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CDM exam 2 > Diabetes lecture 1 > Flashcards

Diabetes lecture 1 Flashcards

1
Q

Type 1 diabetes

A

autoimmune β-cell destruction, usually leading to absolute insulin deficiency

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2
Q

Type 2 Diabetes

A

progressive loss of β-cell insulin secretion frequently on the background of insulin resistance

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3
Q

Gestational diabetes (GDM)

A

diabetes that is first diagnosed in the 2nd or 3rd trimester that is not clearly preexisting type 1 or type 2 diabetes

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4
Q

Other causes of diabetes

A

Genetic defects

Disease of the exocrine pancreas (cystic fibrosis, pancreatitis)

Drug-induced hyperglycemia

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5
Q

Pathophysiology of Type 1

A

-Defect in pancreatic β-cell function&raquo_space; deficiency of insulin
and amylin
-Relative increase in glucagon – disequilibrium is created
with insulin
-Increase in BG fails to suppress production of glucagon
-Effects metabolism of fat, protein, and CHOs
-Protein and fat breakdown occurs because of lack of insulin
– results in weight loss
-Ketoacidosis will result if no treatment

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6
Q

Type 1

A

decreased insulin leads to increase glucose

glycogen and protein breakdown cause keto-acidosis

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7
Q

Stages of Type 1

A

Stage 1: autoimmune, normoglycemic, pre-symptomatic

Stage 2: Autoimmune, dysglycemic, pre-symptomatic

Stage 3: Autoimmune, hyperglycemia, symptomatic

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8
Q

Rate of progression of Type 1 is dependent on

A

Age at first detection

Number of autoantibodies

Autoantibody specificity

Autoantibody titers

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9
Q

Pathophysiology of Type 2

A

Genetic predisposition and lifestyle –> insulin resistance –> B cell decompensation –> insulin resistance and B cell failure

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10
Q

Factors of Type 2 leading to hyperglycemia

A 
impaired insulin secretion in pancreas
increased glucagon secretion in pancreas
increased HGP in liver
Neurotransmitter dysfunction in brain 
decrease glucose uptake in muscles 
increased glucose reabsorption in kidney
increase lipolysis in adipose tissue
decreased incretin effect in gut
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11
Q

metabolic defects:

Insulin resistance in muscle

A

ineffective glucose uptake

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12
Q

metabolic defects:

Insulin resistance in liver

A

increase glucose secretion

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13
Q

metabolic defects:

Pancreatic B cell decline

A

reduced insulin secretion

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14
Q

metabolic defects:

increased activity of a-cells in the pancreas

A

higher blood levels of glucagon increase blood glucose levels

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15
Q

metabolic defects:

Increased free-fatty acid levels in the blood from fat cell breakdown

A

more insulin resistance, toxic to beta-cells

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16
Q

metabolic defects:

Loss of incretin function from the gut

A

deficiency/resistance

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17
Q

metabolic defects:

Sodium-glucose cotransporter upregulation in the kidney

A

results in higher blood glucose levels

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18
Q

Risk factors of Type 1

A 
Genetic 
Environmental (poorly defined)
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19
Q

Risk factors Type 2

A 
BMI ≥ 25 kg/m2 (≥ 23 kg/m2 in Asian Americans)
Physical inactivity
Hypertension
HDL < 35 mg/dL and/or TG > 250 mg/dL
First degree relative with diabetes
Women who were diagnosed with GDM
Women with polycystic ovary syndrome
High risk race/ethnicity 
Prediabetes on previous testing
History of CVD
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20
Q

gestational Diabetes risk factors

A

overweight
older age
family history of type 2

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21
Q

gestational diabetes pathophysiology

A

insulin resistance

diminished insulin secretory response

22
Q

Gestational diabetes risks to mother and baby

A 
Macrosomia
Shoulder dystocia
Preeclampsia
Cesarean delivery
Stillbirth
23
Q

Clinical manifestations of hyperglycemia

A

Polyuria (excessive urination)
Polyphagia (excessive hunger)
polydipsia (excessive thirst)

24
Q

Factors that decrease glucose

A

insulin
excess DM medications
increased exercise
alcohol

25
Q

Factors that increase glucose

A 
counter-regulatory hormones 
insufficient DM medications 
other medications 
excess food 
illness
stress
26
Q

Screening for Type 1

A

Autoantibodies

  • Islet cell (ICA)
  • Glutamic acid decarboxylase (GAD65)
  • Insulin autoantibodies (IAA)
  • Tyrosine phosphatases (IA-2 and IA-2β)
  • Zinc transporter 8 (ZnT8)
27
Q

Screening for Type 2

A
  • Starting at age 35
  • Anyone obese (BMI> 25 or >23 in Asian americans) plus 1 more riks factors
  • people with HIV
  • pre-diabetics
  • Women with GDM
28
Q

With normal results, repeat screening for Type 2 every

A

3 years

29
Q

if results indicate pre-diabetes, repeat type 2 screening

A

yearly

30
Q

Fasting plasma glucose

A

no caloric intake for at least 8 hours

31
Q

OGTT

A

75 g anhydrous glucose dissolved in water

Diagnoses more patients than A1C or FPG

32
Q

Hemoglobin A1C

A
  • Reflects glycemic control over previous 2-3 months
  • Strong predictive value for complications
  • Advantages of A1C compared to FPG and

OGTT:

  • Greater convenience (fasting not required)
  • Less day-to-day variations during periods of stress or illness
33
Q

Testing for Diabetes

A

FPG
Casual plasma glucose
OGTT
A1C

34
Q

Hemoglobin A1C

A

Percent glycosylation of
hemoglobin subfraction, A1c

Binding of glucose to hemoglobin A
is a nonenzymatic process that
occurs over the lifespan of a red
blood cell

35
Q

limitations of A1C

A

A1C inaccurately reflects glycemia in conditions that alter red blood cell turnover
o Sickle cell disease
o Pregnancy
o Glucose-6-phosphate dehydrogenase deficiency
o End stage renal disease
o Recent blood loss or transfusion
o Hemodialysis

36
Q

Testing for Type 1

A

Same blood tests as type 2 diabetes

Presence of 2 or more autoimmune markers

Plasma glucose rather than A1C preferred in acute onset

C-peptide useful to differentiate type 1 from type 2
o Levels generally match insulin levels
o Low levels usually = type 1 diabetes

37
Q

Diagnosis Criteria for A1C

A

pre = 5.7-6.4%

diabetes = > 6.5%

38
Q

Diagnosis Criteria for FPG

A

Pre = 100-125 mg/dL

diabetes = > 126 mg/dL

39
Q

Diagnosis Criteria for OGTT

A

pre = 140-199 mg/dL

diabetes = > 200 mg/dL

40
Q

Diagnosis Criteria for random glucose

A

Diabetes = ≥ 200 mg/dL plus classic
symptoms of hyperglycemia
or hyperglycemic crisis

41
Q

FGP and PPG to A1C

A

Higher the A1C, less contribution of PPG, more FPG

42
Q

Goals therapy

A

Attain normoglycemia (or appropriate glycemic control)

Reduce onset and progression of diabetes-related complications

Aggressively address CV risk factors

Improve quality and quantity of life

43
Q

A1C goal

A

< 7%

44
Q

preprandial glucose (fasting) goal

A

80-130 mg/dL

45
Q

peak postprandial glucose

A

< 180 mg/dL

made 1-2 hours after the beginning of meal

46
Q

Children and adolescents

A

less stringent goals to minimize risk of hypoglycemia

47
Q

Goals for pediatrics type 1

A 
A1C = <7.5%
fasting = 90-130mg/dL
bedtime/overnight = 90-150mg/dL
48
Q

Diagnostic criteria for pregnant women using 75-g fasting OGTT

A

Fasting >92mg/dL
1 hour >180 mg/dL
2 hour >153 mg/dL

49
Q

target glucose range for hospitalized patients

A

140-180 mg/dL

50
Q

Goals for older adults (healthy)

A 
A1C = < 7-7.5%
Preprandial = 80-130 mg/dL
Bedtime = 80-180 mg/dL
51
Q

Goals for older adults (complex/intermediate)

A 
A1C = < 8%
Preprandial = 90-150mg/dL
Bedtime = 110-200 mg/dL
52
Q

Goals for older adults (very complex/poor health)

A 
A1C = < 8.5% 
Preprandial = 100-180 mg/dL
Bedtime = 110- 200 mg/dL

CDM exam 2 (12 decks)

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