surgery.
  • Warn patients to stop drug whenever a study requiring iodinated contrast is needed and not restarted until 48 hours later if the renal function permits.
58
Q

How much of a reduction in her A1c from metformin as monotherapy?

A
  • 1-1.5%
  • most therapies for diabetes would result in a 0.5% to 1.5% reduction.
  • The most effective therapeutic classes (with an expected 1%-1.5% A1c reduction):
    • Biguanides (metformin)
    • GLP-1 receptor agonists
  • Does not cause hypoglycemia & weight loss.
  • But a/s wit vitamin B12 deficiency.
    • get “periodic” testing of B12 esp if pt has anemia or symptoms of peripheral neuropathy.
59
Q

drug classes for the treatment of type 2 diabetes mellitus that reduces cardiovascular disease (CVD)

A
  • SGLT2 inhibitors (Empagliflozin, Canagliflozin , and Dapagliflozin)
  • GLP-1 receptor antagonists Liraglutide
  • Although SGLT2 inhibitors have some proven efficacy for primary and secondary prevention of cardiovascular endpoints, their cadioprotective effects are most pronounced in patients with underlying CV disease.
  • Liraglutide has been show more beneficial than other GLP-1 in reducing CV endpoints (CV death, non-fatal MI, or stroke).
60
Q

if A1C > 7.5…

A
  • lifestyle modifications, metformin, AND [would need dual therapy]:
  • GLP-1 receptor agonists, SGLT2 inhibitors, DPP-4 inhibitors, TZDs, colesevelam (a bile-acid sequestrant that lowers LDL and improves glycemic control), bromocriptine-QR (Cycloset), alpha-glucosidase inhibitors, sulfonylureas, non-sulfonylurea secretagogues (aka the “glinides” or meglitinides), amylinomimetic agents (amylin agonist), and insulin are all treatment optiåons that can accompany metformin
61
Q

which diabetic treatment options are injectable form

A
  • The GLP-1 receptor agonists, pramlintide (Similin), and most insulins
62
Q

If initial A1c > 9%

A

start with insulin (w/ or w/o other agents), esp if have sx’s of diabetes

if not at goal at 3 months (< 7%), triple therapy or tx with insulin may be needed

63
Q

metformin MOA

A

reduces A1c 1-1.5%

in the liver to reduce gluconeogenesis; in the skeletal muscles to decrease insulin resistance

64
Q

Glucagon like peptide (GLP1) agonist [Albiglutide, dulaglutide , exenatide, liraglutide, lixisenatide, and samaglutide] MOA

A
  • reduce 1-1.5% a1c
  • in pancreas, stimulates insulin secretion & prevent beta-cell apoptosis
65
Q
  • Sulfonylureas MOA:
    • 1st generation: Chlorpropamide, tolazamide, tolbutamide;
    • 2nd generation: Glyburide, glipizide, glimepiride
A
  • 1-1.5%
  • Enhance insulin secretion from the pancreas by interacting with the ATP-sensitive potassium channels in the beta cell membranes
66
Q

thiazolidinediones (Pioglitazone)

A

1-1.5% reduced

  • Increases insulin sensitivity of skeletal muscle, adipose tissue, and the liver
67
Q

Non-sulfonylurea secretagogues MOA (Repaglinide and nateglinide)

A

Enhance insulin secretion from the pancreas by interacting with the ATP-sensitive potassium channels in the beta cell membranes (structurally different than the sulfonylureas)

68
Q

Sodium glucose co transporter 2 (SGLT2) inhibitors MOA (Canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin)

A
  1. 5-1% A1c reduction
    * Inhibits the SGLT2 membrane protein in the proximal tubule, which results in decreased renal glucose reabsorption and increased urinary glucose excretion.
69
Q

Dipeptidyl peptidase 4 (DPP-4) inhibitors (Alogliptin, linagliptin, saxagliptin, and sitagliptin) MOA

A

Slows degradation of GLP-1 and glucose-dependent insulinotropic peptides (GIPs)

70
Q

what other 2 non insulin drugs can be used to tx DM 2 but shouldn’t be used as mono therapy

A

bile acid sequestrant Colesevelam (Welchol) and Bromocriptine

71
Q

major adverse effects of biguanides (metformin)

A
  • metallic taste, nausea, diarrhea, abdominal pain, lactic acidosis (rare – but potentially fatal); B12 deficiency
  • Doesn’t cause hypoglycemia
72
Q

major adverse effects of GLP-1 agonists (Albiglutide, dulaglutide , exenatide, liraglutide, lixisenatide, and samaglutide)

A

nausea, vomiting, diarrhea; renal impairmentan acute renal failure associated with dehydration caused by GI toxicity; injection-site reactions; risk of acute pancreatitis; thyroid C-cell hyperplasia; possible risk of thyroid C-cell carcinoma

73
Q

major adverse effects of SGLT2 inhibitors (canagliflozin, dapagliflozin, empagliflozin, and ertugliflozin)

A
  • genital mycotic infections; Fournier’s gangrene; volume depletion; decreased eGFR; acute kidney injury; hypotension; fractures; hyperkalemia; hypermagnesemia, hyperphosphatemia; euglycemic diabetic ketoacidosis
74
Q

major adverse effects of DPP-4 inhibitors (alogliptin, linagliptin, saxagliptin, and sitagliptin)

A

pancreatitis, hypersensitivity reactions, hypoglycemia if used in conjunction with sulfonylureas; fatal hepatic failure; possible worsening of heart failure; possible and severe joint pain

75
Q

How to start insulin based on A1c?

A
  • if a1c < 8%, total daily dosing 0.1-0.2 units per kg of body weight
  • if a1 > 8%, total daily dosing 0.2-0.3 units per kg
  • start with Basal (long acting) insulin
  • STOP/reduce sulfonurleas therapy when starting basal insulin
76
Q

rapid acting (Lispro (humalog), aspart (novolog, fiasp), Glulisine (Apidra))

onset, peak, duration

A
  • Onset 5-15 mins
  • Peak 30-90 mins
  • Duration 4-6 hrs
77
Q

short acting - (regular insulin (Humulin R, novolin R))

onset, peak, duration

A
  • Onset 30-60 mins
  • Peak 2-3 hrs
  • Duration 8-10 hrs
78
Q

Intermediate (isopahen insulin, NPH, humulin N, nonovlin N)

onset peak duration?

A
  • Onset 2-4 hrs
  • Peak 4-10 hrs
  • Duration 12-18 hrs
79
Q

Long acting insulin (Glargine (Lantus, Basaglar, Toujeo)

onset peak duration?

A
  • Onset 2 to 4 hours, no peak, Duration 20 to 24 hours
  • Detemir (Levemir) – Onset 2 to 4 hours, Peak 3 to 9 hours, Duration 6 to 24 hours
  • Degludec (Tresiba) – Onset 1 hour, Peak 9 hours, Duration greater than 42 hours
    *
80
Q

screening recommendations for DM 1 peds

A
  • NEPHROPATHY: Annual screening for albuminuria with a random spot urine sample for albumin/creatinine ratio after child is 10 years old or older and has had diabetes for at least 5 years. (normal spot ACR < 30 mg/dg)
  • RETINOPATHY: Annual comprehensive and dilated eye exam after age 10 and when child has had T1DM for at least 3 to 5 years, then annually after
  • NEUROPATHY: Annual compressive foot exam starting at age 10 or after puberty has started (whichever is earlier) after diabetes duration of 5 years.
  • HYPERTENSION: Cuff blood pressure at time of diagnosis and every office visit thereafter. Elevated blood pressure should be confirmed on 3 separate days with DM 1
  • DYSLIPIDEMIA: Fasting lipid panel starting at age 10. If LDL cholesterol is less than 100 mg/dL, then repeat every 3 to 5 years. If abnormal, monitor yearly. Initial therapy should consist of optimizing glucose control and medical nutrition therapy using a Step 2 American Heart Association (AHA) diet. Statin therapy is recommended after making lifestyle changes if LDL cholesterol is greater than 160 mg/dL, or greater than 130 mg/dL with 1 or more cardiovascular risk factors. Remember that statins are contraindicated in pregnancy, so consider birth control in adolescents who require statin therapy.
  • THYROID DISEASE: Screen for thyroid disease with thyroid stimulating hormone (TSH) soon after diagnosis and improvement in glucose control. Also, consider testing for antithyroid peroxidase and antithyroglobulin antibodies soon after the diagnosis. If TSH is normal, repeat every 1 to 2 years, or sooner if patient has symptoms of hypothyroidism, thyromegaly, abnormal growth rate, or unexplained glucose variation.
  • CELIAC DISEASE: Screen for celiac disease with either tissue transglutaminase or deamidated gliadin antibodies, along with serum immunoglobulin A (IgA) level, soon after diagnosis. Recommendations for screening also include if the patient has a first-degree family member with celiac disease, growth failure, weight loss or failure to gain weight, gastrointestinal (GI) symptoms (diarrhea, flatulence, abdominal pain, or other concerns for malabsorption), or recurrent unexplained hypoglycemia or worsening of glycemic control.
81
Q

What are the available methods for delivery of insulin and monitoring blood glucose?

A
  • Insulin injection
  • Insulin pump
  • Wireless insulin pump (“Pod” style)
  • Continuous glucose monitor (CGM)
  • “Artificial pancreas”
82
Q

clinical manifestations of congenital hypothyroidism

A
  • >95% of NB’s have no or little clinical manifestations at birth
  • if present, lethargy, hypotonia, hoarse cry, feeding problems, constipation, macroglossia, open posterior fontanelle, umbilical hernia, dry skin, hypothermia, and prolonged jaundice.
  • Goiter is uncommon
    • only in infants with genetic defects in thyroid hormone synthesis
83
Q

Why and how are newborns screened for hypothyroidism?

A
  • TH essential for growth and neurological development in childhood.
    • Longer the condition goes undetected, the lower the IQ.
  • For newborn screening, use TSH testing then (T4) testing if TSH levels high
    • other places do both TSH and T4 levels
    • repeat screening at 2 weeks in case of delayed onset of hypothyroidism.
  • TSH screening alone will not identify infants with central hypothyroidism, while infants with subclinical hypothyroidism can only be detected by TSH testing.
  • don’t exclude hypothyroidism in Newborn screening if have high index of suspicion
84
Q

How is congenital hypothyroidism treated?

A
  • start Synthroid (levo) asap
  • initial dosing neonates 10-15 mcg/kg/day
  • tablets >> suspensions
    • better for dosing
    • crush into breast milk, formula, water
  • do not give with Ca, soy, iron supp
85
Q

What is the most common cause of acquired childhood hypothyroidism in the United States?

A
  • Hashimoto thyroiditis (also called chronic lymphocytic thyroiditis)
  • early to mid-puberty
  • autoimmune condition that may occur by itself or in association with other autoimmune diseases such as type 1 diabetes mellitus, Addison disease, juvenile idiopathic arthritis, or systemic lupus erythematosus.
  • increased prevalence in individuals with Down syndrome and Turner syndrome
86
Q

What are the common clinical manifestations of Hashimoto thyroiditis?

A
  • decline in linear growth, weight gain (usually minimal), fatigue, constipation, cold intolerance, poor school performance, bradycardia, dry skin, proximal muscle weakness, delayed relaxation phase of deep tendon reflexes, irregular menstrual periods, and delayed puberty. Rarely, acquired childhood hypothyroidism presents with precocious puberty.
  • thyroid gland is usually enlarged and firm with pebbly texture, or goiter.
    • atrophic thyroid glands (rather than a goiter) → final stage of thyroid failure in Hashimoto thyroiditis.
87
Q

What lab workup should you obtain for hashimotos thyroiditis?

A
  • Thyroid function tests (TSH and free T4) and thyroid antibodies (thyroid peroxidase antibody and thyroglobulin antibody) [will be high]
    • Initial findings of hypothyroidism may be elevated serum TSH concentrations and normal free T4 concentrations (subclinical hypothyroidism). As thyroid failure progresses, serum free T4 concentrations fall (overt hypothyroidism).
88
Q

What is the treatment of choice for Hashimoto thyroiditis?

A

Levothyroxine

goal: normalization of serum TSH values (no need to monitor thyroid antibodies)

89
Q

The most common physical finding in a child with congenital hypothyroidism is:

A Open posterior fontanelle

B Macroglossia

C Hypotonia

D Normal physical exam

A

Most children with congenital hypothyroidism do not have clinical manifestations of hypothyroidism due to the presence of maternal thyroid hormones or a small amount of thyroid tissue in the infant. If present, signs and symptoms of congenital hypothyroidism may include lethargy, hypotonia, hoarse cry, feeding problems, constipation, macroglossia, open posterior fontanelle, umbilical hernia, dry skin, hypothermia, and prolonged jaundice

90
Q

The most common cause of congenital hypothyroidism is:

A Abnormal development of the thyroid gland

B Decreased thyroid-stimulating hormone (TSH) levels

C Hashimoto thyroiditis

D Inborn error in thyroxine synthesis

A

Approximately 85% of cases of congenital hypothyroidism are due to thyroid dysgenesis, which includes agenesis, hypoplasia, and ectopy. Approximately 10% to 15% of cases of congenital hypothyroidism are due to inborn errors of thyroxine synthesis which are inherited in autosomal recessive pattern. Hashimoto thyroiditis is the most common cause of acquired hypothyroidism. Central hypothyroidism is due to disruption in the hypothalamus or pituitary leading to decreased TSH levels, and is a rare cause of congenital hypothyroidism.

91
Q

Which of the following lab abnormalities is associated with subclinical hypothyroidism?

A Low TSH and normal free T4

B Low TSH and high free T4

C Elevated TSH and normal free T4

D Elevated TSH and low free T4

A

C Elevated TSH and normal free T4

Subclinical hypothyroidism is characterized by elevated TSH and normal free T4. Overt hypothyroidism is characterized by elevated TSH and low free T4. Low TSH and normal free T4 is characteristic of subclinical hyperthyroidism. Low TSH and high free T4 is characteristic of overt hyperthyroidism.

92
Q

What is the most common cause of hyperthyroidism in children? In adults?

A
  • Graves disease is the most common cause of hyperthyroidism in children and adults.
  • autoimmune condition in which antibodies bind and activate the thyrotropin (aka TSH) receptor. Graves disease accounts for more than 95% of childhood and adolescent cases of hyperthyroidism, with a peak incidence of 11 to 15 years of age (female predominance).
  • In adults, Graves disease accounts for 50% to 80% of cases of hyperthyroidism, with a peak incidence between 40 and 60 years of age (again female predominance), although it can occur at any age.
  • may occur in conjunction with other autoimmune diseases, including type 1 diabetes mellitus, hypoparathyroidism, Addison disease, myasthenia gravis, vitiligo, and pernicious anemia.
93
Q

What are other causes of hyperthyroidism?

A
  • Hyperfunctioning thyroid nodules, thyrotoxic phase of autoimmune Hashimoto thyroiditis (so-called Hashitoxicosis, caused by release of preformed thyroid hormone from the inflamed thyroid gland), and factitious hyperthyroidism from exogenous thyroid hormone.
94
Q

What are clinical manifestations of Graves disease?

A
  • Weight loss, heat intolerance, difficulty sleeping, tremor, increased frequency of defecation, irritability, and menstrual irregularity.
  • Tachycardia, palpitations, and widened pulse pressure.
    • Atrial fibrillation common if > 50 yrs
  • Children
    • behavioral disturbances, decreased attention span, difficulty concentrating, emotional lability, and hyperactivity.
    • upper percentiles for height. Rare findings include localized dermopathy (pretibial myxedema) and thyroid acropachy (clubbing).
  • tremors, a shortened relaxation phase in deep tendon reflexes, fatigue, and proximal muscle weakness.
  • Graves ophthalmopathy
    • Proptosis, periorbital edema, & inflammation
  • Gynecomastia, reduced libido, and erectile dysfunction.
95
Q

What are typical lab results in Graves disease?

A
  • low/undetectable TSH, elevated T4
  • T3 may also be elevated, and some individuals may have low TSH, normal free T4, and elevated T3. Thyrotropin receptor antibodies (TRAbs) are present in 95% of affected patients.
  • Thyroid peroxidase and antithyroglobulin antibodies may be positive
  • Thyroid stimulating immunoglobulins (TSI) may also be positive but this test has less sensitivity and a negative result does not exclude Graves disease.
96
Q

other studies for graves disease

A
  • 24-hour radioiodine uptake:
    • measure uptake at 4 and 24 hours
    • high: graves, toxic nodular goiter
    • low: inflamed/destructed gland (thyroiditis), iodine exposure
  • 24-hour radioiodine scan:
    • do same time uptake
    • differentiates from Graves disease, toxic adenoma, and toxic multinodular goiter.
    • Graves disease,
      • generally diffuse and homogenous
      • focal in a toxic adenoma and heterogeneous with multiple areas of focal increased and suppressed uptake in toxic multinodular goiter.
  • Pertechnetate thyroid scan:
    • Provides an image of the thyroid and can distinguish between Graves disease, toxic adenoma, and toxic multinodular goiter.
    • only 20 minutes to perform; but no numerical measurement of uptake and cannot be used to dose radioiodine therapy.
97
Q

if hyperthyroid and have irregular heart rhythm, get

A

ECG to determine atrial fibrillation is present

98
Q

In postmenopausal women and other patients at risk for bone loss with hyperthyroidism

A

get a bone-density test should be obtained.

99
Q

Large goiters can be associated with airway or esophageal obstruction. If an affected patient has difficulty breathing or swallowing,

A
  • CT or MRI of the neck should be obtained
100
Q

What are the 3 modalities available for the treatment of Graves disease?

A
  • antithyroid medication
    • reduce thyroid hormone production and block its effect peripherally.
    • methimazole (for 2nd/3rd trimester) and propylthiouracil( for 1st trimester): inhibit thyroid hormone production.
      • methamizole SE pruritic papular or urticarial rash, granulocytopenia or agranulocytosis (which typically is accompanied by fever, sore throat, mouth sores, and other systemic symptoms consistent with infection) and hepatitis.
    • BB for cardiovascular findings.
  • radioiodine ablation of the thyroid gland
    • orally administered iodine-131 concentrates in the thyroid gland and induces cell death.
  • surgical thyroidectomy
    • surgery if fail initial medical therapy, relapse after cessation of antithyroid drugs, have significant drug reactions, have large goiters, or severe ophthalmopathy.
    • complications: hypoparathyroidism and recurrent laryngeal nerve damage. As with RAI, permanent hypothyroidism is the goal of therapy.
      *
101
Q

Which of the following lab abnormalities is associated with subclinical hyperthyroidism?

A

C Low TSH and normal free T4

Low TSH and normal free T4 is characteristic of subclinical hyperthyroidism. Low TSH and high free T4 is characteristic of overt hyperthyroidism. Subclinical hypothyroidism is characterized by elevated TSH and normal free T4. Overt hypothyroidism is characterized by elevated TSH and low free T4.

102
Q

In hyperthyroidism due to Graves disease, what are the expected findings on 24-hour radioiodine uptake and thyroid scan?

A

Increased uptake with diffuse homogenous appearance on scan

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