Endocrine Flashcards

1
Q

What is the name of the eye pathology associated with Graves disease?

A

Exopthlamos

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2
Q

List the broad effects of T3/4 on the body

A
  1. Metabolic (increase metabolism)
  2. Sympathetic (increase)
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3
Q

What are the treatment options for hyperthyroidism?

A
  1. Carbimazole (inhibits thyroid peroxidase)
  2. Surgery to remove thyroid
  3. radioactive iodine to destroy thyroid
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4
Q

A common side effect of carbimazole aside from hypothyrodisim?

A

Agranulocytosis - WBC deficiency

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5
Q

What does a non-visible JVP usually mean?

A

Hypotension

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6
Q

What are the Adrenal cortex zones and what do they make?

A

GFR - Glomerulosa, Fasciculata, Reituclaris.
Salty, Sweet, Sexy.
Aldosterone, Glucocorticoids, Androgens.

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7
Q

What causes Cushing’s Disease?

A

Pituitary adenoma causing ACTH overrelease

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8
Q

Name 2 each of ACTH dependant and independant Cushing’s syndrome.

A

ACTH dependant - Cushings disease or ectopic ACTH producing tumour.

ACTH independant - adrenal adenoma, exogenous steroids.

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9
Q

Which test could differentiate between Cushing’s disease and an ecoptic ACTH tumour?

A

Dexamethasone suppression test (should shut off pituitary ACTH).

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10
Q

Name a primary and secondary cause of adrenal insufficiency.

A

Primary - Addison’s disease
Secondary - stopping long term steroids

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11
Q

Bronze gums are a red flag for what?

A

Addison’s disease

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12
Q

Why does Cushing’s disease cause red striae, muscle weakness and poor healing?

A

Striae - decreased collagen
Weakness - gluconeogenesis
Healing - immune suppression

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13
Q

What are the three hormones in the cortisol ladder and where are they made?

A

CRH - hypothalamus
ACTH - pituitary
Cortisol - adrenals

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14
Q

What is the must common cause of Cushing’s syndrome?

A

Iatrogenic - steroids.

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15
Q

How can Cushing’s cause HTN?

A

Cortisol has minor mineralocorticoid actions, so it will increase Na absorption and water retention.

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16
Q

What are the molecules involved in osteoclast vs osteoblast activity and how is estrogen involved? How is cortisol involved?

A

Osteoblasts make RANK-L which activates osteoclasts. OPG blocks RANK-L.
Estrogen ups OPG.
Cortisol inhibits osteoblast activity and promotes osteoclast activity.

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17
Q

Why is normal ACTH levels and huge cortisol levels abnormal?

A

Huge cortisol levels should cause very low ACTH levels, even if they are ‘normal’ that is still atypical.

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18
Q

Outline the steps in T3/4 production.

A

Iodine enters thyroid follicular cell.
Thyroglobulin (TG) is made is the thyroid follicular cell.
TG is exported into lumen by exocytosis.
Thyroid peroxidase iodinated tyrosine residues of the TG. Can have 3 or 4.
TGs paired.
Endocytosis of TG back into Thyroid Follicular cell.
Proteolysis to split TGs.
Release into body by MCT8 channel.

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19
Q

Which thyroid carrying protein has the best affinity for T3/4?

A

Thyroid Binding Globulin - main carrier

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20
Q

Does the blood have more T3 or T4?

A

T4 - better at travelling due to longer half life, is converted to T3 in cells because T3 is more potent.

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21
Q

What organelle is the site of cholesterol production and what molecule is needed to assist?

A

Mitochondria, needs StAR.

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22
Q

What are the 2 steps of steroid production?

A
  1. Cytochrome p450 turns cholesterol into pregnenolone
  2. Pregnenolone into progesterone by hydroxysteroid dehydrogenase
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23
Q

Which hormone classes form homodimers, which form heterodimers, which have cytosolic receptors and which have nucleic receptors?

A

T3/4 - heterodimer (has T in it, nucleus).
Steroids - homodimer, cytoplasm

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24
Q

Which two hormones are trophic for prolactin and which molecule inhibits prolactin?

A

PRF and TRH (weirdly), dopamine shuts off prolactin

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25
Q

What are somatotropin, somatostatin and somatomedin and where are they made?

A

Somatotropin is Growth Hormone
Somatostatin is inhibitory and is made in the hypothalamus.
Somatomedin are the insulin like growth factors (IGF) made from GH in liver. - does all the hard work

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26
Q

What is the tropic hormone for GH and what is it in balance with?

A

GHRH from hypothalamus, in balance with somatostatin

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27
Q

Compare cretinism to dwarfism and which hormones cause each?

A

Cretinism - low T3/4 in childhood
Dwarfism - low GH in childhood

28
Q

How do Type 1 Hypersensitivities work?

A

Type 1 = allergies.
IgE made by B cells sensitises mast cell FC receptor.
Re-exposure to the allergen will allow the IgE imbedded on the Mast cells to cross link causing massive histamine release.

29
Q

Outline the origin and function of PTH and Calcitonin.

A

PTH - parathyroid
- stimulates vit D activation
- promotes kidney Ca absorption
- bone degradation
- osteoclasts up

Calcitonin - C Cell of thyroid.
- inhibits vit D
- lowers kidney Ca resorb
- inhibits gut Ca absorb
- inhibits osteoclasts

30
Q

Chronic B12 deficiency can lead to what?

A

Nerve damage and inability to activate folate - anemia.

31
Q

What deficiencies are vegans at risk of?

A

Meat and dairy baby: Fe, Ca, B12, Vit D. (and zinc)

32
Q

Side effects of hypercortisolemia?

A
  • weight gain
  • muscle wasting
  • hyperglycemia
  • HTN due to salt retention
33
Q

What is congenital adrenal hyperplasia and what impact does it have on hormones?

A

Enzyme that makes corticoids is shot so adrenals just make androgens and HEAPS of them as ACTH is trying to get cortisol cooking.
Leads to hirsutism in females, abnormal growth or adrenal crisis in males.

34
Q

What is fludrocortisone?

A

Really great drug that acts as a powerful mineralocorticoid

35
Q

Which molecules control aldosterone release?

A

Mostly ANG2 but a bit of ACTH too.

36
Q

Which histological types makeup the anterior pituitary and how will you remember them?

A

Split into acidophils (pink) and basophils (purple), acidophils make prolcatin and GH so think ‘big pink tits’ - rest made by basophils.

37
Q

What is the most common pituitary adenoma type, 2nd?

A

-prolactinoma - amennorhea in females, asymptomatic in men
- GH adenoma is 2nd, causes acromegaly
-corticotroph adenoma is 3rd

38
Q

What is the mechanism of Addison’s disease?

A

Autoimmune adrenalitis - Ig kills cortex of adrenals.

39
Q

List the 4 adrenal neoplasms I need to know.

A

2x cortical and 2x medullary. One each of benign and malignant.
Cortical: Adrenal Adenoma (benign but cause hormone release). Adrenal carcinoma (very poor prognosis).

Medullary:
Pheochromocytoma - benign - catecholamine disease.
Neuroblastoma - malignant. (kids).

40
Q

What is the most common cause of acute adrenal insufficiency?

A

Stopping corticosteroids suddenly

41
Q

Symptoms of hypercalcaemia?

A

Bones, Moans (Neuro), Stones, Groans (GIT)

42
Q

What is someone likely to have if they have multiple primary endocrine tumours in different locations?

A

MEN syndrome - Multiple Endocrine Neoplasms Syndrome

43
Q

Describe a classic patient with hyperthyroidism?

A

Thin, hot, sweaty bugs (bug eyes).

44
Q

What is the target of Hashimoto’s?

A

IgG to thyroid peroxidase (TPO).

45
Q

Describe the histology of Graves vs Hashimotos.

A

Regular thyroid - follicles look like big crinkle cut chips.
In Graves - these are breaking down and may be filled with clear vacuoles.

In Hashimotos - these are full of purple - WBC.

46
Q

What is the gold standard pathology test for thyroid nodules?

A

Fine Needle Aspirate - not biopsy.

47
Q

Discuss the epidemiology of singular thyroid nodules.

A

More common in women but worse in men.
A bigger worry if in young people.
Hot nodule = taking up iodine, not likely to be a malignancy (cold is bad).

48
Q

What are the 4 thyroid cancers I need to know and describe their histology.

A
  1. Follicular adenoma
  2. Follicular Carcinoma - looks same as above, need resection.
  3. Papillary carcinoma - most common thyroid malignancy. Ground glass nuclei, orphan annie eyes. Coffee bean nuclei.
  4. Medullary carcinoma - from C cells of thyroid. 100% chance if they have MEN syndrome.
49
Q

How could you differentiate between patients with Cushings vs Metabolic Syndrome.

A

The SKIN - affected in Cushings, not in Metabolic syndrome.

50
Q

If the source of a Cushing’s Syndrome is in the adrenal, what will the contralateral adrenal look like.

A

very atrophied due to negative feedback.

51
Q

How to treat symptoms of hyperthyroidism?

A

B- Blocker.

52
Q

Main feature of pituitary adenoma on histo?

A

Cellular monomorphism - pituitary should be full of 3 different cell types, any 1 dominating is a giveaway.

53
Q

What does hypocalcaemia cause?

A

Muscle cramps and mouth tingles

54
Q

What stain is used for medullary thyroid carcinoma?

A

Congo red to detect amyloid

55
Q

name 4 conditions common in MEN Syndrome

A

Parathyroid hyperplasia, medullary thyroid carcinoma, pituitary adenoma, pheochromoctyoma

56
Q

Name 3 important functions of the microbiome?

A
  • Maintaining gut and immune function
  • bacteria supply us with SCFA, Vit K, folate etc
  • energy supply - around 15% of body energy
57
Q

Compare alpha and beta microbiota diversity

A

Alpha - diversity within a sample
Beta - diversity between samples

58
Q

What is free C peptide?

A

A molecule made in insulin production, it indicates insulin is being made.

59
Q

What does cortisol do to skin?

A

Skin thinning

60
Q

Which molecule inhibits prolactin?

A

Dopamine

61
Q

What hormone type is made on demand?

A

Steroids

62
Q

What impact will congenital adrenal hyperplasia have on ACTH?

A

Raised as it is trying to make cortisol and aldosterone

63
Q

Why can a thyroid goiter impact the voice?

A

Impedes on recurrent laryngeal nerve

64
Q

How will non-functional pituitary adenomas impact pituitary function?

A

Mass effect tends to limit pituitary function.

65
Q

Which test would be best to assess presence of acromegaly?

A

IGF-1 concentration