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CMS200 > Week 5- Hypothyroid > Flashcards

Week 5- Hypothyroid Flashcards

1
Q

what is hypothyroid

A

inadequate production of T4 T3 by thyroid gland

OR

insufficient stimulation by hypothalamus (TRH) or pituitary gland (TSH)

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2
Q

iatrogenic hypothryoid

A

from medical exam or treatment

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3
Q

primary vs secondary vs tertiary hypothyroid

A

primary @ thyroid (t4 t3)

secondary (AKA central) @ pituitary (TSH)

territory (AKA central) @ hypothalamus (TRH)

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4
Q

what type of hypothyroid (1,2,3) is most common

A

primary (95% of cases) are at the thyroid gland level

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5
Q

ethology of primary hypothyroidism’s (5)

A
  1. iodine deficiency
  2. autoimmunity
  3. transient
  4. congenital abnoramilties
  5. infiltrative thyroid disease (rare)
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6
Q

what is most common cause of hypothyroid in North America

A

autoimmune

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7
Q

2 types of autoimmune hypothryoid? which is common?

A
  • chronic autoimmune thyroiditis (Hashimoto thyroiditis) - most common
  • subacute granulomatous thyroiditis (de Quervain disease) - rare
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8
Q

what is transient causes of primary hypothryoid?

A

postpartum thyroiditis, pregnancy, silent thyroiditis, subacute thyroiditis, thyroiditis associated with TSH receptor-blocking antibodies

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9
Q

what congenital abnormalities can cause primary hypothryoid?

A

aplasia/agenesis of thyroid, dyshormonogenesis

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10
Q

what is infiltrative thyroid diseases that can cause primary hypothryoid

A

(rare): amyloid goiter, black thyroid, cystinosis, diffuse lipomatosis, hereditary hemochromatosis, langerhans cell histiocytosis, reidel’s thyroiditis, sarcoidosis, scleroderma

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11
Q

what is the most common cause of central (secondary and tertiary) hypothyroid

A

pituitary adenomas

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12
Q

etiology of central (secondary + tertiary) hypothyroidism (7)

A
  • pituitary tumors
    -sheehan syndrome
    -lymphocytic hypophysitis

– brain tumors compressing hypothalamus
- thyroid releasing hormone (TRH) resistance
- TRH deficiency

  • radiation therapy to the brain
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13
Q

what is Sheehan syndrome

((etiology of central (secondary + tertiary) hypothyroidism))

A

a rare condition involving injury to your pituitary gland
following extreme blood loss during childbirth

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14
Q

what is lymphocytic hypophysitis

((etiology of central (secondary + tertiary) hypothyroidism))

A

a rare, autoimmune condition of the pituitary gland

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15
Q

iatrogenic hypothryoid

A

MEDICATIONS
- amiodarone
- antibiotics: rifampin, ethionamide
- anti-convuslants: phenytoin, carbamazepine
- anti-neoplastics: tyrosine kinase inhibitors
(sunitinib, imatinib), bexarotene, interleukin-2,
- dopamine - opioids
- prednisone
procedures
anti-CTLA-4 and anti-PD-L1/PD-1
- interferon-α -
- lithium
- perchlorate -
- phenobarbital
- stavudine
- thalidomide

PROCEDURES
-radiotherapy to head or neck area
-thyroid radioactive iodine -therapy thyroid surgery

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16
Q

effects of thyroid hormones on the body (and therefore hypothyroid is opposite)

A

increase metabolism
increase body heat
increase GI motility
neuronal development
SNS (fight or flight)- increase HR, RR, mental alertness

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17
Q

impacts of low thyroid hormones on body functions

A
  • skin: reduced sweating, skin discoloration, coarse hair (or loss), brittle nails, non-pitting edema, periorbital edema
  • hematologic: hypocoagulability (bleeding risk), pernicious anemia
  • cardiovascular: bradycardia, pericardial effusion, diastolic hypertension
  • respiratory: shortness of breath on exertion, rhinitis, decreased exercise capacity
  • gastrointestinal: constipation, decreased taste, nonalcoholic fatty liver disease
  • reproductive: menstrual irregularities, decreased libido, infertility, miscarriage,
    erectile dysfunction, delayed ejaculation, reduced sperm morphology
  • neurologic: hashimoto encephalopathy, myxedema coma
  • muscular: weakness, cramps, myalgias (high serum creatine kinase)
  • mental: depression, anxiety, poor concentration, decreased short-term memory
  • metabolic: hyponatremia, hyperlipidemia, hypercholesterolemia, hyper-
    homocysteinemia, hyperuricemia, reduced drug clearance (e.g. hypnotic, opioid)
  • weight gain
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18
Q

what does hypothyroid do to cause symptoms (2 main effects)

A

generalized slow metabolism or accumulation of polysaccharides in interstitial spaces

generalized slow metabolism causes constipation, weight gain, fatigue, brittle nails, bradycardia, slow speeach

the accumulation of polysaccharides causes things to do with water retention and swelling (puffy face, pleural effusion, pericardial effusion, weight gain)

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19
Q

common symptoms of hypothyroid

A
  • weight gain
  • fatigue, lethargy, depression
  • weakness, dyspnea on exertion, arthralgias or myalgias, muscle cramps
  • menorrhagia
  • constipation
  • dry skin, hair changes (dryness, thinning, loss)
  • headache, paresthesias, carpal tunnel syndrome, raynaud syndrome
  • cold intolerance
  • voice changes
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20
Q

common clinical findings in hypothyroid

A
  • bradycardia
  • diastolic hypertension
  • thin, brittle nails
  • thinning hair or alopecia (including lateral 1⁄3 of eyebrow thinning)
  • peripheral edema
  • puffy face and eyelids
  • skin pallor or yellowing (carotenemia)
  • delayed relaxation of deep tendon reflexes
  • goiter (chronic autoimmune hypothyroidism: firm, then shrinks with fibrosis)
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21
Q

what is a goiter

A
  • enlargement of the thyroid gland, can be diffuse, nodular or multinodular
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22
Q

what is an endemic goiter from

A

iodine deficiency

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23
Q

physiologic goiter

A

adolescence and pregnancy

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24
Q

when can a goiter be a symptoms of hyperthyroidism

A

Grave disease, toxic nodular/multinodular goiter thyroid cancer or infiltrative disease (e.g. sarcoidosis)

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25
Q

when a goiter can be a symptom of inflammatory disorders (thyroiditis)

A

autoimmune, postpartum,
silent, radiation, subacute, suppurative

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26
Q

what type of thyroid condition are gaiters most common in

A

can be euthyroid, hypothyroid or hyperthyroid - most goiters are euthyroid

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27
Q

management for goiter

A

referral for ultrasound, fine-needle aspiration biopsy (if nodule), treatment varies with serum findings

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28
Q

symptoms for autoimmune hypothryoid

A

none alone have a high LR+ when combine multiple symtpoms get a better picture

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29
Q

what is euthyroid sick syndrome

A

often seen in hospitalized settings (patients with severe critical illness, deprivation of calories, and following major surgeries)

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30
Q

what is ridel thyroiditis

A

a rare inflammatory disease of the thyroid, causing compression and fibrosis of the thyroid and adjacent tissues

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31
Q

what is subacute thyroiditis

A

an immune reaction of the thyroid gland that often follows an upper respiratory infection

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32
Q

what is thyroid lymphoma

A

a rare thyroid malignancy where lymphoid cancer cells cause the thyroid gland to rapidly enlarge

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33
Q

if TSH is normal but symptoms persists; what things may co-exist with hypothryoid too

A

anemia (vitamin B12 or iron deficiency) autoimmune (rare)
- adrenal insufficiency (aka. Addison’s disease)
- atrophic gastritis with pernicious anemia
- celiac disease or gluten sensitivity
- diabetes mellitus type 1
- rheumatoid arthritis chronic kidney disease liver disease menopause
mental health disorder (i.e. depression, anxiety or somatoform disorder) obstructive sleep apnea
viral infection (e.g. mononucleosis, lyme disease, HIV)

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34
Q

things that can causes aberrations in lab tests: high TSH

A

Acute psychiatric illness (transient,14%) Anti-mouse antibodies
Antithyrotropin antibodies
Anti-TSH receptor antibodies Autoimmune disease (assay interference)
Drugs Amiodarone
Amphetamines Atypical antipsychotics Dopamine agonists Heroin Phenothiazines Exercise before testing
Following prolonged primary hypo- thyroidism
Heterophile antibodies
Laboratory error
Macro-thyrotropin
Nonadherence to thyroid replacement therapy
Older adults (especially women) Pituitary TSH hypersecretion Recovery from acute nonthyroidal illness (transient)
Strenuous exercise (acute)
Sleep deprivation (acute)
TSH resistance

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35
Q

what factors may cause aberrations in lab tests: low t4 and t3

A

Acute psychiatric illness Cirrhosis
Familial thyroid-binding globulin deficiency
Laboratory error Nephrotic syndrome Severe illness Drugs
Androgens
Antiseizure drugs (Carbamazepine, Phenobarbital, Phenytoin)
Asparaginase Carbamazepine (T4) Chloral hydrate Corticosteroids
Diclofenac (T3), naproxen (T3) Didanosine
Fenclofenac
5-Fluorouracil
Halofenate
Imatinib
Mitotane
Nicotinic acid
Oxcarbazepine
Phenobarbital
Phenytoin
Salicylates, large doses (T3 + T4) Sertraline
Stavudine T3 therapy (T4)

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36
Q

what 2 natural health products to be aware of affecting thyroid levels in labs

A
  1. biotin
  2. st johns wort
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37
Q

what does biotin do to thyroid levels

A

falsely high fT4 and fTA3
falsely low TSH

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38
Q

does biotin affect thyroid function

A

no- but looks like it on labs

does not impair thyroid function but can interfere with laboratory testing
falsely high fT4 and fT3
falsely low TSH
- appears as hyperthyroidism or thyroid replacement dosing is too high
- avoid interference by having patients discontinue biotin at least 48hr prior to
testing

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39
Q

what does st johns warts do to thyroid

A

transiently elevated TSH levels (no effect on fT4)

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40
Q

TSH and fT4 is primary vs central (secondary or tertiary) hypothryoid

A

central= low TSH, low fT4

primary= high TSH, low fT4

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41
Q

what is central hypothyroid

A

hypothyroidism due to insufficient stimulation by thyroid stimulating hormone (TSH) of an otherwise normal thyroid gland; can be secondary (pituitary) or tertiary (hypothalamus) in origin

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42
Q

how common is central hypothyroid

A

< 1% of hypothyroid cases

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43
Q

what could cause central hypothyroid in children

A

craniopharyngiomas, hx of cranial irradiation (brain or hematological cancer)

44
Q

what could cause central hypothyroid in adults

A

pituitary macroadenomas, pituitary surgeries or post-irradiation
transient: sick euthyroid syndrome, over-replacement of T4 (primary hypothyroidism)

45
Q

what are the symptoms ofd central hypothyroidism

A

hypothryoid symptoms but milder

46
Q

diagnosis of central hypothryoid via blood markers

A
  • low serum fT4, relatively low serum TSH
47
Q

management of central hypothyroidism

A

referral - TRH Stimulation Test

48
Q

what is subclinical hypothyroidism

A

endocrine disorder presenting with elevated TSH but normal thyroxine (fT4)

49
Q

symptoms of subclinical hypothyroid

A

asymptomatic (most often) or hypothyroid symptoms

50
Q

diagnosis of subclinical hypothyroid (blood markers)

A
  • elevated TSH > 4.0 mIU/L; fT4 within range

serum TSH and fT4 +/- symptoms +/- TPO antibodies

51
Q

when would you treat vs when would you not treat subclinical hypothryoid

A

treat: TSH >10, TPO antibodies present, patient symptomatic or has CVD risk factors (i.e. high cholesterol)

dont treat: if TSH between 4-10mIU/L

treatment recommended if TSH >10 mIU/L, TPO antibodies present, patient is symptomatic or has cardiovascular risk factors (e.g. ↑ cholesterol)
if TSH is 4.0 - 10.0 mIU/L, monitor TSH q6-12mo

52
Q

prognosis of subclinical hypothyroid

A

60% resolve without intervention within 5yrs, 2-6% develop overt thyroid dysfunction (if anti-TPO present, risk is up to 50% over 20 yrs)

  • increased risk of fracture, ischemic heart disease and heart failure if TSH > 10 mIU/L
53
Q

primary hypothryoid

A

endocrine disorder presenting with elevated serum TSH and low thyroxine (fT4)

54
Q

what other diseases does primary hypothryoid usually present with

A

autoimmune disease (e.g. T1DM, celiac disease), Down or Turner syndrome

55
Q

what is the diagnosis for primary hypothryoid via blood

A

high TSH, low fT4

  • high thyrotropin (TSH) > 4.0 mIU/L, low thyroxine (fT4) < 12 pmol/L
  • thyroid peroxidase antibody (anti-TPO) testing does not help diagnosis, but
    indicates autoimmune etiology
56
Q

how to manage primary hypothyroid

A

thyroid hormone replacement therapy (T4)

57
Q

CTFPHC screening recommednations

A

dont screen in asymptomatic and non pregnant

  • The Canadian Task Force on Preventive Health Care (CTFPHC) strongly recommends against screening for thyroid dysfunction in asymptomatic, nonpregnant adults
  • not likely to confer clinical benefit, but could lead to unnecessary treatment for some patients and consume resources
  • treating asymptomatic adults for screen-detected hypothyroidism may result in little to no difference in clinical outcomes
58
Q

current evidence for screening

A

The US Preventive Services Task Force (USPSTF) states that current evidence is insufficient to assess the balance of benefits and harms of screening for thyroid dysfunction in nonpregnant, asymptomatic adults

59
Q

management for primary vs subclinical vs secondary hypothryoid

A

primary: Levothyroxine
(T4 replacement therapy)

subclinical: if TSH > 10 mIU/L + positive thyroid antibodies, cardiovascular risk, or treatment-resistant depression then consider Levothyroxine
(T4 replacement therapy)

secondary: brain MRI (for tumor)

60
Q

what happens to thyroid hormone in pregnancy

A

20% to 40% increase in thyroid hormone requirement as early as 4 weeks

61
Q

what does estrogen do to thyroid hormones

A

estrogen-mediated increase in thyroid-binding globulin, increased volume of
distribution of thyroid hormone, as well as the placental metabolism and
transport of maternal thyroxine

also thyroid gland size icnrease

62
Q

what trimesters levels for TSH, fT4, fT3 (chart of slide 36)

A

TSH increases over the trimesters
ft4 and ft3 decrease slightly

63
Q

what happens to thyroid antibodies in pregnancy

A

thyroid antibodies decrease drastically later in pregnancy; so dont test for autoimmune thyroid then bc worst be accurate

64
Q

what’s the hypothryoid that would happen in prgnengcy

A

chronic autoimmune hypothryoid

around 1%

65
Q

what are the effects of having hypothryoid in pregnancy

A
  • miscarriage
  • gestational hypertension
  • pre-eclampsia
  • anemia
  • postpartum hemorrhage
  • abruptio placentae
  • preterm birth + low birth weight - fetal neurocognitive deficits
66
Q

what can thyroid hormone replacement therapy do in perngnacy

A

(levothyroxine, LT4):
- little to no effect on hypertensive disorders and placental abruption
- reduces miscarriage, preterm birth
- improves fetal intellectual development

67
Q

what has the highest odds ratio in hypothyroid related complications in pregnancy

A

post partum thryioditis risk

68
Q

if known to have hypothryoid before prenancy what should u do to medication dose

A

increase

increase thyroxine by 30% once pregnancy is confirmed unless preconception TSH <1.5 mIU/L

69
Q

postpartum thryoidistis

A

abnormal TSH level within the first 12 months postpartum in the absence of a toxic thyroid nodule or thyrotoxin receptor antibodies

increased risk of permanent hypothyroidism

70
Q

what increases risk of postpartum thyroiditis

A

risk increased in T1DM and those with thyroglobulin (TG) or thyroperoxidase (TPO) autoantibodies

71
Q

postpartum thyroiditis symptoms

A

can mimic the fatigue typically following delivery or postpartum depression
43% present with symptoms of hypothyroidism; 32% present with symptoms of hyperthyroidism; 25% of patients present with symptoms of hyperthyroidism followed by hypothyroidism and then recovery

72
Q

postpartum thyoiditis’ hyper vs hypo labs

A
  • hyperthyroid state: low serum TSH, high-normal fT4 and fT3
  • hypothyroid state: high serum TSH, low-normal fT4
73
Q

hypothyroidism and relative risk of other autoimmune diseases; what does it increase the most with

A

Addisons disease

74
Q

hypothyroid and celiac disease ; what needs to happen to medications for thyroid ? what can alter these changes?

A

increase meds, but maybe not if go gluten free

increased therapeutic dose (nearly 50% more) needed for patients with hypothyroidism and celiac disease
- dose often can be reduced by following a gluten-free diet
- gluten-free diet doesn’t significantly affect thyroid antibody levels

75
Q

Addison disease/ adrenal insufficiency

A

an acquired primary adrenal insufficiency due to autoantibodies causing destruction of adrenal cortical tissue; rare, but potentially life-threatening emergency

76
Q

symptoms of Addison disease

A

fatigue, generalized weakness, weight loss, nausea, vomiting, abdominal pain, dizziness, tachycardia, and/or postural hypotension; hyperpigmentation

77
Q

what do you need to diagnose addisons

A

low cortisol high ACTH
low Na, high K

  • morning cortisol (<140nmol/L) combined with ACTH (2x upper limit)
  • low Na+, high K+ and hypotension
78
Q

what to treat addison

A

referral for ACTH stimulation for confirmation and comanagement

79
Q

prognosis of addison

A

up to 50% of patients may develop another autoimmune disease adrenal crisis if not treated (hypoglycemia, hypotension, shock, death)

80
Q

hypothyroid and Addison

A

thyroid hormone replacement may precipitate an adrenal crisis in unrecognized patients:
- pain in back, abdomen or legs
- vomiting + diarrhea leading to dehydration and low blood pressure
- progresses to loss of consciousness and death

81
Q

what has good LR- in Addison/ primary adrenal insufficiency

A

AM cortisol >380
serum basal cortisol >350

therefore if dont see these things than rule out lol idk

82
Q

what is the order of treatment for hypothyroid and Addison/adrenal

A

1st Addison than hypo

  • in patients with suspected or known adrenal insufficiency, testing and treatment for adrenal insufficiency should be done first
  • adrenal insufficiency can be associated with subclinical hypothyroidism that is reversible with treatment of adrenal insufficiency
  • in confirmed adrenal insufficiency, thyroid tests should be reassessed following adequate treatment of adrenal insufficiency
83
Q

what heart thing does hypothryoid increase

A

increased risk of coronary artery disease in overt hypothyroidism

84
Q

what does hypothryoid effect on the heart

A
  • reduces cardiac output, cardiac contractility and heart rate
  • increases peripheral vascular resistance
  • increases atherosclerotic risk factors, most notably:
  • hypercholesterolemia
  • diastolic hypertension
85
Q

what effect can thyroid replacement therapy have on the heart

A

((precipitate acute coronary syndrome or an arrhythmia))

thyroid replacement therapy increases heart rate + contractility (therefore myocardial oxygen demand), and can precipitate acute coronary syndrome or an arrhythmia - start with low dosing thyroid replacement and proceed slowly

86
Q

what happens with hypothyroidism and age? what to do with meds?

A
  • TSH increases with age, but fT4 does not
  • thyroid replacement therapy started at lower doses than in younger patients
87
Q

reasons why a stable TSH may become abnormal

A
  • change in adherence (e.g. missing a dose) or timing relative to eating
  • malabsorption (e.g. celiac disease, helicobacter pylori gastritis)
  • pregnancy
  • initiation of new medication:
  • androgens or estrogens
  • heroin / methadone
  • medications that decrease absorption (see next slide)
  • medications that reduce levothyroxine conversion to T3 (amiodarone,
    high-dose beta-adrenergic agonists, glucocorticoids)
  • medications that may reduce serum protein binding of levothyroxine
    (carbamazepine, phenytoin)
  • SSRI or tricyclic antidepressants
  • tamoxifen
88
Q

what medication can reduce levothyroxine absorption and should therefore be taken 4 hours before or after

A
  • bile acid sequestrants (e.g. colesevelam, cholestyramine, colestipol)
  • calcium carbonate
  • ferrous sulfate
  • intragastric pH elevation via hypochlorhydria
  • antacids (e.g. aluminum, magnesium)
  • proton pump inhibitors - simethicone
  • sucralfate
  • ion exchange resins (e.g. sodium polystyrene sulfate, sevelamer)
  • orlistat
89
Q

how does levothyroxine effect diabetes medication

A

may increase dosing of diabetes medications to achieve glycemic control

90
Q

levothyroxine and food interactions

A

patients who regularly consume walnuts, dietary fibre, soybean flour, cottonseed meal or grapefruit juice may need higher doses of levothyroxine

91
Q

ketamine therapy and levothyroxine interactions

A

concurrent use may result in significant hypertension and tachycardia

92
Q

oral anticoagulants and levothyroxine

A

may increase effects

93
Q

SSRIs and TCAs interact with levothyroxine

A

may increase therapeutic and toxic effects

94
Q

sympathomimetic and levothyroxine

A

concurrent use may increase risk of cardiac event in patients with coronary artery disease

95
Q

complication of hypothyroid if left untreated, patient at risk of:

A
  • cognitive impairment
  • susceptibility to bacterial pneumonia
  • developing megacolon
  • developing cardiovascular disease (including heart failure)
  • rhabdomyolysis (may lead to kidney dysfunction)
  • infertility and miscarriage
  • myxedema
  • mortality
96
Q

what is a myxoedema coma

A

rare, severe, life-threatening manifestations of hypothyroidism

97
Q

who and when is myedema coma most likely in

A

female, > 60 yrs, winter
inadequate/interrupted treatment, undiagnosed hypothyroidism, or presence of acute illness (e.g. sepsis, stroke, heart failure, infection (e.g. pneumonia), trauma), medications (sedatives, antidepressants, hypnotics, anesthetics, opioids, etc)

98
Q

what are symptoms of myxoedema coma

A

altered mental status (lethargy, impaired cognition, confusion, coma), seizure(s), abdominal pain, N/V, respiratory failure, fluid/urine retention (incl. ascites)

99
Q

what clinical manifestations that are of myxoedema coma

A
  • hypothermia (<35.5°C), hypotension, bradycardia, hypoventilation
  • non-pitting edema, hyponatremia, hypoglycemia, arrhythmia(s), dry skin
100
Q

management for myxedema coma

A

911 emergency

101
Q

when to refer to an endocrinologist for hypothyroid

A
  • age 18 yrs or younger
  • elusive euthyroid state
  • myxedema, suspected
  • pregnancy
  • simultaneous presence of another endocrinopathy
  • structural changes in thyroid gland (e.g. goiter, nodule)
  • symptoms do not improve or worsen after treatment with levothyroxine (T4)
  • unstable ischemic heart disease
102
Q

hypothyroid symptoms from

generalized slow metabolism or accumulation of polysaccharides in interstitial spaces

A

weight gain
fatigue
sensitive to cold
constripation
dry skin
puffy face
hoarse voice
muscle weakness
thin hair
slow HR
depsesssion
impaired memroy
enlarged goiuter
irregular periods

103
Q

PAGE 59 CHART

A

REALLY GOOD FOR DIFFERENTIATION THE HYPOTHYROID TYPES

104
Q

when to test antibodies for hypothyoid

A

antibodies aren’t routinely tested since majority of cases are autoimmune

105
Q

subclinical hypo treat

A
  • subclinical hypothyroidism often resolves on its own, but treatment may reduce risk of fracture, ischemic heart disease and heart failure if TSH > 10mIU/L

CMS200 (18 decks)

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