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Tp2. Metabolism, Endocrinology and Haemology > Type 1 And 2 Diabetes > Flashcards

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
Q

What is T2DM

A

Insulin resistance
Dysfunction of the beta cells

26
Q

What is the typical triad for the T1DM

A

Polyuria (increased urination)
Polydispia (increased thirst)
Weight loss

27
Q

What are the symptoms of DKA

A

weight loss
Polyuria
Polydispia
Tachycardia
Dehydration
Acetone breath
Shortness of breath
Abdominal pain (from the acids)

28
Q

How does diabetes lead to osmotic diruesis

A

Too much glucose to the kidney
Above renal threshold
Would not reabsorb
Goes to urine

29
Q

What are the symptoms of a hyperglycaemic hyperosmolar state

A

Hypovolemia (increased water loss)
Hyperosmolarity (increased reabsorbtion of water due to the high glucose)
Severe hyperglycaemia

30
Q

Why would people with T2DM not have DKA

A

They would still produce the insulin
So this would stop them from developing it

31
Q

Why does weight loss mainly happen in the T1DM

A

Not producing the insulin
Insulin would be a main anabolic reactant and allow anabolism
Would mainly have catabolism now
Breakdown = weight loss

32
Q

What are the markers for type 1 diabetes

A

Islet cell antibodies (ICA)
Antibody’s to GAD (glutamic acid decarboxylase)
Antibody’s to insulin (tyrosine phosphatatases)

33
Q

What is metabolic syndrome

A

Metabolic disease that can lead to cardiovascular disease
Symptoms:
Obesity
Insulin resistance
Dyslipidemia
Hypertension

34
Q

What is Charcot neuroarthropathy

A

Normally would come from the neuropathy
Destruction of the joints and the bones of the foot, loss of sensation

35
Q

What happens to the proteins when would have the depletion of the NADPH

A

Causes increased disulfide bond formation
Would then alter the protein function in the cell

36
Q

What would the sorbitol accumulation do to the cell

A

Osmotic damage

37
Q

What are the types of autonomic neuropathy

A

Cardiac autonomic neuropathy
Gastrointestinal neuropathies
Genitourinary disturbances

38
Q

What do you get when you have cardiac autonomic neuropathy

A

Resting tachycardia
Orthostatic hypotension (the fall in the blood pressure when you standup)

39
Q

What do you get when you have gastrointestinal neuropathy’s

A

Gastroparesis
Diarrhoea
Constipation

40
Q

What do you get when you have genitourinary disturbances

A

Sexual dysfunction
Bladder dysfunction

41
Q

What are the genes that are associated with diabetes

A

HLA - DR3
HLA - DR4

Tp2. Metabolism, Endocrinology and Haemology (16 decks)

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