Endocrine Disorders Flashcards

(38 cards)

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?

25
What test can be done to confirm amcromegaly?
Glucose tolerance test - increase in glucose should feedback to stop GH release
26
What other affects can prolactoma have on the body other than milk production?
Menstrual disruption In males reduced labido
27
If an adenoma is suspected of the pituitary gland what should be done?
check hormones size of pituitary Vision
28
What cancers are assoicated with acromegally?
Colon Cancer
29
What is Sick Euthyroid?
Low levels of TSH and T3, T4 due to the patients being systemically ill. the thyrod gland still functions though
30
What are the diagnostic criteria for diabetes type II? and name some tests
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
What anti bodies are most commonly seen with type I diabetes?
Anti - glutamic acid decarboxylase (GAD) Islet Cell anti bodies Insulin auto-antibodies
32
What is a common finding in the urine of type I diabetics at time of diagnosis?
Ketones
33
What are the main causes of adrenal insufficiency disease?
Auto immune - addisons tuberculous spread malignancy
34
in the setting of adrenal insufficiency what is the first line of treatment?
Intravenous hydro cortisone
35
What must one think when a patient presents with known Addisons and is cortisol crisis?
Are they acutely unwell and not increased their dosage in response to this - leading to the cortisol being used elsewhere
36
How does ADH reach the pituitary?
Via nerves
37
What affect does cortisol have on bones and why?
makes them more fragile. Increases bone resorption
38
What is the result of taking exogenous steroids?
Negative feedback to hypothalamus and pituitary. reduced CRH and ACTH and cortisol atrophy of adrenal glands. - dangerous if they come off them quickly