Endocrine Disorders Flashcards

1
Q

What does Hashimotos cause antibodies against?

A

Thyroid Peroxiase

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2
Q

What would you expect to see in a staining of Hashimotos thyroud tissue?

A

Lymphocyte infiltration - lots of blue

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3
Q

What is connective like in Hashimotos?

A

Fibrotic

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4
Q

What is the second most common cause of hypertension accounting for the most common cause of secondary hypertension?

A

Primary Aldosteronism - excessive release of aldosterone indepentant of the RAS system

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5
Q

What is Euvolemic?

A

Where the patient doesn’t appear to fluid overloaded. The total amount of Na2+ is normal but there is too much water retention and thus it is diluted - hypotonic.

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6
Q

In patients with SIADH, why does the brain swell and what is an important management of this?

A

As the fluid becomes hypotonic, fluid moves into the brain cells causing swelling.

In response the cells will pump out Na2+, K+, Cl- and glutamate in an effort to reduce the osmotic drive. If then treated too quickly with a hypertonic solution the fluid will be pulled out the cell too quickly and cause osmotic demylination

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7
Q

What are the most common causes of hypercalcaemia?

A

Primary hyperparthyroidism: where the negative feedback isn’t adjusted and the cheif cells continue to release PTH which continues to break down bone and reabsorb Ca2+
- usually due to a small adenoma

Malignancy: Releasing PTH- related peptide.

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8
Q

How do you differentiate between primary hyperparathyroidism and malignancy?

A

In primary the levels of PTH should be high.

If PTH is low then suggestive of malignancy as the high levels of Ca2+ are regulating the PTH levels normally.

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9
Q

Whats the treatment for hypercalcaemia?

A

Bisphosphonates

parathyroidectoma

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10
Q

What are the stages in Cushing’s diagnosis?

A
  1. assess levels of high cortisol. Midnight salivary test.
  2. Dexamethason suppression test - to assess whether there is actual high levels of cortisone
  3. Source the cause. Measure ACTH levels.
    - if low then adrenals is cause
  • if high establish source of ACTH
    Give CRH and see if the levels of ACTH increase. If they don’t it is an ectpoic source.
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11
Q

In Addison’s disease what would you expect the U&Es to be like and why?

A

Low Na2+ - lack of aldosterone production reabsorbing Na2+ and water

High K+ - lack of aldosterone excreted K+

High Urea - dehydration

Low Glucose is possible as well as there is lack of regulation for gluconeogenesis

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12
Q

What test can be done to establish the source of adrenal insufficiency?

A

Short SYNACTH test. If primary it will have no effect and levels of ACTH should already be high.

If secondary then increased cortisol production

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13
Q

What drug is given for replacement of aldosterone?

A

Fludrocortisone

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14
Q

What are the antibodies of Grave’s disease? and what are they known as?

A

IgG antibodies that bind to the TSH receptor.

Long acting thyroid stimulators

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15
Q

What infections are associated prior to Grave’s disease?

A

Yersinia Enterocolitica

E. Coli

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16
Q

In type II diabetes, what are the collective pathologies associated with development of insulin intolerance? and what are they termed?

A
  • central obesity
  • hypertension
  • dyslipidaemia
  • Fasting glucose is high

Metabolic syndrome

17
Q

There is associated insulin receptor gene dysfunction in diabetes type II, what other things may be seen with this?

A

Acanthosis Nigricans - under armpit dark spots

Hyperandrogenism - excessive androgen production

18
Q

What are the broad stages of DM Type II pathologenesis?

A

Insulin resistance leading to increased insulin secretion.

  • increased fatty deposits in muscles and liver
  • adipocytokines release - inducing low inflammation
  • hyperplasia and hypertrophy of beta cells

Beta cells fail

  • build up of Amylin in cells
  • reduction in insulin production
19
Q

Outline processes of diabetic nephropathy:

A

thickened of basement membrane and hyaline arteriosclerosis of the efferent vessels

buldging of the basement membrane causing the gaps between podocytes to increase

*this all leads to intial hyperfiltrations

Mesengial cells respond by increasing collagen production to support excessive forces - lowering GFR

20
Q

What are some symptoms of Grave’s disease?

A

Graves opthalmopathy

  • Proptosis
  • diploia

Pretibial Myxoedema

Finger clubbing

21
Q

What are the common causes of hyperthyroidism? and what tests can be useful for differentiation?

A

Graves

Toxic multinodular goitre

Toxic Adenoma

TSH: to assess whether it is primary or secondary

Antibodies:

  • TSH Receptor Antibodies
  • thyroperioxidase Antibodies

Radioisotope - distinguish between mutlinodular and adenoma

22
Q

When would someone have high T3 but low T4?

A

When been treated with synthetic T3

23
Q

What technique can be used to assess the thyroid?

A

Fine needle aspiration

24
Q

What is the drug that can be given for the treatment of acromegaly?

A

Somatostatin

25
Q

What test can be done to confirm amcromegaly?

A

Glucose tolerance test - increase in glucose should feedback to stop GH release

26
Q

What other affects can prolactoma have on the body other than milk production?

A

Menstrual disruption

In males reduced labido

27
Q

If an adenoma is suspected of the pituitary gland what should be done?

A

check hormones

size of pituitary

Vision

28
Q

What cancers are assoicated with acromegally?

A

Colon Cancer

29
Q

What is Sick Euthyroid?

A

Low levels of TSH and T3, T4 due to the patients being systemically ill.

the thyrod gland still functions though

30
Q

What are the diagnostic criteria for diabetes type II? and name some tests

A

Diagnosis is based on two different lab findings:

  • HbA1c >48mmol/mol (6.5%)
  • fasting plasma glucose >6.9mmol/L
  • random plasma glucose test >11.1mmol/L

this is conjunction with clinical findings - polydipsia etc.

31
Q

What anti bodies are most commonly seen with type I diabetes?

A

Anti - glutamic acid decarboxylase (GAD)

Islet Cell anti bodies

Insulin auto-antibodies

32
Q

What is a common finding in the urine of type I diabetics at time of diagnosis?

A

Ketones

33
Q

What are the main causes of adrenal insufficiency disease?

A

Auto immune - addisons

tuberculous spread

malignancy

34
Q

in the setting of adrenal insufficiency what is the first line of treatment?

A

Intravenous hydro cortisone

35
Q

What must one think when a patient presents with known Addisons and is cortisol crisis?

A

Are they acutely unwell and not increased their dosage in response to this - leading to the cortisol being used elsewhere

36
Q

How does ADH reach the pituitary?

A

Via nerves

37
Q

What affect does cortisol have on bones and why?

A

makes them more fragile. Increases bone resorption

38
Q

What is the result of taking exogenous steroids?

A

Negative feedback to hypothalamus and pituitary.
reduced CRH and ACTH and cortisol

atrophy of adrenal glands.

  • dangerous if they come off them quickly