Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho > Thyroid disease > Flashcards

Thyroid disease Flashcards

1
Q

Another name for Hyperthyroidism (HT)

A

thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Another name for Hypothyroidism (HoT)

A

myxedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What causes the formation of a goiter/ what is a goiter

A

goiter’s are inflammed thryoid glands

Prolonged elevation of TSH cause them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a thyroid nodule?

A

an overgrowth of cells that can be benign or cancerous - overgrowth of cells can be called neoplasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is neoplasm

A

an overgrowth of cells that can be benign or cancerous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the thyroid anatomy

A

hyoid bone
larynx
pyramidal lobe
right lobe and left lobe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is thyroidal peroxidase

A

catalyzes iodine oxidizes so it can then interact with thyroglobulin and form T4 and T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the two major cells in the thyroid and thier fucntions?

A

Follicular cells
- trap dietary iodine and transport it to colloid along with enzyme thyroidal peroxidase
-produce and secret thyroid hormone T3 and T4

Parafollicular cells
- secrete calcitonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the full names of T3 and T4

A

T3 - Triiodothyronine
T4 - Thyroxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain Thyroid hormone synthesis

A

The TSHR receptor on the outside of colloids is stimulated via TSH (whihc is produced from the pituitary gland)

Upon stimulation, it stimulates thyroglobulin, thyroid peroxide and iodine channels

idoien cahnnels allow idoine to enter collloid

iodine and thyroglobulin work together to form T3 and T4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which thyroid hormone is more widely found?

A

T4 - 90%
T3 - 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Before stimulation by TSH, how are the thyroid hormones found?

A

T3 and T4 are attached to thyroglobulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When the thyroid hormones are released what happens?

A

they bind to protein, are lipid-soluble, and diffuse from the follicle to the circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Discuss how thyroid hormone produce an effect when they are lipid soluble

A

since they are lipid soluble they travel bound to a protein

Only a small percanetge dissolve in plasm as free hormone and are ble to cross directly to their traget cell

T3 bind to its receptor and exerts its action, mediated thorugh alternation in gene transcript

T4 is acted on by cellualr enzymes that cleave one iodine unit converting it to active T3 form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What releases TSH

A

TRH - thyroid releasing hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What kind of disease is HT

A

autoimmune disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are some causes of HT

A
  • ingestion of thyroid hormone preparations or excess iodine
  • pituitary adenoma
  • hypothalamic disease
  • Inflammation: toxic thyroiditis of Hashimoto disease and sub-acute thyroidtis
18
Q

what is Hasimoto’s thyroditis

A

thyroid follicular cell destruction with release of preformed T4 and T3

19
Q

what is grave diseas

A

causes HT

  • antibodies stimulate TSHR and we have excess T3 and T4 release
20
Q

What are the classifications of HT and based on what criteria

A

primary: The thyroid gland is affected so T3 and T4

secondary: Hypophysis affects TSH

tertiary: Hypothalamus affected so TRH

ectopic: struma ovarii

21
Q

When in life do we get graves disease?

A

2 or 3 decades of life

22
Q

What HLA types make you more susceptible to graves disease?

A

HLA B-8, DR3 - caucasians
Bw46 and B5 - asaians
B17 - blacks

23
Q

Graves disease more common in male or females?

A

females

24
Q

Graves diseas is what kind of disease what’s it characterized by?

A

autoimmune disorder
- TSH-R (stim) antibody present in 90 % of cases

  • serum levels correlate poorly with severity
25
Q

Causes of graves disease?

A
  1. genetic
  2. molecular mimicry - TSH receptor
  3. Suppressor T lymphocyte defect
26
Q

Pathogenis of graves disease

A

defect in T helper cell allows for B cell generation in response to thryoid antigens producing antibodies,

Inflammation of orbit due to sensitization of T celler cells

27
Q

Histology of Graves disease

A
  • colloid scant
  • packed follicular with columnar epithelium
  • scattered lymohocytes
28
Q

Clinical manifestations of HT

A

Behavioral changes: insomnia, restlessness, tremor, irritability, palpitations, heat intolerance, diaphoresis, inability to concentrate,

Increase appetite and dietary intake

paradoxical weight loss

Scant menses

29
Q

Some more complicated clinical manifestations

A
  • thyromegaly
  • exophthalmos
  • widening of the palpebral fissure resulting in exposed sclera
  • vision changes (blindness), photophobia
30
Q

Key features of primary HT

A
  • undetectable levels of TSh however elevated serum T3 and T4
31
Q

how to confirm the presence of graves diseases and rule out the presence of thyroid neoplasm

A

24-hour radioactive iodine uptake study

32
Q

What is a thyroid storm?

A

dangerous levels of thyroid hormone acutely release
- life-threatening thyrotoxicosis

33
Q

S and S of thyroid storm

A
  • elevated temp, palpitations, arrhythmias, tachycardia
  • extreme restlessness, agitation, and psychosis
  • VND, and jaundice
34
Q

Acquired HoT thru what means?

A
  1. primary lymphocytic thyrodidtis (Hasimotot or autoimmune thyroidtis)
  2. Irradtion of thyroid galnd
  3. surgical removal of thyroid gladn
  4. iodine defieincfy
35
Q

Idoine in HoT

A
  • is essential for T3 and T4 synthesis
  • defeincy leads to lack of T3 and T4 but not thyrogloblulin levels
  • therefore ther is insuffient hormone to inhibit TSH secretion
  • increased TSH cause cells to secret large amounts of thyroglobulin, which leads to a goiter
36
Q

Secondary causes of HoT

A

Defects in TSH production that result from:

  • severe head trauama
  • cranial neoplasms
  • brain infections
  • cranial irradiation
  • neurosurgical procedures
37
Q

Clinical manifesttaions in infants

A
  • dull appearance, thick produlent tongue and lips, prolonged nenatal jaundice, poor mucle tone, bradycardia, mottled extremeites, hoarse cry, umbilical hernia
38
Q

Clinical manifestations in children/adults

A
  • decreas basal metbolic rate, weakness, lethargy, cold intolerance, decreased apapetite, bradycardia, narrowed pulse pressure, mild/moderate weight gain, elevated cholesterol and triglycerides, enlarged thyroid, dry skin, constipation, depression, difficulties with memory and concentration, menstrual irregulairty
39
Q

What does myxedema results from?

A

-prolonged/severe defienciy - edema due to accumulation of glycoaminoglycans in the interistal space

40
Q

what can myxedema patient present with? and what can it progress to?

A
  • altered mental status, altered temperature regulation, history of precipitating event (trauma/sepsis/infections)
  • can progress to myxedema coma and life-threatening condition
41
Q

Diagnosis of HoT

A
  • elevated TSH
  • later in the disease low levels of T3 and T4
42
Q

what results in low levels of TSh and T3 and T4

A

Hypothalamic-pituitary dysfunction

Patho (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions