The release of paracrine substances from the endothelium as well as other transport phenomena is stimulated by increased shear stress on the endothelial cells that line the arteries buy endep 10 mg on line medications list template. These factors are instrumental in stimulating capillary growth and endothelial repair and may be the link between the growth of new blood vessels in skeletal muscle and periodic increases in muscle blood flow during aerobic exercise training discount endep 10 mg overnight delivery medicine 853. In atherosclerosis generic endep 50mg overnight delivery medications to treat anxiety, plaque formation is reduced in areas of high shear but increased in low shear areas of arteries (see Clinical Focus 11. This results in mitotic activation of arterial smooth muscle cells, which migrate into the intima, as well as the activation of monocytes, which transform into macrophages that engulf lipid to become foam cells. These factors stimulate intimal thickening and smooth muscle cell growth with infiltrates the intima. These processes create an inwardly directed growth of the arterial wall, which encroaches on the arterial lumen and creates the appearance of fatty streaks on the inner arterial wall. Over time, this streak grows with the accumulation of extracellular matrix proteins, the development of a fibrous cap over the atheroma, and the development of a lipid- laden necrotic core-containing debris, foam cells, crystallized cholesterol, and calcium deposits. Atherosclerotic plaques usually only develop in a portion of the circumference of the arterial wall. The wall opposite the plaque can actively contract in response to vasoconstrictor stimuli, whereas the wall beneath the plaque becomes weakened, creating an arterial aneurysm that can rupture. Atherosclerotic plaques stimulate platelet aggregation and blood clot formation that can totally occlude an artery. Furthermore, the plaque is friable and can rupture, spilling debris into the arterial lumen, which further stimulate clot formation. Plaque rupture in the arteries of the heart is a primary cause of death from heart attack. Branch points and curvatures alter flow velocity and shear stress at the arterial wall; these are decreased along the inner curvature of a flow stream and at the upstream edge of branch points. It is well known that plaque formation in the vascular system does not occur either uniformly or totally randomly in the vascular tree. Instead, it develops at branch points and bifurcations and along the inner curvature of arteries. The anatomic characteristics of the coronary arteries, the bifurcation of the common carotid arteries, and the entry to the renal arteries make these regions especially susceptible to the accumulation of atherosclerotic plaques and thus place the blood supply to the heart, the brain, and the kidneys at risk. Normally, blood cells flow in a streamlined or bullet-shaped profile with the concentric layers of fluid flow in arteries as illustrated in Figure 11. In three dimensions, this can be envisioned as a set of thin telescoping cylindrical layers projecting from the inner arterial wall out uniformly to the center of the vessel. Flow velocity is highest in the center of a streamline blood flow and lowest adjacent to the inner arterial wall. However, if total flow velocity becomes too high in an artery, the kinetic energy of the flow streams overcomes the tendency of the fluid layers to stick together from viscous forces. Turbulence is a wasteful process that dissipates pressure energy in the cardiovascular system, which could otherwise be used to produce flow. The tendency to produce turbulent flow is expressed in a mathematical term called the Reynolds number, Re. The Reynolds number is a measure of the ratio of kinetic energy in the system (which will pull fluid layers apart) and the viscous component of the system (which holds the fluid layers together). It is represented by (9) where ρ = fluid density, D = inner vessel diameter, v = flow velocity, and η = blood viscosity. Clearly, large-diameter vessels, high flow velocity, and low blood viscosity favor turbulence in the cardiovascular system. Certain diseases, such as atherosclerosis and rheumatic fever, can scar the aortic or pulmonic valves, creating narrow openings and high flow velocities when blood is forced through them. A clinician can detect this problem by listening to the noise created by the resultant turbulence. The fluid dynamic properties of blood are more complicated than they are for a simple homogenous fluid such as water because blood is a suspension of proteins and cells in an aqueous medium. The presence of proteins and cells in blood has two important hemodynamic consequences. First, blood viscosity increases exponentially as the blood hematocrit increases (Fig. Thus, as the hematocrit increases, the flow resistance against which the heart must pump increases, which substantially increases the cardiac workload. Although there are some pathologic instances in which a patient’s hematocrit can increase because of overproduction of red blood cells (e. This can occur in severe dehydration, loss of plasma from severe burns, or inappropriate loss of water through the renal system as a consequence of kidney disease. Secondly, red blood cells tend to clump if blood flow velocity is sluggish (see Fig. This clumping raises blood viscosity, which can be a negative complicating factor in any condition that adversely diminishes the overall flow output of the heart, such as circulatory shock or heart failure. Thus, the resistance to flow is higher in a slow-moving arterial stream than in one that moves with high velocity. Axial streaming of cells in flowing blood Application of Poiseuille’s law to fluid dynamics assumes that the fluid is homogeneous, that is, it is made of one element of uniform composition, such as water. Although all suspensions are nonhomogeneous fluids, the properties of blood cells flowing in arteries are such that blood behaves hemodynamically as if it were a homogeneous fluid. Blood cells tend to compact densely in the center of the flow stream, leaving a thin layer of cell-free plasma against the vascular wall. As such, blood flows more as a compact bulk fluid than as a mixed conglomeration of particles in suspension. For this reason, Poiseuille’s law can be applied to the cardiovascular system as it was written. However, axial streaming of blood does tend to separate this bulk flow into two components of different viscosities. The fluid near the vessel wall is essentially cell-free plasma and has a viscosity of only 1. In large vessels such as the aorta, this low-viscosity layer is only a small percentage of the average viscosity of the flow stream. Thus, for all practical purposes, the viscosity of the blood flowing through the entire aortic cross-section can be considered to be 4 cP. However, in small arterioles (<300 μm interior diameter) and capillaries, this thin layer becomes a greater percentage of the total volume contained within the vessel and thus contributes a greater percentage to the total viscosity of the blood traveling through those vessels. When fluid flows through these smaller vessels, fluid viscosity, as a whole, decreases. This is called the Fahraeus-Lindqvist effect, and it is responsible for reducing blood viscosity, and therefore, flow resistance when blood flows through extremely small vessels such as capillaries. This makes it easier for blood to flow through vessels that otherwise have extremely high resistances.
One week later intraocular pressure is normal cheap endep generic medications similar buspar, and intraocular inflammation has subsided purchase discount endep on-line medicine wheel images. The patient returns 2 days later with recurrence of pain and photophobia and return of intraocular inflammation buy endep 10 mg free shipping medicine 93 3109. A useful rule is to decrease steroids by no more than half of the previous dose, especially in herpetic keratouveitis, in which rebound inflammation is frequent. Sometimes patients abruptly stop the eyedrops when they feel better and then suffer rebound inflammation. The resulting changes in the ocular surface can cause ocular discomfort, scarring, and, in severe cases, loss of vision and perforation. The outer layer is a thin lipid layer produced by the meibomian glands, which open along the upper and lower lid margins. The middle layer, the thickest, is composed of aqueous produced from the main and accessory lacrimal glands. Also, an abnormal lid contour as in ectropion or lid tumor, or poor blinking found in Bell’s palsy. It supplies oxygen from the atmosphere to the corneal epithelium, washes away debris, and has antibacterial properties due to IgA, lysozyme, and lactoferrin present within it. It covers the villus surface of the corneal epithelium, converting it from a hydrophobic surface to a hydrophilic one thus allowing the aqueous layer to lubricate the cornea. Patients with cicatricial ocular pemphigoid, Stevens-Johnson syndrome, chemical burns (especially alkali), and graft-versus-host disease in bone marrow transplantation may have dry eye. Patients with other conjunctival disorders that accompany conditions such as aniridia may also have dry eyes. A normal blink reflex, normal lid anatomy and contour, and a normal corneal epithelium. Burning, irritation, foreign body sensation, light sensitivity, and blurred vision. Usually, the symptoms are worse in the afternoon and evening and better on awakening. A dry or dusty environment may cause more difficulties in patients with dry eye then others. Symptoms are worse in low humidity environments, such as those with central air and in an airplane, during prolonged reading and driving with a decreased blink rate due to increased concentration, and windy conditions. In the early stages, ocular symptoms may be more impressive than what is found on the examination. Signs of dry eye include a decreased tear meniscus, debris in the tear film, conjunctival injection, and superficial punctate keratitis and conjunctivitis. Abnormal fluorescein or rose bengal staining of the corneal and conjunctival epithelium in the exposed interpalpebral fissure (at 3 and 9 o’clock) of the lower third of the cornea is often present. In more severe disease, filamentary keratitis can develop as well as corneal scarring. Rheumatoid arthritis is the most common, but systemic lupus erythematosus, Wegener’s granulomatosis, scleroderma, systemic sclerosis, and primary biliary cirrhosis may also be associated. Women are more likely to develop this than men, probably in relation to changes in hormone levels. It can occur in patients in their 20s and 30s, but may be overlooked unless patients are specifically questioned about symptoms. Rose bengal stains mucin and epithelial cells that are dead or devitalized, but still in place. If a patient has a normal exam, but describes typical dry eye, treatment should still be instituted. Lacrisert is a solid form of artificial tear placed in the lower cul-de-sac that melts over a period of 12 hours. It will blur vision, but may be necessary during the day if exposure is a significant problem, as in Bell’s palsy. Patients should also be counseled to avoid conditions with low humidity such as central air heating, to prevent air from blowing into their eyes as from an air conditioner vent at home or in the car, and to use a humidifier while sleeping and at work if possible. Lubrication may need to be increased while flying, as airplane cabins have very low humidity, and while reading or studying, as the blink reflex is decreased. What if the patient uses tears six to eight times a day and returns with red, painful eyes and more superficial punctate keratitis? Patients who use tears every 2 hours or more may benefit from closing the lower puncta. Occasionally, epiphora may result from overflow tearing and the plug can quickly be removed in the office. If the patient is comfortable with this, but the plug falls out, permanent closure can be done by using cautery. Between 10% and 20% of the tear film is drained through the upper puncta, and these may be closed subsequently if the lower lid punctal closure is not adequate to control symptoms. Frequent tear use may make symptoms worse if the patient is sensitive to the preservatives. Occlude the lower lid puncta first and then proceed to upper lid punctal occlusion. A patient with punctal occlusion returns with more irritation and burning since the procedure was done. If a patient has significant blepharitis, the symptoms can worsen after punctal occlusion. The debris is trapped and not drained and now has a higher concentration than before. Topical cyclosporine (Restasis) has been used recently as it decreases cell-mediated inflammation of the lacrimal tissue and ultimately can increase tear production. Patients need to use it twice a day for 1–3 months to get a response and then continue for up to 6 months or more. Acetylcysteine is a mucolytic agent used to break up mucous in patients that have filamentary keratitis and mucous plaques. Systemic medications that can decrease tear production include antimuscarinics (scopolamine, Detrol), antihistamines, lithium, diuretics, estrogens (including birth control pills), antihypertensives (b-blockers, a-agonists), antidepressants, chemotherapy agents, antipsychotics, marijuana, and morphine. Corneal dystrophies are bilateral, inherited, noninflammatory, commonly progressive alterations of the cornea that are usually not associated with any other systemic condition. Because each dystrophy may exhibit a spectrum of clinical manifestations, examining multiple family members frequently aids in establishing the diagnosis. In contrast to dystrophies, degenerations are unilateral or bilateral aging changes that are not inherited. Examples are Meesmann’s juvenile epithelial dystrophy, epithelial basement membrane dystrophy, and corneal dystrophies of Bowman’s layer. Epithelial basement membrane dystrophy is by far the most common anterior membrane dystrophy. Areas of extra basement membrane result in maplike and/or fingerprint changes as well as intraepithelial microcysts.
One study has reported an association between keratoconus and false chordae tendineae in the left ventricle cheap endep 10mg with visa medicine 014. The relationship between various connective tissue diseases and keratoconus suggests a common defect in the synthesis of connective tissue order 50 mg endep visa medicine 3x a day. Keratoconus has been described in association with various ocular diseases order 75 mg endep fast delivery symptoms webmd, including retinitis pigmentosa, Leber’s congenital amaurosis, vernal conjunctivitis, floppy eyelid syndrome, corneal endothelial dystrophy, and posterior polymorphous corneal dystrophy. Vision becomes progressively more blurred and distorted with associated glare, halos around lights, light sensitivity, and ocular irritation. Corneal topography can document the presence of keratoconus even before keratometric or slit- lamp findings become apparent. Placido rings of light are reflected off the cornea, and corneal curvature is derived from the distance between the rings and displayed as a color-coded map. An irregular light reflex with scissoring on retinoscopy can be appreciated through the dilated pupil. As the disease progresses, the cornea steepens and thins with irregularity of the mires on keratometry and development of obvious keratoconus on slit-lamp examination. The characteristic sign of keratoconus on topography is inferior midperipheral steepening (Fig. Numerous studies have tried to develop quantitative topographic parameters to define keratoconus. However, it may be difficult to make a definitive diagnosis of keratoconus based on topographic findings alone. This is of particular importance in patients seeking refractive surgery because the results of the surgery are poorly predictable in patients with keratoconus. Patients with apparently normal corneas may have inferior midperipheral steepening >1. It is difficult to know whether such patients represent a forme fruste of keratoconus and, as such, should be dissuaded from considering refractive surgery. These instruments also present standard placido disc color maps as well as thickness measurements all across the cornea. The additional information can be helpful in differentiating between forme fruste or early keratoconus and asymmetric astigmatism in nonkeratoconic corneas. The earliest slit-lamp signs of keratoconus are apical thinning and steepening, usually located inferior to the center of the pupil. As the keratoconus progresses, the thinning and ectasia become more prominent with the development of apical scarring that begins in the anterior stroma and then appears in the deeper layers of the stroma (Figs. Fine linear striae become apparent in the deep stroma just anterior to Descemet’s membrane, usually oriented vertically or obliquely. They can be made to disappear when the intraocular pressure is transiently raised by applying external pressure to the globe. Moreover, in some mild cases of keratoconus, the pressure from rigid gas-permeable contact lens wear can induce the formation of such striae, which disappear when the lens is removed. A Fleischer ring is commonly seen outlining the base of the cone, the result of hemosiderin Figure 13-3. Apical thinning and scarring pigment deposition within the deeper demonstrated in slit beam. A Fleischer ring may outline the cone only partially but, as the ectasia progresses, tends to become a complete circle with more dense accumulation of pigmentation that is best appreciated while viewing the cobalt blue filter on the slit lamp. Subepithelial fibrillary lines have been described in a concentric circular fashion just inside the Fleischer ring. The source of these fibrils is unknown but has been postulated as epithelial nerve filaments. Cobalt blue illumination demonstrating Bowman’s membrane are sometimes Fleischer ring outlining the extent of the cone. In the more advanced stages, when the eye is rotated downward, the corneal ectasia causes protrusion of the lower lid, which is known as Munson’s sign. The onset of keratoconus characteristically occurs in the mid to late teens, progressing slowly for several years before stabilizing. As the disease progresses, the corneal thinning and ectasia become more prominent with increasing apical scarring. Two types of cones have been described: (1) a small round or nipple-shaped cone that tends to be more central in location, and (2) an oval or sagging cone that is usually larger and displaced inferiorly, with the thinning extending close to the inferior limbus. Progression of keratoconus tends to manifest as increased thinning and protrusion, although enlargement of the cone also occurs with extension peripherally. Ruptures in Descemet’s membrane allow aqueous to enter into the corneal stroma, resulting in marked thickening and opacification of the cornea that is usually restricted to the cone. The involved stroma becomes massively thickened with large, fluid-filled clefts, overlying epithelial edema, and bulla formation. Rarely, a fistulous tract may develop, with resultant leakage of aqueous through the fluid-filled stroma and epithelium on the corneal surface. The corneal edema gradually resolves over weeks to months as endothelial cells adjacent to the rupture in Descemet’s membrane enlarge and migrate across the defect, laying down new Descemet’s membrane. With healing, scarring tends to flatten the cornea, thereby facilitating the possibility of subsequent contact lens fitting. Some corneas with acute hydrops tend to develop stromal neovascularization that increases the potential risk of graft rejection if corneal transplantation becomes necessary. Acute hydrops is more common in patients with Down syndrome and vernal kerato- conjunctivitis, presumably related to the repeated trauma of eye rubbing in these patients. Most cases of acute hydrops resolve spontaneously, requiring supportive treatment with topical hyperosmotic agents such as 5% sodium chloride drops and/or ointment to promote corneal deturgescence. Some patients with acute hydrops complain of severe photophobia and benefit from the use of topical steroids and/or cycloplegic agents. In addition, topical steroids should be instituted in patients with signs of corneal neovascularization. Once the hydrops has resolved, the patient can then try to resume contact lens wear if the central cornea has not become excessively scarred. Most histopathologic studies of keratoconic corneas are performed on advanced cases that require penetrating keratoplasty. In addition, most patients were previous long-term contact lens wearers, which also may affect the histopathologic findings. The apical epithelium tends to be flattened and thinned with scattered fragmentation and dehiscence of the epithelial basement membrane. Iron can be demonstrated in the epithelial cells outlining the cone, corresponding to the Fleischer ring. Among the most characteristic histologic changes of keratoconus are breaks in Bowman’s membrane that are sometimes filled with epithelium and/or stromal collagen. Ultimately, the anterior corneal stroma may become replaced with irregularly arranged connective tissue. Depending on the stage of the reparative process, breaks in Descemet’s membrane with curled edges subsequently become covered by adjacent endothelial cells that slide over and lay down new membrane. The corneal endothelial cells tend to be normal, although they may exhibit increased pleomorphism. However, as the keratoconus progresses and the amount of irregular astigmatism increases, patients become unable to obtain satisfactory vision with spectacle correction.
Not seen in paroxysmal nocturnal hemoglobinuria is: insignifcant and the person is not on any medication order endep with amex treatment stye. His blood pressure is 120/80 mmHg discount 10 mg endep free shipping medicine vs nursing, pulse is (c) Decreased leukocyte alkaline phosphatase 72/mm buy endep 25 mg otc treatment zit, temperature is 36. A 20-year-old man John Abraham is transported to the emergency department within 20 minutes of sustain- release hemoglobin. If it is presumed that he may have (a) Cirrhosis and hepatocellular carcinoma lost about 1. A 16-year-old female Gitika notices that her urine (b) Decreased hematocrit becomes red after she is given sulfonamides for (c) Decreased blood pressure treatment of a urinary tract infection. Both urine and (d) Decreased red blood cell count serum test positive for free hemoglobin, and the urine 95. The dis- smear shows normocytic and normochromic red cells trict has high endemicity of malaria. Dubey gives him primaquine chemoprophylaxis following substances is most likely responsible for for Plasmodium vivax malaria. Singh develops anemia, (a) Alpha-chain of hemoglobin hemoglobinemia, and hemoglobinuria. Special studies (b) Beta-chain of hemoglobin will likely reveal an abnormality in which of the fol- lowing? An infant presents with mild anemia, jaundice, and (c) Intrinsic factor splenomegaly. A 38-year-old male Kritesh presents to his physician The parents state that several relatives have also with the complaints of sudden onset of fever, chills suffered from a similar illness. A 6yrs old child belonging to Punjabi family with past history of blood transfusions presented with (b) Acute myelomonocytic leukemia hemoglobin 3. A 14-year-old male Kaalu is brought to the emergency (b) One altered peptide of HbS migrates faster towards room with high grade fever, chest pain, and dyspnea. Evaluation today the polymer and cause sickling of the red blood cells reveals a hematocrit of 23% and reticulocyte count of (d) Lowering the concentration of deoxygenated HbS 9%. Several hours after being admitted, the patient dies can prevent sickling in the hospital. At autopsy, the patient’s spleen is frm and brown; this fnding is most likely related to: 111. The hemoglobin electrophoresis shows (e) Target cell are present the following: Hb A 60% and Hb S 40%. Sickle cell anemia is the clinical manifestation of sickle cell anemia and thalassemia major? Hemoglobin H disease is caused by deletion of: Most Recent Questions (a) A single a globin gene (Karnataka 2009) (b) Two a globin genes 121. Which of the following regarding Bombay blood group (d) Relative excess of β, γ, and δ chains is false? In sickle cell anemia defect is in which chain: (b) Lack of H, A and B substance in saliva (a) Alpha chain (b) Beta chain (c) Lack of antigens of several blood group systems (c) Both the chains (d) None of these (d) H, A and B antibody will always be present in serum 121. Which of the following is the genotype of a person with (a) Altered stability blood group A? A 18 year old Afro American boy presenting with a non anticoagulant will you use for sending your sample? Most (c) Potassium oxalate + sodium fuoride likely cause is: (d) Tri Sodium citrate (a) Trinucleotide repeat 127. Molecular pathogenesis of α thalassemia involves (c) Polychromasia (a) Mutation in transcription sequence (d) Elliptocytosis (b) Gene deletion 128. One of the common variants of sickle cell anemia (d) Electrolyte imbalance frequently marked by lesser degree of haemolytic anemia and greater propensity for the development of 129. Stored plasma is defcient in (a) HbA (b) HbA (a) Factors 7 and 8 2 1 (c) HbA (d) HbA (b) Factors 5 and 7 1c 1b (c) Factors 5 and 8 141. Bence Jones protein in urine are due to the presence of (d) Factors 5, 7 and 8 (a) Light chain of monoclonal immunoglobulins (b) Heavy chain of monoclonal immunoglobulins 141. Carbohydrate present in blood group substance is (c) Light chain of polyclonal immunoglobulins (a) Fucose (b) Deoxyribose (d) Heavy chain of polyclonal immunoglobulins (c) Ribulose (d) Ribose 141. Erythropoietin is normally released from the kidney in response to hypoxic or anemic conditions. The proerythroblast (option c) is the frst recognizable cell in the red cell lineage. The reticulocyte (option d) is the enucleated cell just before the mature red blood cell. It is not directly stimulated by erythropoietin, but increases in number as a result of the increase in precursors. The commonest cause is metastatic cancer, most often carcinomas arising in the breast, lung, and prostate. This is due to disturbance of mechanisms regulating the egress of red cells and granulocytes from the marrow. Though it has the name purpura, but the platelet count in this condition is normal. Conditions with altered albumin globulin ratio High Albumin Globulin Ratio Low Albumin Globulin Ratio • Hypothyroidism • Overproduction of globulins in conditions like multiple myeloma, chronic infections and • Hypogammaglobulinemia in some autoimmune diseases. So, hemoglobin = 4 globins + 4 heme groups Since each heme molecule contains an iron, so total iron atoms present in hemoglobin are 4 in number. Release of O2 from oxy Hb at the tissues is accompanied by uptake of protons due to lowering of the pKa of histidine residues. If whole blood is allowed to clot and the clot is removed, the remaining fuid is called serum. Ferroportin is a transmembrane protein that transports iron from the inside of a cell to the outside of it. It makes it possible to see the reticuloflamentous pattern of ribosomes characteristically precipitated in these live immature red blood cells. Please be clear of the concept friends that the reticulocyte count is increased when the megaloblastic anemia is being treated with vitamin B12 and folate supplementation i. The presence of red cells that are macrocytic and oval (macro-ovalocytes) is highly characteristic. There is presence of marked variation in the size (anisocytosis) and shape (poikilocytosis) of red cells. Nucleated red cell progenitors occasionally appear in the circulating blood when anemia is severe. Granulocytic precursors also display dysmaturation in the form of giant metamyelocytes and band forms.
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