Diabetes lecture 1 Flashcards by Annika Larson

Type 1 diabetes

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

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Type 2 Diabetes

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

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Gestational diabetes (GDM)

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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Other causes of diabetes

Genetic defects

Disease of the exocrine pancreas (cystic fibrosis, pancreatitis)

Drug-induced hyperglycemia

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Pathophysiology of Type 1

-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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Type 1

decreased insulin leads to increase glucose

glycogen and protein breakdown cause keto-acidosis

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Stages of Type 1

Stage 1: autoimmune, normoglycemic, pre-symptomatic

Stage 2: Autoimmune, dysglycemic, pre-symptomatic

Stage 3: Autoimmune, hyperglycemia, symptomatic

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Rate of progression of Type 1 is dependent on

Age at first detection

Number of autoantibodies

Autoantibody specificity

Autoantibody titers

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Pathophysiology of Type 2

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

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Factors of Type 2 leading to hyperglycemia

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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metabolic defects:

Insulin resistance in muscle

ineffective glucose uptake

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metabolic defects:

Insulin resistance in liver

increase glucose secretion

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metabolic defects:

Pancreatic B cell decline

reduced insulin secretion

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metabolic defects:

increased activity of a-cells in the pancreas

higher blood levels of glucagon increase blood glucose levels

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metabolic defects:

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

more insulin resistance, toxic to beta-cells

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metabolic defects:

Loss of incretin function from the gut

deficiency/resistance

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metabolic defects:

Sodium-glucose cotransporter upregulation in the kidney

results in higher blood glucose levels

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Risk factors of Type 1

Genetic 
Environmental (poorly defined)

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Risk factors Type 2

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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gestational Diabetes risk factors

overweight
older age
family history of type 2

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gestational diabetes pathophysiology

insulin resistance

diminished insulin secretory response

Gestational diabetes risks to mother and baby

Macrosomia
Shoulder dystocia
Preeclampsia
Cesarean delivery
Stillbirth

Clinical manifestations of hyperglycemia

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

Factors that decrease glucose

insulin
excess DM medications
increased exercise
alcohol

Factors that increase glucose

``` counter-regulatory hormones insufficient DM medications other medications excess food illness stress ```

Screening for Type 1

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

Screening for Type 2

- 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

With normal results, repeat screening for Type 2 every

3 years

if results indicate pre-diabetes, repeat type 2 screening

yearly

Fasting plasma glucose

no caloric intake for at least 8 hours

OGTT

75 g anhydrous glucose dissolved in water Diagnoses more patients than A1C or FPG

Hemoglobin A1C

- 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

Testing for Diabetes

FPG Casual plasma glucose OGTT A1C

Hemoglobin A1C

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

limitations of A1C

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

Testing for Type 1

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

Diagnosis Criteria for A1C

pre = 5.7-6.4% diabetes = > 6.5%

Diagnosis Criteria for FPG

Pre = 100-125 mg/dL diabetes = > 126 mg/dL

Diagnosis Criteria for OGTT

pre = 140-199 mg/dL diabetes = > 200 mg/dL

Diagnosis Criteria for random glucose

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

FGP and PPG to A1C

Higher the A1C, less contribution of PPG, more FPG

Goals therapy

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

A1C goal

< 7%

preprandial glucose (fasting) goal

80-130 mg/dL

peak postprandial glucose

< 180 mg/dL | made 1-2 hours after the beginning of meal

Children and adolescents

less stringent goals to minimize risk of hypoglycemia

Goals for pediatrics type 1

``` A1C = <7.5% fasting = 90-130mg/dL bedtime/overnight = 90-150mg/dL ```

Diagnostic criteria for pregnant women using 75-g fasting OGTT

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

target glucose range for hospitalized patients

140-180 mg/dL

Goals for older adults (healthy)

``` A1C = < 7-7.5% Preprandial = 80-130 mg/dL Bedtime = 80-180 mg/dL ```

Goals for older adults (complex/intermediate)

``` A1C = < 8% Preprandial = 90-150mg/dL Bedtime = 110-200 mg/dL ```

Goals for older adults (very complex/poor health)

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