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Assessment Exam 4 > DM > Flashcards

DM Flashcards

1
Q

What are some hyperglycemia-producing hormones?

A

Glucagon, epinephrine, growth hormone, cortisol

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2
Q

What is the role of glucagon in the glucose counterregulatory system?

A

Stimulating glycogenolysis & gluconeogenesis, inhibiting glycolysis

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3
Q

What is the most common endocrine disease? What is the prevalence of this disease in adults?

A

Diabetes mellitus. 1 in 10

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4
Q

What leads to microvascular and macrovascular complications in diabetes mellitus?

A

Increased circulating glucose levels

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5
Q

What causes Type 1a diabetes?

A

T-cell-mediated autoimmune destruction of β cells

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6
Q

What characterizes Type 1b diabetes?

A

Rare disease of absolute insulin deficiency

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7
Q

What causes Type 2 diabetes?

A

Defects in insulin receptors and post-receptor intracellular signaling pathways

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8
Q

What age is Type I diabetes usually diagnosed? What percentage of all DM cases does Type 1 Diabetes account for?

A

Before age 40. 5-10%

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9
Q

What is the autoimmune cause of Type 1a diabetes?

A

Exact cause unknown

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10
Q

How long is the pre-clinical period of B-cell antigen production before symptoms appear? How much B cell function is lost before hyperglycemia sets in?

A

9-13 yrs
80-90%

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11
Q

What symptoms are associated with hyperglycemia in Type 1 Diabetes?

A

Fatigue, weight loss, polyuria, polydipsia, blurry vision, hypovolemia, ketoacidosis

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12
Q

What percentage of diabetes mellitus cases does Type 2 Diabetes account for? How long may Type 2 Diabetes normally be present before diagnosis?

A

> 90%
4-7 years

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13
Q

What is a concerning trend regarding Type 2 Diabetes in recent years?

A

Increasingly seen in younger patients and children

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14
Q

What happens in the initial stages of Type 2 Diabetes? What occurs as Type 2 Diabetes progresses?

A

Insensitivity to insulin on peripheral tissues leads to increased pancreatic insulin secretion
Pancreatic function decreases and insulin levels become inadequate

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15
Q

What are the 3 main abnormalities seen in Type 2 Diabetes?

A

Increased hepatic glucose release, impaired insulin secretion, insufficient glucose uptake in peripheral tissues

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16
Q

What is type 2 diabetes characterized by?

A

Insulin resistance in skeletal muscle, adipose & liver

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17
Q

What are the causes of insulin resistance in type 2 diabetes?

A

Abnormal insulin molecules, Circulating insulin antagonists, Insulin receptor defects

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18
Q

What are acquired and contributing factors to type 2 diabetes?

A

Obesity and sedentary lifestyle

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19
Q

How can type 2 diabetes be diagnosed?

A

Fasting blood glucose, HbA1c

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20
Q

What is the preferred initial drug treatment for DM2?

A

Metformin

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21
Q

How does Metformin work in the body?

A

Enhances glucose transport

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22
Q

What are the potential side effects of Sulfonylureas?

A

Hypoglycemia, weight gain, cardiac effects

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23
Q

When is insulin necessary in diabetes mellitus cases?

A

All DM1 cases and 30% DM2 cases

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24
Q

What type of insulin provides glucose control at mealtimes?

A

Rapid acting (Lispro, Aspart)

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25
Q

Which type of insulin is considered basal/intermediate acting?

A

NPH, Lente

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26
Q

What leads to ‘hypoglycemia unawareness’?

A

Repetitive hypoglycemic episodes

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27
Q

What can neuroglycopenia result in?

A

Fatigue, confusion, h/a, seizures, coma

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28
Q

How should hypoglycemia be treated?

A

PO or IV glucose

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29
Q

What is Diabetic Ketoacidosis? What type of diabetes is it most commonly found in?

A

Complication of decompensated DM.
DM1

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30
Q

What is the mortality rate associated with Diabetic Ketoacidosis?

A

1-2%

31
Q

What can trigger DKA in DM1 patients?

A

Infection/illness

32
Q

How does high glucose levels contribute to DKA?

A

Exceeds renal reabsorption threshold

33
Q

What metabolic processes lead to liver overproduction of ketoacids in DKA?

A

Tight coupling of gluconeogenesis & ketogenesis

34
Q

What is the loading dose of insulin for DKA treatment? The low dose infusion rate of insulin for DKA treatment?

A

0.1u/kg Regular
Low Dose 0.1u/kg/hr

35
Q

What electrolytes should be supplemented in DKA treatment?

A

k+, phos, mag, sodium

36
Q

Why is it important to correct glucose and sodium levels simultaneously in DKA treatment?

A

Avoid cerebral edema

37
Q

What is Hyperglycemic Hyperosmolar Syndrome characterized by? What age group does Hyperglycemic Hyperosmolar Syndrome normally occur in?

A

Severe hyperglycemia, hyperosmolarity & dehydration

DM2 >60 y/o

38
Q

How does Hyperglycemic Hyperosmolar Syndrome evolve?

A

Over days to weeks with persistent glucosuric diuresis

39
Q

What occurs when the glucose load exceeds maximum renal glucose absorption?

A

Mass solute diuresis

40
Q

What are some symptoms of Hyperglycemic Hyperosmolar Syndrome?

A

Polyuria, polydipsia, hypovolemia, HoTN, tachycardia, organ hypoperfusion

41
Q

What can hyperosmolarity lead to in Hyperglycemic Hyperosmolar Syndrome?

A

Coma

42
Q

How does the acidosis in Hyperglycemic Hyperosmolar Syndrome compare to DKA?

A

Pts have some degree of acidosis, but not as severe as DKA

43
Q

What is the treatment for Hyperglycemic Hyperosmolar Syndrome?

A

Fluid resuscitation, insulin bolus + infusion, electrolytes

44
Q

What is the mortality rate of Hyperglycemic Hyperosmolar Syndrome?

A

10-20%

45
Q

What is peripheral neuropathy? Where are the initial symptoms of peripheral neuropathy seen?

A

Distal symmetric sensorimotor polyneuropathy

Starts in toes/feet

46
Q

How does peripheral neuropathy progress?

A

Progresses proximally

47
Q

What are the effects of losing large sensory and motor fibers in peripheral neuropathy?

A

Decreased light touch & proprioception

48
Q

How does the loss of small nerve fibers impact patients with peripheral neuropathy?

A

Neuropathic pain

49
Q

What can lead to the development of ulcers in peripheral neuropathy?

A

Unnoticed injuries

50
Q

How can peripheral neuropathy lead to significant morbidity?

A

Recurrent infections & amputation wounds

51
Q

What are some treatments for peripheral neuropathy?

A

Optimal glucose control, NSAIDs, antidepressants, anticonvulsants

52
Q

What is retinopathy characterized by?

A

Microvascular changes

53
Q

What visual impairments can result from retinopathy?

A

Color loss to blindness

54
Q

How can the progression of retinopathy be reduced?

A

Glycemic & BP control

55
Q

What is autonomic neuropathy and what parts of the body can it affect?

A

Caused by damaged vasoconstrictor fibers, impaired baroreceptors, ineffective cardiovascular activity

56
Q

What are some cardiovascular symptoms of autonomic neuropathy?

A

Resting tachycardia, loss of HR variability, progresses to ortho-HoTN & dysrhythmias

57
Q

What are some gastrointestinal symptoms of autonomic neuropathy?

A

N/V, early satiety, bloating, epigastric pain

58
Q

How can gastrointestinal symptoms of autonomic neuropathy be managed?

A

Glucose control, small meals, prokinetics

59
Q

What systems should be emphasized in the preoperative evaluation for diabetes mellitus?

A

Cardiovascular, renal, neurologic, musculoskeletal

60
Q

Why is silent ischemia possible in diabetic patients with autonomic neuropathy?

A

Autonomic neuropathy predisposes to ischemia

61
Q

When should a stress test be considered in diabetic patients?

A

Multiple cardiac risk factors, poor exercise tolerance

62
Q

How should hydration status be managed in diabetic patients preoperatively?

A

Meticulous attention, avoid nephrotoxins, preserve renal blood flow

63
Q

What is a potential concern related to autonomic neuropathy in the perioperative period?

A

Dysrhythmia, hypotension risk

64
Q

How can gastroparesis impact diabetic patients perioperatively?

A

Increased aspiration risk

65
Q

What should be done with oral hypoglycemic and noninsulin injectable drugs preoperatively?

A

Hold them

66
Q

What is an insulinoma?

A

Rare pancreatic tumor secreting insulin

67
Q

What demographic does insulinoma present more often in?

A

Twice as much in women, in 50s-60s

68
Q

What is the diagnostic criteria for insulinoma based on?

A

Whipple triad

69
Q

What are the components of the Whipple triad for diagnosing insulinoma?

A

Hypoglycemia with fasting, Glucose <50 with symptoms, Symptoms relief with glucose

70
Q

What is the preoperative treatment for insulinoma and its mechanism?

A

Diazoxide inhibits insulin release from B cells

71
Q

What other treatments can be considered for insulinoma?

A

Verapamil, phenytoin, propranolol, glucocorticoids, octreotide

72
Q

Is surgery curative for insulinoma?

A

Yes

73
Q

What may occur during intra-op for insulinoma surgery?

A

Hypoglycemia then hyperglycemia

74
Q

Why is tight glycemic control paramount in insulinoma management?

A

To manage postoperative glycemic fluctuations

Assessment Exam 4 (9 decks)

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