Download - Bimbingan UKMPPD (UKDI) - Interna 1 (Endokrin, Pulmonologi)

7/26/2019 Bimbingan UKMPPD (UKDI) - Interna 1 (Endokrin, Pulmonologi)

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INTERNA 1

Endokrin

Pulmonologi

Bimbel UKDI MANTAP


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Bimbel UKDI MANTAP

ENDOKRIN


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DiabetesMelitus

DislipidemiaSindrom

Metabolik

Hipertiroid danTirotoksikosis

HipotiroidHiperparatiroidHipoparatiroid

DiabetesInsipidus

CushingsSyndrome

AddisonDisease

Bimbel UKDI MANTAP

MATERI


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Bimbel UKDI MANTAP

Metabolic actions of insulin


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Diabetes Melitus

Suatu kelompok penyakit metabolikdengan karakteristik hiperglikemia

karena kelainan pada

Kerja insulin (resistensiinsulin) di hati

(peningkatan produksiglukosa hepatik) dan dijaringan perifer ( otot

dan lemak)

Sekresi insulin oleh selbeta pankreas

Atau keduanya

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Bimbel UKDI MANTAP

Destruksi sel islet B pankreas yang secara dominan disebabkanoleh proses autoimun (90%) dan idiopatik (10%)insulin (-)glukagon plasma meningkat, sel B pankreas gagal beresponterhadap semua stimuli insulinogenikbutuh insulin eksogen

Diabetes Melitus Tipe 1


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Kadar glukosa darah rata-rata antara 70-110 mg/dlmempertahankan metabolisme sel

makanan(karbohidrat)

diserap(yeyunum)

sistemportal hati

monosakarida

sel target

glukosa

GLUT

insulin

transkripsi

mRN

reseptor insulin

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Bimbel UKDI MANTAP

Diabetes Melitus Tipe 2

Resistensi insulin di selsel betamasih bs kompensasisekresiinsulinhiperinsulinemiasel

beta lelahinsulin hiperglikemi awal (hny saat postprandial)insulin makin

glukosa puasa (hepar memecahglukosa)hiperglikemi fase lanjutmemperberat gangguan sekresiinsulinGLUKOTOKSISITAS dan

LIPOTOKSISITAS (krn resistensi

insulin jg lipolisis )FFAgangg uptake glukosa , gangg

sekresi insulin)


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Faktor Risiko DM tipe 2

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Faktor risiko yang tidak bisadimodifikasi

Ras dan etnik

Riwayat keluarga dengandiabetes (anakpenyandang diabetes)

Usia > 45 tahun Riwayat melahirkan bayi

dengan BB lahirbayi>4000 gram atauriwayat pernahmenderita DMgestasional (DMG)

Riwayat lahir denganberat badan rendah,kurang dari 2,5 kg

Faktor risiko yang bisadimodifikasi

Berat badan lebih (IMT >23 kg/m2)

Kurangnya aktivitas fisik

Hipertensi (> 140/90

mmHg) Dislipidemia (HDL < 35

mg/dL dan atautrigliserida > 250 mg/dL)

Diet dengan tinggi guladan rendah serat

Faktor lain yang terkaitdengan risiko diabetes

Penderita PolycysticOvary Syndrome (PCOS)atau keadaan klinis lainyang terkait dengan

resistensi insulin Penderita sindrom

metabolik memilikiriwayat toleransi glukosaterganggu (TGT) atauglukosa darah puasaterganggu (GDPT)

sebelumnya Memiliki riwayat penyakit

kardiovaskular, sepertistroke, PJK, atau PAD(Peripheral ArterialDiseases)


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Pemeriksaan penyaring dilakukan pada mereka yang mempunyairisiko DM namun tidak menunjukkan adanya gejala DM

Pemeriksaan penyaring dapat dilakukan melalui pemeriksaan

kadar glukosa darah sewaktu atau kadar glukosa darah puasa.

Untuk kelompok risiko tinggi yang tidak menunjukkankelainan hasil, dilakukan ulangan tiap tahun.

Bagi mereka yang berusia >45 tahun tanpa faktor risiko lain,pemeriksaan penyaring dapat dilakukan setiap 3 tahun.

Bimbel UKDI MANTAP

SkriningDM


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What is prediabetic?

Prediabetes

Kondisi dimana

kadar gula darahterlalu tinggi untukdianggap normal,tetapi tidak cukuptinggi untukdilabelkan sebagai

diabetes.

GDPT (Glukosa Darah Puasa Terganggu)

Glukosa plasmapuasa didapatkanantara 100125mg/dL(5,66,9mmol/L) danpemeriksaan TTGOgula darah 2 jam BBI

+ 10 %

Faktor-faktor yang menentukan kebutuhan kalori

Jenis Kelamin

Wanita sebesar 25 kal/kgBB

Pria sebesar 30 kal/kgBB.

Umur

Dikurangi 5% usia 40-59 tahun,

Dikurangi 10% usia 60 -69 tahun

Dikurangi 20% usia > 70 tahun.

Aktivitas Fisik atau Pekerjaan

+ 10% dari kebutuhan basal diberikan padakedaaan istirahat,

+ 20% aktivitas ringan,

+ 30% aktivitas sedang,

+ 50% aktivitas sangat berat.

Berat Badan

Kegemukan dikurangi sekitar 20-30%

Bila kurus ditambah sekitar 20-30% sesuaidengan kebutuhan untuk meningkatkan BB.

Untuk tujuan penurunan berat badan jumlahkalori yang diberikan paling sedikit

1000-1200 kkal perhari untuk wanita

1200-1600 kkal perhari untuk pria.

Total kalori dibagi dalam 3 porsi besar untukmakan pagi (20%), siang (30%), dan sore (25%),

serta 2-3 porsi makanan ringan (10-15%) diantaranya


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Karbohidrat

Karbohidrat yang dianjurkan sebesar 45-65% total asupan energi.

Makanan harus mengandung karbohidrat terutama karbohidrat berserat tinggi.

Pemanis alternatif dapat digunakan sebagai pengganti gula, asaltidak melebihi batas aman konsumsi harian(Accepted Daily Intake)

Lemak

Asupan lemak dianjurkan sekitar 20-25% kebutuhan kalori. Tidak diperkenankan melebihi 30% total asupanenergi.

Lemak jenuh < 7% kebutuhan kalori

Lemak tidak jenuh ganda < 10%, selebihnya dari lemak tidak jenuh tunggal.

Bahan makanan yang perlu dibatasi adalah yang banyak mengandung lemak jenuh dan lemak trans antara lain:daging berlemak dan whole milk.

Anjuran konsumsi kolesterol


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Bimbel UKDI MANTAP

3

PELATIHAN

JASMANI

Frekuensi: jumlah olahraga perminggu sebaiknya dilakukan secarateratur 3-5 kali per minggu

Intensitas: ringan dan sedang (60-70% Maximum Heart Rate)

Durasi: 30-60 menit

Jenis: latihan jasmani endurans (aerobik) untuk meningkatkankemampuan kardiorespirasi seperti jalan, jogging, berenang, dan

bersepeda.

CONTINOUS, latihan yang dilakukanharus terns-menerus

(berkelanjutan) selama 50-60 menittanpa berhenti.

RHYTHMICAL, latihan dilakukansecara berirama dan teratur, tidak

asal-asalan.

INTERVAL, latihan yang dilakukansebaiknya dilaksanakan secara

berselang-seling, kadang cepat,tetapi kadang juga lambat tetapitanpa berhenti. Misalnya jalan

cepat, kadang berlari, kemudianjalan cepat lagi.

PROGRESSIVE, Arti dari tahap iniadalah latihan dilakukan secarabertahap dengan beban latihan

ditingkatkan secara perlahan-lahan.

ENDURANCE, merupakan latihanketahanan, untuk meningkatkan

kesegaran jantung dan pembuluhdarah penderita.


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Bimbel UKDI MANTAP

Farmakoterapi DiabetesMelitus Tipe 1


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INTERVENSI

FARMAKOLOGIS

DM TIPE 2

4

Cheng A, Fantus G. Can Med Assoc J 2005;172:21326.. Barnett A. Int J Clin Pract 2006;60:145470. Prez Lpez G, et al. Nefrologia. 2010;30:61825.

Liver

Muscle

PancreasIntestines

Circulatory System

Glucose

FFA

MetforminTZD

FFA

release

GLP-1

agonist

Insulin

release

AGI

Glucose

absorption

Intestinal

lipase inhibitor

Carbohydrates

Fat

TZDMetformin

Blocks

Promotes

DPP-4

inhibitor

Adipose

AGI: -glucosidase inhibitors; DPP-4: dipeptidyl peptidase-4; FFA: free fatty acid; TZD: thiazolidinedione

SU


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Konsensus PERKENI 2011:

9% 9-10% >10%

Kadar HbA1c

GHS

Gaya Hidup Sehat

Penurunan BB

Mengatur diit

Latihan Jasmani

teratur

GHS

+

Monoterapi

Met, SU, AGI,

Glinid, TZD,

DPP-IV inh

GHS

+

Kombinasi

2 obat

Met, SU, AGI,Glinid, TZD,

DPP-IV inh

GHS

+

Kombinasi3 obat

Met, SU, AGI,

Glinid, TZD,

DPP-IV inh

GHS+

Kombinasi

2 obat

Met, SU,

AGI, Glinid,

TZD

+

Basal

Insulin

GHS

+

Insulin

Intensif

Catatan

1. Dinyatakan gagal bila dengan

terapi 2-3 bulan tidak mencapai

target HbA1c


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Berdasarkan

cara kerjanya,OHO dibagimenjadi 5golongan

(PERKENI 2011):

Pemicu sekresiinsulin (insulinsecretagogue):

sulfonilurea danglinid

Peningkatsensitivitasterhadapinsulin:

metformin dan

tiazolidindion

Penghambatglukoneogenesis (metformin)

Penghambatabsorpsiglukosa:

penghambatglukosidase

alfa.

DPP-IV inhibitor

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Sulfonilureas

First line treatment in non obese patients withtype 2 DM

Stimulating a receptor on the surface cellsclosing K+ channel and opening Ca++ channel

insulin release

Bimbel UKDI MANTAP

Sulphonylurea

Efficacy Safety, Tolerability and Adherence

HbA1c reduction of 1-2%

FPG reduction of 40-70 mg/dl

Associated with hypoglycaemia

and weight gain.

Precaution :long acting SU(elderly, hepar-renal insuffisient,

cardiovascular, malnutrisi)

Long term use NOT

RECOMMENDED


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Sulfonylurea Length of

action

Begins of

action

Daily dose

(mg)

Route of

excretion

Glibenclamide 1624h 24h 1,2515 R = 50%, B = 50%

Gliclazide 1024h 24h 40320 R = 70%, B = 30%

Glipizide 624h 24h 2,540 R = 80%, B =20%

Chlorpramide 2472h 24h 100500 Renal

Tolbutamide 610h 24h 1001000 Renal

Glimepiride 24h 24h 1 - 6 R = 40%, B =60%

gliquidon 18 - 24h 2 - 4h 30 - 120 R = 5%, B = 95%

Bimbel UKDI MANTAP

Interaksi ObatMeningkatkan Aksi SU

Warfarin

Sulfonamid

Salisilat

Fenilbutazon

Propranolol

Kloramfenikol

Ketoconazol

Interaksi ObatMenurunkan Aksi SU

Diuretik

Kortikosteroid

Kontrasepsi Oral

Fenitoin

Fenobarbital

Rifampisin


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Bimbel UKDI MANTAP

Glinide

Efficacy* Safety, Tolerability and Adherence

HbA1c reduction of 0.5-1.5%

FPG reduction of 20-60 mg/dl

PPGreduction of 75-100mg/dl

Associated with weight gain. Associated with a much lower

incidence of hypoglycemia.

Taken just before or with meals,

and the stimulation of thepancreas is limited only to a brief

time around meals.


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Bimbel UKDI MANTAP

METFORMIN

Mekanisme Obat

Mempunyai efekutama mengurangiproduksi glukosa hati

(glukoneogenesis)

Memperbaikiambilan glukosa

perifer.

Memberikan efek samping mual. Untukmengurangi keluhan tersebut dapat

diberikan pada saat atau sesudah makan.

Terutama dipakai padapenyandang diabetes gemuk


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Bimbel UKDI MANTAP

Metformin

Efficacy*Safety, Tolerability and

AdherenceContraindications Advantages

HbA1c : 1-2%

FPGreduction

of 40-70 mg/dl

Associated with

diarrheaand

abdominal

discomfort

Latic acidosis if

improperly

prescribed

Renal

insufficiency

Liver failure

Heart failure

Severe

gastrointestinal

disease

Do not cause

hypoglycaemia

when used as

mono-therapy

Do not cause

weight gain;

may contribute

to weight loss


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Bimbel UKDI MANTAP

TIAZOLIDINEDION

Tiazolidinedion (pioglitazon) berikatan padaPeroxisome Proliferator Activated Receptor Gamma

(PPAR-g), suatu reseptor inti di sel otot dan sel lemak.

Golongan ini mempunyai efek menurunkanresistensi Insulin dengan meningkatkan jumlah

protein pengangkut glukosa, sehinggameningkatkan ambilan glukosa di perifer.

Tiazolidinedion dikontraindikasikan pada pasiendengan gagal jantung kelas I-IV karena dapatmemperberat edema/retensi cairan dan juga

pada gangguan faal hati.

Pada pasien yang menggunakan tiazolidinedionperlu dilakukan pemantauan faal hati secara

berkala


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Thiazolidinediones

Efficacy*Safety, Tolerability and

AdherenceContraindications Advantages

HbA1c

reduction of

0.5-1.5%

FPG reduction

of 20-55 mg/dl

Associated with

weight gain and

edema

Contraindicated

in patients withabnormal liver

function

Warnings

regarding risk of

fractures

May exacerbateor precipitate

congestive heart

failure

Liver disease,

heart failure or

history of heart

disease

Pregnancy andbreast feeding

Reduced levels

of LDL-

cholesterol and

increased level

of HDL-

cholesterol


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Acarbose

Act byinhibiting

disaccharidases in the

small bowel

Delayenzymatic

digestion of

complexcarbohydratedelay

absortiongradual fluxin of glucose

concetrationin portalvessels

Reducingpostprandialhyperglycemi

a (HbA1c:0,5%)

Side effects:

Significantcarbohydratemalabsorptio

nflatulence,abdominal

bloating anddiarrhoea

Reduced thestarting doseof 50 mg/day

andmaintenance

50-100 mgeach meal

Take eachdose with

the first biteof each main

meal.

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Carbohydrate

absorption

Duodenum Jejunum Ileum

Without acarbose

With acarbose

Jejunum

Ileum

Jejunum

Ileum

Without acarbose With acarbose

Carbohydrate

absorption

Carbohydrate

Acarbose delays carbohydrate absorption

Bimbel UKDI MANTAP

Intestinalcarbohydrate

absorption is retarded

by -glucosidase

inhibition1. Lower pp blood glucose

increase

2. Carbohydrates come into

lower intestinal sections

and induce there the

release of the intestinalhormone GLP-1


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Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin (DPP IV-Inhibitor)

Exenatide, Liraglutide (GLP 1 Agonist )

Bimbel UKDI MANTAP

Glucagon-like peptide-1 (GLP-1)merupakan suatu hormon

peptida yang dihasilkan oleh sel L

di mukosa usus.

Peptida ini disekresi oleh selmukosa usus bila ada makananyang masuk ke dalam saluran

pencernaan.

GLP-1 merupakan perangsangkuat penglepasan insulin dan

sekaligus sebagai penghambat

sekresi glukagon.

Namun demikian, secara cepatGLP-1 diubah oleh enzimdipeptidyl peptidase-4 (DPP-4),menjadi metabolit GLP-1 (9,36)-

amide yang tidak aktif.

Sekresi GLP-1 menurun pada DM

tipe 2, sehingga upaya yangditujukan untuk meningkatkanGLP-1 bentuk aktif merupakanhal rasional dalam pengobatan

DM tipe 2.

Peningkatan konsentrasi GLP-1

dapat dicapai dengan pemberianobat yang menghambat kinerjaenzim DPP-4 (penghambat DPP-

4), atau memberikan hormon asliatau analognya (analogincretin=GLP-1 agonis).

Slide 39


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DPP- 4 inhibitorsand GLP1 Agonist

Drucker DJ et al. Nature 2006;368:1696705. Idris I, et al. Diabetes Obes Metab 2007;9:15365. Barnett A. Int J Clin Pract 2006;60:145470. Gallwitz B, etal. Diabetes Obes Metab 2010;12:111.

DPP-4: dipetidyl peptidase-4; GI: gastrointestinal; GIP:glucose-dependent insulinotropic polypeptide; GLP-1: glucagon-like peptide

Increases and prolongs

GLP-1 effect on -cells

Increases and prolongs GLP-1

and GIP effects on -cells

Food intake

Stomach

GI tract

Intestine

-cells

Pancreas

Glucose-dependent

insulinsecretion

-cellsDPP-4inhibitor

Glucose-dependent

glucagonsecretion

Incretins(GLP-1, GIP)

DPP-4

* GIP does not inhibit glucagon secretion by -cells

Improve IncretinActivity and Correct theInsulin:Glucagon Ratio

Slide 40


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DPP-4 inhibitors

DPP-4 inhibitors

Efficacy* Safety, Tolerability and Adherence

HbA1c reduction of 0.5-

1%

FPG reduction of 20

mg/dl

PPGreduction of 45-55

mg/dl

Generally well tolerated

Low risk of hypoglycemia

Notassociated with weight gain Upper respiratory tract infection

has been reported in clinical

studies

Most require only once daily

administration

Ahrn B. Expert Opin Emerg Drugs 2008;13:593607. Gallwitz B, et al. Diabetes Obes Metab 2010;12:111. Amori RE, et al. JAMA 2007;298:194206.

Saxagliptin, FDAs Endocrinologic and Metabolic Drugs Advisory Committee Briefing Document for April 2009 Meeting: NDA 22 -350. Available at:http://www.fda.gov/OHRMS/DOCKETS/ac/09/briefing/2009-4422b1-02-Bristol.pdf. (accessed Nov 2010). Aschner P, et al. Diabetes Care 2006;29:26327.

* Efficacy depends on existing blood glucose levels


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Waktu Penggunaan OHO

Bimbel UKDI MANTAP

Sulfonilurea : 15-30 menit sebelum makan

Repaglinid; Nateglinid : sebelum/sesaat sebelum makan

Acarbose : bersama makan pada suapan pertama

DPP IV inh : Sebelum /bersama makan

Metformin : pada sebelum/saat/sesudah makan

Tiazolidinedion : tidak bergantung pada jadwal makan


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INDIKASI INSULIN

Penurunan beratbadan yang cepat

Hiperglikemia beratyang disertai ketosis

Ketoasidosis diabetikHiperglikemiahiperosmolar

nonketotik

Hiperglikemia denganasidosis laktat

Gagal dengankombinasi OHO dosis

optimal

Stres berat (infeksisistemik, operasi besar,

IMA, stroke)

Kehamilan dengan

DM/diabetes melitusgestasional yang tidak

terkendali denagnperencanaan makan

Gangguan fungsi ginjaldan hati yang berat

Kontraindikasi dan ataualergi terhadap OHO.

Bimbel UKDI MANTAP

Efek Samping

Hipoglikemia Reaksi imunologi terhadap insulin yang

dapat menimbulkan alergi insulin atauresistensi insulin

Penambahan berat badan

HipokalemiaHbA1c > 10%

GDP > 250 mg/dl

GDS > 300 mg/dl


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Insulin preparat

Onset ofaction

(Minutes)

Peakaction

(Minutes)

Effectiveduration of

action(hours)

Insulin prandial (mealrelated)

Human Insulin short

actingInsulin Regular, (Actrapid,Humulin R)

30-60 30-90 3-5

Insulin analog rapidacting

Insulin lispro (Humalog R) 5-15 30-90 3-5

Insulin glulisine (Apidra) 5-15 30-90 3-5

Insulin aspart (Novo Rapid) 5-15 30-90 3-5

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Insulin preparat

Onset ofaction

(hours)

Peak action(hours)


action(hours)

Insulin intermediateacting

NPH (Insulatard,

Humulin N)

2-4 4-10 10-16

Insulin long-acting

Insulin glargine (lantus) 2-4 No peak 18-26

insulin detemir (Levemir) 2-4 No peak 22-24

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Bimbel UKDI MANTAP

Insulin preparat

Onset ofaction

(minutes)

Peak action(hours)


action(hours)

Insulin Campuran(Premix)

70% NPH 30% Reguler(Mixtard, Humulin 30/70)

30-60 Dual 10-16

70% Insulin AspartProtamin

30% Insulin Aspart(Novomix 30)

10-20 Dual 15-18

75% Insulin LisproProtamin

25% Insulin Lispro

(Humalog Mix 25)

5-15 Dual 16-18


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Terapi Insulin Intensif

Defisiensi insulin mungkin merupakan defisiensi insulin basal, prandial, atau keduanya.Defisiensi insulin basalhiperglikemi pada puasaDefisiensi insulin prandialhiperglikemia setelah makan

Bimbel UKDI MANTAP

1st

target:GD Basal

1sttarget:

GDBasal

Insulin Basal(kerja sedang/ panjang) /

OHO

Dosisdisesuaikan

(Algoritma 3-0-

3)

Target GDBasaltercapai

Target A1CBELUM

2ndTarget:

GDPP

Insulin Premix /Insulin Short-

acting


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Time of day (hours)

400

300

200

100

006.00 06.0010.00 14.00 18.00 22.00 02.00

Plasma

glucose(mg/dl)

Normal

Meal Meal Meal

20

15

10

5

0

Plasmaglucose

(mmol/l)

Suntikkan 10 iu Levemir sekali sebelum tidur. Atur dosisnya (+3 atau -3) setiap 3 hari sampai GDP

mencapai target :

< 100 mg/dL (Perkeni 2011)

Hyperglycaemia due to an increase in fasting glucose

T2DM

Fix the Fasting First

Profile T2DMGDP, mencapai target

Bimbel UKDI MANTAP

1 kali insulin basal + 1 kali insulin prandial (basal plus)

1 kali basal + 2 kali prandial (basal 2 plus)

1 kali basal + 3 kali prandial (basal bolus).

Kombinasi Basal + Prandial

Ti i d i i li b l


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Titrasi dosis insulin basal

(Algoritma 3-0-3)

Bimbel UKDI MANTAP

Blonde L et al. Diabetes Obes Metab. 2009; 11(6):623-631

Starting dose:When initiating Levemir, startinsulin-nave patients with type 2 diabetes on10 units once-daily dosage or 0.1 to 0.2units/kg daily dosage with the evening meal orat bedtime and titrate accordingly.


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Premix and Basal Therapy

Factor Premix Insulin Basal TherapyGlucose target Both FPG and PPG Primarily address FPG

Percentage of patients

achieving HbA1C target

More patients achieve

HbA1C target using premix

insulin

Lower number of patients

achieve target compared to

premix insulin

Bimbel UKDI MANTAP

Basal Insulin OD or BID

HbA1C 7-8% HbA1C > 8%

FPG > 110 mg/dl FPG 73-110 mg/dl

Switch to NovoMix 30 BIDTitrate basal to

achieve

FPG 110 mg/dl


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Cara pemakaian insulin

PETUNJUK MEROTASI LOKASI PENYUNTIKAN

1. Pasien tidak dianjurkan untuk menyuntik pada

lokasi yangsama dalam 1 bulan berturut-turut.

2. Lokasi penyuntikan antara satu dengan yang lain

sebaiknya berjarak 2,5 cmBimbel UKDI MANTAP

Avoid intramuscular injection, especially

in the thigh area

Penyuntikan insulin kerja cepat lebihdianjurkan di daerah abdomen karenapenyerapan lebih cepat.

Di daerah lengan, paha, dan pantatuntuk insulin kerja menengah ataukerja panjang karena penyerapan lebihlambat.

Kriteria Pengendalian DM


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Kriteria Pengendalian DM

Bimbel UKDI MANTAP

Target Pencapaian Penderita DM(Perkeni,2011)

Tanpa Resiko

Kardiovaskular

Dengan Resiko

Kardiovaskular

IMT 18,5-23 kg/m2 18,5-23 kg/m2

GDP 100 mg/dl 100 mg/dl

GD2JPP < 140 mg/dl < 140 mg/dl

HbA1c < 7% < 7%

SBP 130mmHg 130mmHg

DBP 80mmHg 80mmHg

LDL

Kolesterol

< 100 mg/dl < 70 mg/dl

Glycemic recommendation fornon-pregnant adult with DM

(ADA, 2014)Value

GDP 70130 mg/dl

GD2JPP < 180 mg/dl

HbA1c < 7%


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Bimbel UKDI MANTAP

KOMPLIKASI KRONIK DM


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Komplikasi

DM

Ketoasidosis diabetik

Hiperosmolar non ketotik

Hipoglikemia

Akut:

Makroangiopati: Pembuluh koroner, vaskular perifer, vaskular otak

Mikroangiopati: kapiler retina, kapiler renal, Neuropati

Cardiomyopathy (DCM-diabetic cardiomyopathy)Lipotoxicity, glucose toxicity, ROS

Rentan infeksi (immunocompromised)

Disfungsi Ereksihiperglikemia berefek langsung menurunkan produksi NO & meningkatkanmediator vasokonstriksi

Diabetic foot: makro (vaskular perifer) + mikro (longstanding peripheral neuropathy)

Kronik:

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O S ODiabetic

retinopathy

Mikrovaskuler

DiabeticNephropathy

Mikrovaskuler

Cardiovascular

disease

Makrovaskuler

Stroke

Makrovaskuler

Diabetic

neuropatiDiabetic Foot

Kombinasi

Vaskulopati dan

neuropati


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Komplikasi Akut: HIPOGLIKEMIA

Keadaan dimana kadarglukosa darah < 60 mg/dl,atau kadar glukosa darah 250 mg/dl

pH arteri


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Hyperosmolar Hyperglycemic State (HHS)


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Hyperosmolar Hyperglycemic State (HHS)

Trias: hiperglikemia, hiperosmolar,dehidrasi

Kriteria dx ADA:

Glukosa darah >600 mg/dl

Osmolaritas serum efektif 320mOSm/kg

Dehidrasi hingga (8-12) L denganpeningkatan BUN

pH arteri 7.3

HCO3 15 mEq/L (rendah)

Ketonuria minimal, ketonemia (-)

Gangguan kesadaran

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Perbandingan DKA vs HHS


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KOMPLIKASI KRONIK DM:

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Nefropathydiabetic


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Kaki diabetik

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KLASIFIKASI WAGNER(0) Kulit intak/ utuh

(1) Tukak superfisial

(2) Tukak Dalam (sampai

tendo, tulang)(3) Tukak Dalam dengan

Infeksi

(4) Tukak dengan gangren

pada 1-2 jari kaki(5) Tukak dengan gangrenluas seluruh kaki


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Managementof Foot Ulcers

Metabolic

Control

InfectionControl

VascularControl

MechanicControl

WoundControl

International Working Group on the Diabetic Foot 2007

1

2

3

45

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DISLIPIDEMIA

Definisi: kelainan metabolisme lipid yg ditandai dgnkolesterol total, LDL, TG, serta HDL

Klasifikasi:

Dislipidemia primer: kelainan genetik dislipid moderat echiperkolesterolemia poligenik dan dislipidemia kombinasi

familial Dislipidemia sekunder: disebabkan penyakit lain seperti DM,

hipotiroidisme, peny hati obstruktif, SN, obat (progestin,steroid anabolik, kortikosteroid, beta blocker)

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DISLIPIDEMIA

Pemeriksaan1. skrining: adult >20 y.o

2. Cara: kol total, LDL, HDLtdk perlu puasa. TG harus

puasa 12-16 jam. KadarLDL dpt dihitung dgrumus Friedewald

Rumus ini hny berlaku bilakadar TG


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CHD Risk Assessment BasedOn NCEP

Risk Category 10-year risk Identification

Low risk < 10% 0-1 risk factor

Moderate risk < 10% 2+ risk factors

Moderately high risk 10% to 20% 2+ risk factors

High risk > 20% CHD or CHD risk equivalent

Grundy SM, et al. NCEP Report. Circulation 2004;110:227-239


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NCEP-ATP III

Non-coronary

forms of

atherosclerotic

disease

Peripheral arterial disease

Abdominal aortic aneurysm

carotid artery disease (TIA or

stroke of carotid origin or 50%

obstruction of a carotid artery)

DiabetesFasting blood glucose of 126mg/dL or greater

2+ risk factors with 10-year risk for hard CHD 20%

NCEP-ATP III Cut points for TLC and drug therapyin different risk categories


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in different risk categories

Risk Category Initiate TLC Consider drug therapy

High risk (10-year risk 20%):

CHD or CHD equivalent

100 mg/dl 100 mg/dl

(100 mg/dl: drug optional)

Moderately high risk

(10-year risk 10% to 20%):

2+ risk factors

130 mg/dl 130 mg/dl

(100-129 mg/dl drug optional)

Moderate risk

(10-year risk 10%):

2+ risk factors

130 mg/dl 160 mg/dl

Lower risk

(10-year risk 10%):

0-1 risk factor

160 mg/dl 190 mg/dl

(160-189 mg/dl: drug optional)

Grundy SM et al Circulation 2004;110:227-39

Risk Level Based on


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ESC/EAS 2011 Guidelines

Known CVD includes ischemic stroke and PADType 2 diabetes or type 1 diabetes with TOD such as microalbuminuria

CKD with eGFR


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Bax, Jeroen et al; EHJ; 2011;32:1769-1818

ESC Intervention Strategies Depending on Total CV


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Total CV

Risk(SCORE)

%

LDL C (mg/dL)


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AHA 2013

Intensity of Statin Therapy


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High-Intensity Statin

Therapy

Moderate-Intensity Stain

Therapy

Low-Intensity Statin

Therapy

LDLC 50% LDLC 30% to


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*Therapeutic Lifestyle Changes


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Lifestyle Intervention


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Lifestyle Interventions aimed to:

Lower LDL-C Increase HDL-C Lower TG

Reduce dietary saturated fat

Increase dietary fiber

Reduce total amount of dietary carbohydrate

Reduce alcohol intake

Increase habitual physical activity

Reduce excessive body weight

Quit smoking

Reiner Z, et al. EHJ;2011:32:1769-1818

y


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StatinsMechanism of Action


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[email protected]@works

1. Reduce hepatic cholesterol synthesis (HMG CoA),

2. lowering intracellular cholesterol,

3. Upregulation of LDL receptor removal apo E-B containing lipoprot. from the liver

4. the uptake of non-HDL from circulation.

LDL receptormediated

hepatic uptake of LDL

and VLDL remnants

Serum VLDL remnants

Serum LDL-C

Cholesterol

synthesisLDL receptor

(BE receptor)

synthesisIntracellular

Cholesterol

Apo B

Apo E

Apo B

Systemic CirculationHepatocyte

LDL

Serum IDL

VLDLR

VLDL

HMGCoA

HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) reductaseinhibitors

HMG CoA Reductase Inhibitors (Statins)


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( )

Common side effects

Headache, Myalgia, Fatigue, GI intol. Flu-like symptoms

Myopathy occurs in 0.2 to 0.4% of patients

Rare cases of Rhabdomyolysis

Who uses statins in impaired renal function combining statins with fibrates

Muscle toxicity requires the discontinuation of statin

Increase in liver enzymes

serious problems are veryrareOccurs in 0.5 to 2.5% of cases in dose-dependent

manner

Current Overview of Statin-Induced


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Muscle Side Effects

Pasternak Use and Safety of Statins. J AM Coll Cardiol2002;40:567-72.

Classification of Muscle Adverse Events with Statins

Condition Definitions (ACC/AHA NHLBI)

Myopathy

Myalgia

Myositis(may also be

called Myopathy)

Rhabdomyolysis

Disease of the muscles, which may be acquired or inherited

Muscle ache or weakness without increases in creatine kinase levels

Common complaint is muscle aches or joint pain

Incidence of complaints is generally reported as about 5% with statins Some patients have mild-to-moderate elevations of CK without muscle

complaints

Muscle aches, soreness or weakness and associated with elevated creatinekinase levels, generally > 10 x ULN

Incidence - rare with statins

Most likely to occur in persons who have complex medical problems and/orwho are taking multiple medications

Muscle symptoms with marked CK elevations (typically substantially greaterthan 10 x ULN) and with creatinine elevation (usually with brown urine andurinary myoglobin)

Incidence - very rare

Without clinical intervention, rhabdomyolysis can be life-threatening


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Statin Monitoring and Goals of Therapy

Statin Monitoring and Goals of Therapy. A Reference Guide. ACC Tool.

Ezetimibe


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et be

Ezetimibe selectively inhibits absorption of cholesterol

at the brush border membrane in the intestinal lumen.Bimbel UKDI MANTAP

Statin monotherapy:inhibits endogenouscholesterol synthesisEzetimibe monotherapy:inhibits dietary cholesterolabsorption & reabsorption

of biliary cholesterolStatin + Ezetimibe:inhibits cholesterolsynthesis and absorption,leads to greater LDL-Creduction


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FibrateBimbel UKDI MANTAP

Nicotinic Acid


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Nicotinic Acid

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C l i


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Conclusion

Lifestyle intervention remains an essential modality in

clinical management.

Elevated LDL-C is the primary target of treatment and

should be treated to target according to the risk category

Absolute LDL-C target should be achieved before minimal

target is considered

Rosuvastatin has the better outcome in lowering LDL

Statins Bile acid resisn:

Cholestyramin: take it with the largest


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Patient Instructions& Counseling

Usually administered in theevening because most hepaticcholesterol production occursduring the night

Atorvastatin may be given anytime of the day because of itslonger half-life

You may take this medicinewith or without food

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y gmeal

Titrate dose slowly to avoid GI side effect

The powder cannot be used in dry form. Itcan be mixed with water, fruit juice, milk,& with food such as thin soup or with milkin breakfast cereal until completelydissolved. The patient must drink thismixture right away

Counsel patient to rinse the glass with

liquid to ensure ingestion of all resin Increase fluid intake

Dose other drugs 1 hour before or 4 hoursafter resin

Fibrates:

Gemfibrozil should be taken twice daily 30

minutes before meals

Fenofibrate can be taken with food once daily

Monitor muscle toxicity, especially when used

with statins

Metabolic syndrome


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Metabolic syndrome

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Definisi Sindrom Metabolik


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Definisi Sindrom Metabolik

Sekumpulan berbagai faktor risiko terjadinya penyakitkardiovaskularterkait aterosklerosis

Terkumpulnya berbagai faktor risiko metabolik padaseseorang, yang memberikan peningkatan risiko untuk

terjadinya kelainan kardiovaskular

Three or more of the following five features are requiredfor diagnosis: enlarged waistline, low HDL cholesterol,

increased blood pressure, increased plasma triglycerides,and increased fasting plasma glucose (Grundy et al., 2005)

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Glandula

tiroid

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Tahapan sintesis hormon tiroid:

1. Inside trapping: sel folikel secara

aktif mengambil iodida (I-) dr

sirkulasi.2. Organifikasi

oksidasi: iodida diubah menjadi

iodium oleh peroksidase (I-I)

iodinisasi: tirosin + iodium

monoiodotirosis (MIT) dan

diiodotirosin (DIT)3. Coupling: penggabungan DIT dan

MIT menjadi T4 dan T3. Jumlah T4

lnh bny tp efek metabolitnya lbh

lemah. Mereka beriikatan dgn

tiroglobulin dan disimpan di

dalam koloid4. sekresi: protease lisosom akan

melepaskan ikatan T4 dan T3

dengan tiroglobulin, dan dilepas

ke sirkulasi.

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EPIDEMIOLOGI GANGGUAN TIROID


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EPIDEMIOLOGI GANGGUAN TIROID

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TIROTOKSIKOSIS & HIPERTIROIDISM


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TIROTOKSIKOSIS & HIPERTIROIDISM

TIROTOKSIKOSIS:Manifestasi klinis kelebihan

hormon tiroid yg beredar dalam

sirkulasi

HYPERTHYROIDISM:

Tirotoksikosis yg diakibatkan

oleh kelenjar tiroid yg hiperaktif

(radioactive neck-uptake )

PENYEBAB TIROTOKSIKOSIS

Hipertiroidiesm

e primer

Tirotoksikosis

tanpa

hipertiroidisme

Hipertiroidisme

sekunder

Peny Graves

Gondokmultinodular

toksik

Adenoma toksik

Karsinoma tiroid

Struma ovarii

(ektopik)Mutasi TSHr gen

Hormon tiroid

ekstrogenberlebih

(faktisia)

Tiroidits

subakut (viral

atau De

Quervain)Destruksi

kelenjar:

amiodaron,

radiasi,

adenoma, infark

TSH-secreting

tumorTirotoksikosis

gestasi (trim 1)

Resistensi

hormon tiroid

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Tirotoksikosis

HipertiroidInflamasi

Ingesti


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Indeks Wayne


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untuk hipertiroid

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Interpretation:> 19: toxichyperthyroidism< 11: euthyroidism11-19: equivocal.

Diagnosticaccuracy of 85%.


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Primary

Hypofunctio

n

Secondary

Hyperfunctio

n

Primary

Hyperfunctio

n

Pituitary

Failure

Normal

range

THYROTRO

PIN(TSH)LEVEL

Low

Normal

High

Low Normal High

THYROID HORMONE LEVEL

Subclinical

Hypofunction

Subclinical

Hyperfunction

PENYAKIT GRAVE

( / )


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(Parrys disease / Basedowsdisease)

PATOGENESIS

- Hipertiroid gangguan

mekanisme homeostasisi yang

mengontrol sekresi

- Gangguan berasal : thyroid

stimulating immunoglobulin

(TSI) - limphosit (IgG).- Antibodi berikatan dengan

reseptor TSH (TRAb)

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PENYAKIT GRAVE


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PREVALENSI Dapat padasemua umur, umumnya

dekade tiga & empat

Rasio wanita : pria = 7 :1

Faktor genetik :frekuensi

Penyakit tiroid -autoimun

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...PENYAKIT GRAVE


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Manifestasi:

- S&S hipertiroid- Graves ophthalmopathy: Wide palpebral aperture

(Dalrymples sign), Lid lag (von Graefes sign), Staring orfrigthened expressions, Infrequent blinking (Stellwagssign),

Absence of farehead wringkling on upward (Joffroys sign),Inability to keep converged (Mobiussign), Diplopia, Swellingof orbital contents and puffiness of the lids, Chemosis,corneal injection/ulceration, Exophthalmus, Decreased visualacuity, retinal edema/hemorrhages, optic nerve damage

- Thyroid dermopathy: pretibial myxedema, indurated plak,orange-skin appearance

- Thyroid acropachy: manifests as clubbing finger

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OCULAR SIGNS & SYMPTOMS

Wide palpebral aperture


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- Wide palpebral aperture(Dalrymplessign)

- Lid lag (von Graefessign)

- Staring or frigthened expressions- Infrequent blinking (Stellwags

sign)

- Absence of forehead wringkling onupward (Joffroyssign)

- Inability to keep converged

(Mobius sign)- Diplopia

- Swelling of orbital contents andpuffiness of the lids

- Chemosis, cornealinjection/ulceration

- Exophthalmus

- Decreased visual acuity, retinaledema/hemorrhages, optic nervedamage

GRAVES DISEASE


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THYROID EXAM

Diffuse toxic goiter,less symetric.

Thrills and bruits are

important but oftenabsent.

Thrills (palpable) andbruits (audible) sign ofturbulence associatedwith an increased rateof flow throughturtuos vessel.

CARDIAC MANIFESTATION

Tachycardia

Atrial fibrillation

LVH and strain on ECG

Premature atrial/ventricularcontractions

Congestive heart failure

Angina with/without coronary arterydisease

Myocardial infarction

Resistance to some drug effects(digoxin)

Residual cardiomegaly

Systolic BP Diastolic BP

Pulse pressure 50-80 mmHg

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Diagnosis Penyakit Graves


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Anamnesis dan Pemeriksaan Jasmani

Pemeriksaan laboratorium

TSH menurun

FT4meningkat

T3T3Toksikosis

Sidik tiroid

Graves:Uptake iodinemeningkat(hot nodule)

Tiroiditis:

uptakerendah

USG

Kurang adamanfaat

BAJAH

Tidak biasadilakukan(hanya kalau

disertai noduldingin)

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Diagnosis Penyakit Graves

Treatment of Hyperthyroidism


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Treatment of Hyperthyroidism

Anti-thyroid

Drugs

Radioactive

Iodine

Surgery

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Kelompok obat Efeknya Indikasi

Obat Anti Tiroid

-Propiltiuurasil (PTU) 100-

Menghambat sintesis hormon

tiroid dan berefek imunosupresif

Pengobatan lini pertama pd

Graves.


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Propiltiuurasil (PTU) 100

200 mg/6-8 jam, maintain

50-100 mg

-Metimazol-Karbimazol

tiroid dan berefek imunosupresif

PTU jg menghambat konversi

T4T3

Graves.

Obat jangka pendek

prabedah/praRAI

Beta blocker

-Propranolol 20-40 mg/6 jam

-Metoprolol

-Atenolol

-Nadolol

Mengurangi dampak hormon

tiroid pd jaringan

Obat tambahan, kdg obat

tunggal pd tiroiditis

Bahan mengandung iodin

-Kalium iodida

-Sol lugol

-Na ipodat

-Asam iopanoat-Iodine Radioactive Therapy

Menghambat keluarnya T4 dan

T3, menghambat produksi T4

dan T3 serta produksi T3

ekstratiroidal

Persiapan tiroidektomi.

Pd krisis tiroid.

Bukan utk pengobatan rutin

Obat lainnya

-Kalium perklorat

-Litium Karbonat

-Glukokortikoid

Menghambat transpor yodium,

sintesis dan keluarnya hormon,

memperbaiki efek hormon di jar

dan sifat imunologis

Bukan indikasi rutin.

Pada subakut tiroiditis berat,

dan krisis tiroid

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PTU MMI300 d il i 3 di id d d 15 t 30 /d i l d


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300 mg daily in 3 divided doses.

Severe hyperthyroidism or very

large goiters, initial dosage may beincreased to 400 mg/day, up to600 to 900 mg/day.

The maintenance dosage is 100 to150 mg/day.

15 to 30 mg/day as a single dose.

15 mg/day for mild hyperthyroidism

30-40 mg/day for moderatelyhyperthyroidism.

60 mg/day for severe hyperthyroidism.

The daily dose is divided into 3 dosesadministered every 8 hours.

The maintenance dose is 5-15 mg/day

Duration of action from 12 to 24 h Duration of action even longerPO peak serum concentrationsoccurring in one hour

Side effects of are less clearlyrelated to dose.

Side effects are dose-related


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Methimazole

(Tapazole)Propylthiouracil

(PTU)

Dosage Range: 5-20 mg qd, BID, TID 50-200 mg TID

Half Life: 4-6 hours 75 minutes

Pregnancy/Lactation: preferred

Cost: ~$20-40/month ~$10-20/month:

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Hyperthyroidism:Adjunctive Therapy


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j py

Iodine: Severe Hyperthyroidism Inhibits thyroid hormone synthesis/release, Decrease the vascularity of the thyroid gland

Should not be used for long-term therapy , Will delay 131I

SSKI (50 mg iodide/drop) LugolsSolution (5-10% KI, 8 mg iodide/drop)

Beta Blockers: For palpitations, Afib with RVR Propranolol, 40-200 mg dalam 4 dosis

Atenolol 25-50 mg sekali sehari

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Goiter Toxic(Hyperthyroidism

present)


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Goiter

berdasarkanpemeriksaan

klinis

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Diffuse(graves) Nodule

Uninodular(toxic adenoma)

Multinodular(toxic multinodular

goiter)

Goiter Non Toxic(No Hyperthyroidism

present)

Diffuse Nodule

Uninodular Multinodular

Endemic goiter/simple

goiter

(defisiensi yodium)

Sporadic goiter

(faktor lingkungan/genetik)

Endemic goiter S di it


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Endemic goiter

Occurs in geographic areas

where the soil, water, and foodsupply contain only low levelsof iodine.

The term endemicis used whengoiters are present in morethan 10% of the population in agiven region.

Such conditions are particularlycommon in mountainous areasof the world, including the Alps,Andes, and Himalayas, where

iodine deficiency is widespread.

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Sporadic goiter

There is a striking female preponderance

and a peak incidence at puberty or inyoung adult life.

Sporadic goiter can be caused by anumber of conditions, including theingestion of substances that interferewith thyroid hormone synthesis.

In other instances, goiter may result fromhereditary enzymatic defects thatinterfere with thyroid hormone synthesis,all transmitted as autosomal-recessiveconditions (dyshormonogenetic goiter;see above).

Diagnosis Treatment


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Diagnosis Anamnesis: biasanya gejala

kearah obstruksi sepertidisfagia apabila benjolan

besar

Inspeksi

Palpasi Tes fungsi Hormon : T4/T3,

TSH, RAIU

Foto rontgen leher (melihat

keparahan obstruksi) USG

Scan Tiroid

FNAB (bila curiga tiroid)

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Treatment

Levotiroksin Pembedahan (bila

obstruktif)

Edukasi

-makan makananmengandung tinggi

yodium seperti ikan

laut,garam beryodium

-Iodinisasi air minum didaerah endemik

KRITERIA DIAGNOSTIK KRISIS TIROID


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60 : highly likely

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Thyroid Storm A clinicaldiagnosis at the end of a

hyperthryoid continuum Hipertermia

Mental Status Changes

Cardiovascular Collapse Precipitatants in hyperthyroid

patients:

surgery sepsis

iodine loads

post-partum

Endocrine emergency (Mortality20-50%)

KRISIS TIROID


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Umum : rehidrasi dan koreksi elektrolit (NaCl dan cairan lain) dan kalori (glukosa), vitamin,

oksigen, obat sedasi, kompres es

Mengkoreksi hipertiroidisme dgn cepat:

a. Memblok sintesis hormon baru: PTU dosis besar loading 600-1000 mg diikuti 200 mg PTU/4 jam dengan dosissehari total 1000-1500 mg

b. Memblok keluarnya hormon dgn sol lugol 10 gtt/6-8 jam atau SSKI (larutan kalium iodida jenuh) 5 gtt/6 jam c. Menghambat konversi perifer dari T4T3 dgn propranolol, ipodat, beta blocker dan/atau kortikosteroid

Pemberian hidrokortison dosis stress (100 mg/8 jam) atau deksametason 2mg/6 jam (karenaada defisiensi steroid relatif akibat hipermetabolisme dan menghambat konversi perifer T4).

Antipiretik: asetaminofen

Tx faktor pencetus

HIPOTIROID


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HIPOTIROID

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HIPOTIROID


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Definition:

Deficiency of thyroid hormone

Causes:

Primary (TSH high) ~95%

Secondary (TSH low) ~5%

Relatively common:

2% adult women, 0.2% adultmen

>60: 6% adult women; 2%adult men

May be higher in select groups

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TANDA DAN GEJALA HIPOTIROID


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Onset:Usually Gradual

Goiter Risk Factors:Age >60, female, history of

thyroid disease, history of radiotherapy

to head/neck, family history of thyroid

disease, lithium or amiodarone therapy.

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Pasien dengan hipotiroid bisa sajamengalami gejala fisik dan mental

yang tidak spesifik

Kelelahan/ mengantuk

Mudah kedinginan

Kram otot

Mengalami kenaikan berat badan meskipun

diet dan berolahraga Depresi

Konstipasi

Periode menstruasi yang abnormal dan/ataumasalah kesuburan

Rambut atau kuku yang tipis dan rapuh dan/atau kulit kering

Muka, tangan dan kaki bengkak

Nyeri otot

Libido menurun

MyxedemaPenebalan, edema non pitting pada jaringan lunak


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Billewicz diagnostic index


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g

(Jarang dipakai)Interpretation:

25: hypothyroidism

-30: exclude the

disease

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Autoimmune Thyroiditis(Hashimotos, Chronic Lymphocytic)


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Autoimmune destruction of thyroid tissue

High titers of anti-thyroid antibodies

Lymphocytic Infiltration of thyroid gland, fibrosis

Firm, non-tender diffuse goiter

#1 cause of hypothyroidism (70%)

western countries Usually permanent

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Treatment of Hypothyroidism


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Treatment of Hypothyroidism

Replace with levo-thyroxine(L-T4)

Monitor thyroid function testsevery 6-8 weeks until steady

dose is achieved; goal is tonormalize TSH in most cases

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LEVOTIROKSIN

l h


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Pilihan pertama

Dapat dipakai untuk Tx koma miksedema Aman untuk ibu hamil

Dosis awal : 50-100 mcg PO 1 x/hari

dinaikkan 25-50 mcg/3-4mgg s/d eutiroid dan kadarTSH normal

Dosis rumatan : 100-200 mcg PO 1/hr

Lansia/Kardiovaskuler : dosis awal 25-50 mcg PO

1x/hr, dosis dinaikkan 25 mcg/4mgg s/d eutiroiddengan TSH normal

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KOMA MIKSEDEMA


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Wanita usia lanjut, infeksi, obat,paparan lingkungan (paparanudara dingin), keadaan terkait

metabolik.Tanda & gejala : riwayat

hipotiroid lama, hipotermi berat

(


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tiroiditis post partum

Induksi obat : defisiensi, farmakologik ( medikasimedia kontras) struma nodusa, amiodaron

Infeksi : tiroditid supurativ, tiroiditis paska infeksiviral

Idiopatik : struma multinoduler toksik

Iatrogenik : tirotoksikosis faktitia

Malignitas : adenoma toksik, hiperfungsi nodultunggal

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Penanganan Koma Miksedema


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Perawatan pra-rumah sakit Perawatan Instalasi Darurat Medis1. Resusitasi awal : intavena2. Monitoring jantung & terapi O2indikasi3. Ventilasi mekanik : penurunan respirasi4. Evaluasi penyebab penurunan kesadaran : glukosa

darah, oksimetri5. Dugaan klinis : hormon tiroid intravena6. Obati faktor pencetus7. Hipotensi membaik dengan kristaloid8. Hipotermi : selimut/pemanasan

9. Hindari : sedatif, narkotik, anestetik

Konsultasi : rawat intensif

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Terapi utama : hormon tiroid

1 I t h ti h ti d PJK


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1. Intavena : hati hati pada PJK

Monitor detak jantung, hentikan bila aritmiaa. Levothyroxine : bolus awal 200-500 mkg

IV/via NG, ruwatan 100-200 mkg/hari IV / viaNG

b.Liothyronine (lebih cepat) : bolus 50 mkg IVpelan dilanjutkan 25 mkg IV/ 8jam sam paimembaik, kemudian 25 mkg/ 12 jam atau 5- 20

mkg IV pelan/4-12 jam (umumnya 12 jam)

2. Oral : kasus ringanMulai dosis kecil dinaikkan pelan pelan

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Parathyroid Gland


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Hyperparathyroidism


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Primary Hyperparathyroid


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Primary hyperparathyroidism is one of the most common endocrine disorders, and it isan important cause of hypercalcemia.

In patients with primary hyperparathyroidism, serum PTH levels are inappropriatelyelevated for the level of serum calcium, whereas PTH levels are low to undetectable inhypercalcemia because of nonparathyroid disease

The frequency of the various parathyroid lesions underlying the hyperfunction is asfollows:

Adenoma 75-80%

Primary hyperplasia (diffuse or nodular) 10-15%

Parathyroid carcinoma < 5%

Primary hyperparathyroidism is usually a disease of adults and is more common inwomen than in men by a ratio of nearly 3:1.

The signs and symptoms of hyperparathyroidism reflect the combined effects ofincreased PTH secretion and hypercalcemia.

Primary hyperparathyroidism has been traditionally associated with aconstellation of symptoms that included "painful bones, renal stones,


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y p p , ,abdominal groans, and psychic moans".

Bone disease includes bone painsecondary to fractures of bonesweakened by osteoporosis or osteitisfibrosa cystica.

Nephrol i thiasis(renal stones) occursin 20% of newly diagnosed patients,with attendant pain and obstructive

uropathy. Chronic renal insufficiencyand a variety of abnormalities in renalfunction are found, including polyuriaand secondary polydipsia.

Gastrointestinal disturbances

include constipation, nausea, pepticulcers, pancreatitis, and gallstones.

Central nervous system alterations

include depression, lethargy, andeventually seizures.

Neuromuscular abnormalities

include complaints of weakness andfatigue.

Cardiac manifestations includeaortic or mitral valve calcifications (or

both).

Secondary hyperparathyroidism


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Caused by any condition associated witha chronic depression in the serumcalcium level because low serum calciumleads to compensatory overactivity ofthe parathyroid glands.

Renal failure is by far the most common

cause of secondary hyperparathyroidismalthough a number of other diseases,including inadequate dietary intake of

calcium, steatorrhea, and vitamin Ddeficiency,may also cause this disorder.

Hypoparathyroid


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PTH deficiency results in hypocalcemia

- Primary hypoparathyroid: inadequate PTH activity

Low PTH with a concomitant low calcium level

- Secondary hypoparathyroid: a physiologic state in which

PTH levels are low in response to a primary process thatcauses hypercalcemia

Low PTH and serum calcium level is elevated

- Pseudohypoparathyroidism: A rare familial disorderswith target tissue resistance to PTH

PTH concentration is elevated as a result of resistance toPTH caused by mutations in the PTH receptor system

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Hypoparathyroid Clinical Manifest


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The classic findings on physical examination ofpatients with neuromuscular irritability are Chvostek

signand Trousseau sign.

The hallmark of hypocalcemia is tetany, which is

characterized by neuromuscular irritability, resulting fromdecreased serum ionized calcium concentration.

These findings can range from circumoral numbness orparesthesias (tingling) of the distal extremities and to life-

threatening laryngospasm and generalized seizures.

Mental status changes can include emotional instability anxiety and depression confusional


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Mental status changescan include emotional instability, anxiety and depression, confusionalstates, hallucinations, and frank psychosis.

Intracranial manifestationsinclude calcifications of the basal ganglia, parkinsonian-likemovement disorders, and increased intracranial pressure with resultant papilledema.

Ocular diseaseresults in calcification of the lens leading to cataract formation.

Cardiovascular manifestationsinclude a conduction defect, which produces a characteristicprolongation of the QT interval in the electrocardiogram.

Dental abnormalitiesoccur when hypocalcemia is present during early development. Thesefindings are highly characteristic of hypoparathyroidism and include dental hypoplasia,failure of eruption, defective enamel and root formation, and abraded carious teeth.

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Treatment


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The mainstay of treatment is a combination oforal calcium with pharmacological doses of

vitamin Dor its potent analogues. Phosphate

restriction in diet may also be useful with orwithout aluminum hydroxide gel to lower

serum phosphate level.

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Diabetes Insipidus


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Definisi: kondisi volume urin yg banyak(>3L/hr) krn gangguan resorbsi air oleh ginjal

yg disebabkan sekresi ADH oleh hipofisis

posterior (DI sentral) atau gangguan responginjal terhadap ADH (DI nefrogenik)

SS: poliuria, polidipsia, dehidrasi, gejala

hipernatremia

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Etiologi...


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DI sentral -Idiopatik

-Kongenital: defek pada gen ADH, DIDMOAD syndrome

(resesif autosomal: DI, DM, atrofi optik, dan tuli/Wolframs

synd)

-Tumor: kraniofaringioma, metastasis, tumor hipofisis

-Trauma: hipofisektomi, head injury-Infiltrasi: histiositosis, sarkoidosis

-Vaskular: Sheehans syndrome

-Infeksi: meningoensefalitits

DI nefrogenik -Inherited

-Metabolik: Kalium, kalsium

-Obat: litium, demeklosiklim

-CKD

-Post uropati obstruktif

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WATER DEPRIVATION TEST


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INTERPRETASI WATER DEPRIVATION TEST

Normal Osmolalitas urin >600 mOsm/kg (kemampuan

mengkonsentrasi urin normal)

Polidipsia primer/psikogenik Urin terkonsentrasi, tp kemampuanmengkonsentrasikan urin masih kurang dr

normal >400-600 mOsm/kg

DI sentral Osmolalitas urin NAIK >600 mOsm.kg SETELAH

pemberian desmopressin

DI nefrogenik Osmolalitas urin TIDAK NAIK setelah

pemberian desmopressin

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ADRENAL CORTEX. The three tissue layers secrete, in the same order, the following corticosteroids:

1. Mineralocorticoids (zona glomerulosa only), which act on the kidneys to control electrolyte balance. Theprincipal mineralocorticoid is aldosterone, which promotes Na retention and K excretion by the kidneys.

2. Glucocorticoids (mainly zona fasciculata), especially cortisol (hydrocortisone); corticosterone is a less potentrelative. Glucocorticoids stimulate fat and protein catabolism, gluconeogenesis, and the release of fatty acidsand glucose into the blood. This helps the body adapt to stress and repair damaged tissues. Glucocorticoidsalso have an antiinflammatory effect and are widely used in ointments to relieve swelling and other signs of

inflammation. Long-term secretion, however, suppresses the immune system.3. Sex steroids (mainly zona reticularis), including weak androgens and smaller amounts of estrogens. Androgens

control many aspects of male development and reproductive physiology. The principal adrenal androgen isdehydroepiandrosterone (DHEA) (de-HY-dro-EPee- an-DROSS-tur-own). DHEA has weak hormonal effects initself, but more importantly, other tissues convert it to the more potent androgen, testosterone. This source isrelatively unimportant in men because the testes produce so much more testosterone than this. In women,however, the adrenal glands meet about 50% of the total androgen requirement.

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Systemic Effects of Glucocorticoids


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Definitions


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Cushings syndrome: chronic glucocorticoid excess.

The commonest cause is steroid tx. Endogenous cases

are much rarer: 85% are due to ACTH, of these a

pituitary adenoma (Cushings disease) is the

commonest cause.

Cushings disease: pituitary gland releases too much

adrenocorticotropic hormone (ACTH). Cushing's

disease is caused by a tumor or excess growth(hyperplasia) of the pituitary gland.

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CushingsSyndrome

Signs andSymptoms

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Cushings SyndromeClinical features


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Most reliable differentiating signs from

obesity are those of protein wasting:

Thin skin Easy bruising

Proximal weakness

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Cushings SyndromeEtiology


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ACTH-independent (ACTH due tonegative feedback) (Factitious): iatrogenik

Unilateral Adrenal adenoma (10%)

Adrenal carcinoma (5%)

Bilateral Macronodular Hyperplasia

(AIMAH) (


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Addison Disease


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Addison disease is adrenocortical insufficiency due to the

destruction or dysfunction of the entire adrenal cortex.

It affects both glucocorticoid and mineralocorticoid function.

The onset of disease usually occurs when 90% or more ofboth adrenal cortices are dysfunctional or destroyed.

Idiopathic autoimmune Addison disease tends to be morecommon in females and children.

The most common age in adults is 30-50 years, but the

disease could present earlier in patients with: polyglandularautoimmune syndromes, congenital adrenal hyperplasia(CAH), or if onset is due to a disorder of long-chain fatty acidmetabolism.


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Pemeriksaan Penunjang


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Rapid ACTH stimulation test:

-Blood is drawn in 2 separate tubes for baselinecortisol and aldosterone values.

-Synthetic ACTH (1-24 amino acid sequence) in a doseof 250 mcg (0.25 mg) is given IM or IV.

-Thirty or 60 minutes after the ACTH injection, 2more blood samples are drawn; one for cortisol andone for aldosterone.

Interpreting rapid ACTH stimulation test:

Two criteria are necessary for diagnosis:


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Two criteria are necessary for diagnosis:(1) an increase in the baseline cortisol value of 7mcg/dL or more(2) the value must rise to 20 mcg/dL or more in 30 or60 minutes, establishing normal adrenal glucocorticoidfunction.

In patients with Addison disease, both cortisol andaldosterone show minimal or no change inresponse to ACTH.

When the results of the rapid ACTH do not meet the 2criteria mentioned above, further testing might berequired to distinguish Addison disease from secondaryadrenocortical insufficiency.

A random plasma cortisol value of 25 mcg/dL or greatereffectively excludes adrenal insufficiency of any kind.

PULMONOLOGI


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COPD Asma TB Pneumonia

Bronkiektasis Atelektasis Efusi pleura Flu Burung

Lung abscess Lung cancer

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Chronic Obstructive Pulmonary Disease


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COPD Guidelines

KEY POINT :


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Bronkitis kronik (Dx Klinis)Kelainan saluran napas yangditandai oleh batuk kronikberdahak minimal 3 bulan

dalam setahun, sekurang-kurangnya 2 tahun berturut -

turut, tidak disebabkanpenyakit lainnya.

Emfisema (Dx Patologis)Suatu kelainan anatomis paruyang ditandai oleh pelebaran

rongga udara distal

bronkiolus terminal, disertaikerusakan dinding alveoli.

(kerusakan permukaanpertukaran gas pada paru)

COPD

KEY POINT :

Persistent airflowlimitation

Progressive

Chronic inflammatory

Noxious particles orgases

Response to Bronchodilators


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ASTHMA

SABA

Tolerance

Dosed PRN

LABA

Monotherapy assoc.

with increased frequency

of exacerbations

Little tolerance

Anticholinergic Efficacious in acute attack

COPD

SABA

No tolerance

Regularly dosed

LABA

Monotherapy assoc.

with decreased frequency

of exacerbations

Little tolerance

Anticholinergic Efficacious in stable

disease

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COPD: Risk Factors


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Exposures

Smoking (generally 90%): Perokok aktif/ pasif/ mantan perokokDerajat berat merokok (indeks Brinkman):- Ringan : 0-200- Sedang : 200-600- Berat : > 600

Outdoor/indoor air pollution Occupational dust/chemicals

Childhood infections (severe respiratory, viral)

Socioeconomic status

Host factors Alpha1-antitrypsin deficiency (


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Gejala Keterangan

Sesak Progresif

Bertambah berat dengan aktifitas

Persisten

Batuk Kronik Hilang timbul dan mungkin tidak

berdahak

Batuk Kronik Berdahak Setiap batuk kronik berdahak dapat

mengindikasikan PPOK

Riwayat Terpajan Faktor Risiko Asap rokok

Debu

Bahan kimia di tempat kerjaAsap dapur

Riwayat Keluarga PPOK

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Anamnesis

Pursed - lips breathing

Barrel chest (diameter antero - posterior dan transversalsebanding)

Pemeriksaan Fisik


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Penggunaan otot bantu napas

Hipertropi otot bantu napas Pelebaran sela iga

Bila telah terjadi gagal jantung kanan terlihat denyut venajugularis di leher dan edema tungkai

Penampilanpink puffer atau blue bloater

Inspeksi

Pada emfisema fremitus melemah, sela iga melebarPalpasi

Pada emfisema hipersonor dan batas jantung mengecil, letakdiafragma rendah, hepar terdorong ke bawah

Perkusi

Suara vesikuler N, atau melemah

Terdapat ronki dan atau mengi pada waktu bernapas biasa ataupada ekspirasi paksa

Ekspirasi memanjang

bunyi jantung terdengar jauh

Auskultasi


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Pemeriksaan Lanjutan


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Spirometri (FEV1/FVC 0,70 post bronchodilator)

Radiologi: Foto thorax PA dan lateral

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Emfisema:Hiperinflasi, hiperlusen, ruangretrosternal melebar, diafragmamendatar, jantung menggantung

Bronkitis kronik :Normal/Corakan bronkovaskulerbertambah pada 21 % kasus

Diagnosis Banding COPD


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MANAGE STABLECOPD


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Kriteria PPOK stabil:

Tidak dalam kondisi gagal napas akut pada gagal napas kronik

Dapat dalam kondisi gagal napas kronik stabil, yaitu hasil analisa gasdarah menunjukkan PCO2 < 45 mmHg dan PO2 > 60 mmHg

Dahak jernih tidak berwarna

Aktivitas terbatas tidak disertai sesak sesuai derajat berat PPOK (hasilspirometri)

Penggunaan bronkodilator sesuai rencana pengobatan

Tidak ada penggunaan bronkodilator tambahanPrescribeTreatment

Pharmacologic

Non-pharmacologic

Rehabilitation

Exercise training

Nutritioncounseling

education

Oxygen therapy

Surgical interventions

III: SevereII: ModerateI: Mild

IV: Very Severe


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FEV1/FVC < 70%

FEV1 > 80% predicted

FEV1/FVC < 70%

50% < FEV1 < 80%predicted

FEV1/FVC < 70%

30% < FEV1 55%), anemia, orleukocytosis

GOLD Pocket Guide to COPD Diagnosis Management and Prevention

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Management of COPD Exacerbations

Controlled oxygen therapy


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Administer enough to maintain PaO2 > 60 mmHG or SaO2 88-92%

Monitor patient closely for CO2 retention or acidosis

Bronchodilators (inhaled)

Increase doses or frequency

Combine 2agonists and anticholinergics

Use spacers or air-driven nebulizers

Consider adding IV methylxanthine (aminophylline) if needed

Antibiotics

IF breathlessness and cough are increased AND sputum is purulent and increased in volume

Choice of antibiotics should reflect local antibiotic sensitivity for the following microbes:

S. pneumoniae

H. influenzae

M. catarrhalis

Glucocorticosteroids (oral or IV)

Recommended as an addition to bronchodilator therapy

If baseline FEV1 < 50% predicted

30-40 mg oral prednisolone x 10 days OR nebulized budesonide

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Management of COPD Exacerbations


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Ventilatory Support Decrease mortality and

morbidity

Relieve symptoms

Used most commonly in

Stage IV, Very Severe COPD Forms:

Non-invasive usingnegative or positivepressure devices

invasive/mechanical withoro- or naso-tracheal tubeOR tracheostomy

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COMPLICATIONS OF COPD


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ASMA


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Obstruksiintermiten

aliran udaranapas


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Karakteristikasma

Inflamasisaluran

napas

Bronchialhyperrespon

siveness

Airway Remodelling


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Kerusakan epithel (penggundulan)

Hiperplasi sel goblet dan Hipersekresi mukus

Pembesaran kelenjar submukosal

Penebalan membran basal

Infiltrasi sel inflamasi, dominasi eosinofil dan

sel mast

Penebalan lapisan otot polos.


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Essential steps in the Management ofAsthma to Achieve Control:


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Establish thediagnosis

Assess severityImplement

asthma

treatment

Set goals forcontrol of asthma

Prevent/avoidancemeasures

Pharmacotherapy

Achieveand

monitorcontrol

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A. ASTHMA DIAGNOSIS

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STEP 1


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Suspect asthma onbasis of symptomsand signs, particularlyif there is variability

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Reversibility based on Spirometry


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B. ASSESSMENT OF SEVERITY OR

CONTROL

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C. ASTHMA TREATMENT

Preventative/Avoidance Measures

Pharmacotherapy

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Preventative/Avoidance Measures

A Avoid exposure to personal and second-hand tobacco smoke


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A. Avoid exposure to personal and second hand tobacco smoke

B. Avoid contact with furry animals

C. Reduce pollen exposure

D. Reduce exposure to house dust mite

E. Avoid sensitizers and irritants (dust and fumes) which aggravateor cause asthma, especially in the workplace

F. Avoid food and beverages containing preservatives

G. Avoid drugs that aggravate asthma such as beta-blockers(including eye drops) and aspirin and non-steroidal anti-inflammatory drugs

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PHARMACOTHERAPY


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Take when necessary

Cause BRONCHODILATATION

symptoms acutelycough wheeze/tightness

(A) RELIEVERS :

Act only on airway smooth muscle spasm

Take regularly, even when well

Relieve:

mucosalswelling

secretionsirritability of

smooth muscle

(B) CONTROLLERS :

underlying INFLAMMATIONand/or cause prolongedbronchodilatation

ASTHMA DRUG CLASSIFICATION


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D. ACHIEVE AND MONITOR CONTROL

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Managing partly/uncontrolled patients

Check the inhaler technique


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Check the inhaler technique

Check adherence andunderstanding of medication

Consider aggravation by:

Exposure totriggers/allergens at homeor work

Co-morbid conditions: GIreflux, rhinitis/sinusitis,cardiac

Medications: Beta-blockers,NSAIDs, Aspirin

Consider stepping up treatment Consider need for short course

oral steroids

Review self-management plan

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Reasons for referral to a specialist


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Persatuan Dokter Paru Indonesia 2003


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SERANGAN ASMA

Oksigen: Pada serangan asma segera berikan