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Thera VI > 03 Thera VI Management of DM Complications Mak > Flashcards

03 Thera VI Management of DM Complications Mak Flashcards

1
Q

Which patients have a higher risk of getting hypoglycemia?

A

Patients on medications that promote insulin release (Insulins, Sulfonylureas, Meglitinides)

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2
Q

When is hypoglycemia a concern?

A

In patients using fast acting and long-duration agents. Elderly with dementia. Long standing DM with defective counter-regulation (no glucagon release when glucose levels are low)

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3
Q

What is the primary complication of DM that leads to hospitalization?

A

Hypoglycemia

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4
Q

What is the 15-15-15 rule for hypoglycemia?

A

Give 15g of carbohydrates, wait 15 minutes, check glucose levels. If still low you can repeat

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5
Q

What are good quick carbohydrates to help with hypoglycemia?

A

Avoid high fat content (slows sugar absorption). Choose simple sugar (fruit juices, hard candies, glucose tablets). Glucose Gel (best choice)

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6
Q

What are the doses for glucagon injections (SQ, IM, IV)?

A

Adult: 1mg. Pediatric: 0.5mg (if over 20kg use adult dose)

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7
Q

What is done in the ER for hypoglycemia?

A

50ml D50W

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8
Q

What are the three main symptoms of Diabetic Ketoacidosis?

A

Kussmahl Breating (d/t acidosis, deep breaths). Glucose level >300s, usually >500s. Fruity breath/UA + Ketones

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9
Q

What type of DM is Ketoacidosis primarily found?

A

T1DM

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10
Q

What is the main contributor to the formation of Ketoacidosis?

A

Absolute Insulin Deficiency

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11
Q

What are the primary complications of HHS?

A

An increase in: Glucagon, Catecholamines, Cortisol, and Growth hormone. THese all lead to Hyperglycemia, which ultimately leads to Hyperosmolarity due to dehydration

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12
Q

What are the primary complications of DKA (Diabetic Ketoacidosis)?

A

Same as HHS (Hyperglycemia and Hyperosmolarity) as well as Ketoacidosis due to an absolute insulin deficiency

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13
Q

What type of DM patient is DKA primarily found in?

A

T1DM

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14
Q

What type of DM patient is HHS primarily found in?

A

More T2DM

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15
Q

What is the difference in symptom duration for DKA and HHS?

A

DKA: < 2 days. HHS: > 5 days

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16
Q

What is the difference in plasma glucose for DKA and HHS?

A

DKA: > 250. HHS: > 600

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17
Q

What is the difference in arterial pH for DKA and HHS?

A

DKA: more acidic

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18
Q

What are the difference in the U and S ketones for DKA and HHS?

A

Very high in DKA, low for HHS

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19
Q

What is the difference in the serum osmolality in DKA and HHS?

A

DKA: variable. HHS: > 320

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20
Q

What is the difference in the serum sodium in DKA and HHS?

A

DKA: 100-nl. HHS: nl-high

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21
Q

What is the difference in the CNS status of DKA and HHS?

A

DKA: alert to stupor. HHS: stupor/comatose

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22
Q

What is the difference in mortality for DKA and HHS?

A

DKA: 3-10%. HHS: 10-20%

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23
Q

What are the signature presentations of Diabetic Ketoacidosis (DKA)?

A

Moderate hyperglycemia (exacerbated 3Ps). Moderate dehydration (sunken eyes, tachycardia). Decreased Na, HCO3, pH, increased BUN/Scr. Large serum or urinary ketones

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24
Q

What are the precipitating factors of DKA?

A

Infection. Inadequate insulin dosing. Severe physical or emotional stress

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25
Q

What is the treatment of DKA and HHS?

A

Fluid replacement (need to alter therapy to avoid cerebral edema). Insulin infusion (decrease PG by 50-70 in 1st hour). Potassium replenishment. Bicarbonate (?): consider only if pH < 7.0

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26
Q

What should the normal diet look like?

A

2000 kcal/day: 60% CHO, 20% Protein, 20% Fat

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27
Q

Why is Fiber good for DM patients?

A

T2DM patients can significantly lower glucose and insulin levels (by 10%) if they eat a high fiber diet. Higher fiber content diet reduced incidence of GDM. 25g/d for women, 38g/d for men

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28
Q

What is the relationship between smoking and DM?

A

Increases risk of morbidity and premature deaths (increases macro- and microvascular complications). Associated with development of type 2 DM

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29
Q

What needs to be considered for DM patients and immunization?

A

Influenza vaccine annually to all DM patients > 6 months of age. Pneumococcal polysaccharide vaccine to ALL diabetic patients > 2 years (one time revaccination for those >64 years previously immunized < 65 years if > 5 years ago

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30
Q

What are the biggest risk reductions with 1% decline in annual mean A1c?

A

Microvascular disease (37%). PVD (43%)

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31
Q

When do DM patients usually get Diabetic Retinopathy (DR)?

A

> 20 years DM history or onset before 30. Almost all have retinopathy. 1/2 have proliferative disease. More prevalent in T1DM

32
Q

What are the risk factors for Diabetic Retinopathy (DR)?

A

Age, genes, beyond puberty. HTN, dyslipidemia, smoking, pregnancy, nephropathy

33
Q

What is the result of accumulation of fluid within the retina?

A

Diabetic Macular Edema (DME). Typically cause moderate visual loss in T2DM

34
Q

What is the result of vascular wall distortions of the eye?

A

Nonproliferative Diabetic Retinopathy (NPDR)

35
Q

What is the result of Neovascularization of the eye?

A

Proliferative Diabetic Retinopathy (PDR). Typically causing visual loss in T1DM

36
Q

What is the screening for retinopathy like for T1DM?

A

Screen > 10 yo, dilated/comprehensive eye exam within 5 years after onset of disease

37
Q

What is the screening for retinopathy like for T2DM?

A

Screen at time of diagnosis. Repeat annually; q2-3 years acceptable if there has been 1 or more normal exam. Screen during first trimester in pre-existing diabetes and 1 year postpartum

38
Q

What is the current treatment for diabetic retinopathy?

A

No current treatment prevents or cures diabetic retinopathy

39
Q

What can improve and slow down diabetic retinopathy (not cure or prevent)?

A

Glycemia and dyslipidemia therapy

40
Q

What is Nephropathy like in DM patients?

A

ESRD more common in T1DM. Renal Insufficiency common in T2DM, elderly, HTN

41
Q

What does Microalbuminuria lead to?

A

Macroalbuminuria, which leads to Scr doubling. Scr doubling leads to ESRD (if no dialysis, 7 month survival). ESRD leads to CVD

42
Q

What happens when the kidneys function to remove water, urea, creatinine, metabolic wastes, preserve acid-base and electrolyte balance fails?

A

N/V/A, metallic taste. Edema, electrolyte imbalance (high K). Pruritus. Fatigue, cramps, change in mental status

43
Q

What happens when the kidneys function to regulate blood pressure fails?

A

HTN, CHF, Atherosclerosis

44
Q

What happens when the kidneys function to Synthesize erythropoietin fails?

A

Anemia, bleeding risk, also neutropenia

45
Q

What happens when the kidneys function to form 1,25 dehydroxy-vitamin D fails?

A

Skeletal fractures, osteomalacia, altered calcium and phosphate metabolism

46
Q

When should screening for nephropathy for T1DM be done?

A

Urine analysis at puberty, or 5 years after diagnosis. If positive do quantitative analysis

47
Q

When should screening for nephropathy for T2DM be done?

A

Urine analysis at diagnosis. If positive, do quantitative analysis

48
Q

When should urine analysis for nephropathy not be done?

A

During periods of urinary albumin excretion (UAE): UTI, hematuria, acute febrile illness, short-term hyperglycemia, vigorous exercise, uncontrolled HTN, HF

49
Q

What can having a high proteinuria do for T2DM?

A

Increases incidence of CHD and Stroke

50
Q

How is kidney function estimated?

A

Modified Diet in Renal Disease (MDRD). GFR = 186 x (Scr ^ -1.154) x (age ^ -0.203) x (0.742 if female) x (1.210 if AA)

51
Q

What are two Nephroprotective agents used?

A

ACE-I or ARBs

52
Q

What is the only FDA approved ACE-I for nephroprotection?

A

Captopril. Not used much due to BID dosing

53
Q

What other ACE-I are clinically used for nephroprotection?

A

Enalapril. Lisinopril. Benazepril. Ramipril

54
Q

Do ACE-I need renal adjustment?

A

Yes, all of them

55
Q

What are the only FDA approved ARBs for nephroprotection?

A

Losartan. Irbesartan

56
Q

What other ARBs are clnically used for nephroprotection?

A

Valsartan. Candesartan. Telmisartan

57
Q

Do ARBs need renal adjustment?

A

No, none of them do

58
Q

Whats the general information on Diabetic Neuropathy?

A

Affects 60-70% patients. Same frequency in T1DM and T2DM. Earliest detectable signs of long term complications. AA at higher risk than caucasians. Taller people at higher risk

59
Q

What is Sensory Motor (peripheral) or Distal Symmetric Polyneuropathy?

A

Pain, numbness, tingling, burning of extremities

60
Q

What is Autonomic Neuropathy?

A

Neurogenic bladder. Sexual dysfunction. Gastroparesis. Fecal incontinence. Decreased or absent response to light, decreasing pupil size

61
Q

What is the mechanism of nerve damage that leads to Neuropathy?

A

Sorbitol Aldose Reductase Pathway (Polyol Pathway): Increased AGEs lead to inflammatory process, decreased synthesis of NO lead to vasoconstriction and decrease circulation

62
Q

What are the FDA approved agents for Diabetic Peripheral Neuropathy?

A

Pregabalin. Duloxetine. Tapentadol ER. Often unresponsive to simple analgesics or even opiates

63
Q

What is Cardiac Autonomic Neuropathy (CAN)?

A

Damage of nerves supplying the heart

64
Q

What are the symptoms of CAN?

A

Resting tachycardia > 100bpm. Dizziness/vertigo. Exercise intolerance. Orthostatic hypotension (drop of 20 mmHg upon standing). Sudomotor dysfunction. Impaired neurovascular function. Brittle diabetes; hypoglycemic autonomic failure

65
Q

What is the treatment for CAN?

A

Rising slowly. Compression stocking. Fludrocortisone. Midodrine

66
Q

What is Gastroparesis?

A

Occurs in 20-60% of patients. Causes bloating, early satiety, reflux, vomiting, abdominal pain, loss of appetite, constipation. Suspect in patients with erratic glucose control

67
Q

What is the treatment for Gastroparesis?

A

Frequent and smaller meals with low fiber/fat. Metoclopramide

68
Q

What is the treatment for sexual dysfunction often seen in DM patients?

A

IP prostaglandins, papaverine, phentolamine, atropine. Vacuum pumps. Surgical implants. Sildenafil

69
Q

What is the symptomology of Peripheral Vascular Disease (PVD or PAD)?

A

Asymptomatic. Intermittent claudication to rest pain. Nonhealing wounds and gangrene, infections, nerve damage (foot ulcers/infections, dental caries/infections)

70
Q

When doing a foot exam, what should be you look for as a sign of risk for foot ulceration?

A

Venous filling time of > 20 seconds. Waxy skin, hair loss, distal digital cooling

71
Q

How do you perform the 10-g monofilament test on feet?

A

Place the device perpendicular to the skin, with pressure applied until the monofilament buckles. Hold in place for 1 second and then release

72
Q

What are some diabetes associated infections?

A

Fungal infections (Tinea pedis, Vaginitis). Bacterial Infections (UTIs, Cellulitis, Vaginitis, Foot ulcers). Dental infections (Gum disease, Dental caries/root canal)

73
Q

How should symptomatic Peripheral Arterial Disease (PAD) be treated in DM patients?

A

Exercise rehabilitation, compression stocking. Pentoxyfyline, cilostazol. Treatment of ischemic foot (debridment, footwear, dressings). Treatment of infection. Analgesics. Revascularization (bypass)

74
Q

What are nonmodifiable risk factors for cardiovascular complications (CAD, MI, PVD, CVA)?

A

Duration of DM, age, genetics, race, and gender

75
Q

What are modifiable risk factors for cardiovascular complications (CAD, MI, PVD, CVA)?

A

Hyperglycemia. HTN. Dyslipidemia. Smoking. Diet and lifestyle

76
Q

What is the ADA/AHA/ACC recommendations for use of ASA for primary prevention of CV events in patients with: 10 year risk of CVD events > 10%, most men > 50, women > 60 with smoking, HTN, dyslipidemia, premature CVD FHx, albuminuria?

A

Low does ASA use for prevention is REASONABLE for adults with diabetes and no previous history of vascular disease who are at increased CVD risk and who are not at increased risk for bleeding

77
Q

What are the ABCs for DM care?

A

A: A1c < 7%. B: Blood pressure < 130/80. C: Cholesterol LDL < 100

Thera VI (27 decks)

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