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533 > Final: Thyroid/DM > Flashcards

Final: Thyroid/DM 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 [high TSH]
    • thyroid is the problem
    • autoimmune (most common)
    • drugs
  • Secondary aka centra hypothyroidism [low TSH]
    • damage to pituitary/tumor
    • Less commo
  • pituitary adenoma hypothyroidism
    • ​low TSH low T4
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3
Q

hypothyroidism risk factors

A
  • Amiodarone (contains iodine)
  • Female
  • Older age
  • Iodine deficiency
  • Irradiation 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

thyroid function tests

A
  • TSH most sensitive indicator of thryoid function
    • ​Order TSH first! If abnormal, order free T4
  • HypERthyroid (TSH < 0.3), hypOthyroid (TSH > 4), euthyroid 0.3-4)
  • If abnormal TSH = check thyroid peroxidase TPO antibody
    • Will be elevated in chronic autoimmune thyroiditis (Hash/Graves)
  • 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 CAD or >65 yrs
  • Recheck TSH in 1-2 months 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 have established hypothyroidism and taking levothyroxine and she becomes pregnant, requirements during pregnancy are higher by dose increasing by 30%
    • 1st: < 0.5-2.5
    • 2nd & 3rd: < 3
  • monitor TSH every 4 weeks until 30 weeks, then once in 3rd trimester
  • after pregnancy, reduce dose and recheck TSH 6 wks later
  • if on birth control pills, need to increase dose
    • Estrogens partially block the action of thyroid hormones, making them less effective.
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8
Q

Referral hypothyroid pt to endocrinology if

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
  • Painful, tender, thyroiditis
  • 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
  • 3 months post partum onset
  • thyrotoxic/hyperthyroid then 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 causing hypERthyroidism
  • 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
  • hypERthyroidism = Low TSH, Elevated T4
  • Thyrotropin receptor antibodies
    • Positive in 98% of patients with untreated Graves’
    • Helps confirm diagnosis
  • Elevated 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

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 (no serum bc serum glucose varies 10-20% while plasma varies 1-3% in testing)
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21
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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22
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 (3 year intervals if normal screening)
  • Screen younger than 45 yrs old if 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
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23
Q

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

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

AND:

  • 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)
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24
Q

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

A
  • highest in the decade after 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
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25
Q

range for impaired fasting glucose

range for impaired oral glucose tolerance test

A

fasting: blood sugar 100-125

(if results give 1 impaired and 1 126, further testing needed to confirm diagnosis)

oral: 140-199

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26
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
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27
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)
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28
Q

tests to order to diagnose type ONE 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
  • 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.
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29
Q

consider screening what other autoimmune diseases soon 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.
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30
Q

when is metformin safe to use?

A
  • Metformin is SAFE to use if > 30 GFR
  • No in:
    • ​lactic acidosis
    • CHF
    • severe renal function < 30 GFR
    • live faiure
    • heavy alochol use
    • underoing major surgery
  • stop metformin if doing study with iodine contrast and begin again 2 days later
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31
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)
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32
Q

when is bariatric surgery considered?

A

if BMI > 35 or can be < 30 if have chronic conditions (db, HTN or cardiovac dz)

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33
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
    • Adults: A1c goal: < 7%.
    • Children/adolescents: < 7.5%
  • 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
    • Adult goal: SBP < 140 / < 90
    • Children and adolescents: < 130 / < 80 OR < 90th % 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→ start on statin
    • Get lipid profile at the time of diagnosis, and at least q 5 years after if < 40 yrs old
    • 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 yearly for DM 2
      • DM1, starting age 10 yrs with 5 yr dx duration
        • if have foot deformities, or ulcers = screen every visit
    • 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.
    • Screening for diabetic gastroparesis
  • Screening for retinopathy
    • Dilated retinal exam
      • DM 2: time of dx then q 1-2 years
      • DM 1: > 10 yrs old for DM 1 for 5 yrs +
  • Screening for nephropathy
    • DM 2: Serum creatinine at least YEARLY to get GFR
    • DM 1: child is at least 10 yrs old with at least 5 year diagnosis, get yearly
    • 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 (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, get PCV13 first, then 6 to 12 months later PPSV23.
    • Flu vaccine yearly when > 6 months with diabetes
    • Hepatitis B vaccine 19 yrs and older
  • Tobacco use assessment
34
Q

what is used instead of micro and macroalbuminuria?

A

persistent albuminuria for >30 mg (abnormal)

35
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
36
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)
37
Q

if A1C is <7.5%…

A

mono therapy for 3 months:

  • 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

38
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.
39
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.
40
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).
41
Q

if A1C > 7.5…

A
  • lifestyle modifications, metformin, AND [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
42
Q

which diabetic treatment options are injectable form

A

GLP-1 receptor agonists, pramlintide (Similin), and most insulins

43
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

44
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
45
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
46
Q

thiazolidinediones (Pioglitazone)

A

1-1.5% reduced

  • Increases insulin sensitivity of skeletal muscle, adipose tissue, and the liver
47
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)

48
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.
49
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)

50
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

51
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
52
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
53
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
54
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
55
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
56
Q

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

A
  • Onset 2-4 hrs
  • Peak 4-10 hrs
  • Duration 12-18 hrs
57
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
    *
58
Q

screening recommendations for DM 1 peds

A
  • NEPHROPATHY: Yearly 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: Yearly dilated eye exam after age 10 and when child has had T1DM for at least 3 to 5 years
  • NEUROPATHY: Yearly compressive foot exam starting at age 10 or after puberty has started (whichever is earlier) after diabetes duration of 5 years.
  • HYPERTENSION: 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 if LDL > 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 : TSH soon after diagnosis and improvement in glucose control.
    • 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: Get tissue transglutaminase or deamidated gliadin antibodies, and serum immunoglobulin A (IgA) level, soon after diagnosis.
    • esp if 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.
59
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”
60
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
61
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.
  • NB Screening: TSH testing, if high, get (T4) testing
    • repeat at 2 weeks (for delayed onset)
  • 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 suspicion
62
Q

How is congenital hypothyroidism treated?

A
  • start Synthroid (levo) asap 10-15 mcg/kg/day
  • tablets -> crush into breast milk, formula, water
  • do not give with Ca, soy, iron supp
63
Q

What is the most common cause of acquired childhood hypothyroidism in the U.S.?

A
  • Hashimoto thyroiditis (aka chronic lymphocytic thyroiditis)
  • early to mid-puberty
  • can be a/s with type 1 diabetes mellitus, Addison disease, juvenile idiopathic arthritis, or lupus
  • higher in Down syndrome and Turner syndrome
64
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.
  • 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.
65
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).
66
Q

What is the treatment of choice for Hashimoto thyroiditis?

A

Levothyroxine

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

67
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

68
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.

69
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.

70
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.
71
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.
72
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.
73
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.
74
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.
75
Q

if hyperthyroid and have irregular heart rhythm, get

A

ECG to determine atrial fibrillation is present

76
Q

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

A

get a bone-density test should be obtained.

77
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
78
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.
      *
79
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

80
Q

what do thyroid scans/imaging assess?

A
  • the causes of hypERthyroidism (Graves, toxic nodules, thyroiditis) or functional of a nodule (NOT thyroid function)
  • iodine isotope scans
  • U/S = anatomy of gland and differentials solid from cystic nodules and for fine needle easpiration
81
Q

Diagnostic criteria for diabetes mellitus

A

Fasting blood/plasma glucose > 126

or oral glucose tolerance test (75g) with plasma glucoes > 200 mg 2 hrs after getting glucose

or A1C > 6.5

or 2 hour 75g oral glucose tolerance test > 200 at 2 hours

**need to do 2 tests on 2 different days to be diagnostic

82
Q

Metformin monitoring

A

metformin reduces A1c 1-1.5% (most are 0.5-1.5%)

doesn’t cause hypoglycemia

monitor vitamin B12 (causes deficiency)

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