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CAS 3 > Disorders of the Thyroid Gland > Flashcards

Disorders of the Thyroid Gland Flashcards

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1
Q

What happens when iodine availability is insufficient:

A
  • T3 and T4 are inadequately synthesized
  • TSH increases
  • Goitrogenesis
  • conversion of T4 to T3 is enhanced
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2
Q

________ is the inhibition of thyroid hormones biosynthesis by blocking Thyroglobulin iodination

A

Wolff-Chaikoff effect

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3
Q

what is thyrotoxicosis

A

Hypermetabolic state caused by elevated circulating levels of free T3 and T4.

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4
Q

describe Primary hyperthyroidism

A

to thyroid pathology. It is the thyroid itself that is behaving abnormally and producing excessive thyroid hormone

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5
Q

Secondary hyperthyroidism is the condition ______

A

where the thyroid is producing excessive thyroid hormone as result of overstimulation by thyroid stimulating hormone. The pathology is in the hypothalamus or pituitary

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6
Q

graves accounts for 85% of __________cases

A

Thyrotoxoicosis

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7
Q

Hyperthyroidism Presentation

A

increased BMR:
peripheral T4 —>T3, binds nuclear receptor, transcription of cellular genes
* weight loss ( increased appetite)
* heat intolerance
* Warm flushed smooth sweaty skin
-Overactive sympathetic system:

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8
Q

Warm flushed smooth sweaty skin in hyperthyroidism is due to

A

– increased blood flow & peripheral vasodilatation to increase heat loss

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9
Q

Overactive sympathetic system in hyperthyroidism is clinically manifested as

A

Tremor, nervousness, emotional changes, diarrhea with fat malabsorption/steatorrhea (hypermotility)
eyelid lag & staring gauze- sympathetic overstimulation of sup tarsal muscle

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10
Q

MSK in hyperthyroidism is clinically manifested as

A

Wasting, weakness (myopathy)
* Osteoporosis, Increased Serum calcium & Alkaline phosphatase

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11
Q

CVS in hyperthyroidism is DUE TO:

A

Earliest & most prevalent
increased beta-adrenergic receptor expression

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12
Q

CVS in hyperthyroidism is clinically manifested as

A

-Increased heart rate
-Increased contractility & myocardial oxygen demand
-peripheral vasodilation (dec. SVR)
- DEC. DBP, increase SBP/PP

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13
Q

Laboratory findings- Hyperthyroidism

A
  • Increased serum T4, decreased serum TSH
  • Increased I uptake ( dec. Thyroiditis & patient taking excess hormones)
  • Hyperglycemia ( increased glycogenolysis)
  • Hypocholesterolemia ( increased LDL receptor synthesis)
  • Hypercalcemia ( increased bone turnover)
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14
Q

Exogenous Hyperthyroidism lab dx:

A

Increased Free thyroxine, decreased TSH, low or undetectable thyroglobulin

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15
Q

determine the dx:
eye symptoms
hyperthyroidism symptoms
proptosis/expthalamos
pretibial myexedema
opthalmopathy
TSH receptor antibodies

A

Graves disease

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16
Q

most common cause of endogenous hyperthyroidism (85%)
* 20-40 years
* F>M ( 10 times), 1.5 – 2% women in US

A

graves disease

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17
Q

graves disease genetic susceptibility

A

HLA DR3

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18
Q

graves disease inhibitory T-cell receptor

A

CTLA-4.

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19
Q

Pathogenesis of Graves disease

A

Autoimmune disorder – autoantibodies against multiple thyroid proteins- most importantly TSH receptor (thyrotropin)
-Thyroid-stimulating immunoglobulin (TSI) 90% patients (IgG antibody)
-Thyroid growth stimulating immunoglobulin
-TSH binding inhibitor immunoglobulin

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20
Q

graves disease triad manifestations:

A
  1. Hyperthyroidism - diffusely enlarged, hyper functional thyroid
  2. Infiltrative ophthalmopathy with resultant exophthalmos - 40% of
    patients
  3. A localized, infiltrative dermopathy (pretibial myxedema & exopthalmos)
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21
Q

pathogenesis for Exophthalmos & pretibial myxedema

A

Fibroblasts and adipocytes behind orbit and overlying skin express TSH receptor. (Glycosaminoglycan build up ( Chondroitin sulphate and hyaluronic acid)

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22
Q

what findings are directly linked to thyrotrophin receptor antibodies they are specific to
Graves disease and not found in other causes of hyperthyroidism.

A

Exophthalmos & pretibial myxedema-

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23
Q

Describe the GROSS morphology of Graves Disease

A

Gland diffusely and symmetrically enlarged
smooth surface. Capsule intact
C/s soft meaty- resembling muscle

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24
Q

Describe the Microscopy morphology of Graves Disease

A

-follicular epithelial cells are tall, columnar,
and crowded.
● Formation of small papillae. That lacks
fibrovascular cores.
● The colloid is pale, with scalloped margins.
● Lymphoid infiltrates ( T cells, scattered B cells
and plasma cells), are present throughout the
interstitium; germinal centers may be seen.

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25
clinical features for hyperthyroidism
- Tachycardia and palpitations - Nervousness & diaphoresis - Heat intolerance - Weakness & tremors - Diarrhea - Weight loss despite a good appetite -cardiac dysrhythmias and sudden death
26
acute, life-threatening complication of hyperthyroidism that presents with multisystem involvement.
thyroid storm ( thyrotoxic crisis)
27
pathogenesis of GOITER
DIFFUSE MULTINODULAR -Low-iodine diets (lack of seafood or iodized salt) Diets high in "goitrogens,“- cabbage, cassava that block iodine uptake
28
clinical presentation
F > M * Frequently asymptomatic * Goiter * Enlarged thyroid gland * Multiple colloid nodules * Areas of degeneration - Calcification - Cyst formation - Hemorrhage
29
Multinodular Goiter path:
-hormonally silent -manifest as toxic multinodular goiter or Plummer syndrome with thyrotoxicosis secondary to development of *autonomous nodules that function independent of TSH stimulation.* - Low risk for malignancy
30
Multinodular Goiter macroscopic:
Multilobulated, asymmetrically enlarged glands, may attain massive size. * cut surface: irregular nodules containing variable amounts of brown, gelatinous colloid. * Older lesions: fibrosis, hemorrhage, calcification, and cystic change
31
Multinodular Goiter microscopic:
Colloid-rich follicles lined by flattened, inactive epithelium. * Areas of follicular epithelial hypertrophy and hyperplasia
32
Hypothyroidism occurring during infancy or early childhood
Cretinism
33
important preventable cause of mental retardation (cretinism)
newborn screened for hypothyroidism.
34
Causes of cretinism
- iodine deficiency - maternal hypothyroidism (early pregnancy) - dyshormonogenetic goitre (rare) -(Inborn metabolic errors in the fetus that interfere with the normal synthesis of thyroid hormones) - lingual thyroid (thyroid removal )
35
cretinism clinical features
* Impaired CNS & bone growth * Mental retardation * Short stature * Coarse facial features * Protruding tongue * Umbilical hernia
36
Hypothyroidism occurring in older children and adults.
Myxedema
37
most common cause of primary hypothyroidism
hashimoto thyroiditis
38
TSH or T4/T3 estimation is the most sensitive test for primary hypothyroidism
TSH
39
Myxedema clinical features
* Slow physical and mental activity * Cold intolerance * Overweight * Low cardiac output * Constipation and decreased sweating * Cool pale thick skin * Hypercholesterolemia *diastolic HTN - sodium and water retention hyporeflexia - loss of later eyebrows (hertoghe sign)
40
hypothyroidism lab features
!Free T4 - decreased !TSH – Primary hypothyroidism * Increased – Secondary hypothyroidism * Decreased hypercholesterolemia- decreased synthesis of LDL receptors
41
diagnosis: Sudden fall in temperature * Reduced heart rate * Reduced blood pressure * Confusion * Coma hyperthermia
Myxedema Coma
42
pathogenesis of Myxedema Coma
Severe complication of hypothyroidism occurring mostly in older female patients; * altered mental status with or without coma.
43
causes of myxedema coma
Precipitating factor is usually present, which may include urinary tract infection or sepsis, trauma, or a side effect of medication.
44
classic signs of myxedema coma
Altered mentation, hypothermia, hypotension * Signs and symptoms of hypothyroidism.
45
Disorder T4 Free T4 TSH Graves
Increased Increased Decreased
46
Taking excess hormone :T4 Free T4 TSH
Increased Increased Decreased
47
Early phase thyroiditis :T4 Free T4 TSH
Increased Increased Decreased
48
Primary hypothyroidism:T4 Free T4 TSH
Decreased Decreased Increased
49
Secondary hypothyroidism (hypopituitarism) :T4 Free T4 TSH
Decreased Decreased Decreased
50
Increased TBG – (excess estrogen) :T4 Free T4 TSH
Increased Normal Normal
51
Reduced TBG –(Androgens/ anabolic steroids) :T4 Free T4 TSH
Decreased Normal Normal
52
Most common non- iatrogenic/ non- idiopathic cause of hypothyroidism in USA
Hashimoto thyroiditis
53
pathogenesis of hashimoto
- Autoimmune disease process * Antibodies against Thyroglobulin and Thyroid peroxidase - Destruction of follicles → antigen exposure (usually hidden) HLA-DR5
54
Hashimoto thyroiditis epidemiology
45 and 65 years of age * F>M 10:1 to 20:1. * Diffuse goiter
55
Risk for B cell lymphoma ( Marginal zone)
Hashimoto thyroiditis
56
Gross morphology of Hashimoto thyroiditis
Pale diffusely enlarged thyroid gland
57
Microscopic morphology of Hashimoto thyroiditis
-Lymphocytic infiltration with germinal centers. * Follicle atrophy * Epithelial “Hürthle cells” changes * Eosinophilic epithelial cells
58
Postpartum thyroiditis MOA
-Pregnancy is understood to be associated with reduced immunity to protect fetus from unwanted exposure to maternal immune system. -At the end of pregnancy the suppressed immunity is suddenly escalated, leading to the slow evolution of autoimmune response to thyroid auto-antigens, resulting in thyroiditis.
59
Postpartum thyroiditis occurs during
-occurs within a year of pregnancy * painless diffuse thyromegaly * destruction is followed by sudden release of stored thyroid hormone in blood causes hyperthyroidism transiently (1-3 months).-->hypothyroidism (4-8months) due to depletion of stores --> recovery to euthyroid state.
60
Postpartum thyroiditis lab values
Elevated thyroglobulin in hyperthyroid state – due to destruction of thyroid follicles & release of colloid * Decreased radioiodine uptake * decreased blood flow on Doppler Ultrasound * associated with HLA-D and HLA-B haplotypes. * Thyroid peroxidase (TPO) auto-antibody is significantly associated
61
subacture thyroiditis is also knnown as
– Granulomatous Thyroiditis – DeQuervain thyroiditis
62
epidemiology of subacute thyroiditis
- Second most common form of thyroiditis - Most common cause of a painful thyroid - Females > Males; 30-50 years
63
clinical features of subacute thyroiditis
post viral syndrome -pain, fever, fatiigue, myalgia assc. HLAB35
64
microscopy of subacute thyroiditis
Granulomatous inflammation to extravasated colloid with lymphocytes, histiocytes, multinucleated giant cells. - self limited prognosis
65
determine diagnosis: -Rare disease of unknown etiology - Destruction of thyroid gland - Dense fibrosis and chronic inflammation
REIDEL’S THYROIDITIS
66
REIDEL’S THYROIDITIS associated with inflammatory fibrosclerotic conditions (____)
mediastinal or retroperitoneal fibrosis, sclerosing cholangitis) * F > M; Middle age
67
gross morphology of REIDEL’S THYROIDITIS
Tan gray, woody, avascular & no lobules apparent
68
microscopic morphology of REIDEL’S THYROIDITIS
* No normal lobular pattern * Follicles are obliterated * extensive inflammation - consists of plasma cells (IgG-4 producing), lymphocytes, macrophages and eosinophils * dense fibrous tissue - infiltrates adjacent skeletal muscle/ airways mimicking malignancy
69
__________- ___________- _________is abnormal thyrid function test in normally functioning thyroid occuring in a setting of non thyroid illness hospitalized pts
Euthyroid Side Syndrome
70
pathogenesis of Euthyroid Side Syndrome
dec. thyroid hormones may limit catabolissm during illness - cytokines downregulate thyroid hormone synthesis
71
lab findings :Euthyroid Side Syndrome
dec T3 N/INC. T4 INC. Reverse T3 N/dec. TSH dec. TBG
72
Scalloping of the coloid tissue is commonly found in biopsy of :
Graves disease
73
what is the rx for graves disease
B-blockers thioamide radioiodine ablation
74
what diagnosis presents with "hard as wood " non tender thyroid gland
reidel fibrosing thyroiditis

CAS 3 (10 decks)

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