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Anästhesie (Subject) / Krankheitsbilder (Lesson)

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• Epiglottitis Bakterium: H. influenzae Typ B Alter: 2-5 Jahre Symptome: Fieber, Dyspnoe, Stridor. KEIN Husten im Ggs zu Tracheobronchitis (Croup) Therapie: Beruhigung. Epinephrin vernebelt. Atemwegssicherung am besten in der Klinik unter Tracheotomiebereitschaft. Tubus eine Nr kleiner. (Penicillin), Cefotaxim, Chloramphenicol i.v.    
• Aldosteron: Steuerung Sekretionsreiz: Hyperkaliämie, Hyponatriämie, Volumenmangel, Hypotonie Stimulation durch ACTH, beta-Stimulation Hemmung durch ANP, Dopamin  
• Schlafapnoe Assoziation mit Art HT, DM, Reflux, schwieriger Intubation
• Phäochromozytom siehe essential clinical anaesthesia 669 90% in Nebenniere, 10% bilateral Symptome: Schwitzen, Herzklopfen, Kopfschmerzen, Synkope Urin: Vanillinmandelsäure, Metanephrin. Heute: freies Metanephrin Plasmalevel, ggf. Clonidinsupressionstest Ziel periop.: Normovolämie, Normotonie, normoglykämie Medis: Caciumkanal-Blocker, Alpha1-Blockade vor Betablockade (Phenoxybenzamin), Mg (antiadrenerg, direkt vasodilatierend), Nitroprussid
• Gastrektomie Spätkomplikationen perniziöse Anämie (Vit b12 Mangel wegen fehlendem intrinsic factor) Frühdumping: Reservoir Magen fehlt--> Kohlenhydrate im Dünndarm entziehen Wasser + Parasympatishe Aktivität --> Volumenmangelschock Spätdumping: 2 h nach Essen: überschiessende Insulinsekretion --> Herzrasen, Hypoglykämie  
• Sichelzellanämie HbS. Präzipiert in desoxygeniertem Zustand -> Sichelform der Erys -> Verstopfung der Mikrozirkulation. Hämolyse Komplikation: Autosplenektomie Diagnostik: Hämoglobinelektrophorese Erbgang: autosomal kodominant/ rezessiv
• Glucose-6-Phosphatdehydrogenasemangel (Flavismus) x chromosomal rezessiv Auslöser: ASS, Metamizol, Sulfonamide, Vit K, Malariamittel u.v.m.                           Infekte, Stress, metabolische Azidose Cave: Hämoglobinurie mit Nierenversagen    
• Post punctional Headache: blood patch Relief of headache may occur immediately or within 24 hours.  Epidural blood patch performed around 48 hours postpartum has a 60-90% cure rate at first attempt.   Geb's Handbuch S34
• Long-QT-Syndrom > Torsade de Pointes a) genetisch: Kalium- oder Natriumkanal-Veränderungen b) medikamenten induziert Tricyclic antidepressants (Imipramine) Major tranquilisers Amiodarone Antihistamines Erythromycin  Ciprofloxacin Ferner assoziiert mit: Hypokalaemia Hypocalcaemia Hypothermia Th: Prävention von Arrhythmien: Betablockade. Zur Sicherheit implantierter Defibrillator  
• Post partale Blutung Ergometrin: Cave: System. Vasokonstriktion. KI: Präeklampsie! Carboprost (Prostaglandin): Cave: Bronchospasmus, bes. bei Asthmatikern
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• Renal tubuläre Azidose   Renal-tubuläre Azidose Typ I (distal-tubuläre Sekretionsstörung für Protonen). Als Kompensation werden mit Kalium und Natrium Kationen ausgeschieden. Renal-tubuläre Azidose Typ II (proximal-tubuläre Rückresorptionsstörung für Bicarbonat aufgrund von Carboanhydratasemangel). Von klinischer Relevanz sind der Natrium- und Kaliumverlust, die Volumendepletion und die Aktivierung des Renin-Angiotensin-Aldosteron-Systems (RAAS). Renal-tubuläre Azidose Typ IV (hyperkaliämische Azidose). verminderte Rückresorption von Natrium im Bereich des distalen Tubulus, bei der H+-Ionen und Kalium tubulär nur unzureichend sezerniert werden Typ I und II: Hypocalziämie!    
• Trigeminus Neuralgie u.a. Kopfschmerzen Trigeminal neuralgia is neuropathic pain in the distribution of the trigeminal nerve. Episodes of paroxysmal shooting or sharp natured pain occur typically provoked by stimuli such as light touch, eating, washing, talking or air currents on the face. Patients may describe 'electric shock-like pain'. Pain is more common in the maxillary (V2) and mandibular (V3) divisions of the trigeminal nerve than the ophthalmic division (V1). It is more frequently seen in patients over 50-years-old and in those with multiple sclerosis but can occur in young adults. It is typically unilateral, although may be bilateral in multiple sclerosis. The cause is not always known. Many patients are found to have an aberrant vascular loop compressing the nerve on MRI scan. Other potential causes include micro-vascular aneurysms, tumours, arachnoid cysts in the cerebellopontine angle or secondary to traumatic events such as car accidents. There are no specific investigations to diagnose trigeminal neuralgia. However, clinical assessment of cranial nerve function should be carried out due to the association with multiple sclerosis and also brain tumours. Any abnormalities should prompt cerebral imaging. There is an argument for cerebral imaging in all patients as MRI can be used to detect vascular compression of the trigeminal nerve near the pons. If this is the case micro-vascular decompression of the aberrant vessel provides immediate pain relief in approximately 75% of patients. Cluster headaches are classically felt as a deep dull aching pain in the retrobulbar, cheek and chin area lasting several hours. Giant cell arteritis is commonly felt as a continuous pain the forehead, temple and neck area and may be associated with jaw claudication. Atypical facial pain may occur in any area and be of various characteristics. Post-herpetic neuralgia is the persistence of pain in the affected dermatomes, after the resolution of an acute herpes zoster infection (shingles). The diagnosis is usually made if pain persists or arises at least three months after the skin lesions are healed. The commonest areas affected are in the thoracic dermatomes and the ophthalmic division of the trigeminal nerve.
• Kryoglobulinämische Vaskulitis Kryoglobuline sind in der Kälte präzipitierende lmmunglobulinkomplexe (reversibel, < 10 °C), meist lgM-IgG-Komplexe (wobei monoklonales lgM als Autoantikörper mit polyklonalem lgG reagiert) 3 Typen: Typ 1: Monoklonales Kryoglobulin, meist lgM (z.B. MM, M. Waldenström u.a.) Typ lI: Mono-und polyklonale Immunglobuline are seen in bacteriral endocarditis, hepatitis C, hepatitis B, Epstein-Barr, and cytomegalovirus Typ III: Polyklonale Immunglobuline (z.B. bei rheumatischen Erkrankungen) are seen in spirochaetal disease, coccidiomycosis, malaria, systemic lupus erythematosus, rheumatoid, Sjogren's, scleroderma and mixed essential cryoglobulinaemia. At.: 1. Essenzielle Kryoglobulinämie 2. Sekundäre Kryoglobulinämie: HCV-Infektion, HBV-Infektion, maligne Lymphome, Kollagenose, Plasmozytom, M. Waldenström u.a. KL.: arterielle Thromben, Akral betonte, palpable Purpura, Arthralgien, membranöse Glomerulanephritis mit Hämaturie, Proteinurie (50%), Neuropathie, Hypokomplementärämie    CAVE: Cold agglutinins cause red cell agglutination at 4°C and may be seen in mycoplasma pneumonia.
• Child-Pugh classification Within the Child-Pugh classification the following five elements are assessed or measured in order: Ascites Grade of encephalopathy Serum bilirubin (μmol/L) Serum albumin  (g/L) Prothrombin time or INR.
• Porphyrie Pathogenese: excess production and excretion of porphyrins and their precursors Ursache: Enzymdefekt im Hämstoffwechsel Auslöser: Stress, infection, pregnancy, menstruation, starvation and certain drugs may precipitate acute attacks. auslösende Medis: Barbiturates (thiopental and methohexital) Steroids Alcohol Clonidine Amiodarone Progestogens Sulphonamides (Cotrimoxazol) Phenytoin Etomidate Ketamin Safe Opiates Gentamicin and penicillins Chlorpromazine. Chloral hydrate  Aspirin, Paracetamol siehe auch Tab Rep. heck 628  
• autonomic neuropathy Features of an autonomic neuropathy include: Postural hypotension Cardiac conduction defects Bladder dysfunction Gastrointestinal disturbances including delayed gastric emptying pupils constrict or dilate slowly in response to changes in light intensity reduced response to hypoglycaemia Postural (also known as orthostatic) hypotension is an abnormal decrease in blood pressure-of at least 20 mm Hg systolic and 10 mm Hg diastolic-within three minutes of standing upright.
• COPD Patients with mild COPD (60 - 79% of the predicted FEV1) are often unknown to their GP. Those with moderate COPD (40 - 59% predicted) are seen intermittently seen by the GP, whilst those with severe disease (< 40% predicted) have frequent hospital and GP visits. Asthma (not emphysema) is associated with an increased (or normal) transfer factor,whereas COPD is associated with a decreased transfer factor. Transfer Factor: Korrektur des Immunsystems in überreaktiven Zuständen ( Autoimmunkrankheiten, Allergien)  Immunologische Wirkungsweise des Transfer Factors  Stimulierende Wirkung auf  lymphopoetische Stammzellen Stimulierende Wirkung auf  Monozyten und Granulozyten, Stimulation der Phagozytoseaktivität Stimulierende Wirkung auf CD4-Zellen und CD8-Zellen. Gleichgewichtsregulation der TH1-Zellen und TH2-Zellen Aktivierung der NK-Zellen  
• Laktatazidose characterised by an elevated arterial blood lactate level and an increased anion gap ([Na + K] - [Cl + HCO3]) of > 20 mmol.  It can be a consequence of overproduction and/or reduced metabolism of lactic acid. The main sites of lactate metabolism are the liver and kidney  There are two recognised types of lactic acidosis: Type A is due to Tissue hypoxia Inadequate tissue perfusion and Anaerobic glycolysis which may be seen in cardiac arrest, shock, hypoxaemia and anaemia. Management involves reversing the underlying cause of tissue hypoxia.        2.  Type B occurs in the absence of tissue hypoxia. The causes include: Hepatic failure Renal failure Diabetes mellitus Pancreatitis Infection and Drugs (aspirin, ethanol, methanol, biguanides and intravenous fructose). Optimising tissue oxygen delivery, correcting the cause and infusions of intravenous sodium bicarbonate form the mainstay of treatment. Peritoneal dialysis has been used in resistant cases.
• Metabolische Alkalose Metabolic alkalosis is a primary increase in serum bicarbonate (HCO3-) concentration which occurs as a consequence of a loss of H+ from the body or a gain in HCO3-. There are many causes of metabolic alkalosis but they can be divided into Chloride-responsive alkalosis (urine chloride <20 mEq/L) Chloride-resistant alkalosis (urine chloride >20 mEq/L) and Other causes, including alkali-loading alkalosis. Ingestion of large doses of non-absorbable antacids (for example, magnesium hydroxide) may generate metabolic alkalosis by a rather complicated mechanism. diuretics and the external loss of gastric secretions Volume depletion also stimulates aldosterone secretion, which enhances sodium ion reabsorption in the collecting duct and increases hydrogen ion and potassium secretion in this segment. penicillin: hypokalaemic metabolic alkalosis by distal delivery of non-reabsorbable anions with an absorbable cation such as Na+.
• Transfusionsreaktion: ABO incompatibility. Antibodies bound to red cells in the body can cause red cell destruction by two major mechanisms: intravascular and extravascular. Intravascular: Red cells are destroyed in the bloodstream with consequent release of haemoglobin into the circulation. The antibodies that can cause this type of reaction, that is, IgM or IgG anti-A or anti-B, cause rapid activation of the complement cascade usually by the classical pathway. Extravascular: Intact red cells are removed from the circulation by cells of the mononuclear phagocyte system situated in the liver and spleen. Red cells coated with IgG or sensitised with complement to the C3 stage, but which do not proceed through the cascade to the C5b-C9 lytic complex, may interact with mononuclear phagocytes, notably the macrophage. Extravascular red cell destruction results in breakdown products of haemoglobin, such as bilirubin and urobilinogen, in the plasma and urine. This type of red cell destruction can be caused by IgG, anti-D and other rhesus antibodies. Non-immune haemolytic transfusion reactions occur when red blood cells (RBCs) are damaged before transfusion resulting in haemoglobinaemia and haemoglobinuria without significant clinical symptoms. Non-haemolytic febrile transfusion reactions are usually caused by cytokines from leukocytes in transfused red cell or platelet components, causing fever, chills, or rigors. In the setting of transfusion administration, a fever is defined as a temperature elevation of 1°C. Patients with hereditary C1-inhibitor deficiency may have recurrent attacks of angioedema when transfused with standard plasma containing blood components.
• Prolaktinom A prolactinoma may present with Amenorrhoea Bitemporal hemianopia due to chiasmal compression Reduced bone mineral density (BMD) associated with longstanding hypo-oestrogenism and Hypopituitarism (zB TSH- Mangel)
• Horner Syndrom Horner's syndrome results from interruption of the sympathetic innervation to the head. It was originally described with cervical lesions causing damage to the T1 contribution to the cervical sympathetic chain, but may be due to lesions anywhere along the sympathetic pathway. The features of Horner's include Partial ptosis Miosis (contraction) Apparent enophthalmos Lack of sweating and Nasal stuffiness on the affected side Miosis occurs due to paralysis of the dilator pupillae and ptosis is due to paralysis of the sympathetic muscle fibres transmitted via the oculomotor nerve to the upper eyelid. Horner's may follow Operations on, or injuries to, the neck in which the cervical sympathetic chain is damaged Malignant invasion from lymph nodes or adjacent tumour or Spinal cord lesions at the T1 segment.
• Serotonerges Syndrom Symptome: excitation, hyperpyrexia, hypertension, profuse sweating, and rigidity. This may progress to seizures, coma, and death.   Auslösende Medikament:  Monoamine oxidase inhibitors (MAOIs) Pethidine Tricyclic antidepressants Selective serotonin reuptake inhinitors (SSRIs) Antibiotics (linezolid) Opiates (meperidine, fentanyl, pentazocine) Tramadol Antiemetic agents (ondansetron, granisetron, metoclopromide) Over-the-counter cough medications (dextromethorphan) Lithium Antimigraine drugs (sumatriptan) Drugs of abuse (methylenedioxymethamphetamine or "ecstasy"). Differenzialdiagnose: neuroleptic malignant syndrome. This is an idiopathic reaction to dopamine antagonists, a condition that is defined by: A slow onset Bradykinesia or akinesia "Lead pipe" muscular rigidity Hyperthermia Fluctuating consciousness Autonomic instability. Signs and symptoms of the neuroleptic malignant syndrome typically evolve during several days, in contrast to the rapid onset and hyperkinesia of the serotonin syndrome. Knowledge of the precipitating drug also helps in distinguishing between syndromes: dopamine antagonists produce bradykinesia, whereas serotonin agonists produce hyperkinesia.
• Lungenfibrose It can be caused by chemical agents including: Paraquat Antimitotic drugs  MTX Busulphan Amiodaron Asbestos Aspiration of gastric contents Fumes.
• Hypoxic pulmonary vasoconstriction Hypoxic pulmonary vasoconstriction (HPV) is the reflex constriction of pulmonary arterioles in response to low a PO2 (below 80 - 100 mmHg; 11 - 13 kPa) in adjacent alveoli. It is independent of the innervation to the vessel walls and can occur when blood with a high PO2 is perfused through lung which has a low alveolar PO2. Thus a low PO2 in the alveoli has been shown to influence hypoxic pulmonary vasoconstriction (HPV) more than a low PO2 in the blood. HPV results in the blood flow being directed away from poorly ventilated areas of the lung and helps to reduce the ventilation/perfusion mismatch. Volatile anaesthetic agents reduce HPV in animals, but in adults the evidence is less convincing, although it certainly does not increase the effect. 20 parts per million (ppm) of nitric oxide will inhibit the HPV response.
• E. coli Infekt- Antibiose? Escherichia coli is a Gram negative bacillus which produces penicillinases, but it remains sensitive to numerous antibiotics. Bacterial resistance to antibiotics is a major problem and where possible sensitivities should be checked before blind treatment of infections is commenced. Ampicillin and amoxicillin are broad spectrum antibiotics active against non-beta lactamase producing Gram positive and Gram negative organisms. They are inactivated by penicillinases and since up to 50% ofEscherichia coli strains are now resistant, they would be an unsuitable choice. Co-amoxiclav consists of amoxicillin and the beta-lactamase inhibitor clavulanic acid. Thus it is active against beta-lactamase producing bacteria that are resistant to amoxicillin, including strains of Escherichia coli. Cefuroxime is a cephalosporin that is resistant to inactivation by bacterial beta-lactamases and so may be used against Escherichia coli. Ciprofloxacin has a 6-fluoro substituent which confers enhanced antibacterial potency against both Gram positive and Gram negative organisms, including Escherichia coli.
• hyperprolactinaemia is associated with the following... ...Acromegaly is associated with hyperprolactinaemia either through stalk compression or co-secretion of prolactin with growth hormone. Dopamine agonists, for example, bromocriptine, suppress prolactin secretion, whereas dopamine antagonist, for example, metoclopramide do cause an increase in prolactin levels.  Pregnancy is associated with elevated prolactin levels. Treatment of pituitary tumours with radiotherapy does cause an elevated prolactin level in the acute stage although hypopituitarism ensues later, which is believed to relate to hypothalamic involvement and reduced dopaminergic control.
• Le-Fort-Frakturen Le-Fort-I : horizontaler Oberkieferbruch. Das Knochenfragment erinnert an eine Oberkiefer-Totalprothese Le-Fort-II: pyramidenförmigen Oberkieferabsprengung Le-Fort-III: vollständiger Abriss des Mittelgesichts von der Schädelbasis. Diese hohe Absprengung der Maxilla liegt im oberen Teil des Mittelgesichts. Trotz regelrechter Ausheilung „auf dem Röntgenbild“ kann es zu Schädigungen von neurovaskulären Bündeln kommen - der N. supraorbitalis, N. infraorbitalis, N. facialis (r. frontalis).
• M. Bechterew Assoziiert mit: Herz: Asociated with a higher risk for cardiovascular diseases: ischemic heart disease, peripheral vascular disease, congestive heart failure aortic regurgitation and conduction disturbances, congestive heart failure. Lunge: restrictions in chest expansion due to costovertebral rigidity   Niere:  IgA nephropathy and secondary amyloidosis (selten) WS: Atlantoaxial subluxation  Fracture of ankylosed spine 
• Fallot-Tetralogie Right ventricular outflow tract obstruction (pulmonary stenosis) Ventricular septal defect (VSD) Deviation of the origin of the aorta to the right so that it overrides the VSD Concentric right ventricular (RV) hypertrophy Therapie: Reparative surgery, which is usually performed electively in the first year of life permits over 85 percent of children to survive to adulthood Severely symptomatic cyanotic newborns may require intravenous prostaglandin (also known as alprostadil) to maintain ductal patency and pulmonary flow pending more definitive therapy An occasional infant with increased pulmonary blood flow requires digoxin and diuretics for heart failure. These drugs should be discontinued as RV obstruction progresses knee-chest position to increase systemic vascular resistance, which promotes movement of blood from the right ventricle into the pulmonary circulation rather than the aorta. intravenous morphine and a fluid bolus. The mechanism of action of morphine is unclear, while fluids improve RV filling and pulmonary flow. intravenous beta blockers (eg, propranolol or esmolol) can be administered. The presumed mechanism of benefit is relaxation of the right ventricular outflow tract (RVOT) with improved pulmonary blood flow. If this is insufficient, systemic afterload can be increased with intravenous phenylephrine Blalock-Taussig shunt: aorta-to-pulmonary artery connection (palliative procedure for infants who may not be acceptable candidates for intracardiac repair due to prematurity, hypoplastic pulmonary arteries, or coronary artery anatomy) Intracardiac repair: patch closure of the ventricular septal defect and enlargement of the RVOT. The latter is accomplished by relieving pulmonary stenosis, resecting infundibular and subinfundibular muscle bundles and if necessary by a transannular patch, creating unobstructed flow from the RV into the pulmonary arteries    
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• Hypophysenadenom The pituitary gland is an important part of the neuro-endocrine axis. It is found in the sella turcica of the sphenoid bone at the base of the skull. Superiorly it is related to the hypothalamus, third ventricle and visual pathways and laterally to cranial nerves III, IV, V and VI, the cavernous sinuses and internal carotid arteries. Pituitary tumours account for approximately 10-15% of all intracranial tumours. Most are benign adenomas. Symptoms can be related to the over-secretion of pituitary hormones (most commonly prolactin, growth hormone or ACTH), the under-secretion of hormones, or due to localised or generalised pressure effects. Local pressure can cause compression of the optic chiasm and visual field defects, most commonly a bitemporal hemianopia. This is due to compression of the nasal retinal fibres that convey the visual impulses from the temporal vision as they cross to the contralateral sides at the optic chiasm before continuing to the optic tracts.
• Mydriasis Mydriasis/pupillary dilatation is associated with Third nerve palsy Mydriatics such as anticholinergics and Tricyclics due to their anticholinergic effect. It is not associated with SSRIs.
• hereditäres Angioödem C1-Esterase-Inhibitor-Mangel (quantitativ oder qualitativ). Autosomal dominant. C1-Esterase-Inhibitor: Kontrolle der Aktivierung des Komplementfaktors C1
• Lagerungsschäden  The length of time spent in an abnormal position will increase the likelihood of problems and possible litigation. The eyes and optic nerves are at risk from direct pressure from surgical instruments, elbows resting over the face and when in the prone position. The brachial plexus and its terminal braches are at risk from stretching or external pressure particularly in the lateral position. The lithotomy position can damage not only the saphenous and common peroneal nerves (pressure from the poles) but also the femoral and obturator nerves. Neuronal injury is usually temporary and function is returns with time, but occasionally damage is permanent.
• Central cord syndrome   Mögliche Ursache: Hyperextension bei Intubation. Is the most common incomplete spinal cord lesion. The spinal cord is injured in central grey matter and results in proportionally greater loss of motor function to upper extremities than lower extremities with variable sensory sparing; The nerve fibres responsible for lower extremity motor and sensory functions are located in the most peripheral part of the cord, whereas fibres controlling the upper extremity and voluntary bowel and bladder function are more centrally located; the sacral tracts are positioned on the periphery of the cord and are usually spared from injury. This type of injury is associated with cervical spondylosis and extension in the elderly or hyperextension injury in middle age.  
• Anterior spinal artery infarction The anterior spinal artery is a single long anastomotic channel that lies at the mouth of the anterior central sulcus and supplies the circulation to the anterior two thirds of the spinal cord. Eight to ten unpaired anterior medullary arteries are branches of the larger afferent aorta and vertebral and iliac arteries. These feed into the anterior spinal arteries. The largest anterior medullary artery, the great anterior medullary artery of Adamkiewicz, which is susceptible to occlusion with neurologic deficit, is located at the lumbar enlargement, usually at L2 on the left side (but may be at any point from T8 to L2). Infarction of the anterior spinal artery causes motor paralysis below the level of the lesion due to interruption of the corticospinal tract, and loss of pain and temperature sensation at and below the level of the lesion. Proprioception and vibratory sensation is preserved, as it is in the dorsal side of the spinal cord. Aortic disease has produced spinal infarction in a variety of situations including dissecting aneurysm; aortic surgery, especially with aortic cross-clamping above the renal artery, atherosclerotic embolisation; aortography; and aortic thrombosis.
• Brown-Sequard syndrome   Ursache: halbseitige Läsion des Rückenmarks durch trauma, neoplasm and multiple sclerosis. Teilweise Kreuzung der Bahnen resultiert in:   ipsilateral upper motor neurone paralysis and loss of proprioception contralateral loss of pain and temperature sensation.     
• Cauda equina syndrome The spinal cord ends at L1 and L2 at which point a bundle of nerves travel downwards through the lumbar and sacral vertebrae (L1-5 and S1-4). Injury to these nerves will cause partial or complete loss of movement and sensation in this distribution Faecal incontinence  impotence  Urinary retention 
• Karzinoid/ Neuroendokrine Tumoren Spezielle NET-Formen sind z. B. VIPome, Gastrinome, Insulinome oder Phäochromozytome.    Karzinoid-Syndrom (durch Serotonin): Trias Diarrhoe (Durchfall), Flush (Erröten) und Hedinger-Syndrom (kardiale Manifestation des Karzinoid-Syndroms), inkl. Rechtsherzbelastung durch endokardfibrosen, pulmonalart. Hypertonie und Bronchospasmus (Asthma).
• Kurzdarmsyndrom nach Resektion von Dünndarm Symptome Durchfällen  Fettstühle  Mangelversorgung mit Wasser, Makro- und Mikro-Nährstoffen (Eiweiß, Fett, Elektrolyte, Calcium, Magnesium, wasser- und fettlösliche Vitamine, insbesondere Vitamin B12)  Gewichtsverlust Überproduktion (Hypersekretion) von Magensäure (Gastric inhibitory polypeptide – GIP, Vasoactive intestinal polypeptide – VIP aus Jejunum). Lactose-Unverträglichkeit durch Wegfall des in bestimmten Darmschleimhautabschnitten sitzenden Enzyms Laktase. Gallensteinbildung (Ileum-Resektion -> Gallensäurenresorption vermindert. Cholesterin fällt aus) Nierensteinbildung: Calcium bindet an Fettsäuren statt an Oxalat -> Resorption von Oxalat > Oxalatsteine. Gallensäuren stimulieren im Dickdarm Sekretion von Wasser und Elektrolyten 
• Hypertroph-obstruktive Kardiomyopathie genetisch bedingte Hypertrophie des Myokards im linken Ventrikel (meist Septum) > Obstruktion des linksventrikulären Ausflusstrakts und verminderte Auswurfleistung.   Ausserdem eingeschränkte Dehnbarkeit und erhöhte Druckbelatung. Folge: Fkt.st. li. Vorhof und erhöhtes Risiko für Vorhofflimmern. Therapie: Vermeidung körperlicher Belastung, Calciumantagonisten, Beta-Blocker. Transkoronare Ablation der Septumhypertrophie. Transaortale subvalvuläre Myektomie. Kontraindikation: Positiv inotrope Medikamente: Digitalis, Sympathomimetika. Nitrate.
• Thalassämie meist Mutation des ß-Giobingens -+ verminderte Produktion von ß-Ketten -+ kompensatorisch gamma-oder delta-Ketten vermehrt. Ineffektive Erythropoese mit intra-und extramedullärer Hämolyse.  Heterozygot (leichte Form): -HbF: ln 50% der Fälle leicht erhöht -HbA2: Immer erhöht  Homozygot: HbF: Immer stark erhöht · HbA2: Unterschiedliche Befunde    Vgl:  Hämoglobinkonstellation der normalen Erythrozyten: Neugeborene: HbA (aa/ßß): ca. 20% HbA2 (aa/delta): ca. 0,25% HbF (aa/gamma): ca. 80%    Erwachsene: HbA (aa/ßß): 97 % HbA2 (aa/delta): 2,5 % HbF (aa/gamma): Spur(< 0,5 %) 
• Dystrophia myotonica: Anästhesieprobleme wenig cardiopulmonale Reserve (Cardiomyopathie, Schwäche Atemmuskeln) Risiko für Aspiration erhöht (verzögerte Magenentleerung) übermässige Wirkung von Iv Anästhetika, nicht depolarisierenden Mm. relaxantien, Opioiden Succi und ACHE I. verursachen verlängerte Mm. Kontraktion (Problem bei Laryngoskopie und Beatmung)  
• SIADH associated with: Pneumonia Bronchial small cell carcinoma Haferzell-lungen-CA Pulmonary tuberculosis Subarachnoid haemorrhage Head injuries Meningitis, etc. medikamentös-induziert (Thiazid-Diuretika, Vasopressin, Oxytocin, Serotonin-Wiederaufnahmehemmer = SSRI, trizyklische Antidepressiva, Carbamazepin, Vincristin, Cisplatin u.a.)  Transient SIADH commonly occurs post-operatively.   euvolaemic hyponatraemia.  Keine Ödeme, da Wasserretention nur ca. 3-4 l beträgt.  Hyponatriämie (oft < 110 mmol/1), Hypoosmolalität des Serums  Trotz hypotoner Extrazellularflüssigkeit wird ein konzentrierter (hypertoner) Urin ausgeschieden (> 300 mOsm/kg H20, Na > 20 mmol/l).  Plasma-ADH normal bis erhöht Therapie A) Kausal: z.B. bei entzündlichen Erkrankungen Spontanbesserung bei Therapie des Grundleidens. Ev. Absetzen auslösender Medikamente u.a.  B) Symptomatisch:  • Bei asymptomatischer leichter Hyponatriämie keine Therapie  • Flüssigkeitsrestriktion (500 -800 ml/d)  • Vasopressinrezeptor-Antagonisten: Vaptane, z.B. Tolvaptan (Samsca®) können eine Aquarese mit Anstieg des Serumnatriums bewirken. Die Therapie muss stationär eingeleitet werden, da eine genaue Dosistindung mit Kontrollen des Serum-Natriums erforderlich ist. CYP3A4-WW u.a. NW sind zu beachten.  "It may respond to demeclocycline" Nur bei lebensbedrohlicher Wasserintoxikation (Na+ i.S. < 100 mmol/1) vorsichtige Infusion hypertoner Na Cl-Lösung (Natrium i.S. darf maximal um 10 mmol/1 in 24 h steigen) und Gabe von Furosemid zur Steigerung der Diurese (bei zu schnellem Anstieg des Serum-Natriums Gefahr der zentralen pontinen Myelinolyse!).   
• Addison-Krise   M. Addison:   = primärer NNR-Insuffizienz. Versiegen sämtlicher Kortikosteroide; (hingegen ist die Aldosteronproduktion bei den sekundären Formen infolge ACTH-Mangel nur wenig betroffen)    Symptome: 1. Schwäche und rasche Ermüdbarkeit 2. Pigmentierung der Haut und Schleimhäute, ev. Vitiligo 3. Gewichtsverlust und Dehydratation 4. Niedriger arterieller Blutdruck 5. Abdominelle Beschwerden (Übelkeit, Erbrechen, Abdominalschmerzen, Durchfälle, Obstipation) 6. Verlust der Sekundärbehaarung bei der Frau (Androgenmangel) u.a.  Therapie 1. Glukokortikosteroid: 15 -25 mg Hydrocortison in 2-3 Dosen;  2. Mineralokortikoid: Fludrecortison (Astonin H®): Dosis so wählen, dass die Plasmareninaktivität in der oberen Norm liegt (0,05-0,2 mg/d). 3. Zusätzliche Gabe von DHEA = Dehydroepiandrosteron: Kann als androgenes Steroid bei Frauen, die über Libidoverlust klagen, sinnvoll sein.    Addison-Krise = akute NNR-Insuffizienz    Exsikkose, BlutdruckabfalL Schock, Oligurie   Pseudoperitonitis   Ev. Durchfälle und Erbrechen   Hypoglykämie, metabolische Azidose  Anfangs unternormale Temperaturen, später Exsikkose-Fieber   Delir, Koma    Ursachen einer akuten NNR-Insuffizienz:   Waterhouse-Friderichsen-Syndrom = hämorrhagische lnfarzierung der Nebennieren infolge Menin-gokokkensepsis -Blutungen (Marcumar, Neugeborene) Operative Entfernung der Nebennieren Fehlende Dosisanpassung bei Patienten mit NNR-Insuffizienz und Infekten anderen Belastungen, Bewußtlosigkeit, Brechdurchfall u.a.  Therapie nach Abnahme einer Blutprobe zur Bestimmung von Certisol und ACTH! 1. 0,9 % NaCI und 5 % Glukose-lnfusion -Gesamtdosis von 0,9 % NaCI-und Glukoseinfusion in Abhängigkeit vom Ausmaß der hypotonen Dehydratation (ZVD, Serum-Natrium) und vom Blutzucker. Keine K+-haltigen Lösungen! Langsamer Ausgleich der Hyponatriämie (Gefahr der zentrale pontinen Myelinolyse). Ev. Ausgleich einer metabolischen Azidose. 2. Hydrocortison: 100 mg i.v., danach 200 mg/24 h (in Glukose 5 %) oder synthetisches Glukokortikosteroid in äquivalenter Dosis.       
• CUSHING-SYNDROM = HYPERKORTISOLISMUS Symptome: 1. Fettstoffwechsel: Umverteilung der Depotfette: Vollmondgesicht, Stiernacken, Stammfett-sucht; supraklavikuläre Gruben durch Fettpolster verstrichen; Hypercholesterinämie 2. Eiweißstoffwechsel: Osteoporose mit ev. Knochenschmerzen, Myopathie mit Muskelschwund, Adynamie; 3. Kohlenhydratstoffwechsel: Diabetagene Stoffwechsellage 4. Hämatopoetisch: Leuko-, Thrombo-und Erythrozyten erhöht; Eosinophile und Lymphozyten vermindert 5. Hypertonie (85 %) 6. Haut: Schlechte Wundheilung, Neigung zu Akne, Furunkulose, Ulzera, Auftreten von Striae rubrae, Atrophie der Haut 7. Bei Frauen Virilismus, Hirsutismus, Zyklusstörungen 8. Bei Kindern Wachstumsstillstand 9. Psychische, ev. psychotische Veränderungen 10. Hypokaliämie (5 %) infolge Uberproduktion von Mineralokortikoiden ist rel. selten und dann verdächtig auf NNR-Tumor oder ektope ACTH-Produktion.   
• Hypocalcämie With hypocalcaemia, neuromuscular, neural and cardiovascular abnormalities predominate. Neural hyperexcitability causes smooth and skeletal muscle contractions. Neural findings include: Dementia or overt psychosis Irritability Confusion Hallucinations Extrapyramidal manifestations and Seizures. Cardiovascular findings include: Bradycardia/tachycardia Signs of heart failure Prolongation of QT interval Refractory hypotension and Arrhythmias.
• Awareness The main risk factors are: 1. Use of neuromuscular blocking agents. 2.Light planes of anaesthesia: Caesarean section (1 in 250) Cardiac anaesthesia (1 in 100) Major trauma (1 in 20) Impaired CVS function Bronchoscopy Difficult intubation 3. Anaesthetic errors. 4. Equipment failure. 5. Patient factors: Parmacogenetic factors Enzyme inducing agents. The incidence of awareness for procedures such as elective inguinal hernia repair is no higher than 0.1-0.2%. Whilst DC cardioversion is a very short procedure that can be carried out under "deep" sedation, general anaesthesia is the preferred option with an incidence of awareness of 0.3%.
• Occulomotoriuslähmung In surgical third nerve palsy, ptosis and mydriasis are evident and the eye looks 'down and out'. These features reflect loss of innervation to all the major structures supplied by the oculomotor nerve. Oculomotor nerve palsy causes ptosis due to paralysis of levator palpebrae superioris. The eye is rotated down and out due to the unopposed actions of the superior oblique and lateral rectus muscles. Surgical (compressive) causes of a third nerve palsy disrupt the parasympathetic pupillomotor fibres on the periphery of the nerve causing mydriasis. In contrast, medical (ischaemic) causes of a third nerve palsy leave the superficially located parasympathetic fibres relatively unaffected and the pupil is spared. Ptosis, anhydrosis and miosis is the classic triad of Horner's syndrome and reflects loss of sympathetic innervation to the tarsal muscle of the upper lid, facial skin and dilator pupillae, respectively.
• Emphysem, LuFu In bullous emphysema the air spaces are > 1 cm in diameter. If the bullae are not significantly ventilated then lung mechanics and carbon monoxide transfer reflect properties of non-bullous lung. The characteristic abnormality in bullous emphysema is a large difference between lung volumes measured by body plethysmography / radionucleotide techniques and helium equilibrium. Whole body plethysmography is superior for lung volume analysis to helium diffusion Static lung compliance is increased  the ratio of FEV1/FVC is decreased TLCO is decreased and KCO (which is TLCO / alveolar volume) is also reduced.

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