Endocrinology Flashcards
What are the main CAUSES of hyperthyroidism
- primary - thyroid makes too much TH
2.Secondary- pathology in hypothalamus or pituitary - too much TSH - Grave’s disease- autoimmune- TSH receptor antibodies cause primary hyperthyroidism
4.Toxic multi nodular goitre- Plummers disease- over 50s - Thyroiditis
What is a thyroid storm/ how do you manage it ?
Thyrotoxic crisis - usually due to surgery or infection etc- fever, tachy and delirium
Treat with: Fluid rhesus, anti arrhythmic meds and beta blockers
What is the management of hyperthyroidism ?
1st line- Carbimazole for 12-18 months
Once levels are normal continue maintenance
Higher doses of carbimazole will block all TH and levothyroxine will need to be given
2nd line- Propythiouracil- but high risk of liver damage
Both meds cause agranulocytosis - pt’s vulnerable to infection- BE AWARE OF SORE THROATS
Radioactive iodine- no pregnant 6 months , limit contact with children and pregnant women
B blockers for symptoms
Surgery
What are the main causes of hypothyroidism ?
- Primary hypo- thyroid doesn’t make enough T3/T4 - negative feedback so high TSH
- Hashimoto’s thyroiditis (Autoimmune) - primary
-Iodine deficiency (most common) - primary
- Treatment for hyperthyroidism
- Lithium/ amiodarone medications
- Secondary hypo- pituitary not enough TSH- low T3/T4
-Pituitary adenoma
-Surgery to pituitary
-Radiotherapy
-Sheehans syndrome
-Trauma
What is the treatment for hypothyroidism?
Oral levothyroxine (synthetic T4)
-Dose titrated every 4 weeks based on TSH level
What is the difference between Cushing’s disease and syndrome and what are the main presentations?
Cushing’s syndrome= too much cortisol produced in the body for some reason
Cushing’s disease- = specific Pituitary adenoma secreting adrenocorticotrophic hormone stimulating excess cortisol from adrenal glands
High levels of glucocorticoids (cortisol)
-Moon face -Central obseity -Abdominal striae -Buffalo hump -Proximal limb muscle wasting
-hirsutism (male facial hair) -easy bruising poor skin healing -Hyperpigmentation of the skin
Metbolix effects
HTN Cardiac hypertrophy Type 2 diabetes Dyslipidaemia Osteoporosis
Mental health effects
Anxiety Depression Insomia
What are the causes of Cushing’s syndrome
-Cushings disease - pituitary adenoma
-Adrenal adenoma
-Paraneoplastic syndrome (Small cell lung cancer)
-Exogenous steroids
How do you test for Cushing’s
Dexamethasone suppression test - tells you when the problem is inside the body and not from exogenous steroids
Normal response is suppressed cortisol when dexamethasone given due to negative feedback
Low dose overnight - given to exclude Cushing’s
Low dose 48 hr- in suspected cushings
High dose in 48hrs - determines cause of cushing’s
Or 24hr urinary free cortisol
What would the findings be in a Dexamethasone suppression test for
1. Normal
2. Pituitary adenoma
3. Adrenal Adenoma
4.Ectopic Steroids
- Cortisol suppressed in all tests and ACTH normal
- Pituitary adenoma Low dose test not suppressed but high dose of dex will surprise cortisol - Cortisol but ACTH will still be high as pituitary tumour is producing this
- Adrenal adenoma- cortisol will not be suppressed in either doses as tumour is secreting cortisol but ACTH will be low as pituitary won’t be producing much
- No suppression for either doses and high ACTH
What are the two main types of hyperaldosteronism
- Primary- adrenal glands make too much aldosterone, low renin as high blood pressure surprises it - due to bilateral hyperplasia of adrenal glands, adrenal adenoma (Conn’s syndrome) or familial
- Secondary- high renin stimulating excessive adolsterone release- due to low BP in kidneys- Renal artery stenosis, HF, liver cirrhosis and ascites
What is the screening test for hyperaldosteronism
Aldosterone to renin ratio
High aldosterone to low renin= primary
High aldosterone to high renin = secondary
What is the management of hyperaldosteronism
- Treat underlying cause - percutaneous renal artery angioplasty via fem artery / remove adrenal adenoma
Aldosterone antagonists - spironolactone
What are the 3 types of Adrenal insufficiency
Low cortisol
1. Addison’s disease- when the adrenal glands are damaged - autoimmune
- Secondary- inadequate ACTH doesn’t stimulate the adrenal glands - damage to pituitary gland (adenoma/ sheehans syndrome)
- Tertiary- inadequate CRH from the hypothalamus - from patients taking long term oral steroids
What is the presentation of adrenal insufficiency
Fatigue, muscle cramps/ weakness, dizzy/fainting/ thirst/ craving salt, weight loss, abdominal pain, depression, low libido, bronze hyperpigmentation (excess ACTH stimulates melanocytes to produce melanin)
What investigations/ findings are present in adrenal insufficiency
High potassium and low sodium
Hypoglycaemia
High creatinine and urea
Hypercalcaemia
What is the test used to diagnose Adrenal insufficiency?
Short synthacthen test - JFK was short - check blood cortisol 30 and 60 mins
- In healthy adrenal glands the extra ACTH will stimulate high cortisol
-Primary adrenal insufficiency (Addison’s)- cortisol will not increase- Adrenal glands not working- won’t be stimulated by ACTH
Long synacthen test - used to choose between primary and secondary - in secondary insufficiency- ACTH will be low as not being produced normal so only the amount given in the fake dose is there
Management of adrenal insufficiency
-hydrocortisone (glucocorticoid)- replaces cortisol and fludrocortisone (mineralocorticoid) - Replaces aldosterone
Patients given steroid card and ID tag
Family members taught how to give IM hydrocortisone
Why are steroid doses important in Adrenal insufficiency
Doses should not be missed and if sick doses should be doubled
What is Addisonian/ Adrenal crisis/ How is it treated
Hypotension. LOC, hypoglycaemia, hyperkalaemia caused by infection trauma or acute illness in patients
Do not perform investigations treat if suspected
ABCDE approach
-IM/IV hydrocortisone (100mg then infusion of 6hrly doses)
-IV fluid resus
-Correct hypoglycaemia with dextrose
-Monitor electrolytes and fluid balance
What is the main presentation of DKA
-Hyperglycaemia -Dehydration -ketosis -Metabolic acidosis (low bicarb) -Potassium imbalance
Polyuria/dipsia -N&V -Dehydration -Weight loss -Hypotension
Criteria
Hyperglycaemia HB>11mmol/L
Ketosis- Ketones >3mmol/L
Acidosis pH below 7.3
How is DKA treated
Escalate
FIG-PICK
Fluids-IV fluid resus - 1L normal saline for 1st hr then 1L every 2 hrs
Insulin- Fixed rate infusion - act rapid 0.1 units/kg/hr
Glucose-monitor and only add glucose to infusion when it goes below 14mmol/L
Potassium- Add potassium to IV fluids every hr initially - do not exceed 10mmol/Hr
Chart fluid balance
Ketones- monitor blood ketones, pH and bicarb
*Don’t stop insulin infusion and fluids until patient is eating and drinking and has restarted subcut insulin
What is pre- type 2 diabetes and type 2 diabetes
Pre-diabetes- HbA1c- 42-47mmol/L
Diabetes HbA1c over 48mmol/L
What are the treatment options of type 2 diabetes
- First line- weight loss and exercise with diet
- First line mediation- Metformin
If QRISK is over 10% add an SGLT2 inhibitor (dapagliflozin) ** this one most likely in second line but potential side effect is DKA
- Second line medication- add to metformin a sulfonurea, pioglitazone, DPP-4 inhibit or SGLT2 inhibit
- Third line- triple therapy- metformin and two second line drugs
Insulin therapy by specialist diabetic nurse
If triple therapy fails and BMI over 35 can give GLP-1 mimetic
What does metformin do
Increase insulin sensitivity and decrease glucose production by liver
No weight gain
What do SGLT2- inhibitors do
- all end in gliflozin
-Block the sodium glucose transporter protein in proximal tube of kidneys - less glucose absorbed and more in urine
Can cause hypoglycaemia, urine infections, glucose in urine , weight loss, DKA
Putting a patient on this then counsel them for DKA
What is a sulfonurea
Gliclazide- stimulates release of insulin from the pancreas
Cause weight gain and hypoglycaemia
What are DDP-4 inhibitors or GLP-1 mimetics
GLP1 is an incretin which reduces blood sugar
DDP-4 inhibits incretins
So a DDP-4 inhibitor med will allow incretins to work
GLP-1 mimetics - exenatide etc are subcut injections and can be used for weight loss
