TREATMENT AND COMPLICATIONS OF DIABETES 1.2 Flashcards
1
Q
What is diabetes mellitus?
A
“A chronic metabolic disorder characterized by hyperglycemia due to defects in insulin secretion. action or both.”
2
Q
What are the main types of diabetes?
A
“Type 1. Type 2.Gestational and Other specific types.”
3
Q
What causes Type 1 diabetes?
A
“Autoimmune destruction of pancreatic beta cells leading to absolute insulin deficiency.”
4
Q
What causes Type 2 diabetes?
A
“Insulin resistance and relative insulin deficiency due to genetic and lifestyle factors.”
5
Q
What is gestational diabetes?
A
“Glucose intolerance diagnosed during pregnancy that usually resolves postpartum.”
6
Q
What are classic symptoms of diabetes?
A
“Polyuria. polydipsia. polyphagia and unexplained weight loss.”
7
Q
What is HbA1c and its diagnostic cutoff for diabetes?
A
“Glycated hemoglobin; ≥6.5% indicates diabetes.”
8
Q
What is the fasting plasma glucose (FPG) diagnostic cutoff for diabetes?
A
“≥126 mg/dL (7.0 mmol/L) on two separate occasions.”
9
Q
What is the 2-hour plasma glucose cutoff in an OGTT for diabetes?
A
“≥200 mg/dL (11.1 mmol/L) after a 75g glucose load.”
10
Q
What is the random plasma glucose cutoff for diabetes diagnosis?
A
“≥200 mg/dL (11.1 mmol/L) with symptoms of hyperglycemia.”
11
Q
What is the preferred initial treatment for Type 2 diabetes?
A
“Lifestyle modifications and metformin.”
12
Q
What is the mechanism of action of metformin?
A
“Decreases hepatic glucose production and increases insulin sensitivity.”
13
Q
What are the side effects of metformin?
A
“GI upset (diarrhea, nausea) and lactic acidosis (rare).”
14
Q
What are the rapid-acting insulins?
A
“Lispro. Aspart. Glulisine.”
15
Q
What are the long-acting insulins?
A
“Glargine. Detemir. Degludec.”
16
Q
What is diabetic ketoacidosis (DKA)?
A
“A life-threatening complication of diabetes characterized by hyperglycemia, ketosis, and metabolic acidosis.”
17
Q
What are signs and symptoms of DKA?
A
“Kussmaul respiration. fruity breath. dehydration. altered mental status.”
18
Q
What is the treatment for DKA?
A
“IV fluids. insulin. potassium replacement and correction of acidosis.”
19
Q
What is hyperosmolar hyperglycemic state (HHS)?
A
“Severe hyperglycemia without ketosis. leading to dehydration and altered mental status.”
20
Q
What is the Somogyi effect?
A
“Rebound hyperglycemia due to nocturnal hypoglycemia triggering counterregulatory hormones.”
21
Q
What is the Dawn phenomenon?
A
“Early morning hyperglycemia due to reduced insulin sensitivity and increased cortisol.”
22
Q
What are microvascular complications of diabetes?
A
“Retinopathy. nephropathy and neuropathy.”
23
Q
What are macrovascular complications of diabetes?
A
“Cardiovascular disease. stroke and peripheral artery disease.”
24
Q
What is the first-line treatment for diabetic nephropathy?
A
“ACE inhibitors or ARBs to reduce proteinuria and protect kidneys.”
25
What screening tests are recommended for diabetic complications?
"Annual eye exams. urine albumin-to-creatinine ratio. foot exams and lipid panels."
26
What is the target HbA1c for most diabetics?
"<7.0% to reduce complications."
27
What is the mechanism of action of sulfonylureas?
"Stimulate insulin release from pancreatic beta cells."
28
What are the side effects of sulfonylureas?
"Hypoglycemia and weight gain."
29
What is the mechanism of action of GLP-1 receptor agonists?
"Increase insulin secretion. decrease glucagon. slow gastric emptying and promote weight loss."
30
What is the mechanism of action of SGLT2 inhibitors?
"Block glucose reabsorption in the kidneys. leading to glycosuria and reduced blood glucose."
31
What is neuropathy?
A heterogeneous condition with diverse clinical manifestations, occurring in ~50% of individuals with long-standing type 1 and type 2 diabetes.
32
What are the types of diabetic neuropathy?
Diffuse neuropathy (distal symmetrical polyneuropathy and/or autonomic neuropathy), mononeuropathy, radiculopathy/polyradiculopathy.
33
What factors correlate with diabetic neuropathy?
Duration of diabetes, glycemic control, BMI, smoking, cardiovascular disease, hypertriglyceridemia, hypertension.
34
What is the most common type of diabetic neuropathy?
Distal Symmetric Polyneuropathy (DSPN).
35
What are the clinical features of distal symmetric polyneuropathy?
Distal sensory loss, pain, classic 'stock-glove' sensory loss, numbness, tingling, sharpness, burning, hyperalgesia, paresthesia, dysesthesia.
36
What physical exam findings suggest DSPN?
Loss of ankle deep-tendon reflexes, abnormal position sense, muscular atrophy or foot drop.
37
Why is DSPN a major concern?
It increases the risk of foot ulceration and falls due to loss of protective sensation.
38
How is DSPN screened?
Annually, 5 years after diagnosis of type 1 DM, at the time of diagnosis of type 2 DM.
39
What is autonomic neuropathy?
Autonomic dysfunction involving the parasympathetic and sympathetic systems, affecting multiple organ systems.
40
What are cardiovascular manifestations of autonomic neuropathy?
Decreased heart rate variability, resting tachycardia, orthostatic hypotension.
41
What is gastroparesis?
Delayed gastric emptying leading to anorexia, nausea, vomiting, early satiety, and bloating.
42
What are genitourinary symptoms of autonomic neuropathy?
Bladder emptying abnormalities, erectile dysfunction, retrograde ejaculation, neurogenic bladder.
43
What is hypoglycemia unawareness?
A condition where autonomic dysfunction reduces counter-regulatory hormone release, preventing the detection of hypoglycemia.
44
What is mononeuropathy?
Atypical form of neuropathy affecting isolated cranial or peripheral nerves (CN 3 & 6) or presenting as mononeuritis multiplex.
45
What is radiculopathy/polyradiculopathy?
Radiculo-plexus neuropathy or thoracic radiculopathy.
46
What are the key management strategies for diabetic neuropathy?
Improved glycemic control, avoidance of neurotoxins (alcohol, smoking), vitamin supplementation (B12, folate), patient education, and pharmacologic treatment (duloxetine, pregabalin, gabapentin, TCAs, venlafaxine, carbamazepine, tramadol, capsaicin).
47
What are the primary GI symptoms of diabetic autonomic neuropathy?
Gastroparesis (delayed gastric emptying), constipation, diarrhea, GERD.
48
What is the preferred management for gastroparesis?
Smaller, more frequent meals, low-fat and low-fiber diet, avoiding opioids and GLP-1 receptor agonists, metoclopramide for severe cases, H2RAs/PPIs for GERD.
49
What is diabetic cystopathy?
A progressive bladder dysfunction leading to urinary hesitancy, incontinence, and recurrent UTIs due to poor bladder contractility.
50
What is the leading cause of nontraumatic lower extremity amputation in the U.S.?
Diabetes mellitus.
51
What factors contribute to diabetic foot ulcers?
Neuropathy, abnormal foot biomechanics, PAD, poor wound healing, repeated minor trauma.
52
What are risk factors for diabetic foot ulcers?
Male gender, diabetes duration >10 years, peripheral neuropathy, foot abnormalities, PAD, smoking, poor glycemic control, diabetic nephropathy.
53
What is the most common site of diabetic foot ulcers?
Plantar surface of the foot.
54
What is the Wagner Classification used for?
Classifying diabetic foot ulcers and guiding management.
55
What are common infections in diabetics?
Rhinocerebral mucormycosis, emphysematous infections, 'malignant' otitis externa, bacterial infections.
56
What vaccinations are recommended for diabetics?
Pneumococcus, annual influenza, SARS-CoV-2 vaccine.
57
What is the most common dermatologic manifestation of diabetes?
Xerosis and pruritus.
58
What is diabetic dermopathy?
Pigmented pretibial papules, also known as 'diabetic skin spots,' resulting from minor mechanical trauma.
59
What is acanthosis nigricans?
Hyperpigmented velvety plaques on the neck, axilla, or extensor surfaces, associated with severe insulin resistance.
60
What are the acute complications of severe hyperglycemia?
Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS).
61
What is the most common precipitating factor for DKA/HHS?
Infection.
62
What differentiates DKA from HHS?
DKA presents with metabolic acidosis and ketosis, while HHS has severe hyperglycemia, increased serum osmolality, and marked volume depletion.
63
What are the key therapeutic goals in managing DKA/HHS?
Restore circulatory volume, normalize glucose and plasma osmolality, clear ketones, correct electrolyte imbalances, treat underlying causes.
64
What is the formula for calculating serum osmolality?
2(Na) + (BUN/2.8) + (Glucose/18).
65
What medications should be considered for cardiovascular protection in diabetics?
ACE inhibitors, ARBs, statins, aspirin, beta-blockers (post-MI), SGLT-2 inhibitors, GLP-1 receptor agonists.
66
What is the blood pressure target for diabetics?
Generally <130/80 mmHg.
67
What lipid-lowering therapy is recommended for diabetics with CVD?
High-intensity statin therapy (atorvastatin, rosuvastatin), possibly ezetimibe or PCSK9 inhibitors if LDL goals are not met.
68
What is the first-line antihypertensive for diabetics?
ACE inhibitors or ARBs, often combined with beta-blockers, thiazide diuretics, or calcium channel blockers.
69
What are the primary macrovascular complications of diabetes?
Coronary artery disease, myocardial infarction, stroke, peripheral artery disease.
70
What nonpharmacologic measures help reduce cardiovascular risk in diabetics?
Weight loss, exercise, stress management, smoking cessation, dietary changes.
71
What is the underlying pathophysiology of diabetic ketoacidosis (DKA)?
Relative or absolute insulin deficiency combined with counterregulatory hormone excess (glucagon, catecholamines, cortisol, and growth hormone), leading to increased gluconeogenesis, glycogenolysis, and ketone body formation in the liver.
72
What are the key counterregulatory hormones involved in DKA?
Glucagon, catecholamines, cortisol, and growth hormone.
73
What is the endpoint of uncontrolled DKA?
Ketonemia and metabolic acidosis.
74
What are the classic symptoms of DKA?
Nausea, vomiting, abdominal pain, polyuria, polydipsia, shortness of breath.
75
What are the classic signs of DKA?
Kussmaul respirations (deep rapid breathing) and fruity odor on the breath (due to increased acetone).
76
What is a potential complication of DKA, especially in children?
Cerebral edema, often associated with rapid correction of hyperglycemia.
77
What are the main differential diagnoses for DKA?
Starvation ketosis, alcoholic ketoacidosis (bicarbonate usually >15 meq/L), and other forms of increased anion-gap acidosis.
78
What laboratory findings confirm the diagnosis of DKA?
Hyperglycemia (serum glucose >250 mg/dL), ketosis, metabolic acidosis (serum bicarbonate <15-18 mmol/L, increased anion gap).
79
What is a distinguishing lab finding of euglycemic DKA?
Serum glucose may be minimally elevated or even normal.
80
What laboratory abnormalities indicate intravascular volume depletion in DKA?
Elevated BUN and creatinine.
81
What is the purpose of a nitroprusside tablet or stick in DKA diagnosis?
To detect urine ketones, although it primarily detects acetoacetate and not β-hydroxybutyrate.
82
What are the criteria for ICU admission in DKA?
pH <7.00, labored respiration, or impaired level of arousal.
83
What initial fluid therapy is recommended for DKA?
2-3 L of 0.9% saline or lactated Ringer’s over the first 1-3 hours (10-20 mL/kg per hour).
84
What is the initial insulin regimen for DKA?
IV bolus of 0.1 units/kg regular insulin, followed by continuous IV infusion at 0.1 units/kg per hour.
85
When should insulin be withheld in DKA treatment?
If initial serum potassium is <3.3 mmol/L, insulin should be withheld until potassium is corrected.
86
What is the target blood glucose range during DKA management?
8.3-11.1 mmol/L (150-200 mg/dL).
87
What electrolyte levels should be monitored in DKA?
Serum K, Na, Mg, Cl, bicarbonate, phosphate.
88
What are common precipitating factors for DKA?
Infection (pneumonia, UTI, sepsis), inadequate insulin administration, infarction (cerebral, coronary, mesenteric, peripheral), pancreatitis, drugs (e.g., cocaine), pregnancy.
89
What are the main physical exam findings in DKA?
Tachycardia, dehydration, hypotension, tachypnea/Kussmaul respirations, abdominal tenderness, lethargy, obtundation, cerebral edema, possibly coma.
90
What is the major difference between DKA and hyperglycemic hyperosmolar state (HHS)?
DKA involves ketosis and metabolic acidosis, while HHS has severe hyperglycemia and hyperosmolality without significant ketosis or acidosis.
91
What is the pathophysiology of hyperglycemic hyperosmolar state (HHS)?
Relative insulin deficiency leads to increased hepatic glucose production and osmotic diuresis, causing profound dehydration and hyperosmolality.
92
What are the key clinical features of HHS?
Profound dehydration, altered mental status, hypotension, tachycardia, and substantially higher mortality than DKA.
93
What are the hallmark laboratory findings in HHS?
Plasma glucose >1000 mg/dL, hyperosmolality (>350 mOsm/L), prerenal azotemia, minimal or absent acidosis and ketonuria.
94
What is the typical patient profile for HHS?
Elderly patient with type 2 diabetes, several weeks of polyuria, weight loss, and diminished oral intake leading to mental confusion, lethargy, or coma.
95
What are the precipitating factors for HHS?
Serious concurrent illness such as myocardial infarction or stroke.
96
What is the primary management approach for HHS?
Similar to DKA: aggressive fluid replacement, insulin therapy, and treating underlying precipitating factors.
97
Why is dehydration more pronounced in HHS than in DKA?
HHS has a longer duration of illness, leading to more severe fluid losses before diagnosis.
