DIABETES MELLITUS: ACUTE AND CHRONIC COMPLICATIONS Flashcards
(115 cards)
1
Q
What are the acute complications of diabetes?
A
Diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), and hypoglycemia.
2
Q
What symptoms are characteristic of hyperglycemia?
A
Patients may report the ‘3 P’s’: polyuria, polydipsia, and polyphagia, along with blurry vision and fatigue.
3
Q
What is DKA, and how common is it?
A
DKA stands for diabetic ketoacidosis. It occurs more often in patients with type 1 diabetes and accounts for 140,000 hospital admissions in the U.S. each year.
4
Q
What three elements are required for the diagnosis of DKA?
A
- Uncontrolled hyperglycemia (blood glucose usually > 250 mg/dL)
- Metabolic acidosis (pH < 7.3)
- Increased ketone concentrations
5
Q
What is the mortality rate for DKA?
A
Currently, the mortality rate for DKA in the U.S. and European countries is about 2%, but 10% in countries with limited resources.
6
Q
Is DKA exclusive to type 1 diabetes?
A
No, patients with type 2 diabetes may also develop DKA under severe insulin deficiency.
7
Q
What are the key factors leading to DKA?
A
- Insulin deficiency
- Elevated levels of counterregulatory hormones (epinephrine, glucagon, cortisol, growth hormone)
8
Q
What are common precipitating factors for DKA?
A
- New diagnosis of diabetes
- Omission of insulin doses
- Infection
- Myocardial infarction
- Pancreatitis
- Stroke
- Alcohol use
- Insulin pump malfunction
9
Q
What are the symptoms and signs of DKA?
A
- Nausea and vomiting
- Abdominal pain
- Polyuria
- Polydipsia
- Fatigue
- Weight loss
10
Q
Fill in the blank: The leading cause of death in children and young adults with type 1 diabetes is _______.
A
DKA
11
Q
What is the case fatality rate for mortality in the hospital for DKA from 2000 to 2014?
A
Decreased from 1.1% to 0.4%.
12
Q
True or False: Patients with ketosis-prone diabetes (KPD) are diagnosed when they present with DKA.
A
True
13
Q
What symptoms may indicate severe DKA?
A
- Kussmaul respirations
- Fruity breath resulting from acetone production
14
Q
What demographic has the highest occurrence of DKA?
A
Young adults, ages 18 to 25 years.
15
Q
What is the age-adjusted rate of DKA hospitalizations from 2009 to 2014?
A
Increased dramatically by 54.9%.
16
Q
Fill in the blank: The catabolism of fat stores increases serum concentrations of free fatty acids, which are then oxidized to _______ in the liver.
A
ketone bodies
17
Q
What is the most common precipitating factor for DKA in the United States?
A
Failure to adhere to insulin therapy.
18
Q
What is required for the diagnosis of DKA?
A
Laboratory findings:
* Hyperglycemia (blood glucose usually ≥ 250 mg/dL)
* Anion gap metabolic acidosis (pH ≤ 7.3; HCO3 ≤ 18 mEq/L; anion gap > 15)
* Positive serum or urine ketones
19
Q
What is euglycemic DKA?
A
DKA with blood glucose levels lower than 250 mg/dL in situations such as:
* Pregnancy
* Starvation
* Alcohol use
* Insulin therapy
* Use of SGLT-2 inhibitors
20
Q
How is the anion gap calculated?
A
Anion gap = sodium [Na+] - chloride [Cl-] - bicarbonate [HCO3-]
21
Q
What are the key measures for treating DKA?
A
Key measures include:
* Volume repletion
* Correction of electrolyte abnormalities
* Insulin therapy to correct hyperglycemia and ketonemia
* Identification and treatment of precipitating events
22
Q
How quickly can DKA resolve with appropriate treatment?
A
DKA often resolves within 10 to 18 hours if treatment is instituted promptly.
23
Q
What factors should be monitored in DKA treatment?
A
Monitor:
* Volume status
* Mental status
* Urine output
* Basic metabolic panels
* Serial vital signs
24
Q
Should ketones be monitored in the management of DKA?
A
Yes, but point-of-care beta-hydroxybutyrate measurements are preferred over the nitroprusside method.
25
When can intravenous insulin infusion be discontinued after DKA treatment?
Intravenous insulin can be discontinued when:
* Acidemia has resolved
* Clinical improvement is observed
* Patient can tolerate oral intake
* Precipitating causes have been addressed
26
What is HHS?
HHS stands for hyperglycemic hyperosmolar state.
27
Who is most likely to develop HHS?
Elderly patients with type 2 diabetes who have an impaired thirst mechanism or cannot access free water.
28
What are common symptoms of HHS?
Symptoms include:
* Polyuria
* Polydipsia
* Blurred vision
* Weakness
* Decreased mental status
* Signs of dehydration
29
Why do people with HHS generally not have ketoacidosis?
Patients with HHS have sufficient insulin to suppress lipolysis and ketone generation.
30
How can one distinguish between DKA and HHS?
Distinguishing features:
* DKA: increased acidemia with ketonemia
* HHS: little to no ketones, normal serum bicarbonate, elevated serum osmolality > 320 mOsm/kg
31
Can a patient present with both DKA and HHS?
Yes, patients may have features of both ketoacidosis and hyperosmolarity.
32
What is the plasma glucose level (mg/dL) for mild DKA?
250
33
What is the arterial pH range for moderate DKA?
7.00 to < 7.24
34
What is the serum bicarbonate level (mEq/L) in mild DKA?
15–18
35
Is urine to serum ketones positive in severe DKA?
Yes
36
What is the mental status of a patient in severe DKA?
Stupor/coma
37
What is the effective serum osmolality (mOsm/kg) for HHS?
320
38
What arterial pH indicates severe DKA?
< 7.00
39
What is the serum bicarbonate level (mEq/L) in moderate DKA?
10–15
40
What is the plasma glucose level (mg/dL) for HHS?
600
41
What is the mental status of a patient in moderate DKA?
Alert/drowsy
42
What is the urine to serum ketones status in mild DKA?
Positive
43
What is the anion gap in severe DKA?
Variable
44
What is the b-hydroxybutyrate level (mmol/L) in mild DKA?
3.0
45
In terms of mental status, what is a common finding in HHS?
Stupor/coma
46
What is needed for the diagnosis of HHS?
The following findings are needed for diagnosis:
* Serum glucose of > 600 mg/dL
* Serum osmolality of > 320 mOsm/kg
* Ketones absent
## Footnote
Effective osmolality is calculated using the formula: sodium ion (mEq/L) x 2 + glucose (mg/dL)/18 + blood urea nitrogen (BUN) (mg/dL)/2.8.
47
What is key to the treatment of HHS?
Adequate volume repletion is key to the treatment of HHS.
## Footnote
Patients with HHS are extremely volume depleted.
48
What role does insulin play in the treatment of HHS?
Insulin therapy is important but secondary; correction of volume loss is the critical element in management.
## Footnote
This differs from the treatment for DKA, where insulin deficiency is the most important factor.
49
Describe the signs and symptoms of hypoglycemia.
Common symptoms include:
* Shakiness
* Diaphoresis
* Irritability
* Hunger
* Fatigue
Neuroglycopenic symptoms may include confusion, unusual behavior, visual disturbances, and loss of consciousness.
## Footnote
Severe hypoglycemia can lead to intoxicated appearance, slurred speech, clumsiness, and seizures.
50
What are common reasons patients with diabetes become hypoglycemic?
Common reasons include:
* Missed/delayed meals after insulin
* Excessive prandial/correctional insulin
* Too much basal insulin
* Physical activity without adjustments
* Renal disease
Other causes include liver failure, cardiac failure, sepsis, critical illness, untreated adrenal insufficiency, untreated hypothyroidism, and starvation.
## Footnote
Insulinomas are rarely a cause in diabetes patients but are considered in the differential diagnosis.
51
Which diabetes medications are most commonly associated with hypoglycemia?
The medications include:
* Insulins
* Sulfonylureas
* Meglitinides (repaglinide, nateglinide)
## Footnote
These account for the vast majority of hypoglycemia cases in diabetes patients.
52
What diabetes medications are associated with a low risk of hypoglycemia?
The following medications rarely cause hypoglycemia:
* Metformin
* Acarbose
* Thiazolidinediones
* Dipeptidyl peptidase-4 inhibitors
* GLP-1 receptor agonists
* SGLT-2 inhibitors
## Footnote
May cause mild hypoglycemia when combined with medications that carry a higher risk.
53
Do patients with type 1 diabetes and type 2 diabetes have the same risk of hypoglycemia?
No, patients with type 1 diabetes are two to three times more likely to develop hypoglycemia compared to type 2 diabetes patients.
## Footnote
Risk factors include advancing age, intensive glycemic control, renal disease, and decreased cognitive function.
54
What is hypoglycemia unawareness?
Absence of hypoglycemic symptoms when blood glucose levels decrease into the hypoglycemic range
## Footnote
Typically occurs after multiple, recurrent episodes of hypoglycemia, leading to a lowered glucose threshold for counterregulatory hormone release
55
Is hypoglycemia unawareness reversible?
Yes, with strict avoidance of hypoglycemia for weeks to months, patients often regain awareness
## Footnote
This process may vary based on individual circumstances
56
How is hypoglycemia treated in a conscious patient?
15 g of oral carbohydrates such as:
* Glucose tablets or gel
* Half cup (4 oz) of juice or regular soda
* 1 cup (8 oz) of milk
* 1 tablespoon of honey
* Three 3-packs of SweeTARTS
* Three rolls of Smarties
## Footnote
These options provide quick glucose replenishment
57
What should be done if a patient is unconscious and severe hypoglycemia is suspected?
Inject glucagon subcutaneously or intramuscularly and call emergency services
## Footnote
Glucagon stimulates immediate glycogenolysis in the liver and should be administered by someone trained
58
What are the key elements of education needed to prevent and avoid hypoglycemia?
Key elements include:
* Recognizing symptoms of hypoglycemia
* Proper treatment of hypoglycemia
* Familiarity with high-risk situations
* Dietary and exercise modifications
* Medication adjustments
* Glucose monitoring methods
## Footnote
Education should be reviewed at every visit and involves meticulous surveillance by healthcare providers
59
What are the common long-term complications of diabetes mellitus?
Complications are divided into:
* Microvascular: retinopathy, diabetic kidney disease, neuropathy
* Macrovascular: atherosclerotic cardiovascular disease (coronary heart disease, cerebrovascular disease, peripheral arterial disease)
## Footnote
Diabetic foot ulcers are multifactorial and cannot be neatly classified
60
Why do complications develop in individuals with diabetes?
Develop due to:
* Uncontrolled hyperglycemia
* Insulin resistance
* Hyperinsulinemia
* Associated conditions like dyslipidemia, hypertension, and obesity
## Footnote
These factors lead to increased oxidative stress, inflammation, and toxic products of abnormal glucose metabolism
61
What fundamental factors need to be managed to prevent microvascular complications?
Hyperglycemia, hypertension, and dyslipidemia must be well controlled
## Footnote
Effective management of these factors is crucial for prevention
62
How common is diabetic retinopathy?
Affects almost 100 million people globally; most common cause of new blindness cases in adults aged 20 to 74 in developed countries
## Footnote
Glaucoma and cataracts also occur earlier and more frequently in diabetic patients
63
What are the different types of diabetic retinopathy?
Nonproliferative diabetic retinopathy (NPDR), proliferative diabetic retinopathy (PDR), diabetic macular edema (DME)
## Footnote
NPDR is the earliest detectable stage, while PDR indicates a more advanced stage.
64
What findings are associated with nonproliferative diabetic retinopathy (NPDR)?
Microaneurysms, retinal hemorrhages, intraretinal microvascular abnormalities (IRMAs), venous caliber changes
## Footnote
NPDR is characterized by these findings during retinal examination.
65
What characterizes proliferative diabetic retinopathy (PDR)?
Preretinal neovascularization
## Footnote
PDR indicates a more advanced stage of diabetic retinopathy.
66
What is diabetic macular edema (DME)?
Abnormal retinal thickening and cystoid macular edema due to breakdown of the blood-retina barrier
## Footnote
DME can occur at any stage of diabetic retinopathy and is the most common cause of visual loss.
67
What are the treatment options for diabetic retinopathy?
Focal and panretinal laser photocoagulation, intravitreal injections of anti-VEGF, intravitreal steroids, vitreoretinal surgery
## Footnote
These treatments are designed to manage advanced disease (PDR and/or DME).
68
What percentage of adults with diabetes develop chronic kidney disease (DKD)?
Approximately 35%
## Footnote
DKD disproportionately affects middle-aged African Americans, Native Americans, and Hispanic Americans.
69
What are manifestations of diabetic kidney disease (DKD)?
Albuminuria, decreased glomerular filtration rate (GFR), glomerular hematuria, abnormalities of urinary sediment, imaging study abnormalities
## Footnote
Not all individuals with DKD and reduced eGFR have increased albuminuria.
70
What is a key treatment for diabetic kidney disease (DKD)?
Good control of blood glucose and blood pressure, especially with ACE inhibitors or ARBs
## Footnote
This can prevent or slow the progression of established DKD.
71
What types of diabetic neuropathies exist?
Distal symmetric sensorimotor polyneuropathy, autonomic neuropathy, focal limb neuropathies, mononeuropathies, entrapment syndromes, diabetic amyotrophy, diabetic truncal radiculopathy, acute sensory neuropathy
## Footnote
Distal symmetric sensorimotor polyneuropathy is the most common type.
72
What is the progression pattern of diabetic neuropathies?
Sensory and autonomic neuropathies progress gradually; mononeuropathies and acute painful neuropathies may be severe but short-lived
## Footnote
The natural histories of diabetic neuropathies are not well defined.
73
What contributes to the pathogenesis of diabetic neuropathies?
Metabolic abnormalities within nerves and/or Schwann cells, microvascular injuries
## Footnote
In distal symmetric polyneuropathy, progressive axonal degeneration occurs.
74
What are common symptoms of distal symmetric polyneuropathy?
Numbness, prickling, tingling, stabbing, burning, electrical shocks, aching pains
## Footnote
Symptoms typically start in the toes and travel proximally.
75
What is the diagnosis process for distal symmetric polyneuropathy?
Diagnosis is a process of exclusion, considering other possible causes
## Footnote
Conditions to consider include chronic inflammatory demyelinating polyneuropathy, vitamin B12 deficiency, hypothyroidism, and uremia.
76
What is the role of tight glycemic control in diabetic neuropathy?
Prevents progression of neuropathy but does not reduce pain in distal symmetric polyneuropathy
## Footnote
FDA-approved therapies for painful diabetic neuropathy include pregabalin and duloxetine.
77
Fill in the blank: The most common type of diabetic neuropathy is _______.
Distal symmetric sensorimotor polyneuropathy
78
What are common complications in patients with diabetes related to foot health?
Diabetic foot ulcers, insensate feet, foot infections, foot deformities, peripheral artery disease, amputations
## Footnote
Foot deformities include Charcot foot.
79
What are risk factors for diabetic foot ulcers and amputations?
Poor glycemic control, peripheral neuropathy, cigarette smoking, foot deformity, preulcerative callouses, peripheral artery disease, previous foot ulcers, prior amputations, visual impairment, DKD (especially ESRD on dialysis)
## Footnote
DKD stands for Diabetic Kidney Disease.
80
What are key components of proper foot care for diabetic patients?
Daily skin and nail assessment, visual or palpation surveillance, use of well-fitting shoes, proper wound care
## Footnote
Custom-fitted shoes may be necessary in select circumstances.
81
What are the clinical features of diabetic autonomic neuropathy?
Hypoglycemia unawareness, resting tachycardia, orthostatic hypotension, gastroparesis, constipation, diarrhea, fecal incontinence, erectile dysfunction, neurogenic bladder, sudomotor dysfunction
## Footnote
Sudomotor dysfunction can involve increased or decreased sweating.
82
How can cardiac autonomic neuropathy be detected?
Decreased heart rate variability with deep breathing, resting tachycardia, orthostatic hypotension
## Footnote
Cardiac autonomic neuropathy is independently associated with mortality.
83
When do patients with diabetes typically develop gastroparesis?
10 to 15 years after diagnosis for type 1 diabetes; longer for type 2 diabetes
## Footnote
Symptoms include esophageal dysmotility, diarrhea, and constipation.
84
What is the gold standard for diagnosing gastroparesis?
Gastric-emptying scintigraphy
## Footnote
Must exclude mechanical obstruction and gastric or peptic ulcers first.
85
What conditions must be met for a valid gastric-emptying scintigraphy result?
Discontinue drugs affecting gastric emptying, fast overnight, consume a standard low-fat radiolabeled meal, glucose values < 275 mg/dL
## Footnote
Delayed gastric emptying defined as > 60% retention at 2 hours or > 10% retention at 4 hours.
86
What are limitations of gastric-emptying scintigraphy?
Low sensitivity for mild gastroparesis, potential overdiagnosis in women, intraindividual variation, test meal may not reflect actual meals
## Footnote
Physiologic delay of gastric emptying may occur in women.
87
What is diabetes-related distress?
Affective state from worry about adherence to diet, exercise, and blood glucose monitoring, leading to feelings of fear, anxiety, and burnout
## Footnote
It negatively impacts diabetes management and outcomes.
88
How does diabetes-related distress correlate with patient demographics?
Higher in younger patients, females, nonwhite patients, patients with higher BMI, and insulin-treated patients
## Footnote
Level of distress not associated with duration of diabetes.
89
How common is depression in people with diabetes?
Two to three times more common than in the general population
## Footnote
Depression may be a risk factor for developing diabetes.
90
What is the pooled relative risk for developing depression in individuals with preexisting diabetes?
1.15
## Footnote
Depression is linked to an increased risk of developing diabetes by up to 60%.
91
What are standard measures for the prevention of atherosclerotic cardiovascular disease (ASCVD) in persons with diabetes?
Smoking cessation, lowering blood pressure, lowering LDL cholesterol levels, regular physical activity, and a healthy dietary pattern
## Footnote
Healthy dietary patterns emphasize intake of fruits and vegetables, reduced saturated fat, and low-fat dairy products. The Mediterranean diet and the DASH diet align with these recommendations.
92
What is the recommended intensity of LDL lowering for individuals with diabetes compared to those without?
Greater for individuals with diabetes
## Footnote
This is in comparison to individuals of low to moderate ASCVD risk without diabetes.
93
What dietary patterns are recommended for the prevention of ASCVD in persons with diabetes?
Mediterranean diet, DASH diet
## Footnote
Both diets emphasize fruits, vegetables, and low saturated fat.
94
What is the recommended daily dosage of low-dose aspirin for individuals with a 10-year ASCVD risk of ≥ 10%?
75–162 mg per day
## Footnote
This measure is part of additional preventive strategies.
95
Should individuals with diabetes be screened for coronary artery disease and peripheral arterial disease?
Yes
## Footnote
Screening methods include resting electrocardiography, ankle-brachial index, and electron beam CT for CAC score.
96
What are reasonable screening choices for assessing coronary artery disease (CAD) and peripheral arterial disease (PAD)?
Resting electrocardiography, ankle-brachial index, electron beam CT for CAC score
## Footnote
Stress myocardial perfusion imaging is not indicated in asymptomatic individuals at low or intermediate ASCVD risk.
97
What are the cornerstones of secondary ASCVD prevention in individuals with diabetes?
Smoking cessation, regular physical activity, heart-healthy diet, weight loss, good blood pressure control, statin and aspirin use
## Footnote
Glucose-lowering therapy with ASCVD risk reduction agents should also be considered.
98
What landmark trials demonstrated the importance of good glycemic control in preventing diabetic microvascular complications?
DCCT/EDIC, UKPDS
## Footnote
These trials also showed a legacy effect on macrovascular complications.
99
What recent trials confirmed the importance of good glycemic control for preventing microvascular complications, particularly kidney disease?
ACCORD, ADVANCE
## Footnote
These trials highlighted the significance of glycemic control in diabetes management.
100
What was the primary outcome of the ACCORD trial regarding intensive glycemic control?
No difference in three-point major adverse cardiovascular event (MACE) rates
## Footnote
MACE includes nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascular causes.
101
What was a significant finding regarding mortality in the ACCORD trial's intensive treatment group?
Increased all-cause mortality, primarily due to cardiovascular-related death
## Footnote
The trial was stopped early due to these findings.
102
What relationship was observed between hemoglobin A1c (HbA1c) and mortality in the intensive treatment group of the ACCORD trial?
Higher risk for mortality in subjects with baseline HbA1c > 8.5%
## Footnote
This suggests that achieving target glycemia is crucial.
103
What were the outcomes of the ADVANCE and VADT trials in terms of intensive glycemic control?
Did not show increased mortality or adverse cardiovascular outcomes but also did not show improved cardiovascular outcomes
## Footnote
This was observed in patients with longstanding type 2 diabetes.
104
Fill in the blank: The Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications (DCCT/EDIC) demonstrated the importance of good _______ in preventing diabetic microvascular complications.
glycemic control
105
True or False: Intensive glycemic control is always beneficial for preventing cardiovascular events in individuals with diabetes.
False
## Footnote
The ACCORD trial showed increased mortality in the intensive treatment group.
106
What are the basic principles of diabetic ketoacidosis (DKA) management?
1. Volume repletion
2. Correction of electrolyte abnormalities
3. Insulin therapy for hyperglycemia and ketonemia
4. Identification and treatment of precipitating event(s)
107
Under what conditions can patients be transitioned off intravenous insulin infusion in DKA?
When:
* Acidemia and elevated anion gap have resolved
* Patient is clinically improved and can tolerate oral intake
* Precipitating causes have been addressed
* Insulin infusion rate has been stable for at least 6 hours at 2-3 units/hr or lower
* Glucose is well-controlled
108
What are the key differences between DKA and hyperglycemic hyperosmolar state (HHS)?
DKA:
* Significantly acidemic
* Ketonemia present
* Elevated anion gap
HHS:
* Little to no ketones
* Normal serum bicarbonate levels
* Serum osmolality > 320 mOsm/kg
* Severe hyperglycemia (glucose > 600 mg/dL)
109
What serum osmolality is indicative of hyperglycemic hyperosmolar state (HHS)?
Serum osmolality > 320 mOsm/kg
110
What is hypoglycemia unawareness?
Occurs when a patient has had recurrent hypoglycemia, lowering glucose levels and triggering the release of counterregulatory hormones
111
How can hypoglycemia unawareness be reversed?
By strict avoidance of hypoglycemia for a period (weeks to months)
112
What does hypoglycemia-associated autonomic failure (HAAF) consist of?
Hypoglycemia unawareness and impaired counterregulatory hormone responses
113
What are the manifestations of diabetic kidney disease (DKD)?
1. Albuminuria
2. Decreased glomerular filtration rate (GFR)
3. Glomerular hematuria
4. Other abnormalities of urinary sediment
5. Abnormalities on imaging studies
114
How do diabetic neuropathies progress?
Sensory and autonomic neuropathies progress gradually, while mononeuropathies, radiculopathies, and acute painful neuropathies present acutely and resolve completely
115
What is the best strategy for prevention of ASCVD in patients with diabetes?
1. Smoking cessation
2. Regular physical activity
3. Heart-healthy diet
4. Weight loss (if needed)
5. Statin and aspirin use
6. Good blood pressure control
7. Glucose-lowering agent for high-risk patients or those with established ASCVD
