Type 1 And 2 Diabetes Flashcards

1
Q

What are the non-insulin drugs

A

The insulin sensitisers
Secretagogues
Stimulating the glucosuria

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2
Q

What are the type of insulin sensitisers

A

Metoformin
Thiazolidinediones
(Both would decrease the hepatic secretion of glucose)

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3
Q

What are the types of secretagogues

A

Sulfonolureas
DPP-4 inhibitors
GLP-1 receptor agonists (suppress glucagon secretion)

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4
Q

What are the drugs that would stimulate glucosuria

A

SGLT-2 AGONIST

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5
Q

What does HbA1c do
(Glycated haemoglobin)

A

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

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6
Q

What is blood glucose monitoring and continuous glucose monitoring

A

Would show the snapshot levels of glucose concentration in the blood

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7
Q

What is the mangement of T1DM

A

Insulin
Pancreas and sometimes renal transplants
Education on management
Needing some diet advice

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8
Q

What is the management for T2DM

A

Weight loss
Diet plans
Insulin and non-insulin drugs

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9
Q

How would hypoglycaemia be caused

A

Medication
Lowed glucose levels

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10
Q

What is the whipped triad of hypoglycaemia

A

Low blood glucose levels
Symptoms and signs consistent with hypo
Symptoms and signs go when increase blood glucose levels

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11
Q

What is the difference between neurogenic and neuroglycopenic symptoms

A

Neurogenic when have interaction of the adrenergic and cholinergic systems
Neuroglycopenic when have the damage to the brain

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12
Q

Why it too much blood glucose bad

A

Toxic
Glucose + NADPH — ——— sorbitol and NADP+
Sorbitol would cause osmotic damage to the cells
ENZYME: ALDOSE REDUCTASE

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13
Q

What is non-enzymatic glycosylation

A

Glucose would attach to the free amino acids
Would change the 3d structure of the protein
Would change the function of the protein

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14
Q

What are the macro vascular complication of diabetes

A

Cerebral vascular complications
Coronary artery disease
Peripheral artery disease

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15
Q

What are the micro vascular complications caused

A

Retinopathy
Neuropathy
Nephropathy

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16
Q

What is diabetic retinopathy

A

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

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17
Q

What is diabetic neuropathy

A

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)

18
Q

What is diabetic nephropathy

A

Albuminuria (protein in the urine)
Hypertension
Kidney damage and loss of function

19
Q

What is diabetic ketoacidosis

A

Production of the ketoacids as would not have enough glucose within the cells

20
Q

What is DKAs pathology

A

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)

21
Q

How does low insulin effect the adipose tissue

A

More lipolysis as break down of the stored fats

22
Q

How would low insulin effect the skeletal muscles

A

Break down of protein that would release the amino acids

23
Q

How does low insulin effect the liver

A

Gluconeogenesis of the amino acids and the lipids released

24
Q

What is T1DM

A

Autoimmune disease (t killer and macrophages on the islets cells)
Not producing insulin

25
What is T2DM
Insulin resistance Dysfunction of the beta cells
26
What is the typical triad for the T1DM
Polyuria (increased urination) Polydispia (increased thirst) Weight loss
27
What are the symptoms of DKA
weight loss Polyuria Polydispia Tachycardia Dehydration Acetone breath Shortness of breath Abdominal pain (from the acids)
28
How does diabetes lead to osmotic diruesis
Too much glucose to the kidney Above renal threshold Would not reabsorb Goes to urine
29
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
30
Why would people with T2DM not have DKA
They would still produce the insulin So this would stop them from developing it
31
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
32
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)
33
What is metabolic syndrome
Metabolic disease that can lead to cardiovascular disease Symptoms: Obesity Insulin resistance Dyslipidemia Hypertension
34
What is Charcot neuroarthropathy
Normally would come from the neuropathy Destruction of the joints and the bones of the foot, loss of sensation
35
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
36
What would the sorbitol accumulation do to the cell
Osmotic damage
37
What are the types of autonomic neuropathy
Cardiac autonomic neuropathy Gastrointestinal neuropathies Genitourinary disturbances
38
What do you get when you have cardiac autonomic neuropathy
Resting tachycardia Orthostatic hypotension (the fall in the blood pressure when you standup)
39
What do you get when you have gastrointestinal neuropathy’s
Gastroparesis Diarrhoea Constipation
40
What do you get when you have genitourinary disturbances
Sexual dysfunction Bladder dysfunction
41
What are the genes that are associated with diabetes
HLA - DR3 HLA - DR4