Obesity is the oldest and still the most common metabolic disorder in humans. It has been depicted in sculptures of ancient civilizations, and until the 20th century was considered an aesthetic problem or ideal of beauty in some cultures. Today, obesity is classified as one of the most common diseases of modern civilization, affecting around 15% of the global population. The causes of obesity are complex and include genetic, cultural, social, metabolic and physiological factors interacting with lifestyle habits like diet and physical activity level. Prevention is key to reducing the burden of diseases associated with obesity.
Obesity is the oldest and still the most common metabolic disorder in humans. It has been depicted in sculptures of ancient civilizations, and until the 20th century was considered an aesthetic problem or ideal of beauty in some cultures. Today, obesity is classified as one of the most common diseases of modern civilization, affecting around 15% of the global population. The causes of obesity are complex and include genetic, cultural, social, metabolic and physiological factors interacting with lifestyle habits like diet and physical activity level. Prevention is key to reducing the burden of diseases associated with obesity.
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. Uvod
• Celijakija ili glutenska enteropatija je
kronična bolest TANKOG CRIJEVA koja
nastaje zbog trajne nepodnošljivosti glutena.
• Klinički je obilježena MALAPSORPCIJOM.
• Histološki postoji totalna i suptotalna atrofija
crijevnih resica uz hiperplaziju
Lieberkühnovih kripti.
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3. Uvod
• Odstranjenje glutena iz prehrane dovodi do
potpune kliničke i histološke remisije, a
ponovno izlaganje glutenu izaziva recidiv
bolesti.
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4. Tipična klinička slika u ranoj
dječjoj dobi
• opća pothranjenost
• kronični proljev
• steatoreja
• velik distendiran trbuh
• osobita razdražljivost djeteta
• gubitak apetita (rijetko i pojačanje apetita)
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6. Etiologija i patogeneza
• Bjelančevina gluten, a posebice njezina u
alkoholu topljiva frakcija glijadin, izazivaju
nenormalnu imunosnu reakciju u sluznici
crijeva.
• Gluten nalazimo u pšeničnom brašnu, grizu,
keksima, pahuljicama, raženom i ječmenom
zrnu.
• Nema ga u zobi, kukuruzu i riži.
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7. Etiologija i patogeneza
• Posljedica imunosne reakcije je kronična
upala crijevne sluznice s tipičnim histološkim
nalazom.
• Bolest se javlja u 3-5% krvnih srodnika prvog
reda, a u 10% njih postoje asimptomatske
mikroskopske promjene na sluznici crijeva.
• HLA-DQ2 (80%), HLA-DQ8 (20%)
• HLA-B8, HLA-DR3, HLA-DR7
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8. Etiologija i patogeneza
Dojenje smanjuje rizik od pojave
bolesti.
Infekcija adenovirusom tip 12
može povećati rizik za pojavu
celijakije.
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9. Klinička slika
• Razvoj bolesti je postupan.
• Simptomi su u početku nespecifični.
• Stolice postaju učestalije, mekše i
vodenastije.
• Proljevi se javljaju intermitentno.
• Anoreksija postaje sve izraženija.
• Dijete zaostaje ili čak gubi na težini.
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10. Klinička slika
• Katkad bolest počinje kao akutni infektivni
proljev poslije kojeg se stolice ne popravljaju,
a opće stanje djeteta nazaduje.
• Kronični proljev je glavni simptom.
• U fazi potpuno razvijene kliničke slike stolice
su učestale, obilne, pjenušave, masne i jako
smrdljive.
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11. Klinička slika
• U dojenčadi, koja se hrani s puno mlijeka,
stolice mogu biti dosta guste, tvrde, velike,
blijedosive.
• Zaudaraju na užeglu mast od kalcijevih
sapuna koji nastaju iz kalcija i neresorbiranih
masnih kiselina.
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12. Klinička slika
• Pothranjenost i opća tjelesna slabost su više
ili manje uvijek izražene.
• Stalno se pogoršavaju zbog velikog gubitka
energije obilnim stolicama.
• Distenzija trbuha je vrlo uočljiv nalaz.
• Zbog prekomjerne fermentacije u crijevu i
hipotonije muskulature, crijeva su
meteoristična.
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13. Klinička slika
• Stijenka trbuha je hipotonična i hipotrofična.
• Trbuh je velik i mlohav.
• Psihičke su promjene česte.
• Bolesno dijete postaje sve razdražljivije i
negativističnije.
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14. Latentna glutenska enteropatija
• To su djeca koja su imala normalnu
histološku sliku crijevne sluznice uz hranu s
glutenom.
• Nakon određenog vremena, pri ponovnoj
biopsiji, se nađe atrofija resica koja se
popravlja na bezglutensku prehranu.
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15. Preosjetljivost na gluten s blagom
enteropatijom
• Histološka slika sluznice pri prvoj biopsiji je
normalna.
• Uz bezglutensku dijetu nestanu klinički
simptomi i protutijela.
• Katkad ponovljena biopsija ipak pokaže
atrofiju resica.
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18. Histološki nalaz
• U sluznici jejunuma crijevne su resice
deformirane, zdepaste, skraćene ili potpuno
nestale.
• Lieberkühnove kripte su dublje nego
normalno.
• Lamina propria je infiltrirana limfocitima,
plazma-stanicama i eozinofilima.
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19. Histološki nalaz
• Epitelne su stanice vakuolizirane, a među
njima se u povećanom broju nalaze
pojedinačni limfociti (karakterističan nalaz).
• Aktivnost crijevnih epitelnih enzima četkaste
prevlake (laktaza, enterokinaza) je smanjena.
• Imunoflourescentnom pretragom se nađe
povećan broj stanica koje sadržavaju IgA i
IgM.
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20. Histološki nalaz
Opisane promjene se mogu još
naći i kod:
• crijevne lablijaze
• preosjetljivosti na kravlje
mlijeko
• teške pothranjenosti
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21. Dijagnoza
• tipični PH nalaz sluznice jejunuma u vrijeme dok
je dijete na glutenskoj prehrani
• kliničko poboljšanje (za nekoliko dana ili tjedana)
i nalaz normalne (ili samo malo abnormalne)
crijevne sluznice (tek za nekoliko mjeseci ili
godinu-dvije) nakon isključenja glutena iz
prehrane
• klinički ili samo histološki relaps bolesti 6 mjeseci
nakon ponovnog uvođenja glutena u prehranu
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22. Dijagnoza
• endomizijska protutijela klase IgA u serumu
bolesnika poslije 2. godine života
• antitijela na tkivnu transglutaminazu (IgA)
Uz bezglutensku dijetu treba nakon 6-12
mjeseci očekivati normalizaciju seroloških
testova.
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24. Celijakična kriza
• To je najteža akutna komplikacija.
• Obično bude izazvana crijevnom infekcijom u
djeteta s nedosljedno provođenom dijetom.
• Javlja se u djece s celijakijom do 2. g. života.
• Očituje se akutnim i iznenadnim pogoršanjem
bolesti.
• Obilno i žestoko povraćanje, te drastični proljevi
vrlo brzo izazivaju dehidraciju, acidozu i kolaps.
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25. Diferencijalna dijagnoza
Celijakija
• tipičan početak u dobi između 6 i 12
mjeseci
• tipična klinička slika
• lab. znakovi malapsorpcije
• test opterećenja ksilozom je
pozitivan
• tipične histološke promjene u
mukozi jejunuma
• pozitivna endomizijska IgA-
protutijela i anti-TTG u serumu
• poboljšanje bolesti uz dijetu bez
glutena, pad titra protutijela
Cistična fibroza
• raniji početak bolesti
• izraziti simptomi kronične
bolesti pluća
• teška pothranjenost
• jaki hipoproteinemički edemi
• povećana konc. klorida u znoju
• značajno smanjena aktivnost
enzima u duodenalnom soku
(zamućen, grudičast ili
gelatinozan duodenalni sok)
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26. Diferencijalna dijagnoza
Lamblijaza
vegetativni oblici
intestinalne
lamblije u svježem
duodenalnom soku
(ključan nalaz)
Nepodnošljivost disaharida
• vodenaste stolice, kisele s
niskim pH i pozitivnim testom na
reduktivne supstancije
• pozitivan oralni test opterećenja
disaharidom
• pozitivan test izdaha vodika
• smanjena aktivnost disaharidaze
u bioptatu mukoze jejunuma
• brzo poboljšanje dijetnom
prehranom bez određenog
disaharida
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27. Diferencijalna dijagnoza
Alergijska nepodnošljivost
proteina kravljeg mlijeka
• anamneza prehrane
• pozitivni alergijski
testovi na goveđi
laktoglobulin
• brzo poboljšanje
bolesti dijetnom
prehranom bez kravljeg
mlijeka
Sindrom iritabilnog kolona
• školsko dijete ili
adolescent
• naizmjence opstipacija i
proljev
• katkad sluzave stolice
• boli u trbuhu
• emocionalna labilnost
• opće stanje, rast i razvoj
nisu poremećeni
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28. Liječenje
doživotno dijetno liječenje hranom bez
glutena
isključenje svih proizvoda od pšenice,
raži i ječma
dozvoljeni su riža, kukuruz i po nekim
autorima zob
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29. Liječenje
• Treba dodavati vitamine, osobito vitamin D,
najbolje u obliku vodene suspenzije.
• Preparati Fe su potrebni (svaki dan) sve dok
se ne izliječi sideropenična anemija.
• Vitamin K se daje samo u slučajevima
krvarenja ili kada je smanjena aktivnost
protrombina.
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30. Liječenje
• Kratkotrajna peroralna primjena KS je
indicirana u bolesnika kod kojih je proljev
uporan i ne reagira na dijetnu terapiju.
• Celijakičnu krizu je potrebno liječiti u bolnici
zbog postojanja dehidracije, acidoze,
hipokalemije, hipokalcemije i/ili šoka.
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31. Liječenje
• U tvrdokornim slučajevima potrebno je dijete
hospitalizirati i pribjeći potpunoj
parenteralnoj prehrani u tijeku više dana ili
tjedana dok se opće stanje djeteta ne popravi
i sluznica jejunuma djelomično ne oporavi.
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