Endocrine Flashcards
Describe the hormones and feedback loops from the hypothalamus and pituitary (mnemonic)
Hypothalamus releases releasing hormones (CRH, TRH, GnRH, GHRH) other than dopamine that inhibits prolactin. Also makes oxytocin and ADH that are stored in posterior pituitary.
The anterior pituitary secretes (peptide): follicle SH, luteinizing H, adrenocorticotropic H, thyroid SH, prolactin, growth H (TP FLAG)
ACTH, FSH, LH, TSH all have negative feedback from their hormones at pituitary and hypothalamus. Prolactin and GH just have effect on hypothalamus (no secondary gland)
What is released by the posterior pituitary
ADH and oxytocin
What are the actions of insulin and glucagon
Insulin decreases amount of serum glucose. It suppresses hepatic glucose output (glycogenolysis and gluconeogenesis) and the breakdown of fat and muscle. It increases uptake into sensitive tissues: liver, muscle (glycogen + protein synthesis), fat (lipogenesis).
Glucagon increases hepatic insulin output, increases from glycogenolysis + gluconeogenesis (from lactic acid and amino acids), reduces peripheral glucose uptake, stimulates lipolysis + muscle breakdown
What are the complications of diabetes
Microvacular: retinopathy, nephropathy, neuropathy
Macrovascular: stroke, MI, renovascular, limb ischaemia + ulcers
Others like erectile dysfunction, frequent infections, poor healing of wounds, autonomic neuropahty
What are the symptoms of diabetes
Fatigue, polyuria + polydipsia, unintentional weight loss, opportunistic infections, slow wound healing
Long term: blurred vision, altered sensation in hands and feet, areas of darkened skin - acanthosis nigricans
What are the test result values to diagnose diabetes
HbA1c > 48 (6.5%) (repeat after 1m if no symptoms); > 42 prediabetes
Fasting plasma glucose >7
2 hours after 75g oral glucose > 11.1
Random glucose > 11.1
What is recommended by NICE to manage T2DM
Structured education program, low-glycaemic and high-fibre diet, exercise, healthy BMI, antidiabetic drugs, monitor and manage complications (regular checks)
What are the treatment targets for diabetics
HbA1c of 48 for new patients, 53 for patients requiring more than one medication
What class of drugs are second line in T2DM and why, when are they first line
SGLT2 inhibitors (dapagliflozin) protect against cardiovascular disease and CKD
To be offered alongside metformin when Qrisk >10%
Risk of UTI / thrush, risk of DKA
Describe the mechanisms of action of the different classes of antidiabetic drugs used
Metformin (biguanide): increases insulin sensitivity / peripheral glucose uptake, inhibits gluconeogenesis in liver + intestinal absorption
Sodium-glucose co-transporter-2 inhibitors (flozins): increased glucose excretion / reduced reabsorption in kidneys, lowers blood pressure; direct cardiac protection / improved function?
Sulfonylureas (glicazide): stimulates insulin release
DPP-4 inhibitors (alogliptin): prevents breakdown of GLP-1 and GIP hormones - increased insulin and decreased glucagon, do not cause hypos
Glucagon-like peptide-1 receptor agonist (semaglutide (ozempic)): enhances glucose dependent insulin secretion and suppressed glucagon release
What classes of drugs are used in diabetic patients with hypertension, CKD, neuropathic pain
HTN: ACE
CKD with albumin:creatinine >3 ACE; ACR > 30 dapagliflozin
Neuropathic: amitriptyline / dulozetine / gabapentin / pregabalin
Describe a hyperosmolar hyperglycaemic state
Similar to DKA without the ketones, enough insulin to prevent ketoacidosis but not enough to prevent hyperglycaemia. Usually a precipitating event like infection, glucose starts being excreted by kidneys, water follows leading to dehydration (osmotic diuresis). Large risk of cerebral oedema
Polyuria, polydipsia, dehydration, tachycardia, hypotension, confusion to coma / seizures
IV fluids, slow insulin infusion + potassium, VTE prophylaxis
Describe the bloods taken for a new diagnosis of T1DM
Baseline: glucose, HbA1c, U+Es, FBC, ketones
Other autoimmune: TFTs + TPO, anti-TTG
Abnormal presentation: C-peptide and specific T1DM autoantibodies
What in a history would make a patient more likely to be T1DM than T2DM
Peak age 10-14; suspect in child with normal diabetic symptoms
In adults: ketosis, rapid weight loss, age <50, BMI <25, personal / family history of autoimmune
Presenting with DKA: dehydration, n+v, abdo pain, tachypnoea, tachycardia, lethargy
T2DM in a child: strong family history, obese, black / asian, no insulin requirement, evidence of insulin resistance
Describe the different types of insulin and common regimes
Rapid acting - before meals (Humalog, novorapid). Isophane - cheap. Pre mixed - different % of short and long (NovoMix). Long acting analogues - bedtime
BD - twice premixed by pen (good for T2DM). QDS - rapid acting before meals and long acting overnight. Once daily before bed - initial in T2DM. Insulin pump - continuous infusion
What is the pathogenensis of diabetic ketoacidosis
Body has no available glucose or glycogen, fatty acids made into ketones as last resort
Kidneys can only compensate for acidosis for so long
Glucose in urine draws water with it causing dehydration (osmotic diuresis)
Lack of insulin means no potassium driven into cells
Cerebral oedema due to dehydration and hyperglycaemia (water extra - intracellular)
How is ketoacidosis monitored and treated
Venous blood gas, blood ketones (or urinalysis) + glucose, U+Es (measure potassium), FBC
Blood glucose >11.1, blood ketones >3, blood pH <7.3
Correct hydration over 48h (too fast - cerebral oedema), fixed rate insulin infusion, give dextrose and potassium, treat underlying cause, consider sodium bicarbonate and and VTE prophylaxis
What are the symptoms of hypoglycaemia
Start feeling hungry / shaky / sweaty, autonomic (trembling, palpitations), neuroglycopenic (confusion, drowsiness, seizures)
What are the causes of hyper and hypothyroidism
Hyperthyroidism / thyrotoxicosis (overproduction): Graves’ (Trab, TPO), toxic multi nodular goitre, toxic adenoma, thyroiditis
Hypothyroidism: primary 99% - Hashimoto’s (anti TPO, anti Tg, most common), atrophic hypothyroidism, iodine deficiency (most common global), thyroidectomy, lithium
What is the pathogenesis of Grave’s
Grave’s: autoimmune, genetic + environmental (smoking big precipitant), Abs mimic TSH causing goitre and hyperthyroidism, also receptors on orbital fibroblasts and adipocytes (inflammation, fibrosis, fat deposit)
