tentiran endokrin.pptx

7/30/2019 Tentiran Endokrin.pptx

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DWS 2010

ETIOLOGIC CLASSIFICACTION

I. Type 1 (-cell destruction leading to absolut deficiency)

A. Immune mediatedB. Idiopathic

II. Type 2

Predominantly insulin resistance + relative insulin

deficiency

Predominantly secretory defect + insulin resistance

III. Other specific types

IV. Gestasional diabetes mellitus

ADA. The Expert Committee,1997

Type 1 + Type 2 = 70 95% of diabetes


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Type 1 Type 2

Clinical Features

Age at onset

Onset

Weight Spontaneous ketosis

Chronic complication

Epidemiology

Prevalence

Sex

Insulin (C-peptide) level

Genetics

Concordance in twins

HLA asoociation

Pathology

Islet cell mass

Insulitis at onset

Immunology Associated with other

endocrinopathy

Anti-islet ell immunity

Humoral

Cell mediatedl

Usually < 30

Acute

Non obeseCommon

(++)

0,5%

Male prepdominancece

/ (-)

40%

(+) (DR3/DR4)

Severely reduced

Present

Frequent

60 80% at onset

35 50% at onset

Usually > 40

Insidious

ObeseRare

(++)

2%

Female predominance

/ N /

70 90%

(-)

Moderately reduced

?

Frequent

5 20%

< 5%

DWS 2010


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1. Symptoms (+)Casual plasma glucose > 200 mg%

(11.1 mmol/L)

or

2. FPG 126 mg% (7.0 mmol/L)

2. During OGTT

2h post 75 g glucose load 200 mg/dl

DWS 2010

.

(The Expoert Committee,1997)Fasting at least 8 h


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Normal IFG or IGT Diabetes

FPG< 100 mg/dl

IFG :FPG 100; < 126 mg/dl

FPG 100; < 126 mg/dl

2-hPG < 140 mg/dl

FPG 126 mg/dl2-hPG 200 mg/dl

Symptoms of

diabetes and causal

plasma glucose

concentration

200 mg/dl

2-hPG< 140 mg/dl IGT :FPG < 106 mg/dl

2-hPG 140; < 200 mg/dl


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Aggressive Treatment Driven by Target (AIC< 7%)

Early Combinations Oral agent oral agent

Oral agent insulin

Aggressive Insulin Treatment


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Circulation

Glucose

FFA

Liver Muscle

Pancreas

Blocks

Promotes

Adipose

Intestines

Fat

Carbohydrates

AGI

Intestinal lipase inhibitor

Insulin secretagogues

Biguanide

Biguanide

Glucoseabsorption

FFA absorption

TZD

TZD

FFA release

RESUME MECHANISM OFACTION OF OAD

DPP IVINHIBITOR


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FASTING BLOOD GLUCOSEPOST PRANDIAL BLOODGLUCOSE

Metformin

TZD

Long acting secretogoue

Basal insulin

AGI

Short actingsecretogogue

Rapid / short actinginsulin


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Pancreatic output :

basal prandial

Basal insulin : the amount of insulin necessary to prevent fasting

gluconeogenesis (fasting hyperglycemia) and ketogenesis

Prandial insulin : the amaount of insulin necessary to cover meals

without development of posprandial hyperglycemia


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Prandial HyperglycemiFasting Hyperglycemia

Insulin basal

Long-acting SUMetforminGlitazone

Insulin prandial

Short-acting SUGlinide

GlitazonesAcarbose

Incretin based


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Glucose

Adiposetissue

Gut

Stomach

Liver

Sulphonylureas andGlinides

BiguanidesMuscle

Pancreas

Insulin

a-glucosidase inhibitors

Thiazolidinediones

DPP-4

inhibitors

DPP-4

GLP-1

GLP-1analogues .


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Progressive deterioration of -cell function

Lifestyle changes

Oral agents

BasalAdd basal insulin and titrate

Basal plusAdd prandial insulin at main meal

Basal bolusAdditional prandial

doses as neededFBG above target

HbA1c above target

HbA1c abovetarget

FBG at target

HbA1c above target

Adapted from Raccah D et al. Diabetes Metab Res Rev 2007;23(4):257-64.


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T2DM is a progressive disease characterizedby increased insulin resistance and decreasingpancreatic -cell function.1

At diagnosis, patients may have already lostapproximately 50% of -cell function.2

An ideal treatment strategy for T2DM shouldprovide:

Continuity of care as the disease progresses;

Flexibility to adapt to individual needs.

1. Bergenstal RM. In: Textbook of Diabetes Mellitus, 3rd

edition: John Wiley & Sons; 2004: pp. 995-1015.2. Holman RR. Diabetes Res Clin Pract 1998;40(Suppl 1):S21-5.


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* Check HbA1c every 3 months until HbA1c


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1. ADA. Diabetes Care 2006;29(Suppl 1):S4-S42.2. ADA. Diabetes Care 2006;29(Suppl 1):S43-8.

3. IDF. Global Guideline for Type 2 Diabetes. Brussels: International Diabetes Federation, 2005.

http://www.idf.org/webdata/docs/IDF%20GGT2D.pdf.4. Nathan DM et al. Diabetologia 2006;49:1711-21.

* DCCT referenced assays: normal range 4-6%; ** 1-2 hours postprandial; ADA and ADA/EASD guidelines recommend HbA1c levels as close to normal (


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DiabeticRetinopathy

Leading causeof blindnessin working age

adults1

DiabeticNephropathy

Leading cause ofend-stage renal disease2

Cardiovascular

Disease

Stroke2 to 4 fold increase incardiovascularmortality and stroke3

DiabeticNeuropathy

Leading cause ofnon-traumatic lowerextremity amputations5

8/10 diabetic patientsdie from CV events4

1 Fong DS, et al.Diabetes Care 2003; 26 (Suppl. 1):S99S102. 2Molitch ME, et al.Diabetes Care 2003; 26 (Suppl. 1):S94S98.3 Kannel WB, et al.Am Heart J1990; 120:672676. 4Gray RP & Yudkin JS. In Textbook of Diabetes 1997.

5Mayfield JA, et al.Diabetes Care 2003; 26 (Suppl. 1):S78S79.


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Diabetic Neuropathy (DN) are among the mostfrequent complications of diabetes mellitus, leadingto great morbidity and mortality.

Neuropathy is generally considered to be related to

duration and severity of hyperglycaemia.However it may also occur acutely even withhypoglycaemia

Epidemiologic data suggest that approximately 30%to 50% of people with type 2 diabetes have a distalperipheral neuropathy.

The major morbidity is foot ulceration, which canlead to gangrene and ultimately to limb loss.

Diabetic neuropathy is a small-fiber disease


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Table 4: Symptoms and signs of autonomic neuropathy.

1. Cardiovascular

Postural hypotension

Resting tachycardiaPainless myocardial infarction

Sudden death (with or without association with general anaesthesia)

Prolonged QT interval

2. Gastrointestinal

Oesophageal motor incoordination

Gastric dysrhythmia, hypomotility (gastroparesis diabeticorum)

Pylorospasm.

Uncoordinated intestinal motility (diabetic diarrhoea, spasm)

Intestinal hypomotility (constipation)

Gallbladder hypocontraction (diabetic cholecystopathy)

Anorectal dysfunction (faecal incontinence)


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Table 4: Symptoms and signs of autonomic neuropathy (continued)

3.Genitourinary

Diabetic cystopathy (impaired bladder sensation, atonic bladder,

post micturition dribbling, detrusor hyporeflexia or hyperreflexia)

Male impotence

Ejaculatory disorders

Reduced vaginal lubrication, dyspareunia

4. Respiratory Impaired breathing control (?)

Sleep apnoea ?

5.Thermoregulatory

Sudomotor

Vasomotor

6. Pupillary

Miosis

Disturbances of dilatation

Argyll Robertson pupil


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Pain is the most common symptom which could besuperficial, deep or aching.

The management of pain is often difficult anddisappointing

Treatment of Neuropathic Pain Adjuvant Analgesics

: Antidepressants Anticonvulsants Analgesic antiarrhythmics Sympatholytic agents

Topical agents NMDA receptor antagonists Opioids Other

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