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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
Cancer Therapy induced thyroid disorders
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
Two types of hyperthyroidism and examples
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) 2. Secondary hyperparathyroidism - pituitary adenoma - molar pregnancy (HCG) - iatrogenic overdose - gestational thyrotoxicosis
27
Clinical manifestations Hyperthyroidism undiagnosed
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
Laboratory diagnosis Hyperthyroidism
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
Differential diagnosis Radioactive Iodine uptake
1. Low uptake - auto-immune thyroiditis - infectious thyroiditis - * hyperthyroidism due to release of thyroid hormone stored in colloid cells (not due to increased synthesis) 2. High uptake - graves disease - toxic multi nodular goitre - toxic thyroid adenoma *hyperthyroidism due to increase synthesis and release of thyroid hormone
30
Treatment Hyperthyroidism
1. Thionamides - Methionazole (MMI) - propylthiouracil (PTU) 2. radioactive iodine therapy I-131 - radioactive destruction of follicular cells 3. Surgical resection
31
Graves Disease Pathophysiology
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
Graves Disease Incidence
Most common cause of hyperthyroidism Females > males 80% cases
33
Graves Disease Distinguishing Clinical S&S
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
Toxic Multi-Nodular Goitre Pathophysiology
Primary hyperthyroidism Also called Plummer's disease less common Follicular cells produce thyroid hormone without TSH stimulation
35
Distinguishing clinical S&S Toxic Multi-nodular goitre
1. No opthalmopathy (exopthalmous) 2. No dermopathy (pre-tibial myxoedema; acropathy) 3. No TSI (thyroid stimulating immunoglobulins, IgG) - develops slowly
36
Clinical S&S of hyperthyroidism (thyrotoxicosis)
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
Hyperthyroidism Complication
Thyroid storm also known as thyrotoxic crisis
38
Pathophysiology Thyroid Storm
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
Treatment Thyroid Storm
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
Hypoparathyroidism Etiology
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
Laboratory diagnostics Hypoparathyroidism
Serum PTH (low) serum calcium (low) serum phosphate (high) serum magnesium (aetiology r/o) serum vitamin D (low?)
42
Normal physiology Hypertrophy of thyroid gland
pregnancy adolescents
43
Physiological function Parathyroid hormone
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
Hypoparathyroidism Pathophysiology
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
Clinical S&S Hypocalcemia
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
Long term complications of hypocalcemia
Parkinsonian syndrome - calcification basal ganglia Bone deformities - bow legs Hypoplasia teeth
47
Clinical S&S hyperphosphatemia
Worsening hypocalcemia: inhibits activation vitamin D Worsening CVD: atherosclerosis, hypertension, L sided HF
48
Treatment Hypoparathyroidism
1. Vitamin D supplimentation 2. Calcium supplimentation (prevention hypocalcemia) 3. magnesium supplimentation (if hypo magnesium is the cause)
49
Anatomy Parathyroid glands
Posterior to thyroid gland 2-6 glands per person
50
Hyperparathyroidism Classifications and etiology
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
Differential laboratory diagnosis hyperparathyroidism
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
Primary hyperparathyroidism Etiology
85% parathyroid adenoma 15% parathyroid hyperplasia 1% carcinoma
53
Clinical S&S Primary hyperparathyroidism
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
Hypercalcemia effect on kidney tubule function
Renal tubular dysfunction - alkaline urine (decrease H+ excretion, HCO3- reabsorption) --> infections - metabolic acidosis - resistance to ADH (diabetes insipidus), polyuria, polydipsia, dehydration - kidney stones
55
Clinical S&S Secondary hyperparathyroidism
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
Treatment Primary Hyperparathyroidism
Remove the adenoma, parathyroid hyperplasia or carcinoma Supplementation with vitamin D, calcium
57
Treatment Secondary hyperparathyroidism
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
Endocrine Glands
- pineal gland - pituitary gland - parathyroid gland - thyroid - thymus - adrenal gland - pancreas - ovary - testes
59
Endocrine system Hypothalamus-Pituitary System Function
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
Endocrine system and aging
Decrease receptor function Decrease hormone synthesis and secretion endocrine gland atrophy

Year 1: Patho/Pharm (45 decks)

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