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Clin Med II > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What disease is the leading cause of ESRD?

A

DM

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2
Q

What two types of DM have the potential to be reversed?

A

T2DM and GDM

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3
Q

Obstructive sleep apnea, age-specific hip fx, cognitive impairments/dementia, hep C, and DM distress are what?

A

Potential subsequent comorbidities

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4
Q

Pt w/ impaired fasting glucose (IFG) of 100-125 is concerning for what?

A

Prediabetes

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5
Q

Pt w/ impaired glucose tolerance (IGT) of 140-199 is concerning for what?

A

Prediabetes

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6
Q

A pt w/ HbA1c of 5.7-6.4% is concerning for what?

A

Prediabetes

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7
Q

The continuum of risk for DM is curvilinear. What does this mean?

A

As glucose measurements/ A1c rises, DM risk rises disproportionately

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8
Q

Prediabetes places you are increased for what two diseases?

A

DM and CV disease

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9
Q

When is metformin considered for a prediabetic pt? (3)

A

If BMI ≥ 35 age < 60 women w/ prior GDM

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10
Q

What is the first line tx for prediabetic pt?

A

Life style modification (education, preventions, behavior lifestyle intervention, weight loss)

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11
Q

What form of diabetes is due to an absolute insulin deficiency?

A

Type 1 DM

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12
Q

What form of DM is due to an autoimmune destruction of B-cell, resulting in presence of islet cell and/or GAD-65 Ab?

A

Type 1 DM

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13
Q

If pt is prediabetic, how often do you need to test for development of T2DM?

A

Annually

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14
Q

In a prediabetic pt, what disease must you also screen for and tx?

A

ASCVD (screen annually, used 10 yr risk calculator)

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15
Q

Is the rate of B-cell destruction in T1DM pt the same for each pt?

A

No, it is variable

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16
Q

T1DM is most common in what ages?

A

Children and young adults

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17
Q

Is a pt with T1DM at risk for other autoimmune disorders?

A

Yes (thyroid disease, celiac disease, pernicious anemia)

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18
Q

What is the classic triad of T1DM?

A

Polyuria, polydipsia, polyphagia

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19
Q

DKA is more common in T1 or T2DM?

A

T1

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20
Q

Weight loss, nocturia and blurry vision are sx associated with T1 or T2DM?

A

T1

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21
Q

Is T1 or T2DM most common?

A

T2 (90-95%) T1 (5-10%)

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22
Q

Does T2DM develop quickly or gradually?

A

Gradually

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23
Q

Obesity, specifically in what area of the body, is associated with an increased risk of DM?

A

Visceral/abdominal obesity

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24
Q

Hyperglycemia, insulin resistance and relative insulin deficiency are characteristics of what form of DM?

A

T2DM

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25
Q

Insulin resistance impair glucose utilization by insulin sensitive tissues. What does this result in?

A

Results in increase insulin production

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26
Q

What happens to the B-cell mass over time in pts w/ T2DM?

A

B-cell failure (burnout)

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27
Q

Polyuria, polydipsia, nocturia, and blurry vision are sx of what form of DM?

A

T2DM

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28
Q

Chronic skin infections/poor wound healing, genital yeast infections, and acanthosis nigricans are sx of what form of DM?

A

T2DM

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29
Q

Who do you screen for for T2DM? (2)

A
  1. All adults @ 45 y/o 2. BMI ≥ 25 & 1 RF
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30
Q

What are the four risk factors for T2DM?

A
  1. Positive family history 2. HTN (≥140/90 or on meds) 3. dislipidemia (HDL < 35 or TG > 250) 4. severe obesity
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31
Q

If diabetes screen is normal. At what yearly minimum should you retest the pt?

A

3 year intervals (consider more frequent testing if increased risk factors/initial test results)

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32
Q

All DM pts should receive what during their during the annual exam?

A

Comprehensive foot exam

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33
Q

What vitamin level should oyu check in pts w/ DM?

A

Vit. B 12

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34
Q

Results of what test might be skewed by anemia/ hemoglobinopathies (high RBC turnover), race, or pregnancy?

A

HbA1c

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35
Q

Fasting plasma glucose <100 is normal, prediabetic or DM?

A

normal

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36
Q

Fasting plasma glucose 100-125 is normal, prediabetic or DM?

A

Pre-DM

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37
Q

Fasting plasma glucose ≥126 is normal, prediabetic or DM?

A

DM

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38
Q

Oral glucose tolerance <140 is normal, prediabetic or DM?

A

normal

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39
Q

Oral glucose tolerance 140-199 is normal, prediabetic or DM?

A

pre-DM

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40
Q

Oral glucose tolerance ≥200 is normal, prediabetic or DM?

A

DM

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41
Q

HbA1c < 5.7% is is normal, prediabetic or DM?

A

normal

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42
Q

HbA1c 5.7-6.4% is is normal, prediabetic or DM?

A

pre-DM

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43
Q

HbA1c ≥6.5 % is is normal, prediabetic or DM?

A

DM

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44
Q

DX of DM requires what?

A

Requires two abnormal testsfrom the same sample or two separate test samples

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45
Q

If asx pt is tested for DM and OGTT is 180, but HbA1c is 6.5% can you dx pt w/ DM?

A

No. Need to recheck the lower lab value. *DX Requires two abnormal test from the same sample or two separate test samples

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46
Q

If pt resents with classic DX sx and random plasma glucose 200 can you dx pt w/ DM?

A

Yes

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47
Q

What is the leading cause of morbidity and mortality in DM pts?

A

ASCVD/Macrovascular complications (CHD, cerebrovascular disease, PAD, HF) (DM pts are 2x more likely to die of stroke of MI vs those w/o DM)

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48
Q

DM is an independent RF for what disease?

A

ASCVD (= leading cause of morbidity and mortality in

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49
Q

What is the tx to prevent macrovascular complications in DM pts? (4)

A

Lifestyle mod, BP control, lipid management, antiplatelets (aspirin, clopidogrel)

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50
Q

Diabetic kidney disease is aka what?

A

Nephropathy

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51
Q

T or F: DM is the leading cause of renal failure in the US?

A

TRUE

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52
Q

A clinical Dx of DM nephropathy is supported by what findings? (2)

A

Albuminuria and/ or reduced GFR (in the absence of signs/ sxs of other primary causes of kidney damage)

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53
Q

DM pts should be screened annually for nephropathy. What two things do you need to measure?

A
  1. urinary albumin-to-creatinine ratio (UACR) - 2-3 specimens of UACR collected within 3-6 month period should be abnormal before considered albuminuria 2. eGFR
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54
Q

When do you start screening for T1DM for nephropathy?

A

start @ ≥ 5 years from diagnosis

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55
Q

When do you start screening for T2DM for nephropathy?

A

start @ time of dx

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56
Q

What medication can you use along side intensive glycemic and BP control in the treatment of DM nephropathy?

A

ACE-I or ARBs

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57
Q

Will every pt w/ DM get retinopathy?

A

No. Prevalence strongly related to duration of DM and level of glycemic control

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58
Q

What is avascular complication of T1 and T2DM?

A

Retinopathy

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59
Q

Is retinopathy an erly or late disease stage disease finding?

A

Late. - Gradual onset, no sx until very late stage of disease

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60
Q

Retinal hemorrhages, yellow lipid exudates, and cotton wool spots are concerning for proliferative or nonproliferative retinopathy?

A

Nonproliferative

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61
Q

Neovascularization at the disc is concerning for proliferative or nonproliferative retinopathy?

A

Proliferative

62
Q

When do you perform an initial dilated & comprehensive eye exam in a T1DM pt?

A

w/in 5 yrs of DM dx

63
Q

When do you perform an initial dilated & comprehensive eye exam in a T2DM pt?

A

At time of DX

64
Q

When can you considered performing a detailed eye on a DM pt every 1-2 years? (2)

A

If no evidence of retinopathy for 1+ annual eye exam & glycemia is well controlled

65
Q

If any level of DM retinopathy is present, how often must a dilated retinal exam must performed?

A

At least annually

66
Q

What is the tx plan for DM retinopathy?

A

Refer to ophthalmologist to prevent vision loss

67
Q

Pt presents with distal symmetic polyneuropathy in a “stocking glove” patten, what should you be concerned about?

A

DM Neuropathy

68
Q

Pain, dysesthesias (burning and tingling), numbness, and loss of protective sensation (LOPS) are concerning for what disease?

A

Neuropathy

69
Q

LOPs are a RF for diabetic foot ulcers. What is the most useful dx test?

A

Monofilament test. Failure to detect cutaneous pressure at any site = high risk for future ulceration Later stage signs/ sxs: loss of vibratory sensation/ altered proprioception, decreased/ abs

70
Q

What is the leading cause of nontraumatic LE amputations?

71
Q

How often should a comprehensive foot eval be performed for T1DM pts?

A

Start @ 5yrs post dx

72
Q

How often should a comprehensive foot eval be performed for T2DM pts?

A

At time of dx

73
Q

If concern for vascular disease due to presence of claudication and decreased peal pulses what test should you perform?

74
Q

The follow are RF for what is not properly cared for? Superficial diabetic foot ulcer, charcot arthropathy (rocker bottom foot).

A

Full thickness diabetic foot ulcer, +/- amputaion

75
Q

A monofilament test + any 1 of the following: pinprick, temp, vibration sensation, ankle reflexes will test for what?

A

Neuro - protective sensation

76
Q

T or F: DM autonomic neuropathy can lead to sx of hypoglycemia unawareness, gastroparesis, and sexual dysfunction?

A

TRUE Autonomic dysfunction = wide spectrum of sx across several system.

77
Q

If pt has absolute insulin deficiency, what would you expect their C peptide level to be?

78
Q

What are possible presenting comorbidities in a DM pt? (6)

A

: ASCVD, hypothyroidism, CKD, hyperlipidemia, HTN, liver function testing (fatty liver or NASH)

79
Q

The “ominous octet” all lead to what? Islet beta cell → impaired insulin secretion Islet alpha cell → increased glucagon secretion Increased hepatic glucose production Neurotransmitter dysfunction Decreased glucose uptake Increased glucose reabsorption Increased lipolysis and reduced glucose uptake Decreased incretin effect

A

Hyperglycemia

80
Q

What are the approved meds for DM + MACE (major adverse CV events)?

A

SGLT-2 inhibitors and GLP-1 agonist

81
Q

What lab values should be managed in a DM pt? (5)

A

HbA1C, urine microalbumin, BP, lipids, anti-platelet therapy

82
Q

When is insulin used?

A

Severe hyperglycemia (A1C ≥ 10% and glucose level ≥ 300 mg/dL)

83
Q

When metformin monotherapy or multiple drug regiments is inadequate in treatment, what is the next treatment step?

84
Q

What are the SEs of insulin? (4)

A

Hypoglycemia, weight gain, hunger, nausea

85
Q

There is a particularly high risk of hypoglycemia with what insulin preparation?

86
Q

When is premixed insulin used?

A

Pts who are stable on insulin and diet is relatively the same or w/ poor adherence to basal-bolus regimen

87
Q

What are the 2 guidelines used to start insulin treatment?

A

Fix fasting glucose first and begin with Basal insulin (titrate up)

88
Q

If fasting glucose is normal but A1C is elevated, what should you consider?

A

Overbasalization, consider adding meal-time/ bolus insulin (do not continue to increase basal dosing, only half of TDD should be basal)

89
Q

If fasting glucose is normal but A1C is elevated due to overbasalization, there is risk for what?

A

Hypoglycemia (esp nocturnal)

90
Q

If you want tighter control of glucose levels at meal times or if meal times vary throughout day, what should you consider?

A

Refer to endo, consider calculations

91
Q

What type of device can be used with or without pump and measures patterns of glucose levels?

A

Continuous glucose monitors

92
Q

An insulin pump allows for continuous infusion of what?

A

Rapid acting insulin

93
Q

When should you consider using an insulin pump?

A

If testing/ injecting multiple times/ day and cannot achieve normal HbA1C or have frequent hypoglycemia

94
Q

What type of insulin is aka “mealtime” or “correction” insulin and what are the different types?

A

Rapid acting Humalog, NovoLog, Apidra

95
Q

What are the different types of short acting insulin and how is it used?

A

Regular insulin (Novolin R, Humulin R) Bolus but not commonly used

96
Q

What are the different types of intermediate acting insulin and how is it used?

A

NPH insulin (Humulin N, Novolin N) Basal but not commonly used

97
Q

What is the use for long acting (basal) insulin and what are the different types?

A

Reaches bloodstream several hrs after injection, lower glucose levels fairly evenly over 24 hr period, “background” insulin Lantus, Levemir, Tresiba

98
Q

What is 1st line treatment for T2DM and when do you begin this tx?

A

Metformin, start @ diagnosis

99
Q

What are the benefits of Metformin? (2)

A

↓ risk of CV death, beneficial effect on LDL

100
Q

What are the SEs of Metformin? (2)

A

GI (better w/ ER), vit B12 depletion (neuropathic sx)

101
Q

If a pt is on Metformin, what must be done prior to surgery or contrast dye injection?

A

Hold med until renal fxn has normalized

102
Q

Metformin is contraindicated for CKD with a GFR of what?

A

GFR < 30 (should be avoided if GFR 30-45)

103
Q

What is the black box warning for Metformin?

A

lactic acidosis

(can also cause metabolic acidosis)

104
Q

Aside from CKD and lactic acidosis/ metabolic acidosis, what are other contraindications of Metformin? (3)

A

DKA, hepatic disease, acute/unstable HF

105
Q

What must be monitored for a pt on Metformin? (3)

A

GFR, liver enzymes, B12

106
Q

What is important due to the fact that GLP-1 agonists are injectable meds?

A

Pt adherence

107
Q

What drug class treats T2DM as well as slows gastric emptying → weight loss (titrate dosing), and has the potential to ↑ beta cell # and function?

A

GLP-1 agonists (-tides)

108
Q

What drugs are used for T2DM and MACE? (3)

A

Liraglutide, semaglutide, dulaglutide

109
Q

What T2DM drug is given weekly (depots under skin) and should be avoided with GFR < 30?

110
Q

What are the SEs of GLP-1 agonists? (3)

A

N/V/decreased appetite, acute pancreatitis, thyroid c-cell tumor risk (Black Box)

111
Q

What are the contraindications for the GLP-1 agonists? (2)

A

Hx pancreatitis, Hx gastroparesis

112
Q

What T2DM drugs act to slow breakdown of GLP-1, restore insulin/ glucagon to physiologic levels, and result in a modest decrease in HbA1C?

A

DPP-4 inhibitors (-gliptins)

113
Q

How are the DPP-4 inhibitors eliminated?

A

Renal elimination, EXCEPT linagliptin = liver/ GI elimination

114
Q

What are the SEs of the DPP-4 inhibitors? (2)

A

Peripheral edema, acute pancreatitis

115
Q

What are the precautions with the DPP-4 inhibitors? (3)

A

Renal impairment, risk of pancreatitis, HF

116
Q

The SGLT-2 inhibitors (-gliflozin) are used to treat T2DM and also cause what?

A

Weight loss

117
Q

Which SGLT-2 inhibitors have been shown to ↓ CV events?

A

Canaglifozin and Empagliflozin

118
Q

What are the SEs of the SGLT-2 inhibitors? (3)

A

DKA (reduced availability of carbs and reduced insulin), diuresis (caution w/ eldery & hypotensive pts), lower limb amputation risk (Canagliflozin- black box)

119
Q

What is the contraindication to treatment with a SGLT-2 inhibitor?

120
Q

What is the precaution to treatment with an SGLT-2 inhibitor?

A

Genitourinary/ mycotic infections

121
Q

What should be monitored for a pt on an SGLT-2 inhibitor? (3)

A

GFR, hydration, hyperkalemia

122
Q

What are the TZDs? (2)

A

Pioglitazone, Rosiglitazone

123
Q

What are the uses of the TZDs?

A

T2DM (early tx), high insulin resistance

124
Q

What are the SEs for TZDs? (4)

A

Weight gain, edema/fluid retention, reduces bone density/↑ bone fx risk, CHF (black box)

125
Q

What are the contraindications to treatment with TZDs? (2)

A

CHF, active bladder CA

126
Q

What should be monitored for a pt on TZDs?

127
Q

The sulfonylureas are used in the early treatment of T2DM. What drugs are included in this class? (3)

A

Glyburide, Glipizide, Glimepride

128
Q

What are the SEs for the Sulfonylureas? (3)

A

Hypoglycemia (highest risk), weight gain, progressive disease process of DM

129
Q

What are the contraindications to treatment with sulfonylureas? (2)

A

Sulfa allergy, elderly

130
Q

What is the Somogyi Effect and what is it common with?

A

Morning hyperglycemia in response to undetected nocturnal hypoglycemia

Common w/ excessive exogenous insulin

131
Q

What is the Dawn Phenomenon?

A

Morning hyperglycemia due to elevated a.m. hormone levels (HGH, cortisol, epi)

132
Q

What is the treatment for hypoglycemia?

A

Oral glucose (tabs, juices, etc.), IV glucose, glucagon

133
Q

When is glucagon used in the treatment of hypoglycemia?

A

If pt unwilling to consume orally (train caregivers)

134
Q

If oral glucose is used to treat hypoglycemia, what guidelines should be followed? (3)

A

Avoid fats, recheck BG after 15 min, f/u w/ snack

135
Q

What is the triad associated with DKA?

A

Hyperglycemia, ketonemia, acidemia

136
Q

What hyperglycemic emergency presents with hyperglycemia, ketonemia, acidemia (rapid onset), is potentially fatal, and is more common in T1DM?

137
Q

What are the 2 most common etiologies of DKA?

A

Absence of insulin (T1), elevation of counter-regulatory hormones

138
Q

What abnormalities are caused by DKA? (general)

A

Extreme metabolic derangements

139
Q

What are the precipitating events of DKA?

A

4 s’s → sepsis (infection), skipping insulin doses, sickness, stress (surgery)

140
Q

The following sxs are associated with what?

Dehydration, polydipsia/polyphagia, N/V, abd pain, weight loss, shock (severe cases)

A

DKA (hyperglycemic emergency)

141
Q

On PE you note Kussmaul respirations, fruity breath, tachycardia/tachypnea, AMS, decreased skin turgor, orthostatic hypotension. What should you be concerned for?

142
Q

The following labs might be ordered upon suspicion of what hyperglycemic emergency?

Glucose, UA, serum ketones, BMP, CBC, ABG

143
Q

What is an arterial pH and venous pH used for respectively for DKA?

A

Arterial pH needed to diagnosis DKA, venous pH needed to monitor treatment

144
Q

What is the treatment for DKA? (5)

A

Hospitalize, IV insulin, restore volume deficits, correct electrolyte abn, tx underlying cause

145
Q

Non-ketotic Hyperglycemic Hyperosmolar Syndrome (NKHS or HSS) is defined as what?

A

Profound hyperglycemia (>600)

(more common in T2DM)

146
Q

What is the etiology for NKHS/ HSS?

A

Insulin deficiency + increased counter regulatory hormones

147
Q

What are the precipitating events for NKHS or HSS? (2)

A

I’s → illness or infection (PNA or UTI)

148
Q

The following are sxs for what condition?

Osmotic diuresis, NOT acidotic, absent/ minimal ketones in urine or blood (b/c body still has functioning insulin)

149
Q

On PE you note AMS, polyuria, polydipsia, weakness, tachycardia, hypotension, dehydration, shock. What should you be concerned for?

150
Q

What is the treatment for NKHS/ HSS? (5)

A

Hospitalize, IV insulin, restore volume deficits, correct electrolyte abn, tx underlying cause

Clin Med II (12 decks)

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