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Year 1: Patho/Pharm > Thyroid PATHO > Flashcards

Thyroid PATHO Flashcards

1
Q

Synthesis of Thyroid Hormone

A
  1. Iodide active transport into follicular cells
  2. peroxidase enzyme oxidizes to iodine (blocked by MMI)
  3. Thyroglobulin combines iodine and tyrosine to make mono/di-iodotyrosine
  4. Coupling to make T3 (triiodothyronine) or T4 (tetraiodothyronine) (blocked by MMI)
  5. Stored in colloid cells (1 month supply)
  6. T4 converted to T3 in periphery (blocked by PTU and cortisol)
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2
Q

Drugs that block peripheral conversion of T4 to T3

A
  • Propylthiouracil
  • Cortisol
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3
Q

Amount of T4 vs. T3
Compare half lives and fate

A

Majority secreted thyroid hormone is T4
T4 protein bound
half life 7 days
heptaic metabolism
converted to periphery into T3
80% T3 comes from T4

T3 free
half life is 1 day
hepatic metabolism
minority secreted hormone is free T3

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4
Q

Three Biological Functions
Thyroid Hormone

A
  1. Energy
    - Increase BMR
    - increase heat production
    - increase breakdown of glycogen, lipid, muscle, bone
    - increase oxygen consumption and demand
  2. Growth and development
    - bone, muscles, CNS
    - essential for normal development
    - screen in pregnancy and neonates
  3. Heart
    - Increase cardiac output, heart rate, conduction, contraciltity
    - increase oxygen demand and consumption
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5
Q

MOA
Thyroid hormone

A

T3 bioactive form
transcription factor
binds DNA (more tightly than T4)
gene expression
influences BMR, cardiac, growth and development

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6
Q

Negative feedback loop
hypothalamus-pituitary-thyroid

A
  1. Hypothalalmus
    - releases thyrotropin releasing hormone (TRH)
  2. Pituitary
    - releases thyroid stimulating hormone (TSH) from anterior pituitary
  3. Thyroid gland
    - binds to thyroid stimulating hormone (TSH)
  4. Increase iodide uptake
  5. hypertrophy gland
  6. Increase synthesis thyroid hormone
  7. increase secretion thyroid hormone

Thyroid hormone
- T3 and T4
- negatively feedback to decrease release TSH and TRH

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7
Q

How does a goitre develop?

A

Excess stimulation of the thyroid gland by TSH
Results in gland hypertrophy

Ex.
primary hypothyroidism
secondary hyperthyroidism

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8
Q

Serum tests to assess Thyroid function

A

TSH thyroid stimulating hormone

Free T3 and Free T4

*Low TSH = secondary hypothyroidism

*high TSH, low T3 and low T4 = primary hypothyroidism

High T3 = hyperthyroidism

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9
Q

Two types of Hypothyroidism
Example causes

A
  1. primary hypothyroidism
    - thyroid gland dysfunction

Examples
- Iatrogenic: surgery, radioactive iodine, amiodarone, lithium
- congenital hypothyroidism
- iodine deficiency
- autoimmune (Hashimoto’s thyroiditis, postpartum thyroiditis, silent painless thyroiditis)
- Subacute painful thyroiditis (De Quevain’s Thyroiditis) ; Acute painful thyroiditis (infection)

  1. secondary hypothyroidism
    - outside of the thyroid gland
    - pituitary or hypothalamus gland dysfunction

Examples
- tumour
- hemorrhage, clot: stroke
- brain surgery
- trauma

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10
Q

Clinical S&S
Hypothyroidism

A

CNS: fatigue, lethargy, depression, sleep disturbances, decrease IQ

Cardio: Decrease CO, BP, HR, decreased peripheral perfusion

Energy: Decrease BMR, hypoglycaemia, weight gain, constipation, brittle hair, skin, nails, pale puffy face, peripheral edema, cool extremities, cold intolerance

Fertility: infertility, heavy menstruation

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11
Q

Laboratory diagnostics
Hypothyroidism

A

Primary hypothyroidism
- High TSH
- Low free T3 and Low free T4
- *goitre

Secondary hypothyroidism
- Hypothalamus: Low TRH -> low TSH -> Low T3 and T4
- Pituitary: High TRH -> low TSH -> low T3 and T4
- *no goitre

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12
Q

Life threatening complication of
Untreated Hypothyroidism

A

Myexedema Coma

Triggers: Stress, trauma, opioid use, sedatives, infection, *old age high risk

Medical emergency:
- Decreased LOC, coma
- Hypothermia (non-shivering)
- Hypotension (hypovolemic shock)
- Hipoglicemia
- Lactic acidosis
- Death

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13
Q

Pharmacological treatment
Hypothyroidism

A

Levothyroxine (T4)
Lifelong therapy

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14
Q

Most common thyroid disorder

A

hypothyroidism
females > males

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15
Q

Examples of Autoimmune Thyroiditis

A

Auto-immune Thyroiditis
- Hashimoto’s
- Silent painless
- post-partum (up to 1 year)

Infectious
- De Quervain thyroiditis (post viral infection)
- Acute infectious thyroiditis (bacterial infection)
*painful

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16
Q

Clinical Course of Thyroiditis

A
  1. Hyperthyroidism
  2. Hypothyroidism
  3. Euthyroidism OR hypothyroidism sustained

Hyperthyroidism
- inflammation of the thyroid gland
- causes release of stored thyroid hormone
- thyrotoxicosis like symptoms
- fever, swelling gland, enlargement, painful/painless, thyrotoxicosis

S&S Thyrotoxicosis:
palpitations, tachycardia, tremors, sweating, heat intolerance, racing thoughts, insomnia, etc.

Hypothyroidism
- gland unable to function (synthesize and secrete thyroid hormone)

S&S hypothyroidism
lethargy, fatigue, depression, confusion, dry skin, brittle hair, nails, hypoglycaemia, cold intolerance, constipation, low BP, HR, CO, pale periphery, edema

Duration hormone replacement
6-12 months
trial period off medication to see if euthyroid OR permanent

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17
Q

Pharmacological treatment thyroiditis

A

Subacute/painful thyroiditis (De Quervain post viral thyroiditis) & acute infectious thyroiditis (bacterial infection)
- antibiotics
- NSAIDS, corticosteroids for pain

Hypothyroid phase
- thyroid replacement therapy

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18
Q

Auto-immune Thyroiditis

A

Anti-thyroid peroxidase antibodies
Anti-thyroid thyroglobulin antibodies

  • Hashimoto’s
  • silent/painless
  • post-partum
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19
Q

Congenital Hypothyroidism
Incidence, cause, window for treatment

A

Females > males

treatment window: 3-12 weeks

Cause:
- radiation
- auto-immune disease
- iodine deficiency
- TSH deficiency

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20
Q

Clinical S&S
Congenital Hypothyroidism

A

*3-12 weeks

Myexedema vocal cords, tongue
- protruding tongue
- hoarse cry
- dysphagia

CSN: fatigue, lethargy, sleep

MSK: short stature, hypotonic muscles, hernias, potbelly

CARDIO: cold, mottled, bradycardia, poor cardiac output

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21
Q

Treatment window for congenital hypothyroidism

A

3-12 weeks
Permanent growth, development, CNS impairment

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22
Q

Treatment Congenital Hypothyroidism

A

Thyroid replacement therapy for 3 years
Test 3 years if euthyroid

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23
Q

Thyroid Cancer
Cellular Pathophysiology

A
  1. Papillary & Follicular carcinoma
    - most common
    - Euthyroid (normal thyroid levels)
  2. Medullary cancer (parafollicular cells, C cells)
    - less common
    - high calcitonin level
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24
Q

Thyroid Cancer
Clinical S&S

A

Dysphagia
hoarse voice
difficulty breathing
Goitre or nodules
Euthyroid

*Treatment sometimes will cause hypothyroidism secondary to iatrogenic intervention (surgery, radiation, etc.)

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25
Q

Cancer Therapy induced thyroid disorders

A
  1. chemotherapy and radiation
    - hypothyroidism
  2. Tyrosine Kinase Inhibitors (TKI)
    - solid cancers (kidney, GI, thyroid)
    - Survival 2x greater if hypothyroidism develops > subacute > euthyroid

Hypothyroid = survival

26
Q

Two types of hyperthyroidism and examples

A
  1. Primary hypothyroidism
    - thyroid gland hypersynthesis and secretion of thyroid hormone

Examples
- Grave’s disease
- toxic multi-nodular goitre (Plummer’s disease)
- toxic nodular adenoma (follicular cell)
- Auto-immune thyroiditis (post-partum, Hashimoto’s, silent painless thyroitidis - first stage)

  1. Secondary hyperparathyroidism
    - pituitary adenoma
    - molar pregnancy (HCG)
    - iatrogenic overdose
    - gestational thyrotoxicosis
27
Q

Clinical manifestations
Hyperthyroidism undiagnosed

A

Hair: thinning hair

Eyes: exopthalmous

CNS: insomnia, racing thoughts, anxiety, aggitation

Heart: palpitations, tachydysrhythmias, increased cardiac output, angina

BMR: diarrhea, weight loss, hyperglycaemia, heat intolerance, sweaty

MSK: hyperreflexia, pre-tibial edema

28
Q

Laboratory diagnosis
Hyperthyroidism

A
  1. Primary hyperthyroidism
    - TSH low (negative feedback)
    - free T3 and free T4 high
  2. Secondary hyperthyroidism
    - TSH normal/high
    - free T3 and free T4 high
29
Q

Differential diagnosis
Radioactive Iodine uptake

A
  1. Low uptake
  • auto-immune thyroiditis
  • infectious thyroiditis
    • hyperthyroidism due to release of thyroid hormone stored in colloid cells (not due to increased synthesis)
  1. High uptake
  • graves disease
  • toxic multi nodular goitre
  • toxic thyroid adenoma
    *hyperthyroidism due to increase synthesis and release of thyroid hormone
30
Q

Treatment
Hyperthyroidism

A
  1. Thionamides
    - Methionazole (MMI)
    - propylthiouracil (PTU)
  2. radioactive iodine therapy I-131
    - radioactive destruction of follicular cells
  3. Surgical resection
31
Q

Graves Disease
Pathophysiology

A

Hyperthyroidism

Type II hypersensivity reaction
formation of Thyroid stimulating immunoglobulins (TSI) IgG which bind the TSH receptor

Stimulates
1. thyroid gland hypertrophy
2. increased iodide uptake
3. increase thyroid synthesis and secretion

32
Q

Graves Disease Incidence

A

Most common cause of hyperthyroidism
Females > males
80% cases

33
Q

Graves Disease
Distinguishing Clinical S&S

A
  1. Opthopathy
  2. Dermopathy

Opthalmopathy

  • Lid and global lag (SNS overactiviation)
  • Exophthalmos (WBC infiltrates, connective tissue proliferation and edema, protrusion)
  • Other: papilledema, blurred vision, irritation, abrasions

Dermopathy

  • Pre-tibial Myxedema
  • Thyroid Acropachy (clubbing toes, fingers)
    • myofibroblasts have TSH receptors, proliferation connective tissue, edema
34
Q

Toxic Multi-Nodular Goitre
Pathophysiology

A

Primary hyperthyroidism
Also called Plummer’s disease
less common

Follicular cells produce thyroid hormone without TSH stimulation

35
Q

Distinguishing clinical S&S
Toxic Multi-nodular goitre

A
  1. No opthalmopathy (exopthalmous)
  2. No dermopathy (pre-tibial myxoedema; acropathy)
  3. No TSI (thyroid stimulating immunoglobulins, IgG)
  • develops slowly
36
Q

Clinical S&S of hyperthyroidism (thyrotoxicosis)

A

CNS: agitation, insomnia, racing thoughts

Heart: palpitations, increased CO, increased oxygen demand, angina pain, tremors

BMR: weight loss, sweating, heat intolerance, diarrhea, dry hair

MSK: increased tendon reflexes

37
Q

Hyperthyroidism Complication

A

Thyroid storm
also known as thyrotoxic crisis

38
Q

Pathophysiology
Thyroid Storm

A

Trigger: stress, infection, surgery, trauma, labour

Massive increase in thyroid hormone release

HEART: increase HR, conduction, contraciltity, high output heart failure (> 8L/minute); hypertension

CNS: aggitation, delirium, coma

BMR: extreme increase in BMR, increase oxygen demand (not met by supply), metabolic acidosis; hyperglycaemia; hyperthermia

39
Q

Treatment
Thyroid Storm

A

ICU admission
Death within 48 hours

  1. Sedation
  2. Cooling
  3. anti-thyroid medications (propylthiouracil, radioactive iodine)
  4. thyroid resection
  5. corticosteroids (block conversion T4 to T3)
  6. beta blockers (slow HR, contractility, conduction)
  7. Correct fluid, electrolyte, acid-base imbalances
40
Q

Hypoparathyroidism
Etiology

A
  1. Surgical removal of thyroid gland (parathyroid glands located behind thyroid)
  2. Genetic: familial hypoparathyroidism (DiGeorge Syndrome)
  3. Hypomagnesium (alcoholism, malnutrition, amino glycoside antibiotics)
  4. Receptor mutation (pseudoparahypothyroidism - high PTH, hypocalcemia, hyperphosphatemia)
41
Q

Laboratory diagnostics
Hypoparathyroidism

A

Serum PTH (low)
serum calcium (low)
serum phosphate (high)
serum magnesium (aetiology r/o)
serum vitamin D (low?)

42
Q

Normal physiology
Hypertrophy of thyroid gland

A

pregnancy
adolescents

43
Q

Physiological function
Parathyroid hormone

A

Pulsatile release

  1. PTH –> osteoclast activation –> bone reabsorption –> increase serum calcium
  2. PTH –> Kidney –> increase vitamin D activation; increase calcium reabsorption and phosphate excretion
  3. Vitamin D –> increase GI absorption of calcium

Continual low level release
- bone formation

44
Q

Hypoparathyroidism
Pathophysiology

A

Low PTH
1. BONE: no bone reabsorption –> hypocalcemia
2. KIDNEY: decrease vitamin D activation, increase absorption phosphate
3. GI: decrease GI absorption calcium

Result:
Hypocalcemia
hyperphosphatemia
low Vitamin D (1,25-dihyroxyvitamin D)

45
Q

Clinical S&S
Hypocalcemia

A

CRAMPS

C: Convulsions
R: Reflexes hyperactive
A: Arrhythmias (prolonged QT interval)
M: Muscle spasms (calves, feet, tetany, weakness, laryngeal spasms, dysphagia)
P: positive signs (Chvostek- cheek, Trousseau - carpal tunnel spasm
S: sensation (paraesthesias, mouth, extremities)

46
Q

Long term complications of hypocalcemia

A

Parkinsonian syndrome
- calcification basal ganglia

Bone deformities
- bow legs

Hypoplasia teeth

47
Q

Clinical S&S hyperphosphatemia

A

Worsening hypocalcemia: inhibits activation vitamin D

Worsening CVD: atherosclerosis, hypertension, L sided HF

48
Q

Treatment
Hypoparathyroidism

A
  1. Vitamin D supplimentation
  2. Calcium supplimentation

(prevention hypocalcemia)

  1. magnesium supplimentation (if hypo magnesium is the cause)
49
Q

Anatomy
Parathyroid glands

A

Posterior to thyroid gland
2-6 glands per person

50
Q

Hyperparathyroidism
Classifications and etiology

A
  1. Primary
    - parathyroid adenoma
    - hyper secretion PTH
  2. Secondary
    - Low vitamin D or low calcium
    - Causes:
    - Kidney disease: cannot synthesize Vitamin D
    - GI disease: cannot absorb vitamin D or calcium
    - Dietary deficiency
    - Medications: AEDs (carbamazepine, phenytoin, phenobarbital) increase vitamin D metabolism; Laxatives
  3. Tertiary
    - prolonged compensation secondary hyperparathyroidism
    - bone reabsorption
51
Q

Differential laboratory diagnosis
hyperparathyroidism

A

primary hyperparathyroidism
- high PTH
- high calcium
- high vitamin D
- low phosphate
- ethology: tumour secretes PTH

secondary hyperparathyroidism
- low calcium
- low vitamin D
(Deficiency kidney, GI, medication -> low vitamin D, calcium)
- high PTH

Tertiary hyperparathyroidism
- very high PTH
- high calcium
- high phosphate (bone reabsorption to compensate)
- low vitamin D

52
Q

Primary hyperparathyroidism
Etiology

A

85% parathyroid adenoma
15% parathyroid hyperplasia
1% carcinoma

53
Q

Clinical S&S
Primary hyperparathyroidism

A
  1. Hypercalcemia
    - anorexia, nausea, vomiting
    - arrhythmias, MI
    - insulin resistance
    - bone pain, muscle weakness
    - kidney stones, diabetes insipidus, UTI, metabolic acidosis
    - confusion
  2. Hyperphosphatemia
    - Worsening CVD: hypertension, atherosclerosis, L ventricular HF
  3. High vitamin D
    - same symptoms as hypercalcemia
    - anorexia, nausea, vomiting, confusion
    - polyuria, polydipsia, diuresis (osmotic diuresis)
    - kidney stones
    - UTI
    - metabolic acidosis
54
Q

Hypercalcemia effect on kidney tubule function

A

Renal tubular dysfunction

  • alkaline urine (decrease H+ excretion, HCO3- reabsorption) –> infections
  • metabolic acidosis
  • resistance to ADH (diabetes insipidus), polyuria, polydipsia, dehydration
  • kidney stones
55
Q

Clinical S&S
Secondary hyperparathyroidism

A
  1. hypocalcemia
  2. Low vitamin D
  3. high or low phosphate

S&S hypocalcemia
CRAMPS
- convulsions
- hyper reflexia
- arrhythmias , long QT
- muscle spasms, tetany, laryngospasms
- Positive: + Chvostek, +trousseau
- Sensation: numbness/tingling/mouth/extremities

*differential is laboratory PTH value

56
Q

Treatment
Primary Hyperparathyroidism

A

Remove the adenoma, parathyroid hyperplasia or carcinoma

Supplementation with vitamin D, calcium

57
Q

Treatment
Secondary hyperparathyroidism

A

R/O cause
- kidney disease
- vitamin D and Calcium deficiency
- mediation
- GI absorption

*supplementation with Vitamin D or Calcium
phosphate restricted diet
Calcimimetics (increase parathyroid sensitivity to calcium to decrease release)

58
Q

Endocrine Glands

A
  • pineal gland
  • pituitary gland
  • parathyroid gland
  • thyroid
  • thymus
  • adrenal gland
  • pancreas
  • ovary
  • testes
59
Q

Endocrine system
Hypothalamus-Pituitary System
Function

A
  1. releasing hormones
  2. trophic hormones
  3. endocrine gland

Bind to receptors

  1. intracellular (lipid hormones: thyroid hormone, steroid hormones (estrogens, glucocorticoids, mineralocorticoids, progestin, testosterone), arachidonic acid derivatives (prostaglandins, leukotrienes, thromboxanes)
  2. extracellular

Too much hormone = down regulation receptors
Too little hormone = up regulation receptors

Negative and positive feedback loops

60
Q

Endocrine system and aging

A

Decrease receptor function
Decrease hormone synthesis and secretion
endocrine gland atrophy

Year 1: Patho/Pharm (39 decks)

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