Patrick Bradshaw PhD

• Assistant Professor, Epidemiology

https://publichealth.berkeley.edu/people/patrick-bradshaw/

We can focus our attention on one voice out of many at a party acne location meaning generic permethrin 30 gm overnight delivery, on the smell of faint perfume acne essential oils permethrin 30 gm buy lowest price, or on the texture of an intriguing surface acne y estres purchase permethrin online now. Despite these considerations acne upper lip generic permethrin 30 gm buy line, neurobiologists have focused most of their research on visual spatial attention acne tretinoin cream 005 order permethrin master card. This is reasonable because humans tend to be highly visual and because most forms of attention have a strong spatial component. Overt versus Covert Spatial Attention When your attention is drawn to a particular location in space, what do you do Most of the time you turn your head, or at least your eyes, toward the location of interest. These orienting movements are sensible because they aim your retinal and acoustic foveae at the attended location, thereby maximizing your ability to gather information from that site. Sometimes, of course, we choose to inhibit these orienting movements and shift our attention to areas in our peripheral vision. Although covert spatial attention is relatively rare in everyday life, it is important for researchers because it allows shifts in attention to be studied without the confounding effects of orienting movements. Involuntary Attention Some stimuli draw our attention automatically, without involvement of our will and sometimes even against it. This kind of involuntary attention is also known as bottom-up, stimulus-driven, or exogenous attention. Its key characteristic is that the target of our attention is determined by some external stimuli and not by our goals or intentions. As William James put it, in cases of involuntary attention the stimulus is a sense-impression, either very intense, voluminous, or sudden-in which case it makes no difference what its nature may be, whether sight, sound, smell, blow, or inner pain-or else it is an instinctive stimulus, a perception which, by reason of its nature rather than its mere force, appeals to some of our normal congenital impulses and has a directly exciting quality. These stimuli differ from one animal to another, and what most of them are in man: strange things, moving things, wild animals, bright things, pretty things, metallic things, words, blows, blood, etc. As you can see, many of the stimuli that attract our involuntary attention indicate potential threats or benefits. However, our attention is also drawn to stimuli that have no intrinsic significance but simply stand out from the background. A single yellow flower on a green lawn, for example, will command our involuntary attention. By aiming our attention, if not our eyes and heads as well, toward salient stimuli, we can assess more thoroughly their true significance. If we then determine that the stimuli are not interesting after all, our attention moves on. For example, you can intentionally focus your attention on a specific person at a party, on the sound of specific instrument in a piece of music, or on the words in front of you. Voluntary attention is also used to search for a specific item among many distractors. When you look at the images in (a), the red circle rapidly "pops out" of the background, even when the number of blue circles is increased (left vs. In contrast, it takes more time to find a red circle among a mix of blue circles and red stars (B). In such a task, you must examine each stimulus in turn (serially), and the time to find the target increases with the number of distractors. This sort of conjunctive analysis requires the voluntary movement of attention from one object to another until the "search image" is found. A historically important study of voluntary spatial attention was performed by Hermann von Helmholtz at the end of the 19th century. A small hole in the center of the card let light shine through from behind the card. Therefore, when Helmholtz looked inside the box, he could see only a spot of light at the center of the card. A Without inside attention Helmholtz then set off a flash of lightselectivethe box. However, when Helmholtz decided before the flash to attend to a specific portion of the card, then the flash allowed him to read the letters there. The most important conclusion Helmholtz drew from this experiment is that even covert attention improves perception. As mentioned earlier, overt attention improves perception because the retinal and acoustic foveae are aimed at the attended location. Keeping his eyes fixed on the light, he triggered a flash inside the box to illuminate the card. Because helmholtz kept his eyes fixed on the pinhole, the shift in his attention was covert. This is important because it shows that covert spatial attention serves a valuable function. Furthermore, experimenters can use this spatially selective enhancement of perception to determine whether their test subjects are covertly attending to specific locations. Without these effects on perception, covert attention would not just be outwardly invisible, it would be completely undetectable and impossible to study experimentally. This finding suggests that the salience of stimuli that catch our involuntary attention is being computed in parallel rather than serially. Specifically, it suggests that separate populations of neurons are scrutinizing each region of space for the presence of salient stimuli. This conclusion, in turn, implies that stimulus salience is computed by neurons with relatively small spatial receptive fields. Another clue to how neurons compute stimulus salience is that pop-out stimuli can vary from the background in many different aspects, including color, luminance, shape, and movement. Furthermore, attention-grabbing objects usually differ from the background in more than one respect. The black fly on the white wall, for example, becomes even more salient once it begins to move. Therefore, overall stimulus salience is probably computed by neurons that receive converging information about multiple stimulus features (color, motion, etc. The Saliency Map Based on such considerations, neuroscientists have built computer models of how visual salience is computed. In addition, "inhibition of return" decrements the salience of winning locations, ensuring that attention does not get stuck. Different parts of the saliency map then compete with one another, using a winner-take-all algorithm, to determine which region is most salient. An additional mechanism, called inhibition of return, makes a winning location temporarily less salient after its victory, thus ensuring that attention does not "get stuck" on just a single location (we will return to this shortly). Compared to what humans consider most interesting in an image, and where they aim their eyes, the computer models perform well, suggesting that they are realistic. Much research has focused on the parietal and frontal eye fields (which you may recall from Chapter 11), but these regions are also involved in voluntary attention. Another region that appears to be involved in computing the sort of involuntary, bottom-up saliency that generates pop-out effects is the superior colliculus. As you learned in Chapter 11, the superior colliculus receives topographic retinal input, as well as topographic projections from multiple cortical areas. In addition, the superior colliculus is heavily involved in targeted eye and head movements. This, too, is consistent with the saliency map hypothesis, given that involuntary attention is normally associated with orienting reflexes. Finally, the superior colliculus receives somatosensory and auditory inputs, which could mediate involuntary shifts of attention to salient touches or sounds. This experiment is conceptually similar to the awake brain stimulation experiments we discussed in Chapter 12, except that the experimenters in this case were trying to alter perception indirectly by activating neurons that effect a change in covert spatial attention. The first step in this experiment was to train a monkey on the same sort of direction discrimination task that we discussed in Chapter 12. Once the monkey was good at reporting the average direction of the moving dots, the task was made more difficult by having the dots move totally randomly throughout most of the screen. Only in one relatively small portion of the visual field did most of the dots move coherently (in the same direction). The monkey managed to perform this task correctly, using just its peripheral vision (the eyes had to stay focused on a central fixation point). Under these conditions, the task was essentially impossible unless the monkey was covertly paying attention to that particular region of space. Of course, given what you learned in Chapter 11, you would expect strong how Does the Brain Generate and Direct attention The experimenters solved 70 this problem by reducing current intensity until the electrical stimulation no longer elicited an eye movement. Because the perceptual improvement on the moderately difficult trials was evident only when the moving dots were presented in the eye movement field, rather than elsewhere, we can conclude that the boost in performance resulted from a specific shift in covert attention rather than some more general mechanism (such as increased arousal). Overall, this experiment revealed that stimulation of the superior colliculus can guide covert, as well as overt, spatial attention. As we scan a scene with our Higher order eyes, we look first at the most salient feature; but then our eyes move on. Once our attention has shifted, it tends not to return to its earlier target for at least a few hundred milliseconds. The mechanisms underlying V1 this inhibition of return remain obscure, but they probably include a temporary suppression of neural activity at the "winning" location in the saliency map. Recent studies with barn owls suggest an important role for Superior colliculus Reticular inhibitory neurons in the lateral tegmental nucleus, which are reciprocally interconformation nected with the superior colliculus. These tegmental neurons probably ensure that only one winner at a time is selected, but how this winner is "chosen" and then supRetina pressed remains unclear. This question remains unanswered, but the mechanism probably involves projections from the superior colliculus to the pulvinar nucleus of the thalamus. Because these projections are excitatory and topographically organized, increased activity in one part of the superior colliculus may, by way of the pulvinar, enhance neural activity in multiple visual cortical areas, and do so in a spatially specific manner. This idea remains to be tested, but pulvinar lesions are known to cause deficits in visual spatial attention. Neural Correlates of Voluntary Attention By definition, voluntary attention is controlled by the subject, rather than external stimuli. This form of attention is sometimes referred to as top-down attention, highlighting its dependence on "executive" control, and contrasted with bottom-up, involuntary attention. Attention Selectively Enhances Neural Responses In the laboratory, voluntary attention is commonly studied in cued spatial attention tasks. In these tasks, subjects are trained to look at a central fixation point, where they are presented with an instructive cue (such as an arrow) that instructs them to direct their attention to a specific location on a computer screen (often just to the left or right of the fixation point). Then a visual stimulus is presented either at the location where the subject was instructed to attend or, in control trials, at some other location on the screen. When monkeys are used in such experiments, they are trained to make a specific hand or eye movement as soon as they identify the stimulus. Although the monkeys in such experiments are highly trained, the shifts in attention are voluntary (top-down) because the monkeys are choosing to cooperate. The key finding to emerge from such experiments is that monkeys generally react more rapidly when the stimuli appear at the attended location. This is consistent with our own experience, as paying attention to a specific location allows us to respond more rapidly to what is happening there, compared to non-attended locations. Overall, such experiments have shown that monkeys are as capable of covert voluntary spatial attention as we are. Importantly, monkeys performing these cued spatial attention tasks can be used to study the neural bases of voluntary attention in considerable detail. Monkeys were trained to direct their attention either to the left of the fixation point or to the right (top right and bottom right of the figure, respectively). If they correctly identified the stimuli at the attended location, they received a juice reward. Simultaneously, the experimenters recorded the orientation preferences of V4 neurons to stimuli in their receptive fields. They also function in controlling attention, -200 -100 0 specifically the voluntary shifts of visual spatial attention Time before response (ms) that we discussed in the previous section. FeF neurons increased their firing rates found the target, the monkeys had to make an eye movewhenever the attentional spotlight reached their receptive field. For neurons whose receptive field coincided with the target stimulus (B), ment straight to the target to obtain a reward. For reaction time data indicated that the monkeys typically neurons whose receptive field was counterclockwise to the target began their covert serial search on the right side of the stimulus (C), firing rates increased roughly 80 ms before the eye movestimulus array and then searched in a clockwise direction. This increase in activity might be the result of the attentional spotlight reaching the target stimulus, or it could be some sort of premotor activity commanding the trained eye movement response. To see why this is important, consider what would happen if attention simply increased neural responses to all stimuli. Such an indiscriminate increase in response strengths would add more noise to the neural representation of the stimulus and decrease its efficiency. By boosting responses selectively, covert attention makes it easier for animals to discriminate between similar stimuli, a feature that would often be useful. In other words, the deficits may occur in a variety of spatial coordinate frames (see Chapter 11), but are usually associated with the left side of the affected spatial frame. Important for our discussion here is that the deficits in hemispatial neglect tend to be neither sensory nor motor but attentional (as the term "neglect" implies). For example, when hemispatial neglect patients are tested in a peripheral cueing task, they can see stimuli in the left half of their visual field, but they are slow to react when targets appear there, especially when their attention had been focused on the right. Furthermore, you may wonder how lesions in the inferior parietal and Right hemisphere damage temporal lobes can impact the attention-related circuits that pass through the more dorsally located frontal and parietal eye fields. When regions of damage for multiple normal activity of the dorsal parineglect patients are mapped onto a reference brain (bottom panel), overlap tends to be maximal etal cortex, which results from disin the inferior parietal and superior temporal cortices and at the junction between the two (the ruptions of activity in more ventral more overlap, the warmer the color in this figure). Lesions of the posterior parietal cortex, for example, interfere with motor attention as well as with the execution of visually guided hand movements. Similarly, lesions of the frontal eye field or superior colliculus lead to deficits in visual attention, but they also interfere with eye and head movements.

Syndromes

• What other medical problems have you had?
• Cough
• Flu-like symptoms
• No menstruation (amenorrhea)
• Malnutrition (when severe)
• Your doctor or nurse will tell you when to arrive at the hospital.
• Penile pain
• Ruptured bronchial tube

Noncaseating Sarcoid Granulomas the prognosis is favorable with a variable clinical course skin care products for rosacea order cheap permethrin on-line. Summary of Obstructive Versus Restrictive Pattern Variable Obstructive Pattern skin care doctors discount permethrin 30 gm online. Chronic bronchitis is a clinical diagnosis made when a patient has a persistent cough and copious sputum production for at least 3 months in 2 consecutive years skin care coconut oil purchase permethrin now. Clinical findings include cough skin care for acne buy permethrin master card, sputum production skin care 2012 purchase 30 gm permethrin with visa, dyspnea, frequent infections, hypoxia, cyanosis, and weight gain. Microscopic examination demonstrates hypertrophy and hyperplasia of bronchial mucous glands (Reid index equals the submucosal gland thickness divided by the bronchial wall thickness between the pseudostratified columnar epithelium and the perichondrium; normal ratio is 0. Complications include increased risk for recurrent infections; secondary pulmonary hypertension leading to right heart failure (cor pulmonale) and lung cancer. Emphysema is the term used when destruction of alveolar septa results in enlarged air spaces and a loss of elastic recoil. The 4 types of emphysema are named for the anatomical distribution of the septal damage. On gross examination, the lungs are overinflated and enlarged, and have enlarged, grossly visible air spaces. Clinical findings include progressive dyspnea, pursing of lips and use of accessory respiratory muscles to breathe, barrel chest (increased anteriorposterior diameter), and weight loss. Manifestations Related to Area of Involvement Centriacinar (Centrilobular) Proximal respiratory bronchioles involved, distal alveoli spared Most common type (95%) Associated with smoking, air pollution Distribution: worse in apical segments of upper lobes -1-antitrypsin deficiency Distribution: entire lung; worse in bases of lower lobes Panacinar (Panlobular) Entire acinus involved Asthma is due to hyperreactive airways, which undergo episodic bronchospasm when triggered by certain stimuli. Microscopic examination of sputum cytology may show Curschmann spirals (twisted mucus plugs admixed with sloughed epithelium), eosinophils, or CharcotLeyden crystals (protein crystalloids from broken down eosinophils). In patients dying from disease, autopsy findings include mucus plugs, increased mucous glands with goblet cell hyperplasia, inflammation (especially with eosinophils), edema; hypertrophy and hyperplasia of bronchial wall smooth muscle, and thickened basement membranes. Bronchial Changes in Asthma Bronchiectasis is an abnormal permanent airway dilatation due to chronic necrotizing inflammation. Causes are diverse, and include bronchial obstruction by foreign body, mucus, or tumor, necrotizing pneumonias, cystic fibrosis, and Kartagener syndrome. It is characterized clinically by bronchiectasis, chronic sinusitis, and situs inversus (a congenital condition where the major visceral organs are anatomically reversed compared with their normal anatomical positions). On gross examination, bronchiectasis shows dilated bronchi and bronchioles extending out to the pleura. Complications include abscess, septic emboli, cor pulmonale, and secondary amyloidosis. Clinically, patients show dyspnea, tachypnea, hypoxemia, cyanosis, and use of accessory respiratory muscles. On gross pathologic examination affected lungs are heavy, stiff, and noncompliant. Microscopically, there is intra-alveolar edema, and hyaline membranes line the alveolar spaces. Treatment is based on treating the underlying cause and on supporting respiration with mechanical ventilation. Respiratory distress syndrome of the newborn (hyaline membrane disease of newborns) is caused by a deficiency of surfactant. It is associated with prematurity (gestational age of <28 weeks has a 60% incidence), maternal diabetes, multiple births, male gender, and cesarean section delivery. Clinically, infants are normal at birth but within a few hours develop increasing respiratory effort, tachypnea, nasal flaring, use of accessory muscles of respiration, an expiratory grunt, and cyanosis. Chest radiograph may demonstrate bilateral "ground-glass" reticulogranular densities. Respiratory distress syndrome of the newborn can sometimes be prevented if labor can be delayed and if corticosteroids are used to mature the lung. Chronic interstitial lung disease is a term describing heterogeneous lung disorders which share similar symptomology but vary in prognosis. Lung biopsy findings can be paired with clinical information to aid in therapeutic management/palliative care. After exposure to a sensitizing agent such as moldy hay, patients present with a febrile acute reaction or a chronic disease with weight loss. Biopsy shows peribronchiolar acute and chronic interstitial inflammation +/- noncaseating granulomas. Occupation-associated pneumoconiosis is a common cause of chronic interstitial lung disease. It is considered separately here to show the full spectrum of disease since neoplasia may occur during its course. Key factors affecting their development include the type of aerosol and its ability to stimulate fibrosis; the dose and duration of exposure; and the size of the particle, with only particles <10 microns entering the alveolar sac. Occupations in which asbestos exposure may occur include shipyard work, insulation and construction industries, brake-lining manufacture. Amphibole asbestos is more pathogenic than serpentine asbestos, and is highly associated with mesotheliomas. Pulmonary biopsy may demonstrate asbestos bodies that have become coated with iron (ferruginous bodies). The tumor grossly encases and compresses the lung; microscopic exam exhibits carcinomatous and sarcomatous elements (biphasic pattern), while electron microscopy shows long, thin microvilli on some tumor cells. Family members also have increased risk of cancer due to the worker bringing home clothing covered with asbestos fibers. It is seen most frequently with occupational exposure (sandblasters, metal grinders, miners). The pulmonary pathology shows dense nodular fibrosis of the upper lobes which may progress to massive fibrosis; birefringent silica particles can be seen with polarized light. Patients present with insidious onset of dyspnea that is slowly progressive despite cessation of exposure. Asbestos Fibers in Lung Tissue · Berylliosis is an allergic granulomatous reaction due to workplace exposure to beryllium in the nuclear, electronics, and aerospace industries. Pulmonary edema is fluid accumulation within the lungs, usually due to imbalance of Starling forces or endothelial injury. The pathology grossly shows wet, heavy lungs (usually worse in lower lobes), while microscopic examination shows intra-alveolar fluid, engorged capillaries, and hemosiderin-laden macrophages (heart-failure cells). Clinical Correlate Dietary drugs fenfluramine and phentermine have been associated with primary pulmonary hypertension. The etiology varies and can include chronic obstructive pulmonary disease and interstitial disease (hypoxic vasoconstriction); multiple ongoing pulmonary emboli; mitral stenosis and left heart failure; congenital heart disease with left to right shunts (atrial septal defect, ventricular septal defect, patent ductus arteriosus); and primary (idiopathic) pulmonary hypertension, typically in young women. Pulmonary hypertension may also damage the heart, leading to right ventricular hypertrophy and then failure (cor pulmonale). Major risk factors include cigarette smoking, occupational exposure (asbestosis, uranium mining, radiation, etc. Clinical features include cough, sputum production, weight loss, anorexia, fatigue, dyspnea, hemoptysis, and chest pain. Obstruction may produce focal emphysema, atelectasis, bronchiectasis, or pneumonia. Grossly, it causes a peripheral gray-white mass, and the tumor may develop in areas of parenchymal scarring (scar carcinoma). The precursor lesion-atypical adenomatous hyperplasia-progresses to adenocarcinoma in situ (noninvasive well-differentiated tumor <3 cm) and to minimally invasive tumor (invasion no more than 5 mm) before progressing to invasive adenocarcinoma. Squamous cell carcinoma arises from bronchial epithelium after a progression: metaplasia dysplasia carcinoma in situ invasive carcinoma Pathologically, the tumor grossly causes a gray-white bronchial mass, usually centrally located. Microscopically, well-differentiated tumors show invasive nests of squamous cells with intercellular bridges (desmosomes) and keratin production ("squamous pearls"). This neuroendocrine tumor is very aggressive, with rapid growth and early dissemination. Small Cell Carcinoma with Crush Artifact in the Lower Left Field Pathologically, gross examination demonstrates central, gray-white masses. Microscopic examination shows small round or polygonal cells in clusters, and electron microscopy shows cytoplasmic dense-core neurosecretory granules. Large cell carcinoma has large anaplastic cells without evidence of differentiation. Intrathoracic spread of lung cancer is to lymph nodes, particularly hilar, bronchial, tracheal, and mediastinal; pleura (adenocarcinoma); and lung apex causing Horner syndrome (Pancoast tumor). Note Horner Syndrome causes ipsilateral: · · · · Ptosis Miosis Anhidrosis Enophthalmos Extrathoracic sites of metastasis include adrenal (>50%), liver, brain, and bone. Treatment of non­small cell lung cancer is with surgery, and treatment of small cell lung cancer is with chemotherapy and radiation. Bronchial carcinoids occur in a younger age group (mean age 40 years) and typi- cally produce a polypoid intrabronchial mass or plaque; it is characterized on light microscopy by small, round, uniform cells growing in nests (organoid pattern), and on electron microscopy by cytoplasmic dense-core neurosecretory granules. Bridge to Pharmacology Erlotinib (Tarceva) is used to treat non­small cell lung cancer, pancreatic cancer, and other types of cancers that have failed a prior trial of chemotherapy. It typi- cally causes multiple, bilateral, scattered nodules; common primary sites include breast, stomach, pancreas, and colon. Carney triad is the finding of a hamartoma with a predominantly cartilaginous component (pulmonary chondroma), an extra-adrenal paraganglioma and a gastric gastrointestinal stromal tumor. Risk factors include smoking, alcohol, and frequent cord irritation (professional singing or lecturing). It can be due to traumatic penetrating chest wall injuries or spontaneous rupture of apical blebs in typically tall young adults (spontaneous pneumothorax). The term tension pneumothorax is used if a life-threatening shift of thoracic organs across midline occurs. Densely Black Appearance on Chest X-Ray of a Pneumothorax Hemothorax is the presence of blood in the pleural cavity. Atelectasis is an area of collapsed or unexpanded lung and can occur secondary to obstruction, compression, contraction, or lack of surfactant. Bacterial pneumonia is an acute inflammation and consolidation (solidification) of the lung due to a bacterial agent. Lobar pneumonia causes consolidation of an entire lobe and is most commonly caused by infection with Streptococcus pneumoniae. Bronchopneumonia causes scattered patchy consolidation centered around bronchioles and can be due to a wide variety of bacterial agents. Lung abscess is a localized collection of neutrophils (pus) and necrotic pulmonary parenchyma and may occur following aspiration, pneumonia, obstruction, or septic emboli. Atypical pneumonia causes interstitial pneumonitis without consolidation and can be due to viral agents and Mycoplasma pneumoniae. Obstructive airway disease is characterized by increased resistance to airflow secondary to obstruction of airways, whereas restrictive lung disease is characterized by decreased lung volume and capacity. Chronic bronchitis is a clinical diagnosis made when persistent cough and copious sputum production have been present for at least 3 months in 2 consecutive years. Emphysema is associated with destruction of respiratory bronchioles or alveolar septa, resulting in enlarged air spaces and a loss of elastic recoil, and producing overinflated, enlarged lungs. Asthma is due to hyperreactive airways, resulting in episodic bronchospasm when triggered by stimuli that may include allergens, respiratory infections, stress, exercise, cold temperatures, and drugs. Bronchiectasis is an abnormal permanent airway dilatation due to chronic necrotizing infection; most patients have underlying lung disease such as bronchial obstruction, necrotizing pneumonias, cystic fibrosis, or Kartagener syndrome. Acute respiratory distress syndrome is due to diffuse damage to the alveolar epithelium and capillaries, resulting in progressive respiratory failure that is unresponsive to oxygen treatment. Causes include shock, sepsis, trauma, gastric aspiration, radiation, oxygen toxicity, drugs, pulmonary infections, and many others. Pulmonary edema is fluid accumulation within the lungs that can be due to many causes, including left-sided heart failure, mitral valve stenosis, fluid overload, nephrotic syndrome, liver disease, infections, drugs, shock, and radiation. Most pulmonary emboli arise from deep vein thrombosis in the leg and may be asymptomatic, cause pulmonary infarction, or cause sudden death. Pulmonary hypertension is increased pulmonary artery pressure, usually due to increased vascular resistance or blood flow. Major risk factors are cigarette smoking, occupational exposures, air pollution, and "scarring. Mesotheliomas are rare, highly malignant neoplasms that can involve the pleura and are closely related to prior asbestos exposure. Pneumoconiosis is a fibrosing pulmonary disease caused by inhalation of an aerosol, such as mineral dust, particles, vapors, or fumes. Caplan syndrome is the term used for the combination of pneumoconiosis (due to many different agents) and rheumatoid arthritis. Asbestosis can cause pulmonary fibrosis, bronchogenic carcinoma, and malignant mesotheliomas. Berylliosis can cause an acute pneumonitis or granulomatous disease with fibrosis of the lungs. Hypoplasia is failure of a kidney (usually unilateral) to develop to normal weight; In a Nutshell Oligohydramnios (Potter) Sequence Renal agenesis Oligohydramnios Fetal compression Flattened facies and positional abnormalities of hands and feet the hypoplastic kidney has a decreased number of calyces and lobes. Horseshoe kidney is a common congenital anomaly that is found in 1 in 600 abdom- inal x-rays. The kidneys show fusion, usually at the lower pole; affected individuals have normal renal function but may be predisposed to renal calculi. Clinically, patients are asymptomatic with normal renal function until middle age, and then present with renal insufficiency, renal stones, hematuria, and hypertension or with abdominal masses and flank pain. On gross pathologic examination, the kidneys have massive bilateral enlargement with large bulging cysts filled with serous, turbid, or hemorrhagic fluid. Microscopic examination shows functioning nephrons present between the cysts; the cysts arise from the tubular epithelial cells of the kidney. Extrarenal manifestations include cysts of the liver, pancreas, and lungs; berry aneurysms of the circle of Willis; mitral valve prolapse; and colonic diverticula. Gross Pathology of Polycystic Kidneys 144 Chapter 15 · Renal Pathology Renal dysplasia is the most common renal cystic disease in children, in whom it causes an enlarged renal mass with cartilage and immature collecting ducts. Acquired polycystic disease is seen in renal dialysis patients and is associated with a small risk of developing renal adenomas and renal cell carcinoma. Simple retention cysts of the kidney are common in adults and occasionally cause Medullary diseases with cysts · Medullary sponge kidney can cause nephrolithiasis but is otherwise innocuous.

In fact skin care 08 buy permethrin in india, the force with which the stapes pushes on the oval window membrane is at least 13 times as large as the force with which the tympanic membrane pushes on the malleus acne face 30 gm permethrin buy free shipping. In reaction to very loud sounds acne 9 dpo permethrin 30 gm with visa, reflexive contraction of two small middle ear muscles (attached to the tympanic membrane and the stapes) can greatly reduce the degree to which vibrations are amplified within the middle ear skin care zamrudpur order cheap permethrin line. The portion of our inner ear involved in hearing is called the cochlea (from the ancient Greek word for "snail with spiral shell") skin care jogja discount 30 gm permethrin. Flexible joints link the malleus to the incus, and the latter to the stapes; the stapes, in turn, is attached to the thin membrane of the oval window. Because of these linkages, any movement of the tympanic membrane causes an opposite movement of the oval window. Incus Stapes Eustachian tube Oval window Round window Tympanic membrane Middle ear how Do We hear Sounds Inner and outer hair cells, as well as numerous supporting cells, are located on top of the thin basilar membrane. The half of the cochlear tube that extends from the oval window to the apex of the cochlea is called the scala vestibuli; the other half is called the scala tympani. It extends from the apex to the round window, which is a thin membrane quite similar to that of the oval window. Consider that vibrations of the oval window membrane generate sound waves within the cochlear tube. The resulting pressure changes at the round window cause it to vibrate just as the oval window does (although the two membranes move in opposite directions). Now imagine what would happen if the membrane of the round window were replaced with inflexible bone. Because the cochlear fluid is incompressible and the walls of the cochlea are stiff, any attempts to displace the cochlear f luid by pushing on the oval window would be futile. Because the basilar membrane is flexible, it tends to vibrate at right angles to the longitudinal sound waves passing through the scala tympani. Deflections toward row 1 pull on the tip links, as shown in the two scanning electron micrographs on the right. Displaying enormous technical skill, von Békésy dissected the cochleae out of cadavers from many different species and observed the vibrations of the basilar membrane in response to sounds at various frequencies. These hairs, called stereocilia, are neither hairs nor cilia, but modified microvilli. The ~3,500 inner hair cells of the human cochlea form a single, spiraling row near the inner edge of the basilar membrane. Most important is that inner hair cells are purely sensory, whereas outer hair cells perform both sensory and motor functions. As you will learn in Chapter 8, the outer hair cells are capable of causing basilar membrane vibrations and, thereby, amplifying some of the vibrations caused by sound. Converting Membrane Vibrations into Ion Currents Whenever sounds cause the basilar membrane to vibrate up and down, the stereocilia of the inner hair cells vibrate sideways. As sound waves travel up and down the cochlea, this tectorial membrane vibrates up and down, just as the basilar membrane does. As a result of this arrangement, the basilar and tectorial membranes slide sideways against one another as they how Do We hear Sounds Because of this displacement, up­down vibrations of the two membranes cause the fluid between them to slosh back and forth sideways (slightly). These fluid movements, in turn, deflect the stereocilia sideways, usually by less than 1 µm. You also need to know that the tips of the shorter stereocilia (in rows 2 and 3) contain ion channels that, in their open state, allow K+ and Ca 2+ ions to flow into the stereocilia and depolarize them. Finally, you need to know that these ion channels open whenever the stereocilia bend toward the tallest stereocilia and close whenever they bend the opposite way. When the stereocilia bend away from the tallest stereocilia, the tip links are slack; when they move in the other direction, the tip links are tight and pull on the stereocilial tips. Although the molecular identity of the mechanosensitive ion channels in stereocilia remains debatable (transmembrane channel-like proteins appear to be involved), experimental evidence supports their existence. These data are consistent with the hypothesis that tip links open calcium channels by actively pulling on the tips of row 2 and 3 stereocilia. Hair Cell Neurotransmitter Release the depolarization of hair cell stereocilia opens voltage-gated Ca 2+ channels that then allow more Ca 2+ ions to flow down the electrical potential and concentration gradients into the hair cell. As you may recall from Chapter 2, increases in intracellular Ca 2+ concentration trigger synaptic vesicle release in axon terminals. They develop from extraneural ectoderm, generate no action potentials, and lack axons. Bending the stereocilia toward row 1 opens Ca2+ and K+ permeable ion channels in the tips of row 2 and 3 stereocilia. Over time, this influx causes membrane depolarization and elevates Ca2+ concentration throughout much of the hair cell, including the row 1 stereocilia. Myosin molecules (red rectangles) act as molecular motors that move along the stereocilium, adjusting tip link tension. Indeed, the ribbon synapses of hair cells can release substantial amounts of glutamate for prolonged periods of time. When the terminals become sufficiently depolarized, action potentials are triggered. This arrangement does not fit the neuronal stereotype you learned about in Chapter 2 because these neurons appear to have two axons emerging from their cell body. As it turns out, most peripheral sensory neurons also have such axon-like dendrites. As we discussed in Chapter 2, membrane depolarization in most neurons leads to a gradual opening of voltagegated K+ channels through which K+ ions move out of the cell and repolarize the membrane. How can this work in hair cells if, as we just learned, K+ tends to rush into (rather than out of) hair cells Therefore, the opening of K+-permeable channels causes K+ to flow from the endolymph into the stereocilia, down into the body of the hair cells, and then out into the perilymph. At every step of this pathway, K+ ions are flowing down their concentration gradient, which means that the hair cells do not need to spend much metabolic energy pumping K+ ions back out. Hair cells also differ from typical neurons in that their depolarization involves essentially no Na+ influx. This, too, saves energy because there is no need to pump Na+ ions back out across the hair cell membrane after a depolarization. The fact that cochlear hair cells have little need for metabolic energy probably explains why they, in contrast to most sensory cells, are not adjacent to a dense capillary bed. This work is not performed by the cochlear hair cells but by specialized epithelial cells in a structure called the stria vascularis. When the blood supply to the stria vascularis is disrupted, or when ion transport in these cells is blocked, then the endolymph becomes depleted of K+ ions and cochlear hair cells rapidly cease functioning. Thus, the cochlear hair cells have essentially "outsourced" much of the metabolic work required for auditory transduction to the stria vascularis cells. This is a good design feature because placing a dense capillary bed on top of the basilar membrane (which is where it would have to be to feed the cochlear hair cells) would dampen the basilar membrane vibrations that are so critical for sensing sound. Because the two vowels contain a different mix of frequencies, they excite a different (although overlapping) set of cochlear hair cells. Use of such cochlear implants can help the deaf understand speech, especially if they were born deaf (~1/2,000 live births) and received the implants as babies, or if they became deaf in adulthood, long after they learned to speak. Despite differences across manufacturers, most cochlear implants are fundamentally similar. For example, most employ some sort of volume control to boost soft sounds and attenuate loud ones. In addition, most cochlear implants decompose incoming sound into several frequency bands. Importantly, the current pulses for each frequency band, or channel, are applied to different electrodes in keeping with the principle of cochlear tonotopy. Surgical complications during the initial implantation are relatively rare, but replacing old or damaged implants is difficult. Yet another worry is that children who grow up with cochlear implants may feel estranged from the sign-language-using deaf community but not be full members of the hearing community either. Simple tonal melodies are A Sound processor hardly recognizable, andand transmitter not perceived as such. In addition, it is possible to fine-tune the rate at which stimulus pulses are presented through the various electrodes and to disable any electrodes that are ineffective or, on stimulation, create unpleasant sensations. Current is passed between each of these electrode contacts and a ground electrode (not shown) that is usually implanted outside of the cochlea. Sounds containing multiple frequencies activate multiple groups of hair cells at several locations along the cochlea. All our central nervous system has to do is to monitor which hair cells are activated. If you want an analogy, imagine a very clever deaf person who can infer what sounds a piano is producing by noting carefully which piano keys a pianist is depressing. To answer this question, recall that tip links open ion channels when the stereocilia bend toward the tallest stereocilia. The louder the sound, the greater the degree of stereocilial bending, the greater the degree of hair cell depolarization, and the more neurotransmitter is released during each cycle of the sound wave. Furthermore, the more neurotransmitter is released by a hair cell, the greater the odds that action potentials are triggered in the postsynaptic axons. Other things being equal, this means that the average firing rate of axons in the auditory nerve increases with sound amplitude. After all, we generally perceive sound frequency as being independent of sound amplitude (imagine how musicians would feel if the pitch of their instrument depended on how loud they played). Mainly by analyzing the temporal pattern of action potentials in the auditory nerve. Because only one direction of stereocilial bending generates hair cell depolarization, auditory nerve fibers tend to fire only during one half of each cycle in the sound pressure wave. Therefore, the temporal pattern of action potentials in the auditory nerve correlates with sound frequency. This arrangement, in turn, allows auditory neurons in the brain to determine the frequency of an incoming sound by analyzing the temporal pattern of firing in auditory nerve fibers. The details of how this temporal analysis might be performed are controversial and complex. However, none of these complexities invalidate the notion that cochlear tonotopy plays a major role in the perception of sound frequencies, especially for complex sounds. It is useful, therefore, to step back and highlight a few common principles of sensor organization. One such principle is that the information sensors provide is incomplete and variable. Another common theme is that, in most sensory systems, key stimulus parameters are represented in an orderly, map-like fashion. Variability in Sensor Range Biological sensors generally respond to a limited subset of all possible stimuli within their sensory modality (vision, hearing, somatosensation, etc. Photoreceptors, for 194 Chapter 6 Sensors I: remote Sensing instance, respond most strongly to light within a relatively narrow range of wavelengths, and auditory hair cells respond most strongly to sounds of a particular frequency. Neuroscientists refer to this kind of stimulus selectivity as sensors being "tuned" to a specific range of stimuli, or they may speak anthropocentrically of sensors "preferring" a particular subset of stimuli. Sometimes the preference is due to the specificity of the receptor molecules expressed by a sensor; in other instances, the preference arises from the physical environment in which a sensor is embedded. Below some threshold level of intensity, a stimulus cannot be sensed at all; and once a sensor is activated maximally, further increases in stimulus intensity cannot be discerned. From a mechanistic perspective, these limitations arise from how the sensors and their associated structures are built. However, many sensor limitations exist not because it was physically impossible for evolution to overcome them but because evolution favored sensors tuned to the subset of all possible stimuli that is important for survival or reproduction. Given that sensing is metabolically expensive, it is adaptive for organisms to focus on what is most important for members of their species. Moreover, flooding the brain with all sorts of irrelevant sensory signals would hardly be beneficial; as it is, we struggle to keep our sensory world from becoming "one great blooming, buzzing confusion" (as William James put it in 1890). The strongest evidence in favor of the hypothesis that sensors evolved to focus on biologically important stimuli is that sensor limitations differ across species, often dramatically. For example, many insects and birds can detect ultraviolet radiation; some snakes find prey by means of infrared sensors; and bats, as well as dolphins, can hear ultrasound. Turtles and homing pigeons can sense magnetic fields; and many fishes, as well as the platypus, are able to detect weak electric fields (see Box 6. For example, most fishes and salamanders cannot hear frequencies above ~2 kHz; and dolphins and their relatives, the whales, have lost their main olfactory sense. Thus, the point is not that other animals perceive a broader range of stimuli than we do but that each species senses a different range of stimuli. This conclusion is important to keep in mind when you are designing (or interpreting) behavioral experiments on non-humans. Even within an individual, sensor sensitivity can vary dramatically as it is adjusted to current conditions. Adaptation to prolonged stimuli also occurs in the olfactory system, where Ca 2+ accumulation in the olfactory sensory neurons reduces the signal amplification provided by the olfactory transduction cascade (through a variety of mechanisms). As a rule, such changes in sensitivity ensure that sensors do not respond to steady "background" stimuli. A major benefit of such background adaptation is that it leaves the sensors exquisitely sensitive to changes in stimulation. There is, however, a downside to the changeability of sensor sensitivity, namely the loss of information about absolute stimulus levels. If you look at the headlights of a car at night, for instance, they will seem brighter than they would in daylight, largely because your vision is more sensitive when it is generally dark. To determine the absolute intensity of those car lights, you have to use a light meter.

The clinical presentation of Mycobacterium tuberculosis includes fevers and night sweats acne fulminans order permethrin 30 gm overnight delivery, weight loss acne 8 yr old girl order permethrin 30 gm without prescription, cough skin care doctors order discount permethrin on line, and hemoptysis acne yeast buy permethrin paypal. The term Ghon complex refers to the combination of the Ghon focus and secondarily-involved hilar lymph nodes with granulomas acne questions generic permethrin 30 gm buy line. Most primary pulmonary tuberculosis lesions (95%) will undergo fibrosis and calcification. Sites that may become involved include meninges; cervical lymph nodes (scrofula) and larynx; liver/spleen, kidneys, adrenals, and ileum; lumbar vertebrae bone marrow (Pott disease); and fallopian tubes and epididymis. It may be asymptomatic, or presenting symptoms may include cough and shortness of breath; fatigue and malaise; skin lesions; eye irritation or pain; and fever or night sweats. Most often, the disease is first detected on chest x-ray as bilateral hilar lymphadenopathy or parenchymal infiltrates. The noncaseating granulomas that are characteristic of sarcoidosis may occur in any organ of the body. In the lung, they typically form diffuse scattered granulomas; lymph node involvement may cause hilar and mediastinal adenopathy. Skin, liver and/or spleen, heart, central nervous system, bone marrow, and gastrointestinal tract are also frequent targets of the disease. Eye involvement can be seen in Mikulicz syndrome (involvement of the uvea and parotid). In practice, this means that the diagnosis is considered when a biopsy shows features characteristic of sarcoidosis (such as noncaseating granulomas, Schaumann bodies [laminated dystrophic calcification], and asteroid bodies [stellate giant cell cytoplasmic inclusions]). There are no pathognomonic microscopic features though, and the diagnosis requires clinicopathologic correlation. Glomerular diseases may be divided into those originating in the kidney and those caused by systemic disease (secondary). There is a decreasing incidence in the United States; children are affected more often than adults. The crescents are composed of fibrin, parietal epithelial cells, monocytes, and macrophages. Immunofluorescence shows granular deposits of IgG and C3 throughout the glomerulus within the capillary walls and some mesangial areas. Renal biopsy findings include hypercellularity, crescents, and fibrin deposition in glomeruli. By electron microscopy, there are no deposits, but there is glomerular basement membrane disruption. Even with treatment (plasma exchange, steroids, and cytotoxic drugs), the prognosis is poor because of risks of severe and life-threatening pulmonary hemorrhage and renal failure. Immune-complex mediated crescentic glomerulonephritis · Any of the immune complex nephritides can cause crescent formation. Crescent Formation in Rapidly Progressive Glomerulonephritis, as Seen with Trichrome Stain IgA nephropathy (Berger disease) is the most common cause of glomerulonephritis in the world, being particularly common in France, Japan, Italy, and Austria. IgA nephropathy can be associated with celiac sprue and Henoch-Schönlein purpura or can be secondary to celiac sprue or liver disease. The pathogenesis is unknown, but may be related to a possible entrapment of circulating immune complexes with activation of the alternate complement pathway; it may also be related to a genetic predisposition. This antibody stabilizes C3 convertase, which leads to enhanced degradation and low serum levels of C3. Light microscopy demonstrates a lobulated appearance of the glomeruli due to mesangial and endothelial cell proliferation and/or deposition of subendothelial immune complex deposits. It is characterized by hereditary nephritis, hearing loss, and ocular abnormalities. Hearing loss (leading to sensorineural deafness) and various ocular abnormalities of the lens and cornea can occur. Electron microscopy shows alternating thickening and thinning of basement membrane with splitting of the lamina densa, causing a "basketweave" appearance. Most cases (85%) are idiopathic; in most of these cases, autoantibodies cross-react with podocyte antigens. Membranous glomerulonephritis may also be caused by drugs (penicillamine), infections (hepatitis virus B and C, syphilis, etc. It has also been associated with malignant carcinomas of the lung and colon, and there may be a genetic predisposition. Electron microscopy shows subepithelial deposits along the basement membranes with effacement of podocyte foot processes. The clinical course is variable and may lead to spontaneous remission, persistent proteinuria, or end-stage renal disease. Minimal change disease (also called lipoid nephrosis and nil disease) is the most common cause of nephrotic syndrome in children. Light microscopy shows normal glomeruli with lipid accumulation in proximal tubule cells (lipoid nephrosis). Electron microscopy shows effacement of epithelial (podocyte) foot processes, microvillous transformation, and no immune complex deposits. The prognosis is excellent because treatment with corticosteroids produces a dramatic response in children. Focal segmental glomerulosclerosis is a very common cause of nephrotic syndrome that occurs in all ages. Light microscopy shows focal segmental sclerosis and hyalinization of glomeruli; focal segmental glomerulosclerosis initially affects the glomeruli along the medullary border. Electron microscopy shows effacement of foot processes in nonsclerotic regions and increased mesangial matrix in sclerotic segments. There is frequently a poor response to steroids, with the overall prognosis being poor (most progressing to chronic renal failure), though children do better than adults. Initials Secondary glomerulonephritis is glomerular disease that is secondary to other dis- Diabetes causes nodular glomerulosclerosis, hyaline arteriolosclerosis, and diabetic microangiopathy. Clinically, diabetic patients may develop microalbuminuria that can progress to nephrotic syndrome. Sclerotic Nodules (arrows) of Nodular glomerulosclerosis (Kimmelstiel-Wilson syndrome), kidney (Kimmelstiel-Wilson Syndrome) Associated with Diabetes Systemic lupus erythematosus can cause various patterns of damage to the kidney with clinical features that can include hematuria, nephritic syndrome, nephrotic syndrome, hypertension, and renal failure. Clinical features include anemia, anorexia, malaise, proteinuria, hypertension, and azotemia. On pathologic examination, the kidneys are grossly small and shrunken; microscopic exam shows hyalinization of glomeruli, interstitial fibrosis, atrophy of tubules, and a lymphocytic infiltrate. It can be due to many causes, including medications, infections, acute pyelonephritis, systemic lupus erythematosus, lead poisoning, urate nephropathy, or multiple myeloma. Pyelonephritis affects females much more than males, but the incidence increases in older males with prostatic hyperplasia. Causative organisms include gram-negative enteric bacilli, Escherichia coli, Proteus, Klebsiella, and Enterobacter. Predisposing factors include urinary obstruction, vesicoureteral reflux, pregnancy, urethral instrumentation, diabetes mellitus, benign prostatic hyperplasia, and other renal pathology. Symptoms can include fever, chills, and malaise; dysuria, frequency, and urgency; and costovertebral angle tenderness. Scarring can be seen at the upper and lower poles of the kidney, with associated calyceal blunting. Microscopically there is interstitial fibrosis and inflammation with thyroidization of the tubule. This hypersensitivity reaction presents a couple of weeks after drug exposure with fever, eosinophilia, rash, and hematuria. Clinical Correlate It may be difficult to distinguish cystitis from pyelonephritis. The condition is due to decreased blood flow caused by severe hemorrhage, severe renal vasoconstriction, hypotension, dehydration, or shock. The prognosis is excellent if the patient survives the underlying disease, and if the patient had no preexisting kidney disease. Magnesium ammonium phosphate ("struvite") stones are associated with infection by urea-splitting bacteria (proteus), and these stones often form large staghorn calculi. Struvite (Magnesium Ammonium Phosphate) Stone Forming Staghorn Calculi · Pathology. Most stones are unilateral stones that are formed in the calyx, pelvis, and urinary bladder. Clinically, it causes progressive irreversible azotemia, normocytic anemia, platelet dysfunction, renal osteodystrophy, and hypertension. Renal Artery Stenosis as Demonstrated by Angiogram Benign nephrosclerosis is caused by hypertension. The kidneys have a finely gran- ular external surface and on microscopy show hyaline arteriolosclerosis, tubular atrophy, interstitial fibrosis, and glomerulosclerosis. Malignant (accelerated) hypertension can damage the kidney, causing fibrinoid necrosis of arterioles, glomerulitis, and hyperplastic arteriolosclerosis. Clinically, it causes cerebral edema, papilledema, retinal hemorrhage, intracerebral hemorrhage, and oliguric acute renal failure. Renal infarction is due to thrombi from the left side of the heart, atheroembolic disease, and vasculitis. Sickle cell anemia can cause medullary infarctions due to blockage of blood flow in the medullary vessels, which can result in asymptomatic hematuria, loss of urine concentrating ability, renal papillary necrosis, and pyelonephritis. Diffuse cortical necrosis can cause anuria; the condition can occur with obstetric emergencies and disseminated intravascular coagulation. The papillary adenomas share the same chromosomal gains as papillary renal cell carcinoma. In 10% of cases, the "classic" triad occurs: · Hematuria · Palpable mass · Flank pain © Katsumi M. Gross examination typically demonstrates a large, solitary yellow mass found most commonly in the upper pole. The tumor often invades the renal vein and may extend into the inferior vena cava and heart. Microscopic examination reveals a tumor containing 3 elements: metanephric blastema, epithelial elements (immature glomeruli and tubules), and stroma. Treatment is surgery, chemotherapy, and radiation, which as a combined therapy yields an excellent prognosis. Transitional cell carcinomas can involve the renal pelvis as well as the urinary bladder. Specific causes include renal stones, retroperitoneal fibrosis, benign prostatic hyperplasia, and cervical cancer. If complete obstruction occurs suddenly, necrosis of the renal papillae may result. Retroperitoneal fibrosis is usually an idiopathic condition causing severe fibrosis of the retroperitoneal area, which can entrap the ureters. Some cases show sclerosing conditions in other body sites and are associated with elevated serum IgG4. Exstrophy of the bladder is a developmental failure of the formation of the abdominal wall and bladder which leaves the bladder open at the body surface. The etiology of cystitis varies, with important causes including organisms, notably from fecal flora (Escherichia coli, Proteus, Klebsiella, Enterobacter); radiation cystitis (may follow radiation therapy); and chemotherapy agents such as cyclophosphamide (hemorrhagic cystitis). Symptoms include frequency, urgency, dysuria, and suprapubic pain; systemic signs such as fever and malaise are uncommon. Predisposing factors include benign prostatic hypertrophy, bladder calculi, and cystocele. Malakoplakia is a bladder inflammatory pattern associated with a defect in macro- There is an increasing incidence of urinary bladder tumors; males are affected more than females, and peak incidence is age 40-60. Risk factors include: · Cigarette smoking and occupational exposure to azo dye production (transitional cell carcinoma) (both due to 2-naphthylamine) · Chronic bladder infection with Schistosoma haemotobium (squamous cell carcinoma) (Africa including Egypt and the Middle East) Bladder cancer usually presents with painless hematuria, but it may also cause dysuria, urgency, frequency, hydronephrosis, and pyelonephritis. Precursors of invasive transitional cell carcinoma can arise from a flat or papillary lesion. Other bladder tumors include papillomas, adenocarcinoma, and embryonal rhabdomyosarcoma. Migratory Eggs of Schistosoma haemotobium Surrounded inflammation in theby Densewall, which predisposes to squamous cell carcinoma bladder Inflammation in the Bladder Wall Miscellaneous bladder conditions · Acquired diverticuli can complicate urinary tract outlet obstruction due to benign prostatic hyperplasia or other causes. Bilateral renal agenesis is incompatible with life, but persons with unilateral agenesis may have adequate renal function. Other congenital anomalies of the kidney include hypoplasia, horseshoe kidney, and abnormal locations. Autosomal recessive polycystic kidney disease presents in infancy with progressive renal failure. Autosomal dominant polycystic kidney disease presents in adulthood with renal insufficiency, hematuria, and hypertension. Renal dysplasia is the most common renal cystic disease in children and may cause a renal mass and renal failure. Nephronophthisis-medullary cystic disease complex may progress to renal failure, but medullary sponge kidney is generally innocuous. Glomerular diseases can present with either nephritic syndrome or nephrotic syndrome. Nephritic syndrome is characterized by hematuria, hypertension, azotemia, oliguria, and proteinuria <3. Acute post-streptococcal glomerulonephritis is associated with subepithelial immune complex deposits (subepithelial humps) by electron microscopy, occurs 2­4 weeks after a streptococcal infection of the throat or skin, and usually causes nephritic syndrome in children. Anti-glomerular basement membrane antibody-mediated crescentic glomerulonephritis is characterized by a smooth and linear pattern of IgG and C3 by immunofluorescence. Rapidly progressive glomerulonephritis is characterized microscopically by hypercellular glomeruli with crescent formation in Bowman space. IgA nephropathy is characterized by mesangial deposits of IgA and C3, is the most common cause of glomerulonephritis worldwide, and tends to produce recurrent gross hematuria in children and young adults. Membranoproliferative glomerulonephritis is characterized microscopically by mesangial proliferation and basement membrane splitting and clinically may produce a nephritic pattern, a nephrotic pattern, or a mixed pattern.

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