Endocrine Disorders Flashcards
What does Hashimotos cause antibodies against?
Thyroid Peroxiase
What would you expect to see in a staining of Hashimotos thyroud tissue?
Lymphocyte infiltration - lots of blue
What is connective like in Hashimotos?
Fibrotic
What is the second most common cause of hypertension accounting for the most common cause of secondary hypertension?
Primary Aldosteronism - excessive release of aldosterone indepentant of the RAS system
What is Euvolemic?
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.
In patients with SIADH, why does the brain swell and what is an important management of this?
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
What are the most common causes of hypercalcaemia?
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.
How do you differentiate between primary hyperparathyroidism and malignancy?
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.
Whats the treatment for hypercalcaemia?
Bisphosphonates
parathyroidectoma
What are the stages in Cushing’s diagnosis?
- assess levels of high cortisol. Midnight salivary test.
- Dexamethason suppression test - to assess whether there is actual high levels of cortisone
- 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.
In Addison’s disease what would you expect the U&Es to be like and why?
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
What test can be done to establish the source of adrenal insufficiency?
Short SYNACTH test. If primary it will have no effect and levels of ACTH should already be high.
If secondary then increased cortisol production
What drug is given for replacement of aldosterone?
Fludrocortisone
What are the antibodies of Grave’s disease? and what are they known as?
IgG antibodies that bind to the TSH receptor.
Long acting thyroid stimulators
What infections are associated prior to Grave’s disease?
Yersinia Enterocolitica
E. Coli
In type II diabetes, what are the collective pathologies associated with development of insulin intolerance? and what are they termed?
- central obesity
- hypertension
- dyslipidaemia
- Fasting glucose is high
Metabolic syndrome
There is associated insulin receptor gene dysfunction in diabetes type II, what other things may be seen with this?
Acanthosis Nigricans - under armpit dark spots
Hyperandrogenism - excessive androgen production
What are the broad stages of DM Type II pathologenesis?
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
Outline processes of diabetic nephropathy:
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
What are some symptoms of Grave’s disease?
Graves opthalmopathy
- Proptosis
- diploia
Pretibial Myxoedema
Finger clubbing
What are the common causes of hyperthyroidism? and what tests can be useful for differentiation?
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
When would someone have high T3 but low T4?
When been treated with synthetic T3
What technique can be used to assess the thyroid?
Fine needle aspiration
What is the drug that can be given for the treatment of acromegaly?
Somatostatin
What test can be done to confirm amcromegaly?
Glucose tolerance test - increase in glucose should feedback to stop GH release
What other affects can prolactoma have on the body other than milk production?
Menstrual disruption
In males reduced labido
If an adenoma is suspected of the pituitary gland what should be done?
check hormones
size of pituitary
Vision
What cancers are assoicated with acromegally?
Colon Cancer
What is Sick Euthyroid?
Low levels of TSH and T3, T4 due to the patients being systemically ill.
the thyrod gland still functions though
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.
What anti bodies are most commonly seen with type I diabetes?
Anti - glutamic acid decarboxylase (GAD)
Islet Cell anti bodies
Insulin auto-antibodies
What is a common finding in the urine of type I diabetics at time of diagnosis?
Ketones
What are the main causes of adrenal insufficiency disease?
Auto immune - addisons
tuberculous spread
malignancy
in the setting of adrenal insufficiency what is the first line of treatment?
Intravenous hydro cortisone
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
How does ADH reach the pituitary?
Via nerves
What affect does cortisol have on bones and why?
makes them more fragile. Increases bone resorption
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
