12. Managing diabetic patients and their complications Flashcards

1
Q

What is impaired fasting glucose?

A

Impaired fasting glucose is a condition where blood glucose levels are higher than normal but not high enough to be diagnosed as diabetes.

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2
Q

What is impaired glucose tolerance?

A

Impaired glucose tolerance is a condition where blood glucose levels are higher than normal but not high enough to be diagnosed as diabetes.

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3
Q

What is type 1 diabetes?

A

Type 1 diabetes is a form of diabetes caused by autoimmune destruction of beta cells in the pancreas, leading to absolute insulin deficiency.

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4
Q

What is type 2 diabetes?

A

Type 2 diabetes is a form of diabetes caused by a progressive loss of beta cell insulin secretion, often in the context of insulin resistance.

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5
Q

What is gestational diabetes mellitus?

A

Gestational diabetes mellitus is a form of diabetes that is diagnosed during the second or third trimester of pregnancy and was not present before pregnancy.

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6
Q

What are the different general categories of diabetes according to the WHO-2006 classification?

A

The different general categories of diabetes according to the WHO-2006 classification are type 1 diabetes, type 2 diabetes, gestational diabetes mellitus, and specific types of diabetes due to other causes.

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7
Q

What are the possible causes of drug-induced diabetes?

A

Glucocorticoid use, treatment of HIV/AIDS, and organ transplantation can cause drug-induced diabetes.

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8
Q

What are the possible causes of exocrine pancreas-related diabetes?

A

Cystic fibrosis and pancreatitis can cause exocrine pancreas-related diabetes.

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9
Q

What is precision diabetology?

A

Precision diabetology is a novel approach to diabetes treatment that involves identifying subgroups of patients with similar characteristics and tailoring treatment to their specific needs.

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10
Q

What are the different types of acute complications of diabetes?

A

The different types of acute complications of diabetes are hypoglycemia, hyperglycemic ketoacidosis (DKA), and hyperglycemic hyperosmolar nonketotic coma (HHNK) or nonketotic hyperosmolar syndrome (NKHS).

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11
Q

What is hypoglycemia?

A

Hypoglycemia is a condition where blood glucose falls below 3 mmol/L, which is the blood glucose achieved during prolonged starvation in a healthy individual.

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12
Q

What is the new type of hypoglycemia?

A

The new type of hypoglycemia is called “pressuring or biomechanical” hypoglycemia, which can be detected using continuous glucose monitoring (CGM) even when there are no symptoms.

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13
Q

What is the definition of biochemical hypoglycemia?

A

Blood glucose below 3 mmol/L without symptoms.

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14
Q

What is the definition of pressuring or biomechanical hypoglycemia?

A

A new type of hypoglycemia characterized by altered mental and/or physical status requiring assistance, detected by CGM.

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15
Q

What are the three levels of hypoglycemia severity?

A

Level 1: 3.0-3.9 mM/L, Level 2: <3.0 mM/L, Level 3: severe event-characterized altered mental and/or physical status requiring assistance.

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16
Q

What is the mechanism of insulin overdose as a risk factor for hypoglycemia?

A

Insulin overdose can lead to hypoglycemia, depending on the time and type of insulin used.

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17
Q

How does decreased endogenous glucose production contribute to hypoglycemia?

A

Decreased endogenous glucose production, caused by alcohol abuse or certain medications, can lead to hypoglycemia.

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18
Q

What is the effect of intensive insulin therapy on insulin sensitivity?

A

Intensive insulin therapy can increase insulin sensitivity, which can lead to hypoglycemia.

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19
Q

What is the effect of renal failure on insulin secretion?

A

Renal failure can decrease insulin secretion, which can lead to hypoglycemia.

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20
Q

What is the “15/15” rule for treating hypoglycemia?

A

15g CHO, 15 min BG-check, if needed repeat 15 g CHO, 15 min BG-Check.

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21
Q

What is the recommended treatment for severe hypoglycemia?

A

Glucagon i.m. (Glucagon Hypokit) or nasal (Baqsimi) or IV glucose.

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22
Q

What is the recommended treatment for hypoglycemia in T2DM caused by insulin administration?

A

Hypoglycemic antidiabetic (SU, glinide): eating, drinking.

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23
Q

What is the recommended treatment for hypoglycemia in T2DM caused by acarbose treatment?

A

Acarbose treatment alone with glucose.

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24
Q

What is the recommended treatment for hypoglycemia in T2DM if there is a loss of consciousness?

A

Drink 10-40 ml of 40% glucose (slowly), then 5% glucose infusion permanently, accompanied by a meal.

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25
Q

Why should glucagon not be used to treat recurrent hypoglycemia?

A

It may induce repeated hypoglycemia.

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26
Q

What are the recommended treatments for other recurrent hypoglycemia?

A

Diazoxide, steroid.

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27
Q

What is the mechanism of action of glucagon?

A

It increases blood glucose levels by stimulating glycogenolysis and gluconeogenesis.

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28
Q

What is the recommended treatment for hyperglycemia in diabetic ketoacidosis?

A

Insulin therapy and fluid replacement.

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29
Q

What is the prognosis for diabetic ketoacidosis?

A

Hospital deaths from diabetic ketoacidosis are rare with proper treatment.

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30
Q

What is the most common cause of death in children and adolescents with T1DM?

A

Diabetic ketoacidosis (DKA).

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31
Q

What are the most important prognostic factors for DKA?

A

Older age, severe underlying disease/triggering disease, severe hypothermia.

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32
Q

What are the biochemical causes of ketosis?

A

Glucose deficiency (starvation ketosis), absolute or relative insulin deficiency, increase in counterregulatory hormones/insulin (stress ketosis-alcoholic ketoacidosis).

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33
Q

What are the causes of DKA?

A

Insulin deficiency (non-administration, manifestation of newly onset diabetes, insulin pump treatment), stressful situation (AMI, stroke, infection, premenstrual, acute pancreatitis), drug (cocaine, “disco-drugs”: ecstasy), lack of compliance.

34
Q

What are the diagnostic criteria for DKA?

A

High blood sugar, usually >13.9 mmol/L, arterial blood pH 5 mmol/L.

35
Q

What are the diagnostic criteria for DKA?

A

High blood sugar, usually >13.9 mmol/L; Arterial blood pH 5 mmol/L; Hyperamylasemia; False positive serum creatinine increase (ketone bodies); Nonspecific leukocytosis (10,000-15,000/?L).

36
Q

What are the clinical appearances of DKA?

A

Dry, warm skin with reduced turgor; Polyuria, polydipsia, weight loss; Abdominal pain and tenderness (differential diagnosis of acute abdomen!); Kussmaul-breathing-acetone breath (fruit scent); Dehydration symptoms (tachycardia, hypotension, minute volume reduced); Normal or low body temperature.

37
Q

What are the symptoms of DKA?

A

Acute dilated gastritis, erosive gastritis; Hematemesis, coffee-sleeper-like vomiting; Brain edema; Stupor, somnolence, coma with or without neurological symptoms; Hyperkalemic cardiac arrest; Hypokalemia arrhythmia; Fever.

38
Q

What is the differential diagnosis of DKA?

A

Kitabchi AE et al Diabetes Care 24:131-153, 2001.

39
Q

What is the treatment scheme of DKA?

A
  1. 1st hour: 1000 ml physiological NaCl infusion; 2. 2nd hour: 1000 ml physiological NaCl + 2 gr KCl; 8E Human regular insulin (HRI) IV bolus + 8E Human.
40
Q

What is the treatment scheme for DKA in the first hour?

A

1000 ml physiological NaCl infusion, 2nd hour: 1000 ml physiological NaCl + 2 gr KCl, 8E Human regular insulin (HRI) IV bolus + 8E Human regular insulin infusion v. bolus, pH correction (below 7.0) - 400 ml of 4.2% NaHCO3 in 3-4 hours (in parallel with NaCl).

41
Q

What is the treatment scheme for DKA from the 3rd hour until blood sugar reaches 13 mmol/L?

A

Every hour (until blood sugar reaches 13 mmol/L) 500 ml physiological NaCl + 1 gr KCL + 8 E HRI infusion v iv bolus.

42
Q

What should be done if the baseline blood glucose value is ~50 mmol/L 25 mmol/L?

A

The NaCl infusion should be “enriched” with 20 ml of 40% dextrose solution.

43
Q

What is the transition treatment for insulin when 13 mmol/L is reached in DKA?

A

If the nearest obligate insulin delivery time is within 3 hours: 8-12 E HRI sc. If it’s over 3 hours: 12-16 E HRI sc.

44
Q

What is the mortality rate of HHNK?

A

15-20%.

45
Q

What are the most important prognostic factors for HHNK?

A

Older age, severe underlying disease/triggering disease, severe hypothermia.

46
Q

What are the basic factors of the pathophysiology of HHNK?

A

Extracellular hyperglycemia.

47
Q

What are the basic factors of HHNK pathophysiology?

A

Extracellular hyperglycemia, increased hepatic glucose outflow, reduced peripheral sugar expenditure.

48
Q

What is the major cause of HHNK?

A

Acute disease/illness, large-scale consumption of sugary drinks, certain medicines.

49
Q

What are the clinical appearances of HHNK?

A

Symptoms develop slowly, extreme hyperglycemia is also possible, polyuria, polydipsia, progressive disturbance of consciousness, worsening symptoms of exsiccation, consequential prerenal azotaemia, many times central nervous system seizures.

50
Q

What are the principles of therapy for HHNK?

A

The principles of treatment are still unclear today. Insulin treatment: according to the same principles as in diabetic ketoacidosis. Slow, gradual reduction of blood sugar (4-5 mmol/l per hour). Do not reduce blood sugar below 14 m.

51
Q

What is the recommended rate of gradual reduction of blood sugar during insulin treatment?

A

4-5 mmol/l per hour.

52
Q

What is the maximum blood sugar level that should not be exceeded during the first day of insulin treatment?

A

14 mmol/l.

53
Q

What is the leading cause of end-stage renal insufficiency in diabetes?

A

Microvascular complications.

54
Q

What is the leading cause of CVD mortality in diabetes?

A

Microvascular complications.

55
Q

What is the leading cause of blindness among the working-age population in diabetes?

A

Microvascular complications.

56
Q

What is the leading cause of non-traumatic lower limb amputations in diabetes?

A

Microvascular complications.

57
Q

What are some patients able to do after the metabolic is settled during insulin treatment?

A

Some patients can be kept in balance without insulin.

58
Q

What are some risk factors for ulcers or amputations?

A

Poor glycemic control, peripheral neuropathy with LOPS, cigarette smoking, foot deformities, pre-ulcerative callus or corn, PAD, history of foot ulcer, amputation, visual impairment, CKD (especially patients on dialysis)

59
Q

What is the recommended frequency for a comprehensive foot evaluation to identify risk factors for ulcers and amputations?

A

At least annually

60
Q

When should patients with evidence of sensory loss or prior ulceration or amputation have their feet inspected?

A

At every visit

61
Q

What should be obtained prior to assessing current symptoms of neuropathy and vascular disease?

A

A prior history of ulceration, amputation, Charcot foot, angioplasty or vascular surgery, cigarette smoking, retinopathy, and renal disease

62
Q

What are some symptoms of neuropathy that should be assessed in diabetic patients?

A

Pain, burning, numbness.

63
Q

What type of patients should be referred to foot care specialists for ongoing preventive care and lifelong surveillance?

A

Patients who smoke or who have histories of prior lower extremity complications, loss of protective sensation, structural abnormalities, or peripheral arterial disease.

64
Q

What is the recommended preventive foot self-care education for all patients with diabetes?

A

General preventive foot self-care education.

65
Q

When is the use of specialized therapeutic footwear recommended for diabetic patients?

A

It is recommended for high-risk patients with diabetes including those with severe neuropathy, foot deformities, ulcers, callous formation, poor peripheral circulation, or history of amputation.

66
Q

What are some symptoms of diabetic autonomic neuropathy that should be looked for in all diabetics?

A

Acute heart failure/pulmonary edema, collapse, vomiting, ketoacidosis of unknown origin/unexplained hyperglycemia.

67
Q

What is the abbreviation for Type 2 diabetes mellitus?

A

T2DM.

68
Q

What does CVD stand for?

A

Cardiovascular diseases.

69
Q

What does HF stand for?

A

Heart failure.

70
Q

What does CKD stand for?

A

Chronic kidney disease.

71
Q

What percentage of patients with T2DM who are not yet cardiorenally affected during their lifetime develop some cardiorenal comorbidity?

A

80%.

72
Q

What is the recommended therapy for patients with known ASCVD to reduce the risk of cardiovascular events?

A

ACE inhibitor or angiotensin receptor blocker therapy.

73
Q

How long should b-blockers be continued in patients with prior myocardial infarction?

A

At least 2 years after the event.

74
Q

Can metformin be continued for glucose lowering in patients with type 2 diabetes with stable heart failure?

A

Yes, if eGFR remains >30 mL/min.

75
Q

Should metformin be avoided in unstable or hospitalized patients with heart failure?

A

Yes.

76
Q

What is the recommended treatment for patients with type 2 diabetes and established ASCVD, multiple ASCVD risk factors, or diabetic kidney disease?

A

A sodium-glucose cotransporter 2 inhibitor with demonstrated cardiovascular benefit is recommended to reduce the risk of major adverse cardiovascular events and heart failure hospitalization.

77
Q

What is the recommended treatment for patients with type 2 diabetes and established ASCVD or multiple risk factors for ASCVD?

A

A glucagon-like peptide 1 receptor agonist with demonstrated cardiovascular benefit is recommended to reduce the risk of major adverse cardiovascular events.

78
Q

What is the recommended treatment for patients with type 2 diabetes and established heart failure?

A

A sodium-glucose cotransporter 2 inhibitor may be considered to reduce the risk of heart failure hospitalization.

79
Q

What is the recommended glucose-lowering regimen for patients with type 2 diabetes who have established ASCVD or established kidney disease?

A

A SGLT2 inhibitor or GLP-1 receptor agonist with demonstrated cardiovascular disease benefit is recommended as part of the glucose-lowering regimen.

80
Q

What is the recommended use of loop diuretics in patients with heart failure?

A

Loop diuretics can be used to treat fluid overload in patients with heart failure, but should be avoided in unstable or hospitalized patients with heart failure.

81
Q

What is a sodium-glucose cotransporter 2 inhibitor?

A

It is a medication that can be considered to reduce the risk of heart failure hospitalization.

82
Q

How can a sodium-glucose cotransporter 2 inhibitor reduce the risk of heart failure hospitalization?

A

By inhibiting the reabsorption of glucose and sodium in the kidneys, leading to increased urinary excretion of both and a reduction in blood volume.