gejala total

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THT Pseudocroup peradangan subglotis akut Demam Batuk non produktif Memburuk pada malam hari Sianosis Serak, kadang2 Peradangan subglotis sampai glottis (rima glottis sempit) Hiperemis ringan plika vokalis X foto : Steeple sign Virus THT Epiglotitis supraglotik dan epiglotis, akut Demam ringan, odinofagi ringan, bisa berat Drooling Batuk jarang Gejala berkembang sangat cepat, tdk spesifikà sumbatan mendadak (2-24 jam)à emergency Udem epiglotis, plika ariepiglotika, aritenoid dan supraglotis Penimbunan saliva di hipofaring Daerah plika vokalis dan subglotis normal Tidak disarankan melakukan laringoskopi Laringoskopi direct à cherry red app X- foto soft tissue colli lateral à Thumb sign H. Influenza tipa B THT Laringitis difteri Serak, batuk, sesak, stridor inspirasi, panas tinggi Bullneck Pseudomembran Aspirasi Trakea Batuk Demam Sesak nafas Stridor Lihat separah apa (x foto, BGA) THT Trakeitis akibat sekunder infeksi virus Batuk yang dalam (mirip croup) Panas tinggi Nyeri dada Udem dan hiperemis pada trakea 1. Kultur S. aureus

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Page 1: Gejala Total

THT Pseudocroupperadangan subglotis akut

• Demam • Batuk non produktif • Memburuk pada malam

hari • Sianosis • Serak, kadang2

Peradangan subglotis sampai glottis (rima glottis sempit)Hiperemis ringan plika vokalisX foto : Steeple sign

Virus

THT Epiglotitissupraglotik dan epiglotis, akut

Demam ringan, odinofagi ringan, bisa beratDroolingBatuk jarangGejala berkembang sangat cepat, tdk spesifikà sumbatan mendadak (2-24 jam)à emergency

Udem epiglotis, plika ariepiglotika, aritenoid dan supraglotis

Penimbunan saliva di hipofaring

Daerah plika vokalis dan subglotis normal

Tidak disarankan melakukan laringoskopi

Laringoskopi direct à cherry red app

X- foto soft tissue colli lateral à Thumb sign

H. Influenza tipa B

THT Laringitis difteri Serak, batuk, sesak, stridor inspirasi, panas tinggiBullneck

Pseudomembran

Aspirasi Trakea • Batuk • Demam • Sesak nafas • Stridor

Lihat separah apa (x foto, BGA)

THT Trakeitisakibat sekunder infeksi virus

• Batuk yang dalam (mirip croup)

• Panas tinggi • Nyeri dada • Serak (kadang) • Sesak nafas • Kadang nyeri telinga

Udem dan hiperemis pada trakea

1. Kultur dari nasofaring /trakea

S. aureus

THT Benda Asing Trakea-bronkus

Bisa batuk2

Trakea:Batuk paroksimal mendadak Sianosis / asfiksia bising / wheezeAudibel slap ( benda bergerak )Flutter atau palpatory thrillRetraksi dinding dada

Foto rongen paru Bronkoskopi

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Sterm fremitus dan auskultasi lemah

Bronkus:Rasa tersumbat / tercekik batuk paroksismal Bising di bronkus Stem fremitus kanan dan kiri beda Auskultasi lemah pada bronkus yang tersumbat

Segmen:Segmen : Perasaan tersumbat dan tercekik Batuk paroksismal Bising pada segmen yang kena Auskultasi melemah pada segmen yang kena

“Symtomless interval”

THT Adenoitis Kronik - Tidur mendengkur - Rinore - Batuk-batuk - Kurang pendengaran - Facies adenoides :- Palatal phenomena :

negatif - Adenoid membesar

Bakteri

THT Tonsilitis Akut - Sakit telan / odinofagi

- Lesu - Suhu naik - Sakit kepala dan

sakit di otot-otot - Kadang-kadang

batuk, serak, nafas bau

- Otalgia

Tonsil : - hiperemi - edema -

permukaan / kripte tertutup detritus.Uvula : hiperemis dan edemaFaring : Hipersekresi

BakteriVirus

THT Tonsilitis Kronik - Sakit telan ringan (pancingen)

- Lesu - Kurang nafsu makan - Sakit kepala

- Tonsil :* Hiperemis, edema?* Kripte melebar,

detritus?* Permukaan benjol2

Page 3: Gejala Total

- Ngantukan Panas nglemeng/meriang/subfebril

* Atropi/hipertrofi

THT Faringitis Akut - Faring terasa kering - Odinofagi - Otalgia-refered pain- Berdahak :Encer → Mukoid → Lengket - Sakit kepala - Febris

Mukosa faring :1. Bengkak (udem)2. Merah (hiperemi)3. Lendir : serus

- Suhu badan naik - Kel. Limfe leher membesar

Bakteri?

THT Faringitis Kronik - Diskomfort di tenggorok

- Rasa kering di tenggorok à tipe atrofi

- Rasa selalu ada lendir di tenggorok à tipe hipertrofi

- Batuk-batuk - Kemerahan mukosa

faringPembesaran kel. Limfe leher

Bentuk atrofi:* Mukosa kering * Mukosa atrofi * Mukosa mengkilat

Bentuk hipertrofi:* Mukosa banyak lendir * MUkosa tidak rata

Faktor disposisi

THT Abses Peritonsil - Panas - Nyeri telan (spontan)- Buka mulut terbatas

(trismus)- Ngiler (droling)

- ”Hot potato’s voice” - Droling - Uvula udem, deviasi

ke sisi sebelah - Tonsil membesar

(sering sebelah)- Trismus

Kel. Limfe di bawah angulus mandibula

Bakteri

THT Parotitis Supuratif pre/post aurikula à sudut rahang bawah, discharge purulendysgeusia dan limfadenopati servikalparah, mungkin ada yang disertai demam , abses pada ruang parafaringeal, termasuk angina Ludwig ’ s

bakteri

THT Abses Submandibula (Ludwig’s Angina)

- Sakit gigi M I – M III bawah

- Bengkak submandibula :* Keras (SPT-papan)* Unilateral

- Sakit spontan

Bakteri

Page 4: Gejala Total

- Trismus Komplikasi :

- Udem laring à Dispnea

- Mediastinitis à Abses mediastinum

- Tromboplebitis à Trombus ke otak

THT Obstructive Sleep Apnea Syndrome (OSAS)

Pernafasan abnormal selama tidur

Kantuk berlebih siang hari

Kelainan nasal, faringeal, laryngeal, neurologis/ congenital, farmakologik

THT Cystic Higroma (cystic lymphangioma)

Bisa juga di tempat lain, tapi sering di leherDlm kehamilan, congenital, atau saat masa perkembangan (makin membesar).

Amniosintesis atau CVS USG pedigree - Pemeriksaan infeksi

virus lainnya - Pencarian tanda hisrops

amnion

THT Kista Brankialis I : preaurikula II : sudut mandibula, submandibulaIII : sering mengalami abses tiroid à DD Kista BrakialisIV : di laring (jarang)

CT Scan à gold standard Gambaran lesi homogen

Neuro SPONDILOSIS SERVIKALIS

• dull aching pain, unilateral / bilateralintermiten /

konstan, diprovokasi dengan

Penunjang : (bila ada defisit neurologik)

• X foto polos vertebra servical

Page 5: Gejala Total

rotasi leher • kaku , spasme dan

tenderness• Nyeri kepala bangun

tidur ~ TTH

• MRI • EMG

• Berhubungan dg pekerjaan : mengetik, menggambar, sekretaris

• Faktor stress dan ketegangan mental

Nyeri kencang• Mobilitas leher :

terbatas • Palpasi : tenderness

difus / terbatas ~ trigger spot

FROZEN SHOULDER (Nyeri bahu)

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Carotico-cavernous fistule

CCF symptoms include bruit (a humming sound within the skull due to high blood flow through the arteriovenous fistula), progressive visual loss, and pulsatile proptosis or progressive bulging of the eye due to dilatation of the veins draining the eye. Pain is the symptom that patients often find the most difficult to tolerate.

Patients usually present with sudden or insidious onset of redness in one eye, associated with progressive proptosis or bulging.

They may have a history of similar episodes in the past.

Retinitis Pigmentosa

Rod cells gradually lose their ability to respond to light

GK : nictalopia, constricted visual field

Fundus : bone sicule-like pigment, arteriolar narrowing, pallor of disc (variable)

T : vit A palmitate, DHA, hindari cahaya, no high-dose vit E

Stargardt Disease

GK : gradual impairment of central vision, presentation on second decades

S : fovea atrophy surrounded by discrete yellowish round or pisciform flecks at the level of RPE, if flecks are widely scattered disebut fundus flavimaculatus

T : low vision aid, light protection

Myopic degeneration

Krn myopia à elongation of eye à thinning RPE and choroid (>-6 D, axial length >26 mm), liable to glaucoma and cataract

T : optical correction, pressure control, sclera buckling

ARMD (Age related macular disease)

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GK : early – central vision may be blurred or distorted, objects looking unusual size/shape and straight lines appearing wav or fuzzy (over several months)

S : dry armd (90%) : drusen/yellowish debris in retina, atrophic

Wet armd (more progressive) : choroidal neovascularization

Chorioretinitis toxoplasma

GK : unilateral, mild ocular pain, blurred vision, new onset of floating spots

S : granulomatous iritis, vitritis, optic disc swelling, neuroretiniits, vasculitis, white-yelllow choreoretinal lesions, may be old inactive in the fellow eye

Diabetic retinopathy

S : non-proliferative : mircroaneurism, dot & blot intraretinal hemorrhage, hard exudates, dilatation and beading of retinal vein

Proliferative : neuvascularization on disc or else where

Hypertensive retinopathy

HTN can affect choroid, retina and n.II

- Nerve fiber layer micro-infarcts (Cotton wool spots) due to disruption of axoplasmic transport (lap ganglion keluar)

- Dot/blot and flame shaped hemorrhage

Traction/drawing to retina

GK : flashes

C : exudativa (uveal effucsion infection/inflammation), rhegmatogenous (retinal break), tractional (proliferative DR)

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Indirect carotid-cavernous sinus fistulas tend to cause fewer, less serious symptoms. This is because of their relatively low rate of blood flow. Direct fistulas usually require more urgent attention. For both types, symptoms may include:

a bulging eye, which may pulsate a red eye an eye which protrudes forwards double vision loss of vision an audible swish or buzz coming from your eye weak or missing eye movements pains in your face ringing in your ears headaches nosebleeds

GIANT CELL ARTERITIS

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Giant cell arteritis is an inflammation of the lining of your arteries — the blood vessels that carry oxygen-rich blood from your heart to the rest of your body. Most often, it affects the arteries in your head, especially those in your temples. For this reason, giant cell arteritis is sometimes called temporal arteritis or cranial arteritis.

Giant cell arteritis frequently causes headaches, jaw pain, and blurred or double vision. Blindness and, less often, stroke are the most serious complications of giant cell arteritis.

Can varyGenerally, signs and symptoms of giant cell arteritis include:

Persistent, severe head pain and tenderness, usually in your temple area

Vision loss or double vision

Scalp tenderness — it may hurt to comb your hair or even to lay your head on a pillow, especially where the arteries are inflamed

Jaw pain (jaw claudication) when you chew or open your mouth wide

Sudden, permanent loss of vision in one eye

Fever

Unexplained weight loss

Diagnosis

o help diagnose giant cell arteritis, you may have some or all of the following tests:

Physical exam. In addition to asking about your symptoms and medical history, your doctor is likely to perform a thorough physical exam, paying particular attention to your temporal arteries. Often, one or both of these arteries are tender with a reduced pulse and a hard, cord-like feel and appearance.

Blood tests. If your doctor suspects giant cell arteritis, you're likely to have a blood test that checks your erythrocyte sedimentation rate — commonly referred to as the sed rate. This test measures how quickly red blood cells fall to the bottom of a tube of blood. Red cells that drop rapidly may indicate inflammation in your body.

You may also have a test that measures C-reactive protein (CRP), a substance your liver produces when inflammation is present. The same tests may be used to follow your progress during treatment.

Biopsy. The best way to confirm a diagnosis of giant cell arteritis is by taking a small sample (biopsy) of the temporal artery. Because the inflammation may not occur in all

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parts of the artery, more than one sample may be needed. The procedure is performed on an outpatient basis during local anesthesia, usually with little discomfort or scarring. The sample is examined under a microscope in a laboratory.

If you have giant cell arteritis, the artery will often show inflammation that includes abnormally large cells, called giant cells, which give the disease its name. Unfortunately, a biopsy isn't foolproof. It's possible to have giant cell arteritis and still have a negative biopsy result. If the results aren't clear, your doctor may advise another temporal artery biopsy on the other side of your head.

Although a temporal artery biopsy is the standard test for diagnosing giant cell arteritis, imaging tests may also be used for diagnosing giant cell arteritis and for monitoring treatment. Possible tests include:

Magnetic resonance angiography (MRA). This test combines the use of magnetic resonance imaging (MRI) with the use of a contrast material that produces detailed images of your blood vessels. Let your doctor know ahead of time if you're uncomfortable being confined in a small space because the test is conducted in a tube-shaped machine.

Doppler ultrasound. This test uses sound waves to produce images of blood flowing through your blood vessels.

Positron emission tomography (PET). Using an intravenous tracer solution that contains a tiny amount of radioactive material, a PET scan can produce detailed images of your blood vessels and highlight areas of inflammation.

K : loss of vision, aortic aneurysm, stroke

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GLAUKOMA

sindrom:

- optic neuropati (cupping/excavation)

- visual field defect (arcuate)

- TIO tinggi (30%)

RF : DM, HTN

myopia, hipermetropia

2 mekanisme : TIO naik atau krn perfusi yg kurang

Open Angle (POAG)

chronic progressive, incidious, sometimes asymptomatic until relatively late (thief of sight)

familial tendency

Angle Closure (PACG)

Prodromal/SubAcute

elevated IOP are of short duration, key: history (short episode of unilateral pain, redness, blurring vision+halos around the light)

Acute

emergency

IOP raise rapidly (severe pain, redness, blurring vision)

Chronic Angle Closure

GK mirip open angle

ada faktor predisposisi

dever develop acute rise in IOP but form peripheral anterior synechia (PAS)

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Absolute glaucoma

end result of any uncontrolled glaucoma, IOP still high, redness, visus 0, often painfull, optic nerve atrophy

Degenerative glaucoma

visus 0, bullous keratopathy (often painfull) atrofi iris, atrofi ciliary body, cataract

DEFEK JALUR PENGLIHATAN

(liat gambar slide)

Papiledema

GK : nyeri kepala, muntah, bisa defisit neurologis dan penurunan kesadaran,

visus umumnya N, kecuali sudah kronis (atrofi papil), pelebaran bintik buta (di lap pandang)

T : disc swelling, batas kabur, hiperemis, vasculature melear dan berkelok, perdarahan dan eksudat peripapil, Paton's line

Optic Neuritis

- Papilitis

GK : penurunan visus subakut (2-7 hari), gangguan penglihatan warna dan kontras, nyeri gerak bola mata

T : visus turun, lap pandang tu/ sentral skotoma, refleks pupil menurun, papil udem, hiperemis pelebaran vena

- Neuritis retrobulber

patient sees nothing, docotor seen nothing

ISCHEMIC OPTIC NEUROPATHY

Stroke mata (nonarteritic anterior ischemic optic neuropathy)

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stroke mata, a. siliaris posterior brevis

FR : hipertensi, DM, hiperkolestrol

GK : peurunan visus mendadak, tanpa rasa sakit

T : refleks pupil menurun, papil udem sektoral atau menyeluruh, kepucatan

Compresi

Toxic and Nutritional

Traumatic

Hereditary

Pupil

RAPD/Marcus Gunn Pupill

defek sistem afferent, yg ipsi direct refleknya melambat

Tonic pupil

reaksi pupil thd sinar berkurang

krusakan pd ggl siliaris atau n. siliaris brevis

Horner's syndrome

miosis, ptosis, anhidrosis

krn simpatisnya terganggu