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Clinical Nutrition 3 > Diabetes Complications > Flashcards

Diabetes Complications Flashcards

1
Q

Examples of acute complications?

A
  • Hypoglycemia

- Hyperglycemic emergencies

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2
Q

Two kinds of hyperglycaemic emergencies?

A
  • DKA

- Hyperosmolar

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3
Q

Chronic complications?

A

-Microvascular and Macro-vascular complications

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4
Q

Microvascular complications?

A
  • Diabetic retinopathy
  • Diabetic nephropathy
  • Diabetic neuropathy
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5
Q

Macro-vascular complications?

A
  • Stroke

- CVD disease

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6
Q

What are the risks of macrovascular complications?

A
  • There is a 2-4 fold increase in CVD mortality and stroke

- 8/10 diabetic patients die from CV event

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7
Q

What is the definition of hypoglycemia/

A

1) Development of neurogenic or neuroglycopenic symptoms
2) Low blood glucose (<4 mmol/L if on Insulin or IS)
3) Response to CHO load

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8
Q

T/F someone without diabetes with a blood glucose <4 mmol/L is considered hypoglycemic

A

F

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9
Q

Examples of neurogenic (autonomic) symptoms?

A
  • Trembling
  • Palpitations
  • Sweating
  • Anxiety
  • Hunger
  • Nausea
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10
Q

Examples of neuroglycopenic symptoms?

A
  • Difficulties concentrating
  • Confusion
  • Weakness
  • Drowsiness
  • Vision changes
  • Difficulty speaking
  • Dizziness
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11
Q

Mild hypoglycaemia?

A
  • Autonomic symptoms present

- Individual is able to self-treat

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12
Q

Moderate hypoglycemia?

A
  • Autonomic and neuroglycopenic symptoms

- Individual is able to self-treat

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13
Q

Severe hypoglycemia?

A
  • Requires assistance of another person
  • Unconsciousness may occur
  • Plasma glucose is typically <2.88 mmol/L
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14
Q

What is the MAIN indication of severe hypoglycemia?

A

When assistance is required from another person

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15
Q

List 6 medical risk factors for severe hypoglycemia

A
  • Prior episode of severe hypoglycemia
  • Current low A1C (<6.0%)
  • Long duration of insulin therapy
  • Hypoglycemia unawareness
  • Autonomic neuropathy
  • CKD
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16
Q

What are social/demographic factors than can increase risk for severe hypoglycemia?

A
  • Low economic status, food insecurity
  • low health literacy
  • Pre-school age children, pregnancy, adolescence and elderly
  • Cognitive impairment
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17
Q

What are the 5 steps to address hypoglycemia?

A

1) Recognize autonomic or neuroglycopenic symptoms
2) Confirm BG <4.0 mmol/L
3) 15 g CHO and retest if BG is >4 mmol/L is 15 mins, retreat or needed
4) Eat usual snack or meal due at that time of day or snack w/ 15 g CHO plus protein

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18
Q

Is 15 g of CHO usually enough?

A

No, and average required is much higher

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19
Q

Example of 15 g simple CHO?

A
  • 15 g glucose tablets
  • 15 ml or 3 packets sugar dissolved in water
  • 150 ml of juice or regular soft drink
  • 6 Lifesavers
  • 15 ml honey
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20
Q

What is under-treating a hypo?

A

Not having enough CHOs

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21
Q

What is over-treating a hypo?

A

Having 100 g of glucose before bed to avoid hypo during the night (way too much)

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22
Q

How do we treat severe hypoglycemia in unconscious people with no IV access?

A

1) Treat with 1 mg of glucagon subcutaneously or intramuscularly
2) Call 911
3) Discuss with diabetes health-care team

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23
Q

What are two kinds of glucagon used to treat hypoG?

A
  • Injectable glucagon

- Nasal glucagon

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24
Q

Which glucagon injection treatment is similar to an epipen?

A

GlucaGen Hypokit

-Must reformulate prior to injection

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25
Q

When is 1/2 a dose used for glucagon injection? In GlucaGen?

A
  • 1/2 dose if <20 kg

- 1/2 dose if <25 kg or 6-8 years old

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26
Q

What are the two types of hyperglycaemic emergencies?

A
  • Diabetic ketoacidosis (DKA)

- Hyperosmolar Hyperglycaemic State (HHS)

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27
Q

HHS is seen most commonly in what kinds of diabetes?

A

Mainly seen in T2DM, where there is still some insulin being produced

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28
Q

What is the MAIN difference between DKA and HHS

A

In HHS, there is still some preliminary insulin produced

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29
Q

Describe the pathophysiology of HHS

A

There is a deficiency of insulin, which leads to hyperglycemia and consequently a loss of water and electrolytes.. Therefore, the volume depletion and corresponding electrolyte deficiency will lead to the hyperosmolarity (as blood glucose levels remain high)

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30
Q

Describe the pathophysiology of DKA

A

In absolute insulin deficiency, there will be (1) up-regulation of lipolysis, B-oxidation and formation of ketone bodies which will lead to the change in pH. (2) Flux of glucose from increased glucagon and lack of insulin

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31
Q

Provide 4 medical or tangible risks associated with developing DKA

A
  • Lower BMI
  • Preceding infection
  • Adolescent girls
  • Age
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32
Q

Which age group will have a 3x higher risk of developing DKA?

A

Age <2 years

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33
Q

Why are adolescent girls more prone to developing DKA?

A

Due to tendency to withold insulin to avoid weight-gain (type of ED)

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34
Q

What are 5 social and environmental risks associated with developing DKA?

A
  • Ethnic minorities
  • Lower socioeconomic status
  • Lack of private health insurance
  • Lower parental education
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35
Q

What are signs consistent with DKA?

A
  • ketoacidosis
  • ECFV contraction
  • Milder hyperosmolarity
  • Normal to high glucose
  • May have decreased LOC
  • Hypokalemia
  • MUST use insulim
  • Absolute insulin deficiency and increased glucago
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36
Q

What are signs consistent with HHS?

A
  • Minimal acid/base problems
  • ECFC contraction
  • Hyperosmolarity
  • Marked hyperglycemia
  • Marked decrease LOC
  • Hypokalemia
  • May need insulin
  • Relative insulin deficiency
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37
Q

(T/F) HHS required insulin to reverse

A

F

May require insulin

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38
Q

(T/F) DKA can be present with normal blood glucose levels

A

T

Check ketones to confirm

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39
Q

T/F) DKA has the greatest hyperosmolarity

A

F

Milder hyperosmolarity

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40
Q

(T/F) HHS has the most severe consequences in terms of LOC

A

T

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41
Q

(T/F) HHS primarily has a flux of FFA to the liver

A

F

Slight insulin can still inhibit lipolysis, therefore there is less FFA or B-oxidation, mostly gluconeogenesis from skeletal muscle) and glycogenolysis

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42
Q

What contributes to the dehydration in HHS?

A

The gluconeogenesis and glycogenolysis leads to hyperglycemia, which will cause chronic diuresis, and therefore dehydration

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43
Q

What are the two clinical presentation of DKA?

A
  • Hyperglycemia

- Acidosis

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44
Q

Signs and symptoms of hyperglycemia in DKA?

A
  • Polyuria, polydipsia, weakness

- ECFV contraction

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45
Q

Signs and symptoms of acidosis in DKA?

A

Hunger, nausea, vomiting, abdo pain

-Kussmaul respiration, acetone-odoured breath, altered sense

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46
Q

When is measuring urine ketones particularly important?

A
  • Type 1
  • GDM
  • Previous GDM patient s
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47
Q

What does elevated level of ketones indicate?

A

Impending or established ketoacidosis

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48
Q

When are the 5 instances which diabetics should test their ketones? (CAPSS)

A
  • Acute illness accompanied by elevated BG
  • Stress
  • Consistently elevated BG levels (>14 mmol/L)
  • Symptoms of ketoacidosis
  • Pregnancy
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49
Q

In the morning, would we expect our ketone test to be positive?

A

Yes if fasting

-Doesn’t indicate DKA,

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50
Q

(T/F) There is normally no ketones in the urine

A

F

Usually in the urine, however usually in amounts below the limit of detectability

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51
Q

In what populations are up to 30% of first morning urine specimens + for ketones?

A

In pregnant women

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52
Q

What may cause a false-positive ketone test?

A

-Sulfhydryl drugs (captopril)

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53
Q

What may cause false-negative ketone tests?(2)

A
  • Test strips expose to air for extended periods of time

- Highly acidic specimens (such as after large intakes of ascorbic acid)

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54
Q

(T/F) Urine ketone tests are reliable for diagnosing or monitoring the treatment of ketoacidosis

A

F

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55
Q

What is the preferable method to diagnose and monitor ketoacidosis? What does it quantify?

A
  • Blood ketones

- Will quantify b-OH butyrate acid

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56
Q

What is the MOST common cause of DKA?

A

Insulin omission

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57
Q

What are other causes of DKA?

A 
-New diagnosis
of diabetes
-Infection/sepsis
-MI
-Thyrotoxicosis
-Drugs
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58
Q

How can we treat DKA?

A

By treating the precipitating factor, and with insulin

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59
Q

What are the microvascular/specific complications of DM?

A
  • Retinopathy
  • Nephropathy
  • Diabetic neuropathy
  • Erectile dysfunction
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60
Q

Macrovascular/non-specific complications in DM?

A
  • Stroke (2-4 fold increase in CVD mortality and stroke)

- CVD (8/10 diabetic patients die from CV events)

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61
Q

What are other non-specific complications of DM?

A
  • Arthritis of lower limbs

- Infections

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62
Q

What are the acute complications of diabetes?

A

-Hypo and hyperglycemia

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63
Q

What are the chronic complications of diabetes?

A

-Specific and non-specific

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64
Q

What 3 complications of diabetes lead to amputations of limps?

A
  • Neuropathy
  • Infections
  • Peripheral artery disease
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65
Q

What si the best way to improve the complications of diabetes?

A

Though tight control of A1C

-Even a 1% decrease in A1C will reduce the risk of complications in T2DM

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66
Q

when there is a 1% reduction in A1C in T2DM patients, which complication is most significantly reduced?

A

43% reduction in lower limb amputation or secondary arterial disease deaths

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67
Q

Chronic complications in vision?

A
  • Retinopathy (most in type I)
  • Glaucoma
  • Cataracts
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68
Q

What is the most common cause of blindness in T1DM patients with diabetic retinopathy?

A

Proliferative retinopathy

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69
Q

What is neuropathy accelerated by?

A

-Smoking, lack of exercise, greater than 4 alcoholic drinks/day

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70
Q

What are two broad categories of neuropathy?

A

-Diffuse and Focal

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71
Q

What is diffuse neuropathy?

A
  • Peripheral (legs, feet, arms, hands)

- Autonomic/Visceral (heart, digestive, sexual organs, urinary tracts, sweat glands)

72
Q

Gastroparesis is the complication fo what kind of neuropathy

A

Diffuse visceral neuropathy

73
Q

What is focal neuropathy?

A

-Eyes, face, mouth, hearing, pelvis, lower back, thigh, abdomen

74
Q

_____ can reverse neuropathy

A

Tight glycemic control (preferably intensive glycemic control)

75
Q

What increases risk of nephropathy?

A

-DM, HTN, Smoking, hyperchol

76
Q

How can we manage nephropathy?

A

-ControlHTN and cholesterol, limit protein to improve GFR

77
Q

Can nephropathy be reversed?

A

NO

-Neuropathy may be reversed

78
Q

What may cause hyperkalemia, despite improving proteinuria?

A

ACEi, will control proteinuria and attenuate HT (risk:benefit)

79
Q

What is the earliest clinical evidence of nephropathy?

A

Microalbuminuria

80
Q

Which medications are OK when GFR <15?

A
  • TZDs

- Some DPP-4 inhibitors

81
Q

Describe the ABCDES in the vascular protection checklist

A
  • A1C: Optimal glycemic control (=7%)
  • Optimal BP control (<130/80)
  • Cholesterol: LDL <2.0 mmol/l or >50% reduction if tx. indicated
  • Drugs to protect heart (ASA)
  • Exercised and healthy eating
  • Smoking cessation
82
Q

What are the 3 drugs to protect the heart? (ASA)?

A
  • ACEi or ARB
  • Statin
  • ASA if indicated
83
Q

Which drugs have demonstrated a CV benefit for those with T2DM with CVD and A1C not a target?

A

-SGLT2i and GLP-1A

84
Q

What did the STENO-2 indicated about CVD prevention in people with T2DM?

A
  • A multifaceted approach is required

- The focus is NOT just on blood-glucose, we need to think of the co-morbidities present

85
Q

In the STENO-2 study, what is considered to prevent CVD in the intensive arm of those w/ T2DM and Microalbuminuria?

A
  • Therapies to achieve targets in glycemia, lipids, BP and albuminuria
  • Multidisciplinary care
  • ASA and ACEi
  • Intensive therapy will help achieve these targets
  • Significant outcomes concerning CVD 21-years follow-up
86
Q

What doe the multifaceted vascular protection strategy include

A

Combining lifestyle (healthy behaviours, weight management, smoking cessation and PA) with medical management (optimal BP, A1C and meds)

87
Q

What are the 4 key macrovascular complications?

A
  • Heart Disease
  • HTN
  • Peripheral vascular disease
  • Atherosclerosis
88
Q

_____ is the greatest risk factor for CVD and poses a ____ greater risk of CAD

A
  • Diabetes

- 2-3 x

89
Q

What does diabetes worsen in short and long-term?

A

Outcomes after CAD event

90
Q

(T/F) If a T1DM is not overweight, they do not have a significant increase in CVD risk

A

F

Hyperglycaemia and AGEs pose significant risk to heart health

91
Q

What is the mediating variable in obesity –> atheroclerosis?

A

Insulin resistance, which drives AGES, Dyslipidemia, endothelial dysfunction, impaired thrombolysis and inflammation

92
Q

Discuss the mechanism of hyperlipidemia in T1DM

A
  • Hyper TF defective removal of chylomicrons and VLDL resulting from impaired LPL activity (insulin dependant)
  • HDL and LDL-C may be normal
93
Q

Discuss the mechanism of hyperlipidemia in T2DM

A
  • Hyper TG due to elevated de novo synthesis from glucose
  • Low HDL-C (due to obesity)
  • LDL-C may be normal
94
Q

What are TG associated components with T2DM and mets?

A
  • Increased TG and TG-rich lipoproteins

- Increased PP TG

95
Q

What are lipoprotein associated components with T2DM and Mets?

A
  • Low apo A1
  • Increased Apo B
  • Increased LDL and smaller size (more atherogenic)
  • Increased oxidized and glycated lipids
96
Q

Who should receive statins? What is it regardless of?

A
  • Clinical CVD OR
  • Age >/= 40 years OR
  • Microvascular complications OR
  • Diabetes >15 yrs and age >30 yrs
  • -> Regardless of baseline LDL
97
Q

Among women with childbearing potential, when should stating be used?

A
  • Only under the presence of proper preconception counselling and reliable contraception
  • Stop statins prior to conception
98
Q

If on therapy, what should the LDL target be?

A

<2.0 mmol/L

99
Q

What does mental illness increase?

A

The risk of diabetes and diabetic complications

100
Q

How much does major depressive disorder increase the risk of T2DM by?

A

60%

101
Q

Reasons for drastic increase in diabetes complications in those w/ depression?

A
  • Non-adherence to medication and self care
  • Functional impairment
  • -> Further increases risks of complications, healthcare costs and risks early mortality
102
Q

Depressive symptoms are present in ___ of people with diabetes

A

30%

  • 10% of people with T2DM
  • Only 5% prevalence in the general population
103
Q

Why does co-morbid depression worsen clinical outcomes in T2DM ? (2)

A
  • Lower levels of physical fitness

- Reduces medication adherence

104
Q

What is A1C a risk predictor of?

A

Mild cognitive impairment and dementia

105
Q

Each ____ elevation in A1C increases the risk of mild cognitive impairment and dementia

A

1%

106
Q

Both ____ & ____ could impact brain function and demential

A

hyper and hypoG

–> The bottom line is good glycemic control is required

107
Q

What are other psychiatric disorders associated with diabetes?

A
  • Mood disorders
  • Anxiety disorders
  • Feeding/eating disorders
  • Schizophrenia
108
Q

What is the issue with psychiatric meds and diabetes?

A
  • May increase/have impacts on weight, A1C, lipid profile, BP an require regular metabolic screening
  • Impacts on their co-morbidities which is undesirable
109
Q

What % of patients with diabetes develop NAFLD ? Which type?

A
  • 70%

- NASH (inflammatory)

110
Q

What does the high incidence of NASH in patients with T2DM lead to?

A

-Liver cirrhosis, HCC

111
Q

(T/F) The same medications use in the Tx of T2DM are also effective in NASH therapy

A

T

112
Q

Which drugs have desirable outcomes for both diabetes and liver?

A
  • Metformin
  • GLP-1
  • TZDs
113
Q

What is the cut-off for HTN in people with diabetes? What does proper BP control result in?

A

> /= 130/80
Where it should be confirmed twice
-24% reduction of CVD events

114
Q

In a patient with diabetes AND CKD or CVD, what is the drug of choice?

A

ACEi o ARB, and may have >/= 2 drug therapies for increased response

115
Q

In patients with diabetes and WITHOUT CKD or CVD, what is the drug of choice?

A
  • ACEi or ARB OR
  • DHB-CCB or Thiazide/Thiazide-like diuretic
  • > /= 2-drug combinations for increased response
116
Q

What should be checked at baseline within 1-2 week of initiation of ACEi or ARB?

A

-Serum potassium and creatinine

117
Q

Combinations of agents that block the ____ should not be used

A

RAAS

118
Q

How many drugs may be required to reach target BP value for those w/ diabetes?

A

More than 3

119
Q

____ of people with T2DM are overweight/obese

A

80-90%

120
Q

What may contribute to weight gain? What can improve glycemic control?

A
  • Antihyperglycemic agents

- 5-10% weight loss

121
Q

What are 2 key strategies for Tx of obesity?

A
  • Healthy behaviour interventions
  • Pharmacotherapy
  • Bariatric Sx
122
Q

Which medications are approved for the Tx of obesity in T2DM?

A
  • Gastrointestinal lipase inhibitor (orlistat)

- GLP-1 receptor agonist (liraglutide)

123
Q

Which warrants more weight–loss, Orlistat or liraglutde?

A

Liraglutide

124
Q

Side effects of orlistat?

A

-Loose stools, GI upset, rare liver failure

125
Q

Nutritional implications of orlistat?

A

-Decrease fat absorption, may require ADEK supplement

126
Q

Side effects of GLP-1RA?

A

-nauseam GI upset, rare gallstones and pancreatitis

127
Q

Nutritional implications of GLP-1RA?

A

-Subcutaneous injectable, increases satiety

128
Q

Which antihyperG meds will have a positive effect on weight? (gain)

A
  • Insulin
  • TZDs
  • Sulfonylureas
  • Meglitinies
129
Q

Which antihyperGs are weight neutral?

A
  • Metformin

- A-glucosidase inhibitors

130
Q

Which antihyperG meds have a negative effect on weight? (loss)

A
  • GLP-1

- SGLT2

131
Q

Criteria for bariatric Sx?

A

-BMI = 40 OR BMI 35-39.9 with co0morbidites

132
Q

When is T2DM control or remission most likely achieved ?

A

In malabsorptive an restrictive procedures (not gastric banding0

133
Q

What is a macrovascular complication of DM which affects digestion?

A
  • Gastroparesis
  • Neuromuscular disorder
  • Could be reversed with good glycemic control
134
Q

What is gastroparesis characterized by?

A

-Delayed gastric emptying, especially with solid food in the absence of mechanical obstruction

135
Q

Prevalence of gastroparesis in diabetes?

A

-30-50%

136
Q

What is the mean age of onset of gastroparesis? Is it more prevalent in men or women?

A
  • 34 yo

- Women (4:1 ratio)

137
Q

What does gastroparesis increase the risk of?

A

-Hyperglycemia, followed by hypoglycemia due to tricky timing with insulin injections

138
Q

recommendations for gastroparesis?

A
  • LOW fibre

- Small freq. meals with higher proportion of LIQUID kcals to meet nutrition needs

139
Q

What should be avoided in gastroparesis?

A

-High protein meals and large-particle meals as they may delay gastric emptying

140
Q

(T/F) Celiac disease is double the prevalence in diabetics compared to general population

A

F

Up to 16 x higher
~16% prevalence vs, ~1% prevalence in general population
–> Only Tx is GF diet for life

141
Q

What is the dawn phenomenon?

A

-An abnormal early morning increase in blood sugar (between 4 AM -8 AM) more common in T1DM than in T2DM

142
Q

Explain the proposed mechanism of dawn phenomenom

A

Fasting glucose levels rise due to increased hepatic glucose which is facilitated by surges of cortisol, Gh and glucagon in the night

  • -> Therefore, when we wake in the morning we are slightly insulin resistant
  • *NOT protective over nocturnal hypoglycemia**
143
Q

In T1DM, what else could explain high blood glucose levels?

A

Potential rebound hyperglycemia after a nocturnal hypoglycemia/somogyi phenomenom

144
Q

What may explain the hyperglycemia following nocturnal hypoG/Somogyu phenomenon?

A

-The pattern of hypoG followed by HyperG as counterregulatory hormones in response to depleted blood glucose will overcompensate, and cause a hyperG (strong stimulation of gluconeogenesis)

145
Q

If nocturnal hypogylcemia, how should we intervene?

A
  • Suggest patient to wake between 2-4 am to monitor BG levels
  • Have a small 15-20 g CHO snack if BG <5 mmol/L prior to bedtime
  • DO NOT treat snack before bedtime with bolus - basal insulin should be enough to cover
146
Q

What are symptoms of nocturnal hypoglycemia?

A
  • Nightmares, sweating, difficulty waking up, morning headache
  • Note that some may be asymptomatic
147
Q

What kind of transplant may resolve or improve diabetes? (in overt T2DM or T1DM)

A
  • Pancreatic or Islet Cell Transplant

- May restore endogenous insulin secretion

148
Q

What does restoration of endogenous insulin secretion result in?

A
  • Improvement in A1C

- Reduction/elimination of HypoG

149
Q

Which transplantation may stabilize microvascular disease?

A

-Islet transplantation

150
Q

Which transplantation may improve microvascular outcomes, lipids, BP, carotid intimal media thickness?

A

Pancreatic transplant

151
Q

Renal transplant options for people with diabetes with ESRD?

A
  • Living donor kidney
  • Cadveric kidney
  • Simultaneous kidney-pancreas
152
Q

Diabetes transplant options for people with functioning renal transplant?

A
  • -> AFTER they have had a kidney transplant, candidates for:
  • Islet transplant
  • Pancreatic transplant
153
Q

If no ESRD, which transplant options are available for T1Dm subjects with lability +/- hypoG?

A

Only islet or pancreas alone

154
Q

Which pancreas graft transplant type will have the greatest survival after 15 years? the worst?

A
  • Simultaneous pancreas kidney (33%)

- Pancreas alone (9%)

155
Q

Insulin independence rate after 5 years in islet allotransplantation?

A

Drops from 70% to 10% in 5 years

156
Q

What are the key points in the diabetes in the elderly checklist? (AIASG)

A
  • Assess for functional dependancy
  • Individualize glycemic targets
  • Avoid hypoG and cognitive impairment
  • Select antihyperG therapy carefully
  • Give regular diets instead of diabetic diets
157
Q

How should glycemic targets in the elderly be individualized?

A

-Based at = 8.5% AIC for frail elderly, but if otherwise healthy, use the same targets as younger people

158
Q

Which antihyperG med should be selected carefully in the elderly?

A
  • Caution with sulfonylureas or TZDs
  • DPP-4i are preferable over sulfonylureas
  • Basal analogues preferable instead of NPH
159
Q

What are the 6 key points in the preconception checklist for women with pre-existing diabetes?

A
  • Use reliable BC until adequate glycemic control
  • Attain pre-conception AIC of =7.0%, and 6.5% if safe
  • May remain on metformin and glyburide until pregnancy,, otherwise switch to insulin
  • Asses for and manage any diabetes complications
  • Folic acid 1 mg/day: 3 months pre-conceptions to at least 12 weeks gestation
  • Discontinue potential embryopathic meds
160
Q

Which medications are potentially embryopathic?

A
  • ACEi and ARB

- Statin therapy

161
Q

What are the 6 key points regarding T2Dm and Indigenous people?

A
  • Are amongst the highest risk populations
  • Prevention strategies are essential
  • Management should be NO different than general population
  • Build a therapeutic relationship
  • Acknowledge that colonizations and it’s ongoing effects on Indigenous health
  • Use the Educating for Equity framework to address social barriers, and apply a cultural approach
162
Q

What are the 6 key components of pre-ramadan diabetes management planning?

A
  • Risk stratification
  • BG monitoring
  • Fluids and dietary advice
  • Excercise advice
  • Medication adjustments
  • When to break the fast?
163
Q

Who is at VERY high risk, and must not fast?

A
  • Poorly controlled T1DM with >9% AIC
  • Severe hypoG within 3 mo, recurrent hypo or hypo unawareness
  • Ketoacidosis within 3 mo
  • Acute illness
  • Pregnancy and diabetes or GDM
164
Q

Which complications put patients at very high risk, and must not face?

A
  • Those with macrovascular complications
  • Renal disease (on dialysis or stage 4/5)
  • Cognitive dysfunction
  • Uncontrolled epilepsy
165
Q

Which groups are at high risk and should NOT fast, an should receive medical advice if fasting

A
  • T2DM with sustained poor glycemic control
  • Well-controlled T2DM on MDI or mixed insulin
  • Pregnant T2DM or GDM controlled by diet only
  • CKOD stage 3 or stable macrovascular complications
  • Performing intense physical labour
  • Well controlled T1DM
166
Q

Which groups are at moderate risk, and can fast with medical advice?

A
  • Well controlled diabetes
  • Treated with/ life-style alone or with metformin, acarbose, DPP-4i or GLP-1RA, SGLT2D inhibitors, TZD or basal insulin in otherwise healthy individuals
167
Q

(T/F) Diabetics on basal insulin should NOT fast due to risk of hypoG

A

F

Can fast if on basal insulin and otherwise healthy

168
Q

Approximately ___ of in-patients have been found to have hyperglycemia

A

1/3

–> Many have pre-existing diabetes prior to admission

169
Q

What are the three adverse effects of hyperglycemia within the context of the hospitalized patient?

A
  • Increased risks of post-op infections and delirium
  • Prolonged hospital stay, resource utilization
  • Increased renal dysfunction and renal allograde rejection in transplant
170
Q

Non-CI BG target ?

A

PP: 5.0-8.0

RandomL <10.00

171
Q

CI BG target?

A

6.0-10.0

172
Q

CABG intraoperatively BG target?

A

5.5-11.1

173
Q

Preoperatively for other Sx BG target?

A

5.0-10.0

174
Q

Acute coronary syndrome BG target?

A

7.0-10.0

175
Q

Labour and deliver bG target?

A

4.0-7.0

Clinical Nutrition 3 (30 decks)

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