Endocrine Flashcards
Triad of symptoms in PCOS
Hyperandrogenism - acne, hirsutism, increased hair growth, deep voice
Marked insulin resistance - acanthosis nigricans + skin tags
Oligomenorrhoea (irregular + inconsistent menstrual flow)
- infertility
- Dysfunctional uterine bleeding
What is type A insulin resistance?
Severe insulin resistance caused by insulin receptor gene mutations producing PCOS
Pathogenesis of diabetic microangiopathy?
Hyperglycaemia in blood + blood vessels (insulin independent entry of glucose into cells) –> glycosylation of BM proteins –> “AGE” deposition –> BV wall damage + leakage of serum proteins into tunica media+ thickening of wall with more BM deposition (type IV collagen) –> hyaline arteriolosclerosis. This –> luminal narrowing –> ischaemia
Three broad categories of effects seen in visceral diabetic neuropathy?
Central: Bells palsy, diplopia
CVS: orthostatic hypotension
GIT: constipation, diarrhoea
Treatment of DKA + HHS
- Fluid replacement with 0.9% isotonic saline – restore circulatory volume + improve tissue perfusion + correct hyperosmolarity
- Low-dose physiological insulin therapy – only administer insulin when hypovolaemia corrected and K+ >3.3mmol/L (insulin drives ECF –> ICF, exacerbates hypovolaemia and low K+).
- Electrolyte correction
- Evaluate + treat underlying cause – get FBCs, ECG, Hb1ac, infectious workup
What are three main features of DKA that you always forget? What are the rest of the features?
DKA:
- Fatigue
- Dehydration
- Fruity breath
Abdo pain
Nausea + vomiting
Kussmaul breathing
What are three main features of HHS that you always forget? What are the rest of the features?
HHS
- Fatigue
- SEVERE dehydration: loss of skin turgor, reduced mucosal hydration, reduced CRT/cyanosis, tachycardia + hypotensive
- Weight loss
Polyuria, polydipsia, polyphagia
Tachypnoea
Fever
What is the incretin effect?
What are the incretins?
What enzyme degrades the incretins?
What happens to incretin effect in T2DM?
Incretin effect = oral glucose stimulates more insulin release than IV glucose due to incretins.
incretins = glucagon-like peptide (GLP-1) and glucose-independent insulinotropic polypeptide (GIP)
Dipeptidyl peptidase 4 (DPP4)
“Incretin” effect is reduced in T2DM – oral glucose stimulates same insulin secretion by pancreas as would IV
3 causes of hypopituitarism + which are most common?
1) Empty sella syndrome:
o Congenital lack of hypothalamic hormones
o Acquired – necrosis, tumours, injury, surgery (most common – final 3).
2) Craniopharyngioma
3) Glioma
Clinical features of hypopituitarism - separate into anterior vs posterior and go by that
Anterior GH: pituitary dwarfism (proportional dwarfism) FSH/LH: infertility, impotence TSH: hypothyroidism ACTH: hypo-adrenalism MSH: pallor
Posterior
ADH: diabetes insipidus central
Post pit: D insipidus
No
Dwarfism in order of commonality
- Achondroplasia – disproportionate, trunk normal, short limbs
- Turner Sy
- Pituitary dwarf – symmetric
Diagnostic test for diabetes insipidus?
Water deprivation test?
Diagnostic test for acromegaly? how does it work>
Oral glucose growth hormone suppression test.
Oral glucose GH suppression test – classic screening for acromegaly. Take baseline HGH – then 2 hours after glucose administration. Meant to be suppressed but isn’t in GH-secreting adenoma
Risk factors for diabetes insipidus nephrogenic
Kidney damage - pyelo, obstruction to outflow
Electrolytes - hypokalamiea, hypercalcaemia
lithium drug
pregnancy
Etoh temporary
Polycystic kidney disease - genetic
Investigations to do for multinodular goitre - justify each, and state what you’d expect in one
- TFT
- USS – screen nodules for any suspicious malignant change
NB: USS not indicated for suspected thyroid dysfunction - Scintilligraphy characteristic feature NTK – uneven radioiodine (1-123) uptake between each nodule
