Summary
Endocrine - Summary
- Course
- Institution
Endocrine - Summary Table of all endocrine conditions organised by history findings, examination findings, investigation findings and management according to Australian guidelines.
[Show more]
Seller
Follow
nikitagoyal
Content preview
Endocrine; Nikita GoyalGliclazide - 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;
The benefits of buying summaries with Stuvia:
Guaranteed quality through customer reviews
Stuvia customers have reviewed more than 700,000 summaries. This how you know that you are buying the best documents.
Quick and easy check-out
You can quickly pay through credit card or Stuvia-credit for the summaries. There is no membership needed.
Focus on what matters
Your fellow students write the study notes themselves, which is why the documents are always reliable and up-to-date. This ensures you quickly get to the core!
Frequently asked questions
What do I get when I buy this document?
You get a PDF, available immediately after your purchase. The purchased document is accessible anytime, anywhere and indefinitely through your profile.
Satisfaction guarantee: how does it work?
Our satisfaction guarantee ensures that you always find a study document that suits you well. You fill out a form, and our customer service team takes care of the rest.
Who am I buying these notes from?
Stuvia is a marketplace, so you are not buying this document from us, but from seller nikitagoyal. Stuvia facilitates payment to the seller.
Will I be stuck with a subscription?
No, you only buy these notes for $7.79. You're not tied to anything after your purchase.
Can Stuvia be trusted?
4.6 stars on Google & Trustpilot (+1000 reviews)
75323 documents were sold in the last 30 days
Founded in 2010, the go-to place to buy study notes for 14 years now