Diabetes mellitus Flashcards
1
Q
What is the prevalence of Diabetes Mellitus (DM) in Mexico in 2018?
A
The prevalence of DM in Mexico in 2018 was approximately 13.7% of the adult population.
2
Q
What was the DM mortality rate in Mexico from 2011 to 2020 per 10,000 people?
A
The DM mortality rate in Mexico from 2011 to 2020 was 7.5 deaths per 10,000 people.
3
Q
How is Diabetes Mellitus (DM) defined?
A
DM is a chronic condition characterized by hyperglycemia (elevated blood glucose levels).
4
Q
What are the four main classifications of Diabetes Mellitus?
A
Type 1 Diabetes
Type 2 Diabetes
Gestational Diabetes
Other specific types (e.g., monogenic diabetes).
5
Q
What causes Type 1 Diabetes (DM1)?
A
DM1 is caused by autoimmune destruction of pancreatic β-cells by lymphocytes, often triggered by genetic and environmental factors (e.g., viruses like Coxsackie, Rubella, or nutrients like cow milk).
6
Q
What are the key tissues involved in glucose regulation, and how does insulin affect them?
A
Adipose Tissue: Insulin increases glucose uptake and lipogenesis, decreases lipolysis.
Muscle: Insulin increases glucose uptake, glycogen synthesis, and protein synthesis.
Liver: Insulin decreases gluconeogenesis and increases glycogen synthesis and lipogenesis.
7
Q
What are the acute complications of Diabetes Mellitus?
A
Hypoglycemia
Diabetic Ketoacidosis (DKA)
Non-Ketotic Hyperosmolar State.
8
Q
What are the chronic microvascular complications of DM?
A
Retinopathy
Neuropathy
Nephropathy.
9
Q
What are the diagnostic criteria for DM according to the ADA?
A
Fasting glucose ≥ 126 mg/dL
Postprandial glucose ≥ 200 mg/dL
HbA1c ≥ 6.5%.
10
Q
What are the treatment goals for Diabetes Mellitus?
A
Reduce symptoms
Prevent acute and chronic complications
Delay disease progression.
11
Q
What are the two main types of DM treatment?
A
Non-Pharmacological: Diet, exercise, and avoiding precipitating factors.
Pharmacological: Oral hypoglycemics and insulin therapy.
12
Q
What is the mechanism of action of Sulfonylureas?
A
Sulfonylureas stimulate insulin secretion by closing K+ ATP channels in pancreatic β-cells, leading to cell depolarization, calcium influx, and insulin release.
13
Q
What are the adverse effects of Metformin (a Biguanide)?
A
The main adverse effect is lactic acidosis, though it is rare.
14
Q
How do Thiazolidinediones (TZDs) work?
A
TZDs bind to PPARγ receptors, increasing insulin sensitivity in adipose tissue, muscle, and liver, and reducing free fatty acids and TNF-α.
15
Q
What is the mechanism of DPP-4 inhibitors?
A
DPP-4 inhibitors increase incretin levels (e.g., GLP-1), which enhances insulin release and suppresses glucagon secretion.
16
Q
What are the benefits of GLP-1 agonists?
A
GLP-1 agonists increase insulin release, suppress glucagon, delay gastric emptying, and promote weight loss.
17
Q
How do SGLT-2 inhibitors work?
A
SGLT-2 inhibitors block glucose reabsorption in the kidneys, increasing urinary glucose excretion and lowering blood glucose levels.
18
Q
What are the types of insulin based on duration of action?
A
Rapid-acting: Starts in 5-10 mins, peaks in 30-90 mins, lasts 2-5 hours.
Short-acting: Starts in 30-60 mins, peaks in 2-5 hours, lasts 6-8 hours.
Intermediate-acting: Starts in 1-2 hours, peaks in 4-12 hours, lasts 12-18 hours.
Long-acting: Starts in 1-2 hours, no peak, lasts up to 24 hours.
19
Q
What are the symptoms of diabetic neuropathy?
A
Burning pain in feet and hands (glove and stocking distribution).
Paresthesias, dysesthesias, and allodynia.
20
Q
What is Charcot foot, and how is it treated?
A
Charcot foot is a progressive foot deformity due to neuropathy. Treatment includes immobilization, non-weight-bearing, and custom footwear. Surgery is reserved for severe cases.
21
Q
What is the goal for HbA1c in diabetic patients?
A
The goal is < 7% for most patients.
22
Q
What are the key pathways involved in diabetic complications?
A
Polyol pathway
Protein kinase pathway
Hexosamine pathway.
23
Q
What is the osmolarity range in a non-ketotic hyperosmolar state?
A
Osmolarity is typically > 320 mOsm/kg, with normal range being 280-300 mOsm/kg.
24
Q
What is Monckeberg’s sign in diabetes?
A
Monckeberg’s sign refers to calcification of medium-sized arteries, often seen in diabetic patients.
25
What is the prevalence of DM in 2018 per state in Mexico?
The prevalence of DM varied by state in Mexico in 2018, with the highest rates in states like Campeche, Tamaulipas, and Hidalgo (over 14%), and the lowest in Chiapas and Quintana Roo (below 10%).
26
What is the mortality rate of DM per state in Mexico?
DM mortality rates per state in Mexico ranged from 6.5 to 9.2 deaths per 10,000 people, with higher rates in northern and central states like Nuevo León, Veracruz, and Mexico City.
27
What are the environmental factors linked to Type 1 Diabetes (DM1)?
Environmental factors for DM1 include viral infections (e.g., Coxsackie, Rubella) and dietary factors (e.g., early exposure to cow milk).
28
What are the key differences between Type 1 and Type 2 Diabetes?
Type 1: Autoimmune, insulin deficiency, often diagnosed in childhood.
Type 2: Insulin resistance, associated with obesity, usually diagnosed in adults.
29
What are the symptoms of Diabetes Mellitus?
Polyuria (excessive urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Fatigue
Blurred vision.
30
What are the macrovascular complications of DM?
Coronary artery disease
Cardiovascular disease (CVD)
Peripheral vascular disease.
31
What is the role of HbA1c in DM diagnosis and management?
HbA1c reflects average blood glucose levels over 2-3 months. It is used for diagnosis (≥ 6.5%) and monitoring (goal < 7%).
32
What are the non-pharmacological treatments for DM?
Diet: Low-carb, high-fiber, balanced meals.
Exercise: Regular physical activity to improve insulin sensitivity.
Lifestyle changes: Weight management and smoking cessation.
33
What are the adverse effects of Sulfonylureas?
The main adverse effect is hypoglycemia, especially in elderly patients or those with irregular eating habits.
34
What is the mechanism of action of Meglitinides?
Meglitinides stimulate rapid, short-acting insulin secretion by closing K+ ATP channels in pancreatic β-cells, similar to Sulfonylureas but with a faster onset and shorter duration.
35
What are the adverse effects of Thiazolidinediones (TZDs)?
Edema (fluid retention)
Anemia
Arthralgia (joint pain)
Increased risk of heart failure.
36
What is the mechanism of α-Glucosidase Inhibitors?
They inhibit brush border enzymes in the small intestine, delaying carbohydrate absorption and reducing postprandial glucose spikes.
37
What are the adverse effects of DPP-4 Inhibitors?
Hypoglycemia (rare)
Headache
Upper respiratory tract infections.
38
What are the benefits of SGLT-2 Inhibitors?
Lower blood glucose levels by increasing urinary glucose excretion.
Promote weight loss.
Provide cardiovascular and renal benefits.
39
What are the adverse effects of SGLT-2 Inhibitors?
Genitourinary infections
Polyuria (excessive urination)
Dysuria (painful urination).
40
What is the insulin dosage adjustment for hospitalized patients?
Blood glucose 150-200 mg/dL: 2 UI
201-250 mg/dL: 4 UI
251-300 mg/dL: 6 UI
301-350 mg/dL: 8 UI
351-400 mg/dL: 10 UI
≥ 401 mg/dL: 12 UI.
41
What are the goals for blood glucose levels in DM management?
Fasting: 80-110 mg/dL
Postprandial: < 140 mg/dL
HbA1c: < 7%.
42
What is the polyol pathway, and how does it contribute to diabetic complications?
The polyol pathway converts glucose to sorbitol, leading to osmotic stress and oxidative damage in nerves, kidneys, and eyes, contributing to neuropathy, nephropathy, and retinopathy.
43
What are the symptoms of diabetic retinopathy?
Blurred vision
Floaters
Gradual vision loss
In severe cases, blindness.
44
What is the clinical severity stratification for diabetic neuropathy (Boulton classification)?
Stage 0: No neuropathy
Stage 1: Asymptomatic neuropathy
Stage 2: Symptomatic neuropathy
Stage 3: Disabling neuropathy.
45
What is the treatment for painful diabetic neuropathy?
Medications: Gabapentin, pregabalin, duloxetine, or tricyclic antidepressants.
Lifestyle changes: Blood sugar control, foot care, and physical therapy.
46
What are the key features of Charcot foot?
Early stage: Warm, swollen, red foot (often mistaken for infection).
Late stage: Joint deformities, rocker-bottom foot, and ulcers.
Pain: Usually absent or mild despite severe damage.
47
What is the role of the hexosamine pathway in diabetic complications?
The hexosamine pathway contributes to insulin resistance and cellular damage by altering protein function through excessive O-GlcNAcylation.
48
What is the significance of the protein kinase pathway in DM complications?
Activation of protein kinase C (PKC) leads to vascular damage, inflammation, and oxidative stress, contributing to retinopathy, nephropathy, and cardiovascular disease.
49
What is the mechanism of action of GLP-1 agonists?
GLP-1 agonists mimic endogenous GLP-1, increasing insulin release, suppressing glucagon, delaying gastric emptying, and promoting satiety.
50
What are the adverse effects of GLP-1 agonists?
Hypoglycemia
Pancreatitis
Nausea, vomiting, and diarrhea.
51
What is the significance of the non-ketotic hyperosmolar state in DM?
It is a life-threatening condition characterized by severe hyperglycemia and dehydration, often seen in Type 2 DM patients, with osmolarity > 320 mOsm/kg.
52
What is the role of OTSR in neurological evaluation for diabetic neuropathy?
OTSR (Osteotendinous Reflexes) are used to assess nerve function and reflex integrity in patients with diabetic neuropathy.
53
What are the key features of symmetrical distal polyneuropathy?
Symptoms: Burning pain, paresthesias, and numbness in a 'glove and stocking' distribution.
Progression: Starts in the feet and moves upward.
54
What are the key features of autonomic neuropathy in DM?
Cardiovascular: Orthostatic hypotension, resting tachycardia.
Gastrointestinal: Gastroparesis, constipation, or diarrhea.
Genitourinary: Erectile dysfunction, bladder dysfunction.
55
What is the significance of the rocker-bottom foot in Charcot foot?
The rocker-bottom foot is a severe deformity caused by midfoot collapse, leading to instability and increased risk of ulcers.
56
What is the prevalence of DM in 2018 per state in Mexico?
The prevalence of DM varied by state in Mexico in 2018, with the highest rates in states like Campeche, Tamaulipas, and Hidalgo (over 14%), and the lowest in Chiapas and Quintana Roo (below 10%).
57
What is the mortality rate of DM per state in Mexico?
DM mortality rates per state in Mexico ranged from 6.5 to 9.2 deaths per 10,000 people, with higher rates in northern and central states like Nuevo León, Veracruz, and Mexico City.
58
What are the environmental factors linked to Type 1 Diabetes (DM1)?
Environmental factors for DM1 include viral infections (e.g., Coxsackie, Rubella) and dietary factors (e.g., early exposure to cow milk).
59
What are the key differences between Type 1 and Type 2 Diabetes?
Type 1: Autoimmune, insulin deficiency, often diagnosed in childhood.
Type 2: Insulin resistance, associated with obesity, usually diagnosed in adults.
60
What are the symptoms of Diabetes Mellitus?
Polyuria (excessive urination)
Polydipsia (excessive thirst)
Polyphagia (excessive hunger)
Weight loss
Fatigue
Blurred vision.
61
What are the macrovascular complications of DM?
Coronary artery disease
Cardiovascular disease (CVD)
Peripheral vascular disease.
62
What is the role of HbA1c in DM diagnosis and management?
HbA1c reflects average blood glucose levels over 2-3 months. It is used for diagnosis (≥ 6.5%) and monitoring (goal < 7%).
63
What are the non-pharmacological treatments for DM?
Diet: Low-carb, high-fiber, balanced meals.
Exercise: Regular physical activity to improve insulin sensitivity.
Lifestyle changes: Weight management and smoking cessation.
64
What are the adverse effects of Sulfonylureas?
The main adverse effect is hypoglycemia, especially in elderly patients or those with irregular eating habits.
65
What is the mechanism of action of Meglitinides?
Meglitinides stimulate rapid, short-acting insulin secretion by closing K+ ATP channels in pancreatic β-cells, similar to Sulfonylureas but with a faster onset and shorter duration.
66
What are the adverse effects of Thiazolidinediones (TZDs)?
Edema (fluid retention)
Anemia
Arthralgia (joint pain)
Increased risk of heart failure.
67
What is the mechanism of α-Glucosidase Inhibitors?
They inhibit brush border enzymes in the small intestine, delaying carbohydrate absorption and reducing postprandial glucose spikes.
68
What are the adverse effects of DPP-4 Inhibitors?
Hypoglycemia (rare)
Headache
Upper respiratory tract infections.
69
What are the benefits of SGLT-2 Inhibitors?
Lower blood glucose levels by increasing urinary glucose excretion.
Promote weight loss.
Provide cardiovascular and renal benefits.
70
What are the adverse effects of SGLT-2 Inhibitors?
Genitourinary infections
Polyuria (excessive urination)
Dysuria (painful urination).
71
What is the insulin dosage adjustment for hospitalized patients?
Blood glucose 150-200 mg/dL: 2 UI
201-250 mg/dL: 4 UI
251-300 mg/dL: 6 UI
301-350 mg/dL: 8 UI
351-400 mg/dL: 10 UI
≥ 401 mg/dL: 12 UI.
72
What are the goals for blood glucose levels in DM management?
Fasting: 80-110 mg/dL
Postprandial: < 140 mg/dL
HbA1c: < 7%.
73
What is the polyol pathway, and how does it contribute to diabetic complications?
The polyol pathway converts glucose to sorbitol, leading to osmotic stress and oxidative damage in nerves, kidneys, and eyes, contributing to neuropathy, nephropathy, and retinopathy.
74
What are the symptoms of diabetic retinopathy?
Blurred vision
Floaters
Gradual vision loss
In severe cases, blindness.
75
What is the clinical severity stratification for diabetic neuropathy (Boulton classification)?
Stage 0: No neuropathy
Stage 1: Asymptomatic neuropathy
Stage 2: Symptomatic neuropathy
Stage 3: Disabling neuropathy.
76
What is the treatment for painful diabetic neuropathy?
Medications: Gabapentin, pregabalin, duloxetine, or tricyclic antidepressants.
Lifestyle changes: Blood sugar control, foot care, and physical therapy.
77
What are the key features of Charcot foot?
Early stage: Warm, swollen, red foot (often mistaken for infection).
Late stage: Joint deformities, rocker-bottom foot, and ulcers.
Pain: Usually absent or mild despite severe damage.
78
What is the role of the hexosamine pathway in diabetic complications?
The hexosamine pathway contributes to insulin resistance and cellular damage by altering protein function through excessive O-GlcNAcylation.
79
What is the significance of the protein kinase pathway in DM complications?
Activation of protein kinase C (PKC) leads to vascular damage, inflammation, and oxidative stress, contributing to retinopathy, nephropathy, and cardiovascular disease.
80
What is the mechanism of action of GLP-1 agonists?
GLP-1 agonists mimic endogenous GLP-1, increasing insulin release, suppressing glucagon, delaying gastric emptying, and promoting satiety.
81
What are the adverse effects of GLP-1 agonists?
Hypoglycemia
Pancreatitis
Nausea, vomiting, and diarrhea.
82
What is the significance of the non-ketotic hyperosmolar state in DM?
It is a life-threatening condition characterized by severe hyperglycemia and dehydration, often seen in Type 2 DM patients, with osmolarity > 320 mOsm/kg.
83
What is the role of OTSR in neurological evaluation for diabetic neuropathy?
OTSR (Osteotendinous Reflexes) are used to assess nerve function and reflex integrity in patients with diabetic neuropathy.
84
What are the key features of symmetrical distal polyneuropathy?
Symptoms: Burning pain, paresthesias, and numbness in a 'glove and stocking' distribution.
Progression: Starts in the feet and moves upward.
85
What are the key features of autonomic neuropathy in DM?
Cardiovascular: Orthostatic hypotension, resting tachycardia.
Gastrointestinal: Gastroparesis, constipation, or diarrhea.
Genitourinary: Erectile dysfunction, bladder dysfunction.
86
What is the mechanism of action of Sulfonylureas?
Sulfonylureas stimulate insulin secretion by closing K+ ATP channels in pancreatic β-cells, leading to cell depolarization, calcium influx, and insulin release.
## Footnote
Example: Glibenclamide 5 mg. Max Dose: 15 mg/day. Adverse Effects: Hypoglycemia.
87
What is the mechanism of action of Meglitinides?
Meglitinides stimulate rapid, short-acting insulin secretion by closing K+ ATP channels in pancreatic β-cells.
## Footnote
Example: Repaglinide 1-2 mg. Max Dose: 16 mg/day. Adverse Effects: Hypoglycemia.
88
What is the mechanism of action of Biguanides?
Biguanides increase glycolysis (glucose breakdown), decrease gluconeogenesis (glucose production in the liver), and decrease glucose absorption in the intestines.
## Footnote
Example: Metformin 500-850 mg. Max Dose: 2 g/day. Adverse Effects: Lactic acidosis (rare), gastrointestinal upset.
89
What is the mechanism of action of Thiazolidinediones (TZDs)?
TZDs bind to PPARγ receptors, increasing insulin sensitivity in adipose tissue, muscle, and liver. They also decrease free fatty acids and TNF-α.
## Footnote
Example: Pioglitazone 15-45 mg. Max Dose: 45 mg/day. Adverse Effects: Edema, anemia, weight gain, increased risk of heart failure.
90
What is the mechanism of action of α-Glucosidase Inhibitors?
They inhibit brush border enzymes in the small intestine, delaying carbohydrate absorption and reducing postprandial glucose spikes.
## Footnote
Example: Acarbose 500 mg. Max Dose: 600 mg/day. Adverse Effects: Flatulence, diarrhea, abdominal discomfort.
91
What is the mechanism of action of DPP-4 Inhibitors?
DPP-4 inhibitors increase incretin levels (e.g., GLP-1), which enhances insulin release and suppresses glucagon secretion.
## Footnote
Example: Sitagliptin 100 mg. Max Dose: 100 mg/day. Adverse Effects: Hypoglycemia (rare), headache, upper respiratory infections.
92
What is the mechanism of action of GLP-1 Agonists?
GLP-1 agonists mimic endogenous GLP-1, leading to increased insulin release, suppressed glucagon secretion, delayed gastric emptying, and promoted satiety.
## Footnote
Example: Liraglutide 0.6-1.8 mg. Max Dose: 1.8 mg/day. Adverse Effects: Nausea, vomiting, diarrhea, pancreatitis (rare).
93
What is the mechanism of action of SGLT-2 Inhibitors?
SGLT-2 inhibitors block glucose reabsorption in the kidneys, increasing urinary glucose excretion and lowering blood glucose levels.
## Footnote
Example: Dapagliflozin 10 mg. Max Dose: 10 mg/day. Adverse Effects: Genitourinary infections, polyuria, dehydration.
94
What are the insulin types based on duration of action?
Rapid-acting: Starts in 5-10 mins, peaks in 30-90 mins, lasts 2-5 hours (e.g., Insulin Lispro).
Short-acting: Starts in 30-60 mins, peaks in 2-5 hours, lasts 6-8 hours (e.g., Regular Insulin).
Intermediate-acting: Starts in 1-2 hours, peaks in 4-12 hours, lasts 12-18 hours (e.g., NPH Insulin).
Long-acting: Starts in 1-2 hours, no peak, lasts up to 24 hours (e.g., Insulin Glargine).
95
What is the insulin dosage adjustment for ambulatory patients?
Start with 0.2-0.6 U/kg/day. Increase by 2-4 units every 3 days based on blood glucose levels.
96
What are the adverse effects of insulin therapy?
Hypoglycemia, weight gain, injection site reactions (e.g., lipodystrophy), allergic reactions (rare).
97
What is the mechanism of action of Sulfonylureas at the cellular level?
Bind to SUR receptors on pancreatic β-cells, close K+ ATP channels, causing cell depolarization, open voltage-dependent Ca2+ channels, increasing intracellular Ca2+, and trigger insulin secretion.
98
What are the secondary pathways involved in Sulfonylureas' mechanism of action?
cAMP pathway: Enhances insulin secretion.
Epac2/Rap1 pathway: Modulates insulin release.
Adrenergic and incretin pathways: Influence β-cell function.
99
What are the key benefits of SGLT-2 Inhibitors beyond glucose control?
Weight loss due to calorie excretion in urine, cardiovascular benefits: Reduced risk of heart failure, renal protection: Slows progression of kidney disease.
100
What are the key differences between GLP-1 Agonists and DPP-4 Inhibitors?
GLP-1 Agonists: Mimic GLP-1 directly, stronger effect, injectable, promote weight loss.
DPP-4 Inhibitors: Increase endogenous GLP-1, oral, moderate effect, weight-neutral.
101
What are the key adverse effects of Thiazolidinediones (TZDs)?
Edema (fluid retention), weight gain, increased risk of heart failure, bone fractures (long-term use).
102
What are the key adverse effects of Metformin?
Gastrointestinal upset (nausea, diarrhea), vitamin B12 deficiency (long-term use), lactic acidosis (rare, but serious).
103
What are the key adverse effects of GLP-1 Agonists?
Nausea and vomiting, diarrhea, pancreatitis (rare), hypoglycemia (when combined with insulin or sulfonylureas).
104
What are the key adverse effects of SGLT-2 Inhibitors?
Genitourinary infections (e.g., yeast infections), polyuria (excessive urination), dehydration and hypotension, diabetic ketoacidosis (rare).
105
What are the key adverse effects of α-Glucosidase Inhibitors?
Flatulence (gas), diarrhea, abdominal discomfort.
