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Endocrine System > Thyroid path & Chemical pathology > Flashcards

Thyroid path & Chemical pathology Flashcards

1
Q

What is Thyrotoxicosis ?

A

Thyrotoxicosis is the hypermetabolic state caused by increased levels of circulating thyroid hormones most commonly due to hyperthyroidism.

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2
Q

True or False? Grave’s disease is as a result of Hypothyroidism.

A

FALSE!! It is as a result of Hyperthyroidism

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3
Q

What are diseases that are as a result of Hypothyroidism?

A
  • Hashimoto’s thyroiditis
  • Iatrogenic : surgery , radiation, drugs
  • Dyshormonogenetic goitre( congenital biosynthetic defect)
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4
Q

What are the most common causes of Hyperthyroidism as a result of over functioning of the Thyroid gland?

A
  • Graves disease( diffuse toxic hyperplasia)
  • Hyper-functioning (“toxic”) multinodular goiter.
  • Hyperfunctional (“toxic”) adenoma of the thyroid
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5
Q

What is the main circulating antibody produced in Grave’s disease?

A

IgG

G for Graves duuhhh

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6
Q

True or False? Grave’s disease is considered a Type I hypersensitivity reaction.

A

FALSE!! It is a Type II sensitivity reaction.

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7
Q

What is the main gene associated with Grave’s disease?

A

HLA- DR3 and HLA-B8.

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8
Q

What are the autoantibodies that are produced in Grave’s disease?

A
  • Thyroid-stimulating immunoglobulin.
  • Thyroid-Growth stimulating immunoglobulin.
  • TSH- binding inhibitor immunoglobulin
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9
Q

Fill in the blanks. “ Multinodular goitre (MNG) is due to _____. “

A

Impaired synthesis of thyroid hormone.

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10
Q

Multinodulular goitre can arise as a result of a deficiency of what nutrient?

A

Dietary iodine

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11
Q

Which autoantibody in Grave’s disease is an IgG anti-body that binds to the TSH receptor and mimics the action of TSH?

A

Thyroid-stimulating immunoglobulin (TSI).

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12
Q

Which autoantibody in Grave’s disease antibodies have been implicated in the proliferation of thyroid follicular epithelium?

A

Thyroid Growth stimulating immunoglobulin .

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13
Q

Which autoantibody in Grave’s disease is anti-TSH receptor antibodies prevent TSH from binding to its receptor on thyroid epithelial cells and in so doing may inhibit thyroid cell function ?

A

TSH-binding inhibitor immunoglobulins.

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14
Q

What happens to the TSH levels if there is an impairment of Thyroid hormone such as in Goitre?

A

Increase in serum TSH

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15
Q

True or False? In goitre, The degree of thyroid enlargement is proportional to the level and duration of thyroid hormone deficiency.

A

TRUE!!

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16
Q

What are the different types of Multinodular goitre?

A

Sporadic or Endemic

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17
Q

When does Endemic goitre occur?

A

Endemic is used when goiters are present in more than 10% of the population in a given region.

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18
Q

What are the clinical features of Multinodular goitre’s?

A

Multiple nodules
Cysts
Haemorrhage
Fibrosis
Dystrophic calcification
Airway obstruction, dysphagia
Superior Vena Cava syndrome
Plummer syndrome

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19
Q

True or False? Thyroid adenomas are malignant.

A

FALSE!! They are benign

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20
Q

Which types of nodules are likely to be neoplastic?

A
  • Solitary nodules
  • Nodules in very young and very old persons.
  • Nodules in males
  • Nodules in males»>nodules in females.
    *Nodules that take up radioactive iodine in imaging studies (hot nodules) are more likely to be benign.
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21
Q

True or False? Cold nodules are likely to be benign while 10% of hot nodules are likely to become malignant.

A

FALSE!! 10% of cold nodules eventually prove to be malignant while Hot nodules are benign.

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22
Q

What are examples of Hot nodules?

A

Toxic adenoma- Produces T3 & T4 independent of TSH.

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23
Q

Which thyroid carcinoma is NOT derived from Thyroid follicular epithelium?

A

Medullary carcinoma

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24
Q

What are the types of Thyroid carcinoma?

A
  • Papillary carcinoma (accounting for more than 85% of cases)
  • Follicular carcinoma (5% to 15% of cases)
  • Anaplastic (undifferentiated) carcinoma (<5% of cases)
  • Medullary carcinoma (5% of cases)
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25
Q

Which gene mutation is associated with Follicular carcinoma of the Thyroid gland?

A

RAS or PI3K/AKT signaling pathway

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26
Q

Fill in the blanks. “ Follicular carcinoma of Thyroid gland is diagnosed only by _______.”

A
  • Invasion through capsule
  • Vascular invasion
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27
Q

What gene mutations are associated with Papillary carcinoma?

A

Activation of the MAP kinase pathway is a feature of most papillary carcinomas.

*RET on chromosome 10q —> leading to fusion gene called ret/PTC.

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28
Q

Which type of Thyroid carcinoma presents with an Optically Clea nuclei ( Orphan Annie eye)?

A

Papillary carcinoma

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29
Q

What are the histological findings in Papillary carcinoma of the Thyroid gland?

A
  • Papillae ( duh)
  • Can be composed of follicles
  • Overlapping nuclei with grooves
  • Optically clear nuclei ( Orphan Annie eye)
  • Nuclei pseudo-inclusions
  • Psammoma bodies in stoma of papillae
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30
Q

Where do Medullary carcinoma arise from?

A

Parafollicular C cells

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31
Q

Fill in the blanks. “ 80% of Medullay carcinoma can be _____ while 20% can be _____.”

A

80%- Sporadic ( 5th & 6th decade)
20%- Familial ( Young adults & kids )

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32
Q

What gene mutation is associated with Medullary carcinoma of the Thyroid gland?

A

RET

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33
Q

In what type of diseases can Familial Medullary carcinoma occur in also?

A

Multiple endocrine neoplasia type 2 (MEN-2) or Familial medullary thyroid carcinoma (FMTC)

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34
Q

Which gene mutation is associated with Anaplastic carcinoma?

A

TP53

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35
Q

Which carcinoma of the Thyroid gland can arise by progression of a well-differentiated papillary or follicular carcinoma?

A

Anaplastic carcinoma

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36
Q

The spread of Papillary carcinoma of the Thyroid gland occurs through what lymph nodes?

A

They spread mainly via lymphatics to cervical lymph nodes

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37
Q

Which type of Thyroid carcinoma is associate with Hürthle cells?

A

Follicular carcinoma

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38
Q

What substance is secreted by Medullary thyroid carcinomas?

A

Calcitonin ( because its occurs from the Parafollicular , C cells)

  • can be used for diagnosis
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39
Q

Which carcinoma of the Thyroid gland can present with Amyloid deposits?

A

Medullary carcinoma

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40
Q

What are symptoms of Cretinism seen in Hypothyroidism?

A
  • Impaired development of the skeletal system and central nervous system.
  • Severe mental retardation.
  • Short stature
  • Coarse facial feature
  • A protruding tongue,
  • Umbilical hernia.
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41
Q

What are the symptoms of Myxedema seen in Hypothyroidism?

A
  • Increased generalized fatigue
  • Increased apathy,
  • Increased mental slug- gishness, which may mimic depression
  • Constipation
  • Decreased sweating
    *Non- pitting edema,
  • Broadening and coarsening of facial features
  • Enlargement of the tongue
  • Deepening of the voice.
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42
Q

True or False? Serum T4 is decreased in Hypothyroidism.

A

TRUE!!

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43
Q

What are examples of Autoimmune Thyroiditis?

A

Hashimoto’s disease
Lymphocytic thyroiditis
Subacute Thyroiditis

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44
Q

Which substance is an intracellular second messenger for secretion of some hormones and neurotransmitters?

A

Calcium

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45
Q

What are the three forms that Calcium are present in the blood plasma?

A
  • Ionized Ca2+
  • Protein Bound
  • Complexed ( citrates, phosphates)
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46
Q

What is the physiologically active form of Calcium in the body?

A

Ionized Ca2+

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47
Q

Calcium is 80% bounded to what Protein in the blood plasma?

A

Albumin

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48
Q

What is the total calcium reference range?

A

2.25 – 2.75 mmol/L.

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49
Q

What is the ionized calcium reference range?

A

1.1 – 1.4 mmol/L.

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50
Q

What are the names of the Calcium regulating hormones?

A
  • Parathyroid hormone (PTH)
  • Calcitriol (1:25-dihydroxycholecalciferol)
  • Calcitonin (minor role).
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51
Q

Fill in the blanks .” Calcium regulating hormones also ____.”

A

Control the inorganic phosphate concentration of the ECF.

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52
Q

Which structure produces Parathyroid hormone?

A

Chief cells

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53
Q

True or False? Parathyroid hormone is a steroid.

A

FALSE!! It is a polypeptide comprising 84 amino acids.

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54
Q

What is the half life of Parathyroid hormone in the blood?

A

3-4 mins

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55
Q

Where does the biological activity reside in PTH?

A

N-terminal 1-34 amino acid sequence.

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56
Q

What is the principal acute regulator of Plasma Calcium?

A

Parathyroid hormone

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57
Q

True or False? Plasma PTH is lowest at about 1/2 am and highest at about 9 am.

A

FALSE!! It is lowest at 9 am and highest in the early morning 1 or 2 am.

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58
Q

What is the mechanism of action for parathyroid hormone in regards to calcium levels?

A

The active hormone is secreted in response to a fall in plasma [Ca2+], and its actions are directed to increase plasma [Ca2+].

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59
Q

What is the name of the receptor that Parathyroid hormone acts on ?

A

The parathyroid hormone 1 receptor & parathyroid hormone 2 receptors

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60
Q

Where are parathyroid hormone 1 receptors located?

A

High levels in bone & kidney

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61
Q

Where are parathyroid hormone 2 receptors located?

A

High levels in the central nervous system, pancreas, testis, and placenta

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62
Q

Fill in the blanks. “Binding of PTH to its receptor activates 2 signaling pathways:______ & _______”

A
  • Increased cyclic AMP
  • Increased phospholipase C
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63
Q

True or False? An increase in plasma [Ca2+] suppresses PTH secretion.

A

TRUE!!

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64
Q

What happens when PTH acts on the kidneys?

A

There is a net effect of lowering glomerular filtration rate (GFR), increasing the reabsorption of calcium and magnesium, and decreasing the reabsorption of phosphate and bicarbonate (increase excretion).

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65
Q

What substance is produced when PTH acts on the kidneys?

A

It stimulates the production of biological active form of Vitamin D- 1,25(OH) 2D.

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66
Q

How does PTH act on the bones?

A

It increases the degradation of bones ( which INCREASES the release of calcium)

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67
Q

True or False? PTH will stimulate Osteoclasts but NOT Osteoblast activity.

A

FALSE!! It will stimulate both Osteoclast & Osteoblast activity.

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68
Q

How does PTH stimulate Osteoclasts?

A

PTH stimulates bone stem cells to develop into osteoclasts

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69
Q

When PTH stimulates Osteoblast activity what other substance is increased?

A

ALP & a calcium-binding protein osteocalcin

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70
Q

Fill in the blanks. “ Most vitamin D3 (Cholecalciferol) is synthesized by the action of ________ on 7-hydrocholesterol precursor in the skin.”

A

Ultraviolet light rays

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71
Q

What is the name of the enzyme that catalyzes the hydroxylation of cholecalciferol with the formation of 25-hydroxycholecalciferol (25-HCC, calcidiol)?

A

25-Hydoxylase

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72
Q

True or False? Vitamin D is actually a hormone than a vitamin.

A

TRUE!!

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73
Q

Which form of Vitamin D is measured in the blood?

A

Calcidiol ( 25- OH or Hydroxy vitamin D)

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74
Q

What is the plasma half life of Calcidiol?

A

15-25 days

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75
Q

Where does Calcidiol undergo hydroxylation to form Calcitriol (1:25-DHCC) - active vit D?

A

In the kidney

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76
Q

What is the name of the enzyme which aids in the formation of Calcitriol from Calcidiol ?

A

1-α hydroxylase

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77
Q

What is the active form of Vitamin D3?

A

Calcitriol (1,25 dihydroxy Vitamin D)

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78
Q

What is the inactive form of Vitamin D3?

A

Calcitroic acid (24,25 - dihydroxy vitamin D)

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79
Q

Where is 1α-hydroxylase enzyme located ?

A

In the proximal convoluted tubules of the nephrons.

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80
Q

The enzyme 1α-hydroxylase is inhibited by what substances?

A

1:25-DHCC (Calcitriol) and by hyperphosphataemia (high phosphate)

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81
Q

The enzyme 1α-hydroxylase is stimulated by what substances?

A

PTH and hypophosphataemia (low phosphate)

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82
Q

What is the name of the enzyme that converts Calcidiol ( 25, hydroxycholecalciferol or 25 HCC) to Calcitroic acid ( 24,25 dihydroxycholecalciferol) ?

A

24-hydroxylase

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83
Q

What are the main actions of Calcitriol?

A
  • Promotes intestinal reabsorption of calcium .
  • Promotes bone mobilization.
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84
Q

What is the name of the calcium- binding protein that promotes the absorption of calcium and phosphate from the gut lumen to the plasma compartment?

A

Calbindin-D

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85
Q

Calcitonin is produced by what cells?

A

Parafollicular or C cells

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86
Q

What is the main target cell for Calcitonin?

A

Osteoclasts

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87
Q

True or False? Calcitonin Increases osteoclast activity but DECREASES osteoblast activity.

A

FALSE!! Calcitonin Inhibits Osteoclasts activity but Increases Osteoblastic activity .

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88
Q

During what conditions are Calcitonin levels increased?

A

Pregnancy & Lactation

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89
Q

What are the actions of Calcitonin?

A
  • It lowers Calcium
  • It inhibits Calcium absorption by intestines
  • Inhibits Calcium reabsorption in the kidney.
  • Inhibits Osteoclasts
  • Promotes deposition of Calcium into bones
90
Q

What are the common cause of Hypercalcemia?

A
  • Malignant disease, e.g. some lung cancers
  • Hyperparathyroidism
  • Vitamin D toxicity (excessive intake
91
Q

What are the uncommon causes of Hypercalcemia?

A
  • Renal failure
  • Sarcoidosis
  • Multiple myeloma
92
Q

What is the most common single presenting complaint from a patient with Primary Hyperparathyroidism?

A

Renal stones

93
Q

What is Primary Hyperparathyroidsim characterised by?

A

Hypercalcemia
Hypercalcuria
Hypophosphatemia
Hyperphosphaturia.

94
Q

What is Primary Hyperparathyroidism?

A

There is the autonomous production of PTH which occurs from a single, parathyroid adenoma (tumour), diffuse hyperplasia (all four glands) or, rarely, parathyroid carcinoma may be responsible.

95
Q

What are the causes of Secondary Hyperparathyroidism ?

A
  • Kidney failure during dialysis
  • Celiac disease
    *Crohn’s disease
    *Severe vit D deficiency
    *Stomach or Intestinal Obesity surgery.
96
Q

In what type of patients is secondary hyperparathyroidism seen?

A
  • It occurs in patients with chronic renal failure or in disorders where there is malabsorption of fat soluble vitamin D.
  • Osteromalcacia &rickets
97
Q

What happens to the Calcitriol production when the phosphate levels are increased?

A

An increase in phosphate level suppresses Calcitriol production .

98
Q

What are the factors implicated in Hypercalcemia of malignancy?

A
  • Tumour necrosis factor,
  • Interleukin -1
  • Prostaglandins.
99
Q

True or False? The very high plasma total calcium usually observed in patients with multiple myeloma reflects increased binding of calcium by paraprotein.

A

TRUE!!

100
Q

Fill in the blanks. “ In Hypercalcemia of malignancy , The malignant plasma cells secrete immunoglobulin of a single class only called a ________.”

A

Paraprotein or monoclonal

101
Q

What is Milk alkali syndrome?

A

Decrease renal excretion of calcium. Ingestion of alkali decreases renal excretion of calcium

102
Q

Which drug can cause Hypercalcemia?

A

Thiazides diuretics

103
Q

True or False? Vitamin D deficiency can cause Hypocalcemia.

A

TRUE!!

104
Q

Which drug can induce enzymes that catabolise vitamin D?

A

Phenytoin

105
Q

What are the causes of Hypoparathyroidism?

A

Thyroid surgery
Parathyroid surgery
Autoimmune
Infiltrative
Familial
Idiopathic

106
Q

What is Pseudohypoparathyroidism?

A

Pseudohypoparathyroidism is a genetic disorder associated primarily with resistance to the parathyroid hormone (body fail to respond to PTH).

107
Q

What are the clinical findings in Pseudohypothyroidism ?

A

Low serum calcium
High Phosphate
High PTH

108
Q

What happens in Type I pseudohypoparathyroidism ?

A

Activation of adenyl cyclase is defective and cyclic AMP is not formed in response to the binding of PTH to its receptor.

109
Q

What happens in Type II Pseudohypoparathyroidism?

A

Cyclic AMP is formed, but the response to it is blocked (defective G proteins).

110
Q

How can one differentiate between Type I and Type II Pseudohypoparathyroidism?

A

By measuring the urinary cyclic AMP levels

111
Q

What is the function of the hypothalamic-pituitary axis ?

A

To regulate hormone function.

112
Q

Fill in the blanks.” Release of TSH from the pituitary gland is stimulated by _____________ from the hypothalamus.”

A

Thyrotropin releasing hormone (TRH)

113
Q

What is the Hypothalamic- Pituitary axis?

A

The hypothalamic-pituitary axis is a classical negative feedback regulatory mechanism in which secretion of thyroid stimulating hormone (TSH) is modulated by thyroid hormones (FT3 & FT4).

114
Q

Where in the body is T4 (Thyroxine) converted to T3 ( Triiofothyronine)?

A

In the kidneys, liver, brain and Skeletal muscle

115
Q

What is the name of the enzyme that converts T4 to T3?

A

Iodothyronine Deiodinase

116
Q

What is an inactive byproduct of Deiodination?

A

rT3 - Reverse T3

117
Q

What is the normal amount of T3 produced on a daily basis?

A

6 mcg/day

118
Q

What is the normal amount of T4 produced on a daily basis?

A

100 mcg/day

119
Q

What is the name of the hormone that stimulates Thyroid gland to release thyroid hormone?

A

Thyroid -stimulating hormone TSH ( Thyrotropin )

120
Q

What substances act at the hypothalamic level by inhibiting mRNA for TRH synthesis?

A

T3 &T4

121
Q

What is the name of the transporter by which iodide enters the follicular lumen from the cytoplasm?

A

Pendrin

122
Q

What is the name of the enzyme that aids in the oxidation of iodide to IODINE?

A

Thyroid peroxidase

123
Q

Where does oxidation of Iodide to Iodine occur?

A

In the colloid

124
Q

Fill in the blanks. “Iodine (I0) is very reactive and iodinates the thyroglobulin at________ in its protein chain. “

A

Tyrosyl residues

125
Q

What are the substances formed at the end of Conjugation?

A
  • Mono-iodotyrosine (MIT)
  • Di-iodotyrosine (DIT)
126
Q

What is the name of the process in T3& T4 synthesis in which adjacent tyrosyl residues are paired together?

A

Conjugation

127
Q

How is the production of T3 & T4 formed?

A

By the coupling iodotyrosyl residues in the thyroglobulin molecule.

( MIT + DIT = T3)
(DIT +DIT = T4)

128
Q

What are the functions of the Thyroid gland?

A
  1. Role in growth
  2. Role in CNS development

3.Stimulates heart rate

  1. Stimulates heart contraction .
  2. Stimulates synthesis of proteins and carbohydrates
  3. Degrade cholesterol & Triglycerides
  4. Enhances beta- adrenergic receptors to catecholamines

8.It increases vitamin requirements

  1. Increase gluconeogenesis & glycogenesis
  2. Increases glucose intestinal absorption
129
Q

Thyroid releasing hormone is produced by ?

A

Hypothalamus

130
Q

True or False? Thyroid releasing hormone is down-regulated by T4.

A

FALSE!! It is down-regulated by T3

131
Q

Fill in the blanks. “ Thyroid stimulating hormone is secreted by _______.”

A

Thyrotrophs of the anterior pituitary.

132
Q

What is the major external regulator of the Thyroid gland?

A

Thyroid stimulating hormone (TSH)

133
Q

Where is the TSH receptor located?

A

On the BASAL surface of the thyroid follicular cell.

134
Q

What happens when there is an INCREASE in plasma TSH?

A
  • Release of formed T3 and T4
  • Increased rate of iodide uptake
  • Increased rate of synthesis
  • Increased size and number of follicles.
135
Q

What happens to the TSH levels in Primary HYPOTHYROIDISM ?

A

They are HIGH !!

136
Q

What is the most sensitive screen test for hyperthyroidism and primary hypothyroidism ?

A

Testing the TSH levels

137
Q

True or False? In Secondary Hypothyroidism the TSH levels is HIGH while in Tertiary Hypothyroidism the TSH levels are Normal.

A

FALSE!! It is appropriately NORMAL or LOW in secomdary & tertiary hypothyroidism

138
Q

Why is the TSH levels high in Primary hypOthyroidism?

A

This occurs because of a loss of feedback inhibition of thyrotropin-releasing hormone (TRH) and TSH production by the hypothalamus and pituitary, respectively

139
Q

True or False? The TSH levels are also INCREASED in individuals with hypO thyroidism caused by primary hypothalamic or pituitary disease.

A

FALSE!! The TSH concentration is NOT increased in individuals with hypo- thyroidism caused by primary hypothalamic or pituitary disease.

140
Q

What is the name of the substance to which thyroid hormones are bound to and transported in the blood?

A
  • Thyroxine-binding globulin (TBG) binds about 70% of plasma T4 and 80% of plasma T3.

*Thyroxine-binding pre-albumin and albumin .

141
Q

What percentage of T4 & T3 are free ( unbound to protein)

A

T4 - 0.05%
T3 - 0.2%

142
Q

What is the normal concentration of Total T4?

A

60 – 150 nmol/L

143
Q

What is the normal concentration of T3?

A

1.0 – 2.9 nmol/L

144
Q

What drugs can cause a DECREASE in Thyroxine - binding globulins ?

A
  • Anabolic Steroids ( Androgens)
  • Glucocorticoids
145
Q

What drugs can cause an INCREASE in Thyroxine - binding globulins ?

A
  • Oral contraceptives ( oestrogens)
  • Heroin or Methadone abuse
  • Clofibrate or 5- Fluorouacil ( Adrucil)
146
Q

Which classification of Thyroid Function tests deals with testing the primary function of the Thyroid Gland?

A

Group I

147
Q

Fill in the blanks.” Group III Thyroid function test measures _____.”

A

The Metabolic effects of the Thyroid hormone.

148
Q

Which classification of Thyroid Function tests deals with the Immunological tests for auto-immune diseases?

A

Group IV

149
Q

Which classification of Thyroid Function tests deals with the measurement of blood levels of thyroid hormones?

A

Group II

150
Q

What are the clinical aspects of Group IV Thyroid function tests?

A

Agar gel diffusion test
Complement Fixation Test

151
Q

Which group of thyroid function tests deals with:
- Radio-iodine uptake
-T3 - suppression test
-TSH - stimulation test
- TRH- stimulation test?

A

Group I

152
Q

Which group of thyroid function tests deals with:
- Basal Metalic rate
- Serum cholesterol level
- Serum creatine
- Serum uric acid
- Serum creatine kinase level?

A

Group III

153
Q

What are the clinical aspects Group II Thyroid function tests?

A
  • Total T3 & T4
  • Free T3 &T4 levels
  • Circulating TSH levels
  • Plasma Tyrosine level
154
Q

What is the normal of TSH?

A

0.4 – 4.0 mU/L

155
Q

What is the concentration of Free T3 (triiodothyronine)?

A

1.5 – 4.1 pg/mL

156
Q

What is the concentration Free T4 (thyroxine)?

A

0.8 – 1.9 pmol/L

157
Q

What are nutrients that can be tested for during Thyroid tests?

A

Vitamin D
Vitamin B12
Iodine
Magnesium
Iron
Zinc

158
Q

What is the autoantibody thyroid test that can be used for suspected Hypothyroidism/ Hashimotos’s?

A

Thyroid Peroxidase Antibodies
(TPO)

159
Q

What is the autoantibody thyroid test that can be used for suspected Hyperthyroidism/ Grave’s?

A

Thyroid Stimulating Immunoglobin (TSI)

160
Q

Fill in the blanks. “ Primary thyroid disease is an abnormality of ________.”

A

Thyroid Gland

161
Q

True or False? Secondary Thyroid disease is abnormality in hypothalamus while Tertiary Thyroid diseases an abnormality in pituitary gland.

A

FALSE!! Second thyroid disease is really an abnormality in PITUITARY GLAND.
Tertiary thyroid disease is abnormality in HYPOTHALAMUS

162
Q

Fill in the blanks. “In Secondary Thyroid diseases, an abnormal amount of __________ is produced .”

A

Thyroid stimulating hormone(TSH)

163
Q

Fill in the blanks. “In Tertiary Thyroid diseases, an abnormal amount of __________ is produced .”

A

Thyrotropin-releasing hormone (TRH )

164
Q

During Hypothyroidism , what happens to the Plasma Free T4 levels?

A

It is DECREASED

165
Q

During Hypothyroidism, what happens to the Plasma Free T3 levels.

A

It remains NORMAL

166
Q

During Hypothyroidism, what happens to the TSH levels?

A

It is INCREASED

167
Q

What are the conditions which can cause an Increase in Radio-active uptake?

A
  • Grave’s disease
  • Toxic multi- nodular goitre
  • Toxic adenoma
  • hCG secreting tumours - hyadatidiform mole
  • choriocarcinoma
  • TSH mediated thyrotoxicosis
  • pituitary tumour
  • pituitary resistance to thyroid hormone
  • Iodine deficiency
168
Q

Fill in the blanks. “ Low uptake or radioactive iodine suggests ______, while high uptake of radioactive iodine suggests _________.”

A

Low uptake suggests THYROIDITIS , high uptake suggests GRAVES DISEASE

169
Q

What are examples of Primary Hyperthyroidism?

A
  • Graves disease
  • Autonomous toxic adenoma
  • Multinodular toxic goitre
    *Iodine Overload , Procor
170
Q

What are examples of Secondary hyperthyroidism ?

A

*TSH -producing pituitary adenoma
* Thyroid hormone resistance
* Gestational thyrotoxicosis

171
Q

What happens to the cholesterol level in Grave’s disease?

A

Decreased serum cholesterol

172
Q

What is the most common anti-thyroid antibody that is present in Hashimoto’s disease?

A
  • Anti-thyroid peroxidase (anti-microsomal antibodies)

*Anti-thyroglobulin antibodies

173
Q

What are the anti-thyroid antibodies present in Grave’s disease?

A
  • Anti-thyroid peroxidase (anti-microsomal antibodies)

*Thyroid stimulating immunoglobulins (thyroid receptor antibodies)

  • Anti-thyroglobulin antibodies
174
Q

True or False? Subacute thyroiditis normally occurs after a viral infection of the lower respiratory tract.

A

FALSE!! Subacute thyroiditis normally occurs after a viral infection of the UPPER respiratory tract.

175
Q

True or False? Subacute thyroiditis is diagnosed based on a very low radioiodine I-123 uptake.

A

TRUE !!!

176
Q

Fill in the blanks. “ Primary Hyperthyroidism is caused by _______.”

A

Thyroid destruction

177
Q

Fill in the blanks. “ Secondary Hyperthyroidism is caused by _______.”

A

*A deficiency of Thyroid Stimulating hormone.

  • Pituitary or hypothalamic neoplasms.
  • Congenital hypopituitarism
  • Pituitary necrosis (Sheehan’s syndrome)
178
Q

What is the treatment of Hashimoto’s disease ?

A

Levothyroxine

179
Q

What is the Pathogenesis of Hashimoto’s thyroiditis
( Chronic lymphocytic thyroiditis) ?

A

Hashimoto’s thyroiditis is an autoimmune disease
in which the immune system reacts against a variety of Thyroid agents.

180
Q

What is the laboratory test used to confirm the diagnosis Hashimoto’s thyroiditis?

A

TSH,T4, andanti-thyroid autoantibodies.

181
Q

What are the laboratory values for Hashimoto’s thyroiditis?

A

High TSH
Low T4
Anti-TPO Ab
Anti-TBG Ab

182
Q

What type of Hypersensitivity is seen is Hashimoto’s disease?

A

Type IV hypersensitivity (cell mediated)

Type II hypersensitive (antibody mediated)

183
Q

Fill in the blanks. “ Secondary Hypothyroidism involves _________.”

A

Decreased activity of the thyroid caused by failure of the pituitary gland.

184
Q

What happens to the TSH levels in Secondary Hypothyroidism ?

A

It is “inappropriately normal” due to the fact that TSH secreted by the pituitary may not be as biologically active, but it is picked up by the assay.

  • results are normally generally low
185
Q

What laboratory findings associated with Secondary Hypothyroidism ?

A

Free T4 (low)
Free T3 (low)
Serum TSH – Results are generally low in secondary hypothyroidism because the pituitary is damaged. However, normal values may be seen.

186
Q

Which additional laboratory tests can be used to help determine the diagnosis of Secondary Hypothyroidism?

A
  • Increased total cholesterol levels
  • Increased liver enzyme (AST)
  • Low serum sodium
  • Low blood glucose
  • Elevated creatine kinase (CK)
187
Q

Which drugs can cause Hypothyroidism?

A

Dopamine ( secondary /Tertiary)
Lithium
Amiodarone
Interferon

188
Q

What is the inner layer of the Adrenal gland called?

A

Adrenal medulla

189
Q

What is the outer layer of the Adrenal gland called?

A

Adrenal cortex

190
Q

What are the main substances secreted by the Adrenal medulla?

A

Catecholamines - Epinephrine & Norepinephrine

191
Q

What substances are secreted by the Adrenal cortex?

A
  • Glucocorticoid - cortisol.
  • Mineralocorticoid - Aldosterone.
192
Q

What are the layers of the Adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
193
Q

Which layer of the Adrenal cortex secretes androgens- androstenedione, dehyroepiandrosterone (DHEA), estrogen, testosterone.

A

Zona Reticularis

  • think rectum - then think male reproductive organ near rectum then think male hormones.
194
Q

Which layer of the adrenal cortex secretes mineralocorticoids- aldosterone ?

A

Zona glomerulosa

  • think glomerulus then think kidney then think water then think aldosterone
195
Q

Which layer of the adrenal cortex secretes glucocorticoids- cortisol, corticosterone?

A

Zona fasiculata

196
Q

What is Cushing’s syndrome?

A

Cushing’s syndrome refers to excess cortisol of any etiology.

197
Q

What is the most common cause of Adrenal Cushing’s syndrome ?

A

Cortisol-secreting adenoma in the cortex of the adrenal gland

198
Q

In Cushing’s syndrome , what happens to the ACTH levels?

A

They are LOW - This is because the tumour will be providing large amounts of cortisol and therefore large amounts of negative feedback on the pituitary.

199
Q

What are the clinical features of Cushing’s syndrome?

A

Truncal Obesity
Moon facies
Buffalo hump
Thinning of skin
Hirsutism (excess hair around mouth and chin )
Hemorrhagic purple-red striae of skin
Glucose- Intolerance

200
Q

What are the different types of Cushing Syndrome?

A
  • ACTH - dependent ( Example - Pituitary
    Cushing syndrome and Ectopic (paraneoplastic) Cushing syndrome.)
  • ACTH - independent - ( Example - Adrenal adenoma or carcinoma)
  • Iatrogenic Cushing syndrome
201
Q

True or False? Pituitary
Cushing syndrome is the ONL ACTH-secreting tumour that is termed Cushing disease.

A

TRUE!!

202
Q

Where is the most common location for an Ectopic (paraneoplastic) Cushing syndrome?

A

Lung ( small cell carcinoma of the lung which can also secret ACTH)

203
Q

What is the name of the test that is primarily used to screen for excess cortisol production (Cushing’s syndrome) and are useful in detecting dysregulated cortisol hypersecretion?

A

Dexamethasone suppression tests (DSTs)

204
Q

What other examples of tumours can give rise to Ectopic (paraneoplastic) Cushing’s syndrome?

A

Carcinoids
Medullary cancer of the Thyroid
PanNETS

205
Q

Which drugs can give a false positive of a High dose Dexamethasone suppression tests (DSTs)?

A

Phenytoin & Rifampicin

206
Q

During the high dose Dexamethasone suppression tests (DSTs), If the ACTH levels are LOW and the cortisol levels is not suppressed it is indicative of what type of Cushing’s syndrome?

A

Adrenal Cushing syndrome

207
Q

During the high dose Dexamethasone suppression tests (DSTs), If the ACTH levels are HIGH and there is Lack of suppression it is indicative of what type of Cushing’s syndrome?

A

Ectopic Cushing syndrome

208
Q

True or False? A serum cortisol concentration < 50 nmol/L (at 0900h) confirms the diagnosis of Addison’s disease).

A

TRUE!!

209
Q

What is the name of the test given that assess the functioning of theadrenal glandsstress response by measuring the adrenal response toadrenocorticotropic hormone(ACTH)?

A

ACTH stimulation test(also called theSynacthen test)

210
Q

What is the function of Aldosterone?

A

Promotes sodium retention and potassium elimination by the kidney.

211
Q

What is Conn’syndrome?

A

This refers to the excess production of the hormone aldosterone from the adrenal glands, resulting in low renin levels.

212
Q

What are the laboratory findings in Conn’s syndrome?

A

High Na
High Chloride
Low Potassium

213
Q

How is the diagnosis of a Pheochromocytoma achieved?

A

Measuringcatecholaminesandmetanephrinesin plasma (blood) or through a 24-hour urine collection.

214
Q

What are the symptoms of a pheochromocytoma?

A

Paroxysmal attacks
Hypertension
Headaches
Diaphoresis ( Sweating)
Palpitations

215
Q

The presence of what substances can confirm the diagnosis of a pheochromocytoma?

A

Vanilllyl Mandelic Acid
Homo Vanillyc acid

  • Breakdown products of catecholamines
216
Q

What is the treatment for a Pheochromocytoma?

A

Alpha- blockers ( Phenoxybenzamine)
Surgical removal of tumour

217
Q

What is the common location for a Pheochromocytoma?

A

Medulla of the adrenal glands

218
Q

What is a pheochromocytoma?

A

Pheochromocytoma (PCC) is a neuroendocrine tumour of the medulla of the adrenal glands that secretes high amounts of catecholamines, mostly norepinephrine, plus epinephrine to a lesser extent.

219
Q

Metanephrine and Normetanephrie are metabolites created by the action of which enzyme?

A

Catechol-O-methyl transferase

220
Q

Which drug can you give you false positive when testing for the diagnosis of a pheochromocytoma using Metanephrine &. Nor-metanephrine?

A

Acetaminophen

221
Q

What is the name of the enzyme that breaks down Metanephrine to Vanillymandelic Acid
(VMA)?

A

Monoamine Oxidase ( MAO)

222
Q
A

Endocrine System (10 decks)

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