"Mali geografi" iz OŠ Dragutina Domjanića su cijelo polugodište (2011.) proučavali litosferne ploče i vulkane i izradili prezentaciju pod vodstvom učiteljice Marije Ujlaki.
"Mali geografi" iz OŠ Dragutina Domjanića su cijelo polugodište (2011.) proučavali litosferne ploče i vulkane i izradili prezentaciju pod vodstvom učiteljice Marije Ujlaki.
Tetrodotoxin is a potent neurotoxin found in marine animals like pufferfish. It blocks sodium channels, preventing action potentials and paralyzing neurons and muscles. Poisoning symptoms range from numbness to respiratory failure and death. The toxin is produced by various bacteria in marine life. While rare, poisoning is more common where pufferfish is regularly consumed. There is no antidote, so treatment focuses on supportive care and monitoring until the toxin is cleared from the body.
1) The Sgarbossa criteria provide guidelines for diagnosing acute myocardial infarction in patients with left bundle branch block (LBB) or ventricular paced rhythm on electrocardiogram (ECG), as these conditions can obscure ECG changes.
2) The original Sgarbossa criteria included three criteria involving concordant or discordant ST segment changes greater than 1mm. The modified criteria expanded this to include proportionally excessive discordant ST elevation.
3) Different types of STEMI are described based on the location of maximal ST elevation, including anterior, inferior, lateral, posterior, and right ventricular STEMI, each with characteristic ECG patterns.
This document discusses interventricular conduction delay and raised intracranial pressure as seen on electrocardiograms (ECGs). It defines interventricular conduction delay and lists various causes including fascicular blocks, bundle branch blocks, ventricular hypertrophy, dilatation, electrolyte abnormalities, toxins, pre-excitation, and arrhythmogenic cardiac conditions. It then discusses raised intracranial pressure and the associated ECG findings of widespread T-wave inversions, QT prolongation, and bradycardia as part of the Cushing reflex, indicating imminent brainstem herniation. Massive intracranial hemorrhages such as subarachnoid hemorrhage are the most common causes
The document discusses various electrolyte abnormalities and their ECG manifestations, including hypercalcemia, hypocalcemia, hyperkalemia, hypokalemia, hypomagnesia, hyperthyroidism, hypothyroidism, and hypothermia. For each condition, it provides the normal and abnormal ranges for the electrolyte levels and describes the associated ECG changes such as peaked T waves, QT prolongation, low QRS voltage, bradycardia, and arrhythmias. The document serves as a reference for clinicians to recognize ECG patterns caused by electrolyte and endocrine abnormalities.
1) Fascicular ventricular tachycardia is the most common form of idiopathic ventricular tachycardia originating from the left ventricle. It typically presents in young patients without structural heart disease.
2) It has characteristic ECG features including a monomorphic ventricular rhythm with fusion complexes and AV dissociation. The QRS duration is between 100-140 ms with a short RS interval of 60-80 ms. It also shows a right bundle branch block pattern and axis deviation.
3) Posterior fascicular ventricular tachycardia, which arises near the left posterior fascicle, shows a right bundle branch block pattern with left axis deviation. Anterior fascicular ventricular tachycardia arises
The document discusses several electrocardiogram (ECG) findings and rhythms including ectopic atrial tachycardia, atrial tachycardia, electrical alternans seen in massive pericardial effusion which produces low QRS voltage, electrical alternans and tachycardia, escape rhythms like junctional escape rhythms where the pacemaker rate decreases down the conducting system, and ventricular escape rhythms. It also discusses the terminology of junctional rhythms and includes literature references.
The document discusses De Winter's T waves, which are characterized by three key findings on ECG: upsloping ST depression in precordial leads, tall symmetric T waves in precordial leads, and ST elevation in aVR. It also summarizes the ECG patterns seen in dextrocardia, including right axis deviation, positive complexes in aVR, and dominant S waves in precordial leads. Finally, it outlines the ECG features of digoxin effect and toxicity, such as biphasic T waves, shortened QT, and the dysrhythmia of supraventricular tachycardia with a slow ventricular response seen in digoxin toxicity.
Massive carbamazepine overdose of more than 50 mg/kg can cause cardiotoxicity due to sodium channel blockade, which may be detectable on ECG as subtle QRS widening or first-degree AV block. Dilated cardiomyopathy is characterized by ventricular dilatation and reduced ejection fraction below 40%, commonly presenting with symptoms of biventricular failure. Chronic obstructive pulmonary disease can cause prominent P waves in inferior leads, exaggerated ST segments, low QRS voltage especially in V4-V6, and may show an SV1-SV2-SV3 pattern.
- Benign early repolarization shows concave ST elevation less than 2 mm with no progression over time, most prominent in V2-V5. Notching at the J-point and concordant T-waves are also seen.
- Beta-blocker and calcium channel blocker toxicity can cause prolonged PR interval and bradycardia. Propranolol toxicity specifically causes QRS widening and positive R' wave in aVR. Sotalol toxicity causes QT prolongation and risk of Torsades de Pointes.
- Bifascicular block is a combination of right bundle branch block with either left anterior or posterior fascicular block, and can be caused by ischemia, hypertension or other
This document discusses atrioventricular nodal reentrant tachycardia (AVNRT). It states that AVNRT is the most common cause of palpitations in structurally normal hearts. It can occur spontaneously or be provoked. There are three main types - slow-fast AVNRT which is most common and shows no visible P waves, fast-slow AVNRT where P waves are visible after the QRS, and slow-slow AVNRT where P waves appear before the QRS. The tachycardia rate is typically between 140-280 beats per minute and is regular. AVNRT occurs due to a reentry circuit within the atrioventricular node.
This document summarizes different types of atrioventricular (AV) blocks seen on electrocardiograms (ECGs). It describes first-degree AV block as a PR interval over 200ms. Second-degree AV block, Mobitz type I (Wenckebach phenomenon) shows progressive PR prolongation until a blocked pulse. Mobitz type II shows intermittent non-conducted pulses without PR prolongation. High-grade second-degree AV block has a P:QRS ratio of 3:1 or higher, with an extremely slow ventricular rate. Third-degree or complete heart block shows no relationship between atrial and ventricular rates. Causes include myocardial infarction, drugs, and conduction system disease. Treatment ranges from
This document provides an overview of several cardiac arrhythmias and conditions including:
1. Accelerated idioventricular rhythm (AIVR), which results when an ectopic ventricular pacemaker exceeds the sinus node rate. AIVR is seen post-myocardial infarction and features a regular rhythm between 50-110 bpm with three or more QRS complexes.
2. Atrial flutter, a supraventricular tachycardia caused by a reentry circuit in the right atrium with a rate of around 300 bpm. The ventricular rate is determined by AV conduction.
3. Atrial fibrillation, the most common sustained arrhythmia characterized by irregularly irregular rhythm without
1) Cardiorenal syndrome commonly occurs in patients with acute decompensated heart failure and is associated with poor outcomes. It involves a complex interaction between hemodynamic alterations and activation of neurohormonal systems that affects both the heart and kidneys.
2) There are five types of cardiorenal syndrome classified based on the inciting cardiac or renal event and the affected secondary organs. Type 1 is acute cardiorenal syndrome due to acute worsening of cardiac function leading to kidney injury.
3) Loop diuretics are the mainstay of treatment for congestion in heart failure but aggressive diuresis may worsen kidney function. Other therapies discussed include inotropic agents, vasopressin antagonists
Categorization of risks and benefits (food additives)Domina Petric
The document discusses various categories of risks associated with food, including foodborne hazards of microbial origin, nutritional hazards, environmental contaminants, naturally occurring toxicants, and food additives. It notes that foodborne diseases of microbial origin pose the greatest risks. Nutritional hazards can arise from deficiencies or excesses. Environmental contaminants can enter the food supply from industrial or natural sources. Naturally occurring toxicants are found in some foods. Food additives present minimal risks when consumed within permitted levels. The document also outlines categories of potential benefits from foods, including health benefits, supply benefits, hedonic benefits, and convenience benefits.
This document discusses the benefits and risks of food additives. The benefits include making foods safer, more nutritious, and longer lasting through the use of preservatives and antioxidants. Additives also provide greater variety of foods and lower prices. However, there are also risks. There is a lack of data on the long term health effects of combinations of additives. Some additives are associated with "junk foods" that are low in nutrients. While direct toxic effects are unlikely at legal levels, some individuals may have hypersensitivity reactions. Some animal studies also indicate potential cancer and reproductive issues, but no direct evidence in humans. The risks must be weighed against the benefits on a case by case basis.
The document discusses different types of food additives and how they are classified. It describes preservatives like antimicrobials, antioxidants and antibrowning agents. Nutritional additives add vitamins, minerals and fiber. Coloring agents and flavors are used to enhance appearance and taste. Texturizing agents modify texture and mouthfeel. Additives are identified by International Numbering System codes or E numbers from the European Union.
Effector phase in immune mediated drug hypersensitivityDomina Petric
This document discusses antibody-mediated and T cell-mediated drug hypersensitivity. It describes how drugs can act as haptens and stimulate T and B cell responses, leading to IgE production and immediate hypersensitivity reactions. It also discusses the p-i concept where drugs can directly interact with T cell receptors and cause reactions without prior sensitization, particularly in the skin which contains many resident immune cells.
1. Small molecule drugs can become immunogenic by undergoing bioactivation into chemically reactive metabolites that covalently bind to proteins, forming hapten-carrier complexes.
2. These complexes are then processed and presented by antigen presenting cells to T cells, stimulating an adaptive immune response.
3. Whether a humoral or cellular immune response develops depends on which proteins are modified by the hapten and whether they are soluble or cell-bound.
2. Definicija
• AR-nasljedna multisistemna bolest koja
zahvaća brojne epitelne organe, a
osobito egzokrine žlijezde.
• Klinički su najvažnije pojave u sluznici
bronha i plućima, u pankreasu, žučnim
vodovima, crijevu, žlijezdama
slinovnicama, žlijezdama znojnicama i
sjemenovodima.
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4. Epidemiologija
• U sjevernoj i zapadnoj Europi incidencija
iznosi 1:2000 do 1:3000.
• Svaka 20.-25. osoba je heterozigotna.
• Incidencija u crnoj rasi je oko 1:20 000, a u
pripadnika žute rase oko 1:100 000.
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5. Etiologija
• CFTR-gen na 7q31.2.
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70% bolesnika u sjevernoj
i zapadnoj Europi.
Ova mutacija uzrokuje
nedostatak molekule
fenilalanina na 508. mjestu
peptidnog lanca.
6. Genski produkt
• CF-transmembranski regulator
(CFTR-cystic fibrosis transmembrane
regulator) je protein koji obavlja
funkciju kloridnog kanala
reguliranog cAMP-om.
• Nadzire protok klorida kroz staničnu
membranu.
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7. Patofiziologija
• Osnovni je poremećaj nemogućnost
zadržavanja dovoljnih količina kloridnih iona
u lumenu bronha uz povećanu resorpciju
Na-iona i vode iz lumena kroz stanice.
• Posljedica je dehidracija sekreta.
• Sekret na respiracijskoj sluznici je zgusnut i
žilav te se teško odstranjuje uobičajenim
fiziološkim mukocilijarnim mehanizmima.
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9. Patofiziologija
Poremećaj prometa elektrolita je praćen
povećanjem elektronegativnog
potencijala respiracijske sluznice
bolesnika.
Taj se potencijal može izravno mjeriti
uživo na nosnoj sluznici (dijagnostika,
procjena učinka eksperimentalnih
lijekova).
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10. Patofiziologija
U izvodnim kanalićima pankreasa, u žučnim
vodovima i djelomično u sjemenovodu pregust
sekret izaziva:
• opstrukciju
• proksimalno cistično proširenje izvodnih
kanalića
• reaktivnu upalu
• fibrozu tih organa
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11. Patofiziologija
Zatajenje funkcije žlijezda znojnica se
očituje povećanom konc. soli u znoju za
razliku od smanjene konc. soli u
respiracijskom sekretu.
Povećana konc. klorida u znoju je glavni
laboratorijski kriterij za dijagnozu
cistične fibroze.
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13. Kronična plućna bolest
• Očituje se u gotovo svih bolesnika sa CF.
• Određuje prognozu bolesti.
• Početak bolesti je vrlo varijabilan.
• Prvi klinički simptom je suh, naporan kašalj,
osobito noću.
• Kasnije su sve očitiji znakovi kronične
bronhoopstrukcije sa slikom kroničnog
bronhitisa i trajnom hiperinflacijom pluća.
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14. Kronična plućna bolest
• Fizikalni nalaz-hiperinflacija i difuzno
oslabljen šum disanja uz poneki diseminirani
hropčić ili krepitaciju.
• U egzacerbacijama bolesti u dojenčadi se
pojavi klinička slika BRONHIOLITISA s
opstruktivnom dispnejom i sipnjom.
• Progresijom bolesti razvije se peribronhalna
fibroza, atelektaze i bronhiektazije uz obilje
žilavog gnojnog sekreta.
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15. Kronična plućna bolest
• Konačna faza bolesti se očituje kao kronična
insuficijencija pluća i cor pulmonale.
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Početak plućne
bolesti
virusi,
pneumokoki,
klebsijela
Poodmakla bolest stafilokok
Kasnije faze bolesti pseudomonas,
katkad seracija,
anaerobi, kandida
ili aspergilus
17. Egzacerbacije plućne bolesti novim sojem
uzročnika ili ranijim uzročnikom
• pojavljuju se periodički sa subakutnom
slikom
• pojačan kašalj
• promjena boje i konzistencije iskašljaja
• smanjeni apetit
• gubitak težine i malaksalost
• nema porasta temperature ni novih
infiltracija vidljvih na RTG-pluća
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18. Alergijska bronhopulmonalna
aspergiloza
• u starije djece i odraslih
• sipnja, migrirajući plućni infiltrati
• povišeni IgE u serumu, pozitivan RAST na
aspergilus
• pojava pozitivne kožne reakcije na aspergilus
• SLIKA BRONHALNE ASTME SA SPECIFIČNIM
GLJIVIČNIM ALERGENOM
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20. Kronična insuficijencija pankreasa
• Očituje se u gotovo 85% bolesnika od prvih
dana bolesti (mekonijski ileus).
Zbog nedostatka pankreasnih i crijevnih enzima
postoji MALDIGESTIJA sa sekundarnom
MALAPSORPCIJOM:
• steatoreja
• povećan gubitak dušičnih spojeva stolicom-
obilne, kašaste, masne ili rijetke smrdljive
stolice
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21. Kronična insuficijencija pankreasa
U neliječenih bolesnika postoje znakovi
sekundarnog nedostatka liposolubilnih
vitamina:
• slabije napredovanje djeteta
• izrazita pothranjenost s
hipoproteinemičnim edemima, osobito
u dojenčadi
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22. Kronična insuficijencija pankreasa
Katkad se poslije
dojenačke dobi pojave
epizode DISTALNE
INTESTINALNE
OPSTRUKCIJE zbog žilave
sluzi i maldigestije.
U prve 2-3 g.
života je čest
PROLAPS
REKTUMA.
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23. Kronična insuficijencija pankreasa
• Endokrina funkcija Langerhansovih
pankreasnih otočića je očuvana do u
kasnu adolescentnu ili odraslu dob,
unatoč opsežnoj fibrozi pankreasa.
• Tek se tada u nekih bolesnika
pojavljuje RELATIVNI NEDOSTATAK
INZULINA S HIPERGLIKEMIJOM.
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24. Bilijarni trakt
• Katkad se bilijarna opstrukcija očituje već u
novorođenačkoj dobi kao KOLESTATSKA
ŽUTICA PRODULJENOG TRAJANJA.
• Može biti tako jaka da klinički podsijeća na
bilijarnu atreziju.
• U starije djece se može razviti kronična bolest
jetre zbog BILIJARNE CIROZE s portalnom
hipertenzijom i varikozitetima jednjaka.
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25. Gubitak Na i klorida znojenjem
• Za vrijeme ljetnih vrućina, osobito u
febrilnog djeteta, može uzrokovati
TEŠKU HIPONATREMIJSKU DEHIDRACIJU
PRAĆENU HIPOKLOREMIČNOM
METABOLIČKOM ALKALOZOM.
•Rijetko to može biti i prvi znak
cistične fibroze.
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26. Tjelesni razvoj
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Ovisi u velikoj mjeri o
nadomjesnom davanju
pankreasnih hormona.
Pubertet je obično odgođen u
prosjeku oko 2 g.
27. Azoospermija i sterilitet
Više od 95% muškaraca sa CF.
Uzrok tome je nerazvijenost sjemenovoda.
Spolne funkcije su normalne.
Postoje muškarci kojima je azoospermija i sterilitet
jedina klinička pojava CF (blage mutacije).
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28. Žene
• Žene sa CF imaju smanjenu fertilnost.
• One s blažim oblikom plućne bolesti
mogu iznijeti trudnoću do kraja.
• U žena s težim oblikom plućne bolesti
može doći do nepopravljivog pogoršanja
plućne funkcije za vrijeme trudnoće, s
letalnim ishodom.
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29. Analiza znoja
Iontoforeza pilokarpin-nitrata:
• pilokarpin potiče lokalnu sekreciju
znoja
• znoj se skupi pomoću filtrirnog papira
ili kapilarnih cjevčica
• dobiveni znoj se analizira na kloride ili
se mjeri električna vodljivost
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30. Analiza znoja
40 mmol/L klorida je normalno.
40-60 mmol/L je granična
vrijednost.
60 mmol/L i više je CF.
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31. Analiza znoja
• U prva 3 mjeseca života konc. klorida iznad
40 mmol/L je već indikativna za CF.
Rijetka stanja s povišenom konc. klorida u
znoju su:
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neliječena adrenalna
insuficijencija
DI (diabetes insipidus)
ektodermalna displazija
32. Kriteriji za dijagnozu cistične
fibroze
jedna ili više karakterističnih fenotipskih pojava za CF ili
CF u brata ili sestre ili
pozitivni novorođenački screening-test
UZ
povećanu konc. klorida u znoju dobivenog iontoforezom
pilokarpina u 2 ili više mjerenja ili
identifikacija dviju mutacija CFTR-gena ili
utvrđivanje abnormalnog električnog potencijala nosne
sluznice što dokazuje poremećaj u transportu iona kroz epitel
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33. Test probira u novorođenčadi
Procjena
aktivnosti
tripsinogena
u krvi.
Pojačana je u
bolesnika sa CF zbog
bijega pankreasnih
enzima iz oštećenog
pankreasa u krv.
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35. Liječenje CF
• fizikalna terapija (perkusija pojedinih
segmenata toraksa, primjena vibratora u
određenim drenažnim položajima prsnog koša)
• inhalacija (0,45% ili 0,9% NaCl)-dovođenje
aerosola u lumen bronha radi razrjeđivanja
bronhalnog sekreta
• inhalacija sintetskog pripravka ljudske DNA-aze
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36. Liječenje CF
• inhalacija AB (gentamicin, tobramicin,
karbenicilin, tikarcilin) radi suzbijanja blaže
egzacerbacije
• AB lijekovi kod kuće, inhalacijom ili
peroralno, po potrebi parenteralno u bolnici,
obično ne kraće od 2 tjedna u maksimalnim
dozama, tj. dok se kliničko stanje i
mikrobiološki nalazi ne poboljšaju
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37. Liječenje CF
• β-agonisti, kromoglikat ili ipratropium su
indicirani u djece koja su razvila sindrom
reverzibilne bronhoopstrukcije, odn. pravu
bronhalnu astmu ili bronhopulmonalnu
aspergilozu
• ibuprofen tijekom 4-godišnje primjene
usporava propadanje pluća
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38. Liječenje CF
• nadomještanje pankreasnih enzima
(održavanje optimalne uhranjenosti,
sprječavanje sindroma distalne opstrukcije
crijeva)
• 1-3 kapsule dražiranih mikrokuglica
osjetljivih na crijevni pH uz svaki obrok, za
dojenčad pripravci u prahu
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39. Liječenje CF
• Dojenčad bolje probavlja pripravke mlijeka s
pretprobavljenim proteinima i sa
srednjolančanim trigliceridima.
• Kod parcijalne distalne opstrukcije crijeva
treba povećati unos tekućine, dodati
omekšivače stolice, nakratko i parafinsko ulje,
uz primjenu klizme izotonične otopine soli.
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40. Liječenje CF
• Kod totalne distalne opstrukcije crijeva daje
se visoka klizma gastrografina uz dovoljan
parenteralni unos tekućine.
• Rijetko je potrebna kirurška intervencija.
• Veći gubitak soli znojenjem se nadoknađuje
većim dodatkom soli u hrani (1-6 g) ovisno o
dobi bolesnika i stanju (ljetne vrućine,
febrilna stanja, veći fizički napori).
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