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Diagnosis and Management > Endocrine Part 1 Adrenal, Thyroid > Flashcards

Endocrine Part 1 Adrenal, Thyroid Flashcards

1
Q

A Closer Look at Hormone Function

  • Releasing hormones from _____ – can be ____tory or ____tory -> anterior pituitary or posterior pituitary
  • Posterior pituitary releases only (1) (considered more part of the nervous system bc made up of axons)
A
  • Releasing hormones from hypothalamus – can be inhibitory or excitatory -> anterior pituitary or posterior pituitary
  • Posterior pituitary releases only argenine vasopressin (considered more part of the nervous system bc made up of axons)
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2
Q

How Hormones Transmit their Signals

  • Water soluble: our ____ or ____ derived hormones travel on their own (insulin, parathyroid hormone) – bind _____ cell surface receptors and acts through the (1) system
    • (1) hormone is the only exception, is lipid soluble, and needs a binding globulin + nuclear receptor
  • Lipid soluble: our ______ derived hormones (corticosteroids, sex hormones testosterone, estradiol) have to – binds to (1) receptors and act through (1)
A
  • Water soluble: our amino acid or protein derived hormones travel on their own (insulin, parathyroid hormone) – bind directly cell surface receptors and acts through the second messenger system
    • Thyroid hormone is the only exception, is lipid soluble, and needs a binding globulin + nuclear receptor
  • Lipid soluble: our cholesterol derived hormones (corticosteroids, sex hormones testosterone, estradiol) have to – binds to nuclear receptors and act through gene transcription
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3
Q

Hypothalamic/Anterior Pituitary/End Organ Chart

A
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4
Q

The Adrenal Cortex – Anatomy and Imaging

Imaging of choice to visualize adrenals (2)

Look for th_____, n______

  1. Signs of non-concerning/functional adrenal nodule =
  2. Signs of a concerning nodule =
A

CT or MRI (cannot visualize with US)

Thickening, Nodules

  1. Homogenous, lipid rich
  2. Heterogenous, non lipid rich interior, bright and dark signal – worrying about pheochromocytoma, adrenal cortical carcinoma, mets from other areas, anything >4cm is concerning, not being smooth
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5
Q

Adrenal Cortex Homeostasis

Hypothalamic hormone (1) → Pituitary hormone (1) → acts on

If the hypothalamus is damaged, can aldosterone still be released?

  1. Glomerulosa to secrete (1) → acts on (1) receptor
  2. Fasciculata to secrete (1) → acts on (1) receptor
  3. Reticulosa to secrete (1) → acts on (1) receptor
A

CRH → ACTH

YES, core regulation of aldosterone by the RAAS system

  1. Aldosterone → Mineralocorticoid receptor (MR)
  2. Cortisol (→ corticosteroid binding globulin) → Glucocorticoid Receptor
  3. Androgens (testosterone, sex hormone binding globulin) → Androgen Receptor
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6
Q

Role of Aldosterone

The Adrenal Cortex- Role in Homeostasis

  • Sodium _____ (preserves ____)
  • Potassium ______
  • R____-A____ mediated
A
  • Sodium absorption (preserve volume)
  • Potassium secretion
  • Renin-ATII mediated
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7
Q

Role of Cortisol

The Adrenal Cortex - Role in Homeostasis

  1. Fuel m_____ – Preserve glucose availability (f___) and increase supply (st___)
  2. Increase peripheral ______ resistance
  3. Increase Hepatic ______ Production (HGP)
  4. P_____ catabolism – substrates available for HGP
  5. ____lysis for HGP
  6. Physiologic effect on b____
  7. Anti-in_____, st____ responses
  8. W____ balance – needed to increase free water clearance
  9. CNS – m___, app____, sl____ stabilization
  10. Vascular responsiveness to vaso______
A
  1. Fuel metabolism – Preserve glucose availability (fasting) and increase supply (stress)
  2. Increase peripheral insulin resistance
  3. Increase Hepatic Glucose Production (HGP)
  4. Protein catabolism – substrates available for HGP
  5. Lipolysis for HGP
  6. Physiologic effect on bone
  7. Anti-inflammatory, stress responses
  8. Water balance – needed to increase free water clearance
  9. CNS – mood, appetite, sleep stabilization
  10. Vascular responsiveness to vasoconstrictors
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8
Q

The Adrenal Cortex- Pituitary Control

(4) major things that trigger release of cortisol?

These serve the basis of how we expect the adrenals to respond to ____ - which is the THE critical question when evaluating an inpatient for adrenal insufficiency

A

Stress

Hypotension

Infection

Hypoglycemia

These serve the basis of how we expect the adrenals to respond to Illness - which is the THE critical question when evaluating an inpatient for adrenal insufficiency

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9
Q

Cortisol Circadian Rhythm*

*This is the basis for the best test for an ambulatory patient when there is a concern about adrenal insufficiency – (1)

A

Basal 8am serum cortisol

(ACTH peaks 6-8am leading to burst of cortisol in the morning)

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10
Q

Primary Adrenal Insufficiency

=

  • Invariably involves loss of adrenal (2) production as well
    • This pathophysiology is how we will differentiate PAI from SAI
  • The adrenal medulla is usually left _____
  • Must be __lateral and involve destruction of __% of the gland before one develops signs or symptoms
A

Bilateral destruction of glucocorticoid producing capabilities of the adrenal cortex

  • Invariably involves loss of adrenal mineralocorticoid and androgen production as well
    • This pathophysiology is how we will differentiate PAI from SAI
  • The adrenal medulla is usually left intact
  • Must be bilateral and involve destruction of 90% of the gland before one develops signs or symptoms
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11
Q

Primary Adrenal Insufficiency Etiology

Most common cause (1)

(5) others

A

Auto-immune Adrenalitis (>70% USA)

  1. Infectious Adrenalitis (TB, HIV, Fungal, Bacterial - meningococcus/waterhouse friedrichson sx)
  2. Carcinoma of lung, renal, breast (rare)
  3. Hemorrhage or Thrombosis (very rare) (sepsis (meningococcus, pseudomonas, staph, s pneumo), Warfarin mediated, Antiphospholipid syndrome)
  4. Drugs (rare) (ketoconazole, ICI, mitotane,) CAH (congenital adrenal hyperplasia)
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12
Q

Primary Adrenal Insufficiency Manifestations*

Destruction of which layers of the cortex?

(2) Differentiating symptoms*

A

Destruction of all three layers of adrenal cortex

Hyperpigmentation dt excess ACTH

Hyperkalemia dt mineralcorticoid deficiency

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13
Q

Secondary Adrenal Insufficiency

=

  • No effect on (1) → no (1)
  • May be (1) or (1) in origin
    • Reduced production of ACTH - no (1)
  • Overtime, the lack of adrenal stimulus by ACTH causes _____ of the adrenal glands
A

Interruption of the hypothalamic-anterior pituitary axis such that a deficit in cortisol production occurs

  • No effect on aldosterone – no hyperkalemia
  • May be hypothalamic or pituitary in origin
    • Reduced production of ACTH – no hyperpigmentation
  • Over time, the lack of adrenal stimulus by ACTH causes atrophy of the adrenal glands
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14
Q

Secondary Adrenal Insufficiency Etiology

(2)

A

Exogenous Glucorticoid Administration (main cause)

Any cause of Hypopituitarism (2nd most common cause- pituitary adenomas)

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15
Q

Exogenous Glucocorticoids in Secondary AI

  • Potential Routes =
  • Many im_____ algorithms – duration (>__ weeks) and dose (>__ mg prednisone) play a significant role – but nothing has been clinically defined
  • There is no clear recommendation for “_____” down a dose to prevent SAI – but ch____ of use, d____, fr____, interfering m_____ and in____ for therapy all play a role
A
  • Oral, ocular, inhaled, transdermal, rectal, or parenteral routes
  • Many imperfect algorithms – duration (>3 weeks) and dose (>5 mg prednisone) play a significant role – but nothing has been clinically defined
  • There is no clear recommendation for “titrating” down a dose to prevent SAI – but chronicity of use, dose, frailty, interfering medications and indication for therapy all play a role
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16
Q

Causes of Hypopituitarism in Secondary AI

  • T____, craniopharyngioma, ra_____, pituitary su____
  • In_____ diseases – Sarcoidosis, Hereditary Hemochromatosis, Histiocytosis X
  • Lymphocytic hy____ – Auto-immune, pregnant women
  • Post-partum pituitary n_____
  • Head tr____
  • Dr___ - ICI
A
  • Tumors, craniopharyngioma, radiation, pituitary surgery
  • Infiltrative diseases – Sarcoidosis, Hereditary Hemochromatosis, Histiocytosis X
  • Lymphocytic hypophysitis (inflammation of pituitary gland) – Auto-immune, pregnant women
  • Post-partum pituitary necrosis
  • Head trauma
  • Drugs - ICI (intracavernosal injection)
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17
Q

Adrenal Insufficiency Non-Specific Symptoms

(seen in both types of AI)

  • F_____, listlessness, f___, abdominal p___, n____, ____ appetite, em____, generalized w____ness, d____ness
  • Weight ____
  • _______ hypotension
  • Concerning symptoms –(3)
    • If a patient with a known history of AI calls with these symptoms – it is clinically reasonable to assume they are in adrenal _____
A
  • Fatigue, listlessness, fever, abdominal pain, nausea, poor appetite, emesis, generalized weakness, dizziness
  • Weight loss
  • Orthostatic hypotension
  • Concerning symptoms – fever, N/V, abdominal pain
    • if a patient with a known history of AI calls with these symptoms – it is clinically reasonable to assume they are in adrenal crisis
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18
Q

Manifestations Specific to Primary AI

(2)

1st symptom, specifically where?

A

Skin Hyperpigmentation

(Palms, dorsal surface of hands, buccal mucosa, sun-exposed areas)

Salt Craving

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19
Q

Associated Symptoms of Secondary AI

Any symptom of hypopituitarism

  • Hypo_____ - sexual dysfunction, loss of libido, ED, oligo- or amenorrhea
  • Hypo_____ – cold intolerance, constipation, fatigue
  • (1) hormone deficiency – not clinically apparent in adults
  • (1) – polyuria, thirst
  • _____ effect – Headache, Visual Field deficits
A
  • Hypogonadism - sexual dysfunction, loss of libido, ED, oligo- or amenorrhea
  • Hypothyroidism – cold intolerance, constipation, fatigue
  • GH deficiency – not clinically apparent in adults
  • DI – polyuria, thirst
  • Mass effect – Headache, Visual Field deficits
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20
Q

Adrenal Insufficiency - Lab Evaluation

Why are these levels low or elevated?

  1. Na =
  2. K+ =
  3. Glucose =
  4. BP =
  5. WBC =
A
  1. Hyponatremia dt cortisol/aldosterone deficiency (salt wasting - only in primary)
  2. Hyperkalemia and Metabolic Acidosis (only in primary)
  3. Hypoglycemia
  4. Hypotension dt salt wasting w concomitant volume depletion/inability to maintain vascular tone from cortisol deficiency
  5. Eosinophilia
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21
Q

Adrenal Insufficiency Diagnostics

There may not be a true gold standard, recall the circadian rhythm

(2)*

  • For inpatient ?
  • After diagnosis made, try to establish level of defect by using ACTH
    • Primary - _____ ACTH
    • Secondary - _____ ACTH
A

Basal 8am serum cortisol

ACTH stimulation tests

  • For inpatient use cortisol levels independent of time
  • After diagnosis made, try to establish level of defect by using ACTH
    • Primary - elevated ACTH
    • Secondary - low or normal ACTH
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22
Q

ACTH Stimulation Testing

=

A

Your pretty much giving a bolus of ACTH and see if adrenals can make cortisol

If primary → still won’t make it bc destruction is in the adrenals

If secondary → can probably make cortisol bc using synthetic ACTH

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23
Q

Basal 8am Cortisol and ACTH Diagnostic Levels

Cortisol level diagnostic for AI?

Cortisol level that rules out AI?

ACTH levels diagnostic for primary AI?

ACTH levels diagnostic for secondary AI?

A

Cortisol <3mcg/dL ~100% specific for AI

Cortisol >16mcg/dL ~100% rules out AI

ACTH >100pg/mL seen uniformly in primary AI

ACTH low/normal in secondary AI

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24
Q

Indeterminate Basal Cortical Levels

Between __ - __

  • For patients whose time is of the essence?
  • Most useful form of emergent/urgent ACTH stimulation test =
A

Cortisol levels between 3-16mcg/dL

  • Test can be performed at any time of day since there is no diurnal variation in response to ACTH
  • High dose, short ACTH stimulation test = 250mcg cosyntropin and drawing plasma cortisol at time 0 and 60min
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25
Q

Interpreting High Dose ACTH Stimulation Test

Normal result =

Abnormal result =

A

Peak cortisol >16mcg/dL

Failure to reach a cortisol of >16mcg/dL is diagnostic of AI

(but have to wait for ACTH level to return to know if PAI or SAI)

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26
Q

Primary AI Treatment

(2) Glucocorticoid replacement, frequency of dosing?

XX (1) XX

(1) Mineralcorticoid replacement for management of (2)

A
  1. Hydrocortisone 10-20mg AM/5-10mg PM (shorter half life)
  2. Prednisone 2.5-7.5 at bedtime (longer half life)

NO dexamethasone bc so potent can Cushing’s

  1. Fludrocortisone 0.05-0.2mg daily for management of BP and K+
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27
Q

Secondary AI Treatment

_______ replacement only, which is first choice?

(2)

A

Glucocorticoid replacement only, hydrocortisone is first choice

Hydrocortisone 10-15mg AM/5-10mg early PM

Prednisone 2.5-7.5 at bedtime

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28
Q

AI Home Precautions

  1. Medic-Alert _____/Fit-bit t___
  2. ____ or ____ dose rules for stress
  3. Rx (1) (or other glucocorticoid) emergency 100 mg IM injection ___ at home (1)
  4. If unable to take PO* pills- use the (1) and call for emergency assistance

*sign of impending adrenal crisis

A
  1. Medic-Alert bracelet/Fit-bit tag
  2. Double or Triple dose rules for stress
  3. Solumedrol (or other glucocorticoid) emergency 100 mg IM injection kit at home Act-o-Vial
  4. If unable to take PO* pills- use the Act-o-Vial and call for emergency assistance
  • Home stress like flu, gastroenteritis – will need to double or triple glucocorticoid dose – to mimic increased stress response*
  • Act-O-vial – fam member is the one that gives it, then call 911*
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29
Q

Adrenal Crisis Symptoms and Labs

Symptoms

  • ________ followed by ____ (usually refractory to fluids and pressors)
  • Abdominal p____and em___
  • O______ hypotension and severe ____ness
  • F____
  • Con____

Clinical lab findings

  • _____natremia
  • _____glycemia
A

Symptoms

  • Hypotension followed by shock (usually refractory to fluids and pressors)
  • Abdominal pain and emesis
  • Orthostatic hypotension and severe weakness
  • Fever
  • Confusion

Clinical lab findings

  • Hyponatremia
  • Hypoglycemia
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30
Q

Adrenal Crisis Treatment

(3)

A

Aggressive IVF (2-3 liters bolus)

Hydrocortisone 100 mg iv t.i.d.

Treat underlying illnesses with Antibiotics, ICU admission

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31
Q

Diseases of Adrenal Cortical Excess

(3)

A

Hyperaldosteronism (Conn’s Syndrome)

Hypercortisolism (Cushing Syndrome)

Hyperandrogenism

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32
Q

Hyperaldosteronism (Conn’s Syndrome)

Etiology (1) vs. (1)

  • BP =
  • Na _____ and K _____
A

Adenoma vs bilateral hyperplasia

  • Hypertension
  • Na retention and K secretion (hypokalemia)
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33
Q

Hypercortisolism (Cushing’s Syndrome)

ACTH dependent most common cause (1)

ACTH independent causes (2)

Pseduo-Cushing’s Syndromes (3)

  • My_____of symptoms
A

Pituitary tumor that releases extra ACTH

Adrenal adenoma or carcinoma , Exogenous administration

Alcoholism, Depression, Obesity

  • Myriad of symptoms
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34
Q

Hyperandrogenism

Etiology (1) seen more commonly than (1)

  • Excess of DHEAS/_____ causing viralization
A

Adrenal cortical carcinoma seen more commonly than adenoma

  • Excess of DHEAS/Testosterone causing viralization
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35
Q

Cushing’s Syndrome Manifestations

More truncal _____, extremities ____

  1. Weight =
  2. Hair =
  3. Bone =
  4. Face =
  5. BP =
  6. Abdominal skin =
  7. Muscle =
  8. Ankle =
  9. Immune =
A

Truncal obesity, thin extremities

  1. Weight gain
  2. Hirsutism
  3. Fractures
  4. Moon Facies
  5. Hypertension
  6. Abdominal red-purple striae
  7. Muscle weakness
  8. Ankle edema
  9. Immune suppression (fungal infections)
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36
Q

Cushing’s Syndrome Definition

=

A

A group of diseases whose common theme is excess glucocorticoid exposure

Patho includes an exacerbation of the underlying actions of glucocorticoids

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37
Q

Cushing’s Syndrome Loss of Circadian Rhythm

What happens to normal cortisol levels around midnight?

In Cushing’s how do we test for a loss of this nadir?

A

Nadir of cortisol at midnight

Midnight salivary free cortisol using cotton swab since midnight plasma cortisol is not really feasible (normally should be low, but will be high in Cushing’s)

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38
Q

Dexamethasone Suppression Test

=

Low-Dose DST =

A

Give 1mg dexamethasone at midnight, comes to lab the next morning to test 8am cortisol – should have low cortisol (<2 mcg/dL) bc you’re suppressing the normal HPA axis, but pts with Cushings will still have high cortisol

Also can be done using 0.5mg Q6 for 48 hours

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39
Q

How do we quantify an abnormal level of free cortisol?

3rd test for Cushing’s

A

24 hour urine free cortisol

(is the quantitative integrated measure of cortisol production in a single day)

(since circadian rhythm makes a morning cortisol insufficient evidence of an excess in cortisol and >90% is bound to CBG/Alb-any excess beyond capacity of CBG/Alb will be free and excreted in urine)

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40
Q

Cushing’s Screenings Summary

Variable sensitivity and specificity of each test depending on value used for diagnosis- ask yourself these questions

Should cortisol be high in the saliva at midnight?

Should cortisol be detectable if we are giving the patient exogenous steroids?

Should cortisol be detectable in excess in the urine?

A

Late night salivary cortisol should be undetectable

1mg dexamethasone should show low AM cortisol

24 hour urine free cortisol should be within the normal range

41
Q

Assess for ACTH dependency in Cushing’s

Once someone tests + for a Cushing’s Syndrome screening test

  • ACTH levels suppressed =
  • ACTH levels detected =
A
  • CT Adrenals (consider macronodular hyperplasia)
  • MRI of pituitary → transphenoidal hypophysectomy
42
Q

Endocrine Hypertension - RAAS

Aldosterone acts on the ____ tubule to?

A

Aldosterone acts on the distal tubule to resorb sodium and excrete potassium

43
Q

Primary Aldosteronism

=

Effects:

  1. BP =
  2. Sodium =
  3. Potassium =
  4. H+ excretion → metabolic _____
  5. Pleiotropic effects – inflammation, microangiopathy, fibrosis
  6. ______ of plasma renin activity
  7. Aldosterone escape (a ____ in response to the expanded ECF) will prevent edema from developing, but ___ persists
  8. Increased risk of _____ disease (MI, CVA, A Fib) and chronic kidney disease
A

“Inappropriately high aldosterone production, relatively autonomous, non-suppressible by sodium loading”

  1. Hypertension
  2. Sodium retention
  3. Potassium excretion → hypokalemia
  4. H+ excretion → metabolic alkalosis
  5. Pleiotropic effects – inflammation, microangiopathy, fibrosis
  6. Suppression of plasma renin activity
  7. Aldosterone escape (a diuresis in response to the expanded ECF) will prevent edema from developing, but HTN persists
  8. Increased risk of cardiovascular disease (MI, CVA, A Fib) and chronic kidney disease
44
Q

Who to test for Primary Aldosteronism (Endocrine Hypertension)

Prevalence of 5-10% of all HTN pts

  1. Age =
  2. Masses on _____
  3. _____ HTN (>3 drugs poorly controlled, 4 drugs needed to control)
  4. _____ HTN (>150/100)
  5. Potassium =
  6. ____ History
A
  1. Young (early onset HTN or stroke)
  2. Adrenal masses
  3. Resistant HTN
  4. Severe HTN
  5. Hypokalemia
  6. Fam hx
45
Q

Primary Aldosteronism Tests

Morning, seated, normokalemic levels of plasma (2), (1) ratio

A

Plasma Aldosterone Concentration

Plasma Renin Activity

PAC/PRA: Aldosterone Renin Ratio (ARR)

46
Q

Interpretation of Aldosterone/Renin Tests

Primary Aldosteronism will show =

Secondary Aldosteronism will show =

Other Mineralcorticoid excess will show =

A

High Aldo, Low Renin

High Aldo, High Renin

Low Aldo, Low Renin

47
Q

Treatment for Primary Aldosteronism

Aldosterone Producing Adenoma (APA) tx =

Idiopathic Bilateral Adrenal Hyperplasia tx =

A

Surgery cures the disease, HTN improves in 30-60% of patients

Medically treated as surgery does not cure the disease (and causes primary adrenal insufficiency)

48
Q

Aldosterone Producing Adenoma Treatment

(1)

100 % cure of _____

30 – 60% cure of ____

Residual HTN after surgery is usually _____ HTN

A

Unilateral adrenalectomy

100 % cure of hypokalemia

30 – 60% cure of HTN

Residual HTN after surgery is usually essential HTN

49
Q

Bilateral Adrenal Hyperplasia Pharm Therapy

(1)-(2)

A

Aldosterone receptor antagonists

Spironolactone

Epleronone

50
Q

How to perform a Thyroid Exam?

(3) lobes of thyroid + the (1)

Thyroid gland engulfs the (1)

A

Stand behind patient and place 3 middle fingers of both hands along midline of neck below chin and gently walk them down.

Right, Left, Pyramidal Lobe, Isthmus

Cricoid cartilage

51
Q

Thyroid Hormone Metabolism

Hypothalamus secretes (1) →

Pituitary secretes (1) →

Thyroid secretes (2) →

Which is the dominant hormone?

Travels through circulation using (1) made by the Liver, ____ hormone is what inhibits pituitary from releasing more TSH

A

Hypothalamus secretes TRH

Pituitary secretes TSH

Thyroid secretes T3, T4

T4 is the dominant hormone

Travels through circulation using binding globulins made by liver, free hormone is what inhibits pituitary from releasing more TSH

52
Q

Producing Thyroid Hormone

Thyroid hormone is stored in the _____ →

Through (1) transcription, uses (1) which adds iodine to protein and produces T3 and T4 using (1)

A

Thyroid hormone is stored in the colloid →

Through mRNA transcription, uses thyroid peroxidase (TPO) which adds iodine to protein and produces T3 and T4 using thyroglobulin (Tg)

53
Q

Transport of Thyroid Hormone

Bound hormone =

Unbound hormone =

Which is the most important level?

  • ____ in TBH = Estrogen, acute hepatitis, drugs, inherited D/O
  • ____ in TBG = Androgen, Nephrotic syndrome, Cirrhosis, glucocorticoids, inherted D/O (XLR)
A

Bound hormone = Inactive form (99%)

Unbound hormone = Free Active form

Free T4 is the most important level

  • Increase in TBG = Estrogen, acute hepatitis, drugs, inherited D/O
  • Decrease in TBG = Androgen, Nephrotic syndrome, Cirrhosis, glucocorticoids, inherted D/O (XLR)
54
Q

T4 and T3 Production

T3 is produced in the _____ and is converted into T3 from ___

Takeaway: Always measure (2)**

A

T3 is produced in the periphery and is converted into T3 from T4

Always measure Free T4 and TSH**

55
Q

Role of Thyroid Hormone

  1. Fetal ____ Development/C__ and S_____Maturation
  2. Basal metabolism =
  3. Cardiac effects =
  4. Sympathetic Nervous System =
  5. Pulmonary =
  6. Hematopoietic =
  7. Gastrointestinal =
  8. Skeletal =
  9. Neuromuscular=
  10. Fuel metabolism – passive hormone – needed but not the primary role of T4/T3 =
  11. Endocrine =
A
  1. Fetal Brain Development/CNS and Skeletal Maturation
  2. O2 consumption and Heat Production
  3. Positive inotropic and chronotropic effects, Enhanced Adrenergic sensitivity
  4. Increase in B-adrenergic receptors and enhances sensitivity to catecholamines
  5. Permissive responses to hypoxia and hypercapnia
  6. Erythropoiesis
  7. Gut motility
  8. Bone turnover (promotes resorption > formation)
  9. Muscle contraction and relaxation
  10. Hepatic gluconeogenesis and glycogenolysis, Lipid synthesis and turnover
  11. Production, responsiveness and metabolic clearance of hormones
  • Thyroid hormone does pretty much everything*
  • Lack of thyroid hormone -> gut motility goes down – risk for ileus, risk for fractures*
56
Q

Tests of Thyroid Function

(2) most important

  • (1) binding protein dependent, used mostly for pregnancy
  • (1) not a useful assessment in most cases, peripheral production
A

TSH - the most informative test, very sensitive, always to be done with measurement of peripheral hormone…

Free T4 - unbound biologically important portion

  • Total T4-binding protein dependent, used mostly for pregnancy
  • Free T3-not a useful assessment in most cases, peripheral production
57
Q

Tests of Thyroid Autoimmunity

(1)* commonly seen in Hashimotos, but a general marker for thyroid autoimmunity

  • (1) as above, but less commonly positive
  • (1) specific marker of Grave’s disease
  • (1) aka thyrotropin binding inhibitory immunoglobulin (TBBII) - also specific for Graves disease
A

TPO (thyroid peroxidase antibody)

  • Thyroglobulin Ab
  • TSIg (thyroid stimulating immunoglobulin) - Graves
  • TRAbs (TSH Receptor antibodies) - Graves
58
Q

Thyroid Imaging

(1)*

Functional Testing

(1)*

A

US (assesses for echogenicity, nodularity, vascularity)

Uptake and Scan - usually for hyperthyroidism

59
Q

Hypothyroidism

=

Most common primary etiologies (4)

T4, TSH levels =

A

A clinical condition of reduced or absent thyroid hormone production

Hashimoto’s (autoimmune) most common

Total thyroidectomy (iatrogenic)

RAI I131 therapy (iatrogenic)

Iodine Deficiency

Low T4, High TSH

60
Q

Primary vs. Secondary Hypothyroidism

Primary Hypothyroidism =

T4 and TSH levels =

Secondary Hypothyroidism =

T4 and TSH levels =

A

Destruction of thyroid gland, Low T4, High TSH

Underactive pituitary gland, Low T4, Low TSH

61
Q

Hashimoto’s Hypothyroidism

=

  1. Most common cause of (1)
  2. General population antibody __ prevalence can range from 8-27%
  3. Risk of hypothyroidism increases with (1) +Ab, but is still low 2-4%/year
  4. More common in what gender?
  5. Associated with other _____ diseases (T1___, Add_____, Vit_____, Pernicious ______ and ____ areata)
  6. Can see other thyroid antibodies such as (1)
  7. What is seen on histology?
A

B and T cells launch autoimmune attack and damage normal thyroid cells, damaged thyroid leaks hormones

  1. Most common cause of primary hypothyroidism
  2. General population antibody + prevalence can range from 8-27% (but do not have Hashimoto’s)
  3. Risk of hypothyroidism increases with TPO +Ab, but is still low 2-4%/year
  4. More common in women
  5. Associated with other autoimmune diseases (T1DM, Addison’s, Vitiligo, Pernicious anemia, Alopecia areata)
  6. TSH receptor antibodies can also be seen
  7. Lymphocytic CD4, CD8 T cells, and B cells infiltration (purple patches in pic)
62
Q

Hypothyroidism Symptoms

  1. General =
  2. Weight =
  3. Extremities =
  4. Temperature intolerance =
  5. Muscle =
  6. GI =
  7. Voice =
  8. Menses =
  9. Sweating =
A
  1. Fatigue and listlessness, slowed mentation
  2. Weight gain – usually with a poor appetite
  3. Edema
  4. Cold intolerance
  5. Proximal muscle weakness
  6. Constipation
  7. Hoarseness – accumulated fluid in the vocal cords
  8. Menorrhagia, Irregular menses or amenorrhea
  9. Decreased sweating
63
Q

Hypothyroidism Signs

  1. Affect =
  2. Skin =
  3. Hair and Nails =
  4. Eyes/Extremities =
  5. BP, HR =
  6. Myocardial contractility =
A
  1. Depressed affect
  2. Cold dry skin
  3. Brittle hair and nails
  4. Periorbital/LE edema (non-pitting)
  5. HTN, Bradycardia
  6. Decreased myocardial contractility
64
Q

Lab Findings in Hypothyroidism

  1. Hgb =
  2. Na =
  3. LFTs =
  4. Inflammatory markers =
  5. Lipid panel =
A
  1. Anemia
  2. Hyponatremia
  3. Abnormalities in liver enzymes
  4. Increased CK
  5. Hypercholesterolemia and Hypertriglyceridemia
65
Q

Consequences of Untreated Hypothyroidism

End stage hypothyroidism =

  • ____cholesterolemia, An____
  • Cardiac, Pulmonary =
  • Neuro =
A

Myxedema Coma

  • Hypercholesterolemia, Anemia
  • CHF, effusions
  • Neurologic abnormalities
66
Q

Hypothyroidism Treatment

(2) Rx

Which is not recommended, and why?

Target range?

A

Levothyroxine (Synthroid) - LT4

Liothyronine LT3 <3/LT4 combo

Liothyronine not recommended bc risk of overtreatment

*At target range is defined by medical conditions, age and other factors (elderly naturally have higher TSH lvls so normal is around 4, theres is 7-8)

67
Q

Levothyroxine Dosing

____mcg/kg = full replacement

Slow replacement recommended for populations at risk for CVD/arrhythmia, particularly (2)

What happens if you miss a dose?

A

1.6mcg/kg = full replacement

Slow replacement for >60, CVD/TD2M patients

T4 has a long half life of 7 days, so missed doses can be given on subsequent days

Takes 5 weeks to get to steady state

68
Q

Hypothyroidism Tx Follow Up

__ week re-check of TFTs after any dose change

Goal for Primary hypothyroidism – At ____ range* (2) values

Goal – Secondary hypothyroidism – ___-level of normal ___ range

A

6 week re-check of TFTs after any dose change

Goal for Primary hypothyroidism – At target range* TSH and FT4

Goal – Secondary hypothyroidism – mid-level of normal FT4 range

69
Q

Levothyroxine Patient Education

When to take it, how?

Do not take with?

If you miss a dose?

Any change in pill (1) or (1) begets a call

Do not take b____ within 5 days of having labs drawn

A

On an empty stomach, 60 min before food or drink, with water only (can be given 2-3 hrs after last meal if more convenient)

Do not take with iron, calcium, soy, other otc, herbals, supplements, prenatal/multi vitamins (is a drug that easily interacts with other things, educate to take alone!)

Okay to take as soon as you remember or following day

Any change in pill color or shape begets a call

Do not take with biotin within 5 days of having labs drawn

70
Q

Algorithm for Pts with Interference in Achieving Euthyroidism

  1. Assess ad____
  2. Change in w____?
  3. Change in man____?
  4. Has the patient started supp____ or new m____?
  5. Has there been a change in thyroxine (1)
  6. Has there been a new diagnosis of ___itis or C____ disease (interfering with absorption)
A
  1. Adherence → pill box or toothbrush recommendation, reminders about safety of taking missed doses
  2. Change in weight?
  3. Change in manufacturer? (pill shape)
  4. Has the patient started supplements or new medications? (absorption, metabolism, thyroiditis, hypophysitis)
  5. Change in thyroxine binding globulin (typically estrogen mediated)
  6. Gastritis or Celiac disease?
71
Q

Features of Myxedema Coma

Which symptom is directly correlated with mortality in some studies?

A

Hypothermia*

72
Q

Treatment of Myxedema Coma

(controversial-no studies support any general recs)

___ stay is mainstay of therapy (5)

(1) 100-500mcg IV once, then 50-100mcg daily
(1) 10-25mcg IV Q8, then 10mcg IV Q8

A

ICU stay is mainstay of therapy

Antibiotics, Steroids, Ventilator support, Warming, Volume resuscitation

Levothyroxine

Liothyronine (the one exception where we give T3)

73
Q

Condition where someone has normal T4 levels, but abnormal TSH

Generally, we will start thyroid hormone replacement if TSH > ___

A

Subclinical Hypothyroidism

treat if TSH >10

74
Q

Thyrotoxicosis

A medical condition of excess thyroid hormone levels

(3)* most cases caused by endogenous overproduction by thyroid gland

(1) by release of preformed thyroid hormone from damage to gland

(1) exogenous administration

A
  1. Grave’s Hyperthyroidism (autoimmune stimulation of thyroid
  2. Toxic Nodule (adenoma-Plummer’s disease) or
  3. Toxic Multinodular goiter

Thyroiditis

Excess Levothyroxine administration (thyrotoxicosis factitia or iatrogenic)

75
Q

Rare causes of thyrotoxicosis

  • (1) producing pituitary adenoma
  • (1) mediated hyperthyroidism - think glycoprotein a and B chains
  • Drugs (3)
A
  • TSH producing pituitary adenoma
  • HCG mediated hyperthyroidism - think glycoprotein a and B chains
  • Amiodarone, Iodine administration, ICI (Immune Checkpoint Inhibitors)
76
Q

Grave’s Disease

(1) stimulates the (1) receptor

  • __-__% of thyrotoxicosis
  • More common in what gender?
  • Risk factors: G____ and En_____, sm_____, MZ rate < than expected, HLA-DR
  • TPO +?
A

Thyroid Stimulating Immunoglobulin (TSIg) stimulates TSH-Receptors

  • 60-80% of thyrotoxicosis
  • More common in females
  • Risk factors: Genetic and Environment, smoking, MZ rate < than expected, HLA-DR<
  • TPO + in many cases
77
Q

Thyrotoxicosis Symptoms

  1. Pal_______
  2. N______ness
  3. Ag______ or irr______
  4. _____ intolerance
  5. Tr_____
  6. Easy Fatigue
  7. Muscle weakness
  8. Weight _____ with good appetite
  9. Blurry or Double Vision
  10. ________ bowel movements
  11. Oligomenorrhea
A
  1. Palpitations
  2. Nervousness
  3. Agitation or irritability
  4. Heat intolerance
  5. Tremor
  6. Easy Fatigue
  7. Muscle weakness
  8. Weight loss with good appetite
  9. Blurry or Double Vision
  10. Frequent bowel movements
  11. Oligomenorrhea
78
Q

Grave’s Disease Pathognomonic Findings

(1) dt cytokines

(1) heard over thyroid gland

(1) found on tibia

A

Ophthalmopathy dt cytokines

Bruit/Thrill heard over thyroid gland

Pretibial Myxedema (NOT that myxedema)

79
Q

Thyroiditis

Pattern of thyroid levels in Thyroiditis?

Etiologies

  • Subacute painful causes = Post ____ infection (de Quervain), G____ cell or Gran______
  • Acute thyroiditis = b_____ cause, symptoms include ____ pain, fluctuance, f___, marked elevated ____
  • Painless (silent) thyroiditis - most common = happens post-_____ (TPO+)
  • Drug induced = (1)*, Am______, IFN a, post-______ contrast load, RAI-131, usually painless
A

Hyperthyroid phase then falls to hypothyroid phase than back to normal (ppl will recover if just one episode)

  • Subacute painful causes = Post viral infection (de Quervain), Giant cell or Granulomatous
  • Acute thyroiditis = bacterial cause, symptoms include severe pain, fluctuance, fever, marked elevated ESR
  • Painless (silent) thyroiditis - most common = happens post-partum (TPO+)
  • Drug induced = ICI*, Amiodarone, IFN a, post-iodinated contrast load, RAI-131, usually painless
80
Q

Thyrotoxicosis Signs

(2)* cardiac signs

  1. Goiter
  2. Warm, moist skin
  3. Proximal myopathy
  4. Eye lid retraction
  5. Gynecomastia (rare)
  6. Systolic Murmur – high output CHF
  7. Wide pulse pressure
A

Tachycardia (ST most commonly)

Atrial arrhythmias – esp. A Fib

  1. Goiter
  2. Warm, moist skin
  3. Proximal myopathy
  4. Eye lid retraction
  5. Gynecomastia (rare)
  6. Systolic Murmur – high output CHF
  7. Wide pulse pressure
81
Q

Consequences of Untreated Hyperthyroidism

(3)*

Others (4)

A

A-Fib*

Osteopenia, Osteoporosis*

Thyroid Storm

Tachycardia, CHF (high output), Angina, Death

82
Q

Importance of Eye Exam in Thyrotoxicosis

What is common to all forms of thyrotoxicosis?

What is only found in Graves?

A

Lid Retraction (white sclera exposed)

Proptosis

83
Q

Thyrotoxicosis Diagnostic Labs

(2)* most specific

A

TSIg (Thyroid stimulating immunoglobulin)

TBII (Thyrotropin binding inhibitory immunoglobulin)

84
Q

Thyrotoxicosis Imaging
(1)*

Explain?

(as long as pt is not pregnant)

A

Uptake and Scan

(where you give radioactive iodine and see if there is increased iodine uptake in the gland meaning that gland is actively making excess thyroid hormone)

top left (normal), bottom left (1 nodule), top right (graves nc bilateral)

85
Q

Hyperthyroidism Pharm Treatment

(2)* first line therapy

(1)* symptom relief

A

Methimazole or PTU

High dose Beta Blockers

86
Q

Methimazole and PTU Considerations

First line therapy for what type of patients ideally?

Precautions for high doses?

Why is PTU not really used? except in (2) conditions

A

Young, low risk patients or depletion therapy in eldery, high risk patients prior to I-131 or surgery

Agranulocytosis precautions - head to ED with pill bottle for CBC if experiencing Fever or Infectious symptoms

3rd most common cause of liver toxicity by medication, rarely indicated except for 1st trimester of pregnancy or thyroid storm

87
Q

Definitive Treatment for Hyperthyroidism

(2)-(1),(2)

A

RAI 131 (radioactive iodine to destroy enough thyroid tissue to become euthyroid)

Surgery - Total thyroidectomy for Graves or TMNG, Hemithyroidectomy for toxic adenoma

88
Q

Tidbits of Hyperthyroidism Treatment

Thionamides

  • Thionamide (ie. methimazole) only inhibits production of ___ hormone, does not interfere w pre-formed hormone release
  • Thionamide use in a patient with (1) will only lengthen hypothyroid phase and cause confusion in interpreting TFT’s
  • So only use (2) to treat thyroiditis

Beta Blockers

  • BB in high doses are the drug of choice to treat which symptomatic relief and suppression of (1)
  • Utilize BB up front and titrate agg_______
  • Establish the _____ of thyrotoxicosis before initiating
A

Thionamides

  • Thionamide (ie. methimazole) only inhibits production of new hormone, does not interfere w pre-formed hormone release
  • Thionamide use in a patient with thyroiditis will only lengthen hypothyroid phase and cause confusion in interpreting TFT’s
  • So only use BB and pain meds to treat thyroiditis

Beta Blockers

  • BB in high doses are the drug of choice to treat which symptomatic relief and suppression of tachyarrhythmia
  • Utilize BB up front and titrate aggressively
  • Establish the etiology of thyrotoxicosis before initiating
89
Q

Hyperthyroidism Chart

A

Uptake is low in thyroiditis bc is damaged cells just leaking out – nothing to hold on to the radioactive iodine

90
Q

Thyroid Storm

  • Precipitated by?
  • Increased risk in in______ treated thyrotoxicosis
  • Avoid point scoring systems – it is a _____ diagnosis!
    • PS – if the patient is calm, afebrile and can take PO without nausea or emesis, it is almost assuredly ____ storm
    • If the patient is agitated, febrile and cannot take PO – treat as _____ until proven otherwise
  • High mortality from _______ causes
    • These patients require the ICU
A
  • Precipitated by acute illness or insult
  • Increased risk in in inadequately treated thyrotoxicosis
  • Avoid point scoring systems – it is a clinical diagnosis!
    • PS – if the patient is calm, afebrile and can take PO without nausea or emesis, it is almost assuredly not storm
    • If the patient is agitated, febrile and cannot take PO – treat as storm until proven otherwise
  • High mortality from cardiovascular causes
    • These patients require the ICU
91
Q

Thyroid Storm Treatment Algorithm

  • High doses of (1) 40 – 60 mg PO q4H (or i.v. beta-blocker)
  • High doses of (1) (PO, NG, PR enema) or PTU (T4->T3 effect)
  • 1 hour after Thionamide dose – can give (1) solution ( it blocks thyroid hormone release)
  • High dose (1) +/-
A
  • High doses of Propranolol 40 – 60 mg PO q4H (or i.v. beta-blocker)
  • High doses of Methimazole (PO, NG, PR enema) or PTU (T4->T3 effect)
  • 1 hour after Thionamide dose – can give Iodine solution ( it blocks thyroid hormone release)
  • High dose steroids +/-
92
Q

Treatment of Subclinical Hyperthyroidism

Takeaway =

A

Subclinical hypothyroidism, can be more lenient and watch but subclinical hyperthyroidism esp in elderly we are worried for A-fib

93
Q

Transient Gestational Thyrotoxicosis

Why does it happen? Do we treat it?

A

Happens bc early in pregnancy HCG levels are elevated which stimulate TSH receptors resulting in high T4

We don’t treat it, will go away once HCG falls after 1st trimester

94
Q

Nodular Thyroid Disease

Commonly associated with what levels of FT4 and TSH?

Usually asymptomatic but monitor for (4) symptoms

Preferred imaging for substernal nodules (1)

Asymptomatic nodules need further workup to rule out? How? and especially for who?

A

Non-toxic/Euthyroid - normal FT4 and TSH

Dysphagia, Dyspnea with arms raised or lying down, Hoarseness, Stridor

CT neck and chest with contrast

Cancer, >1cm usually need a FNA, high risk (fam/radiation hx)

95
Q

Pemberton’s Maneuver

What does it test for?

How to perform it and positive result?

A

Nodular Thyroid Disease

Holding hands up for 2 minutes – thyroid traps large vessels and tracheal compression -will have venous compression/pooling – need to have surgery

96
Q

US for thyroid disease

gives an_____ information

A

Gives anatomic information

97
Q

Thyroid Cancer

(4) major types
(2) risk factors

More commonly seen in what gender, but worse prognosis in what gender?

(1) Cancer diagnosis seen in pts with underlying Hashimoto’s

A

Papillary*, Follicular*, Medullary, Anaplastic

Radiation exposure, Family History

More commonly seen in women, but worse prognosis in men

Non-Hodgkin’s Lymphoma (rare, rapidly enlarging neck mass)

98
Q

Papillary vs. Follicular Thyroid Cancer

(1) most common, (1) 2nd most common

Mainstay of therapy (2) +/- (1)

Follow serum __ as marker of disease

  1. Papillary
    1. Metastasis usually to (1), also to (2)
    2. Prognosis
  2. Follicular
    1. (1) variant is more aggressive
    2. Metastasis =
    3. Prognosis
A

Papillary most common, Follicular 2nd most common

Surgery is mainstay of therapy + RAI using I-131 +/- LT4 suppression

Serum Thyroglubulin (Tg) - is the primary tumor biomarker used to detect recurrence

  1. Papillary
    1. Metastasis usually localized to neck lymph nodes, also to lung, bone
    2. Excellent prognosis
  2. Follicular
    1. Hurthle cell (oncocytic) variant is more aggressive
    2. Hematogenous spread - lung and bone
    3. Slightly worse prognosis

Note: If someone has thyroid Ca history – will probably see low thyroid levels bc want to suppress it to prevent more thyroid CA

99
Q

Effect of COVID on Adrenal Axes?

A

No increased risk for adrenal insufficiency with COVID or being treated with dexamethasone during covid

Diagnosis and Management (36 decks)

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