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Drug Action II > Block 4: Thyroid Patho > Flashcards

Block 4: Thyroid Patho Flashcards

1
Q

What is the pituitary gland?

A

Master gland:
1. produce hormones that are released into the bloodstream
2. Anterior and posterior

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2
Q

Neurohormonal regulation of the pituitary are controlled by what?

A

Hypothalamus

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3
Q

What is the hypothalamus?

A
  1. Neurosecretory hormone secreting cells of the posterior pituitary via the infundibular stalk
  2. Releasing & Inhibitory factors that act on cells in the anterior pituitary via the hypophyseal portal system
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4
Q

What are the causes of hyperpituitarism?

A

Adenoma:
1. Visual field changes
2. Increased intracranial pressure
3. Prolactin (25%)
4. GH (15%)
5. ACTH (15%)

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5
Q

What are the causes of hypopituitarism?

A

Destructive processes:
1. Ischemic injury
2. Radiation or surgery
3. Inflammation and autoimmune
4. Adenomas

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6
Q

What is the posterior pituitary?

A
  1. Comprised of the endings of axons from the cell bodies in the hypothalamus
  2. Axons pass from hypothalamus to the posterior pituitary via the infundibular stalk
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7
Q

What are the hormones secreted by the posterior pituitary?

A
  1. Vasopressin (ADH / AVP): kidneys - water reabsorption
  2. Oxytocin: mammary glands: milk ejection, uterus: uterine contractions
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8
Q

What stimulates vasopression secretion?

A
  1. Large decreases in BV and BP
  2. Small changes above normal plasma osmotic pressure (>285 mOsm/kg)
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9
Q

What is the function of vasopressin on the vasculature?

A
  1. Increases BP in extreme hypovolemia or hypotension
  2. Acts in vasculature via Vasopressin V1a receptors (Gq)
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10
Q

What is the function of vasopressin on renal?

A

ADH causes aquaporins to be inserted in the collecting tubule:
1. Increases water reabsorption
2. Decreases water excretion
3. Increase plasma volume and pressure
4. Act via Vasopressin V2 receptors (Gs)

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11
Q

What happens if ADH is absent?

A

No aquaporins are inserted in collecting duct. Membrane is not permeable to H2O or urea, and no fluid reabsorption occurs

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12
Q

What is the hypersecretion of ADH?

A

SIADH: excessive amount of ADH release

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13
Q

What is the hyposecretion of of ADH called?

A

Diabetes Insipidus:
No ADH released, no response to ADH, or defective V2 vasopressin receptors

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14
Q

What is SIADH?

A

Excessive amount of ADH released:
1. Preventing urinary excretion of water resulting in low plasma osmolality and Na+, and dilute urine
2. High urine osmolality and Na+
3. Hyponatremia:
* Water drawn into the cells affecting the brain
* Most clinical symptoms relate to degree and rate of hyponatremia

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15
Q

What are the causes of SIADH?

A
  1. Loss of neuronal control with uninhibited release of ADH from intracranial disease
  2. Ectopic ADH release from small cell lung cancer
  3. Severe N/V
  4. Drugs: opioids, carbamazepine, chlorpropamide, cisplatin, vincristine, vinblastine, cyclophosphamide, amitriptyline, SSRIs, neuroleptics, bromocriptine, ecstasy (MDMA)
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16
Q

What are the primary sx and labs of DI?

A

Sx:
1. Polyuria
2. Polydipsia
3. Dehydration
4. No hyperglycemia

Labs:
1. Large volumes of dilute urine
2. Decreased specific gravity of urine
3. Decrease urine Na+/osmolarity
4. Normal/elevated Serum Sodium (HYPERNATREMIA)
5. Normal/elevated Serum Osmolality (↑ Serum Na+)

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17
Q

What are the types of DI?

A

Central (neurogenic) DI: Caused by lack of hypothalamic ADH secretion.
Nephrogenic DI: caused by impaired response to ADH in the kidney

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18
Q

What are the causes of central DI?

A
  1. Idiopathic (autoimmune)
  2. Head trauma
  3. Hypophysectomy
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19
Q

What are the causes of nephrogenic DI?

A
  1. X linked genetic mutations: AVPR2 ≈ 90%; AQP2 ≈ 10%
  2. Lithium (chronic)
  3. Renal dx
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20
Q

How do you determine the cause of DI?

A

Water deprivation test: Serum Na+ increases with no change in urine osmolarity (polyuria despite dehydration -> Diabetes Insipidus

Central: Responds to desmopressin, urine osmolality increases, lood for a CNS lesion
Nephrogenic: doesn’t respond to ADH

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21
Q

How does lithium cause nephrogenic DI?

A
  1. Lithium causes nephrogenic diabetes insipidus in up to 40 percent of patients taking lithium
  2. Loss of the ability to concentrate urine is related to the duration of lithium exposure from the inhibition of cAMP second messenger signalling
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22
Q

What is oxytocin?

A

Secreted by hypothalamic oxytocinergic neurons and released in response to neural stimulation

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23
Q

What are the MOA of oxytocin?

A

Specific G protein-coupled receptor (Gq):
1. Increasing uterine contraction
2. Increasing milk ejection

Disorders are rare

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24
Q

Hypothalamus and pituitary are connected via blood vessels converging at the ____?

A

Median eminence by the hypophyseal portal system

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25
Q

What are the types of hormones released by the hypothalamus?

A

Releasing: Causes release of hormones by the anterior pituitary
Inhibiotry: Inhibit secretion of hormones by the anterior pituitary

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26
Q

Describe the feedback control of the hypothalamus?

A
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27
Q

What are the anterior pituitary hormones?

A
  1. Growth Hormone (GH, Somatotropin)
  2. Prolactine
  3. TSH
  4. Adrenocorticotropic Hormone (ACTH)
  5. Follicle-stimulating Hormone (FSH)
  6. Luteinizing Hormone (LH)
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28
Q

What is GH?

A

Primary hormone responsible for regulating body growth, and is important in metabolism

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29
Q

What is prolactin?

A

Females: stimulates breast development and milk production.

Males: involved in testicular function

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30
Q

What is TSH?

A

Stimulates secretion of thyroid hormone & growth of thyroid gland

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31
Q

What is ACTH?

A

Stimulates cortisol secretion by the adrenal cortex

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32
Q

What is FSH?

A

Females: stimulates growth & development of ovarian follicles, promotes secretion of estrogen by ovaries.

Males: required for sperm production

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33
Q

What is LH?

A

Females: responsible for ovulation, formation of corpus luteum in the ovary, and regulation of ovarian secretion of female sex hormones.

Males: stimulates cells in the testes to secrete testosterone

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34
Q

What is Panhypopituitarism?

A

Loss or Absence of > 75% of Anterior Pituitary -> hypopituitarism

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35
Q

What is the cause of Panhypopituitarism? How does it effect the release of hormones?

A

Nonsecretory pituitary adenomas slow onset of hormones depending of causes:
1. ↓ TSH - life threatening (must replace thyroid hormone)
2. ↓ ACTH - life threatening (must replace cortisol)
3. ↓ GH
4. ↓ MSH
5. ↓ LH and FSH

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36
Q

Describe the MOA growth hormone?

A
  1. Growth hormone has metabolic effects on fuel mobilization (anti-insulin), and is a potent stimulator of growth via the actions of IGF-I
  2. Release stimulated by hypothalamic Growth Hormone-Releasing Hormone (GRH or GHRH)
  3. Release inhibited by Somatostatin (or SRIF)
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37
Q

What is somatopause?

A

Human GH is frequently used in pediatric endocrinology to correct growth deficiencies, and occasionally in elderly patients to enhance lean body mass and muscle strength

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38
Q

How does GRH act and what are its clincal products?

A

Activates a G-coupled (Gs) protein receptor that induces release of Growth Hormone (GH)

Sermorelin acetate (Geref): DC’d in US

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39
Q

How is GH secreted?

A

By the anterior pituitary in a pulsatile fashion:
1. Short bursts mostly at night
2. Daytime bursts occur during exercise or stress
3. Greatest amount of GH secretion occurs during the night within the first 1-2 hrs of slow-wave sleep

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40
Q

Other than growth what is stimulated by GH?

A

Formation of IGF1 in liver

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41
Q

What is the primary mediator of GH action?

A

IGF1

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42
Q

What are the primary roles or IGF1?

A

Bound in plasma to IGF-Binding Proteins (IGF-BPs)

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43
Q

What are the outcomes of GH def?

A

Short stature:
1. Postnatal growth retardation
2. Adult GH def

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44
Q

What are the outcomes of GH hypersecretion?

A

Tumor of pituitary somatotrophs:
1. Gigantism: GH excess during early postnatal development
2. Acromegaly: GH excess during adult life (after closure of epiphyseal plates (enlarged extremities, thickened skin)

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45
Q

What are the long term complications of developing acromegaly?

A
  1. Carbohydrate intolerance and Type-2 Diabetes
  2. Hypertension and Congestive Heart Failure (CHF)
  3. Arthritis and Osteoporosis
  4. Reduced life-expectancy if untreated
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46
Q

Prolactin release is controlled by what?

A

Dopamine: an inhibitory factor that decreases secretion

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47
Q

What are the primary target of prolactin?

A

Mammary glands:
1. Induces milk protein synthesis
2. Initiates and maintains lactation

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48
Q

What are the causes of Hyperprolactinemia?

A
  1. Prolactinomas: Most Common Hyperfunctioning Pituitary Adenoma
  2. Antipsychotics and antiemetics with dopamine D2 receptor antagonist activity (prevents the inhibition of GH from dopamine)
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49
Q

What are the clincal effects of hyperprolactinemia?

A
  1. Amenorrhea
  2. Galactorrhea
  3. Loss of libido
  4. Infertility
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50
Q

Describe the structure of the adrenal gland?

A

Cortex is the outer region containing 3 zones:
1. zona glomerulosa - outer zone
2. zona fasciculata - middle zone
3. zona reticularis - inner zone

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51
Q

What is the function of Zona Glomerulosa?

A
  1. Mineralocorticoids - ion (and water) balance: Aldosterone
  2. Stimulates reabsorption of Na+ and secretion of K+ from the kidney
  3. Increases water reabsorption in kidney
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52
Q

What stimulates the release of aldosterone?

A
  1. High K+, low Na+
  2. Angiotensin II
  3. ACTH (under severe stress, high concentrations)
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53
Q

What is Aldosteronism?

A

Hypersecretion of Aldosterone:
1. Increased water and Na+ reabsorption (HTN, edema)
2. Loss of K+ –> May disrupt neuronal and muscle function

54
Q

What are types of primary Aldosteronism?

A

Adrenal Adenoma, Conn’s Syndrome, Congenital Adrenal Hyperplasia:
1. ↑ Aldosterone
2. ↓ Renin
3. ↑ BP
4. ↑ Na
5. ↓ K

55
Q

What are the types of secondary aldosteronism?

A

Pregnancy, CHF, renin producing tumors, renal disease

56
Q

What is the cause of hyposecretion of mineralocoriccoids?

A
  1. Loss of GCC
  2. Decreased aldosterone
  3. Typically associated with Addison’s Disease: cortisol loss
57
Q

What is the function of the Zona Fasciculata?

A
  1. Glucocorticoids - Effects glucose metabolism: corisol (hydrocortisone)
  2. Helps to maintain BG levels
  3. Decreases immune response
58
Q

What are the cotnrols of cortisol release?

A
  1. Stimulated by CRH -> ACTH
  2. Stress
  3. Low plasma glucose concentrations
59
Q

Describe the feedback mechanism of cortisol secretion?

A
  1. CRF or CRH (corticotropic releasing factor/hormone) regulates ACTH secretion in pituitary
  2. ACTH regulates glucocorticoid (cortisol) secretion from adrenal cortex
  3. Feedback loops: ACTH inhibits CRH; cortisol inhibits ACTH
60
Q

What is primary Adrenal Cortisol Insufficiency?

A

Increased ACTH: Chronic (Addison’s disease; Autoimmune (-60%-70%))

61
Q

What is secondary Adrenal Cortisol Insufficiency?

A

Decreased ACTH: Rapid withdraw from exogenous steroid therapy

Reduces CRH and/or ACTH release:
Hypothalamic lesions
Hypopituitarism
Pituitary adenomas (non-functioning)

62
Q

Results of prolonged adrenal insufficiency?

A

Addisonian Crisis/disease:
1. Weakness & Fatigue
2. Hypotension, ↓ Na, ↑ K+
3. Hyperpigmentation is only Seen in only in primary due ↑ ACTH -> ↑ melanotropic activity

63
Q

Importance of tapering GCC?

A

If exogenous chronically administered steroids are rapidly withdrawn, results in an ACTH deficiency and secondary adrenocortical insufficiency.

64
Q

Causes of Adrenocortical Hyperfunction?

A
  1. Hypersecretion of cortisol (Cushing’s Disease)
  2. Hypersecretion of cortisol is usually due to adrenal tumor
  3. Hypersecretion of ACTH due to tumor in pituitary, lungs, kidneys, or pancreas
  4. Exogenous steroids: “Iatrogenic Cushing’s syndrome”
65
Q

How do you test for Adrenocortical Hyperfunction?

A

↑ 24 hr urine free cortisol (↑ plasma cortisol)

66
Q

Describe the MOA of cushings disease?

A
  1. Hypothalamic - Pituitary Disease: ↑ ACTH - Cushing’s Disease
67
Q

Describe the MOA of cushings syndrome?

A
  1. Primary Adrenocortical Hyperplasia/Neoplasia
  2. Ectopic ACTH by Non-Endocrine Neoplasia (Lung, kidney, or pancreas)
68
Q

Sx of Cushing syndromes?

A

Lipid tissue redistribution:
1. Weight Gain
1. Truncal Obesity
1. “Moon” Facies
1. Buffalo Hump

Fragile Skin & easy bruising
Anti-inflammatory effect
Mental Disturbances
Metabolic disturbances:
1. Hyperglycemia: steriod diabetes
2. Loss of muscle and bone mass (atrophy)
3. Water and salt retention (HTN)

69
Q

What is the function of Zona Reticularis?

A
  1. Gonadal Steroids: androgens
  2. contribute to onset of puberty
70
Q

What controls androgen release?

A
  1. Primarily stimulated by ACTH
  2. Gonadal steroids do not provide feedback inhibition of ACTH secretion
71
Q

What cause hypersecretion of androgens?

A

Increased ACTH secretion in Cushing’s disease, or to congenital adrenal hyperplasia or 21b-hydroxylase or 11b- hydroxylase deficiency

72
Q

Presentations of Hypersecretion of Gonadal Steroids?

A

In females: masculinization & male-like Genitalia
In males: hypersecretion of testosterone rapid maturation of reproductive organs and secondary sex characteristics

73
Q

What is the largest endocrine organ?

A

Thyroid

74
Q

Describe the control of thyroid hormone?

A
75
Q

Describe the regulation of the thyroid?

A
  1. TSH binds to receptors that stimulate cAMP and the synthetic mechanisms for secretion of TH
  2. TSH Increases synthesis of Thyroglobulin (Tg)
  3. TSH Increases I- uptake, Iodide is actively transported by a Na+ / Iodine cotransport
  4. Iodination of tyrosine resides on thyroglobulin
  5. Endocytosis of colloid and iodinated thyroglobulin
  6. Degradation of thyroglobulin and release of thyroxine
  7. Free thyroxine (T3 and T4) diffuse out of cell into circulation
76
Q

What is the wolff chaikoff effect?

A
  1. Initial administration of high levels of iodide inhibit thyroid hormone synthesis and release
  2. The negative feedback effect of high intrathyroidal iodide concentrations is reversible and transient
  3. Iodothyroid hormone synthesis and release returns to normal after several days due to increased TSH
  4. iodide administration is not a useful long-term therapy for hyperthyroidism
77
Q

What are the clinical uses of walff chaikoff?

A

Used to manage Thyroid Storm

78
Q

What enzyme synthesizes and secretes thyroglobin into follicular space?

A

Thyroid Peroxidase (TPO)
Tyrosine residues of Thyroglobulin:
1. I- = IODIDE to Io = IODINE
2. Requires H2O2

79
Q

What is the main circulating thyroid hormone?

A

T4

80
Q

What transports thyroid hormone in the blood?

A

Thyroid Binding Globulin

81
Q

Feedback regulation is based on the ___ component of the thyroid hormone?

A

‘free’ T4/T3

82
Q

What factors alter TBG?

A

Increase: estrogen, decreases in free TH
Decrease: adrogens, GCC, cirrhosis, increase free TH

Thyroid hormone is NOT active in the bound form

83
Q

What is the difference between T4 and 3?

A

T4: prohormone
T3: Active TH and has the highest binding affinity for TR, 5’-deiodination occurs at target

84
Q

How can TH activity increase without new synthesis?

A

Convertion of T4 to T3

85
Q

What is the regulation if there is too much TH activity?

A

T4 converts to inactive rT3 by 5-deiodination

86
Q

Describe the conversion pathway of TH?

A
87
Q

What TH has the most potency?

A

T3

88
Q

Describe the MOA of TH?

A
  1. T4 diffuses into the cytoplasm and is converted to T3
  2. Receptor proteins are located in the nucleus:
    * T3 binds to the ligand-binding domain of the thyroid hormone receptor.
    * Other half-site is an RXR receptor which binds the vitamin A derivative, 9-cis-retinoic acid

Thyroid hormone regulates gene expression through Thyroid Hormone Regulatory Elements (TREs) -> promotes or enhances regions of target genes

89
Q

What are THR?

A

TRα 1, 2, & 3 and TRβ 1 & 2

90
Q

Describe the gene regulation of TH?

A

T3 binding can either positively or negatively regulate gene expression depending on the nature of the TRE and the tissue

91
Q

What are the metabolic actions of TH?

A
  1. Regulates basal metabolic rate
  2. Increases oxygen consumption
  3. Permissive metabolic actions:
    * Increases sensitivity of target tissues to catecholamines
    * Elevating lipolysis, glycogenolysis and gluconeogenesis
92
Q

What are the physiological functions of TH?

A
  1. Mediates normal growth and development
  2. Maintains basal metabolic rate and calorigenesis
93
Q

What are the intermediary metabolism functions of TH?

A
  1. Protein metabolism
  2. Carb metabolism: High doses stimulate glycogenolysis to support increased BMR
  3. Lipid metabolism
94
Q
A
95
Q

What are the CV effects of TH?

A
  1. Up-regulates catecholamine receptors (β adrenergics)
  2. Increases sympathetic tone
  3. T3 suppresses activity of Gi-α
96
Q

What are the TH effects on the NS?

A
  1. Critical for normal CNS neuronal development: Congenital hypothyroidism occurs in patients that lack TH
  2. Enhances wakefulness and alertness
  3. Enhances memory and learning capacity
  4. Required for normal emotional tone
  5. Increases speed and amplitude of peripheral nerve reflexes
97
Q

What is a goiter?

A

Endemic goiter: Caused by dietary deficiency of Iodide:
1. Hashimoto’s thyroiditis
2. Subacute thyroiditis
3. Graves Disease (autoimmune activation of the TSH receptor)

98
Q

What are the complications of goiters?

A
  1. Deformation of the trachea
  2. Compression of the blood vessels in the neck
  3. Might require surgery
99
Q

What is observed in a serum thyroid testing/thyroid function test?

A
  1. Thyroid Stimulating Hormone (TSH) (0.5-6 mIU/L): Measues of thyroid function
  2. Free T4 (0.7-1.9 ng/dL): more accurate meassure that TT4
  3. Free T3
  4. TT4
  5. TT3
  6. TSAb (negative): confirmation of Hashimotos and graves
100
Q

Best test for routine screening of thyroid dysfunction?

A

TSH response w/ Free T4

101
Q

When is free T4 and T3 testing necessary?

A

Free T4: Abnormal TSH
Free T3: Abnormal TSH + normal FT4

102
Q

What are you thyroid antibodies?

A
  1. Thyroid Antiperoxidase: TPO (more sensitive)
  2. Antithyroglobulin: Tg
    * TPO + Tg Ab’s assoc w/ Hashimoto Hypothyroidism
  3. TSH Receptor Binding Antibody: TRAb
    * TRAb is considered a gold standard diagnostic test for the autoimmunity of Graves’ disease (GD
  4. Thyroid Stimulating Immunoglobulin: TSI
    * High levels of TSI can indicate the presence of Graves’ disease
    * ophthalmopathy
103
Q

What does an increased RAIU mean?

A
  1. Graves’ Disease
  2. Toxic Nodules (MNG, adenoma)
  3. hCG secreting tumors
  4. TSH mediated thyrotoxicosis
  5. Iodine def
104
Q

What does an decreased RAIU mean?

A
  1. Thyroiditis
  2. Iodine excess
105
Q

What causes hypothyroidism?

A

Congentital hypothyroidism in infancy -> hypothyroidism in adults

106
Q

What is the cause of primary hypothyroidsim? Labs?

A
  1. Most common: Autoimmune thyroid destruction

↓ T3 and T4, ↑ TRH, ↑ TSH

107
Q

TH effects on development?

A
  1. TH is critical for normal development of the skeletal system and musculature.
  2. Congenital hypothyroidism is the term for the constellation of defects resulting from untreated fetal and neonatal hypothyroidism.
108
Q

What are the RF of hypothyroidism?

A
  1. Elders
  2. Postpartum
  3. Radiation exposure
  4. Down syndrome
  5. T1DM
109
Q

Sx of hypothyroidism?

A
  1. Fatigue and weakness
  2. Cold intolerance
  3. Constipation
  4. Weight gain
  5. Myxedema
  6. Ptosis
110
Q

What are the causes of secondary hypothyroidism? Labs?

A
  1. Failure of the pituitary gland <1% of cases
  2. Pituitary tumors, surgery, pituitary radiation, pituitary necrosis, other autoimmune mechanisms

↓ TSH, T3, and T4, ↑ TRH

111
Q

What is tertiary hypothyroidism?

A
  1. Failure of the hypothalamus (very rare)
  2. Hypothalamic tumors, Stroke, Radiation, Trauma

↓ TSH, T3, T4, and TRH

112
Q

What is subacute thyroiditis?

A

Inflammation of the thyroid gland may occur after a viral illness

113
Q

What is lymphocytic thyroiditis?

A

Inflammation of the gland with an accumulation of lymphocytes

114
Q

Prolonged thyroiditis can lead to ___?

A
  1. “leaky,” so that the amount of thyroid hormone entering the blood may be temporarily increased
  2. Hyperthyroid phase lasts 4-12 weeks and may be followed by a hypothyroid phase that can last up to 6 months
115
Q

What is the most common thyroid disease?

A

Hashimoto’s Thyroiditis

116
Q

What is the cause Hashimoto’s Thyroiditis?

A
  1. Autoimmune damage
  2. Thyroid peroxidase Abs
  3. Polyglandular autoimmune diseases: T1DM
117
Q

What are the lab findings of hypothyroidism?

A
  1. polyglandular autoimmune diseases (>10)
  2. Low FT4
  3. TPO Ab (+)
118
Q

What is myxedema?

A

Decompensation of hypothyroidism:
1. ALtered mental status
2. Hyponatremia
3. Hypoglycemia
4. Hypotension and shock
5. Respiratory failure
6. Hypothermia
7. GI disorders and ileus

119
Q

What is the most common overt thyroid disease? Labs?

A

Subclinical Hypothyroidism:
1. Elevated TSH
2. Normal or near normal T3 and T4 levels

May occur with or without symptoms
3-20% will progress to overt hypothyroidism in time

120
Q

What is the most common etiologies of hyperthyroidism?

A
  1. Graves (TSI antibodies)
  2. Toxic multinodular and nodular goiters (thyrotoxicosis)
121
Q

What is primary hyperthyroidism? Labs?

A

Caused by thyroidal dysfunction with an increased release of thyroid hormone:
1. Fatigue
2. Weight Loss
3. Heat Intolerance and Hyperhidrosis
4. Nervousness and Anxiety
5. Palpitations

↓ TSH / ↑ T4 / ↑ T3 / TSI positive

122
Q

How is primary hyperthyroidism diagnosed?

A
  1. Elevated free T4 and Low TSH
  2. T3 level should be done to rule out T3 toxicosis
  3. Antibody measurement: TSI
123
Q

What is Graves?

A

Caused by auto-antibodies directed against the TSH receptor, resulting in continuous stimulation of the thyroid gland to secrete thyroid hormone.

124
Q

What is toxic multinodular goiters?

A

Plummer’s disease:
Nodules which automatously produce TH

125
Q

What is secondary hyperthyroism? Labs?

A

May be due to increased production of TSH from the pituitary gland or TSH-secreting tumors

↑ TSH / ↑ T4 / ↑ T3 / TSI negative

126
Q

What the presentations of Hyperthyroid Eye Disease?

A

Lid lag, lid retraction and stare due to increased adrenergic tone

127
Q

What are true graves ophthalmopathy?

A
  1. Exophthalmos (protrusion of eyeball from socket): Caused by thyroid auto-Ab’s that cross-react with fibroblasts, adipocytes, and myocytes behind the eyes
  2. Inflammatory changes
128
Q

What are non-grave hyperthyroidsim types?

A
  1. TSH secreting tumor
  2. Pituitary resistance to thyroid hormone
  3. Trophoblastic (high secretion of HCG)
  4. Thyroid nodule / multinodular goiter
  5. Thyroiditis (due to Hashimoto’s, usually self-limiting)
129
Q

Hyperthyroidism severity is dependent on?

A
  1. Degree of hormone excess
  2. Duration of excess
  3. Age of patient
  4. Rapidity of disease onset and progression
130
Q

What is thyroid storm?

A

A life threatening hypermetabolic state caused by hyperthyroidism (mortality: 10-30%)

131
Q

What are the common signs of thyroid storm?

A
  1. Fever
  2. Tachycardia
  3. Altered mental status
  4. Diaphoresis

Drug Action II (28 decks)

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