Upload
hendradarmawan4
View
221
Download
0
Embed Size (px)
Citation preview
7/30/2019 Tentiran Endokrin.pptx
1/21
7/30/2019 Tentiran Endokrin.pptx
2/21
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
7/30/2019 Tentiran Endokrin.pptx
3/21
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
7/30/2019 Tentiran Endokrin.pptx
4/21
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
7/30/2019 Tentiran Endokrin.pptx
5/21
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
7/30/2019 Tentiran Endokrin.pptx
6/21
Aggressive Treatment Driven by Target (AIC< 7%)
Early Combinations Oral agent oral agent
Oral agent insulin
Aggressive Insulin Treatment
7/30/2019 Tentiran Endokrin.pptx
7/21
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
7/30/2019 Tentiran Endokrin.pptx
8/21
FASTING BLOOD GLUCOSEPOST PRANDIAL BLOODGLUCOSE
Metformin
TZD
Long acting secretogoue
Basal insulin
AGI
Short actingsecretogogue
Rapid / short actinginsulin
7/30/2019 Tentiran Endokrin.pptx
9/21DWS 2010
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
7/30/2019 Tentiran Endokrin.pptx
10/21DWS 2010
Prandial HyperglycemiFasting Hyperglycemia
Insulin basal
Long-acting SUMetforminGlitazone
Insulin prandial
Short-acting SUGlinide
GlitazonesAcarbose
Incretin based
7/30/2019 Tentiran Endokrin.pptx
11/21DWS 2010
Glucose
Adiposetissue
Gut
Stomach
Liver
Sulphonylureas andGlinides
BiguanidesMuscle
Pancreas
Insulin
a-glucosidase inhibitors
Thiazolidinediones
DPP-4
inhibitors
DPP-4
GLP-1
GLP-1analogues .
7/30/2019 Tentiran Endokrin.pptx
12/21
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.
7/30/2019 Tentiran Endokrin.pptx
13/21
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.
7/30/2019 Tentiran Endokrin.pptx
14/21
* Check HbA1c every 3 months until HbA1c
7/30/2019 Tentiran Endokrin.pptx
15/21
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 (
7/30/2019 Tentiran Endokrin.pptx
16/21
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.
7/30/2019 Tentiran Endokrin.pptx
17/21
7/30/2019 Tentiran Endokrin.pptx
18/21
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
7/30/2019 Tentiran Endokrin.pptx
19/21
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)
7/30/2019 Tentiran Endokrin.pptx
20/21
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
7/30/2019 Tentiran Endokrin.pptx
21/21
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