Endocrinology Flashcards
(40 cards)
Acromegaly
Features
Investigations
Treatment
Mainly caused by a pituitary adenoma.
Spade like hands, large tongue, pronounced jaw, headaches, bitemporal hemianopia, excessive sweating etc.
Complications; DM HTN Cardiomyopathy Colorectal cancer
Investigations- IGF-1 serum test, if high then confirm with OGTT.
Treatment
Trans-sphenoidal surgery is first line.
If can’t access the tumour, or metastatic, or no pituitary adenoma then give somatostatin analogues, GH receptor antagonists or dopamine agonists (bromlcriptine).
Addisons
Features
Investigations
Management
Usually due to autoimmune destruction of the adrenal glands therefore decreased cortisol and aldosterone (primary hypoadrenalism).
Features; lethargy, hypoNa, hyperK, hypoG, weight loss, hyperpigmentation, N+V.
Investigate with a ACTH stimulation (syncathen test), if not available then cortisol levels (9am), if low consider referring for syncathen test.
Treatment:
Glucocorticoid + mineralcoricoid- hydrocortisone (20-30mg/day split but mainly in the morning), fludrocortisone.
Educate pt about their cortisol (*2 in illness)
Addisons crisis
Underlying chronic hypopituitarism exacerbated by sepsis (infection) or surgery, steroid withdrawal.
Shock, pyrexia, collapse.
Manage with 100mg IV/IM hydrocortisone.
Then IV 1L saline over 30-60mine, with dextrose if hypoG
Then continue hydrocortisone 6hrly until stable
Other causes of hypoadrenalism
Primary: Metastasis TBH HIV Anti Phospholipid
Secondary:
Pituitary associated disorder I.e. tumour
Bartters syndrome
Inherited disorder
Equivalent of taking lots of furosemide (loop diuretics)
Carbimazole
Treatment of hyperthyroidism
Mg and Ca
Mg will allow for PTH to be secreted and act at target tissues.
Low Mg will lead to to low Ca therefore hyperexcitability.
Congenital adrenal hyperplasia
Autosomal recessive disorders affecting the adrenal glands ability to produce steroids, resulting in low cortisol. This stimulates release of ACTH from the pituitary, activating the synthesis of androgens.
Can lead to virilisation of female.
Corticosteroids
Low GC, high MC- fludroctortisone
GC, high MC- hydrocortisone
GC, low MC- prednisolone
High GC, minimal MC- dexamethasone, betmethasone
Side effects;
GC- poor insulin regulation, Cushing’s syndrome, peptic ulcer, mania, osteoporosis, weight gain, neutrophilia, immunosuppression etc
MC- fluid retention, HTN.
Need slow withdrawal of steroids if 40mg+ dose for >1wk, if on steroids for >3wks or on a repeated course.
Cushing’s syndrome
Causes
Investigations
Causes are usually exogenous (steroid use).
Endogenous is rarer: Cushings disease (pituitary adenoma) Ectopic ACTH Adrenal adenoma (increase cortisol not ACTH)
Investigate with dexamethasone suppression test (overnight) and 24hr free cortisol in urine test.
T1DM
Autoimmune destruction of the islet cells.
Present at young age, polydypsia, polyuria, weight loss, DKA (dehydration, abdominal pain, acetone breath, vomiting, reduced consciousness).
Need to look at urine for ketones and look at random BG (>/=11.1mM) and fasting BG (>/=7mM)
In the case where overlapping symptoms between T1 and T2 DM then need to look at c-peptide levels and diabetes-specific autoantibodies to decide which type and treatment.
T1DM
Management
Manage with insulin injection- basal/bolts regime.
Monitor HbA1c every 3-6 months- target >/= 6.5%.
Monitor BG 4 times as day, before each meal and sleep.
T2DM
Usually occurs later in life and associated with obesity. Diagnose with HbA1C or BG (fasting/random).
HbA1c may be innacurate in haemoglobinopathies, haemolytic anaemia, HIV, CKD, untreated iron deficiency etc.
Polydypsia, polyuria, usually incidental on BT.
NB 6.0-6.4% HbA1c is prediabetes- need to make lifestyle changes to avoid diabetes within 2yrs.
T2DM management
HbA1c monitoring for 3-6 months, until stable then 6 monthly. Aim for less than 6.5% on lifestyle changes, if doesn’t improve then introduce metformin. If >7.5% on metformin and lifestyle changes then introduce a second drug. If not improvement then triple therapy.
May need insulin therapy if not effective.
Also modify risk factors; QRISK may need statins, HTN may need ACEi.
DM sick day rule
Do not stop anti hyperglycaemic drugs even if not eating as much. Do not stop insulin. Increase fluid intake. Check BG 4hrly Check ketones in urine.
Admit to hospital if BG>20mM despite medication, can’t keep fluid down, persistent diarrhoea, suspected underlying illness (MI), no support at home etc
Diabetic foot disease
Reduced neuropathy
PAD
Need to examine pt pulses, Doppler and response to microfilament touch.
Stratify pt into low risk (simple calluses) to moderate and high risk (previous ulcers, amputations, RRT etc). Keep a closer look on moderate and high risk.
DKA
Diagnosis: pH<7.3 Bicarbonate<15mM Ketones in urine>3mM BG>11mM or known diabetic
Management:
Fluid replacement (usually very dehydrated)
Insulin infusion (IV), when BG<15mM then can introduce dextrose infusion.
K+ infusion since insulin can lower K+ levels
Resolution:
pH>7.3
Bicarbonate>15mM
Ketones in blood<0.6mM
Complications: HypoK+/hyperK+; arrhythmias Cerebral oedema (fluid induced) Thromboembolism AKI
Painful diabetic neuropathy
First line: amitriptyline, pregabalin, gabapentin, duloxetine.
Can consider tramadol
GORD, chronic diarrhoea (at night) also common
Graves’ disease
Common cause of hyperT
Female, 30-40yrs
Typical features of hypoT along with exopthalmus, opthalmoplegia, pretibial myxoedema, clubbing.
Autoantibodies- TSH receptor stimulating antibody.
Manage with anti thyroid drugs- carbimazole starting at 40mg.
Control symptoms with propranolol.
Gynaecomastia
Breast tissue in males due to an increase in oestrogen:testosterone ratio.
Causes: normal puberty, testicular failure, ectopic tumour secretion, hyperT.
Drug causes: Spironolactone (v common), finasteride, cannabis, digoxin, GnRH agonists.
Hashimotos
Common cause to hypoT
Common in females
Typical hypoT symptoms along with firm non tender goitre. Anti-thyroid peroxidase antibodies.
Associated with other autoimmune diseases I.e. T1DM, vitiligo, coeliacs
Treat hypoT with levothyroxine (SE- hyperT, worsening angina, AF, reduced mineral bone density).
Main causes of hyperCa
Primary hyperPTH- in non hospitalised pts
Malignancy- in hospitalised pts. I.e. due to bone metastasis, PTHrP etc
Other causes; acromegaly, Addisons, dehydration, drugs, hyperT, sarcoidosis etc
Hyperosmolar hyperG state
Pt presents with hypovolaemia, increased serum osmolality and hyperG- NEED HDU
Presents with lethargy, tired, altered consciousness, hyper viscosity of blood etc over a few days.
Treat with fluid replacement, gradual correction of BG and gradual correction of osmolality.
Causes of hypoG
Diabetes related: increased insulin or sulfanylureas.
Non diabetic:
Ex- exogenous I.e. alcohol without food (low insulin so therefore high ketones) bodybuilders taking insulin. P- pituitary insufficiency L- liver disease (glucose stored here) A- Addisons I- islet cell tumours (insulinoma) N- non pancreatic neoplasms
