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Primary care of adults 2 > Diabetes (7 questions) > Flashcards

Diabetes (7 questions) Flashcards

1
Q

Basic role of insulin

A

Regulates body’s balance of storage vs mobilization of body stores

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2
Q

Insulin: normal stimulation vs T2DM

A

Normal: beta cells sense rise in glc levels in bloodstream, send enough insulin to lower sugar into normal range (70-105mg/dL)

T2DM: lack of adequate stimulation to lower BG to normal range

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3
Q

Insulin in liver: normal vs T2DM

A
  • Normal: insulin allows glc to be stored as glycogen to be later released during fasting states; promotes conversion of liver glc into fatty acids/inhibits lipolysis
  • T2DM: lack of insulin or sensitivity means body thinks it’s in a fasting state when it’s not and releases glc from glycogen and FAs = high BG and free fatty acids
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4
Q

Insulin in skeletal muscle: normal vs T2DM

A

normal: insulin stimulates storage of glc as muscle glycogen to be used for energy by muscle cell

T2DM: glycogen released b/c body believes it’s in fasting state, but can’t get into cells since glc transporters on cell depend on insulin

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5
Q

What is the renal threshold for hyperglycemia?

A

180 mg/dL - osmotic diuresis occurs leading to significant urinary losses of F & Es

–> progressive dehydration and hyperosmolality

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6
Q

Etiology of Type I DM

A

autoimmune mediated diabetes, insulin producing B-cells are destroyed by an autoimmune process.

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7
Q

Additional risks associated with DMI

A

increased incidence of other autoimmune diseases such as Hashimoto’s thyroiditis, graves disease, pernicious anemia, vitiligo, celiac disease and Addison’s Disease.

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8
Q

DMII etiology

A

strong family Hx - genetics & environment

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9
Q

MODY etiology

A

genetic defect in the b-cell. Genetic defects in insulin action.

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10
Q

Dz of exocrine pancreas that can lead to DM

A

pancreatitis, trauma, pancreatectomy, neoplasm, CF, hemochromatosis

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11
Q

Medications that may cause DMII

A

steroids, HIV meds and some of the psychotropic agents may induce DM.

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12
Q

Clinical manifestations of diabetes mellitus

A
  • polyuria, polydipsia, polyphagia
  • fatigue, blurred vision, headache, paresthesia, recurrent infections (UTI’s, candidiasis,etc.)
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13
Q

Polyuria: DDx

A
  • Diabetes Insipidus
  • Primary Polydipsia
  • UTI or Bladder Dysfunction
  • Must rule out secondary causes such as
    • Excess of counter-regulatory hormones
    • Significant hypokalemia caused by impaired glc tolerance (IGT), diuretic use or hyperaldosteronism
    • Destruction of Beta cells from pancreatitis, hemochromatosis, or drugs
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14
Q

What is diabetes insipidus?

A

polyuria and polydipsia caused by inadequate secretion of vasopressin, the antidiuretic hormone (ADH). Cause is unknown, or trauma to the head which causes damage to the pituitary or a tumor. Causative factor eliminated. If not d/t damage then given vasopressin replacement therapy.

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15
Q

What is primary polydipsia?

A

altered thirst perception with increased thirst and fluid intake followed by polyuria. Prevalent among patients with psychiatric history- i.e. schizophrenia.

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16
Q

What is an excess of counter-regulatory hormones?

A

excess of glucagon, growth hormone, cortisol, catecholamines

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17
Q

What is hyperaldosteronism?

A

production of salt retaining hormone aldosterone by an adrenal adenoma resulting in intravascular volume expansion and renin suppression.

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18
Q

What is hemochromatosis

A

disease manifested with high serum iron and ferritin levels, often requiring routine phlebotomy.

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19
Q

What drugs may cause polyuria?

A

e.g., corticosteroids, pentamadine, nicotinic acid, thyroid hormone, interferon, dilantin, thiazides

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20
Q

Types of Diabetes Mellitus

A
  • Type 1
  • Type 2
  • Latent Autoimmune Diabetes in Adults (LADA)
  • Gestational Diabetes Mellitus
  • Secondary Diabetes
  • Maturity Onset Diabetes of the Young (MODY)
  • Pre-Diabetes (High Risk)- impaired fasting glucose or impaired glucose tolerance
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21
Q

Lab work for Dx type I DM

A

Presence of islet auto-antibodies-glutamic acid decarboxylase (GAD65), insulin autoantibody (IAA), insulinoma-associated protein 2 autoantibody (IA-2A) & zinc transporter 8 antibody (ZnT8A) and C. Peptide

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22
Q

What is LADA?

A

Latent Autoimmune Diabetes in Adults (LADA)

  • slowly progressive form of autoimmune diabetes
  • adult age of Dx,
  • presence of auto-antibodies (usually 1 vs DM1 has 2+)
  • lack of an insulin requirement at the time of diagnosis.
    • short duration of diet / PO Tx before requiring insulin.

Pt.s are usu. Thinner, lower BMI, higher A1c

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23
Q

What is secondary diabetes?

A
  • caused by medications such as zyprexa, abilify, (which contribute to weight gain) along with steroids, some of the meds used to treat HIV (such as Epivir, Retrovir, Norvir)
  • pancreatitis, surgeries (especially involving the pancreas or organ transplantation and meds used in treatment), or diseases of the exocrine pancreas such as cystic fibrosis, ect.
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24
Q

What is MODY?

A

defect in the B-cell function, characterized by onset of hyperglycemia@ an early age, generally before the age of 25 years. At least 3 different gene mutations have been identified which cause impaired insulin secretion without insulin resistance.

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25
Q

What constitutes “impaired fasting glucose”

A

BG 100 - 125

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26
Q

What constitutes “impaired glucose tolerance”?

A

2 hour plasma glucose of 140 to 199mg/dl.

That test is performed w/ a 75-g oral glucose load.

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27
Q

Diagnostic criteria for DM

A
  • Symptoms of diabetes plus a casual/random plasma glucose > 200 mg/dl OR
  • FPG_>_126 mg/dl OR
  • 2-H post-load glucose > 200 mg/dl during an OGTT ** not standard clinically
  • A1C > 6.5 %

must repeat one of last 3 on another occasion.

fasting = no PO intake > 8h

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28
Q

How were OGTT, FPG and A1c numbers set for Dx of DM?

A

thresholds correlate with the presence of retinopathy, basis for these values

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29
Q

“One-step” Dx of GDM

A
  • 24 to 28w gestation w/o prior overt DM
    • 75-g OGTT: PG fasting, 1hr, 2hr
    • Perform AM after an overnight fast of at least 8hr
  • GDM Dx: any one of 3
    • Fasting: ≥92 mg/dL (5.1 mmol/L)
    • 1 h: ≥180 mg/dL (10.0 mmol/L)
    • 2 h: ≥153 mg/dL (8.5 mmol/L)
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30
Q

“Two-step” Dx for GDM

A

24 to 28w gestation w/o prior overt DM

  • STEP 1: 50-g GLT (nonfasting)
    • PG at 1h (step 1)
    • If 1hr PG is ≥140 mg/dL* (7.8 mmol/L), proceed to step 2.
  • STEP 2: 100-g OGTT (fasting)
    • GDM Dx: 2+ of the following
      • Fasting >95
      • 1H >180
      • 2H >155
      • 3H >140

*ACOG recommends lower threshold of 135 if high risk ethnic minority

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31
Q

Does the NIH recommend the one or two step version of the OGTT for Dx of GDM?

A

Two step: lack of evidence for one step, and potential negative consequences for Dxing more women

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32
Q

PEak age for DMI

A

10-14 years

females 10-12, males 12-14

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33
Q

Whites vs other ethnic groups for risk of DM?

A

The risk for type 1 diabetes is higher in whites than for African-Americans, American Indians, Asians and Pacific Islanders or Hispanics, where as the opposite is true for type 2 diabetes.

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34
Q

Mainstays of mgmt for DMI

A
  • Insulin therapy to obtain near normo-glycemia
  • Diet sufficient for growth
  • Exercise
  • Psychological well being
  • Prevention of complications
  • Immunizations
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35
Q

BG goal and A1c goal for 8yo and older

A

SBGM: Fasting & Pre-Prandial BS 70-120
A1C goal less than 7.5% for children and older

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36
Q

Goal A1c for <8yo

A

<8 d/t risk of hypoglycemia

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37
Q

DMI: how often is A1c measured?

A

Quarterly

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38
Q

What is the “honeymoon period”

A

In DMI

In first few weeks of insulin therapy common to see a “honeymoon” period when β cells recover some function. Loss of function then proceeds after a period of up to 6 months or a year.

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39
Q

Risk factors for DMII

A
  • Obesity
  • Hypertension/ Hyperlipidemia
  • Having a baby > 9 lbs
  • Ethnicity
  • Age
  • Women with prior Gestational Diabetes or PCOS
  • Sedentary Lifestyle
  • Impaired Glucose Tolerance or Impaired Fasting Glucose
  • Vascular Disease
  • first-degree relative with diabetes
  • high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander)
  • history of CVD
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40
Q

When should you screen adults <45yo for DMII?

45+?

A
  • <45 BMI > or equal to 25 and 1 or more risk factors
  • 45+: For all patients, particularly those who are overweight or obese, testing should begin at age 45 years.
  • screen now and then every 3 years (yearly if prediabetes)
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41
Q

What does the history portion of a comprehensive evaluation of DM (I or II) consist of?

A
  • Medical History
  • Age and characteristic of onset (i.e. DKA, HHS, lab finding)
  • Symptoms, results of lab tests, A1C records, exams
  • Eating patterns, weight Hx, growth/dev
  • Medications, meal plan, SBGM, diabetes self-management ed
  • Exercise Hx
  • Acute complications- hypo/hyperglycemia
  • Hx and treatment of other conditions
  • Risk factors for CVD, other co-morbid conditions
  • Family HX of Diabetes and other endocrine disorders
  • Lifestyle, cultural, psychological, educational, economic factors
  • Tobacco, ETOH and other controlled substance use
  • Contraceptive, reproductive and sexual Hx
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42
Q

What does the PE portion of a comprehensive evaluation of DM (I or II) consist of?

A
  • Height, weight, BMI
  • BP measurement, including orthostatic when indicated
  • Fundoscopic exam
  • Thyroid palpation
  • Skin exam (acanthosis nigricans and insulin injection sites)
  • Comprehensive foot exam
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43
Q

What does the comprehensive foot exam of DM (I or II) consist of?

A
  • Annual!
  • to identify risk factors predictive of ulcers and amputations
    • Inspection
    • Palpation of dorsalis pedis/posterior tibial pulses
    • Presence /absence of patellar and Achilles reflexes
    • Determination of proprioception, vibration perception threshold using 128-Hz tuning fork, and monofilament sensation using a 10-g monofilament
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44
Q

What does the laboratory evaluation of DM (I or II) consist of?

A
  • A1C (if none from last 3 mths)
  • Fasting Lipid Profile
  • Liver Function tests
  • Spot Urine Alb/Cr ratio
  • Serum Creatinine in adults (in children if proteinuria is present and calculated GFR
  • TSH in all Type 1, dyslipidemia or women over age of 50 years
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45
Q

What referrals may be needed for DM pts (I or II)?

A
  • Eye care professional for yearly dilated eye exam
  • Family planning for women of reproductive age
  • Registered Dietitian for MNT
  • DSME
  • Dentist for comprehensive periodontal exam
  • Mental health professional if needed

MNT= Medical nutrition therapy

DSME=Diabetes self management education

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46
Q

Mgmt of hyperglycemia: what elements support a more stringent approach?

A
  • Low risk associated w/hypoglycemia
  • Newly Dxed DM
  • Long life expectancy
  • No important comorbidities
  • No established vascular complications
  • Resources and support system readily available
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47
Q

Mgmt of hyperglycemia: what elements support a less stringent approach?

A
  • high risk associated w/hypoglycemia
  • Long-standing DM
  • Short life expectancy
  • Severe comorbidities
  • Severe vascular complications
  • Resources and support system limited
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48
Q

Major goal of the mgmt of DMII

A

maintain normoglycemia and to prevent complications.

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49
Q

A1c targets in DMII

A

(6. 0 - 6.5%) - younger, healthier
(7. 5 - 8.0%+) - older, comorbidities, hypoglycemia prone

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50
Q

Preprandia BS target for DM

A

80-130 mg/dL

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51
Q

Postprandial BS target for DMII

A

<180 mg/dL

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52
Q

BP target for DMII

A

<140/90 in most

<130/80 in selected pts

53
Q

LDL goal for DMII

A

< 100

w/overt CVD <70

54
Q

TG goal for DMII

A

<150

55
Q

HDL goal for DMII

A

>50

56
Q

Urine Alb/Cr Ratio for DM II

A

< 30

57
Q

Pharmacologic options for DMII

A
  • Sulfonylureas
  • Non-Sulfonylurea Insulin Secretagogues
  • Biguanides
  • Thiazolidinediones
  • α-Glucosidase Inhibitors
  • Insulin
  • DPP-4 Inhibitors
  • Incretin Mimetics (GLP-1)/ Amylin Analogues
  • SGLT-2 Inhibitors
58
Q

Biguanides: MOA

A
  • Activates AMP-kinase
  • decrease Hepatic glucose production
  • Increase insulin sensitivity – often insulin resistance is the problem & not lack of insulin
59
Q

Biguanides: advantages

A
  • Extensive experience
  • No hypoglycemia
  • Weight neutral
  • ? decrease CVD
60
Q

Biguanides: disadvantages

A
  • Gastrointestinal
  • Lactic acidosis
  • B-12 deficiency
  • Contraindications
61
Q

Biguanides: cost

A

low

62
Q

SUs / Meglitinides: MOA

A
  • Closes KATP channels
    • Stimulate insulin release through β cells

Meg: Quick peak, short duration compared to sulfonylureas

63
Q

SUs / Meglitinides: Advantages

A
  • Extensive experience
  • decrease Microvasc. risk
64
Q

SUs / Meglitinides: Disadvantages

A
  • Hypoglycemia
  • Weight gain
  • Low durability
  • ? Ischemic preconditioning
65
Q

SUs / Meglitinides: Cost

A

Low

66
Q

TZDs: MOA

A
  • PPAR-g activator
  • increase­ insulin sensitivity
67
Q

TZDs: advantages

A
  • No hypoglycemia
  • Durability
  • decreased TGs, ­increased HDL-C
  • ? decreased CVD (pio)
68
Q

TZDs disadvantages

A
  • Gastrointestinal
  • Dosing frequency
  • Modest decrease in A1c
69
Q

TZDs cost

A

high

70
Q

a-GIs: MOA

A
  • Inhibits a-glucosidase
  • Slows carbohydrate absorption
71
Q

a-GIs: Advantages

A
  • No hypoglycemia
  • Nonsystemic
  • decreased Post-prandial glucose
  • ? decreasedCVD events
72
Q

a-GIs: Cost

A

Moderate

73
Q

DPP-4 Inhibitors: MOA

A
  • Inhibits DPP-4, suppress glucagon secretion
  • Increases GLP-1, GIP, Increase glucose-dependent insulin release
74
Q

DPP-4 inhibitors: Advantages

A
  • No hypoglycemia
  • Well tolerated
75
Q

DPP-4 Inhibitors: disadvantages

A
  • Modest decrease A1c
  • ? Pancreatitis
  • Urticaria
76
Q

DPP-4 Inhibitors: cost

A

high

77
Q

GLP-1 receptor agonists: MOA

A
  • Activates GLP-1 R
  • increased Insulin, decreased glucagon
  • decreased gastric emptying
  • increased ­ satiety
78
Q

GLP-1 receptor agonists: Advantages

A
  • Weight loss
  • No hypoglycemia
  • ? Beta cell mass
  • ? CV protection
79
Q

GLP-1 receptor agonists: Disadvantages

A
  • GI
  • ? Pancreatitis
  • Medullary ca
  • Injectable
80
Q

GLP-1 receptor agonists: cost

A

high

81
Q

Amylin mimetics: MOA

A
  • Activates amylin receptor
  • decreased glucagon
  • decreased gastric emptying
  • increased satiety
82
Q

Amylin mimetics: advantages

A
  • Weight loss
  • decreased PPG
83
Q

Amylin mimetics: Disadvantages

A
  • GI
  • Modest decrease A1c
  • Injectable
  • Hypo w/ insulin
  • Dosing frequency
84
Q

Amylin mimetics: Cost

A

high

85
Q

SGLT2 Inhibitors: MOA

A
  • ­increased urinary excretion of glucose
  • decreased reabsorption of glucose prox. segment of the convoluted tubule

sodium / glc cotransporter 2

86
Q

SGLT2 Inhibitors: Advantages

A
  • Weight loss
  • No hypoglycemia
87
Q

SGLT2 Inhibitors: Disadvantages

A
  • UTIs
  • Genital infections
88
Q

SGLT2 Inhibitors: Cost

A

high

89
Q

Can a point of care A1c be used for Dx?

A

No!

90
Q

How do you titrate metformin and what do you tell pt when you start them on metformin?

A

MOA, SE, Titrate up by 500 mg in a week, take with the first bite of food or with meals

91
Q

How often should BG be checked for pts using multiple insulin injections or insulin pump Tx?

A

3+ times daily

92
Q

How often should BG be checked for pts using less freqent insulin injections, noninsulin tx, or medical nutrition therapy alone?

A

could be a useful guide, but no specific number given and may not be truly useful / cost-effective if not on insulin

93
Q

What does HbA1c reflect?

A

reflects mean glycemia over the preceding 2-3 months

94
Q

How often should A1c be checked?

A

adults at target: q6mths

kids: q3mths

95
Q

How is glycemic control best judged?

A

combination of the patient’s self blood glc monitoring (SBGM) and the current A1C result

96
Q

Meaning of A1c values - 6 to 12%

A

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

97
Q

What are the general recommendations of medical nutrition therapy?

A
  • Individualized meal planning include optimization of food choices to meet recommended dietary allowance/dietary reference intake for all micronutrients as needed to achieve treatment goals.
    • For people with diabetes, it is unlikely one optimal mix of macronutrients for meal plans exists
    • The best mix of carbohydrate, protein, and fat appears to vary depending on individual circumstances
98
Q

Goals of Medical Nutrition Therapy

A

Metabolic Control and Balance

  • Maintenance of as near-normal blood glucose levels as possible
  • Prevention and treatment of acute and long-term complications of diabetes
  • Achievement of optimal serum lipid levels
  • Improvement of overall health through optimal nutrition
  • Adequate calories for maintaining/attaining reasonable weights for adults, normal growth and development in children and adolescents, increased metabolic needs during pregnancy and lactation, or recovery from catabolic illnesses
99
Q

Physical Acivity recommendatons for adults

A
  • Adults 150 minutes of moderate physical activity over 3 days/ week….no 2 consecutive days w/o exercise
  • resistance training twice a week (w/o contraindications)
  • In Type 1 adjust the therapeutic regimen to allow safe participation in all forms of physical activity.
100
Q

IZs for patients with DM

A
  • Provide an influenza vaccine annually to all diabetic patients ≥6 months of age
  • Administer pneumococcal polysaccharide vaccine 23 (PPSV23) to all diabetic patients ≥2 years
  • For those > 65 not previously vaccinated receive the pneumococcal conjugate vaccine 13 (PCV13) followed by the PPSV23 in 6-12 months
  • For those > 65 previously vaccinated PPSV23, receive >12 months the PCV13
  • Other indications for repeat vaccination: nephrotic syndrome, chronic renal disease, immunocompromised states
  • Hepatitis B per CDC recommendations (19-59, consider 60+)
101
Q

Recommended pharm therapy for diabetes & htn

A

ACEi or ARB

2+ drugs at max dose for BP targets

1+ antiHTN at bedtime

102
Q

DMI + proteinuria + ACEi - outcome?

A
  • ACEI’s were associated with a 50% reduction in the risk of death, dialysis, and transplantation.
103
Q

How should neuropathy be screened for in DM pts?

How often?

A
  • All patients should be screened for distal symmetric polyneuropathy (DPN) and for signs and symptoms of cardiovascular autonomic neuropathy
    • At diagnosis of type 2 DM with 5 years after diagnosis of type 1
    • At least annually thereafter using simple clinical tests
104
Q

Oral therapies for neuropathy

A

Lyrica, Cymbalta, Gabapentin

Alpha lipoic Acid 600-1200mg QD

105
Q

How / when should initial retinopathy screenings be done?

A
  • Initial dilated and comprehensive eye examination by an ophthalmologist or optometrist
    • Adults and children aged 10 years or older
      with type 1 diabetes
      • Within 5 years after diabetes onset
    • Patients with type 2 diabetes
      • Shortly after diagnosis of diabetes
  • Women with preexisting diabetes/pregnancy
106
Q

How / when should follow-up screenings be done for diabetic retinopathy?

A
  • for type 1 and type 2 diabetic patients should be repeated annually by an ophthalmologist or optometrist
  • Less frequent exams (every 2-3 years) may be considered following 1+ normal eye exams, if recommended by eye care professional
  • Examinations will be required more frequently if retinopathy is progressing (B)
107
Q

Eye exams in women with preexisting diabetes who are pregnant or planning to get pregnant - when and how?

A
  • Comprehensive eye examination
  • Counseled on risk of development and/or progression of diabetic retinopathy
  • Eye examination should occur in the first trimester (B)
  • Close follow-up throughout pregnancy
  • For 1 year postpartum
108
Q

How should nephropathy be screened for in DM?

A
  • Assess urine albumin excretion annually
    • In type 1 diabetic patients with diabetes duration of ≥5 years
    • In all type 2 diabetic patients at diagnosis
  • Measure serum creatinine at least annually
    • In all adults with diabetes regardless of degree of urine albumin excretion
    • Serum creatinine should be used to estimate GFR and stage level of chronic kidney disease, if present
109
Q

Significance of high triglycerides in the setting of hyperglycemia

A

TRIG elevation may be related to the high glucose and once it normalizes the TRIG may normalize, but keep an eye on the lipids

110
Q

Indications for Insulin Therapy in Patients With Type 2 Diabetes

A
  • Maximal doses of oral agents do not control glucose levels
  • Periods of acute injury, stress, infection, or surgery
  • Presence of weight loss, ketonemia and/or ketonuria and/or severe hyperglycemic symptoms
  • Pregnancy
  • Renal disease
  • Allergy or serious reaction to sulfa drugs
111
Q

Recommendations for Insulin Therapy for Type 1?

A

Most people with type 1 diabetes should

  • Be treated with MDI injections (3–4 injections per day of basal and prandial insulin) or continuous subcutaneous insulin infusion (CSII)
  • Be educated in how to match prandial insulin dose to carbohydrate intake, premeal blood glucose, and anticipated activity
  • Use insulin analogs to reduce hypoglycemia risk
112
Q

Initial total daily dose for insulin, Type I?

A

0.4-1.0 u/kg of body weight

113
Q

How many insulin injections per day recommended for DMI?

A
  • Initially 3-4 injections per day in Type 1
  • Basal –Bolus Therapy is recommended
114
Q

How many insulin doses for DMII initially recommended?

A

Initially as bedtime insulin

115
Q

What are the rapid / short acting insulins?

A
  • Aspart (Novolog® - Novo Nordisk)
  • Lispro (Humalog® - Eli Lilly)
  • Glulisine (Apidra® - Sanofi Aventis)
  • Regular Insulin ( Humulin – Eli Lilly, Novolin – Novo Nordisk)
116
Q

What are the intermediate acting insulins?

A
  • NPH (Humulin – Eli Lilly, Novolin – Novo Nordisk)
117
Q

What are the long acting insulins?

A

Detemir (Levemir® - Novo Nordisk)
Glargine (Lantus® - Sanofi Aventis)

118
Q

What are the mixed acting insulins?

A
  • Humalog® 75/25 (Eli Lilly)
  • Novolog® 70/30 (Novo Nordisk)
  • 70/30 Mix ( Novolin -Novo Nordisk, Humulin – Eli Lilly)
119
Q

Rapid-Acting: OPD

A

O: 5-10min

P: 3/4 - 1hr

D: 2hrs

120
Q

Regular insulin: OPD

A

O: 0-1h

P: 2-4h

D: 4-6h

121
Q

NPH: OPD

A

O: 1-4h

P: 6-10h

D: 12-20h

122
Q

Detemir / Glargine: OPD

A

O: 1-2h

P: none

D: 24h

123
Q

Treatmnt for hypoglycemia

A
  • 15-30 gms of simple carbohydrate orally
  • Check BG in 15-20 minutes
  • Can repeat in 15 minutes with 10 -15 gm
  • Snack of 1 protein and 1 carbohydrate 30 minutes later
  • If severe and able to swallow then 30-45 gms simple carbohydrate
  • If unable to swallow glucagon SQ
  • IV Glucose
124
Q

What are the three classes of hypoglycemia?

A

Mild, moderate, severe

125
Q

What symptoms characterize mild hypoglycemia?

A

hunger weakness, shakiness, diaphoresis, pallor, tachycardia, irritability, difficulty concentrating

126
Q

What symptoms characterize moderate hypoglycemia?

A

Impaired CNS function, decreased thinking ability, increased anger, irritability, some changes in mental status, may be able to treat.

127
Q

What symptoms characterize severe hypoglycemia?

A

confusion, drowsiness, progression to seizure activity

128
Q

Criteria for prediabetes Dx?

A
  • FPG 100 to 125 mg/dL

OR

  • 2-h PG in the 75-g OGTT 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0 mmol/L) (IGT)

OR

  • A1C 5.7–6.4%

*For all three tests, risk is continuous, extending below the lower limit of the range and becoming disproportionately greater at higher ends of the range.

Primary care of adults 2 (15 decks)

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