Week 7 diabetes Flashcards
Learn about diabetes and the methods of controlling
What is diabetes mellitus? What characterises the disease?
Metabolic disorder w. multiple causes. Characterised by chronic hyperglycaemia with disturbed carbohydrate, fat and protein metabolism and associated with co-morbidities
Explain glucose regulation in our body and the feedback mechanisms.
High blood sugar: promotes pancreas to release insulin -> cells uptake glucose+ liver turns glucose–>glycogen -> lower BGS
Low blood sugar: pancreas releases glucagon, stimulates liver to degrade glycogen into glucose -> release into periphery –> increase in BGS
Aboriginal peoples have a __x higher incidence of DM, are __x more likely to die from DM
- 10 times
- 13 times
Describe pathophysiology Type 1 DM
Autoimmune disease characterised by absolute deficiency or low levels of insulin production caused by pancreatic B-cell destruction.
Describe pathophysiology Type 2 DM
metabolic defects:
- insulin resistance in peripheral tissue
- pancreatic Beta-cell dysfunction -> low insulin production
List some of the chronic complications of diabetes:
KNIVES
Kidney. nephropathy Nerves: neuropathy damage to sensory, motor, pain, pins and needles Infection: fungal Vasculature Eyes: glaucoma, Skin
coronary artery disease, cerebrovascular disease
what are the short term and long term goal of tx of diabetes?
short term: relieve acute complications
long term: appropriate glycaemia levels, reduce concurrent risks (cardiovascular) and any chronic complications
If type 2 diabetes patients start insulin, they may also take a co-drug. List the drugs/classes of MIITAS and their MOA.
- Metformin: decrease insulin resistance
- Insulin scretagogues: increases insulin secretion
- Incretin therapies: various, new
- Thiazolidinediones: insulin sensitisers
- Acabose: reduce variation in glucose levels
- SGLT2 inhibitor: sodium-glucose co-transporter 2 –> inhibits glucose reabsorption
If type 2 diabetes patients start insulin, they may also take a co-drug. List the drugs/classes of MIITAS and their basic MOA.
- Metformin: decrease insulin resistance
- Insulin scretagogues (sulfonylureas): increases insulin secretion:
- Incretin therapies: various, new
- Thiazolidinediones: insulin sensitisers
- Acabose: reduce variation in glucose levels
- SGLT2 inhibitor: sodium-glucose co-transporter 2 –> inhibits glucose reabsorption
Which first-line drug is used in monotherapy for glycaemia management in type 2 diabetes?
Metformin
A type 2 diabetic patient is taking Metformin, but has resulted in secondary failure. What may happen next?
A second oral antidiabetic may be added to help control HbA1c level.
e. g. Metformin + sulfonylurea
e. g metformin + SGLT2 inhibitor
e. g. metformin + DPP4 inhibitors
For metformin, explain the
- MOA
- GI adverse effects
- tolerability
- hypoglycemic potential
- dosing
- Reduce hepatic glucose production -> increases peripheral use of glucose
- nausea, Vs, Ds, anorexia, rare lactic acidosis
- moderately tolerated (start small dose)
- No
- 1-2g/day over 2/3 doses
Gliptins act on the incretin family. Explain the - MOA - Adverse effects - tolerability - hypoglycemic potential - example of drug
- inhibits DPP-4 enzymes. Acts on GLP-1 to and GIP to increase glucose-dependent insulin secretion, reduce glucagon production, delay gastric emptying
- lacking data
- low risk
- saxagliptin, linagliptin
GLP-1 agonists are injectable agents . Explain the - MOA - Adverse effects - tolerability - hypoglycemic potential - example of drug
- Mimics GLP-1, stimulate insulin secretion
- SIg. nausea/Vs (up to 50%) but lessens
- Liraglutide, Dulaglutide
For the SGLT-2 inhibitors, provide the
- MOA
- Adverse effects
- tolerability
- hypoglycemic potential
- example of drug
- other benefit on organ system
- reduces reabsorption of glucose in the kidney = excretion of excess glucose (mono or dual thx)
- Increase UT//Genital infections, euglycaeimic DKA
- moderate
- low risk
- Dapagliflozin, Empagliflozin
- decrease risk of major cardiovascular events
For the sulfonylureas class, provide the
- MOA
- Adverse effects
- tolerability
- hypoglycemic potential
- example of drug
- increase pancreatic insulin secretion
- hypoglycaemia, weight gain
- moderate
- yes
- gliclazide
For thiazolidinedione class, provide the
- MOA
- Adverse effects
- tolerability
- hypoglycemic potential
- example of drug
- increase peripheral tissue sensitivity tissues to insulin. Decrease hepatic output
- increased risk of peripheral oedema, bone fractures, bladder cancer. worsening of diabetic macular oedema
- moderate
- no
- pioglitazone
For acabose, provide the
- MOA
- Adverse effects
- tolerability
- hypoglycemic potential
- inhibits digestion of carbohydrates in GIT
- flatulence, abdominal bloating
- poor
- no
Describe initial insulin thx program.
- 10 units of intermediate-acting insulin before bedtime as late as possible.
- allows maximum potency at dawn and avoid hypoglycaemia at 2-3am
- hyperglycaemic patients can start on higher dose (20-25 units)
When combining insulin and oral drug thx, patients are put on either a “basal insulin” or “premixed” schedules. What are the pro and cons of either?
Basal insulin: lower risk of nocturnal hypos, once daily. Injected
Premixed: may be more simple if fasting BSL and postprandial glucose are high; once daily before biggest meal. Dosage adjustments complex, risk of hypo and weight gain
