Endocrine conditions Flashcards
Type 1 diabetes who? what? symptoms diagnosis treatment
crisis?
Type 4 hypersensitivity reaction in which T cells attack beta cells in islets of langerhans leading to a lack of insulin production. Link with HLA DR3/DR4. Usually younger presentation, slim build.
Symptoms: may be asymptomatic until late on, polyphagia, polyuria, polydipsia, glucosuria, weight loss
Diagnosis:
Random plasma glucose > 11.1 mmol/L or fasting glucose >7mmol/L. 2 abnormal readings or 1 + symptomatic.
HbA1c > 6.5% normal (48mmol/mol)
Oral glucose tolerance tests
Treat:
Lifelong insulin injection
Diabetic Ketoacidosis (DKA) High glucose in blood and absence of insulin causes muscle protein breakdown and lipolysis of adipose tissue. This catabolic state is what causes weight loss and hunger. Lipolysis produces FFAs which form ketones in the liver, leading to ketoacidosis of the blood. FFAs cannot cross the BBB and brain function can be affected. Hyperkalaemia also ensues. 'Kussmaul' deep laboured breathing may be observed as the individual attempts to remove CO2
Type 2 diabetes what? who? symptoms diagnosis treatment
complications
crisis
Cells become resistant to insulin. beta cells compensate by hyperplasia and hypertrophy, but this is not sustainable and they atrophy, leading to hyperglycaemia.
Parasthesia
Polyuria
Polyphagia
Polydypsia
Obesity, hypertension, genetics, old age
Diagnosis:
Random plasma glucose > 11.1 mmol/L or fasting glucose >7mmol/L. 2 abnormal readings or 1 + symptomatic.
HbA1c > 6.5% normal (48mmol/mol)
Oral glucose tolerance tests
Treat:
1st lifestyle modification, diet/exercise, bp/cholesterol management
2. Oral metformin
Eventually may need insulin injections
complications: hyperglycaemia of blood damages blood vessels leading to
Microvascular: retinopathy, neuropathy (loss pain sensation/reflex, erectile dysfunction)
Macrovascular: CHF, stroke, atherosclerosis -> gangrene, ulceration: foot checks!!
Crisis = hyperosmolar hyperglycaemic state, total body dehydration
Causes of hyperthyroidism
Grave’s (TSHr antibodies) = 70-80%
Toxic multinodular goitre
Pituitary adenoma
Exogenous: Thyroid medication, Iodine
Grave's disease: what? who? symptoms/signs diagnosis treatment
TSH receptor antibodies are produced, which mimic TSH by binding to receptor, stimulating T3 and T4 release. Despite the negative feedback these have on the hypothalamus to produce less TRH, antibodies are still produced so levels continue to rise.
Female, family history, amiodarone, thyroiditis, smoking, stress, high iodine, other autoimmune disease.
Anxiety/irritability, fatigue, weight loss, sweating & heat intolerance, sexual dysfunction, frequent loose stools, tachycardia.
Graves opthalmology: periorbital oedema, lid lag and stare. Goitre. Grave’s dermopathy (rare) - skin lesions on legs
Diagnose:
Low serum TSH (due to negative feedback). TSH receptor stimulating antibodies (TSHR-Ab) raised - DIAGNOSTIC
Treat:
anti-thyroid drugs: carbimazole + thyroxine (‘block and replace’ - to reduce risk of hypothyridism)
surgery
radioiodine
thyroid function tests that indicate hyperthyroidism
Serum TSH is suppressed:
- Due to negative feedback produced by hyperthyroidism
•In secondary hyperthyroidism (pituitary resistance, pituitary secreting adenoma) - TSH will be very elevated and not suppressed since the fundamental problem is with the pituitary
T4 & T3 raised - DIAGNOSTIC:
- T4 is almost always raised
- T3 is more sensitive
Thyroid peroxidase (TPO) and thyroglobulin antibodies are present in 80% of Graves’ but are all found in normal hyperthyroidism
- Ultrasound of thyroid:
• Helps to differentiate Graves’ from toxic adenoma
In a scan, injected iodine is taken up rapidly by the thyroid and appears as hot spots
hypothyroidism
causes?
99% are primary, dysfunction with thyroid gland
secondary = pituitary dysfunction, tertiary = hypothalamic
Primary:
Iodine deficiency
Hashimoto’s thyroiditis (autoimmune)
Hashimoto's thyroiditis What? Who? Symptoms/presentation Diagnosis Treatment
Cytotoxic T cell mediated. Antivodies attack thhyroid gland causing progressive damage, and so less effect of TSH + low T3/T4. Lymphocytic and plasma cell infiltration leads to goitre.
Females, middle -> late age.
Depression, fatigue, weight gain, cold sensitivity, heavy periods, myalgia, joint pain and stiffness
Diagnose
Thyroid function test’s (TFTs):
Serum TSH high (confirm primary hypothyroidism) - increases in an attempt to make thyroid work again
In secondary hypothyroidism the TSH is inappropriately low for the low T4/T3 - since issues is in the pituitary
Serum free T4 low - DIAGNOSTIC for HYPOTHYROID STATE
- Thyroid antibodies and organ specific antibodies e.g. TPO-Ab (thyroid peroxidase antibody) in Hashimoto’s
Treat: levothyroxine, 6mg/kg body weight
Cushing's syndrome, Cushing's disease What? Cause? Presentation/symptoms Diagnose Treat
Syndrome = chronic high levels of cortisol in the blood
Disease = excess ACTH produced by pituitary adenoma leads to excess cortisol
Cause: normally iatrogenic, oral steroids. If not, 80% pituitary adenoma. Other: ectopic ACTH prod. tumour (usually small cell of the lung), adrenal carcinoma
Presents:
Moon face, central obesity, prone to infections, bruising/striae/muscle wastage/thin skin (due to catabolic effect cortisol), mood changes, gonadal dysfunction, short stature, fractures/osteoporosis
Diagnosis: random cortisol. If high…
- dexamethasone suppression test: see if it has negative feedback effect on cortisol production. If not…
- plasma ACTH - if undetectable, look for tumour.
Make sure to do a thorough drug history to look for steroid use!
Treat:
depending on cause…
stop steroids
excise tumour
Conn's syndrome/primary hyperaldosteronism Cause Who/when to suspect Symptoms Diagnose Treat
excess aldosterone independent of RAS
Adrenal adenoma 2/3, bilateral adrenocortical hyperplasia 1/3.
Suspect in hypertensive patients who are young, no fam hist, drug resistant, unusual symptoms. Often asymptomatic. Hypertension, hyperkalaemia -> weakness parasthesia, polyuria, polydipsia.
Diagnose: ECG shows hyperkalaemia. Plasma aldosterone high, not suppressed by fludrocortisone (a mineralocorticoid)
what is secondary hyperaldosteronism?
excess aldosterone caused by increased release of renin from juxtaglomerular cellls - usually due to decreased renal perfusion (due to stenosis, diuretics, CHF, heoatic failure)
What are 3 functioning pituitary tumours and what do they produce?
- Prolactinoma = prolactin
- Cushing’s disease = ACTH
- Acromegaly = growth hormone
Acromegaly
Symptoms
Diagnosis
Treat
Benign tumour of somatotroph cells in ant. pituitary -> increased, continuous GH release (norm. pulsatile). Increases bone and muscle growth, stimulates glucogen release by liver (–> secondary diabetes) as well as having indirect effects due to stimulation of IGF-1 release from liver.
Insulin resistance, peripheral tissue thickening, large features, large jaw, muscle growth and swelling, enlarged heart (leads to various serious complications)
Diagmosis: IGF-1 increases despite receiving glucose (more reliable test than GH as fluctuates less)
GH pulses are disrupted
MRI confirms tumour.
Treat:
surgery: Trans-sphenoidal surgery - to remove tumour and correct/prevent tumour compression of surrounding structures e.g. optic chiasm
somatostatin analogues: ocreotide
, GH receptor agonists, radiotherapy
Thyroid carcinoma Types Symptoms Diagnosis treat
Arising from thyroid epithelial cells: 70% papillary (young people, local) and follicular (middle aged, mets) are well differentiated and good prognosis, anaplastic = aggressive.
Lymphoma, medullary (from calcitonin C cells.)
Symptoms:
Throat lump - thyroid nodules
Cervical lymphadenopathy
Voice hoarseness
Sore throat
Dysphagia
Diagnosis:
bloods - TFTs to rule out hypo/hyperthyroid
Fine needle aspiration, cytology&biopsy
USS thyroid
treat:
LEVOTHYROXINE (T4) to keep TSH reduced as this is a
growth factor for the cancer!
pap. and foll = radioactive iodine ablation, thyroidectomy
ana/lymphoma = palliative
med = thyroidectomy, lymph node removal
adrenal insufficiency:
causes: primary, secondary, tertiary
symptoms
adrenal glands do not produce adequate amounts of cortisol (+ aldosterone)
primary: autoimmune, addison’s
secondary: hypopotuitarism
tertiary: suppression of HPA axis eg by glucocorticoid meds
Symptoms: low cortisol and aldosterone…
Loss skin pigmentation, pallor, fatigue, muscle weakness, weight loss, thirst, polyuria, irritability
Addison's disease what is it? cause symptoms diagnosis treatment
Primary hypoadrenalism: destruction of the adrenal cortex = cortisol, aldosterone, androgen defficiency.
Cause:
Autoimmuneadrenalitis(most): 21-hydroxylase antigen attacks the adrenal cortex, ass with other AI conditions
+ TB. mets, long term steroids
Abdo pain, vitiligo, hyperpigmented palms and new scars, lethargy, tanned skin, depression..
21 hydroxylase antibody is specific test, Hyperkalaemia, hyponatraemia due to low aldosterone. Short synACTHen test.
Treat:
Replace steroids with pred. 3 times daily to mimic circadian rhythm. Double steroids when prescribing.
Nausea, vomiting, abdominal pain, muscle cramps and confusion = adrenal crisis, IV hydrocortisone.
