Diabetes Mellitus Flashcards

1
Q

Diabetes Mellitus: Overview

A

Decreased ability to control blood glucose levels = glucose is primary energy source

Heterogeneous disorder defined by the presence of hyperglycemia and hypoglycemia = dysregulation of plasma glucose

Although type 1 and type 2 diabetes mellitus each have characteristic features, there is some overlap between the two conditions

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2
Q

Type 1 =

A

due to absence of insulin production

no cure

body fails to produce enough insulin

genetics can be a reason for its occurance

require insulin injections for a lifetime

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3
Q

Type 2 =

A

due to cellular insulin resistance

lifestyle changes help

human body resists to produce insulin resistance

insulin is required, oral or injected

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4
Q

Fasting blood glucose

A

no food or fluid for 8+ hours

normal: less than 100 mg/dL
high risk: 100-125 mg/dL
diabetes: 126 mg/dL or higher

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5
Q

Hemoglobin A1c

A

percent of Hgb bound to glucose

normal: less than 5.7%
high risk: 5.7-6.4%
diabetes: 6.5% or higher

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6
Q

Oral Glucose Tolerance Test (OFTT)

A

Adult OGTT Procedure:
Blood draw pre-glucose solution
Drink 8 oz glucose solution
Blood draw 2 hours post

3 tests:
2 hour - adult
2 hour - child
3 hour - pregnancy

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7
Q

OGTT levels and diagnosis

A

less than 140 mg/dL = normal

140 - 199 mg/dL = prediabetes

200 mg/dL or higher = diabetes

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8
Q

2-hour test - adult
OGTT

A

blood drawn before drinking and 2 hours after

8-ounce solution with 75 grams of sugar

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9
Q

2-hour test - child
OGTT

A

blood drawn before drinking and 2 hours after

1.75 grams of sugar per kilogram of body weight

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10
Q

2-hour test - pregnancy
OGTT

A

blood drawn before drinking and at 1, 2, and 3 hours after

8-ounce solution with 100 grams of sugar

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11
Q

Diabetes Mellitus: Diagnostic Criteria

A

A single random glucose level > 200 mg/dL

Two 2-hour (75 g glucose) oral glucose tolerance tests (OGTT) with a level > 200 mg/dL

A fasting glucose level > 126 mg/dL

A1C >6.5%

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12
Q

Important point: Hemoglobin A1C is a determination of ____ and is used for monitoring the disease process

A

the percent of glycosylated hemoglobin

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13
Q

A1C test:

A

a common blood test used to diagnose type 1 and type 2 diabetes and to monitor how well you’re managing your diabetes

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14
Q

A1C test result =

A

reflects your average blood sugar level for the past two to three months

Specifically, the A1C test measures what percentage of your hemoglobin is coated with sugar

The higher your A1C level, the poorer your blood sugar control and the higher your risk of diabetes complications

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15
Q

A1C - Why it’s done

A

Identify prediabetes

Diagnose type 1 and type 2 diabetes

Monitor your diabetes treatment plan

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16
Q

Identify prediabetes

A

If you have prediabetes, you have a higher risk of developing diabetes and cardiovascular disease = early detection

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17
Q

Diagnose type 1 and type 2 diabetes

A

To confirm a diabetes diagnosis in conjunction with glucose tolerance test

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18
Q

Monitor your diabetes treatment plan

A

A1C results are used to establish a baseline A1C level and to monitor therapeutic response to treatment

Example: A1C of 8.5 with diabetes dx = intervention = A1C of 7.5 at 3 month follow up

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19
Q

Higher A1C

A

Higher A1C percentage corresponds to higher average blood sugar levels

Higher A1C levels = higher risk of developing diabetes or complications of diabetes

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20
Q

Normal A1C level:

A

<5.7 percent

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21
Q

A1C level: 5.7 - 6.4 percent

A

prediabetes or impaired fasting glucose = high risk of developing diabetes

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22
Q

A1C level: > 6.5 percent

A

two separate occasions = diabetes

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23
Q

A1C level: > 8 percent

A

diabetes is not well-controlled and higher risk of developing complications of diabetes

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24
Q

For most adults who have diabetes, an A1C level of ____ is a common treatment target.

A

7 percent or less

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25
A1C levels and glucose level
6% = 126 mg/dL 7% = 154 mg/dL 8% = 183 mg/dL 9% = 212 mg/dL 10% = 240 mg/dL 11% = 269 mg/dL 12% = 298 mg/dL
26
symptoms of type 1 diabetes
abnormal thirst and dry mouth frequent urination lack of energy, fatigue blurred vision constant hunger sudden weight lost bed-wetting
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symptoms of type 2 diabetes
excessive thirst and dry mouth frequent and abundant urination lack of energy, extreme tiredness blurred vision recurrent fungal infections of the skin slow healing wounds tingling or numbness in hands and feet
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___ of all cases of diabetes are type 1
5-10%
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___ of all cases of diabetes are type 2
90-95%
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Diabetes Mellitus: Type 1 and Type 2
Worldwide prevalence of type 1 DM and type 2 DM has been increasing over the past three decades = 9.3% in 2019 in adults 20 years or older United States = 13% adults 18 and older
31
Hyperglycemia: Diabetes Mellitus Type 1 and Type 2
Hyperglycemia in all cases is due to a functional deficiency of insulin action Type 1= decrease in insulin secretion by the β cells of the pancreas Type 2 = decreased response to insulin by target tissues insulin resistance Increase in the counter-regulatory hormones = glucagon = oppose the effects of insulin
32
Glucosuria
excretion of glucose in the urine renal threshold for glucose reabsorption (approximately 200 mg/dL) norm = no glucose in urine This causes an osmotic diuresis manifested clinically by polyuria and nocturia = Dehydration results
33
Hyperglycemia: Clinical Manifestations
Glucosuria, Polydipsia, Polyuria, Polyphagia Stimulating thirst that results in polydipsia A significant loss of calories can result from glucosuria: urinary glucose losses can exceed 75 g/d (75 g × 4 kcal/g = 300 kcal/d)
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Polyphagia
excessive hunger high glucose levels lead to increased hunger, increased hunger & eating leads to increased glucose levels cravings are strongest for sugary food
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Polydipsia
excessive thirst excess glucose excreted in urine, fluids depleted with elimination of glucosuria, endocrine system signals thirst
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Glucosuria, Polyuria, polydipsia, and polyphagia are common presenting symptoms in
both type 1 and symptomatic type 2 patients
37
G & 3 Ps =
Weight loss can also occur as a result of both dehydration, loss of calories in the urine, and breakdown of fats and protein
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Type 1 diabetes mellitus
B-cell destruction, usually leading to absolute insulin deficiency autoimmune idopathic
39
Type 2 diabetes mellitus
ranges from predominantly insulin resistant with relative insulin deficiency to a predominant secretory defect with insulin resistance
40
Gestational diabetes mellitus
any degree of glucose intolerance occurring or first being recognized during pregnancy, a time when insulin resistance and B-cell hyperplasia occur normally women diagnoses with gestational DM have a high risk for later developing type 2 DM
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Type 1 Diabetes Mellitus Epidemiology:
Approximately 10% of all DM cases usually occurs in younger patients but can occur at any age
42
Type 1 Diabetes Mellitus Pathogenesis:
Insulin producing pancreatic β-cell destruction may be caused by genetic susceptibility, autoimmune process or viral infection resulting in insulin deficiency Genetic susceptibility in combination with environmental factors is thought to play a critical role in development of type 1 DM
43
Beta cell autoantigens
are thought to be released from beta cells by cellular turnover or damage and are processed and presented to T helper cells by antigen-presenting cells Resulting in Beta cell destruction
44
Glycogenesis:
monosaccharides to glycogen for storage in muscle & liver = excess glucose stored for use later
45
Lipogenesis:
fatty acid + glycerol = fat excess carbohydrates consumed results in fat storage
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Gluconeogenesis:
formation of glucose in the liver from non-carbohydrate sources
47
High Blood Glucose =
insulin secretion & glucagon inhibition
48
Low Blood Glucose =
glucagon secretion & insulin inhibition
49
DKA:
potentially life-threatening, not enough insulin to allow glucose into cells; liver breaks down fat for fuel = ketone byproduct
50
HHS:
serious state occurs with hyperglycemic state; glucose passes into urine pulling excess fluid out of the body; severe dehydration
51
Diabetic Ketoacidosis (DKA)
Life-threatening problem that affects people with diabetes: Type 1>>>>Type2 Increased serum glucose levels stimulates the body to break down fat at a rate that is much too fast. The liver processes the fat into an energy source = byproduct is ketones = causes the blood to become acidic
52
blood pH
Normal blood pH is tightly regulated between 7.35 and 7.45 Lower the pH = acidosis Higher pH = alkalosis
53
Diabetic Ketoacidosis Diagnosis
Hyperglycemia: > 250 mg/dL Ketosis Characterized by a combination of insulin deficiency and glucagon excess Decreased peripheral glucose uptake secondary to insulin deficiency coupled with excess glucagon = hyperglycemia Type 1>>>Type 2 Diabetic ketoacidosis = medical emergency resulting from ketosis and emergent low pH blood level Precipitating factors: Infection, new-onset diabetes mellitus, stress, and insulin deficiency or non-compliance
54
Ketosis:
normal metabolic process - When the body does not have enough glucose for energy, it burns stored fats instead results in a build-up of acids called ketones within the body Some people encourage ketosis by following a diet called the ketogenic or low-carb diet Ketosis leads to diabetic ketoacidosis = build up of ketone bodies
55
DKA: Clinical Presentation
Symptoms: Nausea, vomiting, thirst, abdominal pain, weakness, and fatigue, dehydration Signs: Tachycardia; poor skin turgor and warm and dry skin = Patients also have ketones on breath and altered mental status Laboratory findings: > Hyperglycemia > Metabolic acidosis: pH <7.35 & low HCO3 > Serum ketones: blood & urine
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Type II Diabetes Mellitus Epidemiology: Clinical presentation:
90-95% of cases of diabetes mellitus = usually occurs in older patients (> 40 years) and obese individuals can occur in children as young as 6 years of age clinical presentation: Weakness, weight loss, and susceptibility to infections
57
Type II Diabetes Mellitus Risk factors: Pathogenesis:
Risk factors: sedentary lifestyle, poor nutrition,overweight and obesity Pathogenesis of type 2 diabetes mellitus: Genetic factors play a more important role in type 2 diabetes mellitus than in type 1 diabetes mellitus = Type 2 diabetes mellitus is due to peripheral resistance to insulin and often times inadequate secretion of insulin
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Diabetes Mellitus: Type II Hyperglycemia
Primary: Target tissue resistance to the effects of insulin = hallmark Secondary: Inadequate pancreatic Beta-cell insulin secretion
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Diabetes Mellitus Type II: Obesity
Major driver of the worldwide increase in diabetes prevalence 85% of patients with type 2 DM are obese A 5–10% weight loss in obese individuals with type 2 DM can minimize the disorder Insulin resistance ~ obesity = type 2 DM
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Type II: Stages of development
Insulin sensitivity decreases = insulin-mediated glucose breakdown after a meal is impaired despite increased pancreatic insulin secretion With continued insulin resistance = pancreatic insulin secretion begins to fail = insufficient insulin production Type II DM can become Type II & Type I
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Hyperosmolar Hyperglycemic Leads to Hyperosmolar Nonketonic Coma
Life-threatening = caused by extremely high blood sugar levels Most commonly occurs in people with type 2 diabetes Often triggered by illness or infection Body tries to rid itself of the excess blood sugar by passing it into your urine Untreated = can lead to life-threatening dehydration Urgent medical care Marked hyperglycemia = no metabolic acidosis or ketoacidosis
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Hypoglycemia
A complication of insulin treatment in both type 1 DM and type 2 DM Cause: oral hypoglycemic drugs that stimulate insulin secretion, exercise or fasting
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Hypoglycemia - NON-DIABETIC Individual
low insulin levels with exercise or fasting allow the counter-regulatory hormone-mediated gluconeogenesis, increased hepatic glucose output, and stimulus for increased glucagon secretion = to restore blood glucose levels
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Hypoglycemia - DIABETIC Individual
exogenous insulin dosing & limited glucagon counter-regulation
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Hypoglycemia: Acute Treatment
Rapid oral administration of glucose at the onset of warning symptoms or the intramuscular administration of exogenous glucagon Rebound hyperglycemia can occur after hypoglycemia due to rapid intake of oral glucose and/or actions of counter-regulatory hormones
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Diabetes Mellitus = Increased Risk of Atherosclerosis & Cardiovascular Disease
Not completely understood = diabetes influences atherosclerosis & CVD High blood glucose & High blood pressure = increased risk of endothelial cell damage of blood vessels Decreases HDLs & Increases LDLs Greatest risk Associated with Diabetes: Nephropathy, Retinopathy, Neuropathy, CVD, Skin 65%+ of individuals with uncontrolled diabetes die from heart disease or stroke
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Diabetes Mellitus: Complications pancreas, vessels, kidney, eye
Pancreas: Reduction in number and size of islets Vessels: contributor to atherosclerosis in large & small blood resulting in hypertension Kidney: Microalbuminuria = associated with 10 to 20 x increased risk of progression to diabetic nephropathy = number one cause of ESRD Eye: Retinopathy or retinal vascular disease
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Diabetes Mellitus: Complications PNS, skin (soft tissues), pregnancy
Peripheral nervous system: Peripheral neuropathies (sensory loss >> motor loss); decreased sensation causes diabetics to be more prone to injury, falls & non-traumatic amputations Skin and soft tissue of extremities: Diabetics often develop ulcers and gangrene of the legs, requiring amputation. Decreased sensation causes diabetics to be prone to injury. These patients are unable to feel the damage occurring, and associated damage to vessels leads to poor perfusion that impairs healing Pregnancy: Large-for-gestational age infants are often born to diabetic mothers
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Macrovascular (Large Vessel) Complications
Atherosclerotic macrovascular disease occurs with increased frequency in diabetes = increased incidence of myocardial infarction, stroke, claudication and gangrene of the lower extremities Accounts for significant morbidity and mortality in both types of diabetes Type 2 DM = responsible for approximately 75% of deaths Protective effect of gender is lost in women with diabetes = risk of atherosclerosis is equal to that of men
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Macrovasuclar Disease: Atherosclerosis
Increased risk of atherosclerosis in diabetes = independent risk factor Incidence of hypertension and hyperlipidemia increases 50% and 30% respectively vs age and gender matched norms Diabetes is synergistic with multiple known risk factors to increase atherosclerosis > Smoking > Physical Inactivity > HTN > Hyperlipidemia > Overweight or Obese
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Retinopathy or Retinal Vascular Disease
Leading cause of blindness in developed countries Diabetic retinopathy is present in one-third of all diabetics Increasing in frequency with disease duration = lifetime risk of 90% for type 1 diabetics vs. 60% for type 2 diabetics
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Nephropathy
Most common cause of end-stage renal disease (ESRD) worldwide ESRD occurs more frequently in Type 1>>>Type 2 type 2 DM accounts for more than half of the diabetic population with ESRD because of its greater prevalence Occurs in about 60% of both type 1 and type 2 DM patients Major cause of morbidity
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Diabetic neuropathy can be divided into three major types:
distal, primarily sensory, symmetric polyneuropathy = most common (50% incidence) autonomic neuropathy, occurring frequently in individuals with distal polyneuropathy (>20% incidence) much less common, transient asymmetric neuropathies involving specific nerves, nerve roots, or plexuses
74
Diabetic Foot Ulcers
Occur in 10% of diabetics = can be complicated by osteomyelitis Amputation associated with high mortality = 50% by 3 years post-amputation Diabetic foot ulcers account for over 60% of nontraumatic amputations in the United States
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Risk factors for ulcer development include:
increased injuries in insensate feet owing to symmetric polyneuropathy present in 75–90% of diabetics with foot ulcers can be detected clinically by decreased vibratory and cutaneous pressure sensation and the absence of ankle reflexes macrovascular and microvascular disease present in 30–40% of those with foot ulcers infections caused by alterations in neutrophil function and vascular insufficiency faulty wound healing caused by unknown factors
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Neuropathy: Systemic Distal Polyneuropathy
Demyelination of peripheral nerves = hallmark of diabetic polyneuropathy, affects distal nerves preferentially Usually manifested clinically by a symmetric sensory loss in the distal lower extremities = stocking distribution > Numbness & tingling = paresthesias > Sx begin distally and move proximally > In the hands = Glove Distribution
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Neuropathy: Systemic Distal Polyneuropathy Pathologic features:
demyelination and loss of nerve fibers, accompanied by microvascular lesions, microvascular disease presence of antibodies to autoantigens in patients with neuropathy also suggests a possible immune component to this disorder
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Neuropathy: Autonomic
often accompanies symmetric peripheral neuropathy Occurs more frequently in type 1 DM Can affect all aspects of autonomic functioning = most notably cardiovascular, genitourinary, and GI systems Cardiovascular: Fixed, resting tachycardia and orthostatic hypotension Erectile dysfunction occurs in more than 50% of diabetic men Overflow IncontinenceL Neurogenic Bladder = Loss of bladder sensation and difficulty emptying the bladder Gastroparesis: Motor disturbances can occur throughout the GI tract, resulting in delayed gastric emptying, constipation, or diarrhea Anhidrosis: in the lower extremities can lead to excessive sweating in the upper body as a means of dissipating heat, including increased sweating in response to eating