Co-Director, University of Nevada, Las Vegas School of Medicine
Floaters: it is of gradual onset: Vitreous degeneration with increasing If age and myopia it is of sudden onset with normal vision: Posterior vitreous If detachment with increasing age and myopia it is of sudden onset with diminished vision: Vitreous If hemorrhage with involvement of macula History double vision: it is monocular-due to ocular problem If it is bilateral-due to nervous system damage from brain If stem to ocular muscle antibiotics gas dogs discount vantin master card. Past History Local z z z z Trauma Surgery Refractive error Previous recurrent history of eye disease-anterior uveitis antibiotic withdrawal symptoms order genuine vantin on line. Systemic z z z z z z z z Hypertension Diabetes Hyperlipidemia Arthritis Ulcer in penis Recurrent headache Recurrent vertigo Other systemic events of vasculitis virus gear vantin 100mg mastercard. Family History It may disclose the hereditary conditions-like: z Retinitis pigmentosa z Corneal dystrophies z Early onset cataract antimicrobial copper order vantin 200 mg online. Social History History of smoking or alcohol intake-it may disclose-traumatic, vascular or hypertensive cause as precipitating factor. Eye Disease 689 Examination Eyelids Note the position of eyelids: z Normally in opened eye condition, upper eyelid covers upper margin of iris z In closed eye condition-upper lid and lower lid approximate each other completely. Droping of eyelid-called ptosis-produce narrowing of palpebral fissure-when bilateral, it is due to myasthenia gravis or any other muscle wasting disease Kearns-Sayre syndrome-bilateral ptosis-symmetrical pro gressive, symmetrical external ophthalmophegia, retinal pigmentary degeneration and cardiac conduction defect; short stature, may be deaf. Inspection of lacrimal apparatus z Epiphora: Some obstruction to flow through punctum. Whether there is blockage of nasolacrimal duct-can be tested by pressing the lacrimal sac. Inspection of conjunctiva Conjunctive should be examined for: z Inflammation (congestion or dilatation of blood vessels) z Pallor z Unusual pigmentation z Swelling z Masses z Hemorrhage. Normal conjunctiva Colorpink Small number of blood vessels is usually seen Compare vascularity of two eyes. Conjunctivitis Inflammation of conjunctiva-causes are: z Bacterial z Viral z Fungal z Parasitic z Allergic z Traumatic z Chemical z Idiopathic. Giant Papillary Conjunctivitis Excessive secretion of conjunctival mucus, itchy, development of giant papillae on the tarsal conjunctiva. May be seen in: z Patient with contact lenses z Patient with occular prosthesis z Foreign body in eye. It may be due to allergic conjunctivitis, trauma, proptosis in hyperthyroidism, neurological deficit It may occur in melanoma, hemorrhage. Examination of Sclera Sclera should be examined for z Color z Nodules z Hyperemia Normal sclera is z White z Muddy in darkskin individuals. Scleromalacia Perforans Uncommon painless condition characterized by appearance of dehiscence in the sclera in absence of inflammatory changes. As a result: z Uveal tissue may bulge through dehiscence z Anterior synechia is present. Corneal tissue should be inspected for: z Color z Cloudiness z Ulceration z Opacities. It is bilateral but asymmetrical When the patient is asked to look downwards, keratoconus will be obvious. In case of intermediate and posterior uveitis: z No pain or acting sensation z Blurred vision z Floaters. Differentiation between strabismus and pseudostrabismus: Corneal reflex test of both eyes: If the reflexion is centered in both the eyes-diagnosis is pseudostrabismus. Ophthalmoscopy should be done all following conditions: z Complaining of altered vision z Older than 40 years of age z Neurological disorders responsible for increase intracranial pressure z Patient with diabetes and hypertension. Red Reflex It is the light reflected by the retina-because of its rich vascular supply. Causes of abnormal red eye reflex: All, those are responsible for opacity of light transmitting media, produce abnormal red eye reflex: z Anterior eye structures: Lens-cataract Cornea-scars, abrasion, ulcers. Optic cup: z It is central excavation in optic disc-where retinal vessels exit or enter the optic up z It is not greater than 50 percent of optic disc. Pathologic changes in optic disc Redness of disc: z Retinal vessel occlusion z Papilledema z Polycythemia z Neovascularization of the disc. Pale optic disc: z Normal variant z Myopic eye z Optic atrophy-due to death of axon cells. Optic disc of glaucoma: >50 percent of size of optic disc-occupied by optic cup-pathological cupping-its vertical diameter or oblique diameter is increased-oval cup. Disc size Swelling of optic disc-due to swelling of optic nerve head-is called papilledema.
History Suggestive of Having Sleep Apnea Syndrome z z z z z z z Is the patient snores Early morning headache is due to poor quality of sleep leads to day time somnolence and carbon dioxide retention virus undead order discount vantin on-line. Pneumonia and pleurisy: Caused by: Bronchiectasis Bronchial tumor Aspiration of esophageal content (achalasia cardia) Aspiration of pharyngeal content or vomit (bulbar palsy) Alcoholism Hypogammaglobulinemia Multiple myeloma antibiotics resistance news purchase vantin 200mg fast delivery. Measles or whopping cough: can produce pneumonia in early childhood It can cause wheeze bronchitis or bronchiectasis antibiotics for sinus ear infection order 200mg vantin with mastercard. It Wheezy bronchitis or recurrent bronchitis in childhood: Recurrence of bronchial asthma in adult who have history of childhood asthma or wheezy bronchitis in common bacteria 3d model order vantin 200 mg fast delivery. Chest injuries: Traumatic hemithorax-leads to pleural thickening and splints of chest (frozen chest). Recent history of general anesthetics or loss of consciousness: Inhalation or aspiration of oropharyngeal secretion or foreign body leads to: Aspiration pneumonia Lung abscess. Pregnancy, surgery: Pulmonary embolism Comparison of recent chest radiograph with previous radiograph. Regarding passive smoking the questions are: How much time spared in home with smokers Respiratory System 193 It may produce bronchial asthma in childhood and intercurrent infections. Pets and Hobbies Exposure to pigeons, parrots and other caged birds can cause: Extrinsic allergic alveolitis Bronchial asthma Allergic rhinitis Pneumonia (psittacosis). Acute symptoms usually seen in pigeon fanciers who, few hours after cleaning out the birds, develop cough, breathlessness, flu like symptoms Chronic symptoms seen in budgerigar owners-because they exposed continuously to low dose of antigen-they complain of progressive breathlessness. You may extend your enquiries beyond home because patient may be exposed to birds belonging to friends and relations. Any job involving exposure to noxious agents of respirable size potentially damages the respiratory tract. Personal History z z Intravenous drug user or sexual malpractices may be responsible for unusual pulmonary disorder Toxicities of immunosuppressive drugs. It is commonly seen in: Lung disease Pain Sepsis Obesity Anxiety Fever: Respiratory rate increases 4 breath/minute for every 1 degree rise in body temperature. Bradypnea-less than 10 breaths/minute-occurs in: Hypothyroidism Narcotic use Sedation Diabetic coma. Central apnea: Neuromuscular dysfunction Obstructive sleep apnea: Airway obstruction induced by rapid eye movement sleep. Difference between hyperpnea and hyperventilation: z Hyperventilation: Where vital capacity compromised, thus breath is shallow and increase in rate z Hyperpnea: Due to increase in tidal volume, rate and death are increased z Hypopnea: Respirations is shallow. Respiratory System 197 z z z z z z Cresendo-decresendo pattern last for 30 sec, apneic period last for shorter periods. Causes: Aging Simple sleep High altitude Neurological disorders: Meningitis, bilateral or unilateral cerebral infarction, hemorrhage, traumatic brainstem lesion. Apneustic breathing: Deep inspiratory phase followed by breath holding period and rapid exhalation. Ataxic breathing: Totally anarchic respiration-fibrillation of respiratory center, sudden shift from hyper- to hypoventilation and from hyperpnea to hypoapnea (agonal respiration) Causes: Medullary damage. Grunting respiration: Preterminal grunting or gurgling sound produced by the patient to clear secretions is a death rattle-sign of severe pneumonia with impending It respiratory failure, muscle fatigue and death More frequent in children-short and low pitched noise produced by forced expiration against closed glottis. Pursed-lip respiration: Patient is at risk of expiratory airway closure and air trapping, so they resort to pursed-lip exhalation, as it they are inflating a balloon. Abnormalities in Posture Orthopnea Orthop (upright), pnea (breathing) Dyspnea aggravated in lying down position, relived by upright position. Causes z z z Congestive cardiac failure: Pooling of blood to the dependent areas of the body-reduces venous return and ventricular load. Nonpulmonary or noncardiac: Obesity Massive ascites Bilateral phrenic nerve paralysis. Paroxysmal Nocturnal Dyspnea Characterized by nocturnal spell (paroxysm) of acute dyspnea (air hunger). After 1 to 2 hours of sleep patient awakens, sit upright, lowers the legs by the side of the bed, opens the window to catch the fresh air, after few minutes, he expectorates small amount of frothy sputum, occasionally pink frothy sputum, he feels better enough to go back to sleep. Respiratory System 199 Mechanism In upright posture, peripheral pooling of blood, reduces the venus return, reduces pulmonary congestion. Causes z Acute left ventricular failure z Bilateral apical and bullous lung diseases-both basilar perfusion and lung mechanics are improved. Significant of Platypnea z z Right to left intrapulmonary shunts: In these cases upright posture increases perfusion to lower lobes and worsens the ventilation/ perfusion (V/Q); as a result oxygen desaturation occurs leading to dyspnea; conversely platypnea improves V/Q matching and relieves dyspnea. It occurs in: Multiple recurrent pulmonary emboli Pleural effusion Cirrhosis Arteriovenous malformation. Intracardiac right to left heart shunt: In case of atrial septal defect associated with increased pulmonary resistance-as in case of pleuropericardial or pericardial effusion or postlobectomy or postpneumonectomy. Upright posture reduces the shunt by: Redirecting the blood through atrial septum Decreasing the pressure over right atrium. Physiology Behind Trepopnea Increased perfusion in dependent lung-producing better V/Q matching, better oxygenation and relieves dyspnea. Causes Unilateral lung collapse from: In these situations patient feels better when the good lung is dependent. Contraindication to good lung down: In unilateral lung disease due to spilable material.
It also stimulates nociceptive nerves and may thus be involved in the pain associated with tissue injury antibiotic breastfeeding buy vantin online. The effect of transmural pressure on arteriolar diameter is more complex because arterioles respond both passively and actively to changes in transmural pressure infection with red line buy 200 mg vantin with amex. For example treatment for dogs chewing paws buy generic vantin pills, a sudden increase in the internal pressure within an arteriole produces (I) first an initial slight passive mechanical distention (slight because arterioles are relatively thick-walled and muscular) virus removal programs order vantin cheap online, and (2) then an active constriction that, within sec onds, may completely reverse the initial distention. A sudden decrease in transmu ral pressure elicits essentially the opposite response, that is, an immediate passive decrease in diameter followed shortly by a decrease in active tone, which returns the arteriolar diameter to near that which existed before the pressure change. All arterioles have some normal distending pressure to which they are prob ably actively responding. Therefore, the myogenic mechanism is likely to be a fundamentally important factor in determining the basal tone of arterioles every where. Also, for obvious reasons and as soon discussed, the myogenic response is potentially involved in the vascular reaction to any cardiovascular disturbance that involves a change in arteriolar transmural pressure. For example, skeletal muscle blood flow increases within seconds of the onset of muscle exercise and returns to control values shortly after exercise ceases. This phenomenon, which is illustrated in Figure 7-3A, is known as exercise or active hyperemia (hyperemia means high flow). It should be clear how active hyperemia could result from the local metabolic vasodilator feedback on the arteriolar smooth muscle. Organ blood flow responses caused by local mechanisms: active and small resistance vessels, endothelial flow-dependent mechanisms may assist in propagating the vasodilation to larger vessels upstream, which helps promote the delivery of blood to the exercising muscle. Reactive Hyperemia-In this case, the higher-than-normal blood flow occurs transiently after the removal of any restriction that has caused a period of lower than-normal blood flow and is sometimes referred to as postocclusion hyperemia. For example, flow through an extremity is higher than normal for a period after a tourniquet is removed from the extremity. The magnitude and duration of reactive hyperemia depend on the duration and severity of the occlusion as well as the metabolic rate of the tissue. These findings are best explained by an interstitial accumulation of metabolic vasodilator substances during the period of flow restriction. However, unexpectedly large flow increases can follow arterial occlusions lasting only 1 or 2 s. Autoregulation-Except when displaying active and reactive hyperemia, nearly all organs tend to keep their blood flow constant despite variations in arterial pressure-that is, they autoregulate their blood flow. As shown in Figure 7-4A, an abrupt increase in arterial pressure is normally accompanied by an initial abrupt increase in organ blood flow that then gradually returns toward normal despite the sustained elevation in arterial pressure. The sub sequent return of flow toward the normal level is caused by a gradual increase in active arteriolar tone and resistance to blood flow. Ultimately, a new steady state is reached with only slightly elevated blood flow because the increased driv ing pressure is counteracted by a higher-than-normal vascular resistance. As with the phenomenon of reactive hyperemia, blood flow autoregulation may be caused by both local metabolic feedback mechanisms and myogenic mechanisms. The arteriolar vasoconstriction responsible for the autoregulatory response shown in Figure 7-4A, for example, may be partially due to (I) a "washout" of metabolic vasodilator factors from the interstitium by the excessive initial blood flow and forces that the increase in pressure imposes on the vessel walls. There is also a (2) a myogenic increase in arteriolar tone stimulated by the increase in stretching tissue pressure hypothesis of blood flow autoregulation for which it is assumed that an abrupt increase in arterial pressure causes transcapillary fluid filtration and thus leads to a gradual increase in interstitial fluid volume and pressure. This mechanism might be especially important in organs such as the kidney and brain whose volumes are constrained by external structures. Although not illustrated in Figure 7-4A, autoregulatory mechanisms operate in the opposite direction in response to a decrease in arterial pressure below the normal value. One important general consequence of local autoregulatory mecha nisms is that the steady-state blood flow in many organs tends to remain near the normal value over quite a wide range of arterial pressure. As discussed later, the inherent ability of certain organs to maintain adequate blood flow despite lower-than-normal arterial pressure is of considerable importance in situations such as shock from blood loss. Sympathetic vasoconstrictor nerves are the backbone of the system for controlling total peripheral resistance and are thus essential participants in global cardiovascular tasks such as regulating arterial blood pressure. Sympathetic vasoconstrictor nerves release norepinephrine from their terminal structures in amounts generally proportional to their action potential frequency. Norepinephrine causes an increase in the tone of arterioles after combining with an Ct1-adrenergic receptor on smooth muscle cells. Norepinephrine appears to increase vascular tone primarily by pharmacomechan ical means. Sympathetic vasoconstrictor nerves normally have a continual or tonic firing activity. When the fir ing rate of sympathetic vasoconstrictor nerves is increased above normal, arterioles constrict and cause organ blood flow to fall below normal. Conversely, vasodila tion and increased organ blood flow can be caused by sympathetic vasoconstrictor nerves if their normal tonic activity level is reduced. However, parasympathetic vaso dilator nerves, which release acetylcholine, are present in the vessels of the brain and the heart, but their influence on arteriolar tone in these organs appears to be inconsequential. Parasympathetic vasodilator nerves are also present in the vessels of the salivary glands, pancreas, and gastric mucosa where they have important influences on secretion and motility. In the external genitalia, they are respon sible for the vasodilation of inflow vessels responsible for promoting secretion and erection.
However antibiotic zosyn order 100mg vantin free shipping, there is general agreement that instrumental delivery antibiotics for uti enterococcus purchase vantin uk, fetal blood sampling and use of fetal scalp electrodes should be avoided antibiotic resistant urinary tract infection treatment buy vantin 100mg. Late amniocentesis is sometimes used to identify unaffected fetuses where delivery can safely proceed without intervention infection of the uterus 200 mg vantin otc. It is usually due to maternal medication that interferes with vitamin K, for example, anticonvulsants (phenobarbital, phenytoin), antituberculous therapy or oral anticoagulants. Some studies, but not others, suggest a link between intramuscular vitamin K at birth and later childhood malignancies. In healthy babies, the choice of which route of administration is increasingly being left to parents. D-dimers are increased, but are not specific and can be found in healthy neonates with no evidence of coagulopathy. Intracranial haemorrhage occurs in 10% of cases, with long-term neurodevelopmental sequelae in 20% of survivors. It usually presents in one of two clinical patterns: early onset thrombocytopenia (within 72 hours of birth) and late onset thrombocytopenia (after 72 hours of life) (Table 50. Neonates who have received intrauterine platelet transfusions should be given irradiated platelets to prevent transfusionassociated graft-versus-host disease. Instead, most centres now use a non-invasive approach relying on maternal intravenous IgG therapy during the second half of the pregnancy. In some cases neonatal thrombocytopenia is prolonged and may last up to 12 weeks before spontaneously resolving. Indications for platelet transfusion A number of countries have published consensus guidelines to help decide the indications for platelet transfusion in term and preterm neonates. Neonatal thrombosis: physiology and developmental aspects Neonates have an increased risk of thrombosis (2. This is largely due to the physiologically low levels of many of the inhibitors of coagulation and the frequent use of indwelling vascular catheters. Levels of plasminogen at birth are only 50% of adult values so neonates have a reduced ability to generate plasmin in response to fibrinolytic agents. Screening tests for thrombophilia in neonates the only inherited deficiencies for which there is a proven role in neonatal thrombosis are deficiencies in proteins C and S, which cause purpura fulminans, and deficiency of antithrombin, although presentation in the neonatal period is extremely rare. The role of thrombophilia screening in neonates is controversial, since the significance of any findings remains very difficult to assess, particularly since the risk of recurrence of thrombosis after an episode in the neonatal period is very low (3%). The diagnosis of protein C deficiency is made by the clinical picture and undetectable levels of protein C (<0. Protein-C-deficient heterozygotes rarely present as neonates and have low protein C levels, which may overlap with the lower limit of normal in the first few months of life, delaying diagnosis until 6 months or later. Treatment is with protein C concentrate (40 U/kg, aiming to maintain a plasma level >0. Protein S deficiency presents with identical features; levels of protein S are undetectable (<0. The rarity of thrombosis in neonates with protein S deficiency may in part reflect the relatively high level of active protein S because of the undetectable levels of C4b-binding protein. Antithrombin deficiency Homozygous antithrombin deficiency usually presents later in childhood, but neonatal deep venous thrombosis and inferior vena cava thrombosis have been reported. Treatment of catheter-related thrombosis depends on the severity and extent of thrombosis. If signs progress despite catheter removal, unfractionated heparin or low-molecular-weight heparin should be started using a dosing regimen adapted for neonates. Thrombolytic therapy with urokinase or tissue plasminogen activator has been used successfully for catheter-related thrombosis in neonates, but experience in preterm neonates is very limited. Excellent guidelines for antithrombotic therapy in neonates are regularly updated by the American College of Chest Physicians.
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