The role of a doctor-dentist in early diagnostics and prophylaxis.
Glomerulonephritis and pyelonephritis. Urolithiasis. Etiology, pathogenesis. Diagnostics. Clinical picture. Complications. Principles of treatment. The role of a doctor-dentist in early diagnostics and prophylaxis. As. of prof. Vereshchahina N.Y. What do the kidneys do. 1. remove toxic waste products 2
What do the kidneys do?1. remove toxic wasteproducts2. remove excess waterand salts3. take part in controllingyour blood pressure4. produce erythropoietin(epo for short) which stimulates red cell production from the bone marrow - you get anaemic without this5. help to keep calcium and phosphate in balance for healthy bones6. maintain the blood in a neutral (non-acid) state Signs, which point on kidney affection
main pain in lumbar region, urination disoders, change of urine, oedema. secondary chills, headache, dizziness, vision deranged, heart pain, skin itching, loss of appetite, nausea, vomiting , fever. Pain in lumbar region Pain is caused by: stretching of kidney capsule,
spasm of urethers, inflammation of peryrenal cellular tissue, kidneys infarction. Intensity of the pain feelings can be different from dull, boring pain (at acute and exacerbation of chronic pyelonephritis)-to sharp, very severe pain with an irradiation along ureters,in a groin, in genitals, in the front surface of thigh(nephrocolic which arises up as a result of ureter corking with astone, at his bend, at the trauma of kidneys, kidneys infarction). Urination disoders Oliguriya (decreasing ofurine excretion of less than 500 ml per day). Anurya (complete stop ofurine excretion - symptom of acute kidney insufficiency, mechanical obstacles of urine passage (stone, tumour). Nycturia (advantage of nightly diuresis above daily ( normaly 1:2); Dysuriya (painful urination) Polakiuriya (frequent urination, which combines with polyuria at chronic nephritis, cystitis). Isosthenuria (At disorders of dilution and concentration function of kidneys specific gravity is ) Oedema Often oedema is the first sign of such diseases.
are one among the main symptoms of renal pathology. Often oedema is the first sign of such diseases. Renal oedema can suddenly develop as well as disappear. As a rulethey are located on the face especially on eyeleads (where the subcutaneous fat tissue is more loose ). Sometimes oedema is equally distributed all over the body (anasarka). Oedema have mild consistency, deep elevation of skin is present even inslight pressing on it. Oedema can spread on internal organs and cavities (profound oedema)with accumulation of transsudate in serous cavities pleural, abdominal and pericardial cavities. Uric syndrome. moderate proteinuria (from 100 mg up to 3,5 g a day),
red blood cells in the urine more than 1106/L per day (erythrocyturia), leukocyturia - more than 1106/l per day), custs in urine, bacteriuria, discharging of salts and their cristals with urine cells of renal andtransitional epithelium and other elements of pathological both organized and non- organized renal sediments, The leading symptom in uric syndrome is proteinuria (albuminuria). (custs in urine) (sieges) Nephrotic syndrome. A massive leak of protein (albumin) into the urine (proteinuria) (more than 3,5 gr per day). A low blood level of albumin due to the large amounts lost in the urine (hypoproteinemiamostly because of hypoalbuminemia). An increased level of cholesterol in the blood (hyperlipidemia). Retention of fluid in the body (edema) causing swelling. Hypercoagulation. Renal arterial hypertension.
This is symptomatic hypertension caused by affection of kidneys or renal vessels with following disorders of blood pressure regulation. Elevation of blood pressure is caused by 3 mechanisms: 1.sodium and water retention, 2.activation of pressor system, 3.inhibition of depressory mechanisms. Acute nephritic syndrome.
It is characterized by the abrupt onset (days) of haematuria with red blood cells, casts or dysmorphic red blood cells appearing in the urine, proteinuria, renal impairement (oliguria, uremia, raised urea and creatitine), hypertension due to water and salt retention, edema (usually periodical). What is glomerulonephritis?
Diffuse glomerulonephritis is the general infectious-allergic disease with prevalent and primary envolvement of nephrone glomerular apparatus into thepathological process. Glomerulonephritis is a type of glomerular kidney disease in which the kidneys' filters become inflamed and scarred, and slowly lose their ability to remove wastes and excess fluid from the blood to make urine. Types of glomerulonephritis include kidney disease of diabetes, IgA nephropathy, andlupus nephritis. Classification (by L. Pyrih)
The following forms of glomerulonephrites are determined I. Acute diffuseglomerulonephritis : uric syndrome; nephrotic syndrome (mostlyhaematuria, hypertension and edema are present). II. Subacute fulminant glomerulonephritis. III. Quickly progressing glomerulonephritis. IV. Chronic glomerulonephriis: 1sttype: primary chronic, secondary chronic. 2. syndromes:uric, nephrotic. 3. stages: non-hypertensive, hypertensive; chronic renal failure; 4. phase: exacerbation, remission. Acute glomerulonephritis (AG, lat. - glomerulonephritis cut).
This is acute immune inflammatory lesion of kidneys parenchima with primary damage of glomerules and following involvement of all renal structures into the pathological process. Ethiology and pathogenesis
AG develops 2-3 weeks after acure infectious disease (tonsillitis pharyngitis skarlet fever morerarely etysipelas etc.) caused by -haemolytic streptococcus, group A or by otherbacteriological agents(pneumococus,staphylococcus, viruses). The process develops asa hyperergic reaction of sensebilized organism. Administration of serum preparations, other medical preparations,vaccination, penetration of toxic substances into the organism, deranged venous outflow from kidneys may be the causes of AG. Provoking factors are overooling, dump weather, traumas. 2.Ischaemia of the glomeruli;
Pathological anatomy 1. Enlarged and hyperaemic glomeruli; 2.Ischaemia of the glomeruli; 3. Fibrinoid swelling of the capillary walls, proliferation of their endothelium; 4. Accumulation of coagulated proteinous exudates in the space between the capillary loops and the glomerular capsule, blood stasis, thrombosis of the capillary loops, and hemorrhages. This symptoms are combined in following syndromes: hypertension, uric syndrom, aedema
Uric syndrome is presence of proteinin the urine, blood formed elements, casts. Even at the beginning of the disease urine colour is changed because of blood admixtures. Urine has the colour of meet wastes. Erythrocytes quantity at the peak of the disease is about100200 in a vision field. Hypertension occurs due to activation of renin-angiotensin-aldosterone and sympathoadrenalsystems as well as water and salt retenstion in the organism and inhibition of depressor systems. Blood pressure elevates from insignificant level till mm Hg(systolic) and 120 mm Hg(diastolic one). Main complaints of these patients are: headache, heaviness in the head, dyspnea, palpitation, nausea and sometimes periodical imparement of vision. Data of general inspection:
patients appearance is quite specific and it is called facies nephritic a: skin paleness, swelling of the face and eyeleads edema under the eyes, Patients condition is heavy, his posture in bed may be forced sitting or semirecumbent. Palpation: pulse is full, dull and slow
Palpation: pulse is full,dull and slow. Apex beat is intensified and displaced leftward.Percussion: may reveal fluid in pleural cavity, lung congestion and displacement of left heart border leftward. :Auscultation: bradicardia, I heart sound is weakened, systolic murmur over heart apex,accentuation of the II heart sound over the aorta.In severe cases especially in left ventricular hyperthrophy hallop rhythm occurs. Vesicular breathing is heard over the lungs. Laboratory methods of examination:
Total blood count: moderate leukocytosis anaemia accelerated ESR. iochemical blood analysis increased content of seromucoid, sialic acids fibrinogen, C-reactive protein, antistreptoliase, immune complexes,2- -globulines. Instrumental methods of examination:
Eye grunds: narrowing of arterioles, dilatation of veins, sometimes - aedema of ophthalmic nerve, hemorrhage into the retina. ECG overloading and hyperthrophy of the left ventricle decreased voltage of R, depression of ST interval, T is low of biphasic. X-ray examinationof the chest: probable presence of fluid in pleural cavity signs of lung congestion, enlargement of the right ventricle. Treatment: bed regimen for 1-15 months dry and warm ambient temterature. Diet 7, limitation of salt ( to 05-15 gr a day)liquid. Medicamentous treatment antibiotics for 7-10 days (penicillin or semisynthetic penicillins). Hypotensive agents: sedative (valerian mothewortbromine tranquilizers) antiadrenergic preparations (apressin clonidine metildopum, -bloquers) in combination withsaluretics, losartan (angiotensin converting enzyme inhibitor), perypheric vasodilatators. Diuretics (in edema, heart failure, hypertension). Pathogenetic therapy immunodepressants glucocorticoids agents that improve haemosthasis and microcirculation (indometacin tiklopidine, curantyl heparin). Chronic glomerulonephritis
(glomerulonephritis chronica, ChG) is inflammatory process in renal glomeruli degeneration of canalicular epithelium and progressive development of connective tissue thatresulting in secondary shrinked kidney. Ethiology and pathogenesis. Often ChG develops after acute glomerulonephritis. If information about AG in patients anamnesis is abcent than thay speak about primary form of ChG Clinical picture. In unhypertensive stage: general weakness, quick fatigue, dull boring pain in lumbar region,change of urine colour, edema below eyes and on the face, on the legs. In hypertensive stage: the same plus headache, dizziness, periodical nassal bleeding, dyspnoe, nictural dyspnoe, palpitation. Data of inspection: patients condition is satisfactory in remission but in exacerbation may be severe. Skin is pale, edema are visible on the face (below the eyes (facies nephritica). Sedimentation of uric acid cristals is possible on the skin. Inspection of precordial region: displacement of apex beat leftward from the left midclavicular line. In dilatation of the left ventricleapex beat becomes diffuse. Palpation: Apex beat is intensified, diffuse and displaced leftward
Palpation: Apex beat is intensified, diffuse and displaced leftward.Percussion:the left border of relative heart dullness is displaced leftward from the left midclavicular line inV interspace. Palpation of organs of abdominal cavity: is painful in epigastrium and above the large bowel. In the case of right ventricular failure the liver is enlarged. Auscultation: in patients with left ventricular failure moist rales may be heard in lover parts of the lungs (because of lung congestion).Heart soungs are intensified but later become weakened, accenttuation of the II sound is heard over the aorta, systolic murmur over the apex. In terminal stage pericardial friction sound may be haerd on the hart basis, along the left sternal border and in zone of absolute heart dullness.Blood pressure is elevated up to 200/120 mm Hg. If heart failure develops systolic pressure may decrease but diastolic one is steel high. Chronic glomerulonephritis with nephrotic syndromeis manifested by decreased diuresis,edema and changes in the blood and urine: hypo- and dysproteinaemia (hypergammaglobulinaemia, hypoalbuminaemia), hyperlipidaemia, proteinuria more than3,5 gr/l, casts in urine (hyaline, granular andrarely - ceraceous (waxy). Respiratory infections are frequent because of immunodepression thatprovoke exacerbation of ChG. Eye grounds: retinal arteriosclerosis hemorrhagias focci of degeneration andaffections of n. ophthalmicus(neuroretinopathy). In the stage of renal failure patients condition is heavy. Forced posture (sitting). Deranged conscioussness,sometimes coma.Main complaints are nausea, vomiting, skin dryness and itching, deranged vision, oliguria or anuria. Laboratory examination.Changes in urine: compensatory poliuria, nikturia. Zimnitskys test show hypoisosthenuria, nicturia. Urine density decreases and become monotonous hypoisosthenuria ( ). Creatinine and urea content in the blood may be normal. Proteinuriafrom insignificant till 3-10 gr/l. Casts hyaline granular and ceraceous. Laboratory examination.
Changes in urine are folowing: compensatory poliuria, nikturia. Simnitskys test show hypoisosthenuria, nicturia. Urine density decreases and become monotonous hypoisosthenuria ( ). Due to poliuria products of nitrogen metabolism is possible to evacuate from the organism that is why kreatinine and urea content in the blood may be normal. Proteinuria develops. Its degree may be from insignificant till 3-10 gr/l. It depends on patients diet, physical loading, overcooling etc. On urine sediments there are casts hyaline granular and ceraceous. Laboratory examination.
Changes in urine are folowing: compensatory poliuria, nikturia. Simnitskys test show hypoisosthenuria, nicturia. Urine density decreases and become monotonous hypoisosthenuria ( ). Due to poliuria products of nitrogen metabolism is possible to evacuate from the organism that is why kreatinine and urea content in the blood may be normal. Proteinuria develops. Its degree may be from insignificant till 3-10 gr/l. It depends on patients diet, physical loading, overcooling etc. On urine sediments there are casts hyaline granular and ceraceous. Treatment is performed taking into account clinical variant of the disease, its phase and stage.Patient should avoid overcoolings, physical loadings, psychoemotional stresses.In exacerbation long-standing treatment is indicated. Diet 7, limitation of salt intake to10 gr a day in nephrotic variant gr a day. Treatment In exacerbation long-standing treatment is indicated.
Diet 7, limitation of salt intake to10 gr a day in nephrotic variant gr a day. Medicamentous treatment: In unhypertensive stage - corticosteroids, cytostatics, aminoquinoline derivatives. In hypertensionhypotensive drugs also should be prescrobed(-bloquers methyldopum, apressin etc.). Diuretics (furosemide ethacrynic acid,hydrochlorothiazide) in edema; Anticoagulants and antiaggregants (heparin curantyl indometacin) Hemosorption, plasmapheresis. If infection develops than antibiotics are administered. Nephrotic syndrome is indication for administration of prednisolone mg a day, azathioprine mg a day, heparin Un, aspirin 0,25 gr. In remission stage sanatorium-resorting treatment is useful with warm and dry climate, mineral waters. Ifhigh risk of renal failure and exaggerated asotaemia are presentit is necessary to perform chronic hemodialisis and transplantation of kidney. Prognosis.Duration of patients life depends on clinical form of ChG and functional condition of kidneys.In the stage of chronic renal failure patients are disable. Prophylaxis includes in-time treatment of acute and chronic focci of infection as well as treatment of exacerbations, dyspancery observation. Pyelonephritis Pyelonephritis is a bacterial infection of one or both kidneys. Ethiology: E. Coli, streptococci, staphylococci, proteus and differrent bacterial assotiations, sometimes it may be caused by viruses Provoking factors: disorders of urine outflow (congenital anomalias, stones, obstruction, pareses, paralises etc.); metabolic disorders (diabetes mellitus, gout); iatrogenic diseases (catheterization, cystoscopy); immunodepression (chronic diseases, focci of infection, overcooling). Pathogenesis: Penetration of microorganisms to calicules and renal interstitium byhematogenic or ascending ways (thrugh urinary tract). Classification: unilateral and bilateral, acute and chronic pyelonephritis, primary and secondary. Primary pyelonephritisoccurs when morphological changes in urinary tract are abcent. Secondary pyelonephritisoccurs whenanomalias of kidneys and urinary tract are present which cause disorders of urine outflow(narrowing of ureters or urethra,stones nephroptosis adenoma of prostatic gland etc.). Acute pyelonephritis devides on serous and purulent. Clinical pattern. Acute pyelonephritis (AP) starts from elevation of body temperature up to 38-39 chills headache unilateral or bilateral dull pain in lumbar region dysuria. Nusea, vomiting, myalgias and arthralgias are possible. Patients condition is heavy, toxic shock may develop. Respiration is frequent, vesicular. Tachicardia is present. Tongue is dry and coated. Herpes labialis. Urination is frequent painful sometimes urinary retention develops. Pasternatskys symptom is positive on the affected side. Urine relative density is decreased (1012-1015) Poliuria is possible.
Urine reaction is acid. Leukocyturia and bacteriuria are typical. Non-significant haematuria and proteinuria (till 1 gr/l), casts in urine (hyaline granular and epythelial). Nechiporenkos and Addis-Kakovskys tests are positive.Sometoimesurine is of alkaline reaction and of unpleasant smell, becomes cloudy, salt sediments and purulent flakes are present is it. Microscopic examination:leukocytes, granular custs and erythrocytes on all fision fields. Treatment: ed mode; diet enriched with milk, vegetables and fruits. Alkohol, spicy food preserved food coffee are prohibited. Liquid3 liters a day (wild rose decoction, mineral water). Antibioticotherapy:) penicillin, semisynthetic penicillicnes, hentamycin, claforan ets., b) nitrofurantoin derivatives: nitrofurantoin (0,1 g 34 tablets a day 7-10 days), biseptol-480 (2 tablets 2-3 times a day 2-3 weaks). Spasmolithics and diuretics. In heavy cases catheterization, lawage of calices andbladder with desinfectant solutions. Chronic pyelonephriti (pyelonephritis chronica, ChP ) is a chronic non-specific inflammation of renal interstitium and calicular mucosa with following affection of renal vessels. Ethiology and pathogenesis. Chronic pyelonephritismay be the result of not effective treatment of acute pyelonephritis The main wayof penetration of infection isascending indisorders of urine outflow (kidney stones, anomalias and strictutes (narrowings) ofurinary tract tumors pregnancy etc.). Infection spreads from renal calices to the renal parenchyma. Clinical pattern. There are latent, recidiving, hypertensive, anaemic and asotaemic forms of the disease. Main complaints are elevation of body temperature, chills, pain in the projection of one or two kidneys, headache general weakness fatique dysuria. If the patient develop renal failure, hisappetite is lost, nausea, vomiting, thirst and metheorismus are present. Blood analysis: anaemia leukocytosis neutropenia and lymphopenia thrombocytopenia accelerated ESR. Urine: its density decreases to (hypoisosthenuria). Mild proteinuria (to 1 gr/l),leukocyturia. Nechiporenkos and Kakovsky-Addis tests data: leukocyturia prevails before erythrocyturia. Bacteriologic examination of the urine reveales marked amount of bacteria. Zimnitskys test at the beginning of the disease reveales hyposthenuria and later hypoisosthenuria. Kreatinine and urea clearance are decreased. The level of blood kreatinine and urea rise. X-ray, ultrasonic examination and computer tomography show distension and deformation of renal calices, asymethry, shrinked kidneys. Treatment: to avoid overcoolings and viral respiratory infections; diet 7 (in exacerbation). In anaemia - food rich on iron (strawberries apples);grapes, melon and water-melon. Antibiotics in days courses with breaks for2-3 weaks.nalidixic acid derivatives negram nevigramone; nitrofurantoins biseptol sulfa-drugs of short action (ethazol urosulfane). Vitamins of B group, ascorbic acid antihistamine preparations and spasmolitics. In the case of hypertesion salt intake should be limited to 4-6 gr a day hypotensive drugs should be prescribed. In remission sanatory-resorting treatment is useful . Prognosis is favorable in active treatment and abcense of complications. Prophylaxis of ChP means treatment of chronic infection focci as well as inflammation of urogenital tract, observation of rules of aseptics and antiseptics during instrumental examinations (cystoscopy, catheterization etc.). Urolithiasis is the condition where urinary calculi are formed or located anywhere in the urinary system, or the process of forming stones in the kidney, bladder, and/or ureters (urinary tract). Urinary stones are typically classified by their location in the kidney (nephrolithiasis), ureter (ureterolithiasis), or bladder (cystolithiasis) Predisposing factors for Stone Formation (Who gets kidney stones?)
Abnormal urinary pH: Allergies: Avoid L-Cysteine if you have a genetic disposition to stones. B Vitamin and Magnesium Deficiency: Cadmium: Calcium Supplements: Chemotherapy: Cystinuria: Dehydration: Drug Overdose; Diabetes: Essential Fatty Acid Deficiencies: Excess Sugar: Genetic Predisposition in Humans: Gout: Having very poor mobility; Heavy Metal Poisoning: Hypercalciuria: Hyperoxaluria: Hyperurcosuria: Medications: Metabolic disorders like Overuse of Aspirin; People who have been catheterized for long periods of time; Previous History of Stones: Red meat: Salt Intake: Some medications; Too much Alcohol: Too much caffeine: Draws minerals from the body and acts as a diuretic; Too much Vitamin D: Symptoms of Kidney and Bladder Stones include:
Severe pain or aching in the back on one or both sides Sudden spasms of excruciating pain (renal or uteric colic) usually starting in the back below the ribs, before radiating around the abdomen, and sometimes to the groin and genitalia (see diagram for referred pain because referred pain is often missed Bloody, cloudy, orange or smelly urine Burning sensation during urination Chronic urinary tract infections Depression Disorientation and fatigue Dull pain in low back (often for days) Feeling or being sick Fever and chills Frequent urge to urinate (polakyuria) Loss of appetite Nausea with possible vomiting (like having the flu) Pain in stomach, back or groin (sometimes severe agony compared to the pangs of natural childbirth which responds only to some severe pain medication) Straining to urinate (we call it stranguria)or difficult urination (dysuria) Symptoms and signs of a kidney stone include excruciating, cramping pain
in the lower back and/or side, groin, or abdomen as well as blood in the urine. Diagram showing the typical location of renal colic, below the rib cage to just above the pelvis
Referred pain from kidneys necessary examinations
Blood tests to identify excess amounts of certain chemicals related to the formation of stones . ECG- Can show heart rate and rhythm abnormalities if the stones are caused by an increase in certain minerals (but this choice of diagnostic technique would not be common). Imaging techniques which involve an injection of a special dye that shows up the whole urinary system on x-ray images, revealing stones that cant usually be seen. Examples are: Urinalysis - to look for signs of infection, crystal formation, determine ph (see urinalysis handout.) necessary examinations
Excretory urography where a contrast agent is injected into the blood stream and is then cleared by the kidneys, outlining the kidney, ureters and urinary bladder. Renal angiography where contrast agents are injected into the renal artery to assess the blood flow to the kidney. Retrograde urethrocystography where contrast agent is injected into the urethra to outline the urethra and urinary bladder. Taking an x-ray image stones that contain calcium usually show up white on x-ray imageswhile other stone are translucent (radio-opaque which means you need additional tests). Ultrasound scan this uses high frequency sound waves to produce an image of the internal organs. CT Scan (Non-contrast helical computerized tomography) this produces pictures from a series of x-ray images taken at different angles it is sometimes used to diagnose kidney stones, and is thought to be the most accurate diagnostic test. Urinary stones are classified by their chemical composition (calcium-containing, struvite, uric acid, or other compounds) The most common types of stone is calcium oxalate (dihydrate) - spicules, while the hardest stone is cystine monohydrate. Other stone compositions include triple phosphate, ammonium, magnesium, urate calcium, oxalate, urate, xanthine, etc. Calcium oxalate stones the most common type of stone staghorn stone Depending on the size, most stoneseventually pass on their own within 48 hours 1,4 . TREATMENT OF RENAL STONES BY EXTRACORPOREAL SHOCK-WAVE LITHOTRIPSY For kidney stones that do not pass on their own, a shock waveprocedure called lithotripsy is often used to break up a large stone into smaller pieces to pass. laser lithotripsyA laser fiber is inserted through the working channel of the scope, and laser is directly emitted to the stone. The stone is disintegrated and the remaining pieces are washed out of the urinary tract. This procedure is done under either local or general anesthesia and is considered minimally invasive surgery. This procedure is widely available in most hospitals in the world. PERCUTANEOUS STONE REMOVAL
A nephroscope may be inserted through a nephrostomy tract to remove a stone from the renal pelvis. An ultrasound probe may be used to fragment a staghorn calculus. Conducting ureteral catheterization 0.018 hydrophilic guide photo Phillantus Niruri (Stone Breacker,quiebra piedra,Chanka Piedra,Chanca Piedra) Phyllanthus Niruri Phyllanthus Niruri Extracts of this herb have shown promise in treating a wide range of human diseases. Some of the medicinal properties suggested by numerous preclinical trials are anti-hepatotoxic, anti-lithic, anti-hypertensive, anti-HIV and anti-hepatitis B. However, human trials have yet to show efficacy against Hepatitis B virus. The herbal plant has long been used in Brazil and Peru as an herbal remedy for Kidney stones. Research among sufferers of Kidney stones has shown that, while intake of Phyllanthus niruri didn't lead to a significant difference in either stone voiding or pain levels, it may reduce urinary calcium, a contributing factor to stone growth.In addition, one study conducted on rats showed that an aqueous solution of Phyllanthus niruri may inhibit kidney stone growth and formation in animals who already have stones. To help prevent kidney stones, drink enough water to keep your urine clear. Dietary choices can affect kidney stone development. Weight gain can increase the risk of kidney stones. bearberry parsley watermelon wild carrot field horsetail Figure 32. Adult autosomal dominant
polyeystic kidney disease demonstrated at intravenous urography. Both kidneys are enlarged with irregular contours. The pyelocalyceal systems are splayed and deformed. Intravenous urography
demonstrating crossed renal ectopy. The "left" kidney is located below the right kidney. Fibromuscular dysplasia.
Arteriogram demonstrating several narrowings in the right renal artery of a young woman. Arteriosclerosis. Arteriogram demonstrating arteriosclerosis in the lower abdominal aorta and a stenosis (narrow) of the left renal artery dose to the aorta. THANK YOU FOR YOUR ATTENTION