dr. broto - patologi lingkungan dan keracunan

8/10/2019 Dr. Broto - Patologi Lingkungan Dan Keracunan

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ENVIRONMENTAL DISEASE & PATHOLOGY

Dr.JB.Soebroto.Sp.PA(K)

Rabu 29 oktober 2014Jam 10.00 -12.00

*Everonmental Disease :

Penyakit akibat interaksi

Manusia lingkungan

(Fenomena Bloom?)

* Environmental Pathology :

Penyebab Patogenesis PA.


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PendahuluanLingkungan

- Luas :darat, laut, udaradekat ( lingkup R.Tangga/ lingkup kerja )jauh

- Aneka Ragam Faktor :

Fisik : Mekanik, Suhu, Tek Udara, Suara, Cahaya,Radiasi, Getaran, Listrik

Kimia: Polutan, Asap, Rokok,Industri, Waste,Obat obatan, Racun, insektisida, Makanan,salah makan

Biologi : Bakteri, Virus, Jamur, Parasit, RekayasaGenetik


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Kategori Istilah

Penyakit Lingkungan berdasarkan penyebab dan ruang lingkup :

- Kultural

- Nutrisional

- Okupasional Keselamatan kerja .Patient safety??

- Global Hazard : Potensi bahaya terjadinya kelainan / cidera

Risiko : Perkiraan seberapa besar bahaya menjadikenyataan.

Pemajanan : Kontak faktor penyebab Paparan

Dosis : Takaran fakator penyebab. Hazard - Risiko

Pemajanan/paparan Kerusakan / kelainan / penyakit.

Dosis - Daya tahan tubuh


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Lanjutan.

Organisme mikro

makro : hewan, ular, jamur

Masuk tubuh lewat : mulut, nafas, hidung, mata, kulit (paparan, gigitan)

Penyebab lain Blok-Blok lain Sistema/Organ

Disengaja (tindak kekerasan, bunuh diri)

Tak disengaja (kecelakaan)

Tanda Gejala lokal (organ)

Regional (sistem)

Sistemik komplikasi

Penanganan

Frekuensi: Sering terjadi

Kategorial kompetensi dokter:

1. Datang Rujuk Emergency

II. Datang Observasi Rujuk SpesialisIIIa. Datang Obati Rujuk Spesialis

IIIB. Datang Obati Rujuk Emergency

IV. Datang Obat Tuntas

ENVIRONMENTAL PATHOLOGY


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KONSEP ENVIRONMENTAL PATHOLOGY

Lingkungan & Nutrisi

Penyebab

Masuk tubuh lewat.?

Disengaja,atau

Kecelakaan

Tanda Gejala , Perjalanan Penyakit

Penanganan

(SALING KAIT/ TERGANTUNG)

Berikut tabel-tabel Enviromental & Nutritional Patologyc (Robbins & Gotran

Pathologic Basic of Disease ) 7thEd halaman 415-468


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Exposure

Absorption at portals of entry

Distribution to bodyExcretion

Metabolism

to more toxic

metabolites

Metabolism

to less toxic

metabolites

Metabolism to

conjugation

products

Turnover

and repairDistribution

Interaction with macromolecules( proteins, DNA, RNA, receptors)

Toxic effects

( genetic , carcinogenic, reproductive ,immunotoxic)

ENVIRONMENTAL PATHOLOGY


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Limbah (waste) :-Definisi : Bahan kimia yang terbentuk sebagai sisa

suatu proses kegiatan : manusia; industri; RS

lingkungan (khususnya perkotaan)

- Jenis Limbah : padat; cair; gas; Infeksius(RS)

- Limbah mencemari lingkungan Penyakit

lingkungan

- Diperlukan Risk Assesment kemudian Risk

Manajemen limbah RS

- Pelaku limbah > < Korban Limbah


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Review

Perokok : - PJK + Hypertensi + Hypercholesterol- Kanker- COPD

Cor : - Iskemi (27%

- arrest (37%)- Arteriosklerosis(29%)

- Paru ( 90 %)

- Mulut (92%) - Visika urinaria (50%)

- Laring (82%) - Serviks (30%)- Esofagus(80%) - Pankreas (30%)

- Gaster (20%)


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PNEUMO KONIOSIS

Inhalasi : Debu mineral; Partikel organik & an org ;asap ; uap kimia yang menyebabkan kelainan/reaksi paru berupa : Inert / Inflam; fibrosis ; alergik

; imunologik; neoplastikInhalasi Debu Mineral :

- Arang Antrakosis

- Silika Silikosis

- Asbes Asbestosis mesothelioma

- Berilium Beriliosis


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PENYAKIT LINGKUNGAN GLOBAL1. Global Warming (Infra Merah)

Normal : Sinar matahari Bumi Memantulkan sinarInframerah dibuang ke angkasa luar.

Tidak Normal :terjadi lapisan Green House Gas yangmenghalangi angkasa luar sehingga inframerah kembalimemantul ke Bumi

Green House Gas(lapisan C02, CH4, N2, CFC, H2O): terjadiakibat Green House Efek (Efek rumah kaca) oleh aktifitasmanusia global. Suhu bumi naik (Global Warming) yangmenggangu kesehatan dan merubah pola hidup Vektornyamuk, lalat dll

2. Jendela ozon (Ultra Violet)

Normal Sebelum sinar matahari sampai bumi, sinar U.Vdisaring / ditahan oleh lapisan Ozon;

Lapisan Ozon dirusak (terjadi jendela) oleh Ozon Depleting

Substan : CFC (Creon); HBFC; HCFC;CCL4 sehingga sinarU.V Kontak Iritasi Kulit Manusia Pen akit


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KERACUNAN ULAR BERBISA- Ular berkelenjar racun bertaring (menginjeksikan racun) untuk melumpuhkan mangsanya)

Golongan Elapidolmis : Weling, Sendok, Welang, Cabai, King Kobra

- ToksinHematoksik (cardiovascular)

Pembengkakan, , Nyeri, ..(akibat) trombositopeni

- Neurotoksik (otak-syaraf)

Kelumpuhan kerja syaraf, korban mengantuk, pelupuk mata berat, sesak nafasProtein - Sitotoksik (sel-jaringan)

Komplek langsung (kerusakan jaringan)

- Psikologis cemas kekhawatiran +Syok korban maupun keluarga

aktifitasEnzymmatik

lokal (sekitar tusukan taring) nyeri, perdarahan, memar, melepuh, nekrosis

limfadenopati


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PPPK : 1) Tenang, immobilisasi dengan kayu agar tidak ada pergerakan,

>< penyerapan racun ke darahlimfonode

Tidak boleh: torniket

- insisi

Tak Bermanfaat pengisapan

- Kompres es

Risiko negatif - Antihistamin

-Cortico Steroid

Buang waktu

2) Di Rumah sakit : -perban katun elastis 10cm mengganggu

aliran darah (bisa dikerjakan di lokasi)

3) Dibawa ke Rumah Sakit, dalam posisi nyaman, tenaga, immobilisasi

4) Pertolongan Emergency >< sifat racun , life saving

5) Serum Antibisa ular polivalen

6) ATS, Penicillin Kristal 2gram , analgesik


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Gejala Umum Keracunan Makanan.

Gejala yang timbul beberapa menit sampai 2 jam setelah makan, bisa

berupa :

Peningkatan produksi air mata dan air liur

Pupil yang mengecil

Berkeringat Muntah

Kram perut

Diare

Pusing

Linglung Koma

Kejang (kadangkadang)


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Penanganan

Cuci / bilas/lavase lambung

Perangsang muntah Laborat !

Norit, arang

Dan seterusnya tergantung jenis bahan racun dan akibatnya

Obat Pencahar Infuse Dextrose Nacl (kalau perlu) alat bantu pernafasan O2

Obat Anti nyeri.

Dengan pengobatan yang tepat, biasanya akan terjadi

penyembuhan dalam waktu 24 jam, meskipun bisa terjadikematian dalam waktu beberapa jam.


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CATATANUntuk Keracunan Bahan kaustik (Asam/Alkali kuat) tidak

boleh dilakukan tindakan diatas, karena telah terjadi

proses seperti luka bakar :

Oedema, Bula luka bakar- Kerusakan / Ekskoriasi, Ulkus,

- Peforasi /

Disini kalau perlu dikerjakan Tracheotomi


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Lampiranlampiran

Bahan Efek patologik

Karbon Monoksida Terikat dengan homoglobin, menimbulkan

hipoksiaBahan Pemutih (NAOHCI) Iritasi lokal

Bahan Kaustik (basa atau asam) Iritasi lokal, menimbulkan [erut

Kloroform, karbontetraklorida Dipresi SSP, asidosis metabolik, nekrosis tubulus.

Isopropanolol Gastristis, Depresi SSP.

Merkuri : uap dosis tinggi

uap dosis rendah

Pneumonitis

Tremor, pelupa, gingivitis, ruam kulit, sindrom

nefrotik

Mentanol Depresi SSP, asidosis kebutaan.

Jamur : Amanita muscarin

Amanitaphalloisdes

Sintom parasimpatik : bradikardi, hipotensi

Simtom gastrointinal, syok, konvulasi koma.

BBM (minyak tanah, bensin) Depresi pernapasan, pneuminitis, radang usus

PCB (Polychlorinated biphenyl) Pestisida Klorakne, ganguan penglihatan, ipotensi

Ganguan susunan saraf, kerusakan organorgan

Etanol Alkoholisme akut :Ganguan fungsi SSP, kerusakan hati dan lambung.


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TABLE 9-2 Common Chemiscals at Hazardous Waste Sites

Diteruskan

Acetone DDT, DDE,DDD

Aldrine/Dieldrin 1,1 and 1,2- Diclhorethane

Arsenic Lead

Barium Mercury

benzene Methylene chloride

2-Butanone Nickel

Cadmium Pentachlorophenol

Carbon tetrachloride Polychlorinated biphenyls

Chrordane Tri-and Tetrachloroethylene

Chloroform Toluene

chromium Vinyl Chloride

Cyanide Zinc


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Elimination in urine, bile, or feces

Toxicant

Phase I

reactions:

Hidrolisreduction

oxidation

Primary

metabolite

Phase II

reaction

glucuronidationsulfation

methilation

conjungation

Secondary

metabolisme


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TABLE 9-3 OrganSpecific Carcinogens in

Tobacco Smoke

Lung,Larynx Polycyclic aromatic hydrocarbons 4-

(Methylnitrosoamino)-1-(3-pyridyl)-1-

butanone (NNK) Polonium 210

Esophagus N-Nitrosonornicotine (NNN)

Pancreas NNK (?)

Bladder 4-Aminobiphenyl, 2 -

naphthylamine

Oral cavity (Smoking) Polycyclic aromatic hydrocarbons,

NNK, NNN

Oral cavity ( snuff) NNK, NNN, polonium 210

TABLE 9-3 OrganSpecific Carcinogens in Tobacco Smoke

Lung,Larynx Polycyclic aromatic hydrocarbons 4-

(Methylnitrosoamino)-1-(3-pyridyl)-1-

butanone (NNK) Polonium 210

Esophagus N- Nitrosonornicotine (NNN)

Pancreas NNK (?)

Bladder 4-Aminobiphenyl, 2 - naphthylamine

Oral cavity (Smoking) Polycyclic aromatic hydrocarbons, NNK,NNN

Oral cavity ( snuff) NNK, NNN, polonium 210


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TABLE 9-5 Mechanisme of Disease Caused by Ethanol Abuse

Organ System Lesion Mechanism

Liver Farty change Acute

hepatitis Alcoholic cirrhosis

Toxicity

Nervous system Wernicke syndrome

Korsakoff syndrome

Carebellar degeneration

Peripheral neuropathy

Thaimine deficiency Toxicity

and thiamine deficiency

Nutritional deficiency

Thiamine deficiency.

Cardiovascular system Cardiomyopathy

Hypertesion

Tpxicity Vasopresor

Gastrointestinal tract Gastritis pancreatitis Toxicity

Toxicity


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Skeletal muscle Rhabdomyoisis Toxicity

Reproductive

system

Testicular atrophy

spontaneous

abortion

?

?

Fetal Alcohol

syndrome

Growth

retardation

Mentalretardation

Birth defects

Toxicity


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TABLE 9-6 Common Drugs of Abuse (Farmocology)

Class Molecular Target Example

Opioid narcotics Mu Opioid receptor (agonist) Heroin, Hydromorphone (Dilaudid)

Oxycodone(Percodan,Percocet,Oxycontin)

Methadone (Dolophine)

Meperidine (Demerol)

Sadative- hypnotics GABAA Receptor (Agonist) Barbiturates

Ethanol

Methaqualone (Quaalude)Glutethimide (Doriden)

Ethchlorvynol (Placidyl)

Psychomotor stimulants Dopamin transporter (antagonist)

Serotonim receptor chanel

(antagonist)

Cocaine

Amphetamine

3,4-

methylenedioxymethamphetamine

(MDMA, ecstasy)


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Phencyclidinelike

drugs

NMDA glutamate

receptor chanel(antagonist)

Phencyclidine

(PCP,angel dust)Ketamine

Cananabiniods CBI cannabinoid

receptors (agonists)

Marijuana

Hashish

Necotine Nicotineacrtylcholine

receptor (agonist)

Tabacco Products

Hallucinogens Serotonin 5-HT2

receptors (agonist)

Lysergic acid

diethylamide (LSD)

Mescaline

Psilocybin


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TABLE 9-7 Mechanism of Advers Drug

Reactions(Farmacology)mechanism Example Adverse Effect

Toxicity due to overdose Acetaminophen Liver necrosis anti-

inflammatory

Predicatable reaction based on

pharmacologic mechanism

Nonselemative, nonsteroid

anti-inflammatory digs

Peptic ulcer

Altered drug metabolism

related to:

Thiopurine S-

methyltransferase deficiency

Cytochrome P-450 CYP2C9

variants.

Cytochrome P-450 CYP2D6

variants.

N-acetytransferase, show

acetylator phenotype.

Azathioprine

Oral anticoagulans

Some antipsychotic drugs

Hydralazine

Choramphenicol

Bone marrow failure

Bleeding

Excessive sedation,

parkinsonism

Lupus

Aplastic anemia


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TABLE 9-10 Health Effects of Outdor air Pollutants

Ozone Healthy adults and children

Athletes,outdoor workers

asthematics

Decreased lung fuction

Increased airway reactivity

Lung inflammation

Decreased exercise capacityIncreased hoospitalizations

Nitrogen dioxide Healthy adults

Asthmatics

Children

Increased airway reactivity


Increased respiratory infecton

Sulfur dioxide Healty adults

Patients with chronic lung diseaseAsthmatics

Increased respiratory symptoms

Increased mortalityIncreased hospitalization

Decreased lung function

Acid aerosols Healty adults

Children

Altered mucociliary clearance

Increased respiracory infections

Decreased lung fuctionIncreased hospitalizations

particulates Children

Patiens with chronic lung or heat

disease

Athamatcsasthmatics

Increased respiraory infections


Excess mortality

Increased attacks


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TABLE 9-11 Human Diseases Associated with Occupational Exposures

Pollutant Populations at Risk Effects

Carbone monoxida Aduts and children Acute poisoning

Nitrogen dioxide Children Increased respiratory

infections

Wood Smoke Children Increased respiratory

infections

Formaldehyde Adults and children Eye and nose

irrieation, asthma

Radon Adults and children Lung cancer


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Asbestos fibers Maintenance and

abatement workers

Lung cancer,

mesothelioma

Manufactured mineralfibers

Maintenance andconstructions workers

Skin and airway asthma

Bioaerosols Adults and children Alergic rhinitis, Asthma


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TABLE 9-12 Human Diseases Associated with Occupational Exposuresorgan effect Toxicant

cardiovacular Heart disease Carbon monoxide,lead,

solvents,cobalt, cadmium

Respiratory system Nasal cancer

Lung canzer

Cjhronic obstructive lung disease

Hypersensitivity

Irritation

fibrosis

Isopropyl alchohol, wood dust.

Radon, asbestos, silica,bis

(chloromethy) lether,

nickel,arsenic, chromium,mustard

gas.

Grain dust. Coal dust, cadmium

Beryllium, isocyanates

Ammonia, sulfur oxides,

formaldehyde

Silica, asbestos, cobalt.

Nervous system Peripheral neuropathies

Ataxic gait

Central nervous system depressioncataracts

Solvents, acrylamide, methyl

chloride, mercury, lead, arsenic,

DDTChlordane, toluene, acrylamide ,

mercury

Alcohols, ketones, aldehydes,

solvents

Untraviolet radiation

Urinary system Toxity

Bladder cancer

Mercury, lead, glycol ethers,

solvents

Na hth lamines, 4-


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Reproductive system Male ifertility

Female infertility

teratogenisis

Lead, phthalate

plasticizers

Cadmium, lead.

Mercury, polychlorinated

biphenyls

Hematopoietic system Leukemia Benzene , radon, uranium

Skin Foliculitis and

acneform dermatosis

cancer

Polychlorinated

biphenyls, dioxins,

herbicides

Ultraviolet radiationGastrointestinal tract liver angiosarcomu Vinyl chloride


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TABLE 9-13 Tocix and carcinogenic MetalsLead Renal toxicity

Anemia, colic

Peripheral neuropathy

Insomnia, fatigueCognitive dedeficits

Battery and ammunition workers,

foundry workers, spray painting,

radiator repair

Mercury Renal toxicity

Muscle tremor, dementia

Cerebral palsy

Mental retardation

Chlorine- alkali industry

arsenic Cancer of skin, lung, liver Miners, smelters, oil refinery

workers, farm workers

Beryllium Acute lung irritant

Chonic lung hypersensitivity

? lung cancer

Battery workers, smelters,

welders,soldering

Cobalt and tugsten carbide Lung fibrosis

Asthma

Tool,arkers, grinders, diamond

polishers

Cadmium Renal toxicity

? prostate cancer

Battery woekers, smelters,

welders, soldering

Chromium Cancer of lung and nasal cavity Pigment workers ., smelters , steel

workers

Nickel Cancer of lung and nasal sinuses Smelters, steel workers,

electroplating

9 ff f i l l i id


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TABLE 9-14 HEALTH Effeects of agricultural pesticidescategory Xexample Effects and Associations

Insecticides Organochlorines

DDT

ChordaneMethoxychlor

Organophosphates

Parathion

Daizinon

Malation

Carbamates

Aldicarb

Carbaryl

Botanical agents

Nicotine

Pyrethering

Retenune .

Neurrotoxicity, hepatotoxicity

Neurotoxicity : deleyed neuroohaty

Neurotoxicity ( reversible )Parethesia; lung irritant; allergic dermatitis

Herbicides Aenic compounds

Dinitrophenols

Cholophennoxy herbicides

2,4-D and 2,4,5-T

TCDD

Paraquat

Ateazine

Alachlor

Hyperpigmentation ; gangrene ; anemia; sensory

neuropathy; cancer

Hypertthermia, sweathing

?Lymphoma ; sarcorma

Fototoxicity ; immunotoxicity; cancer

Acute lung injury

?cancer

?cancer

Funggicides Captan

Maneb

benonyl

? Reprodutive toxicity


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Rodenticides Fluoroacetate

Warfarine

strychnine

Cardiac and

respiratory failure

Hemorrhage

Respiratory failure

Fumigants Carbon disulfide

Ethylene dibronide

Phosphine

choropicrin

Cardiac toxicity

Neurotoxicity

Lung edema; brain

demageEye irritation; lung

edema; arrhythmias


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TABLE 921 COMPARASON of Servere Maramus-like and Kwashiorkor-like Secondary Protein-

energy Malnurtrition

Syndrome Clinical setting TimeCourse

Clinicalfeatures

Laboratoryfindings

Prognosis

Marasmus-

like protein

energy

malnutrition

Chronic iliness

(e.g.chronic

lung disease

cancer)

months History of

weight loss

muscle

wastingAbsent

subcutaneou

s fat

Normal or

mnidly

reduced

serumproteins

Variable:

depends on

underlying

disease

Kwashiorkor

-like proteinenergy

malnutrition

acute catabolic

ilines(eg..severe

trauma,burs,

sepsis

Weeks Normal fat

and muscleEderma

Easily

pluckable

hair

Serum

albumin


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TABLE 9-22 Vitamins ; Major functions and Deficiency syndromes

Vitamin Functions Deficiency Syndromes

Fat-soluble VitaminA A component of visual pigment

Maintenance of specialized epithelia

Maintenance of resistance to infection

Night blindness, xerophthalmia,

blindness

Squamous etaplasia

Vulnabili to infection, particularly

measles

Vitamin D Facilitates intestinal absorption of calcium and

phosphorus and nineralization of bone.

Ricketin in children

Osteomalacia in adults

Vitamin E Major antioxidant ; scavenges free radicals Spinocerebellar degeneration

Vitamin K Cofactor in hepatic carboxylation of

procoagulantsfactoers II (prothrombin), VII,IX,

and X ; and protein C and protein S.

Bleeding diathesis

Wather-Soluble

Vitamin B1

(thiamine)

As pyrophosphate, is coenzymes in

decarboxylation reaction

Dry and wet beriberi, Wernicke

syndrome,

?Korsakoff syndrome

Vitamin b2

(riboflamin)

Convereted to coenzymes flavin monocleotide

and flavin adinine dinicleotide, cofactors for many

enzymes in intermediary metabolism

Ariboflavinosis, cheilosis, stomatitis,

glosititis, dermatitis

corneal,vascularization.


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TABLE 9-24 Functions of Trace Metals and Deficiency Syndromes

Iron Essential component of

hemoglobin as well as a number

of iron-containing

mentalloezymes

Hypochromic microcytic anemia

Zinc Component of enzymes,

principally oxidases

Acrodermatitis enteoatyroidusm

Lodine Component of thyroid hormone Terand hypothyroidsm

Selenium Component of glutathione

peroxidase

Myopathy, rarely cardiomyopathy

Copper Component of cytochrome c

oxidase, depamin -hydroxylase,

tyrosinase, lysyl oxidase,and

unknown enzyme involved in

cross-;inking keratin

Muscle weakness, neurologic

defects, hypopignentation,

abnormal collagen cross-linking

Manganese Component of metalloenzymes ,

including oxidoredutases,

hydrolases, and lipases

No well-defined deficiency

syndrome

Fluride Mechanism unknown Dental caries


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Niacin Incorporated into

nicotinamide adenine

dinucletide (NAD) and NAD

phosphate , involved in avariety of redox reactions

Pellagra- three Ds :

dementia, dermatitis diarrhea.

Vitamin B6 (pyridoxine) Derivatives serve as

coenzymes in many

intermediary reactions

Cheilosis, glossitis, dermatitis,

peripheral neuropathy.

Viatamin B12 Required for normal folate

metabolism and DNA

synthesis

Maintenance of myelinization

of spinal cord tracts

Combined system disease

(megabolistic pernicious

anemia and degeneration of

posterolateral spinal cord

tracts)

Vitamin C Servers in many oxidation-

reduction (redox) reactionsand hydroxylation of collagen.

Scurvy

Folata Essential for transfer and use

of 1-carbon units in DNA

syntenis

Megalobastic anemia, neural

tube defects

Pantothenic acid Incorporated in coenzyme A No nonexperimental

ayndrome recognized


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TABLE 9-26 Medical complications associated with Obesity

Gastrointestinal Gallstones, pancreatitis, abdominal hernia, NAFLD (steatosis,

steatohpatitis and cirrhosis) and possibly GERD

Educrine / metabolic Metabolic syndrome, insulin resistence, impaired glucose telorance,

type II dibetes muletus, dyslipidemia, polycystic ovary syndrome

Cardiovarcular Hypertension, coronary aretery disease, congestive heart failure,

arrhyhamias, pulmonary hypertension, ischemic , stroke, venous

stasis, deep vein thrombosis, pulomonary embolus.

Respiratorty Abnormal pulmonary function, obstructive sleep apnea, obesityhypoventilation syndrome

Musculos keletal Ostheorosis, gout, low back pain

Gynecologic Abnormal menses, infertility

Genitourinary Urinary stress incontinence

Ophthalmologic cataracts

Neurologic Indiopathic intracranial hypertension (pseudottumor cerebri)

cancae Esophagus , colon, gallbladder, prostate, breast, uterus, cervix, kidney

Pastoperative events Atelectasis , pneumonia, deep vein thrombosis, pulmonary embolus

dr. broto - patologi lingkungan dan keracunan

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