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Endocrine > Week 1 - Diabetes > Flashcards

Week 1 - Diabetes Flashcards

1
Q

Define diabetes mellitus.

A

A group of metabolic diseases in which an individual has hyperglycemia for one of two reasons. Either the pancreas does not produce enough insulin (absolute deficiency) or the cells do not adequately respond to the insulin which is produced (relative deficiency).

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2
Q

List 4 potential symptoms of diabetes mellitus.

A

Polydipsia, Polyuria, Glycosuria, and blurred vision.

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3
Q

What are three diagnostic characteristics which can be used to diagnose a patient with diabetes mellitus?

A

Fasting glucose > 7.0 mmol/L
Random glucose >11.1mmol/L
HbA(Ic) > 6.5%

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4
Q

What is pre-diabetes an associated risk factor of?

A

Development of diabetes and macrovascular disease.

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5
Q

What recurrent infection can be diagnostic of diabetes mellitus?

A

Recurrent Candida infection, especially in men who otherwise get very few yeast infections.

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6
Q

List two major differences between Type I & Type II diabetes mellitus.

A

Type I: Weight loss & autoimmune disease.

Type II: Associated with obesity & insensitivity to insulin.

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7
Q

What route does insulin take to be activated, what enzymes are involved in this action, and how is endogenous insulin production measured?

A

Pre-Proinsulin –{Prohormone convertase}–> Proinsulin –{Carboxypeptidase}–> Insulin.
Peptide C is a by product of this conversion. For every endogenously derived insulin TWO Peptide C are generated as well.

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8
Q

List the three insulin sensitive tissues.

A

Liver, Adipose, and Muscle {LAM}.

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9
Q

With tight control of blood glucose concentration retinopathy will be _______ for the first two years and ______ in the long run.

A

Worse, Better

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10
Q

What does laser photocoagulation (PPR) target?

A

Ischemic regions of the retina which release angiogenesis stimulation growth factors. {This type of treatment DOES NOT target the invading blood vessels themselves.}

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11
Q

What factor (other than blood glucose concentration) is very beneficial to have tightly regulated in avoiding retinopathy?

A

Blood Pressure

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12
Q

What percentage (of all dialysis patients) start dialysis because of diabetic neuropathy?

A

50%

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13
Q

What are 3 clinical characteristics of nephropathy?

A

Albuminuria, Hypertension, and progressive decline in renal function.

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14
Q

List 5 factors which may influence the development of diabetic retinopathy:

A
  • Blood Pressure
  • Blood glucose concentration.
  • RAS (Renin-Angiotensin System).
  • Lipids
  • Smoking
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15
Q

What percentage of diabetic patients develop neuropathy? What is the most common way for this to present clinically?

A

60% - 70% {Ranging from insignificant to severe}.

Foot ulcers.

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16
Q

Diabetic peripheral neuropathy may present through . . .

A

Cranial nerve palsies, numbness, or extreme sensitivity/pain.

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17
Q

Describe neuropathic foot ulcers. {Other type: Ischemic}

A
  • Pressure is associated with calluses.
  • Ulcers are painless.
  • On the plantar surface of the foot.
  • The feet are warm with dilated veins.
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18
Q

Describe ischemic foot ulcers. {Other type: Neuropathic}

A
  • On the dorsal or lateral surfaces of the foot.
  • Ulcers are painful.
  • Appear “punched out”.
  • The feet are cold, pale, and pulseless.
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19
Q

What is a charcot foot a result of? What is it a major risk factor for?

A

Peripheral neuropathy, Ulceration.
Charcot’s arthropathy involves bone reabsorption and degeneration of a weight bearing joint. Onset is often insidious. May result in ulceration, super infections, or amputation.

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20
Q

What will 70% - 80% of patients with diabetes die from?

A

Cardiovascular Disease {Macrovascular Disease}.

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21
Q

What is CAD?

A

Coronary Artery Disease

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22
Q

What disease is predicted by T2DM diagnosis?

A

Coronary Artery Disease (CAD)

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23
Q

What disease is predicted by T1DM?

A

Diabetic Nephropathy & Diabetic Retinopathy

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24
Q

What percentage of diabetes patients are blind?

A

< 1%. Half of those that are blind have blindness caused by factors other than diabetes.

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25
Q

What cell is damaged and lost in diabetic retinopathy?

A

Pericytes - Contractile cells which wrap around the endothelial cells of capillaries and venules throughout the body.

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26
Q

What are “cotton wool spots”?

A

Ischemic nerve fibres of the eye. These nerve fibres are translucent in healthy individuals but become opaque after the swelling and bloating caused by ischemia.

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27
Q

What causes hemorrhages in the vitreous humour?

A

After ischemia occurs growth factors are released which stimulate angiogenesis. These new blood vessels are weak and grow into the vitreous humour. Eventually they hemorrhage or aneurism.
These vessels may also scar and contract causing retinal detachment.

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28
Q

What hormone may be related to the development of retinopathy?

A

Growth Hormone (GH)

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29
Q

Which type of diabetes is retinopathy more common in?

A

T1DM {Nearly 100% of people with T1DM will develop some degree of retinopathy after having the disease for >10 years}.

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30
Q

What do the beta cells of the Islets of Langerhans produce?

A

Insulin

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31
Q

What do the alpha cells of the Islets of Langerhans produce?

A

Glucagon

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32
Q

What do the delta cells of the Islets of Langerhans produce?

A

Somatostatin

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33
Q

What do the PP cells of the Islets of Langerhans produce?

A

Pancreatic Polypeptide

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34
Q

What exocrine secretions does the pancreas produce?

A

Digestive enzymes.

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35
Q

How many unit of insulin should a resting person inject if they have eaten 20g worth of carbs?

A

4 units, assuming they started with an acceptable [glucose] in their blood.
1 unit of insulin / 5 grams of carbs

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36
Q

What is the target HbA(1c) for patients with diabetes?

A

7%

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37
Q

Insulin (and its analogs) likes to form _______ but must form _______ and _______ to enter the blood.

A

Hexamer, Dimer, Monomers.

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38
Q

What is a typical maximum total daily dose of insulin for a patient for T1DM?

A

1 unit/kg/day.
40% - 50% Basal {Long acting}.
50% - 60% Bolus {With meals}.

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39
Q

What does basal-bolus insulin dosage mean?

A

Patients take a long acting insulin to maintain basal levels throughout the day and night and bolus, short acting, insulin with meals.

40
Q

What does MDI stand for?

A

Multiple Dose Insulin

41
Q

Which two arteries provide blood for the pancreas?

A

The superior and inferior duodenal arteries.

42
Q

Describe the distribution of islet cells in the human pancreas.

A

Heterogenous and random.

43
Q

Insulin is an ________ hormone.

A

Anabolic

44
Q

Name four catabolic hormones.

A

GH, Glucagon, Cortisol, and Epinephrine.

45
Q

What does elevated amino acids do to glucagon secretion?

A

It increases glucagon secretion.

46
Q

What glucose transporter is expressed in muscle tissue with via the stimulation of insulin?

A

GLUT-4

47
Q

1 glucose creates __ pyruvate and __ ATP. The pyruvate subsequently continue to the Kreb’s cycle where they create ~___ more ATP.

A

2, 2, 34

48
Q

Glycerol may be converted into glucose but fatty acids are?

A

Converted into acetyl-coA via beta-oxidation.

49
Q

Which two substances must be absent for ketoacidosis to occur in diabetic patients?

A

Insulin and carbohydrates.

Oxaloacetate is converted into glucose and excess acetyl-coA is stored as acetone and beta-hydroxybutyrate (ketones).

50
Q

What are the glycemic targets for T1DM?

A

Fasting and pre-meal: 4-7 mmol/L
Post-prandial: 5-10 mmol/L
HbA(1c) < 7.0%

51
Q

What is CKD?

A

Chronic Kidney Disease

52
Q

What gene mutations on chromosome 6 result in an increased risk of T1DM?

A

HLA (MHC II)
{DR4/DQ8 - high risk of T1DM}
{DR3/DQ2 - high risk of autoimmune disease}

53
Q

What are the 5 common targets of autoantibodies related to T1DM?

A
  • Islet cells.
  • Glutamic Acid Decarboxylase.
  • Insulinoma-Associated 2.
  • Insulin
  • Zinc-transporter 8.
54
Q

100% of T1DM patients eventually develop antibodies against?

A

Insulin

55
Q

Approximately what percentage of beta cells have been lost by the time of diagnoses in T1DM?

A

~75%

56
Q

The fourth child has a ______ chance of getting diabetes than the first child.

A

Lower

57
Q

T1DM affects more _______ than other races and affects _______ females:males. If your sibling has T1DM you have a ___ chance of acquiring the disease, while an identical twin gives you ____ chance.

A

Caucasians, 1:1, 5%, 25%.

58
Q

What percentage of DM is type 1? Type 2?

A

10%, 90%

59
Q

What age demographic is more likely to get T1DM? T2DM?

A

T1DM typically affects people < 35.

T2DM typically affects people > 35.

60
Q

What percentage of the pancreas is exocrine?

A

The pancreas is 98% exocrine and 2% endocrine.

61
Q

Describe the process of insulin release from pancreatic beta cells.

A

High levels of glucose cause entry of glucose (via GLUT 2 transporters) into pancreatic beta cells. This causes a relative increase in ATP, triggering ATP dependant potassium channels. The potassium efflux depolarizers the membrane which triggers voltage gated calcium channels. Finally, the influx of calcium causes insulin containing vesicles to exocytose from the cell.

62
Q

How is insulin delivered to the liver and what percentage is extracted through first phase metabolism?

A

Insulin travels to the liver via the Hepatic Portal Vein (HPV). 70% is extracted in the first pass.

63
Q

What is the primary function of insulin?

A

Insulin stops the liver from creating glucose (gluconeogenesis) and initiates the conversion of glucose to glycogen.

64
Q

What process keeps glucose inside of cells?

A

Insulin stimulates hexokinase which phosphorylates glucose to glucose-6-phosphate. This prevents it from leaving the cell.

65
Q

By what action does insulin increase cellar glucose uptake?

A

Insulin utilizes a tyrosine kinase receptor pathway to stimulate GLUT 4 transporter movement to the membranes of insulin sensitive tissues (vesicles containing GLUT 4 bind to the membrane).

66
Q

What is gluconeogenesis?

A

Gluconeogenesis is the conversion of glycolysis and Kreb’s cycle intermediates, and other molecules into glucose.

67
Q

What is glycogen?

A

Glycogen is a polymer of on glucose which is synthesized by glycogen synthase in response to insulin. It is broken down by glycogen phosphorylase in response to glucagon and epinephrine.

68
Q

What is special about RBC metabolism?

A

They only use anaerobic metabolism (glycolysis).

69
Q

Describe how triacylglycerides are used for energy?

A

Broken down through lipgloss. Glycogen can be converted to glucose while the fatty acid tails are converted to acetyl coA (via beta oxidation) and enter the Kreb’s cycle from there.

70
Q

In hypoglycaemia, what component of the Kreb’s cycle is removed to make glucose for the brain.

A

Oxaloacetate. This is partially responsible for the pathogenesis of diabetic ketoacidosis.

71
Q

What percentage of T1DM patients have no significant family history of T1DM?

A

90%

72
Q

What percentage of T1DM patients have no detectable autoantibodies (at first)?

A

10%

73
Q

What, besides insulin autoantibodies, is present in 100% or T1DM?

A

Insulitis

74
Q

What does insulin do to increase glucose uptake?

A

Increases the number of GLUT 4 transporters in the cellular membranes.

75
Q

HbA(1c) can be used in most situations. One in which it cannot be used is?

A

Pregnancy

76
Q

What concordance rate do identical twins have for T2DM?

A

> 90% concordance.

77
Q

How is glucagon synthesis inhibited?

A

Islet alpha cells are inhibited by insulin.

78
Q

Why is it thought that apple shaped people (central obesity) have a higher risk of getting T2DM than pear shaped people?

A

Central obesity involves visceral fat deposits while pear shaped people have subcutaneous fat deposits.

79
Q

The risk of microvascular diabetic complications increase with?

A

HbA(1c)

80
Q

Why is renal biopsy not done for diabetic patients with nephropathy?

A

The risk outweighs the need for confirmation. A high likelihood of renal nephropathy already exists.

81
Q

Which cranial nerves are affected by diabetic cranial nerve palsies?

A

III (oculomotor - pupillary sparing, IV (trochlear), and VI (abducens).

82
Q

What are the goals of T1DM therapy? What are we trying to prevent?

A

Physiologic replacement of insulin, achieving near normal glycemia, and to minimize the risk of hypoglycemia.
We are trying to prevent chronic complications.

83
Q

For patients with T2DM, at what point of hyperglycemia should antihyperglycemic agents be initiated with lifestyle management?

A

HbA(1c) > 9%.

Lower than this lifestyle changes alone may be sufficient.

84
Q

Describe when the body begins to raise blood sugar.

A

At a [glucose] of 4 mmol/L insulin is no longer released.
At a [glucose] of 3 mmol/L glucagon is secreted.
At a [glucose] of 1.5 mmol/L individuals go into a coma.
At a [glucose] of 1 mmol/L seizures may occur.
At low [glucose] epinephrine, and then cortisol, are released.

85
Q

What are patients with hypoglycemia (especially T1DM) at risk of developing?

A

Addison’s disease.

86
Q

What should patients be asked if hypoglycemia is suspected?

A

If they have had any episodes of hypoglycemia, surprises (unsymptomatic hypoglycemic incidents), any precipitates, or amy fear of hypoglycemia.

87
Q

How should hypoglycemia be treated?

A

Patient should ingest 15g of carbohydrates, wait 15 minutes, and then measure their blood glucose concentration. If it is below 4 mmol/L the process should be repeated.

88
Q

What is Kussmaul’s breathing?

A

Deep and rapid breathing - the bodies attempt to correct acidosis.

89
Q

How is DKA treated?

A
  • Fluid resuscitation {1-2 L Bolus; IV drip, normal saline with electrolytes}.
  • Insulin IV drip {0.1 units/Kg/Hr} with dextrose added after a few hours to avoid overshooting into hypoglycaemia.
  • IV potassium SLOWLY.
90
Q

How is HHS/HONK treated?

A

Look for causes.

Fluid resuscitation, anticoagulant, and insulin {start with 4 units/hr}.

91
Q

List some common complications of hyperglycemia.

A
  • Cerebral edema.
  • Adult respiratory distress syndrome (ARDS).
  • Sepsis
  • MI
  • Hypokalemia
  • Hypoglycemia
92
Q

List two differences in the presentation of DKA and HHS/HONK.

A

Ketones and acidosis are present in DKA but not in HHS/HONK.

93
Q

What are some causes of DKA?

A

Insulin omission, infection, new diagnoses (non-management), and intercurrent illness.

94
Q

What are some causes of HHS/HONK?

A

Intercurrent illness, infection, MI, dehydration, steroids, and new diagnoses.

95
Q

What do HHS & HONK stand for?

A

Hyperosmolar Hyperglycemic State; Hyperglycemic Osmolar Non Ketotic

96
Q

What is the overall mortality of hyperglycaemic complications?

A

1% - 2%

97
Q

What A(1c) is required for a patient to get an insulin pump in Alberta?

A

<9.0%

Endocrine (6 decks)

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