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CAS 3 > Disorders of the Thyroid Gland > Flashcards

Disorders of the Thyroid Gland Flashcards

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
Q

clinical features for hyperthyroidism

A
  • Tachycardia and palpitations
  • Nervousness & diaphoresis
  • Heat intolerance
  • Weakness & tremors
  • Diarrhea
  • Weight loss despite a good
    appetite
    -cardiac dysrhythmias and sudden death
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26
Q

acute, life-threatening complication of hyperthyroidism that presents with multisystem
involvement.

A

thyroid storm ( thyrotoxic crisis)

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27
Q

pathogenesis of GOITER

A

DIFFUSE MULTINODULAR
-Low-iodine diets (lack of seafood
or iodized salt)
Diets high in “goitrogens,“-
cabbage, cassava that block
iodine uptake

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28
Q

clinical presentation

A

F > M
* Frequently asymptomatic
* Goiter
* Enlarged thyroid gland
* Multiple colloid nodules
* Areas of degeneration
- Calcification
- Cyst formation
- Hemorrhage

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29
Q

Multinodular Goiter path:

A

-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

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30
Q

Multinodular Goiter macroscopic:

A

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
Q

Multinodular Goiter microscopic:

A

Colloid-rich follicles lined by flattened, inactive epithelium.
* Areas of follicular epithelial hypertrophy and hyperplasia

32
Q

Hypothyroidism occurring during infancy or early childhood

A

Cretinism

33
Q

important preventable cause of mental retardation (cretinism)

A

newborn screened for hypothyroidism.

34
Q

Causes of cretinism

A
  • 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
Q

cretinism clinical features

A
  • Impaired CNS & bone
    growth
  • Mental retardation
  • Short stature
  • Coarse facial features
  • Protruding tongue
  • Umbilical hernia
36
Q

Hypothyroidism occurring in older children and adults.

A

Myxedema

37
Q

most common cause of primary hypothyroidism

A

hashimoto thyroiditis

38
Q

TSH or T4/T3 estimation is the most sensitive test for primary hypothyroidism

A

TSH

39
Q

Myxedema clinical features

A
  • 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
Q

hypothyroidism lab features

A

!Free T4 - decreased
!TSH
– Primary hypothyroidism
* Increased
– Secondary hypothyroidism
* Decreased
hypercholesterolemia- decreased synthesis of LDL receptors

41
Q

diagnosis:
Sudden fall in temperature
* Reduced heart rate
* Reduced blood pressure
* Confusion
* Coma
hyperthermia

A

Myxedema Coma

42
Q

pathogenesis of Myxedema Coma

A

Severe complication of hypothyroidism occurring mostly in older female
patients;
* altered mental status with or without coma.

43
Q

causes of myxedema coma

A

Precipitating factor is usually present, which may include urinary tract
infection or sepsis, trauma, or a side effect of medication.

44
Q

classic signs of myxedema coma

A

Altered mentation, hypothermia, hypotension
* Signs and symptoms of hypothyroidism.

45
Q

Disorder T4 Free T4 TSH
Graves

A

Increased Increased Decreased

46
Q

Taking excess hormone :T4 Free T4 TSH

A

Increased Increased Decreased

47
Q

Early phase thyroiditis :T4 Free T4 TSH

A

Increased Increased Decreased

48
Q

Primary hypothyroidism:T4 Free T4 TSH

A

Decreased Decreased Increased

49
Q

Secondary hypothyroidism
(hypopituitarism) :T4 Free T4 TSH

A

Decreased Decreased Decreased

50
Q

Increased TBG –
(excess estrogen) :T4 Free T4 TSH

A

Increased Normal Normal

51
Q

Reduced TBG –(Androgens/ anabolic steroids)
:T4 Free T4 TSH

A

Decreased Normal Normal

52
Q

Most common non- iatrogenic/ non- idiopathic cause of hypothyroidism in USA

A

Hashimoto thyroiditis

53
Q

pathogenesis of hashimoto

A
  • Autoimmune disease
    process
  • Antibodies against Thyroglobulin and
    Thyroid peroxidase
  • Destruction of follicles → antigen exposure (usually hidden)
    HLA-DR5
54
Q

Hashimoto thyroiditis epidemiology

A

45 and 65 years of age
* F>M 10:1 to 20:1.
* Diffuse goiter

55
Q

Risk for B cell lymphoma ( Marginal zone)

A

Hashimoto thyroiditis

56
Q

Gross morphology of Hashimoto thyroiditis

A

Pale diffusely
enlarged thyroid gland

57
Q

Microscopic morphology of Hashimoto thyroiditis

A

-Lymphocytic infiltration with germinal centers.
* Follicle atrophy
* Epithelial “Hürthle cells” changes
* Eosinophilic epithelial cells

58
Q

Postpartum thyroiditis MOA

A

-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
Q

Postpartum thyroiditis occurs during

A

-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
Q

Postpartum thyroiditis lab values

A

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
Q

subacture thyroiditis is also knnown as

A

– Granulomatous Thyroiditis
– DeQuervain thyroiditis

62
Q

epidemiology of subacute thyroiditis

A
  • Second most common form of thyroiditis
  • Most common cause of a painful thyroid
  • Females > Males; 30-50 years
63
Q

clinical features of subacute thyroiditis

A

post viral syndrome
-pain, fever, fatiigue, myalgia
assc. HLAB35

64
Q

microscopy of subacute thyroiditis

A

Granulomatous inflammation to extravasated colloid with lymphocytes, histiocytes, multinucleated giant
cells.
- self limited prognosis

65
Q

determine diagnosis:
-Rare disease of unknown etiology
- Destruction of thyroid gland
- Dense fibrosis and chronic inflammation

A

REIDEL’S THYROIDITIS

66
Q

REIDEL’S THYROIDITIS associated with inflammatory fibrosclerotic conditions (____)

A

mediastinal or retroperitoneal fibrosis, sclerosing
cholangitis)
* F > M; Middle age

67
Q

gross morphology of REIDEL’S THYROIDITIS

A

Tan gray, woody, avascular & no lobules apparent

68
Q

microscopic morphology of REIDEL’S THYROIDITIS

A
  • 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
Q

__________- ___________- _________is abnormal thyrid function test in normally functioning thyroid occuring in a setting of non thyroid illness
hospitalized pts

A

Euthyroid Side Syndrome

70
Q

pathogenesis of Euthyroid Side Syndrome

A

dec. thyroid hormones may limit catabolissm during illness
- cytokines downregulate thyroid hormone synthesis

71
Q

lab findings :Euthyroid Side Syndrome

A

dec T3
N/INC. T4
INC. Reverse T3
N/dec. TSH
dec. TBG

72
Q

Scalloping of the coloid tissue is commonly found in biopsy of :

A

Graves disease

73
Q

what is the rx for graves disease

A

B-blockers
thioamide
radioiodine ablation

74
Q

what diagnosis presents with “hard as wood “ non tender thyroid gland

A

reidel fibrosing thyroiditis

CAS 3 (10 decks)

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