Diabetes Mellitus Type 1 - PowerPoint Presentation

Slide1

Diabetes Mellitus

Type 1

Gary

Strokosch

, MD

Region V Medical Specialist

Type 2

Drew Alexander, MD

Region IV Medical Specialist

November 4, 2013Slide2

Two Main Types of Diabetes

Type 1: formerly known as insulin-dependent diabetes mellitus (IDDM) or juvenile onset diabetes

Type 2: formerly known as non-insulin-dependent diabetes mellitus (NIDDM) or adult onset diabetesSlide3

Type 1 Diabetes

Type 1 accounts for only 10% of all cases of diabetes, but demands daily treatment with insulin.

Type 1 alarms new patients with a variety of symptoms during a brief latency period.Slide4

Diagnosis

A diagnosis of diabetes is made if the fasting glucose is >125 mg/

dL

, or if a 2-hour GTT results in a glucose >200 mg/

dL

.

However, one abnormal glucose value is all that is needed in a patient with classical symptoms of diabetes, such as polyuria or polydipsia.

A HgA1C ≥6.5% was added in 2010.

The diagnosis of diabetes should never be made on the basis of glucose in the urine (glycosuria).Slide5

Glucose Testing

Impaired

Fasting Glucose

75 gm Glucose Tolerance

110-125 mg/

dL

140-200 mg/

dL

Diabetes

Fasting Glucose

75 gm Glucose Tolerance

>125 mg/

dL

>200

mg/

dLSlide6

Glucohemoglobin

HbA

1C

is a measure of integrated glucose control over the preceding 2-3 months and reflects the average life of a red blood cell.

Glucose becomes attached to hemoglobin in a non-enzymatic fashion that is dependent on the average concentration of blood glucose.Slide7

Glucohemoglobin

HbA1

c

Glucose mg/

dL

5

97

(76-120)

6

126 (100-152)

7

154 (123-185)

8

183 (147-217)

9

212 (170-249)

10

240 (193-282)

11

269 (217-314)

12

298

(240-347)

13

326 (260-380)

14

355 (290-410)

15

384

(310-440)Slide8

Historical NotesAbout Types of Diabetes

1550 BC: The oldest description of diabetes was noted to be a

polyuric

condition in ancient Egypt.

In the 5th/6th century BC: The descriptions of diabetes recognized the distinction between two forms of diabetes, one in older, fatter people (type 2), and the other in thin people who rapidly succumbed to their illness (type 1).Slide9

Additional HistoryAbout Diabetes

2nd century AD: Because of the symptom of polyuria,

Aretaeus

of Cappadocia first used the term “diabetes”, which comes from Greek, meaning “siphon” or “pass through”.

10th century AD: Avicenna, living in Arabia, recognized the sugary nature of urine in diabetes.Slide10

Additional HistoryAbout Diabetes

17th century AD: Thomas Willis, physician to King Charles II, rediscovered the sweetness in the urine of subjects with diabetes.

1776: Matthew Dobson showed that urinary sweetness was caused by sugar and was associated with a rise in blood sugar.Slide11

Additional HistoryAbout Diabetes

End of 18th century: John Rollo first used the term “diabetes mellitus” (honey) to distinguish the condition from “diabetes

insipidus

”, or tasteless urine.

1869: Paul

Langerhans

discovered the pancreatic islets that bear his name.Slide12

Additional HistoryAbout Diabetes

1889: Oskar

Minkowski

removed the pancreas from a dog and discovered that the animal developed diabetes.

1893:

Edouard

Laguesse

showed that

Langerhans

’ islets were the endocrine tissue of the pancreas.Slide13

Additional HistoryAbout Diabetes

THE GAME CHANGER!

1921: Frederick

Banting

, Charles Best, James

Collip

& JJR Macleod discovered insulin.

1920s: The first patients with diabetes were treated with insulin.Slide14

Before and after pictures of one of the first people with diabetes to receive Insulin in the 1920sSlide15

History In The Time OfTransplant Development

1955: The primary structure of insulin elucidated by Frederick Sanger.

1969: Dorothy Hodgkin described the three-dimensional structure of insulin using X-ray crystallography.

1980: Recombinant human insulin was introduced.

1996: Insulin analogues were introduced.Slide16

What Causes Type 1 Diabetes?

Type 1 diabetes is cause by an absolute deficiency of insulin, a hormone which is produced in the beta cells of the Islets of

Langerhans

in the pancreas.

Although poorly understood, it is likely that (1) some environmental factor triggers a (2) selective autoimmune destruction of the beta cells in (3) a genetically predisposed individual. Slide17

Age-standardized incidence of type 1 diabetes

in children (per 100,000/year)

Worldwide DifferencesSlide18

Presenting Symptoms

Polyuria / Nocturia

Thirst

Polydipsia

Polyphagia

Weight Loss

KetoacidosisSlide19

Diabetic Ketoacidosis:

A Rapid Onset Life-threatening Complication

Consists of

hypergycemia

, ketosis and acidosis

10-25% of episodes of DKA result from new patients presenting for the first time

30-40% of episodes are from infections

Most of the rest are from stopping insulin

1-2% mortality during each episodeSlide20

Mortality / Morbidity

Prior to 1921 the development of type 1 diabetes meant an almost certain death shortly after diagnosis.

A significant proportion of deaths in young diabetics are attributable to DKA.

Later deaths are more commonly associated with cardiovascular and renal disease.Slide21

Chronic Complications

Retinopathy

: most common cause of blindness in people of working age

Nephropathy

: 20-44% of all new patients needing renal replacement therapy have diabetes

Erectile Dysfunction

: may affect up to 50% of men with long-standing diabetes

Macrovascular Disease

: 2-3 fold increased risk of coronary heart disease and stroke

Foot Problems

: 15% of people with diabetes develop foot ulcers; 5-15% of people with diabetic foot ulcers need amputationsSlide22

Applicant File Review

Three things to remember

Treatment of type 1 diabetes is not optional and without treatment it will inevitably lead to death, as happened prior to 1921.

Some new patients have a “grace period” of weeks or months with minimal need for insulin after starting treatment. Management plans change frequently during the first few months of treatment and can require repeated adjustments of insulin timing and dose.

Highly effective self-management by an adolescent patient is unlikely and is not the criterion for entry into JC.Slide23

Treatment

Insulin

Management of carbohydrate intake

Exercise Slide24

Insulin Development

1921/22: In the US the original insulin was from bovine and later porcine sources

1982: Biosynthetic insulin was introduced

1996: Analogue

insulins

were introducedSlide25

Insulin Names

Generic

a

spart

glulisine

l

ispro

r

egular

NPH

d

etermir

g

largine

Brand

Novolog

Apidra

Humalog

Humulin

R /

Novolin

R

Humulin

N /

Novolin

N

Levemir

LantusSlide26

Insulin Names

Acting

Generic

Brand

Rapid

Aspart

Novolog

Glulisine

Apidra

Lispro

Humalog

Short

Regular

Humulin

R/

Novolin

R

Intermed

.

NPH

Humulin

N/

Novolin

N

Long

Determir

Levemir

Glargine

Lantus

Slide27

Insulin Action

Rapid Acting

Novolog

Apidra

Humalog

Short Acting

Humulin

R

Novolin

R

Onset: 15-30 min

Peak: ½-2

hrs

Duration: <6

hrs

Onset: 30-60 min

Peak: 2-4

hrs

Duration: 6-12

hrsSlide28

Insulin Action

Intermed

. Acting

NPH

Long Acting

Levemir

Lantus

Onset: 1-2 hrs

Peak: 4-14 hrs

Duration: 10-24 hrs

Onset: 1 hr

Peak: none

Duration: 6-24 hrsSlide29

Pre-mixed Insulins

(biphasic)

Novolog

mix:

aspart

protamine

/

aspart

70/30 mix (vials and pens)

Humalog

mix:

lispro

protamine

/

lispro

50/50 mix (vials and pens)

75/25 mix (vials and pens)

Novolin

mix: NPH / regular

70/30 mix (vials)

Humulin

mix: NPH / regular

70/30 mix (vials and pens)

50/50 mix (discontinued in US)Slide30

Treatment Regimens

Pre-mixed insulin twice daily (2 shots daily)

Basal-bolus regimen with rapid acting insulin at the three meals and long acting insulin at bed time (4 shots daily)

Continuous subcutaneous insulin infusion (CSII) or insulin pumps (1 needle insertion every 3 days)Slide31

FRONT

BACK

Injection SitesSlide32

Injection Site Side Effects

Lipohypertrophy

: when insulin is repeatedly injected into the same site there can be a local tropic effect and lead to lumps at the site and compromise absorption of insulin

Lipoatrophy

: immunoglobulin G immune complexes against insulin can form and produce atrophy as well as compromise the action of insulin Slide33

Omnipod Insulin PumpSlide34

Medtronics Insulin PumpSlide35

Medtronics ConnectionsSlide36

Hypoglycemia

When blood glucose falls below 63 mg/dL

The most common side effect of insulin therapy

A barrier to obtaining optimal glycemic control

Most type 1 patients will experience several mild episodes per week and 1-2 severe episodes per year needing outside help

Occurs more frequently in young patients and those under tight glycemic controlSlide37

Hypoglycemia Signs/Symptoms

Autonomic

Sweating

Pins & needles

Feeling hot

Shakiness

Anxiety

Palpitations

Pallor

Neuroglycopenic

Difficulty speaking

Loss of concentration

Drowsiness

Dizziness

Hemiplegia

Fits

Coma

Non-specific

Nausea

Hunger

WeaknessSlide38

Type II Diabetes Mellitus (DM II)

It is the most common glucose disorder

Use of meds: 1994 1:63 and 2007 1:14 youth

Insulin resistance is its dominant feature

R

esistance most often results from unhealthy lifestyle behaviors

Medication often helps as adjunctive therapySlide39

Glucose Disorder: DM II

Genetic,

cytogenic

precursors (to be defined)

Defect in the transport or storage of

insulin

and/or glucose

Defect in fat, liver and muscle cells response

Slow onset of hyperglycemia

and symptomsSlide40

Contributing Factors to DM Type II

Family and parental influence

Cultural/Environmental/Community

Influence

Personal lifestyle behavior influenceSlide41

Variants Inclusive of DM Type I and II

Maturity Onset of Youth (MODY)

Combined Variant DiabetesSlide42

“Ounce of Prevention=Pound of Cure”

Health and wellness

Student life

Academic and trade

HEALS “Healthy Eating and

Active Lifestyles”

TEAP / TUPPSlide43

Onset / Monitoring

Any age where precipitating factors exist

Gradual, slow in onset delaying early

dx

Initial symptoms may wax and wane

More

often diagnosis is made on center

Biochemical testing, monitoring and risks are the same as

DM I

with the exception of glucose swings and mortalitySlide44

Symptoms often Associated with DM II

Loss of energy / stamina and fatigue

Gradual decline in activity and performance

Unusual increase in appetite

Unusual increase in thirst

Increased frequency of urination

Increased frequency awakening to urinate

Often but not always overweightSlide45

Treatment Goals

Medical evaluation and management plans

Address lifestyle behaviors (HEALs on center)

Certified Diabetic Education

Adopt a lifestyle reducing insulin resistance

Lifetime monitoring DM II (CCMP on center)Slide46

Diabetic Education / Management

Wellness team assessing / promoting health

Medical team diagnosing and treating

Measurable change in student’s life behavior

Life time monitoring: CPP, CDP and CTPSlide47

Lifestyle Behavior

Monitor: Weight, BMI, BP, UA,

Fam

Hx

, labs

Monitor Diet: Balance

carbs

, fats and protein

Monitor Daily Activity: Scheduled and not

Monitor Sleep Patterns: Quality lasting @8hrs

Monitor Stress Reduction: MH/ counselor/ RA

Reduce risk behavior

Reduce susceptibility to infectious diseaseSlide48

Common Pharmacologic Adjuncts

Alpha-

glucosidase

Inhibtors

(

ie

Acarbose

)

Biguanides

(i.e., Metformin)

Meglitinides

(i.e.,

Repaglinide

/

Nateglinide

)

Sulfonylureas (i.e.,

Tolazimide

Glimepiride)

Thiazolidinediones

(i.e., Rosiglitazone)

Injectibles

(i.e.,

Exenatide

/

Sitagliptin

)Slide49

Management of DM on a JC Center

When the IDT sees an applicant with DM I or II is this grounds for rejection?

When DM is diagnosed on center, should the wellness team do the work up and begin Rx?

To best manage DM, especially type II, who on center needs to know the students status? Slide50

PRH 6.12, R11: MSWR

Students are medically separated:

when they are determined to have a health condition that significantly interferes with or precludes further training in JC,

when the health problem is too complicated to manage, or

when the necessary treatment will be unusually costly.Slide51

Thank you for your attention.

Questions?