Diabetes Complications Flashcards
1
Q
Examples of acute complications?
A
- Hypoglycemia
- Hyperglycemic emergencies
2
Q
Two kinds of hyperglycaemic emergencies?
A
- DKA
- Hyperosmolar
3
Q
Chronic complications?
A
-Microvascular and Macro-vascular complications
4
Q
Microvascular complications?
A
- Diabetic retinopathy
- Diabetic nephropathy
- Diabetic neuropathy
5
Q
Macro-vascular complications?
A
- Stroke
- CVD disease
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
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
8
Q
T/F someone without diabetes with a blood glucose <4 mmol/L is considered hypoglycemic
A
F
9
Q
Examples of neurogenic (autonomic) symptoms?
A
- Trembling
- Palpitations
- Sweating
- Anxiety
- Hunger
- Nausea
10
Q
Examples of neuroglycopenic symptoms?
A
- Difficulties concentrating
- Confusion
- Weakness
- Drowsiness
- Vision changes
- Difficulty speaking
- Dizziness
11
Q
Mild hypoglycaemia?
A
- Autonomic symptoms present
- Individual is able to self-treat
12
Q
Moderate hypoglycemia?
A
- Autonomic and neuroglycopenic symptoms
- Individual is able to self-treat
13
Q
Severe hypoglycemia?
A
- Requires assistance of another person
- Unconsciousness may occur
- Plasma glucose is typically <2.88 mmol/L
14
Q
What is the MAIN indication of severe hypoglycemia?
A
When assistance is required from another person
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
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
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
18
Q
Is 15 g of CHO usually enough?
A
No, and average required is much higher
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
20
Q
What is under-treating a hypo?
A
Not having enough CHOs
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)
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
23
Q
What are two kinds of glucagon used to treat hypoG?
A
- Injectable glucagon
- Nasal glucagon
24
Q
Which glucagon injection treatment is similar to an epipen?
A
GlucaGen Hypokit
-Must reformulate prior to injection
25
When is 1/2 a dose used for glucagon injection? In GlucaGen?
- 1/2 dose if <20 kg
| - 1/2 dose if <25 kg or 6-8 years old
26
What are the two types of hyperglycaemic emergencies?
- Diabetic ketoacidosis (DKA)
| - Hyperosmolar Hyperglycaemic State (HHS)
27
HHS is seen most commonly in what kinds of diabetes?
Mainly seen in T2DM, where there is still some insulin being produced
28
What is the MAIN difference between DKA and HHS
In HHS, there is still some preliminary insulin produced
29
Describe the pathophysiology of HHS
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)
30
Describe the pathophysiology of DKA
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
31
Provide 4 medical or tangible risks associated with developing DKA
- Lower BMI
- Preceding infection
- Adolescent girls
- Age
32
Which age group will have a 3x higher risk of developing DKA?
Age <2 years
33
Why are adolescent girls more prone to developing DKA?
Due to tendency to withold insulin to avoid weight-gain (type of ED)
34
What are 5 social and environmental risks associated with developing DKA?
- Ethnic minorities
- Lower socioeconomic status
- Lack of private health insurance
- Lower parental education
35
What are signs consistent with DKA?
- ketoacidosis
- ECFV contraction
- Milder hyperosmolarity
- Normal to high glucose
- May have decreased LOC
- Hypokalemia
- MUST use insulim
- Absolute insulin deficiency and increased glucago
36
What are signs consistent with HHS?
- Minimal acid/base problems
- ECFC contraction
- Hyperosmolarity
- Marked hyperglycemia
- Marked decrease LOC
- Hypokalemia
- May need insulin
- Relative insulin deficiency
37
(T/F) HHS required insulin to reverse
F
May require insulin
38
(T/F) DKA can be present with normal blood glucose levels
T
Check ketones to confirm
39
T/F) DKA has the greatest hyperosmolarity
F
Milder hyperosmolarity
40
(T/F) HHS has the most severe consequences in terms of LOC
T
41
(T/F) HHS primarily has a flux of FFA to the liver
F
Slight insulin can still inhibit lipolysis, therefore there is less FFA or B-oxidation, mostly gluconeogenesis from skeletal muscle) and glycogenolysis
42
What contributes to the dehydration in HHS?
The gluconeogenesis and glycogenolysis leads to hyperglycemia, which will cause chronic diuresis, and therefore dehydration
43
What are the two clinical presentation of DKA?
- Hyperglycemia
| - Acidosis
44
Signs and symptoms of hyperglycemia in DKA?
- Polyuria, polydipsia, weakness
| - ECFV contraction
45
Signs and symptoms of acidosis in DKA?
Hunger, nausea, vomiting, abdo pain
| -Kussmaul respiration, acetone-odoured breath, altered sense
46
When is measuring urine ketones particularly important?
- Type 1
- GDM
- Previous GDM patient s
47
What does elevated level of ketones indicate?
Impending or established ketoacidosis
48
When are the 5 instances which diabetics should test their ketones? (CAPSS)
- Acute illness accompanied by elevated BG
- Stress
- Consistently elevated BG levels (>14 mmol/L)
- Symptoms of ketoacidosis
- Pregnancy
49
In the morning, would we expect our ketone test to be positive?
Yes if fasting
-Doesn't indicate DKA,
50
(T/F) There is normally no ketones in the urine
F
Usually in the urine, however usually in amounts below the limit of detectability
51
In what populations are up to 30% of first morning urine specimens + for ketones?
In pregnant women
52
What may cause a false-positive ketone test?
-Sulfhydryl drugs (captopril)
53
What may cause false-negative ketone tests?(2)
- Test strips expose to air for extended periods of time
| - Highly acidic specimens (such as after large intakes of ascorbic acid)
54
(T/F) Urine ketone tests are reliable for diagnosing or monitoring the treatment of ketoacidosis
F
55
What is the preferable method to diagnose and monitor ketoacidosis? What does it quantify?
- Blood ketones
| - Will quantify b-OH butyrate acid
56
What is the MOST common cause of DKA?
Insulin omission
57
What are other causes of DKA?
```
-New diagnosis
of diabetes
-Infection/sepsis
-MI
-Thyrotoxicosis
-Drugs
```
58
How can we treat DKA?
By treating the precipitating factor, and with insulin
59
What are the microvascular/specific complications of DM?
- Retinopathy
- Nephropathy
- Diabetic neuropathy
- Erectile dysfunction
60
Macrovascular/non-specific complications in DM?
- Stroke (2-4 fold increase in CVD mortality and stroke)
| - CVD (8/10 diabetic patients die from CV events)
61
What are other non-specific complications of DM?
- Arthritis of lower limbs
| - Infections
62
What are the acute complications of diabetes?
-Hypo and hyperglycemia
63
What are the chronic complications of diabetes?
-Specific and non-specific
64
What 3 complications of diabetes lead to amputations of limps?
- Neuropathy
- Infections
- Peripheral artery disease
65
What si the best way to improve the complications of diabetes?
Though tight control of A1C
| -Even a 1% decrease in A1C will reduce the risk of complications in T2DM
66
when there is a 1% reduction in A1C in T2DM patients, which complication is most significantly reduced?
43% reduction in lower limb amputation or secondary arterial disease deaths
67
Chronic complications in vision?
- Retinopathy (most in type I)
- Glaucoma
- Cataracts
68
What is the most common cause of blindness in T1DM patients with diabetic retinopathy?
Proliferative retinopathy
69
What is neuropathy accelerated by?
-Smoking, lack of exercise, greater than 4 alcoholic drinks/day
70
What are two broad categories of neuropathy?
-Diffuse and Focal
71
What is diffuse neuropathy?
- Peripheral (legs, feet, arms, hands)
| - Autonomic/Visceral (heart, digestive, sexual organs, urinary tracts, sweat glands)
72
Gastroparesis is the complication fo what kind of neuropathy
Diffuse visceral neuropathy
73
What is focal neuropathy?
-Eyes, face, mouth, hearing, pelvis, lower back, thigh, abdomen
74
_____ can reverse neuropathy
Tight glycemic control (preferably intensive glycemic control)
75
What increases risk of nephropathy?
-DM, HTN, Smoking, hyperchol
76
How can we manage nephropathy?
-ControlHTN and cholesterol, limit protein to improve GFR
77
Can nephropathy be reversed?
NO
-Neuropathy may be reversed
78
What may cause hyperkalemia, despite improving proteinuria?
ACEi, will control proteinuria and attenuate HT (risk:benefit)
79
What is the earliest clinical evidence of nephropathy?
Microalbuminuria
80
Which medications are OK when GFR <15?
- TZDs
| - Some DPP-4 inhibitors
81
Describe the ABCDES in the vascular protection checklist
- 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
What are the 3 drugs to protect the heart? (ASA)?
- ACEi or ARB
- Statin
- ASA if indicated
83
Which drugs have demonstrated a CV benefit for those with T2DM with CVD and A1C not a target?
-SGLT2i and GLP-1A
84
What did the STENO-2 indicated about CVD prevention in people with T2DM?
- A multifaceted approach is required
| - The focus is NOT just on blood-glucose, we need to think of the co-morbidities present
85
In the STENO-2 study, what is considered to prevent CVD in the intensive arm of those w/ T2DM and Microalbuminuria?
- 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
What doe the multifaceted vascular protection strategy include
Combining lifestyle (healthy behaviours, weight management, smoking cessation and PA) with medical management (optimal BP, A1C and meds)
87
What are the 4 key macrovascular complications?
- Heart Disease
- HTN
- Peripheral vascular disease
- Atherosclerosis
88
_____ is the greatest risk factor for CVD and poses a ____ greater risk of CAD
- Diabetes
| - 2-3 x
89
What does diabetes worsen in short and long-term?
Outcomes after CAD event
90
(T/F) If a T1DM is not overweight, they do not have a significant increase in CVD risk
F
Hyperglycaemia and AGEs pose significant risk to heart health
91
What is the mediating variable in obesity --> atheroclerosis?
Insulin resistance, which drives AGES, Dyslipidemia, endothelial dysfunction, impaired thrombolysis and inflammation
92
Discuss the mechanism of hyperlipidemia in T1DM
- Hyper TF defective removal of chylomicrons and VLDL resulting from impaired LPL activity (insulin dependant)
- HDL and LDL-C may be normal
93
Discuss the mechanism of hyperlipidemia in T2DM
- Hyper TG due to elevated de novo synthesis from glucose
- Low HDL-C (due to obesity)
- LDL-C may be normal
94
What are TG associated components with T2DM and mets?
- Increased TG and TG-rich lipoproteins
| - Increased PP TG
95
What are lipoprotein associated components with T2DM and Mets?
- Low apo A1
- Increased Apo B
- Increased LDL and smaller size (more atherogenic)
- Increased oxidized and glycated lipids
96
Who should receive statins? What is it regardless of?
- Clinical CVD OR
- Age >/= 40 years OR
- Microvascular complications OR
- Diabetes >15 yrs and age >30 yrs
- -> Regardless of baseline LDL
97
Among women with childbearing potential, when should stating be used?
- Only under the presence of proper preconception counselling and reliable contraception
- Stop statins prior to conception
98
If on therapy, what should the LDL target be?
<2.0 mmol/L
99
What does mental illness increase?
The risk of diabetes and diabetic complications
100
How much does major depressive disorder increase the risk of T2DM by?
60%
101
Reasons for drastic increase in diabetes complications in those w/ depression?
- Non-adherence to medication and self care
- Functional impairment
- -> Further increases risks of complications, healthcare costs and risks early mortality
102
Depressive symptoms are present in ___ of people with diabetes
30%
- 10% of people with T2DM
- Only 5% prevalence in the general population
103
Why does co-morbid depression worsen clinical outcomes in T2DM ? (2)
- Lower levels of physical fitness
| - Reduces medication adherence
104
What is A1C a risk predictor of?
Mild cognitive impairment and dementia
105
Each ____ elevation in A1C increases the risk of mild cognitive impairment and dementia
1%
106
Both ____ & ____ could impact brain function and demential
hyper and hypoG
| --> The bottom line is good glycemic control is required
107
What are other psychiatric disorders associated with diabetes?
- Mood disorders
- Anxiety disorders
- Feeding/eating disorders
- Schizophrenia
108
What is the issue with psychiatric meds and diabetes?
- May increase/have impacts on weight, A1C, lipid profile, BP an require regular metabolic screening
- Impacts on their co-morbidities which is undesirable
109
What % of patients with diabetes develop NAFLD ? Which type?
- 70%
| - NASH (inflammatory)
110
What does the high incidence of NASH in patients with T2DM lead to?
-Liver cirrhosis, HCC
111
(T/F) The same medications use in the Tx of T2DM are also effective in NASH therapy
T
112
Which drugs have desirable outcomes for both diabetes and liver?
- Metformin
- GLP-1
- TZDs
113
What is the cut-off for HTN in people with diabetes? What does proper BP control result in?
>/= 130/80
Where it should be confirmed twice
-24% reduction of CVD events
114
In a patient with diabetes AND CKD or CVD, what is the drug of choice?
ACEi o ARB, and may have >/= 2 drug therapies for increased response
115
In patients with diabetes and WITHOUT CKD or CVD, what is the drug of choice?
- ACEi or ARB OR
- DHB-CCB or Thiazide/Thiazide-like diuretic
- >/= 2-drug combinations for increased response
116
What should be checked at baseline within 1-2 week of initiation of ACEi or ARB?
-Serum potassium and creatinine
117
Combinations of agents that block the ____ should not be used
RAAS
118
How many drugs may be required to reach target BP value for those w/ diabetes?
More than 3
119
____ of people with T2DM are overweight/obese
80-90%
120
What may contribute to weight gain? What can improve glycemic control?
- Antihyperglycemic agents
| - 5-10% weight loss
121
What are 2 key strategies for Tx of obesity?
- Healthy behaviour interventions
- Pharmacotherapy
- Bariatric Sx
122
Which medications are approved for the Tx of obesity in T2DM?
- Gastrointestinal lipase inhibitor (orlistat)
| - GLP-1 receptor agonist (liraglutide)
123
Which warrants more weight--loss, Orlistat or liraglutde?
Liraglutide
124
Side effects of orlistat?
-Loose stools, GI upset, rare liver failure
125
Nutritional implications of orlistat?
-Decrease fat absorption, may require ADEK supplement
126
Side effects of GLP-1RA?
-nauseam GI upset, rare gallstones and pancreatitis
127
Nutritional implications of GLP-1RA?
-Subcutaneous injectable, increases satiety
128
Which antihyperG meds will have a positive effect on weight? (gain)
- Insulin
- TZDs
- Sulfonylureas
- Meglitinies
129
Which antihyperGs are weight neutral?
- Metformin
| - A-glucosidase inhibitors
130
Which antihyperG meds have a negative effect on weight? (loss)
- GLP-1
| - SGLT2
131
Criteria for bariatric Sx?
-BMI = 40 OR BMI 35-39.9 with co0morbidites
132
When is T2DM control or remission most likely achieved ?
In malabsorptive an restrictive procedures (not gastric banding0
133
What is a macrovascular complication of DM which affects digestion?
- Gastroparesis
- Neuromuscular disorder
- Could be reversed with good glycemic control
134
What is gastroparesis characterized by?
-Delayed gastric emptying, especially with solid food in the absence of mechanical obstruction
135
Prevalence of gastroparesis in diabetes?
-30-50%
136
What is the mean age of onset of gastroparesis? Is it more prevalent in men or women?
- 34 yo
| - Women (4:1 ratio)
137
What does gastroparesis increase the risk of?
-Hyperglycemia, followed by hypoglycemia due to tricky timing with insulin injections
138
recommendations for gastroparesis?
- LOW fibre
| - Small freq. meals with higher proportion of LIQUID kcals to meet nutrition needs
139
What should be avoided in gastroparesis?
-High protein meals and large-particle meals as they may delay gastric emptying
140
(T/F) Celiac disease is double the prevalence in diabetics compared to general population
F
Up to 16 x higher
~16% prevalence vs, ~1% prevalence in general population
--> Only Tx is GF diet for life
141
What is the dawn phenomenon?
-An abnormal early morning increase in blood sugar (between 4 AM -8 AM) more common in T1DM than in T2DM
142
Explain the proposed mechanism of dawn phenomenom
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
In T1DM, what else could explain high blood glucose levels?
Potential rebound hyperglycemia after a nocturnal hypoglycemia/somogyi phenomenom
144
What may explain the hyperglycemia following nocturnal hypoG/Somogyu phenomenon?
-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
If nocturnal hypogylcemia, how should we intervene?
- 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
What are symptoms of nocturnal hypoglycemia?
- Nightmares, sweating, difficulty waking up, morning headache
- Note that some may be asymptomatic
147
What kind of transplant may resolve or improve diabetes? (in overt T2DM or T1DM)
- Pancreatic or Islet Cell Transplant
| - May restore endogenous insulin secretion
148
What does restoration of endogenous insulin secretion result in?
- Improvement in A1C
| - Reduction/elimination of HypoG
149
Which transplantation may stabilize microvascular disease?
-Islet transplantation
150
Which transplantation may improve microvascular outcomes, lipids, BP, carotid intimal media thickness?
Pancreatic transplant
151
Renal transplant options for people with diabetes with ESRD?
- Living donor kidney
- Cadveric kidney
- Simultaneous kidney-pancreas
152
Diabetes transplant options for people with functioning renal transplant?
- -> AFTER they have had a kidney transplant, candidates for:
- Islet transplant
- Pancreatic transplant
153
If no ESRD, which transplant options are available for T1Dm subjects with lability +/- hypoG?
Only islet or pancreas alone
154
Which pancreas graft transplant type will have the greatest survival after 15 years? the worst?
- Simultaneous pancreas kidney (33%)
| - Pancreas alone (9%)
155
Insulin independence rate after 5 years in islet allotransplantation?
Drops from 70% to 10% in 5 years
156
What are the key points in the diabetes in the elderly checklist? (AIASG)
- Assess for functional dependancy
- Individualize glycemic targets
- Avoid hypoG and cognitive impairment
- Select antihyperG therapy carefully
- Give regular diets instead of diabetic diets
157
How should glycemic targets in the elderly be individualized?
-Based at = 8.5% AIC for frail elderly, but if otherwise healthy, use the same targets as younger people
158
Which antihyperG med should be selected carefully in the elderly?
- Caution with sulfonylureas or TZDs
- DPP-4i are preferable over sulfonylureas
- Basal analogues preferable instead of NPH
159
What are the 6 key points in the preconception checklist for women with pre-existing diabetes?
- 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
Which medications are potentially embryopathic?
- ACEi and ARB
| - Statin therapy
161
What are the 6 key points regarding T2Dm and Indigenous people?
- 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
What are the 6 key components of pre-ramadan diabetes management planning?
- Risk stratification
- BG monitoring
- Fluids and dietary advice
- Excercise advice
- Medication adjustments
- When to break the fast?
163
Who is at VERY high risk, and must not fast?
- 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
Which complications put patients at very high risk, and must not face?
- Those with macrovascular complications
- Renal disease (on dialysis or stage 4/5)
- Cognitive dysfunction
- Uncontrolled epilepsy
165
Which groups are at high risk and should NOT fast, an should receive medical advice if fasting
- 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
Which groups are at moderate risk, and can fast with medical advice?
- 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
(T/F) Diabetics on basal insulin should NOT fast due to risk of hypoG
F
Can fast if on basal insulin and otherwise healthy
168
Approximately ___ of in-patients have been found to have hyperglycemia
1/3
| --> Many have pre-existing diabetes prior to admission
169
What are the three adverse effects of hyperglycemia within the context of the hospitalized patient?
- Increased risks of post-op infections and delirium
- Prolonged hospital stay, resource utilization
- Increased renal dysfunction and renal allograde rejection in transplant
170
Non-CI BG target ?
PP: 5.0-8.0
| RandomL <10.00
171
CI BG target?
6.0-10.0
172
CABG intraoperatively BG target?
5.5-11.1
173
Preoperatively for other Sx BG target?
5.0-10.0
174
Acute coronary syndrome BG target?
7.0-10.0
175
Labour and deliver bG target?
4.0-7.0
