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Summary Essential Notes: Endocrinology: Diabetes

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Diabetes
Dx Anti-diabetic drugs
If patient is asymptomatic:
Fasting glucose ≥ 7.0 mmol/L
Type of Mechanism of
Definition chronic condition characterised by abnormally Random glucose ≥ 11.1 mmol/L (or after 75g Side effects
drug Action
raised levels of blood glucose due to insulin insensitivity GTT)
Hypoglycaem
or decreased insulin secretion HbA1c
ia Weight
Types of DM <41 mmol = normal
Insulin - gain
Type 1 autoimmune disorder where the insulin-producing 42-47 mmol = pre-diabetes
Lipodystroph
beta-cells of the pancreas are destroyed by the immune >48 mmol = DM y
system  absolute insulin deficiency  develop ≥ 6.5% (48mmol/mol) is diagnostic of DM
child/early adult < 6.5% doe not exclude
Type 2 most common in the developed world due to Increases insulin
Misleading results may be due to increased GI upset
relative deficiency of insulin due to an excess of adipose sensitivity
RBC turnover Metformin Lactic
tissue Reduced hepatic
General Mx acidosis
‘Not enough insulin to go around’ gluconeogenesis
Principles
Pre-diabetes: Patients who don’t yet meet the criteria for 1. Drug Rx to normalise blood glucose
a formal diagnosis of T2DM but are likely to develop it Sulfonylure Hypoglycaem
2. Monitoring for + Rx any complications
over the next few years a ia
related to DM Stimulate β-cells to
Require closer monitoring + lifestyle interventions such as e.g. Weight gain
weight loss
3. Modifying RF for other conditions e.g. secrete insulin
CVD Gliclazide/ Hyponatraem
Gestational some pregnant women develop raised levels Glimepiride ia
during pregnancy. Important to detect as untreated it Type 1 DM = require insulin
may lead to adverse outcomes for the mother + baby Type 2 DM = medication = 1st Metformin; 2nd
Maturity onset diabetes of the young (MODY) a group of Sulphonylureas, Gliptins, Pioglitazone
1. Metformin Thiazolidin
inherited genetic disorder affecting insulin. Younger Activate PPAR-γ
edione
patients developing similar symptoms to those w/ T2Dm 2. HbA1c > 58 mmol/mol? receptor in
(Glitazones Weight gain
i.e. asymptomatic hyperglycaemia  DKA a. Metformin + Gliptin adipocytes to
) Fluid
Latent autoimmune diabetes of adults (LADA) small group b. OR Metformin + Sulfonylurea promote
e.g. retention
develop later, misdiagnosed as T2DM c. OR Metformin + Pioglitazone adipogenesis + fatty
pioglitazon
Other pathological process that damages the kidney e.g. d. OR Metformin + SGLT-2 acid uptake
e
chronic pancreatitis, haemochromatosis/drugs e.g. inhibitor
glucocorticoids 3. HbA1c > 58 mmol/mol?
Signs + symptoms a. ALL 3
 Type 1 DM weight loss, polydipsia, polyuria b. Insulin Inhibits glucose
 Type 2 DM polydipsia, polyuria (water dragged 4. 3x therapy not SGLT-2
reabsorption in UTIs
out of the body due to osmotic effects of excess effective/tolerated/contraindicated + BMI inhibitors
kidneys
glucose being excreted in the urine)
>35
 DKA abdominal pain, vomiting, reduced
a. Metformin + Sulfonylurea +
consciousness
Ix
GLP-1 mimetic
Metformin not tolerated Nausea +
1. Finger-prick test bedside glucose monitor GLP-1 Incretin mimetic
vomiting
2. One-off blood glucose fasting/non-fasting 1. Gliptin OR Sulfonylurea OR agonist Inhibits glucagon
Pancreatitis
3. HbA1c amount of glycosylated Hb + represents Pioglitazone
average blood glucose over the past 2-3 months 2. HbA1c > 58 mmol/mol?
4. Glucose tolerance test fasting blood glucose is a. 3x therapy
b. Insulin DPP-4 Increases Incretin
taken after which a 75g glucose load is taken High risk of
inhibitor levels
After 2 hrs – another reading pancreatitis
(Gliptin) Inhibits glucagon
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