Diabetes Lecture Flashcards

1
Q

A syndrome with disordered metabolism and inappropriate hyperglycemia due to either a deficiency of insulin secretion or a combination of insulin resistance and inadequate insulin secretion to compensate

A

Diabetes Mellitus

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2
Q

Normally, what is the rate of insulin production

A

1 unit/hour

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3
Q

25 million diabetics in US

>90% are type ___

A

2

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4
Q

2x more common:
African Americans
Hispanics
Native Americans

*genetic predisposition complex but applicable to Type 1 and type 2

A

Diabetes

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5
Q

Polygenetic

at least 30 types of genes associated

A

Type 2 diabetes

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6
Q

Is significant morbidity and mortality associated with both types of diabetes?

A

YES

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7
Q

Primarily auto-immune mediated with presence of islet cell antibodies

*destruction of beta cells in pancreas**

A

Type 1

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8
Q

Catabolic disorder: absence of insulin in response to glucose leads to :

*hyper glycemia

*fat and protein breakdown

A

Type 1

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9
Q

Increase in blood sugar

Glycosuria

Loss of glucose as energy source

…due to?

A

Hyperglycemia (bc of absence of insulin)

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10
Q

Infectious or toxic insult in genetically predisposed individuals;

autoimmune response against altered pancreatic beta cell antigens

A

Type 1 diabetes

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11
Q

What is common in an untreated state of type 1 diabetes?

A

Ketosis

(raised levels of ketone bodies)

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12
Q

Inappropriate fat and protein breakdown (due to absence of insulin in response to glucose) can cause..

A

Ketoacidosis

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13
Q

Mumps

Coxsackie

B-4

Rubella

..these viruses can cause?

A

Type 1 Diabetes (thru damage of pancreas)

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14
Q

Tx of type 1 diabetes

A

Exogenous insulin

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15
Q

Generally in adults, but increasing rates in kids

circulating insulin prevents ketosis, not hyperglycemia

***TISSUE INSENSITIVTY TO CIRCULATING INSULIN… insulin resistance!

A

Type 2 diabetes

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16
Q

Centrally located/ abdominal fat

Omental fat

Fat in liver

increases risk of…

A

Type 2 diabetes

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17
Q

Combination of insulin resistance and defect of beta cells to secrete adequate insulin in response to glucose

*aggrevated by hyperglycemia

A

Type 2 diabetes

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18
Q

Decreased insulin production (destruction of beta cells) occurs over time!

A

Type 2

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19
Q

Strong genetic predisposition!

sedentary lifestyle

A

Type 2

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20
Q

Which percentage of type 2 diabetics are obese?

A

70%

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21
Q

Central/visceral obesity..MAJOR FACTOR IN INSULIN RESISTANCE

A

Type 2

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22
Q

early on…increased insulin production compensates and blood sugar is controlled

(compensation= beta cell hyperplasia)

A

Pre diabetic state

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23
Q

In early type 2…glucose levels will rise despite increased levels of…

A

insulin

(insulin resistance develops)

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24
Q

What happens to insulin levels as the disease progresses?

A

Decrease/declie

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25
Q

Obsesity

Central fat distribution

Storage of fat in muscles

Inactivity

..all contribute to?

A

Insensitivity to insulin

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26
Q

Hepatic insensitivity results in increased gluconeogenesis in spite of presence of….

A

Insulin

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27
Q

Aggressive control of hyperglycemia is essential to preserve..

A

Remaining Beta cell function

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28
Q

What do beta cells produce?

A

Insulin

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29
Q

What do alpha cells produce?

A

Glucagon

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30
Q

What makes up the Islets of Langerhans?

A

Alpha and Beta cells

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31
Q

Major stimulus of ______ secretion is glucose absorbed from food

A

Insulin

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32
Q

Leads to rapid uptake, storage and use of glucose by all tissues (esp liver, muscle, fat)

A

Insulin

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33
Q

Following a high carb meal, _______ is stored in the liver

A

Glycogen

liver stored = ~100 grams of glycogen

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34
Q

Insulin levels drop

glycogen broken down (glycogenolysis)

glucose released into blood

…when does this happen?

A

In between meals/ during fasting

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35
Q

What happens when glycogen stores in the liver are full?

A

Insulin converts exces glucose to fatty acids –> triglycerides –> adipose tissue for storage

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36
Q

Insulin inhibits _________ in liver

A

Gluconeogenesis

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37
Q

_____ “spares” fat. inhibits glucose breakdown

A

Insulin

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38
Q

small amounts of insulin are needed for normal metabolism of…

A

free fatty acids (fat as energy source), when glycogen stores are depleted

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39
Q

In a resting state, muscle energy is supplied by….

A

Fatty acids

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40
Q

Glucose taken up by muscle
*requires little if any insulin, cells are directly permeable to glucose

A

During moderate to heavy exercise

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41
Q

Insulin secretion is HIGH as glucose levels rise

*glucose transported into muscle for storage as glycogen that can later be used for energy during exercise

A

After meals!

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42
Q

Following a meal, insulin promotes _________ synthesis and storage!

A

PROTEIN

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43
Q

Insulin promotes protein synthesis by stimulating transport of _______ into cells

A

Amino Acids

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44
Q

Insulin does what to the break down (catabolism) of protein?

A

Decreases!

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45
Q

Insulin does what to gluconeogenesis in liver?

A

Decreases!

(suppression of gluconeogenesis conserves proteins!)

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46
Q

Insulins suppression of gluconeogenesis conserves…

A

Proteins!

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47
Q

If no insulin, what happens to protein storage?

A

Protein storage stops

muscle broken down! (catabolism)

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48
Q

Which cells in the body are permeable to glucose without insulin

*bc dependent on glucose for energy!

A

Brain cells

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49
Q

Brain cells are easily injured with hypoglycemia

S/S of this….

A

Hypoglycemic shock
fainting, seizures, coma, death

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50
Q

When carbs are present and glucose levels are high

..what is used for energy? does this require insulin?

A

Carbs used for energy

requires insulin!

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51
Q

When glucose and insulin levels are low

..what is used for energy?

A

Fat (lipids) broken down for energy bc no insulin required

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52
Q

Absence of insulin (DM type 1) leads to excessive fat breakdown and abnormal….

A

free fatty acid metabolism

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53
Q

Secreted by alpha cells

increase glucose levels when needed
breaks down glycogen
increases gluconeogenesis

**works rapidly (minutes!) to increase glucose levels

A

Glucagon

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54
Q

Glucagon required ______ stores for major efect

A

Glycogen

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55
Q

What does chronic hyperglycemia do to peripheral insulin resistance?

A

chronic hyperglycemia worsens peripheral insulin resistance

..and eventually destroys beta cells permanently

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56
Q

Exercise increases blood flow to muscles:
**increases muscle mass
**decreases muscle fat storage

result in a diabetic= ?

A

Improved glucose utilization and decreases insulin resistance!

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57
Q

Diet/weight loss results in decreased storage fat deposits

…what is the result in a diabetic?

A

decreased insulin resistance

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58
Q

These lifestyle changes result in:

Decreased hyperinsulinism
Decreased hyperglycemia
potential reversal of impaired glucose tolerance if initiated early

A

Exercise, diet, weight loss

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59
Q

AKA insulin resistance syndrome

increase pts risk of atherosclerosis (3x) when present

*present in about 20% of adults
*often associated with Type 2 DM

A

Metabolic Syndrome

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60
Q

Metabolic syndrome increases a pt’s risk of developing what?

A

3x more likely to develop atherosclerosis

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61
Q
  • *1. Central obesity**
    women: waist circumference > 88 cm
    men: waist circumference >102 cm

2. Hyperglycemia Fasting BS > 110 mg/dL

3. HTN BP > 135/85

4. Increased triglycerides >150 mg/dL

  • *5. Decreased HDL**
    women: <50 mg/dL
    men: <40 d/L
A

3 out of 5 of these = METABOLIC SYNDROME

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62
Q

Polyuria, thirst
Wt loss, weakness
Dehydration
Polyphagia
Ketoacidosis
Hyperosmolality
Complications

Type 1 or Type 2?

A

Type 1

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63
Q

Often asymptomatic early
Polyuria, thirst
Skin infections
Vulvovaginitis
Abn fat distribution
Hyperglycemia
Complications

Type 1 or Type 2?

A

Type 2

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64
Q

Reflects long term control of DM

glucose + Hb

A

Glycated Hb (HbA1C)

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65
Q

A1C reflects state of glycemia over prior…..

A

8-12 weeks

66
Q

Normal A1C range

A

4-6%

67
Q

Dx of diabetes if A1C is over…

A

6.5%

68
Q

An A1C of 5.7-6.4%

A

Prediabetes

69
Q

Goal A1C if diabetic

A

Under 7%

70
Q

Must measure A1C in diabetics every…

A

3-4 months

71
Q

Impaired glucose tolerance, AKA

A

Prediabetes

72
Q

Fasting blood sugar > 126 mg/dL
2 hr GTT BS > 200 mg/dL
Random BS > 200 mg/dL
HbA1c > 6.5%

A

Labs in diabetics

73
Q

FBS: 100-125 mg/dL
2 hr GTT BS: 140-199 mg/dL
HbA1c: 5.7-6.4%

A

labs in prediabetes (impaired glucose tolerance)

74
Q

What will triglycerides and HDL levels look like in obese type 2 diabetics?

A

High triglycerides
Low HDL

75
Q

Low HDL levels in type 2 diabetics correlates with…

A

Macrovascular disease

76
Q

Diabetics age 40-75 with LDL 70-189 without ASCVD

A

Use statins

77
Q

Diabetics with a 10 year ASCVD risk > 7.5%

..what strength of statin therapy?

A

High intensity statin

78
Q

Diabetics with a 10 year ASCVD risk < 7.5%

what intensity statin therapy?

A

Moderate intensity statin therapy

79
Q

Total calories: 25-35 KCAL (less if obese)
Total cholesterol: <300
Protein: 10-35% of calories
Fat: 25-35% of calories
Sat fat: <7% total calories
Carbs: 45-65% total calories
(if type 2, decreased carb calories and replace with monosaturated fats/oils)
Fiber: 20-35 grams

A

Diabetic diet

80
Q

How many alcoholic drinks should a diabetic limit self to?

A

less than 2 a day

81
Q

Retinopathy
Nephropathy
Neuropathy

A

Microvascular diabetic complications

82
Q

CHD
CVD
Stroke
PAD

A

Macrovascular diabetic complications

83
Q

Type 1 diabetics who keep A1C below 7%
decrease microvascular complications by….

A

50-70%

84
Q

Type 2 diabetics who keep A1C below 7%
decrease microvascular complications by…

A

25%

85
Q

Intensive BP control (under 150/80) further decreases…

A

BOTH microvascular and macrovascular complications

86
Q
  • *Pre prandial:** 90-130
  • *Bedtime:** 100-140
  • *Peak post prandial (1 hr)**: <180
  • *2 hr post prandial**: <150
A

Blood glucose goals

87
Q

Adult diabetics with >10% risk for a cardiac event over 10 years

A

put on ASPIRIN

88
Q

Diabetic men over 50, women over 60
with 1 or more major risk factor for CHD

A

Put on ASPIRIN!

89
Q

All adult diabetics with macrovascular (CHD, PVD, CVD) disease

A

Put on ASPIRIN

90
Q

Dose: 75-162 mg/daily

Risks: PUD, gastritis, bleeding

A

Aspirin use in diabetics

91
Q

Decreases hepatic glucose production

*decreases gluconeogenesis
*decreases fasting and post prandial blood sugar

A

Metformin

92
Q

Increases glucose uptake by skeletal muscle

Slows GI absorption of glucose

benefit= does not cause hypoglycemia or weight gain!

A

Metformin

93
Q

Activates AMPK activity, which decreases hepatic gluconeogenesis

A

Metformin

94
Q

Metformin decreases A1c by…

A

1-2%

95
Q

Used in adjunct with diet control of hyperglycemia in Type 2

first line drug therapy for DM Type 2, especially if obese

A

Metformin

96
Q

Does metformin improve hypertriglyceridemia?

A

YES

97
Q

Creatinine >1.5 (males) or 1.4 (females)
GFR under 30
Hepatic insufficiency
Alcoholism

A

Contraindications of metformin

98
Q

How do you start a person on Metformin?

A

Must titrate slowly!

(up to max dose of 2000-2500)

99
Q

SE=

Anorexia, N/V/D
Lactic acidosis

A

Metformin

100
Q

MUST HOLD METFORMIN ON DAY OF TEST AND FOR 48 HOURS IF GETTING CONTRAST

..to avoid?

A

Lactic acidosis

101
Q

Bind to beta cell receptor…increase insulin release!

caution= cause hypoglycemia

used in conjunction with Metformin

A

Sulfonylureas

102
Q

Contraindications: severe renal or hepatic impairment

Adverse effects: hypoglycemia!, weight gain, skin and GI issues

A

Sulfonylureas

103
Q

Glipizide
Glyburide
Glimeperide

..what class of drugs?

A

Sulfonylureas

104
Q

Sensitize peripheral tissues to insulin

(decrease peripheral insulin resistance)

A

TZD drugs

105
Q

Pioglitizone
Roziglitazone

..what class of drugs?

A

TZD drugs

106
Q

Weight gain is common

NO HYPOGLYCEMIA

beneficial effect on lipids

decreases A1c by 1-2%

A

TZD drugs

107
Q

What must you check before starting a patient on a TZD?

A

LFTs!!

108
Q

Can you use TZD drugs in patients with existing HF or LV dysfunction?

A

NO..bc TZD drugs cause fluid retention and edema

109
Q

Competitively inhibit alpha-glucosidase enzymes in the intestines, which digest starch and sucrose

decrease carb absorption in gut
lowers post prandial glucose by 30-50%

lowers A1c by 0.5-1.0%

A

Alpha glucosidase inhibitors

Acarbose

(used for mild DM or adjunct therapy)

110
Q

Why do 60% of patients stop taking alpha glucosidase inhibitors (ie Acarbose)?

A

SE of flatulence and diarrhea (GI issues)

111
Q

Oral Rx for Type 2 DM

inhibits DPP-4, the enzyme that inactivates/degrades incretin hormones

**result in insulin synthesis and release

decreases A1c by 0.5-0.8%
often used in combo wth other drugs, ie Metformin

A

Sitagliptin (Januva)

112
Q

Inhibits SGLT2, a protein in proximal renal tubule that reabsorbs glucose in kidneys

increases glucose excretion!

decreases A1c by ~1%
decreases weight by 5-10 lbs

A

Canaglifoxin (Invokana)

113
Q

Often used along with insulin
Stabilizes insulin dose and helps offset weight gain

A

Canaglifloxin (Invokana)

114
Q

What happens if you combine Canaglifloxin (Invokana) with a sulfonylurea?

A

HYPOGLYCEMIA

115
Q

Adverse effects:

Male/female genital yeast infections
Volume depletion, hypotension
Impaired renal fxn (cant use with GFR under 30)
Can cause hypoglycemia if used with sulfonylurea

A

Canaglifloxin (Invokana)

116
Q

Type 1: mainstay of therapy

Type 2: can be used in adjunct with oral agents or tx for later stages when there is beta cell failure

A

Insulin

117
Q

Human insulin (Humulin) via recombinant DNA and synthetics decreases the amount of…

A

insulin allergies and antibodies

118
Q

Lispro insulin (Humalog)

rapid, short, intermediate or long acting?

A

Rapid!

119
Q

Regular (Humulin-R)

rapid, short, intermediate or long acting?

A

Short

120
Q

Neutral Protamine (Humulin-N)

Rapid, short, intermediate, or long acting?

A

Intermediate

121
Q

Insulin Glargine

Rapid, short, intermediate, or long acting?

A

Long acting

122
Q

Which insulin provides 24 hr coverage with steady state insulin levels

bedtime dosing! once a day

A

Insulin Glargine

123
Q

Onset: 5-15 mins
Peak= 1-1.5 hrs
Duration= 3-5 hours

A

Rapid acting!

Lispro (Humalog)

124
Q
Onset= 30 mins to an hour
Peak= 2-4 hours
Duration= 5-8 hours
A

Short acting

Regular (Humulin-R)

125
Q
Onset= 2-4 hours
Peak= 4-10 hours
Duration= 10-24 hours
A

Intermediate acting

Neutral Protamine (Humulin-N)

126
Q
Onset= 2-4 hours
Peak= none
Duration= 20-24 hours
A

Long acting

Insulin Glargine
(comes in 100u or 300u)

127
Q

Lispro/Asparte is very rapid acting! and is ideal for…

A

pre meal!

128
Q

once a day dosing for basal requirements
CANNOT MIX WITH OTHER INSULINS

A

Insulin Glargine (long acting)

129
Q

Insulin: Lispro or regular

Benefit: tight glycemic control

Drawbacks: costly, skin infections, DKA

A

Insulin pump

130
Q

Incretin mimetics: potentiate insulin secretion

*promotes insulin release
*suppress post prandial glucagon
*delay gastric emptying, promotes satiety
*decreases fasting and post meal glucose

DOES NOT PROMOTE WEIGHT GAIN.
alternative to insulin if pt is obsese and you dont want them to gain more wt

A

GLP-1 receptor agonist

(these are expensive!)

SE= nausea, hypogycemia

131
Q

Exenatide (Byetta)

Liraglutide (Victoza)

What drug class? Which is more potent?

A

GLP-1 receptor agonists

Liraglutide (Victoza) is more potent than Exenatide (Byetta)

132
Q

Pancreas transplant... done in conjunction with renal transplant
85% chance of graft survivial

Islet cell transplant… short term benefits for up to 2 years

A

Other ways to manage DM

133
Q

Weight, BP, postural
A1c
Foot exam..with microfilament
Home monitoring
Psychosocial fxn
Intercurrent illness

..needs to be done how often?

A

3-6 months

134
Q

Lipids
UA
Creatinine
Microalbinuria
Complete PE
Opthalmologist
Dental exam

..should be done how often?

A

Yearly

135
Q

Wt reduction
Diet and exercise
Behavior modification
Decrease adipose stores and regain insulin sensitivity

A

Cornerstone tx for DM type 2

(first line Rx= Metformin)

136
Q

Recent evidence shows best control of A1c under 7% for DM Type 2 occurs once what is added?

A

Insulin

137
Q

Type 1 diabetics should self monitor BS how many times daily?

A

4-6 times

138
Q

MC complication seen with insulin and sulfonylurea

A

Hypoglycemia

139
Q

Sweating
Tachycardia
Hunger
Tremulousness
Nausea

A

Sxs of hypoglycemia

(note: these are masked by beta blockers, esp non selective beta blockers)

140
Q

Hypoglycemic syptoms correlate to blood sugars below…

A

50 mg/dL

141
Q

If a hypoglycemic pt is unconscious or unable to eat, what can you give them?

A

1 mg IM injection of Glucagon

142
Q

15 grams of glucose will increase blood sugar by….

A

25-50 mg/dL

143
Q

Microaneurysms
Hemorrhages
Exudates
Retinal edema

..which type of diabetic retinopathy?

A

Non proliferative

144
Q

Formation of new blood vessels..blindness!
Seen in both Type 1 and Type 2

Type 1: cumulative over years
Type 2: may be developing at time of presentation

..which type of diabetic retinopathy?

A

Proliferative

145
Q

Severity of diabetic retinopathy correlates with…

A

Duration of DM

Glycemic control

146
Q

Tight glycemic control (with an A1c under ___%) is essential to prevent retinopathy

A

7%

147
Q

Retinopathy with smoking and HTN

A

MUCH worse!

148
Q

Common microvascular complication
30-40% of Type 1 will develop over 20 years
15-20% of Type 2

develops as a result of chronic hyperglycemia
and contributed to by uncontrolled HTN

A

Nephropathy

149
Q

Leading cause of end stage renal failure in US

(accelerated in smokers)

A

Nephropathy

150
Q

Losing 30-300 mg albumin/day in urine

how do you detect this?

A

Microalbuminuria

(urine dipstick lacks sensitivity to detect…need radioimmunoassay)

151
Q

If a diabetic has microalbuminuria (even if BP is norm), WHAT MUST THEY BE ON

A

ACE inhibitor

152
Q

BP goal for diabetics

A

Under 140/90

153
Q

>70% of all deaths in diabetics is due to….

A

Atherosclerosis

154
Q

True or false…

DM is considered a coronary risk equivalent

A

TRUE

155
Q

Decreased circulation to skin
+
loss of pain sensation from neuropathy
+
local infection
=
?

A

Skin necrosis/diabetic ulcer

very difficult to tx!

156
Q

Gastroparesis
Diarrhea/constipation
Orthostatic hypotension
Impotence
Cystopathy (decreased bladder sensation)

A

Autonomic neuropathy in diabetics

157
Q

Seen in Type 1 diabetics

Trigger is usually infection, trauma, surgery, MI
(which increases insulin requirements)

S/S: polyuria, polydipsia, abdominal pain, N/V, weakness, fatigue
decreased mentation, stupor and coma can occur

A

Diabetic ketoacidosis (DKA)

158
Q

Increased pulse
Decreased BP
Hypovolemic/dehydration
Rapid breathing
Fruity breath
Abdominal tenderness

A

Diabetic ketoacidosis (DKA)

159
Q

Inadequate insulin resulting in increased blood sugar and increased fat/protein breakdown

result= metabolic acidosis with anion gap

A

Diabetic ketoacidosis (DKA)

160
Q

Glycosuria and osmotic diuresis lead to volume depletion and electrolyte loss/imbalance

Labs:
Blood sugar over 300+
pH less than 7.3
initial serum K often high, but total body K is low

Tx: insulin! replace fluid and K loss

A

Diabetic ketoacidosis (DKA)

161
Q

Repaglinide (Prandin) can be used in a diabetic with what type of allergy

A

Sulfa