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Diabetes Flashcards

(51 cards)

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1
Q

What’s the difference between type a T1 and type b T1

A

Type a: autoimmune

Type b: idiopathic

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2
Q

What genetic factors predispose for T1DM

A

HLa DR3 and DR4. DR2 is protective. IDDM2 and 12 also contributes

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3
Q

What are the steps in the lack of insulin action

A

Hyperglycemia -> glycosuria -> osmotic diuresis -> poluria ->polydipsia -> dehydration -> weight loss

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4
Q

What are the consequences of lipolysis

A

Ketogenesis -> ketosis -> nausea -> acidosis -> compensate with hyperventilation (serious insulin deficiency). Respiratory compensation for metabolic acidosis

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5
Q

What are the macrovascular complications of diabetes

A

Angina, claudication, TIA

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6
Q

What are the microvascular complications of diabetes

A

Retinopathy (as glucose concentration shifts, eye ball and lens will shrink and expand
Neuropathy
Autonomic (abnormal sweating, gastroparesis, diarrhea, postural dizziness, erectile dysfunction, incontinence), radiculopathy
Compression (pain, tingling, weakness in carpal tunnel)
Mononeuritis (more susceptible to damage)

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7
Q

What are the clinical features for T1DM

A

Insulin deficient, ketosis prone, HLA markers, autoimmune, onset peak in adolescence, weight loss

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8
Q

What are the clinical features for T2DM

A

Insulin resistant and deficient, not ketosis prone, polygenic, S Asians, Increases with ageing, associated with obesity

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9
Q

What are the venous plasma glucose levels for diabetes

A

Over 7 fasting and over 11.1 at 2 hours

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10
Q

What are the venous plasma glucose levels for impaired glucose tolerance

A

Less than 7 fasting, (above 7.8 but below 11.1) at 2 hours

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11
Q

What are the venous plasma glucose levels for impaired fasting glucose

A

Above 6.1 but less than 7 at fasting, less than 7.8 at 2 hours

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12
Q

What are the diagnostic criteria for diabetes

A

Symptoms and random plasma glucose over 11.1
Asymptomatic and HbA1c over 48 on 2 occasions, fasting plasma glucose over 7 mmol and/or 2 hour post 75g glucose load over 11.1 on 2 separate occasions

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13
Q

What’s the normal percentage of glucose in urine

A

0.1%, cannot be used to diagnose diabetes

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14
Q

When should HbA1c not be used

A

Blood glucose levels have risen rapidly
Symptomatic children and young people
Symptoms suggesting T1DM
Short duration diabetes symtpoms
Patients are high risk of diabetes who are acutely ill
Taking medication that may cause rapid glucose rise e.g. corticosteroids, anti psychotics
Acute pancreatic damage/pancreatic surgery

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15
Q

How much does glucose concentration fall in plasma and why

A

0.5 mmol over 3 hours due to glycolysis in RBC. Whole blood glucose is 10-15% lower than in plasma

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16
Q

How is capillary glucose testing conducted

A

Prick finger with lancet, obtain blood sample, apply to reagent strip

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17
Q

What are the long term blood glucose control methods

A

Glycated haemoglobin - non enzymatic addition of glucose to amino groups of Hb
Serum fructosamine - glycated albumin. Reference range 200-285

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18
Q

What are the interferences with HbA1c measurement

A

Hb variants (HbF can elevate)
Altered red cell survival (haemolytic anaemia)
Chemically modified Hb (carbamylation in uremia can elevate, acetylation with aspirin can elevated)
Reduced glycation process - vitamin C can lower

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19
Q

What are the steps of ketone metabolism

A

Acetyl CoA form fatty acyl-CoA -> 3-hydroxybutyrate and acetoacetate and saturates in DKA. Acetoacetate and 3-hydroxybutyrate ratio should be similar

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20
Q

What does ketone blood test measure

A

b-hydroxybutyrate
Normal concentration less than 0.6
Over 1.5 clinically significant
Over 3mmol part of triad for DKA

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21
Q

What does ACR measure

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A 
Urine microalbumin (urine albumin and creatinine ratio), helps identify kidney disease that can occur as a complication of diabetes
Persistent microalbuminuria has 20x increased risk of diabetic renal disease
22
Q

What are the measurements for microalbuminuria

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A

ACR over 2.5mg/mmol (men)

ACR over 3.5 mg/mmol (women)

23
Q

What are other causes of increased albumin excretion

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A

UTI, non diabetic renal disease, menstrual contamination, vaginal discharge, uncontrolled hypertension, heart failure, inter-current illness and strenuous exercise

24
Q

What drugs can be used to treat T1DM

25
What drugs can be used to treat T2DM
Biguanides, sulphonylureas, thiazolidinediones, meglitinides, incretins, DPP4 inhibitors, alpha-Glucosidase inhibitors, SGLT2 inhibitors, amylin analogues, insulin
26
What's an example of a biguanide?
Metformin
27
How does biguanide work?
Act through AMPK, increase AMP levels, mTOR (mammalian target for rampamyacin), inhibition of glycerophosphate dehydrogenase -> decrease hepatic gluconeogenesis
28
What do biguanides not have an effect on
Insulin, glucagon, GH, cortisol, somatostatin
29
How does biguanide work
Decrease blood glucose concentration by: decreased hepatic glucose production potentiate insulin action on muscle and adipose tissue stimulation of glycolysis in tissues, stimulates glucose uptake decrease carbohydrate absorption stimulate lactate production decreases LDL and VLDL inhibit expression of genes involved in gluconeogensis
30
What drugs for T2DM cause hypoglycaemia
Sulphonylureas, thiazolidenediones, and insulin
31
What are the side effects of biguanides
Diarrhoea, nausea and metallic taste, rare lactate acidosis, decreases intestinal absorption of folate and vitamin B12
32
What sulphonyureas area used
Glibencalmide, Glipizide
33
What are acute effects of sulphonyureas
Increase insulin release, increase plasma insulin concentration, decrease hepatic clearance of insulin
34
What are chronic effects of sulphonyureas
No acute increase in insulin release but decreased plasma glucose concentration still remains Chronic hyperglycaemia decreases insulin release Down regulation of sulphonylurea receptor
35
What are the side effects of sulphonylureas
Neuroglycopenia (lack of glucose supply to brain) Confusion and coma - take oral glucose If severe give IV glucose, glucagon, adrenaline
36
What meglitinides are used
Repaglinide, nateglinide
37
How do meglitinides work
Take before meals | Close K+ATP channels on beta-cells, share 2 binding sites with sulphonylureas but have their own distinct binding site
38
What thiazolidenediones are used and what are their respective side effects
Trolitazone - live toxicity Rosiglitazone - CV problems Pioglitazone - risk bladder cancer All cause weight gain due to increased differentiation of adipocytes, fluid retention by stimulating amiloride Na+ absorption
39
What is thiazolidenediones mechanism of action
Activates insulin response genes that control carbohydrate metabolism Needs insulin to be effective Reduces insulin resistance in peripheral tissues Reduces glucose production by liver Increases glucose uptake in muscle and adipose tissue potentiates actions of insulin Increase adipocyte number and lipogensis
40
How do SGLT inhibitors work
SGLT2 is found in early proximal tubule, responsible for most absorption of glucose. Inhibitors increase diuresis. SGLT2 inhibitors inhibit glucose re-uptake in kidney
41
What are examples of SGLT2 inhibitors
Dapagliflozin, canaglifozin, empagliflozin -> combined with metformin
42
What alpha-glucosidase inhibitors are used
Acarbose and miglitol
43
How do alpha-glucosidase inhibitors work
Inhibits intestinal brush border alpha-glucosidase Inhibits carbohydrate breakdown and reduce postprandial increase in blood glucose levels Effective in T1DM and T2DM
44
What are incretins
Group of metabolic hormones that stimulate a decrease in blood glucose levels GLP-1 and GLP-2 act on pancreatic beta cells to increase insulin release - found in distal ileum GIP: glucose dependent insulinotrophic peptide or gastric inhibitory peptide K cells in duodenum
45
How do incretins work
``` Given as injection as peptides are not orally active Stimulates insulin release Suppresses glucagon secretion Reduces appetite and body weight Slows gastric emptying Stimulated beta cell number ```
46
How do DPP4 inhibitors work
Blocks DPP4, which breaks down natural incretins
47
How do amylin analgoues work
Amylin is a main component of pancreatic amyloid related to calcitonin Decreases gastric emptying Inhibits glucagon release from alpha cells Promotes satiety Related to beta amyloid and can form aggregates
48
What obesity treatments are used
Orlistat (lipase inhibitor) - causes steatohorrhea Ghrelin antagonists Ghrelin vaccine NPY agonists
49
What are the differences between injected insulin and endogenous insulin
Loss of C peptide Loss of portal:peripheral gradient Weight gain Not controlled endogenously
50
What are rapid acting insulins
Lispro and aspart | Starts to work within half na hour and peak at 1-2 hours
51
What are long acting insulins
Determir (twice a day) Glargine (once a day) Degludec

Diabetes (3 decks)

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