Manolya Flashcards

1
Q

Rash types, classification, on epidermis

A

Less than 1 cm:
Macule:Not raised,faded on pressure( vasodilatation)
Papule: Raised, firm, inflammatory cell aggregation
>1 cm:
Nodule: palpable solid/cystic
Plaque: elevated, psoriasis, mantar enfeksiyonu

Vesicle: içi su dolu, <5mm
Bula: vesicle >5mm
Pustule: Vesicle containing infection, purulent

Petechiae: pinpoint red spots, doesnt fade
Purpura

Differential of:
1.Vesicular:
Coxackievirus
Echovirus
Varicella
Herpes
M-pox
2.petechiae:
Meningococcemia!!
3.Maculopapular: many things

Widespread erythema: strep group A, staph aureus

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2
Q

For history and examination think about

A

Age, season,geolocation,travel history, exposure to insects, animals, ptx, history of vaccines and childhood diseases, immune status of host, medicines

Rash characteristics, distrubiton and progress,, change in morphology, accompanying symptoms, timing w/ fever

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3
Q

1st disease: Measles/Rubella/ kızamık

A

Single strand RNA virus (paramyxovirus)
Late winter, spring
Transmission by droplet and air, very contagious
Rash during viremia

Resp epithelium: primary viremia
Lymphatic tissue: secondary viremia

Signs:
Rhinorrhea
-conjunctivitis(+photophobia)
Dry cough
Fever(peaks at 3 days, subsides after 4 days)
Koplil spots( pathogonomonic): white spots, molar dişler yanı,yanakta, 48 hours before the rash, disappears 2nd day of rash, lymphatic aggregant)
Rash:3-7. day erythematous maculopaular rash, ear-hairline-nape, forehead to trunk and extremities, fades with brown pigmentation)

Lifelong immunity
Transient immunosupression during infection: 1.otitis media 2.pneumonia(mortality 01-03 !)

Hemorhagic measles: hemorhagic rashes that can be fatal, convulsions coma

Risk factors:
Vit A deficiency
Immune deficiency
Malnutrition

DGX:
Clinical findings+(prodromes,fever, rash koplik)
Positive measles IgM/ IgG serology(4 hafta arayla 4 kat artış) or RT-PCR

Differential: kawasaki, kızamıkçık, 5. 6. Disease,ebv, kızıl, adenovirus, mycoplasma
İlaç erupsiyonları? steven johnson toxic epidermal necrolis !?

Treatment: Vit A tedavisi (özellikle 2 yaş altı)

Korunma: kkk aşısı, 1 yaş, 4 yaş 2 doz
Ama vakaların görüldüğü zamanlar 9. Ayda ilave doz
Anneden geçen antikorlar ilk 6-9ay koruyor, aşının etkisini de engelliyor
Canlı aşı olduğu için 6 aydan önce yapılmaz

Post exposure immunuzation: anyone over 6 months for contact
Aşı durumu bilmiyorsan, kızamık şüpheliyle temas: 72 saat içinde aşı

Post exposure IG: <6 months, pregnant, immunosupressed

Subacute sclerosing panencephalitis(SSPE):
Progressive degenerative disorder of CNS 7-10 years after measles

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4
Q

Rubella( kızamıkcık)

A

5-9 yaş grubu
Hafif seyreder. Anne hamileyse congenital rubelladan korkarız
Cervical, suboccipital LAP
Maculopapular rash
Ateş prodromal dönemde, bulaşıcılık 2 hafta devam ediyor
Thrombocytopenia
Arthritis, eklem ağrısı
Encephalitis

People are only resource. Droplet, direct contact, late winter early spring, ıncubation 14-21 days, infectious from 2 days before rash to 7 days after, lifelong immunity. Forscheimer spots. Rash spreads from fave to body in 24 hours. 2nd day quickly fades, rarely 3 days.

Congenital rubella: first trimester:%50-80 infected baby
Cataract, cardiac anomaly, deafness,red purple blueberry muffin spots, meningoencephalitis, low birth weight, newborn IgM +, Ig titer increase, virus isolation

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5
Q

5th disease: Erythema Infectiosum

A

Parvovirus B19
Hafif seyreder
Hemolytic anemia, HIV, kemik iliği nakli durumlarında: aplastic anemia/ krize sebep olur
Pregnancy :hydrops fetalis
Ateş, burun akıntısı, öksürük, YANAKLAR KIPKIRMIZI , okul çağı çocukları, gövdesinde oya şeklinde rash
Döküntü en uzun süren hastalık

Spring,5-15y, respiratory tract and blood, ıncubation 4-14 days, prodrome 2-3 dys, fever, headache, weakness, many are asymptomatic
Rash:macular, plaques, SLAPPED CHEEK, PERORAL PALE, widespread in 1-4 days
Lace like rash on trunk and extremities, for 10-15 days. The rash may recur postinfection with exercise,temperature, stress. Itching, arthritis, arthralgia
Not contagious from onset of rash

yetişkinlerde :Gloves socks appearance: el ayak maculopapular purpuric döküntü, rash

Kızamık döküntüden 4 sonrası 5 gün
Su çiçeği kabuklanana kadar
Parvo döküntü çıktığında bulaştırıcılık kalkar

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6
Q

Infectious mononucleosis

A

EBV!
+CMV, hiv erken tablo
!Membranous Tonsilit, ağrılı cervical LAP, organomegaly, uzamış ateş, maculopapular rash after amoxicillin/ampicillin!
EBV VCA IgM +
Supportive treatment
Relaps edebilir gelecekte

Older children, adolescents
Fever,chills,sweats,,nausea, anorexia,sore throat, post, cervical lymphadenopathy,splenomegaly, malaise
Rash over trunk, extremities, hands, feet

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7
Q

Scarlet fever- kızıl

A

Group A streptococci( faranjit)
3 yaştan sonra görülür
Membranous tonsillit( white exudate like infectious mononucleosis)
White/red strawberry tongue
Petechie on soft palate
Suddenly starts with fever
rash: zımpara gibi, pürüzlü, covers entire body except face in 24 hours, face: forehead and cheeks red,flash like rash
Pallor atound mouth
No constitutional symptoms like kızamık(burun akıntısı gibi)
Pastia sign: linear pigmentation at kıvrım bölgeleri
Treatment: penicillin, 10 gün

Transmission respiratory secretion
İncubation 1-7 days
Sudden fever chills
Vomiting, headache, toxic appearance
Cervical lymphadenopathy
Petechia on palate
Exudative tonsillit

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8
Q

Kawasaki

A

> 5 days fever
+ 4 of these:
Conjunctivit, red tongue-cracked lips, el ayak ödem-erythema of palms, polymorph rash( mostly maculopapular), cervical lenfadenopati

Myocardit peicardit coroner arter genişlemesi, aneurysm
Thrombocytosis at 3 weeks.
A vasculitis

İlk 10 gün ivig, Echo yap

+
Acute period:high fever, conjunctivit,uveit, perianal erythema,strawberry tongue, lip fissure, myocardit, perşcardiy,lymphadenopathy

Subacute(11-30): conjunctivit, fever subsides, thrombocytosis, aneurysm, acral desquamation

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9
Q

6th disease: roseola infantum( gül hastalığı)
/ exanthema subitum

A

Hsv 6/7
Infants
3-5 gün yüksek ateş 39-40
Ateş düştükten sonra döküntü çıkarsa
Birkaç gün içinde kendi iyleşiyor
+occipital adenopathy

Neurotropic virus: febrile convulsion!
İmmunosupressed ptx: dissemine enfeksiyon
encephalopathyi
hemophagocytic syndrome

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10
Q

Chickenpox/ varicella zoster

A

Direct contact, droplet, air!
3 hafta incubation
Hafif ateş, baş ağrısı, soğuk algınlığı sonrası
Vesiculer lezyonlar, içi su dolu, kaşıntılı
Vesiculler farklı evrelerde, hepsi kabuklanana kadar bulaştırıcı(7-10 gün)
İtchy papulles

Complications:
pneumonia
Menengitis, cerebellitis
Myocardit
Reye sendromu
Seconder bacterial cilt enfeksiyonu ! (en sık)
Aplastic crisis
Wegener
Hemorrhagic su çiçeği
+fetal anemic hydrops

Congenital chickenpox:
First 20 week: embryopathy
Last 20 weeks: herpes zoster :)
5d before birth, 2 days after birth: en çok bundan korkarlar

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11
Q

Zona zoster

A

Varicella reaktivasyonu
İmmun sistem zayıflayınca, dermatomal lineda rash( shingles)

Acyclovir/ valacyclovir given to:

immunosupressed patients,
inhale steroid use,
yaşı >13
chronic cilt hastalığı varsa altta yatan,
su çiçeği +aspirin=reyes syndrome( chronic salicylate alan hastalar)
+ unvaccinated adolescents, malignancy, hiv, secondary cases in household contacts, high dose corticosteroid >14 days

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12
Q

Hand foot mouth disease

A

Conxsackie, enterovirus, echovirus
Çocuklarda yaygın, çok bulaşıcı, bir kere geçirince tekrar geçilir
Vesiculer lezyonlar, kaşınır
Direct temas, fecal oral route
Genital, anal lezyonlar da var
Kendi kendine geçiyor
Very contagious for 2 weeks

Complications:
Myocardit, pericardit, meningoencephalit, sudden death

Atypical HFMD: yetişkinde, ağır
Egzema consackium: daha atipik lezyonlar
Generalized HFMD: disseminated, tüm vücutta

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13
Q

Herpes simplex

A

Herpes 1/2

Primary infection: herpetic gingivoSTOMATİTİD: ağız içi beyaz +vesicles, fever, LAP

Neonatal herpes:
Scalp/ neck/ eye Vesicles
Dissemine neonatal herpes( adrenals, liver)
Intracranial, CNS
Encephalit
Herpes 1 by contact, herpes 2 vajinal kanal
Mortal

Intrauterine herpes:
yaygın cilt döküntüleri( hypopigmented, scaling, crusted erosions)

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14
Q

Meningococcemia (purpura fulminans)

A

Fever
Petechiae

En korktukları

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15
Q

Bacterial Meningitis causative organisms

A

Infants <3 months: Group B streptococcus, E.coli
Older infants children: S.pneumonia( pneumococ), N. Meningitis
Adolescents: N. Meningitis

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16
Q

Mechanism of infection for meningitis

A

Nasopharynx colonization

Direct entry( komşu enfeksiyon, trauma, medical device)

Invasion of CNS following bacteremia( infective endocarditis)

17
Q

Predisposimg factors to meningitis

A

Immunodeficiency( asplenia,complement def. Hypogammaglobulinemia,hiv,steroid use, dm)
Anatomic defects(dermal sinus)
Acquired cranial defects( fracture)
Medical device
Parameningeal infections
Recent infection
Recent exposure
Recent travel

18
Q

Presentation, clinical of meningitis

A

Fulminant or grafually progressive

Triad: Fever, neck stifness, abnormal mental status
+ headache, photophobia, nausea/vomiting, Tachycardia, tacyhpnea,hypotension, shock
Petechiae, purpura!
Focal neurologic findings
Seizures
Abnormal mental status
Increased ICP
Systemic findings

INFANTS:
Fever or hypothermia
Bulging fontanelle
Seizures
Jaundice
Respiratory distress
Poor feeding, vomiting, diarhhea
Lethargy, irritability

Meningeal signs:
Nuchal rigidity, headache, photophobia, irritsbility
Nuchal rigidity: limitation of neck flexion, kernig, brudzinski sign

19
Q

N meningitidis

A

Only human nasopharynx
Nasal carriage esp adolescents
Gram - diplococcus, aerobic/ facultative anaerobic
Polysacharide capsule inhibits opsonization and phagoctyosis
6 subgroup causes disease

20
Q

Progession of meningitis - hours

A

0-8h: nonspecific eatly signs like fever sore theoat nausea
9-15hr: classic meningitis signs
16-24: end stage signs like shock and multiple orgn involvemnet

Myalgia higher in bacterial meningitis
Infants at highest risk, then adolescents

21
Q

PE of meningitis

A

Hypotension, tachycardia most common
Petechiae echymosis
Kernig brudzinski
Cold sweats
Partiak clinical response after iv fluids

22
Q

Shock and multisystem involvement in meningitis

A

Peripheral vasoconstriction
Acidosis, hypoxia
Hypotension
Purpura fulminans: low protein C, from meningococcal inf, hemorrhage, necrosis, gangrene( DIC, thrombosis)
(DIC in sepsis)

Focal neurologic signs
Convulsions
Cerebral edema
Myocarditis
Acute abdomen

23
Q

Main toxin in meningitis

A

LOS

High LOS, low plasma in meningitis
Vice versa in meningococcemia

24
Q

Treatment of meningitis

A

4 adet 3rd gen cephalosporins:
1.ceftriaxone
2.cephotaxime
3. Vancomycin
4.penicilline

25
Long term effects of meningitis in surviving patients
Neurologic dysfunction Hearing loss Scars Extremity amputation and growth failure Motor disabilities Cardiovascular, renal problems
26
Prevention of meningitis
Droplet precautions until 24h after antibiyotiks Post exposure prophylaxis: (Contact in 7 days before symptoms appear or in 24 hours after antibiotics) (Ideally İn 24 hours, not after 14 days) 1. Rifampin 2.ciprofloxacin (not before 1 month) 3.ceftriaxone Alternative: azithromycin Immunization: conjugated vaccine+ MEN B MenACWY, Men B vaccines
27
Sepsis
Systemic inflammatory response syndrome (SIRS), immune dysregulation, circulation deramgment, end organ dysfunction SEPSİS: İnfection+ SIRS Severe sepsis: cardiovascular dysfunction, ARDS, or >2 organ systems dysfunctions Septic shock: sepsis+ cardiovascular dysfunction Refractory septic shock: 1.fluid refractory septic shock 2. Catecholamine resistant septic shock
28
Sepsis risk factors and treatment
Immunodef. ,Asplenia, bone marrow/ solid organ transplant, cathether, malignancy, severe intellectual disability with cerebral palsy Sources: respiratory, urinary, gi, ıntra abdominal,genital, bone, joint, cns, skin, burn, cathethers Treatment: INFANTS <28d: 1. Ampicillin ( +vancomycin) 2. 3rd gen Cephalosporin/ Meropenem 3.gentamicin( +acyclovir for HSV) CHİLDREN: 1.Cefotaxime/ ceftriaxone ( +vancomycin) 2.Gentamicin(genitourinary) 3.Anaerobic coverage (gis source) Immunsupresive children/ pseudomanas risk: Cefepim/ carbapenem
29
Hepatitis A
Self limited ilness. Fecal-oral route, contaminated water/food Comtagious Until 1 week before , 33 days after viremia İnactivated by high temp, chlorine, formalin Noncytopathic stage: viral replication, fecal shedding( HAV into bile) Cytopathic stage:portal zone infiltration, necrosis, elevated ALT, liver injury. Excessive host response causes fulminant course. Clinic nonspecific : fever malaise nausea vomiting anorexia, abd discomfort and pain,diarrhea Prodromal: elevated transaminases, hepstomegaly, bilirubin in urine, jaundice Symptomatic: jaundice, lab returns to normal 2-3 months Acute liver failure: <%1 Extrahepatic: maculopapular rash, arthralgia +vasculit,arthrit,encephalit, myelitis, bm suppression, may trigger autoimmune hepatit, rarely relapses so no relapse
30
Hep A dgx and treatment
Diagnosis: Clinical: fever, malaise,diarhea, vomiting, abdominal pain, anorexia, jaundice Elevated transaminases and bilirubin Anti HAV IgM: gold standard for acute infection( remains positive for 6 months) Anti HAV IgG: appears in healing phase and detactable for decades Prevetnion: Routine vaccination: 18m, 24m(1.5, 2 yaş) Hand hygine Pre/post exposure prophylaxis: <2 weeks: hep A vaccine, if <1y only IGIM Treatment: supportive care, self limited: full recovery in 3- 6 months Fulminant hepatic failure: liver transplant