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CDE & BC-ADM Test Prep > Complications > Flashcards

Complications Flashcards

0
Q

Diabetic foot exam should include:

A

Inspection for injury, skin breakdown, etc.
Check foot pulses
LOPS

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1
Q

LOPS test

A

Loss of protective sensation

Test with 10 gram monofilament on foot for feeling

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2
Q

LOPS test options

A

Vibration
Pinprick
Ankle reflexes-vibration
Perception

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3
Q

Severe hypoglycemia is defined as:

A

Level at which patient requires assistance of another person to treat symptoms

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4
Q

Type of diabetes that is risk factor for severe hypoglycemia:

A

Type 1 Diabetes, because normal glucagon response to low blood sugar diminishes, resulting in increased risk for hypoglycemic unawareness.

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5
Q

Why do recurrent hypoglycemic events create extra risk for severe hypoglycemia?

A

Brain adapts to previous hypoglycemia by shifting the sympathetic nervous system response to lower plasma concentration.

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6
Q

In what situation would insulin excess occur in Type 2 using insulin?

A

If using insulin sensitizing med at wrong time or wrong dose.

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7
Q

Does alcohol lead to hypoglycemia?

A

Yes, because it inhibits gluconeogenesis, especially if the person is in starved state.

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8
Q

How is hypoglycemia treated?

A

Ingest 15-20 grams oral carbs, then repeated in 15-20 minutes if symptoms persist or blood glucose still below 70 mg/dl

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9
Q

How is glucagon administered?

A

SubQ or IM

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10
Q

What are the side effects of glucagon?

A

Nausea, vomiting, headache

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11
Q

How is hypoglycemia treated with IV?

A

10-25 grams of 50% dextrose over 1-3 minutes

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12
Q

True or false: alternate site should be used for detecting hypoglycemia?

A

False, only fingertip should be used.

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13
Q

Definition of hypoglycemia:

A

<70 mg/dl

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14
Q

Dosing of oral carbohydrate by glucose level:

A

51-70 mg/dl is 15-20 grams

1 hour away

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15
Q

Examples of 15 grams carbs

A

4 oz fruit juice
7-8 lifesavers
8 oz Fat-free milk
1 tbsp. sugar, jelly, or honey

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16
Q

How much does 10 grams of oral glucose raise plasma glucose levels?

A

40 mg/dl over 30 minutes

Note: 20 grams raise 60 mg/dl over 45 minutes

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17
Q

What are the affects of fat or protein on the oral glucose treatment for hypoglycemia?

A

Protein doesn’t affect it. Fat may slow and prolong the glycemic response.

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18
Q

What is the plasma glucose range for critically ill patients?

A

140-180 mg/dl, with insulin not started until 180 mg/dl

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19
Q

Blood glucose levels for non-critically ill patients in hospital are _____ or less premeal, and random of ______ or less.

A

140 mg/dl premeal, and less than 180 mg/dl random.

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20
Q

Diabetic Ketoacidosis is defined by the following lab values:

A

Plasma glucose >300 mg/dl
Arterial pH < 15 mEq/l
Positive ketones

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21
Q

Common cause of DKA:

A

Infection precipitates about 40% of DKA cases, with omission of insulin on sick days as another common cause. Other reasons include MI, trauma, stress, and surgery.

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22
Q

True or False: a diabetic on insulin therapy who is not eating due to illness should take insulin dose as normal.

A

TRUE

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23
Q

What meds can cause DKA?

A

corticosteroids

Thiazides

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24
Q

What is the definition of DKA?

A

Syndrome of hyperglycemia, ketosis, dehydration, and electrolyte imbalance caused by insulin deficiency.

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25
Q

DKA is most common with which type of diabetes?

A

Type 1

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26
Q

How does insulin deficiency result in DKA?

A

Decreased glucose uptake (Hyperglycemia)’
Excess protein degradation leading to increased hepatic glucose production
Increased action of counter-regulatory hormones, leading to production of free fatty acids that create ketones AND decreasing effectiveness of insuiln

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27
Q

What happens when counter regulatory hormones produce free fatty acids

A

The fatty acids change into ketones, which can result in acidosis when unbuffered.

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28
Q

How does hyperglycemia create electrolyte imbalance?

A

Osmotic diuresis, causing fluid loss and electrolyte depletion.
Excrete ketone bodies, leading to depletion of sodium, potassium, chloride, and fluid.

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29
Q

What are the 3 classic symptoms of DKA?

A

3 Polys:
polydipsia
polyuria
polyphagia

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30
Q

Symptoms of hyperglycemia include:

A

Blurred vision, weakness, lethargy, headache, malaise, and nausea

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31
Q

DKA clinical symptoms:

A 
Dehydration (orthostatic hypotension)
Abdominal symptoms (vomit/pain)
Hyperventilation
Acetone breath with fruity odor
Hypothermia (though may have fever if infection precipitated DKA)
Abdominal pain
Depressed mental status
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32
Q

What is the name for the deep rapid respirations that are result of hyperventilation?

A

Kussmaul

33
Q

What is the definition of orthostatic hypotension?

A

Drop in Systolic BP of 20 mmHg after 1 minute standing compared to baseline where patient is supine.

34
Q

Appropriate management of DKA in those able to ingest fluids:

A

Rehydration as outpatient if they can tolerate 3-5 oz of fluid per hour. Insulin should be supplemented as well

35
Q

Appropriate treatment of moderate to severe DKA:

A

Immediate IV fluid replacement and correction of electrolyte imbalance, along with insulin replacement with fast or short-acting insulin.

36
Q

What is the primary concern with DKA (assuming no cardiac arrest)?

A

Hypovolemia

37
Q

What does fluid replacement correct in DKA treatment?

A

Hypovolemia AND decreases hyperglycemia

38
Q

What must also be corrected with DKA?

A

Potassium

39
Q

Similarities with DKA and HHS?

A

Both are complications of hyperglycemia and have similar precipitating factors.

Both are insufficiency of insulin as well as increased counter-regulatory hormones.

40
Q

What is missing in HHS compared to DKA?

A

ketosis

41
Q

What is HHS?

A

Hyperosmolar Hyperglycemic State

42
Q

What patients are more likely to have HHS and how does it present?

A

Elderly with Type 2, with slower onset and longer duration of symptoms. Causes slow decline in mental status over days/weeks and has higher mortality rate.

43
Q

What patients have DKA?

A

Type 1, and it is usually faster onset compared to HHS.

44
Q

What is the level of hyperglycemia associated with HHS?

A

> 600 mg/dl

45
Q

Why are ketones absent in HHS?

A

Usually enough insulin present to prevent excess fat metabolism. This means less abdominal symptoms seen with DKA.

46
Q

Why does the neurological and cognitive signs (mental status declines and seizures) occur in HHS?

A

Hyperosmolar state from the hyperglycemia causes water to be pulled from body cells, including those in brain.

47
Q

Emergency treatment of HHS includes:

A

Fluid replacement is first, with 0.9% Normal Saline rapidly over the 1st hour and then less concentrated over next hours. Then 5% dextrose may be needed as blood glucose declines.

48
Q

Is insulin needed in HHS treatment?

A

Yes, though conservative as the fluid correction typically corrects the issue.

49
Q

What must be monitored when treating hyperglycemic emergency?

A

Potassium, because it can be profoundly depleted when treating hyperglycemic emergency.

50
Q

Diabetic retinopathy can often be detected with in _ years of diagnosis of Type 1 or 2.

A

5

51
Q

Risk factors for retinopathy:

A 
Hypertension
Pregnancy
Smoking 
Genetics
Hyperlipidemia
Puberty
Renal failure
52
Q

What is retinopathy?

A

Damage to microvasculature supplying the part of the eye responsible for focusing images and light.

54
Q

How does retinopathy result?

A

Hyperglycemic damage causes small hemorrhages and leadake. Neovascularization occurs to compensate for blood loss, but the new vessels are fragile and leak. This causes adhesions between the retina and vitreous. The retina may detach or have vitreous bleeding that causes blindness. Also, macular edema can result.

55
Q

Difference between nonproliferative and proliferative retinopathy

A

Nonproliferative: microaneuryms and vessel leakage on exams, but no vision changes.
Proliferative: neovascularization started and vision impaired (blurring to blind spots)

56
Q

What is the treatment used for proliferative retinopathy?

A

laser photocoagulation, or surgical vitrectomy if retina detached or laser doesn’t resolve.

57
Q

Examples of ocular complications with diabetes

A
  1. Blurred vision (hyperglycemia or when glucose fluctuates)
  2. Cataracts
  3. Open-angled doesn’t occur more common, but the risk is greater when blood glucose isn’t under control
  4. Ischemic optic neuropathy (damage to optic nerve that is irreversible)
58
Q

What percentages of men and women with diabetes have sexual dysfunction?

A

75% and 35%, respectively

59
Q

What is sensory neuropathy?

A

Causes sensory deficits in the distal portions of the lower extremities, or “stocking-glove” distribution

60
Q

How is sensory neuropathy diagnosed?

A

Monofilament
Vibration testing
Temperature sensation
Flex/extend toes and ask to describe

61
Q

What are the palliative treatments for neuropathic pain?

A

Tricyclic antidepressants, anticonvulsants, and capsaicin cream

62
Q

What are autonomic neuropathies?

A

Neurogenic bladder, sexual dysfunction, gastroparesis, intestinal impairment, orthostatic hypotension, cardiac denervation, hypoglycemic unawareness, impaired insulin counter-regulation (brittle Type 1), anhidrosis, slow dilation of pupils

63
Q

What is the most significant cause of morbidity and mortality with autonomic neuropathy?

A

Cardiovascular

56% mortality in 5-10 years of onset

64
Q

Symptoms of autonomic neuropathy on the GI tract

A
  1. Gastroparesis

2. Constipation

65
Q

What is the definition of microalbuminuria?

A

30-299 mg/24 hours

66
Q

What is microalbuminuria a marker for?

A

1st stage nephropathy in Type 1
Marker of nephropathy in Type 2
Increased CV risk

67
Q

What is the definition of macroalbuminuria?

A

> 300 mg/24 hours

This greatly increases the risk for progression to end stage renal disease

68
Q

What is arteriosclerosis?

A

Walls of arteries and veins become thicker and lose elasticity.

69
Q

What is atherosclerosis?

A

Plaque formation within blood vessel walls, especially the arteries.

70
Q

What are the 3 types of macrovascular disease in people with diabetes?

A

Coronary artery
Cerebral vascular
Peripheral vascular

71
Q

True or False: Women with diabetes lose their gender protection from atherosclerosis

A

True

72
Q

Diabetics with CAD are more likely to:

A
  1. Develops at earlier age and more aggressive

2. Have an adverse outcome

73
Q

Diabetics with Cerebral vascular disease are 3-5 times more likely to have what outcome compared to those without diabetes?

A

Death from stroke

74
Q

What accounts for approximately 50% of all lower limb amputations in the US?

A

Peripheral Neuropathy

75
Q

How to prevent macrovascular disease in diabetics?

A
  1. Control HTN (ACE inhibitor)
  2. Smoking cessation
  3. Manage dyslipidemia
  4. Aspirin therapy to help with hypercoagability associated with insulin resistance syndrome.
76
Q

Who should take aspirin?

A

Dose of 81 mg daily for those: Over 40, smoker, HTN, albuminuria, and dyslipidemia.

77
Q

What is most common symptom of PAD?

A

intermittent claudication (cramping in calves, thighs, and buttocks with activity)

78
Q

How is loss of vibratory sensation measured?

A

128-cycle tuning fork or biothesiometer at the big toe

79
Q

How is sensory neuropathy measured?

A

5.07 gram monofilament

80
Q

What is Charcot foot?

A

Complication of diabetes related to peripheral and autonomic neuropathy. Trauma to joints leads to destruction and deformities.

81
Q

What does acute Charcot foot look like?

A

Unilateral swollen, warm foot. Looks like an infection with no skin breakdown. May lose the arch of foot (rocker bottom sole shape).

CDE & BC-ADM Test Prep (13 decks)

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