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Diabetes & Endocrine > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is glycogen?

A

Storage of glucose. Stored in the liver & skeletal muscle

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2
Q

What is glucagon?

A

Antagonist of insulin, secreted from alpha cells in the islets of Langerhans. Which convertes glycogen back into glucose.

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3
Q

What is somatostatin?

A

A hormone that inhibits digestion & absorption. Inhibits secretion of pancreatic hormones.

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4
Q

How is insulin secreted?

A

Glucose enters via GLUT2 transports. Increase in glucose stimulates metabolism -> an increase in ATP. Increase in ATP inhibits an ATP sensitive K+ channel. causes depolarisation which causes the activation of Ca2+, which causes exocytosis of Ca2+ causes the release of insulin too.

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5
Q

Symptoms of DM?

A

Polyuria, polydipsia, weight loss, fatigue, blurred vision.

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6
Q

What are the symptoms of DKA?

A

Hyperventilation, nausea & vomiting, dehydration, weakness, ketone breath, reduces alertness.

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7
Q

Symptoms of HONK?

A

Same as DKA but doesnt have ketosis or acidsis.

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8
Q

WHO criteria for blood glucose test.

A

Random venous plasma >=11.1mmol/L
Fasting venous plasma >= 7mmol/L
HBA1c >48mmol/mL (6.5%)

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9
Q

What is classed as hypoglycemia?

A

blood glucose of less than 4mmol/L.

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10
Q

Treatment of the different severties of Hypoglycemia?

A

Mild :
15-20g rapidly absorbed sugar, then after this you would have a snack or your next meal to have sustained carbohydrates.
Moderate :
1.5 - 2 tubes of glucogel or inter muscular injection of glucagon (1mg)
Severe :
IM glucagon (1mg) or IV glucose (150mL of 10% over 10 - 15 mins)

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11
Q

What are the microvascular complications of type 2 DM?

A

Retinopathy, nephropathy, neuropathy.

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12
Q

Why does microvascular complications occur?

A

Endothelial cells of the retina, kidney, peripheral nervous system allows glucose to enter the cells even in the absense of inslulin.

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13
Q

What should be the first line treatment of Diabetic with hypertension?

A

ACE-i because it has renoprotective effects. Bc studies showed prevented / delayed progression of renal disease.

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14
Q

What is retinopathy?

A

Small haemorages, new blood vesseles form which are fragile which tend to bleed which destroy the retina.

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15
Q

What is nephropathy?

A

Failure of the kidney, and can be cause there to be small amounts of albumin to be found in the urine.

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16
Q

What is neuropathy?

A

Numbess that occurs in both legs, may or may not cause pain, impaired sense of position.

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17
Q

What causes diabetic foot?

A

Peripheral vascular disease, causes poor circulation & ischaemia of lower limbs. Can effect getting antibiotics to the site of infection.

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18
Q

What are the macrovascular complications of DM?

A

Cardio vascular disease.
Hypertension.

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19
Q

Name rapid-acting Insulins.

A

Novorapid, Humalog, Apidra.

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20
Q

Name short acting Insulins.

A

Actrapid, Humulin S, Hypurin porcine neutral.

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21
Q

Name Medium acting Insulins.

A

Insulaterd, Humulin I, Hypurin Porcine Isophane.

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22
Q

Name long acting Insulin.

A

Levemir & Lantus.

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23
Q

Analogue mixture of insulin.

A

Novomix 30, Humalog 50/25.

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24
Q

Mixtures of insulin.

A

Humulin M3, Insuman combi 15,25,50 , Hypurin Porcine 30/70.

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25
Q

Administration sites of insulin.

A

Abdomen (fast absorption)
Thighs (Slower absorption)
Upper arm (Medium absorption)
Buttocks (Slowest absorption)

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26
Q

Name an example of an Sulphonylureas?

A

Glyclazide

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27
Q

MOA of Sulphonylureas?

A

Block the KATP channel causing depolarisation of the membrane potential -> downstream actions and increases the secretion of insulin.

28
Q

What is a side effect of Sulphonylureas, and why is it caused?

A

Can cause hypoglycemia bc insulin secretion is increased even in the absence of glucose.

29
Q

Name an example of a GLP-1 Agonist?

A

Exenatide

30
Q

MOA of GLP-1 Agnosits?

A

Peptide hormone released from the ilium that acts on the GLP-1 Gas coupled receptors in the pancreatic B - cells. Which cause a decrease in gastric emptying, decrease in glucagon secretion and increases in satiety.

31
Q

Name a DPP-4 Inhibitor?

A

Alogliptin.

32
Q

MOA of DDP-4 Inhibitors?

A

GLP-1 has a very short half life, Inhibition of DPP-4 decreases the breakdown of GLP-1 which therefore allows GLP-1 to perform its biological actions for longer.

33
Q

What does metformin do?

A

Decreases gluconeogenesis in liver, increases peripheral glucose uptake & utilisation, improves insulin sensitivity, decreases carbohydrate absorption from the GIT, Decreases lipid synthesis.

34
Q

MOA of Metformin?

A

Inhibits complex 1 -> decreases ATP production, increase in AMP : ATP ratio, inhibition of gluconeogenesis, decrease in ATP -> decrease in CAMP lvls, Activation of AMPK, increase of CAMP, decreases fat synthesis, and an increase in fat oxidation.

35
Q

Name a PPAR gamma Agonist.

A

Pioglitazone

36
Q

MOA of PPAR gamma Agonist?

A

Increase sensitivity of insulin by increasing transcription of genes involved in insulin signalling -> enhancing the effectiveness of insulin.

37
Q

Name an SGLT-2 Inhibitor.

A

Dapagliflozin, empagliflozin

38
Q

MOA of SGLT-2 Inhibitors?

A

These will reduce & therefore increase excretion of glucose in the urine which then decrease the plasma [ ] of glucose.

39
Q

Name a alpha-glucoside inhibitor.

A

Maltase.

40
Q

What is a multiple dose regime?

A

Intermediate/long acting basla once daily at night + multiple short acting at meals times.

41
Q

What are the advantages of Multiple?

A

Flexible if need to delay meal/adjust for exercise.
Suitable for shift workers.

42
Q

Disadvantages of Multiple?

A

More injections.

43
Q

What is a twice daily regime?

A

Short + intermediate acting premixed.

44
Q

What are the advantages of Twice daily?

A

Simple, good control.
Less injections.

45
Q

What are the disadvantages of twice daily?

A

Inflexible, fixed time.
Timed and constant food intake and lifestyle.

46
Q

What is a Once Regime?

A

Intermediate / long acting basal once daily at night. Often used with type 2 diabetics.

47
Q

Starting insluin regime?

A

Start with low doses and increase slowly
Twice daily : 6-10 units BD
Multiple : short 60% & long 40% (4 units TDS & 8 units NOCTE)

48
Q

Adjusting Insulin doses.

A

Adjust doses by 10% alloquots.
Do not omit doses if too low.

49
Q

Storage?

A

Long term storage in fridge loss of 5-10 % poteny at room temp.
Current use keep out of fridge.
1 month out of fridge.

50
Q

Why should longer acting sulphanolureas be avoided in the elderly?

A

Longer acting such as glimperide should be avoided beause it can cause hypoglycaemia.

51
Q

What is the SAR for sulphonylureas?

A

p- subunit on aromatic ring, not amine to avoid antibacterial activity.
Alkyl substituient on urea.

52
Q

What are the main things that cause oxidative stress?

A

Hydrogen peroxide
Superoxide
Hydroxyl radicals

53
Q

What causes polyuria?

A

Osmotic diuresis when blood glucose exceeds renal threshold.

54
Q

What causes polydipsia?

A

Due to resulting fluid & electrolyte loss.

55
Q

Why does weight loss occur in DM?

A

Due to fluid delpletion & increased breakdown of fat & muscle.

56
Q

Why does fatigue occur in DM?

A

Body’s inability to get glucose from blood into cells to meet energy needs.

57
Q

Why does blurred vision occur in DM?

A

Due to blood glucose induced changes in refraction.

58
Q

What is the ETC?

A

Series of biochem reactions in which electrons and hydrogen atoms from NADH and FADH are passed to intermediate carriers and then ultimately react with molecular oxygen to prod water.

59
Q

How is AcetylCoA converted to Ketone bodies?

A

Converted to AcetoacetylCoA
Then converted to 3-hydroxy-3methylglutarylCoA
Which is then converted into acetoacetate -> Acetone.

60
Q

What is the PKC pathway?

A

Excess DHAP converted to Diacyl glycerol (DAG)
DAG activates PKC.
Activated PKC leads to blood-flow abnormalities, capillary and vascular occlusion, pro-inflammatory gene expression, Increased NADPH which is a ROS which causes oxidative stress.

61
Q

What does glutathione do to methylgyoxal

A

Reduces it (DHAP) via the glyoxalase pathway into lactic acid.
same occurs with the polyol pathway but this decreases NADPH which is used to regenereate glutathione.

62
Q

What cells in the islets of langerhands secrete glucagon?

A

Alpha cells.

63
Q

What cells in the islets of langherans secrete insulin

A

Beta cells.

64
Q

What receptotr does insulin act at?

A

RTK.

65
Q

What receptor does glucagon act at?

A

GPCR Gas

Diabetes & Endocrine (7 decks)

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