Endocrine - Summary

Endocrine; Nikita Goyal
Gliclazide - Sulphonylureas – ⇧ insulin secretion from pancreatic β
Diabetes Mellitus: cells (hypoglycaemia risk, DKA risk)
A metabolic disease characterised by elevated blood glucose levels DPP 4 inhibitors - (-liptin)** – ⇧ incretin effect (more likely to get
Ix UTI’s)
Bedside – Dapagliflozin - SGLT2 inhibitors** – ⇧ urinary glucose excretion
 BSL Injectable: Exanetide - GLP-1 agonists** – ⇧ incretin effect
 Retinal Examination - ?Retinopathy INSULIN
 ECG Human insulin
 Urine ACR  Short/intermediate acting
Bloods –  Mixture of short and intermediate acting (biphasic)
 FBE, UEC (ketones - DKA; albuminuria – nephropathy; Analogue insulin
glucosuria), LFTs, TFTs (more predisposed to thyroid  Rapid acting/long acting (basal insulin)
dysfunction)  Mixture of rapid and intermediate acting (biphasic)
 HBA1c >6.5%
 Fasting plasma glucose>7mmol/L Obese patient with chronic kidney disease cannot have metformin,
 Random blood glucose ≥11.1mmol/L sulfonylurea, SGLT2 inhibitors so they have to have insulin.
 2 hr post-load glucose after 75g oral glucose ≥11.1mmol/L Cx
 Random C peptide – undetectable or ↓ in T1DM; ↑ in Macrovascular – Brain (cerebrovascular disease – TIA,
T2DM cerebrovascular accident, cognitive impairment); heart (CAD –
 Lipid Profile – dyslipidaemia - ↓HDL; ↑LDL/TGL coronary syndrome, MI, CCF); extremities (PVD – ulceration,
 Anti-GAD antibodies – T1DM gangrene, amputation
 Hyperglycaemia damages blood vessels leading to
atherosclerosis - i.e decreased blood flow to organs
Microvascular – eyes (retinopathy, cataracts, glaucoma); kidneys
(nephropathy – micro/gross albuminuria, kidney failure); nerves
(neuropathy – autonomic or peripheral)
 Nephropathy – high glucose filtrate causes increased urine
excretion and renin secretion leading to vasoconstriction of
Imaging – renal arterioles and infarction of surrounding tissues
 - leading to destruction of glomeruli
Mx  Neuropathy – high glucose levels can damage nerve fibres
Lifestyle/Non-Pharm: directly
 T1DM – SNAPW will not ensure reversal but will be o Autonomic neuropathy – gastroparesis,
preventative against Cx; diabetes education
autonomic dysfunction (orthostatic hypotension)
 T2DM – SNAPW!!! For three months; diabetes education
o Peripheral neuropathy (+PVD) -> diabetic foot
Review adherence to meds
infections
HbA1c ~7% - Lifestyle; ~8% - 1 oral hypoglycaemic; ~8.5% - 2 oral
o Charcot arthropathy
hypoglycaemic agents e.g metformin + SGLT2
 Goals: Individual HbA1c targets Hypoglycaemia – develops when a person’s blood glucose drops
o Aim is 7% below 4mmol/L
o Aim 6-7% in early diagnosis/young/few  Occurs if too much insulin is administered, but can result
from missing a meal or unplanned physical activity
complications
o May need to aim for 7.5-8% if severe
 Give sugar e.g chocolate or orange juice
 If unconscious – administer glucagon or IV glucose
hypoglycaemia unawareness
o Aim purely for comfort in elderly/palliative
DKA – more common in T1DM
patients - 5-15mmol/L
Insulin deficiency causes counter-regulatory hormone elevation
Pharm: T1DM
(glucagon, catecholamines, GH, cortisol) → ↑ ketones/glucose →
Insulin injection – short-acting + long-acting (mimics basal and post-
osmotic diuresis due to glycosuria (dehydration + electrolyte
meal insulin levels)
abnormalities)
Insulin pumps – very expensive (useful for the young however)
 Sx – abdo pain, N/V, lethargy, drowsiness, deep rapid
respirations, AMS, coma
 Biochemical triad – hyperglycaemia, ketonaemia,
metabolic high anion gap acidosis

Mx – Acute
 Fluid resus
 Insulin infusion to switch off ketone production and reverse
acidosis
 K+ replacement
o Insulin will drive K+ into cells causing
hypokalaemia
o At risk of arrhythmias
 Treat underlying Ax i.e infection
Pharm: T2DM
Oral Hypoglycemic agents - **good for weight Mx + glycaemic
Hyperosmolar Hyperglycaemic State – more common in T2DM
control
Small amounts of insulin present which prevents ketosis by inhibiting
Metformin** – biguanides – ⇧ glucose uptake and ⇩ hepatic glucose
lipolysis
production (cause diarrhoea)

, Endocrine; Nikita Goyal
Characterised by hyperglycaemia, hyperosmolality and dehydration  Polydipsia and polyuria are uncommon
w/o ketosis  Acanthosis nigricans is uncommon
Metabolic acidosis and glycosuria RF – older age, overweight/obesity, black, Hispanic or Native
American ancestry, FHx of T2DM, Hx of gestations diabetes, presence
Mx – Acute of pre-diabetes, physical inactivity, PCOS, HTN, dyslipidaemia or
 Rehydration known CVS disease
 K+ replacement Ax –
 Search for precipitating event Hereditary + env. Factors
 Insulin therapy Associated w/ metabolic syndrome
Pathophys – Peripheral insulin resistance & β Cell dysfunction
Prognosis – DM is a leading cause of death; commonest Cx are MI  Insulin resistance to develops in peripheral tissues which
and ESRF resulting in death; prognosis depends on glycaemic control causes the pancreas to produce more insulin
+ Mx of comorbidities  Eventually insulin production declines
Type 1 Diabetes:  Glucose uptake reduces further ⇨ Hyperglycaemia ensues
Result of an autoimmune response that triggers the destruction of  Loss of insulin leads to ⇧ glucose production and release
insulin producing β cells in the pancreas and results in complete from liver which makes it worse
insulin deficiency  Cells start using fatty acid, therefore ⇧ fatty acid + glucose
Hx – Sudden DKA is usually first manifestation circulating
 Polyuria, polydipsia, nocturia  Lipotoxic and glucotoxic effects on the pancreas ⇨ β cell
 Young age dysfunction
 LOW  Changing microbiota, ⇩ GLP-1 production from the gut or
 Blurred vision inflammatory factors ⇨ β cell failure
 Nausea/Vomiting  Also, an ⇧ in glucose absorption from the gut and kidney ⇨
 Abdo pain ⇧ BG levels
 Tachypnoea
 Lethargy Peripheral insulin resistance can arise due to central obesity which
 Poor wound healing impairs insulin-dependent glucose uptake into cells
Ax – Epi –
Autoimmune β cell destruction in genetically susceptible individuals –  90% of pts w/ diabetes have T2DM
HLA association (HLA-DR3/HLADR4 +ive pts are 4-6x more likely to  Stronger association w/ family history
develop T1DM)  Older onset but the mean age of onset is decreasing
Associated w/ other autoimmune conditions – Hashimoto’s; Type A  More common in Blacks, Hispanics, Aboriginals and Asians
gastritis; Coeliac disease; primary adrenal insufficiency
May be iatrogenic – e.g pancreatectomy Thyroid Disease
Pathophys – Genetic susceptibility, environmental triggers
Hyperthyroidism
Hyperthyroidism: a condition characterised by the overproduction of
thyroid hormones by the thyroid gland; can cause thyrotoxicosis
Thyrotoxicosis: refers to the Sx caused by excessive circulation of
thyroid hormones – caused by thyroid gland hyperactivity
Overt hyperthyroidism – ↑ serum free T4/T3 levels w/ ↓ serum TSH
Subclinical hyperthyroidism – normal serum free T4/T3 levels w/ ↓
serum TSH
Graves Disease – autoimmune associated w/ circulating TSH
receptor autoantibodies leading to overstimulation of thyroid gland
with excess thyroid hormone production
Hx
 Sweating
α cells are spared in T1DM and leads to ⇧ glucagon  Weight loss
Glucagon can exacerbate hyperglycaemia  Emotional instability/erectile dysfunction in men
Autoimmune response w/ production of autoantibodies e.g Anti-GAD  Appetite increase/amenorrhoea/anxiety
that target insulin-producing cells which lead to an absolute insulin  Tremor/tachycardia
deficiency  Intolerance to heat/insomnia/increased reflexes
Epi –  Nervousness
 10% of pts have T1DM  GI problems – goitre, diarrhoea, N/V
 More likely to develop into DKA Examination
 Childhood onset  Graves– exophthalmos, oedema of periorbital tissue,
 More common in Caucasians pretibial myxoedema, diffuse goitre
Type 2 Diabetes:  Palpitations, elevated JVP (CCF)
Characterised by insulin resistance (peripheral cells insufficiently  Tachycardia, irregular pulse, widened pulse pressure
respond to insulin) and pancreatic β -cell dysfunction (impaired  Tremor
insulin secretion) resulting in relative insulin deficiency  Hyperreflexia
 Strong genetic component  Enlarged thyroid (goitre)
 Associated with obesity + sedentary lifestyle  Palmar erythema
Hx  Thin hair, lid lag, lid retraction
 Fatigue Ax –
 Blurred Vision Graves Disease (80%), toxic multinodular goitre (15%), thyroid
 Frequent infections (skin, UTI, candida) adenoma (5%), thyroiditis; rare – TSH-producing pituitary tumours;