Type 1 And 2 Diabetes Flashcards
What are the non-insulin drugs
The insulin sensitisers
Secretagogues
Stimulating the glucosuria
What are the type of insulin sensitisers
Metoformin
Thiazolidinediones
(Both would decrease the hepatic secretion of glucose)
What are the types of secretagogues
Sulfonolureas
DPP-4 inhibitors
GLP-1 receptor agonists (suppress glucagon secretion)
What are the drugs that would stimulate glucosuria
SGLT-2 AGONIST
What does HbA1c do
(Glycated haemoglobin)
Would be a way of measuring the long term glucose concentration (2-3months)
Glucose would attach to the terminal valine of haemoglobin and so can be measured
Not good when would have haemoglobin disorders
What is blood glucose monitoring and continuous glucose monitoring
Would show the snapshot levels of glucose concentration in the blood
What is the mangement of T1DM
Insulin
Pancreas and sometimes renal transplants
Education on management
Needing some diet advice
What is the management for T2DM
Weight loss
Diet plans
Insulin and non-insulin drugs
How would hypoglycaemia be caused
Medication
Lowed glucose levels
What is the whipped triad of hypoglycaemia
Low blood glucose levels
Symptoms and signs consistent with hypo
Symptoms and signs go when increase blood glucose levels
What is the difference between neurogenic and neuroglycopenic symptoms
Neurogenic when have interaction of the adrenergic and cholinergic systems
Neuroglycopenic when have the damage to the brain
Why it too much blood glucose bad
Toxic
Glucose + NADPH — ——— sorbitol and NADP+
Sorbitol would cause osmotic damage to the cells
ENZYME: ALDOSE REDUCTASE
What is non-enzymatic glycosylation
Glucose would attach to the free amino acids
Would change the 3d structure of the protein
Would change the function of the protein
What are the macro vascular complication of diabetes
Cerebral vascular complications
Coronary artery disease
Peripheral artery disease
What are the micro vascular complications caused
Retinopathy
Neuropathy
Nephropathy
What is diabetic retinopathy
Damage to the vessels in the the retina
Proliferative : production of the new blood vessels and so would get haemorrhage
Non-proliferative : microvessel abnormalities (micro aneurysms) and the vessel infarcts
What is diabetic neuropathy
The damage to the nerves
Small: the pain and the dysesthesia (burning and tingling)
Large: numbness and the loss of sensation
(Diabetic foot, leisons, charot neuroathropathy (complete degeneration of the bones and the tendons)
What is diabetic nephropathy
Albuminuria (protein in the urine)
Hypertension
Kidney damage and loss of function
What is diabetic ketoacidosis
Production of the ketoacids as would not have enough glucose within the cells
What is DKAs pathology
The fatty acids released from the liver (fatty Co A)
Made into acetyl Co A and this makes acetoacetone (gives the acetone smell)
Beta-hydroxybutonate goes to urine (so can measure the ketones in the urine)
How does low insulin effect the adipose tissue
More lipolysis as break down of the stored fats
How would low insulin effect the skeletal muscles
Break down of protein that would release the amino acids
How does low insulin effect the liver
Gluconeogenesis of the amino acids and the lipids released
What is T1DM
Autoimmune disease (t killer and macrophages on the islets cells)
Not producing insulin
What is T2DM
Insulin resistance
Dysfunction of the beta cells
What is the typical triad for the T1DM
Polyuria (increased urination)
Polydispia (increased thirst)
Weight loss
What are the symptoms of DKA
weight loss
Polyuria
Polydispia
Tachycardia
Dehydration
Acetone breath
Shortness of breath
Abdominal pain (from the acids)
How does diabetes lead to osmotic diruesis
Too much glucose to the kidney
Above renal threshold
Would not reabsorb
Goes to urine
What are the symptoms of a hyperglycaemic hyperosmolar state
Hypovolemia (increased water loss)
Hyperosmolarity (increased reabsorbtion of water due to the high glucose)
Severe hyperglycaemia
Why would people with T2DM not have DKA
They would still produce the insulin
So this would stop them from developing it
Why does weight loss mainly happen in the T1DM
Not producing the insulin
Insulin would be a main anabolic reactant and allow anabolism
Would mainly have catabolism now
Breakdown = weight loss
What are the markers for type 1 diabetes
Islet cell antibodies (ICA)
Antibody’s to GAD (glutamic acid decarboxylase)
Antibody’s to insulin (tyrosine phosphatatases)
What is metabolic syndrome
Metabolic disease that can lead to cardiovascular disease
Symptoms:
Obesity
Insulin resistance
Dyslipidemia
Hypertension
What is Charcot neuroarthropathy
Normally would come from the neuropathy
Destruction of the joints and the bones of the foot, loss of sensation
What happens to the proteins when would have the depletion of the NADPH
Causes increased disulfide bond formation
Would then alter the protein function in the cell
What would the sorbitol accumulation do to the cell
Osmotic damage
What are the types of autonomic neuropathy
Cardiac autonomic neuropathy
Gastrointestinal neuropathies
Genitourinary disturbances
What do you get when you have cardiac autonomic neuropathy
Resting tachycardia
Orthostatic hypotension (the fall in the blood pressure when you standup)
What do you get when you have gastrointestinal neuropathy’s
Gastroparesis
Diarrhoea
Constipation
What do you get when you have genitourinary disturbances
Sexual dysfunction
Bladder dysfunction
What are the genes that are associated with diabetes
HLA - DR3
HLA - DR4
