Lobarna pneumonija
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Tetrodotoxin
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.
ECG S
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.
ECG I
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
Recommended
Tetrodotoxin
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.
ECG S
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.
ECG I
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
ECG H
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.
ECG F
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
ECG E
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.
ECG D
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.
ECG C
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.
ECG B
- 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
ECG A: AVNRT, AVRT
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.
ECG A: AV blocks
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
ECG A: first part.
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
Cardiorenal syndrome
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)
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.
Benefits and risks of additives
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.
Types of food additives
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 hypersensitivity
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.
T cell stimulation by drugs
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.
Introduction to drug hypersensitivity reactions
This document introduces drug hypersensitivity reactions involving skin. Adverse drug reactions are classified as either type A or type B reactions. Type A reactions are predictable and dose-dependent, while type B reactions are unpredictable and not related to the pharmacological actions of the drug. About 80% of reactions are type A, while type B accounts for 15-20% of reactions. Type B reactions include immune-mediated or allergic drug reactions known as hypersensitivity reactions. Hypersensitivity reactions can be drug intolerance, idiosyncratic, or allergic reactions dependent on immunological mechanisms. Allergic reactions are further classified by the Coombs and Gell system into four types mediated by different antibodies or T lymphocytes.
Drug induced liver injury part II
The document summarizes various biochemical mechanisms that can cause drug-induced liver injury (DILI), including reactions with the cytochrome P450 system and formation of reactive metabolites that damage cellular structures. It also discusses how DILI can trigger both adaptive and innate immune responses through mechanisms like the hapten hypothesis or direct stimulation of T cells. Underlying inflammation from factors like infection may exacerbate DILI by augmenting the toxic response through innate immune system activation.
Drug induced liver injury part I
This document summarizes drug-induced liver injury (DILI). It notes that DILI occurs in 1 in 10,000 to 100,000 people and can cause significant morbidity and mortality. The document outlines various risk factors for DILI, including female sex, age, nutritional status, preexisting liver disease, and concomitant drug usage. It also describes the clinical spectrum of DILI, from elevated liver enzymes to fulminant hepatic failure, and specific types of injury like acute hepatocellular, cholestatic, and mixed injury patterns.
Quasi vitamins, lipoic acid
Lipoic acid is a cofactor that plays an important role in energy metabolism by regulating the flow of carbon into the tricarboxylic acid cycle. It is able to undergo redox reactions that allow it to function as a metabolic antioxidant, reducing reactive oxygen species and free radicals. Clinical trials have shown that lipoic acid can help increase glucose clearance and reduce blood glucose and lipid peroxidation in people with type 2 diabetes. It may also be useful in treating multiple sclerosis by reducing markers of inflammation in the central nervous system. The best dietary sources of lipoic acid are organ meats and dark green leafy vegetables, where it is bound to proteins.
Quasi vitamins, p-aminobenzoic acid
p-Aminobenzoic Acid (pAA) is an essential growth factor for many bacteria species, which use it as a precursor for synthesizing folate. pAA can antagonize the bacteriostatic effects of sulfonamide drugs due to similarities in chemical structure. It has also been found to inhibit fibroblast proliferation and promote reduction of fibrous plaques causing Peyronie's disease. Because pAA metabolism is limited, it can be used as a marker to measure completeness of 24-hour urine collections, with 70-85% appearing in urine after a single oral dose.
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ECG H
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.
ECG F
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
ECG E
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.
ECG D
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.
ECG C
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.
ECG B
- 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
ECG A: AVNRT, AVRT
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.
ECG A: AV blocks
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
ECG A: first part.
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
Cardiorenal syndrome
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)
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.
Benefits and risks of additives
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.
Types of food additives
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 hypersensitivity
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.
T cell stimulation by drugs
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.
Introduction to drug hypersensitivity reactions
This document introduces drug hypersensitivity reactions involving skin. Adverse drug reactions are classified as either type A or type B reactions. Type A reactions are predictable and dose-dependent, while type B reactions are unpredictable and not related to the pharmacological actions of the drug. About 80% of reactions are type A, while type B accounts for 15-20% of reactions. Type B reactions include immune-mediated or allergic drug reactions known as hypersensitivity reactions. Hypersensitivity reactions can be drug intolerance, idiosyncratic, or allergic reactions dependent on immunological mechanisms. Allergic reactions are further classified by the Coombs and Gell system into four types mediated by different antibodies or T lymphocytes.
Drug induced liver injury part II
The document summarizes various biochemical mechanisms that can cause drug-induced liver injury (DILI), including reactions with the cytochrome P450 system and formation of reactive metabolites that damage cellular structures. It also discusses how DILI can trigger both adaptive and innate immune responses through mechanisms like the hapten hypothesis or direct stimulation of T cells. Underlying inflammation from factors like infection may exacerbate DILI by augmenting the toxic response through innate immune system activation.
Drug induced liver injury part I
This document summarizes drug-induced liver injury (DILI). It notes that DILI occurs in 1 in 10,000 to 100,000 people and can cause significant morbidity and mortality. The document outlines various risk factors for DILI, including female sex, age, nutritional status, preexisting liver disease, and concomitant drug usage. It also describes the clinical spectrum of DILI, from elevated liver enzymes to fulminant hepatic failure, and specific types of injury like acute hepatocellular, cholestatic, and mixed injury patterns.
Quasi vitamins, lipoic acid
Lipoic acid is a cofactor that plays an important role in energy metabolism by regulating the flow of carbon into the tricarboxylic acid cycle. It is able to undergo redox reactions that allow it to function as a metabolic antioxidant, reducing reactive oxygen species and free radicals. Clinical trials have shown that lipoic acid can help increase glucose clearance and reduce blood glucose and lipid peroxidation in people with type 2 diabetes. It may also be useful in treating multiple sclerosis by reducing markers of inflammation in the central nervous system. The best dietary sources of lipoic acid are organ meats and dark green leafy vegetables, where it is bound to proteins.
Quasi vitamins, p-aminobenzoic acid
p-Aminobenzoic Acid (pAA) is an essential growth factor for many bacteria species, which use it as a precursor for synthesizing folate. pAA can antagonize the bacteriostatic effects of sulfonamide drugs due to similarities in chemical structure. It has also been found to inhibit fibroblast proliferation and promote reduction of fibrous plaques causing Peyronie's disease. Because pAA metabolism is limited, it can be used as a marker to measure completeness of 24-hour urine collections, with 70-85% appearing in urine after a single oral dose.
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Categorization of risks and benefits (food additives)
Categorization of risks and benefits (food additives)
Effector phase in immune mediated drug hypersensitivity
Effector phase in immune mediated drug hypersensitivity
Lobarna pneumonija
- 2. Uvod • Klasična lobarna pneumonija je uzrokovana PNEUMOKOKOM. • Danas je sve rjeđa. • Bolest klinički počinje u starijeg predškolskog ili školskog djeteta naglom pojavom jakih općih simptoma bez prethodne kataralne respiratorne infekcije.
- 3. Klinička slika • Prvi simptomi su tresavica, visoka temperatura, povraćanje i jaka malaksalost. • Lice je zažareno. • Često postoji labijalni herpes. • Usne su ispucane. • Jezik je suh i bijelo obložen.
- 4. Klinička slika • Prisutna je jaka tahipneja s površnim disanjem koje je praćeno ritmičkim širenjem nosnica. • Česta je bol na desnoj strani toraksa zbog popratnog pleuritisa. • Kašalj je površan, suzdržan i suh.
- 5. Klinička slika • Kad pneumonija zahvati donji desni režanj, može postojati jaka bol u trbuhu (kao kod akutnog apendicitisa). • Uz lobarnu pneumoniju gornjeg režnja često postoji meningealni sindrom, ali lumbalnom punkcijom se dobije normalan nalaz.
- 6. Klinička slika • Temperatura ima tijek kontinue s kritičkim padom između 5. i 9. dana od početka bolesti. • Pri tomu se dijete obično preznoji nakon čega slijedi dosta brz oporavak.
- 7. Fizikalni nalaz • U veće se djece perkusijom čuje skraćen plućni zvuk do mukline. • Auskultacijom se čuje bronhalni šum disanja s bronhofonijom i u kasnijoj fazi bolesti se čuju krepitacije. • U krvnoj slici postoji jaka neutrofilna leukocitoza s pomakom ulijevo. • SE je jako ubrzana.
- 8. Zaključak • Tipični tijek bolesti danas se rijetko vidi. • Obično već 24 h nakon početka liječenja počinje litički pad temperature uz postupan, ali relativno brz oporavak djeteta.
- 9. Literatura: Duško Mardešić i suradnici. Pedijatrija Školska knjiga, Zagreb, 2003.