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ENVIRONMENTAL DISEASE & PATHOLOGY

*Everonmental Disease :
Penyakit akibat interaksi

Manusia ↔ lingkungan
(Fenomena Bloom?): Keturunan – Lingkungan - Perilaku
* Environmental Pathology :
Penyebab  Patogenesis PA.
*Lingkungan rochani : Keluarga, teman, masyarakat , bangsa
Patogenesis : Raga / Fisik ↔ Jiwa ↔ Roch.
‘Bangsa, Ibu Pertiwi saat ini baru sakit jiwa”.
Pendahuluan
Lingkungan
- Luas :darat, laut, udara
dekat ( 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, Rekayasa
Genetik
• Historik Peradaban: - makan
- mobilitas-kerja
- seks
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 menjadi  kenyataan.
• Pemajanan : Kontak faktor penyebab Paparan
• Dosis : Takaran fakator penyebab.
• Hazard - Risiko

Pemajanan/paparan  Kerusakan / kelainan / penyakit.

Dosis - Daya tahan tubuh


NB: Moral Hazard BPJS? : pemerintah, Depkes, BPJS sampai kebawah
Jajaran kesehatan
Pasien masyarakat.
ENVIRONMENTAL PATHOLOGY 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)
Frekuensi: Sering terjadi
Tanda – Gejala lokal (organ) Kategorial kompetensi dokter:
Regional (sistem) 1. Datang Rujuk Emergency
II. Datang Observasi Rujuk Spesialis
Sistemik – komplikasi IIIa. Datang Obati Rujuk Spesialis
IIIB. Datang Obati Rujuk Emergency
IV. Datang Obat Tuntas
Penanganan
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 ) 7th Ed halaman 415-468

(Slide Akhir: 15 Tabel)


ENVIRONMENTAL PATHOLOGY
Exposure

Absorption at portals of entry

Excretion
Distribution to body

Metabolism Metabolism Metabolism to


to more toxic to less toxic conjugation
metabolites metabolites products

Turnover
and repair
Distribution

Interaction with macromolecules


( proteins, DNA, RNA, receptors)

Toxic effects
( genetic , carcinogenic, reproductive ,immunotoxic)
• 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
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%)
PNEUMO KONIOSIS
Inhalasi : Debu mineral; Partikel organik & an org ;
asap ; uap kimia yang menyebabkan kelainan/
reaksi paru berupa : Inert / Inflam; fibrosis ; alergik
; imunologik; neoplastik
Inhalasi Debu Mineral :
- Arang Antrakosis
- Silika Silikosis
- Asbes Asbestosis mesothelioma
- Berilium Beriliosis
PENYAKIT LINGKUNGAN GLOBAL
1. Global Warming (Infra Merah)
Normal : Sinar matahari Bumi Memantulkan sinar
Inframerah “dibuang” ke angkasa luar.
Tidak Normal :terjadi lapisan “Green House Gas” yang menghalangi
angkasa luar sehingga inframerah kembali memantul ke Bumi
“Green House Gas”(lapisan C02, CH4, N2, CFC, H2O): terjadi akibat
Green House Efek (Efek rumah kaca) oleh aktifitas manusia global.
Suhu bumi naik (Global Warming) yang menggangu kesehatan dan
merubah pola hidup Vektor nyamuk, lalat dll
2. Jendela ozon (Ultra Violet)
Normal Sebelum sinar matahari sampai bumi, sinar U.V disaring /
ditahan oleh lapisan Ozon;
Lapisan Ozon dirusak (terjadi “jendela”) oleh “Ozon Depleting Substan”
: CFC (Creon); HBFC; HCFC;CCL4 ,kosmetik sehingga sinar U.V
“Kontak Iritasi” Kulit Manusia Penyakit
KERACUNAN ULAR BERBISA
- Ular berkelenjar racun bertaring (menginjeksikan racun) untuk melumpuhkan “mangsanya”)
Golongan Elapidolmis : Weling, Sendok, Welang, Cabai, King Kobra
- Toksin – Hematoksik (cardiovascular)
Pembengkakan, …, Nyeri, …..(akibat) trombositopeni
- Neurotoksik (otak-syaraf)
Kelumpuhan kerja syaraf, korban mengantuk, pelupuk mata berat, sesak nafas……
Protein - Sitotoksik (sel-jaringan)
Komplek langsung … (kerusakan jaringan)
- Psikologis cemas kekhawatiran +”Syok korban maupun keluarga”

aktifitas
Enzymmatik
lokal (sekitar tusukan taring) nyeri, perdarahan, memar, melepuh, nekrosis –
limfadenopati
PPPK : 1) Tenang, immobilisasi dengan kayu agar tidak ada pergerakan,
>< penyerapan racun ke darah – limfonode
Tidak boleh: – torniket
- insisi
Tak Bermanfaat – pengisapan
- Kompres es
Risiko negatif - Antihistamin
-Cortico Steroid
Buang waktu

2) Di Rumah sakit : -perban katun elastis Ø 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
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 (kadang – kadang)
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 terjadi kematian dalam waktu beberapa jam.
Catatan :
• Untuk 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
LINGKUNGAN ROCHANI
MANUSIA
Fisik / raga ↔ jiwa / daya hidup ↔ roch /
sukma ↔ Roch Allah / Roch suci / Roch
Kebenaran / Roch terang.
↕ Kalifah damai sejahtera
Roch Iblis / Roch jahat / Roch Gelap
Jiwa yang kalah dari pergulatan kemauan tubuh
/ duniawi  sakit / stress  R/ Roch ke Allah
Orandum es us sit, Mens Sana In Corpore Sano.
Firman – Iman – Kedekatan dengan Allah adalah
: sumber kekuatan yang tak terkalahkan
Lampiran – lampiran
Bahan Efek patologik
Karbon Monoksida Terikat dengan homoglobin, menimbulkan
hipoksia
Bahan 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 Pneumonitis
uap dosis rendah Tremor, pelupa, gingivitis, ruam kulit, sindrom
nefrotik
Mentanol Depresi SSP, asidosis kebutaan.
Jamur : Amanita muscarin Sintom parasimpatik : bradikardi, hipotensi
Amanitaphalloisdes 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 organ – organ
Etanol Alkoholisme akut :
Ganguan fungsi SSP, kerusakan hati dan lambung.
TABLE 9-2 Common Chemiscals at Hazardous Waste Sites
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

Diteruskan
Phase I Phase II
reactions: reaction
Primary glucuronidation Secondary
Toxicant Hidrolis
metabolite sulfation metabolisme
reduction
oxidation methilation
conjungation

Elimination in urine, bile, or feces


TABLE 9-3 Organ –Specific Carcinogens in
TABLE 9-3 Organ –Specific Carcinogens in Tobacco Smoke
Tobacco Smoke
Lung,Larynx
Lung,Larynx Polycyclic aromatic
Polycyclic aromatic hydrocarbons
hydrocarbons 4- 4-
(Methylnitrosoamino)-1-(3-pyridyl)-1-
(Methylnitrosoamino)-1-(3-pyridyl)-1-
butanone (NNK) Polonium 210
Esophagus
butanone (NNK) Polonium 210
N- Nitrosonornicotine (NNN)
Esophagus N-Nitrosonornicotine (NNN)
Pancreas
Pancreas NNKNNK(?) (?)
Bladder 4-Aminobiphenyl, 2 -
Bladder naphthylamine
4-Aminobiphenyl, 2 - naphthylamine

Oral cavity (Smoking) Polycyclic aromatic hydrocarbons,


Oral cavity (Smoking) NNK,Polycyclic
NNN aromatic hydrocarbons, NNK,
NNN
• Oral cavity ( snuff) NNK, NNN, polonium 210
Oral cavity ( snuff) NNK, NNN, polonium 210
TABLE 9-5 Mechanisme of Disease Caused by Ethanol Abuse
Organ System Lesion Mechanism

Liver Farty change Acute Toxicity


hepatitis Alcoholic cirrhosis

Nervous system Wernicke syndrome Thaimine deficiency Toxicity


Korsakoff syndrome and thiamine deficiency
Carebellar degeneration Nutritional deficiency
Peripheral neuropathy Thiamine deficiency.

Cardiovascular system Cardiomyopathy Tpxicity Vasopresor


Hypertesion
Gastrointestinal tract Gastritis pancreatitis Toxicity
Toxicity
Skeletal muscle Rhabdomyoisis Toxicity
Reproductive Testicular atrophy ?
system spontaneous ?
abortion
Fetal Alcohol Growth Toxicity
syndrome retardation
Mental
retardation
Birth defects
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) Cocaine


Serotonim receptor chanel Amphetamine
(antagonist) 3,4-
methylenedioxymethamphetamine
(MDMA, ecstasy)
Phencyclidine –like NMDA glutamate Phencyclidine
drugs receptor chanel (PCP,angel dust)
(antagonist) Ketamine
Cananabiniods CBI cannabinoid Marijuana
receptors (agonists) Hashish
Necotine Nicotine Tabacco Products
acrtylcholine
receptor (agonist)
Hallucinogens Serotonin 5-HT2 Lysergic acid
receptors (agonist) diethylamide (LSD)
Mescaline
Psilocybin
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 Nonselemative, nonsteroid Peptic ulcer
pharmacologic mechanism anti-inflammatory digs

Altered drug metabolism Bone marrow failure


related to: Azathioprine Bleeding
Thiopurine S- Oral anticoagulans Excessive sedation,
methyltransferase deficiency Some antipsychotic drugs parkinsonism
Cytochrome P-450 CYP2C9 Hydralazine Lupus
variants. Choramphenicol Aplastic anemia
Cytochrome P-450 CYP2D6
variants.
N-acetytransferase, show
acetylator phenotype.
TABLE 9-10 Health Effects of Outdor air Pollutants
Ozone Healthy adults and children Decreased lung fuction
Athletes,outdoor workers Increased airway reactivity
asthematics Lung inflammation
Decreased exercise capacity
Increased hoospitalizations
Nitrogen dioxide Healthy adults Increased airway reactivity
Asthmatics Decreased lung fuction
Children Increased respiratory infecton
Sulfur dioxide Healty adults Increased respiratory symptoms
Patients with chronic lung disease Increased mortality
Asthmatics Increased hospitalization
Decreased lung function

Acid aerosols Healty adults Altered mucociliary clearance


Children Increased respiracory infections
Decreased lung fuction
Increased hospitalizations

particulates Children Increased respiraory infections


Patiens with chronic lung or heat Decreased lung fuction
disease Excess mortality
Athamatcs Increased attacks
asthmatics
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


Asbestos fibers Maintenance and Lung cancer,
abatement workers mesothelioma

Manufactured mineral Maintenance and Skin and airway asthma


fibers constructions workers

Bioaerosols Adults and children Alergic rhinitis, Asthma


TABLE 9-12 Human Diseases Associated with Occupational Exposures
organ effect Toxicant

cardiovacular Heart disease Carbon monoxide,lead,


solvents,cobalt, cadmium
Respiratory system Nasal cancer Isopropyl alchohol, wood dust.
Lung canzer Radon, asbestos, silica,bis
Cjhronic obstructive lung disease (chloromethy) lether,
Hypersensitivity nickel,arsenic, chromium,mustard
Irritation gas.
fibrosis Grain dust. Coal dust, cadmium
Beryllium, isocyanates
Ammonia, sulfur oxides,
formaldehyde
Silica, asbestos, cobalt.
Nervous system Peripheral neuropathies Solvents, acrylamide, methyl
Ataxic gait chloride, mercury, lead, arsenic,
Central nervous system depression DDT
cataracts Chlordane, toluene, acrylamide ,
mercury
Alcohols, ketones, aldehydes,
solvents
Untraviolet radiation
Urinary system Toxity Mercury, lead, glycol ethers,
Bladder cancer solvents
Naphthylamines, 4-
Reproductive system Male ifertility Lead, phthalate
Female infertility plasticizers
teratogenisis Cadmium, lead.
Mercury, polychlorinated
biphenyls
Hematopoietic system Leukemia Benzene , radon, uranium

Skin Foliculitis and Polychlorinated


acneform dermatosis biphenyls, dioxins,
cancer herbicides
Ultraviolet radiation
Gastrointestinal tract liver angiosarcomu Vinyl chloride
TABLE 9-13 Tocix and carcinogenic Metals
Lead Renal toxicity Battery and ammunition workers,
Anemia, colic foundry workers, spray painting,
Peripheral neuropathy radiator repair
Insomnia, fatigue
Cognitive dedeficits
Mercury Renal toxicity Chlorine- alkali industry
Muscle tremor, dementia
Cerebral palsy
Mental retardation
arsenic Cancer of skin, lung, liver Miners, smelters, oil refinery
workers, farm workers
Beryllium Acute lung irritant Battery workers, smelters,
Chonic lung hypersensitivity welders,soldering
? lung cancer
Cobalt and tugsten carbide Lung fibrosis Tool,arkers, grinders, diamond
Asthma polishers
Cadmium Renal toxicity Battery woekers, smelters,
? prostate cancer 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
TABLE 9-14 HEALTH Effeects of agricultural pesticides
category Xexample Effects and Associations

Insecticides Organochlorines Neurrotoxicity, hepatotoxicity


DDT Neurotoxicity : deleyed neuroohaty
Chordane Neurotoxicity ( reversible )
Methoxychlor Parethesia; lung irritant; allergic dermatitis
Organophosphates
Parathion
Daizinon
Malation
Carbamates
Aldicarb
Carbaryl
Botanical agents
Nicotine
Pyrethering
Retenune .
Herbicides Aenic compounds Hyperpigmentation ; gangrene ; anemia; sensory
Dinitrophenols neuropathy; cancer
Cholophennoxy herbicides Hypertthermia, sweathing
2,4-D and 2,4,5-T ?Lymphoma ; sarcorma
TCDD Fototoxicity ; immunotoxicity; cancer
Paraquat Acute lung injury
Ateazine ?cancer
Alachlor ?cancer
Funggicides Captan ? Reprodutive toxicity
Maneb
benonyl
Rodenticides Fluoroacetate Cardiac and
Warfarine respiratory failure
strychnine Hemorrhage
Respiratory failure
Fumigants Carbon disulfide Cardiac toxicity
Ethylene dibronide Neurotoxicity
Phosphine Lung edema; brain
choropicrin demage
Eye irritation; lung
edema; arrhythmias
TABLE 9 – 21 COMPARASON of Servere Maramus-like and Kwashiorkor-like Secondary Protein-
energy Malnurtrition

Syndrome Clinical setting Time Clinical Laboratory Prognosis


Course features findings

Marasmus- Chronic iliness months History of Normal or Variable:


like protein (e.g.chronic weight loss mnidly depends on
energy lung disease muscle reduced underlying
malnutrition cancer) wasting serum disease
Absent proteins
subcutaneou
s fat
Kwashiorkor acute catabolic Weeks Normal fat Serum poor
-like protein ilines and muscle albumin <2.8
energy (eg..severe Ederma gm/dL
malnutrition trauma,burs, Easily
sepsis pluckable
hair
TABLE 9-22 Vitamins ; Major functions and Deficiency syndromes
Vitamin Functions Deficiency Syndromes

Fat-soluble Vitamin
A A component of visual pigment Night blindness, xerophthalmia,
Maintenance of specialized epithelia blindness
Maintenance of resistance to infection Squamous etaplasia
Vulnabili to infection, particularly
measles
Vitamin D Facilitates intestinal absorption of calcium and Ricketin in children
phosphorus and nineralization of bone. Osteomalacia in adults
Vitamin E Major antioxidant ; scavenges free radicals Spinocerebellar degeneration

Vitamin K Cofactor in hepatic carboxylation of Bleeding diathesis


procoagulants – factoers II (prothrombin), VII,IX,
and X ; and protein C and protein S.
Wather-Soluble
Vitamin B1 As pyrophosphate, is coenzymes in Dry and wet beriberi, Wernicke
(thiamine) decarboxylation reaction syndrome,
?Korsakoff syndrome
Vitamin b2 Convereted to coenzymes flavin monocleotide Ariboflavinosis, cheilosis, stomatitis,
(riboflamin) and flavin adinine dinicleotide, cofactors for many glosititis, dermatitis
enzymes in intermediary metabolism corneal,vascularization.
TABLE 9-24 Functions of Trace Metals and Deficiency Syndromes

Iron Essential component of Hypochromic microcytic anemia


hemoglobin as well as a number
of iron-containing
mentalloezymes
Zinc Component of enzymes, Acrodermatitis enteoatyroidusm
principally oxidases
Lodine Component of thyroid hormone Terand hypothyroidsm

Selenium Component of glutathione Myopathy, rarely cardiomyopathy


peroxidase
Copper Component of cytochrome c Muscle weakness, neurologic
oxidase, depamin β-hydroxylase, defects, hypopignentation,
tyrosinase, lysyl oxidase,and abnormal collagen cross-linking
unknown enzyme involved in
cross-;inking keratin
Manganese Component of metalloenzymes , No well-defined deficiency
including oxidoredutases, syndrome
hydrolases, and lipases
Fluride Mechanism unknown Dental caries
Niacin Incorporated into Pellagra- three “D’s” :
nicotinamide adenine dementia, dermatitis diarrhea.
dinucletide (NAD) and NAD
phosphate , involved in a
variety of redox reactions
Vitamin B6 (pyridoxine) Derivatives serve as Cheilosis, glossitis, dermatitis,
coenzymes in many peripheral neuropathy.
intermediary reactions
Viatamin B12 Required for normal folate Combined system disease
metabolism and DNA (megabolistic pernicious
synthesis anemia and degeneration of
Maintenance of myelinization posterolateral spinal cord
of spinal cord tracts tracts)
Vitamin C Servers in many oxidation- Scurvy
reduction (redox) reactions
and hydroxylation of collagen.
Folata Essential for transfer and use Megalobastic anemia, neural
of 1-carbon units in DNA tube defects
syntenis
Pantothenic acid Incorporated in coenzyme A No nonexperimental
ayndrome recognized
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, obesity
hypoventilation 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