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Pelger-Huët anomaly An inherited benign condition characterized by the presence of functionally normal neutrophils with a bilobed or round nucleus discount chloramphenicol 250 mg on-line oral antibiotics for acne how long. Peripheral membrane Protein that is attached to the cell membrane by protein ionic or hydrogen bonds but is outside the lipid framework of the membrane discount chloramphenicol 500mg online antibiotics for uti pediatric. Petechiae Small discount chloramphenicol 250mg on line infection 5 metal militia, pinhead-sized purple spots caused by blood escaping from capillaries into intact skin. Phagocytosis Cellular process of cells engulfing and destroying a foreign particle through active cell membrane invagination. Phagolysosome A digestive vacuole (secondary lysosome) formed by the fusion of lysosomes and a phagosome. Phase microscopy A type of light microscopy in which an annular diaphragm is placed below or in the substage condenser, and a phase shifting element is placed in the rear focal plane of the objective. This causes alterations in the phases of light rays and increases the contrast between the cell and its surroundings. Phenotype the physical manifestation of an individual’s genotype, often referring to a particular genetic locus. Plasma cell A transformed, fully differentiated B lymphocyte normally found in the bone marrow and medullary cords of lymph nodes. May be seen in the circulation in certain infections and disorders associated with increased serum γ-globulins. The cell is characterized by the presence of an eccentric nucleus containing condensed, deeply staining chromatin and deep basophilic cytoplasm. The large Golgi apparatus next to the nucleus does not stain, leaving an obvious clear paranuclear area. Plasmacytosis the presence of plasma cells in the peripheral blood or an excess of plasma cells in the bone marrow. Plasminogen A β-globulin, single-chain glycoprotein that circulates in the blood as a zymogen. Large amounts of plasminogen are absorbed with the fibrin mass during clot formation. Platelets play an important role in primary hemostasis adhering to the ruptured blood vessel wall and aggregating to form a platelet plug over the injured area. Platelet activation Stimulation of a platelet that occurs when agonists bind to the platelet’s surface and transmit signals to the cell’s interior. Platelet aggregation Platelet-to-platelet interaction that results in a clumped mass; may occur in vitro or in vivo. Platelet factor 4 Protein present in platelet’s alpha granules that is capable of neutralizing heparin. Platelet procoagulant the property of platelets that enables activated activity coagulation factors and cofactors to adhere to the platelet surface during the formation of fibrin. Has the potential to self-renew, proliferate, and differentiate into erythrocytic, myelocytic, monocytic, lymphocytic, and megakaryocytic blood cell lineages. Poikilocytosis A term used to describe the presence of variations in the shape of erythrocytes. If stained with new methylene blue, these cells would show reticulum and would be identified as reticulocytes. Polyclonal gammopathy An alteration in immunoglobulin production that is characterized by an increase in immunoglobulins of more than one class. Polymorphic variants Variant morphology of a portion of a chromosome that has no clinical consequence. Substituents occupy each of the eight peripheral positions on the four pyrrole rings. Portland hemoglobin An embryonic hemoglobin found in the yolk sac and detectable up to eight weeks gestation. Postmitotic pool Also called the maturation-storage pool; the neutrophils in the bone marrow that are not capable of mitosis. Cells spend about 5—7 days in this compartment before being released to the peripheral blood. Primary aggregation the earliest association of platelets in an aggregate that is reversible. Primary fibrinolysis A clinical situation that occurs when there is a release of excessive quantities of plasminogen activators into the blood in the absence of fibrin clot formation. Excess plasmin degrades fibrinogen and the clotting factors, leading to a potentially dangerous hemorrhagic condition. Primary hemostasis the initial arrest of bleeding that occurs with blood vessel/platelet interaction. Primary thrombocytosis An increase in platelets that is not secondary to another condition. A probe is composed of a nucleotide sequence that is complementary to the sequence of interest and is therefore capable of hybridizing to that sequence. Procoagulant An inert precursor of a natural substance that is necessary for blood clotting or a property of anything that favors formation of a blood clot. Progenitor cell Parent or anscestor cells that differentiate into mature, functional cells. Prolymphocyte the immediate precursor cell of the lymphocyte; normally found in bone marrow. It is slightly smaller than the lymphoblast and has a lower nuclear to cytoplasmic ratio. Cytochemically, the cells stain positive for nonspecific esterase, peroxidase, acid phosphatase, and arylsulfatase. The distinguishing feature is the presence of large blue-black primary (azurophilic) granules. The granules contain acid phosphatase, myeloperoxidase, acid hydrolases, lysozyme, sulfated mucopolysaccharides, and other basic proteins. The cell is derived from the pluripotential stem cell and is found in the bone marrow. Prothrombinase complexA complex formed by coagulation factors Xa and V, calcium, and phospholipid. Prothrombin group the group of coagulation factors that are vitamin K-dependent for synthesis of their functional forms and that require calcium for binding to a phospholipid surface. This redistribution of cells accompanies vigorous exercise, epinephrine administration, anesthesia, convulsion, and anxiety states; also called immediate or shift neutrophilia. Pseudo—Pelger-Huët An acquired condition in which neutrophils cells display a hyposegmented nucleus. Unlike the real Pelger-Huët anomaly, the nucleus of this cell contains a significant amount of euchromatin and stains more lightly.
The vessels below the heart level are subjected to pressure caused by the weight of the column of blood extending from the heart to the level of the vessel order chloramphenicol mastercard infection belly button. This increase in pressure has two consequences; the distensible veins give way under the increased hydrostatic pressure discount chloramphenicol 500 mg mastercard infection lung, further distending them cheap chloramphenicol 250mg on line bacteria without cell wall, so that their capacity to accommodate blood is increased. Arteries are less distensible, so they do not expand like the veins to the same gravitational effects. In erect posture, much of the blood from the capillaries pools into the expanded veins, instead of returning to the heart. As venous return diminishes, cardiac output falls, and the effective circulating volume is decreased. Gravity increases pressure in the capillaries, causing excessive fluid to filter out of capillary beds in the lower limbs, producing edema of feet and ankles. Resultant fall in arterial blood pressure on standing from supine position, triggers sympathetic-induced venous vasoconstriction, which moves some of the pooled blood forward. The skeletal muscle pump ‘interrupts’ the column of blood by completely emptying veins blood segments intermittently so that a portion is not subject to the entire column of venous blood from the heart to its level. If a person stands still for a long time, blood flow to the brain is reduced because of the decline in effective circulating blood volume, despite reflexes targeted for maintaining arterial blood pressure, Decreased cerebral blood flow leads to fainting, which returns the person to a horizontal position, thereby eliminating the gravitational effects and restoring effective circulating volume toward normal. Effect of Venous Valves on Venous Return Both venoconstriction and skeletal muscle pump drive blood in the direction of the heart and not backwards because the large veins have one-way valves spaced at 2 - 4 cm gaps, permitting blood to move forward toward the heart but prevent it from moving backward toward the tissue. They also counteract gravitational effects in upright posture by helping minimizing the backflow of blood that tends to occur as a person stands up. Role of Respiratory Activity on Venous Return During respiratory excursions, the pressure within the thoracic cavity averages 5mm Hg less than atmospheric pressure. Blood returning from the lower body parts to heart travels through the chest cavity, where it is exposed to subatmospheric pressure. The venous system of the lower extremity and abdomen is exposed to normal atmospheric pressure. This pressure difference of about 5 mmHg subatmospheric, squeezes blood from lower veins to the chest veins, enhancing venous return. So during exercise, respiratory pump, skeletal muscle pump and venous vasoconstriction enhance venous return. Effect of Cardiac Suction on Venous Return the heart has role in its own filling with blood. During ventricular contraction, the trioventricular valves are pulled downward increasing the atrial cavities, as a result there 170 is transient drop in the atrial pressure, thus increasing vein-to-atria pressure gradient, so that venous return is facilitated. During ventricular relaxation, a transient negative pressure is created in the ventricle, so that blood is ‘sucked in’ from the atria and veins; thus the negative ventricular pressure increasing the vein-to-atria-to-ventricles pressure gradient, further enhancing venous return. The volume of blood returning to the left atrium from the lungs is the same volume, which was released by the right ventricle to the lungs; the output of the right and left ventricles is normally the same. It may be 20 –25 L/min in exercise and in very severe strenuous exercise in a trained athlete 35 – 40 L/min. During anytime, the volume of blood flowing through the pulmonary circulation is the same as flowing through the systemic circulation. Cardiac factors: heart rate & stroke volume, sympathetic stimulation and myocardial contractility; 2. The heart is a “demand pump” adjusting its output to the demand of the body organisms. This action potential spreads through the heart, inducing the heart to contract or have a “heart beat”. Atrial contraction is weakened by a reduction in the slow inward current carried by calcium, reducing the plateau phase. Thus, the heart beats slowly, atrial contraction is weaker, the time between atrial and ventricular contraction is stretched out. These actions are beneficial because parasympathetic controls heart activity in quiet relaxed condition of rest when body is not demanding increase in cardiac output. Sympathetic stimulation increases the rate of depolarization reaching threshold more rapidly mediated via norepinephrine by decreasing potassium permeability by inactivation of potassium channels; greater frequency of action potential and corresponding more rapid heart rate. The overall effect of sympathetic stimulation is to increase heart rate, decrease conduction time, and increase force of myocardial contraction. Heart rate is increased by simultaneous stimulation of sympathetic and inhibition of parasympathetic activity. A decrease in heart rate by stimulating parasympathetic and inhibiting sympathetic activity. These two autonomic branches to the heart in turn are primarily controlled by the cardiovascular control centers in the brain stem. Medullary epinephrine too acts on the heart in a manner similar to postganglionic sympathetic neurotransmitter norepinephrine, thus, reinforcing the direct effects of the sympathetic nerves. Intrinsic control related to the extent of venous return heterometric auto- regulation, a length-tension relationship, or Frank-Starling Mechanism; and 2. Extrinsic control related to the extent of sympathetic stimulation of the heart - the homeometric regulation depending on extrinsic nerves and hormones (medullary catecholamine). Increased End Diastolic Volume Results In Increase in Stroke Volume As more blood returns to the heart, the heart pump more blood but does not empty all the blood it contains. This control depends on the length-tension relationship of cardiac muscle, similar to that of skeletal muscle. An increase in cardiac muscle fiber length increases the contractile tension of the heart on the following systole. The main determinant of cardiac muscle fiber length is the degree of ventricular filling during diastole. The greater the extent of ventricular filling, during diastole, larger is the end-diastolic-volume and more is the heart stretching. Therefore, with more stretch, the longer the initial cardiac muscle fiber length in diastole before contraction in systole. Thus, increased length results in a greater force on the subsequent cardiac contraction, and therefore, a greater stroke volume. The extent of filling is known as ‘preload’, because it is the workload imposed on the heart before contraction begins. The most important of this extrinsic control is the action of cardiac sympathetic nerves and epinephrine; both increase the heart’s contractility leading to more complete ejection. The increased contractility is due to the increased calcium influx triggered by norepinephrine and eipnephrine. Increased cytosolic calcium ion concentration generates more force of contraction through greater cross-bridge cycling than would be possible without sympathetic stimulation. The ability of the heart to increase cardiac output to meet body’s demands as a person grows older, i. It may be on account of reduced norepinephrine from the sympathetic postganglionic neurons; it is related to diminished calcium-mediated exocytosis of neurotransmitter - eventually to do with the calcium channels. During systole, ventricles need to generate sufficient pressure to exceed the blood pressure in the major elastic arteries in order to force open the aortic valve. The arterial blood pressure is referred to as the ‘after-load’, because it is the workload imposed on the heart after the contraction begins. The heart undergoes compensatory hypertrophy for a sustained increase in afterload, enabling it to contract with more force maintaining a normal stroke volume despite the impedance to ejection.
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