Necrosis
Tumor Necrosis Factor-alpha
Receptors, Tumor Necrosis Factor
Receptors, Tumor Necrosis Factor, Type II
Fat Necrosis
Femur Head Necrosis
Kidney Papillary Necrosis
Kidney Cortex Necrosis
Cytokines
Kidney Tubular Necrosis, Acute
Interleukin-1
Apoptosis
Tumor Necrosis Factors
Cells, Cultured
Lipopolysaccharides
NF-kappa B
Interleukin-6
RNA, Messenger
Infectious pancreatic necrosis virus
Lymphotoxin-alpha
Interferon-gamma
Macrophages
Tumor Necrosis Factor Decoy Receptors
TNF-Related Apoptosis-Inducing Ligand
Inflammation
Signal Transduction
Retinal Necrosis Syndrome, Acute
Monocytes
Disease Models, Animal
Dose-Response Relationship, Drug
Caspases
Gene Expression Regulation
Infectious hematopoietic necrosis virus
Liver
Cell Death
Receptor-Interacting Protein Serine-Threonine Kinases
Interleukin-8
Cell Survival
Antigens, CD
Mice, Knockout
Interleukin-1beta
Tumor Cells, Cultured
Arthritis, Rheumatoid
Apoptosis Regulatory Proteins
Gene Expression
Inflammation Mediators
Interleukin-10
Reverse Transcriptase Polymerase Chain Reaction
Receptors, TNF-Related Apoptosis-Inducing Ligand
Up-Regulation
Neutrophils
Immunohistochemistry
Enzyme-Linked Immunosorbent Assay
Caspase 8
Endotoxins
Drug-Induced Liver Injury
Molecular Sequence Data
Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
TNF Receptor-Associated Factor 2
Flow Cytometry
Macrophage Activation
Enzyme Activation
Caspase 3
Pancreatitis, Acute Necrotizing
I-kappa B Proteins
Endothelium, Vascular
Blotting, Western
Rats, Sprague-Dawley
Fish Diseases
TNF Receptor-Associated Factor 1
Pentoxifylline
Transfection
Biological Markers
Base Sequence
Intercellular Adhesion Molecule-1
Leukocytes, Mononuclear
Lung
Macrophages, Peritoneal
Rats, Wistar
Fibroblasts
Nitric Oxide
Down-Regulation
Antigens, CD95
I-kappa B Kinase
Immunoglobulin G
Enzyme Inhibitors
JNK Mitogen-Activated Protein Kinases
ADAM Proteins
Nitric Oxide Synthase Type II
Dental Pulp Necrosis
p38 Mitogen-Activated Protein Kinases
Transcription Factor RelA
Receptors, Tumor Necrosis Factor, Member 25
Cell Division
Reactive Oxygen Species
Skin
Mitogen-Activated Protein Kinases
DNA Fragmentation
Synovial Membrane
Treatment Outcome
Caspase Inhibitors
Transcription, Genetic
Kidney
Myocardium
Shock, Septic
Phosphorylation
Proteins
TNF Receptor-Associated Factor 6
In Situ Nick-End Labeling
Cycloheximide
Carrier Proteins
Receptors, Cell Surface
Reperfusion Injury
Anti-Inflammatory Agents, Non-Steroidal
Alanine Transaminase
Ischemia
Vascular Cell Adhesion Molecule-1
Promoter Regions, Genetic
Chemokine CCL2
Antibodies
Pancreatitis
Receptors, Tumor Necrosis Factor, Member 6b
Oxidative Stress
Caspase 9
Interleukins
Immunologic Factors
Tetradecanoylphorbol Acetate
Nitric Oxide Synthase
Granulocyte-Macrophage Colony-Stimulating Factor
Jurkat Cells
Fas Ligand Protein
Dinoprostone
DNA Primers
Cell Adhesion Molecules
Chemokines
Epithelial Cells
Polymerase Chain Reaction
Leukocytes
Membrane Proteins
Rhabdoviridae
Lymphocyte Activation
Macrophages, Alveolar
Interleukin 1 Receptor Antagonist Protein
Blotting, Northern
Fas-Associated Death Domain Protein
Interleukin-12
Amino Acid Sequence
U937 Cells
Mitochondria
Mice, Inbred Strains
Fibrosarcoma
Microscopy, Electron
Endothelial Cells
Toll-Like Receptor 4
CASP8 and FADD-Like Apoptosis Regulating Protein
Hepatocytes
TNF Receptor-Associated Death Domain Protein
Umbilical Veins
L-Lactate Dehydrogenase
Mice, Transgenic
Granuloma
E-Selectin
C-Reactive Protein
Dendritic Cells
Proto-Oncogene Proteins c-bcl-2
Glycoproteins
Protein Binding
Peroxidase
Rhabdoviridae Infections
Surgical Flaps
RNA, Small Interfering
Interleukin-4
Edema
Rabbits
Recombinant Fusion Proteins
Cell Differentiation
Femur Head
Severity of Illness Index
Cell Nucleus
Systemic infection with Alaria americana (Trematoda). (1/6081)
Alaria americana is a trematode, the adult of which is found in mammalian carnivores. The first case of disseminated human infection by the mesocercarial stage of this worm occurred in a 24-year-old man. The infection possibly was acquired by the eating of inadequately cooked frogs, which are intermediate hosts of the worm. The diagnosis was made during life by lung biopsy and confirmed at autopsy. The mesocercariae were present in the stomach wall, lymph nodes, liver, myocardium, pancreas and surrounding adipose tissue, spleen, kidney, lungs, brain and spinal cord. There was no host reaction to the parasites. Granulomas were present in the stomach wall, lymph nodes and liver, but the worms were not identified in them. Hypersensitivity vasculitis and a bleeding diathesis due to disseminated intravascular coagulation and a circulating anticoagulant caused his death 8 days after the onset of his illness. (+info)Daunorubicin-induced apoptosis in rat cardiac myocytes is inhibited by dexrazoxane. (2/6081)
-The clinical efficacy of anthracycline antineoplastic agents is limited by a high incidence of severe and usually irreversible cardiac toxicity, the cause of which remains controversial. In primary cultures of neonatal and adult rat ventricular myocytes, we found that daunorubicin, at concentrations /=10 micromol/L induced necrotic cell death within 24 hours, with no changes characteristic of apoptosis. To determine whether reactive oxygen species play a role in daunorubicin-mediated apoptosis, we monitored the generation of hydrogen peroxide with dichlorofluorescein (DCF). However, daunorubicin (1 micromol/L) did not increase DCF fluorescence, nor were the antioxidants N-acetylcysteine or the combination of alpha-tocopherol and ascorbic acid able to prevent apoptosis. In contrast, dexrazoxane (10 micromol/L), known clinically to limit anthracycline cardiac toxicity, prevented daunorubicin-induced myocyte apoptosis, but not necrosis induced by higher anthracycline concentrations (>/=10 micromol/L). The antiapoptotic action of dexrazoxane was mimicked by the superoxide-dismutase mimetic porphyrin manganese(II/III)tetrakis(1-methyl-4-peridyl)porphyrin (50 micromol/L). The recognition that anthracycline-induced cardiac myocyte apoptosis, perhaps mediated by superoxide anion generation, occurs at concentrations well below those that result in myocyte necrosis, may aid in the design of new therapeutic strategies to limit the toxicity of these drugs. (+info)Changes in the total number of neuroglia, mitotic cells and necrotic cells in the anterior limb of the mouse anterior commissure following hypoxic stress. (3/6081)
The effects of hypoxic stress (390 mmHg) on the total number of glia, cell division, and cell death in the anterior limb of the anterior commissure were studied. There was a significant (P less than 0-01) fall in the total number of glia following exposure to hypoxia at 390 mmHg for two days. No significant change was observed in the total number of glia between the hypoxic and recovery group one week after return to sea level (ca. 760 mmHg). No change was observed in the number of mitotic figures in the control, hypoxic or recovery groups, but significant falls were observed in the mean number of necrotic cells between both the control and hypoxic groups (P less than 0-05) and the hypoxic and recovery groups (P less than 0-012). The decrease in necrotic cells may be due to a large number of elderly and effete cells, which would normally have undergone degeneration over a period of weeks, dying rapidly after the onset of hypoxia, thus temporarily reducing the daily cell death rate. (+info)A photodynamic pathway to apoptosis and necrosis induced by dimethyl tetrahydroxyhelianthrone and hypericin in leukaemic cells: possible relevance to photodynamic therapy. (4/6081)
The mechanism of cell death induction by dimethyl tetrahydroxyhelianthrone (DTHe), a new second-generation photodynamic sensitizer, is analysed in human leukaemic cell lines in comparison with the structurally related hypericin. DTHe has a broad range of light spectrum absorption that enables effective utilization of polychromatic light. Photosensitization of HL-60 cells with low doses of DTHe (0.65 microM DTHe and 7.2 J cm(-2) light energy) induced rapid apoptosis of > or =90% of the cells. At doses > or =2 microM, dying cells assumed morphological necrosis with perinucleolar condensation of chromatin in HL-60 and K-562 cell lines. Although nuclear fragmentation that is characteristic to apoptosis was prevented, DNA digestion to oligonucleosomes proceeded unhindered. Such incomplete apoptosis was more prevalent with the related analogue hypericin throughout most doses of photosensitization. Despite hypericin being a stronger photosensitizer, DTHe exhibited advantageous phototoxic properties to tumour cells, initiating apoptosis at concentrations about threefold lower than hypericin. Photosensitization of the cells induced dissociation of the nuclear envelope, releasing lamins into the cytosol. DTHe also differed from hypericin in effects exerted on the nuclear lamina, causing release of an 86-kDa lamin protein into the cytosol that was unique to DTHe. Within the nucleus, nuclear envelope lamin B underwent covalent polymerization, which did not affect apoptotic nuclear fragmentation at low doses of DTHe. At higher doses, polymerization may have been extensive enough to prevent nuclear collapse. Hut-78, CD4+ cells were resistant to the photodynamically activated apoptotic pathway. Beyond the tolerated levels of photodynamic damage, these cells died exclusively via necrosis. Hut-78 cells overexpress Bcl-X(L) as well as a truncated Bcl-X(L)tr isoform that could contribute to the observed resistance to apoptosis. (+info)Diet and risk of ethanol-induced hepatotoxicity: carbohydrate-fat relationships in rats. (5/6081)
Nutritional status is a primary factor in the effects of xenobiotics and may be an important consideration in development of safety standards and assessment of risk. One important xenobiotic consumed daily by millions of people worldwide is alcohol. Some adverse effects of ethanol, such as alcohol liver disease, have been linked to diet. For example, ethanol-induced hepatotoxicity in animal models requires diets that have a high percentage of the total calories as unsaturated fat. However, little attention has been given to the role of carbohydrates (or carbohydrate to fat ratio) in the effects of this important xenobiotic on liver injury. In the present study, adult male Sprague-Dawley rats (8-10/group) were infused (intragastrically) diets high in unsaturated fat (25 or 45% total calories), sufficient protein (16%) and ethanol (38%) in the presence or absence of adequate carbohydrate (21 or 2.5%) for 42-55 days (d). Animals infused ethanol-containing diets adequate in carbohydrate developed steatosis, but had no other signs of hepatic pathology. However, rats infused with the carbohydrate-deficient diet had a 4-fold increase in serum ALT levels (p < 0.05), an unexpectedly high (34-fold) induction of hepatic microsomal CYP2E1 apoprotein (p < 0.001), and focal necrosis. The strong positive association between low dietary carbohydrate, enhanced CYP2E1 induction and hepatic necrosis suggests that in the presence of low carbohydrate intake, ethanol induction of CYP2E1 is enhanced to levels sufficient to cause necrosis, possibly through reactive oxygen species and other free radicals generated by CYP2E1 metabolism of ethanol and unsaturated fatty acids. (+info)Tumor suppression in human skin carcinoma cells by chromosome 15 transfer or thrombospondin-1 overexpression through halted tumor vascularization. (6/6081)
The development of skin carcinomas presently is believed to be correlated with mutations in the p53 tumor suppressor and ras gene as well as with the loss of chromosome 9. We now demonstrate that, in addition, loss of chromosome 15 may be a relevant genetic defect. Reintroduction of an extra copy of chromosome 15, but not chromosome 4, into the human skin carcinoma SCL-I cells, lacking one copy of each chromosome, resulted in tumor suppression after s.c. injection in mice. Transfection with thrombospondin-1 (TSP-1), mapped to 15q15, induced the same tumor suppression without affecting cell proliferation in vitro or in vivo. Halted tumors remained as small cysts encapsulated by surrounding stroma and blood vessels. These cysts were characterized by increased TSP-1 matrix deposition at the tumor/stroma border and a complete lack of tumor vascularization. Coinjection of TSP-1 antisense oligonucleotides drastically reduced TSP-1 expression and almost completely abolished matrix deposition at the tumor/stroma border. As a consequence, the tumor phenotype reverted to a well vascularized, progressively expanding, solid carcinoma indistinguishable from that induced by the untransfected SCL-I cells. Thus, these data strongly suggest TSP-1 as a potential tumor suppressor on chromosome 15. The data further propose an unexpected mechanism of TSP-1-mediated tumor suppression. Instead of interfering with angiogenesis in general, in this system TSP-1 acts as a matrix barrier at the tumor/stroma border, which, by halting tumor vascularization, prevents tumor cell invasion and, thus, tumor expansion. (+info)Mycophenolate mofetil inhibits rat and human mesangial cell proliferation by guanosine depletion. (7/6081)
BACKGROUND: Mycophenolate mofetil (MMF) is used for immunosuppression after renal transplantation because it reduces lymphocyte proliferation by inhibiting inosine monophosphate dehydrogenase (IMPDH) in lymphocytes and GTP biosynthesis. In the present study we asked if therapeutic concentrations of MMF might interfere with mesangial cell (MC) proliferation which is involved in inflammatory proliferative glomerular diseases. METHODS: Rat and human MCs were growth-arrested by withdrawal of fetal calf serum (FCS) and stimulated by addition of FCS, platelet-derived growth factor (PDGF) or lysophosphatidic acid (LPA). Different concentrations of MMF (0.019-10 microM) were added concomitantly in the presence or absence of guanosine. MC proliferation was determined by [3H]thymidine incorporation. Cell viability was assessed by trypan blue exclusion. Apoptotic nuclei were stained using the Hoechst dye H33258. Cytosolic free Ca2+ concentrations were determined with the fluorescent calcium chelator fura-2-AM. RESULTS: MMF inhibited mitogen-induced rat MC proliferation with an IC50 of 0.45 +/- 0.13 microM. Human MCs proved to be even more sensitive (IC50 0.19 +/- 0.06 microM). Inhibition of MC proliferation was reversible and not accompanied by cellular necrosis or apoptosis. Addition of guanosine prevented the antiproliferative effect of MMF, indicating that inhibition of IMPDH is responsible for decreased MC proliferation. Early signalling events of GTP-binding-protein-coupled receptors, such as changes in intracellular Ca2+ levels were not affected by MMF. CONCLUSIONS: The results show that MMF has a concentration-dependent antiproliferative effect on cultured MCs in the therapeutic range, which might be a rationale for the use of this drug in the treatment of mesangial proliferative glomerulonephritis. (+info)Bcl-2 alters the balance between apoptosis and necrosis, but does not prevent cell death induced by oxidized low density lipoproteins. (8/6081)
Oxidized low density lipoproteins (oxLDL) participate in atherosclerosis plaque formation, rupture, and subsequent thrombosis. Because oxLDL are toxic to cultured cells and Bcl-2 protein prevents apoptosis, the present work aimed to study whether Bcl-2 may counterbalance the toxicity of oxLDL. Two experimental model systems were used in which Bcl-2 levels were modulated: 1) lymphocytes in which the (high) basal level of Bcl-2 was reduced by antisense oligonucleotides; 2) HL60 and HL60/B (transduced by Bcl-2) expressing low and high Bcl-2 levels, respectively. In cells expressing relatively high Bcl-2 levels (lymphocytes and HL60/B), oxLDL induced mainly primary necrosis. In cells expressing low Bcl-2 levels (antisense-treated lymphocytes, HL60 and ECV-304 endothelial cells), the rate of oxLDL-induced apoptosis was higher than that of primary necrosis. OxLDL evoked a sustained calcium rise, which is a common trigger to necrosis and apoptosis since both types of cell death were blocked by the calcium chelator EGTA. Conversely, a sustained calcium influx elicited by the calcium ionophore A23187 induced necrosis in cells expressing high Bcl-2 levels and apoptosis in cells expressing low Bcl-2 levels. This suggests that Bcl-2 acts downstream from the calcium peak and inhibits only the apoptotic pathway, not the necrosis pathway, thus explaining the apparent shift from oxLDL-induced apoptosis toward necrosis when Bcl-2 is overexpressed. (+info)Necrosis is a type of cell death that occurs when cells are exposed to excessive stress, injury, or inflammation, leading to damage to the cell membrane and the release of cellular contents into the surrounding tissue. This can lead to the formation of gangrene, which is the death of body tissue due to lack of blood supply.
There are several types of necrosis, including:
1. Coagulative necrosis: This type of necrosis occurs when there is a lack of blood supply to the tissues, leading to the formation of a firm, white plaque on the surface of the affected area.
2. Liquefactive necrosis: This type of necrosis occurs when there is an infection or inflammation that causes the death of cells and the formation of pus.
3. Caseous necrosis: This type of necrosis occurs when there is a chronic infection, such as tuberculosis, and the affected tissue becomes soft and cheese-like.
4. Fat necrosis: This type of necrosis occurs when there is trauma to fatty tissue, leading to the formation of firm, yellowish nodules.
5. Necrotizing fasciitis: This is a severe and life-threatening form of necrosis that affects the skin and underlying tissues, often as a result of bacterial infection.
The diagnosis of necrosis is typically made through a combination of physical examination, imaging studies such as X-rays or CT scans, and laboratory tests such as biopsy. Treatment depends on the underlying cause of the necrosis and may include antibiotics, surgical debridement, or amputation in severe cases.
The symptoms of fat necrosis can vary depending on the location and extent of the affected tissue. In some cases, there may be no symptoms at all, while in others, there may be pain, swelling, redness, and warmth in the affected area. If the condition becomes severe, it can lead to the formation of a fat necrosis mass or abscess, which can be painful and tender to the touch.
Fat necrosis is typically diagnosed through imaging studies such as ultrasound, CT scan, or MRI. A biopsy may also be performed to confirm the diagnosis and rule out other conditions.
Treatment of fat necrosis depends on the severity of the condition and can range from conservative measures such as rest, ice, compression, and elevation (RICE) to surgical intervention in more severe cases. In some cases, antibiotics may be prescribed if there is an underlying infection.
Preventing fat necrosis is challenging, but it can be minimized by avoiding trauma or injury to the affected area, maintaining good wound care, and managing any underlying medical conditions that may contribute to the development of the condition.
This can cause pain, stiffness, and difficulty walking. In severe cases, it can lead to complete hip joint dislocation. FHN is typically caused by trauma or aseptic conditions such as osteonecrosis (death of bone cells due to lack of blood supply), sickle cell disease, Gaucher's disease, and long-term use of steroids. Treatment options include conservative management with pain management, physical therapy, and avoiding activities that exacerbate the condition; or surgical intervention such as femoral head osteotomy (cutting and realigning the bone) or hip replacement.
The prognosis for FHN depends on the severity of the condition, with more severe cases carrying a worse prognosis. Early diagnosis and treatment are key to improving outcomes.
Symptoms:
* Blood in urine
* Pain in the back or flank
* Fever
* Nausea and vomiting
Diagnosis:
* Imaging tests like ultrasound, CT scan, or MRI to visualize the papillae and assess any damage
* Biopsy to examine kidney tissue under a microscope for signs of inflammation and scarring
Treatment:
* Antibiotics for infections
* Corticosteroids to reduce inflammation
* Immunosuppressive drugs for autoimmune disorders
* Dialysis in severe cases
Prognosis:
* Mild cases may resolve on their own, but severe cases can lead to chronic kidney disease and potentially kidney failure.
Complications:
* Chronic kidney disease
* Kidney failure
* High blood pressure
* Recurrent infections
Kidney cortex necrosis is a condition where there is death of the cells in the outer layer of the kidney, known as the renal cortex. This can occur due to various reasons such as injury, infection, or inflammation. The symptoms of kidney cortex necrosis may include fever, pain in the flank or abdomen, nausea, vomiting, and blood in the urine.
Diagnosis is typically made through a combination of imaging studies such as CT scans or ultrasound, and laboratory tests to evaluate kidney function. Treatment may involve supportive care to manage symptoms and address any underlying causes, as well as medications to help protect the remaining healthy kidney tissue. In severe cases, dialysis or a kidney transplant may be necessary.
Kidney cortex necrosis can be acute or chronic, and the prognosis depends on the underlying cause and the extent of the damage. Prompt medical attention is essential to prevent further damage and improve outcomes.
In this answer, we will explore the definition of 'Kidney Tubular Necrosis, Acute' in more detail, including its causes, symptoms, diagnosis, and treatment options.
What is Kidney Tubular Necrosis, Acute?
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Kidney Tubular Necrosis, Acute (ATN) is a condition that affects the tubules of the kidneys, leading to inflammation and damage. The condition is often caused by various factors such as sepsis, shock, toxins, or medications.
The term "acute" refers to the sudden and severe nature of the condition, which can progress rapidly within hours or days. The condition can be life-threatening if left untreated, and it is important to seek medical attention immediately if symptoms persist or worsen over time.
Causes of Kidney Tubular Necrosis, Acute
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There are various factors that can cause Kidney Tubular Necrosis, Acute, including:
### 1. Sepsis
Sepsis is a systemic inflammatory response to an infection, which can lead to damage to the tubules of the kidneys.
### 2. Shock
Shock can cause a decrease in blood flow to the kidneys, leading to damage and inflammation.
### 3. Toxins
Exposure to certain toxins, such as heavy metals or certain medications, can damage the tubules of the kidneys.
### 4. Medications
Certain medications, such as antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs), can cause damage to the tubules of the kidneys.
### 5. Infection
Infections such as pyelonephritis or perinephric abscess can spread to the kidneys and cause inflammation and damage to the tubules.
### 6. Radiation necrosis
Radiation therapy can cause damage to the kidneys, leading to inflammation and scarring.
### 7. Kidney transplant rejection
Rejection of a kidney transplant can lead to inflammation and damage to the tubules of the transplanted kidney.
Symptoms of Kidney Tubular Necrosis, Acute
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The symptoms of acute tubular necrosis can vary depending on the severity of the condition and the underlying cause. Some common symptoms include:
### 1. Fatigue
Fatigue is a common symptom of acute tubular necrosis, as the condition can lead to a decrease in the kidneys' ability to filter waste products from the blood.
### 2. Nausea and vomiting
Nausea and vomiting can occur due to electrolyte imbalances and changes in fluid levels in the body.
### 3. Decreased urine output
Acute tubular necrosis can cause a decrease in urine production, as the damaged tubules are unable to filter waste products from the blood effectively.
### 4. Swelling (edema)
Swelling in the legs, ankles, and feet can occur due to fluid buildup in the body.
### 5. Abdominal pain
Abdominal pain can be a symptom of acute tubular necrosis, as the condition can cause inflammation and scarring in the kidneys.
### 6. Fever
Fever can occur due to infection or inflammation in the kidneys.
### 7. Blood in urine (hematuria)
Hematuria, or blood in the urine, can be a symptom of acute tubular necrosis, as the damaged tubules can leak blood into the urine.
## Causes and risk factors
The exact cause of acute tubular necrosis is not fully understood, but it is believed to be due to damage to the kidney tubules, which can occur for a variety of reasons. Some possible causes and risk factors include:
1. Sepsis: Bacterial infections can spread to the kidneys and cause inflammation and damage to the tubules.
2. Toxins: Exposure to certain toxins, such as heavy metals or certain medications, can damage the kidney tubules.
3. Medications: Certain medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics, can cause kidney damage and increase the risk of acute tubular necrosis.
4. Hypotension: Low blood pressure can reduce blood flow to the kidneys and increase the risk of acute tubular necrosis.
5. Shock: Severe shock can lead to damage to the kidney tubules.
6. Burns: Severe burns can cause damage to the kidneys and increase the risk of acute tubular necrosis.
7. Trauma: Traumatic injuries, such as those caused by car accidents or falls, can damage the kidneys and increase the risk of acute tubular necrosis.
8. Surgery: Major surgery can cause damage to the kidneys and increase the risk of acute tubular necrosis.
9. Kidney disease: People with pre-existing kidney disease are at increased risk of developing acute tubular necrosis.
10. Chronic conditions: Certain chronic conditions, such as diabetes and high blood pressure, can increase the risk of developing acute tubular necrosis.
It is important to note that acute tubular necrosis can occur in people with no underlying medical conditions or risk factors, and it is often a diagnosis of exclusion, meaning that other potential causes of the person's symptoms must be ruled out before the diagnosis can be made.
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
The symptoms of acute RNS may include:
1. Severe eye pain
2. Blurred vision or loss of vision
3. Sensitivity to light
4. Redness and swelling of the eye
5. Floaters (specks or cobwebs in vision)
6. Flashes of light
The exact cause of acute RNS is not known, but it is believed to be related to a viral or bacterial infection, trauma, or systemic diseases such as diabetes, high blood pressure, and autoimmune disorders.
Diagnosis of acute RNS typically involves a comprehensive eye exam, including imaging tests such as fluorescein angiography and optical coherence tomography (OCT) to evaluate the retina and optic nerve. Laboratory tests may also be ordered to rule out other causes of vision loss.
Treatment for acute RNS is focused on addressing the underlying cause and managing symptoms. This may include antiviral or antibacterial medications, corticosteroids, and pain management. In severe cases, surgery may be necessary to remove damaged tissue or repair the retina.
Prognosis for acute RNS varies depending on the underlying cause and severity of the condition. In some cases, vision loss may be permanent, while in others, vision can improve with treatment. Prompt medical attention is essential to minimize visual loss and prevent complications.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:
"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."
The ICDCR definition includes several key features of DILI, including:
1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).
The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.
The symptoms of ANP can include:
1. Severe abdominal pain that worsens rapidly within a few days
2. Fever
3. Nausea and vomiting
4. Diarrhea or constipation
5. Blood in stools or vomitus
6. Signs of organ failure, such as decreased blood pressure, tachycardia, and tachypnea
7. Sepsis or infection
8. Pleural effusion or ascites
9. Rhabdomyolysis (breakdown of muscle tissue)
10. Elevated serum levels of inflammatory markers, such as CRP and WBC.
The diagnosis of ANP is based on a combination of clinical features, laboratory tests, and imaging studies. Laboratory tests may include:
1. Elevated serum levels of amylase and lipase
2. Elevated blood urea nitrogen (BUN) and creatinine
3. Increased white blood cell count and elevated C-reactive protein (CRP)
4. Electrolyte imbalance
5. Renal failure
6. Hepatic dysfunction
7. Cardiovascular instability
8. Coagulopathy
9. Hypocalcemia
10. Hyperglycemia
Imaging studies, such as CT scans or MRI, may show:
1. Widespread pancreatic necrosis
2. Inflammation in the surrounding tissues
3. Abscesses or fluid collections in the pancreas or peripancreatic tissues
4. Obstruction of the pancreatic duct
5. Intestinal ischemia or perforation
6. Peritonitis or retroperitoneal abscess
The treatment of ANP involves a multidisciplinary approach, including surgical, medical, and radiological interventions. The goals of treatment are to:
1. Stabilize the patient's vital signs and correct any electrolyte imbalances
2. Manage infection and sepsis
3. Provide supportive care for any organ dysfunction or failure
4. Remove any obstructions or necrotic tissue from the pancreas
5. Promote pancreatic tissue healing and regeneration
6. Prevent further complications, such as pancreatic fibrosis or pseudocyst formation
Surgical interventions may include:
1. Pancreatectomy: removal of the necrotic or infarcted pancreatic tissue
2. Drainage of abscesses or fluid collections
3. Repair of any obstructions in the pancreatic duct
4. Debridement of any infected or necrotic tissue
5. Reconstruction of the pancreas and surrounding tissues
Medical interventions may include:
1. Antibiotics to treat infection and sepsis
2. Pain management with analgesics and sedatives
3. Management of diabetes or other endocrine disorders
4. Supportive care for any organ dysfunction or failure
5. Monitoring of vital signs and laboratory values
Radiological interventions may include:
1. Imaging studies to evaluate the extent of the inflammation and assess the response to treatment
2. Therapeutic interventions, such as endoscopic retrograde cholangiopancreatography (ERCP) or percutaneous drainage of abscesses
The prognosis for ANP depends on several factors, including the severity of the inflammation, the presence of any complications, and the timeliness and effectiveness of treatment. In general, the sooner treatment is initiated, the better the prognosis. Mortality rates for ANP have been reported to range from 5-20%, with higher mortality rates associated with more severe disease and delayed treatment.
Prevention of ANP involves prompt management of any underlying conditions or risk factors that may lead to pancreatitis. This includes:
1. Proper management of gallstones, including cholecystectomy if necessary
2. Treatment of chronic alcoholism and cessation of alcohol consumption
3. Management of hyperlipidemia with appropriate medications and lifestyle modifications
4. Avoiding certain medications that may increase the risk of pancreatitis, such as certain antibiotics and non-steroidal anti-inflammatory drugs (NSAIDs)
5. Maintaining good overall health and avoiding any other potential risk factors for pancreatitis, such as smoking and excessive physical activity.
Some common types of fish diseases include:
1. Bacterial infections: These are caused by bacteria such as Aeromonas, Pseudomonas, and Mycobacterium. Symptoms can include fin and tail rot, body slime, and ulcers.
2. Viral infections: These are caused by viruses such as viral hemorrhagic septicemia (VHS) and infectious hematopoietic necrosis (IHN). Symptoms can include lethargy, loss of appetite, and rapid death.
3. Protozoan infections: These are caused by protozoa such as Cryptocaryon and Ichthyophonus. Symptoms can include flashing, rapid breathing, and white spots on the body.
4. Fungal infections: These are caused by fungi such as Saprolegnia and Achlya. Symptoms can include fuzzy growths on the body and fins, and sluggish behavior.
5. Parasitic infections: These are caused by parasites such as Ichthyophonus and Cryptocaryon. Symptoms can include flashing, rapid breathing, and white spots on the body.
Diagnosis of fish diseases is typically made through a combination of physical examination, laboratory tests, and observation of the fish's behavior and environment. Treatment options vary depending on the type of disease and the severity of symptoms, and can include antibiotics, antifungals, and medicated baths. Prevention is key in managing fish diseases, and this includes maintaining good water quality, providing a balanced diet, and keeping the fish in a healthy environment.
Note: The information provided is a general overview of common fish diseases and their symptoms, and should not be considered as professional medical advice. If you suspect your fish has a disease, it is recommended that you consult with a veterinarian or a qualified aquarium expert for proper diagnosis and treatment.
Osteonecrosis can be caused by a variety of factors, including:
* Trauma or injury to the bone
* Blood vessel disorders, such as blood clots or inflammation
* Certain medications, such as corticosteroids
* Alcohol consumption
* Avascular necrosis can also be a complication of other conditions, such as osteoarthritis, rheumatoid arthritis, and sickle cell disease.
There are several risk factors for developing osteonecrosis, including:
* Previous joint surgery or injury
* Family history of osteonecrosis
* Age, as the risk increases with age
* Gender, as women are more likely to be affected than men
* Certain medical conditions, such as diabetes and alcoholism.
Symptoms of osteonecrosis can include:
* Pain in the affected joint, which may worsen over time
* Limited mobility or stiffness in the joint
* Swelling or redness in the affected area
* A grinding or cracking sensation in the joint.
To diagnose osteonecrosis, a doctor may use a combination of imaging tests such as X-rays, CT scans, and MRI scans to evaluate the bone and joint. Treatment options for osteonecrosis depend on the severity of the condition and can include:
* Conservative management with pain medication and physical therapy
* Bone grafting or surgical intervention to repair or replace the damaged bone and joint.
The symptoms of dental pulp necrosis can include:
* Toothache pain that is often severe and throbbing
* Sensitivity to hot or cold foods and drinks
* Swelling and redness in the gum tissue near the affected tooth
* A bad taste or smell in the mouth
* Discharge of pus from the gums near the affected tooth
If left untreated, dental pulp necrosis can lead to more serious complications such as an abscessed tooth, bone loss, and even sepsis. Treatment options for dental pulp necrosis include root canal therapy, extraction of the affected tooth, or antibiotic therapy if the infection has spread beyond the tooth.
It is important to seek professional dental care if you experience any symptoms of dental pulp necrosis to prevent further complications and maintain good oral health.
Examples of acute diseases include:
1. Common cold and flu
2. Pneumonia and bronchitis
3. Appendicitis and other abdominal emergencies
4. Heart attacks and strokes
5. Asthma attacks and allergic reactions
6. Skin infections and cellulitis
7. Urinary tract infections
8. Sinusitis and meningitis
9. Gastroenteritis and food poisoning
10. Sprains, strains, and fractures.
Acute diseases can be treated effectively with antibiotics, medications, or other therapies. However, if left untreated, they can lead to chronic conditions or complications that may require long-term care. Therefore, it is important to seek medical attention promptly if symptoms persist or worsen over time.
Shock refers to a severe and sudden drop in blood pressure, which can lead to inadequate perfusion of vital organs such as the brain, heart, and lungs. There are several types of shock, including hypovolemic shock (caused by bleeding or dehydration), septic shock (caused by an overwhelming bacterial infection), and cardiogenic shock (caused by a heart attack or other cardiac condition).
Septic refers to the presence of bacteria or other microorganisms in the bloodstream, which can cause a range of symptoms including fever, chills, and confusion. Sepsis is a serious and potentially life-threatening condition that can lead to organ failure and death if left untreated.
Septic shock is a specific type of shock that occurs as a result of sepsis, which is the body's systemic inflammatory response to an infection. Septic shock is characterized by severe vasopressor (a medication used to increase blood pressure) and hypotension (low blood pressure), and it can lead to multiple organ failure and death if not treated promptly and effectively.
In summary, shock refers to a drop in blood pressure, while septic refers to the presence of bacteria or other microorganisms in the bloodstream. Septic shock is a specific type of shock that occurs as a result of sepsis, and it can be a life-threatening condition if not treated promptly and effectively.
Reperfusion injury can cause inflammation, cell death, and impaired function in the affected tissue or organ. The severity of reperfusion injury can vary depending on the duration and severity of the initial ischemic event, as well as the promptness and effectiveness of treatment to restore blood flow.
Reperfusion injury can be a complicating factor in various medical conditions, including:
1. Myocardial infarction (heart attack): Reperfusion injury can occur when blood flow is restored to the heart muscle after a heart attack, leading to inflammation and cell death.
2. Stroke: Reperfusion injury can occur when blood flow is restored to the brain after an ischemic stroke, leading to inflammation and damage to brain tissue.
3. Organ transplantation: Reperfusion injury can occur when a transplanted organ is subjected to ischemia during harvesting or preservation, and then reperfused with blood.
4. Peripheral arterial disease: Reperfusion injury can occur when blood flow is restored to a previously occluded peripheral artery, leading to inflammation and damage to the affected tissue.
Treatment of reperfusion injury often involves medications to reduce inflammation and oxidative stress, as well as supportive care to manage symptoms and prevent further complications. In some cases, experimental therapies such as stem cell transplantation or gene therapy may be used to promote tissue repair and regeneration.
There are several types of ischemia, including:
1. Myocardial ischemia: Reduced blood flow to the heart muscle, which can lead to chest pain or a heart attack.
2. Cerebral ischemia: Reduced blood flow to the brain, which can lead to stroke or cognitive impairment.
3. Peripheral arterial ischemia: Reduced blood flow to the legs and arms.
4. Renal ischemia: Reduced blood flow to the kidneys.
5. Hepatic ischemia: Reduced blood flow to the liver.
Ischemia can be diagnosed through a variety of tests, including electrocardiograms (ECGs), stress tests, and imaging studies such as CT or MRI scans. Treatment for ischemia depends on the underlying cause and may include medications, lifestyle changes, or surgical interventions.
There are several causes of pancreatitis, including:
1. Gallstones: These can block the pancreatic duct, causing inflammation.
2. Alcohol consumption: Heavy alcohol use can damage the pancreas and lead to inflammation.
3. High triglycerides: Elevated levels of triglycerides in the blood can cause pancreatitis.
4. Infections: Viral or bacterial infections can infect the pancreas and cause inflammation.
5. Genetic factors: Some people may be more susceptible to pancreatitis due to inherited genetic mutations.
6. Pancreatic trauma: Physical injury to the pancreas can cause inflammation.
7. Certain medications: Some medications, such as certain antibiotics and chemotherapy drugs, can cause pancreatitis as a side effect.
Symptoms of pancreatitis may include:
1. Abdominal pain
2. Nausea and vomiting
3. Fever
4. Diarrhea or bloating
5. Weight loss
6. Loss of appetite
Treatment for pancreatitis depends on the underlying cause and the severity of the condition. In some cases, hospitalization may be necessary to manage symptoms and address any complications. Treatment options may include:
1. Pain management: Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) or opioids may be used to manage abdominal pain.
2. Fluid replacement: Intravenous fluids may be given to replace lost fluids and electrolytes.
3. Antibiotics: If the pancreatitis is caused by an infection, antibiotics may be prescribed to treat the infection.
4. Nutritional support: Patients with pancreatitis may require nutritional support to ensure they are getting enough calories and nutrients.
5. Pancreatic enzyme replacement therapy: In some cases, pancreatic enzyme replacement therapy may be necessary to help the body digest food.
6. Surgery: In severe cases of pancreatitis, surgery may be necessary to remove damaged tissue or repair damaged blood vessels.
It is important to seek medical attention if you experience persistent abdominal pain or other symptoms of pancreatitis, as early treatment can help prevent complications and improve outcomes.
The exact cause of fibrosarcoma is not known, but it is believed to be linked to genetic mutations that occur during a person's lifetime. Some risk factors for developing fibrosarcoma include previous radiation exposure, chronic inflammation, and certain inherited conditions such as neurofibromatosis type 1 (NF1).
The symptoms of fibrosarcoma can vary depending on the location and size of the tumor. In some cases, there may be no symptoms until the tumor has grown to a significant size. Common symptoms include pain, swelling, and limited mobility in the affected limb. If the tumor is near a nerve, it can also cause numbness or tingling sensations in the affected area.
Diagnosis of fibrosarcoma typically involves a combination of imaging tests such as X-rays, CT scans, and MRI scans, as well as a biopsy to confirm the presence of cancer cells. Treatment options for fibrosarcoma may include surgery, radiation therapy, and chemotherapy, depending on the size and location of the tumor, as well as the patient's overall health.
Prognosis for fibrosarcoma is generally good if the tumor is caught early and treated aggressively. However, if the cancer has spread to other parts of the body (metastasized), the prognosis is generally poorer. In some cases, the cancer can recur after treatment, so it is important for patients to follow their doctor's recommendations for regular check-ups and follow-up testing.
Overall, fibrosarcoma is a rare and aggressive form of cancer that can be challenging to diagnose and treat. However, with early detection and appropriate treatment, many people with this condition can achieve long-term survival and a good quality of life.
Granulomas are formed in response to the presence of a foreign substance or an infection, and they serve as a protective barrier to prevent the spread of the infection and to isolate the offending agent. The granuloma is characterized by a central area of necrosis, surrounded by a ring of immune cells, including macrophages and T-lymphocytes.
Granulomas are commonly seen in a variety of inflammatory conditions, such as tuberculosis, leprosy, and sarcoidosis. They can also occur as a result of infections, such as bacterial or fungal infections, and in the context of autoimmune disorders, such as rheumatoid arthritis.
In summary, granuloma is a term used to describe a type of inflammatory lesion that is formed in response to the presence of a foreign substance or an infection, and serves as a protective barrier to prevent the spread of the infection and to isolate the offending agent.
Example sentences:
1. The rhabdoviridae infections in cattle can cause significant economic losses for farmers, as they can lead to reduced milk production and mortality rates.
2. Scientists are working on developing vaccines against rhabdoviridae infections in pigs, which could help reduce the risk of disease transmission to humans.
There are several types of edema, including:
1. Pitting edema: This type of edema occurs when the fluid accumulates in the tissues and leaves a pit or depression when it is pressed. It is commonly seen in the skin of the lower legs and feet.
2. Non-pitting edema: This type of edema does not leave a pit or depression when pressed. It is often seen in the face, hands, and arms.
3. Cytedema: This type of edema is caused by an accumulation of fluid in the tissues of the limbs, particularly in the hands and feet.
4. Edema nervorum: This type of edema affects the nerves and can cause pain, numbness, and tingling in the affected area.
5. Lymphedema: This is a condition where the lymphatic system is unable to properly drain fluid from the body, leading to swelling in the arms or legs.
Edema can be diagnosed through physical examination, medical history, and diagnostic tests such as imaging studies and blood tests. Treatment options for edema depend on the underlying cause, but may include medications, lifestyle changes, and compression garments. In some cases, surgery or other interventions may be necessary to remove excess fluid or tissue.
There are many different types of liver diseases, including:
1. Alcoholic liver disease (ALD): A condition caused by excessive alcohol consumption that can lead to inflammation, scarring, and cirrhosis.
2. Viral hepatitis: Hepatitis A, B, and C are viral infections that can cause inflammation and damage to the liver.
3. Non-alcoholic fatty liver disease (NAFLD): A condition where there is an accumulation of fat in the liver, which can lead to inflammation and scarring.
4. Cirrhosis: A condition where the liver becomes scarred and cannot function properly.
5. Hemochromatosis: A genetic disorder that causes the body to absorb too much iron, which can damage the liver and other organs.
6. Wilson's disease: A rare genetic disorder that causes copper to accumulate in the liver and brain, leading to damage and scarring.
7. Liver cancer (hepatocellular carcinoma): Cancer that develops in the liver, often as a result of cirrhosis or viral hepatitis.
Symptoms of liver disease can include fatigue, loss of appetite, nausea, abdominal pain, dark urine, pale stools, and swelling in the legs. Treatment options for liver disease depend on the underlying cause and may include lifestyle changes, medication, or surgery. In severe cases, a liver transplant may be necessary.
Prevention of liver disease includes maintaining a healthy diet and lifestyle, avoiding excessive alcohol consumption, getting vaccinated against hepatitis A and B, and managing underlying medical conditions such as obesity and diabetes. Early detection and treatment of liver disease can help to prevent long-term damage and improve outcomes for patients.
1. Influenza (flu): Caused by the influenza virus, which is an RNA virus that affects the respiratory system and can cause fever, cough, sore throat, and body aches.
2. HIV/AIDS: Caused by the human immunodeficiency virus (HIV), which is an RNA virus that attacks the body's immune system and can lead to acquired immunodeficiency syndrome (AIDS).
3. Hepatitis B: Caused by the hepatitis B virus, which is an RNA virus that infects the liver and can cause inflammation, scarring, and cancer.
4. Measles: Caused by the measles virus, which is an RNA virus that affects the respiratory system and can cause fever, cough, and a rash.
5. Rabies: Caused by the rabies virus, which is an RNA virus that attacks the central nervous system and can cause brain damage and death.
6. Ebola: Caused by the Ebola virus, which is an RNA virus that affects the blood vessels and can cause fever, vomiting, diarrhea, and bleeding.
7. SARS-CoV-2: Caused by the severe acute respiratory syndrome-related coronavirus 2 (SARS-CoV-2), which is an RNA virus that affects the respiratory system and can cause COVID-19.
RNA virus infections are often difficult to treat and can be highly contagious, so it's important to take precautions to prevent transmission and seek medical attention if symptoms persist or worsen over time.
Here are some key points to define sepsis:
1. Inflammatory response: Sepsis is characterized by an excessive and uncontrolled inflammatory response to an infection. This can lead to tissue damage and organ dysfunction.
2. Systemic symptoms: Patients with sepsis often have systemic symptoms such as fever, chills, rapid heart rate, and confusion. They may also experience nausea, vomiting, and diarrhea.
3. Organ dysfunction: Sepsis can cause dysfunction in multiple organs, including the lungs, kidneys, liver, and heart. This can lead to organ failure and death if not treated promptly.
4. Infection source: Sepsis is usually caused by a bacterial infection, but it can also be caused by fungal or viral infections. The infection can be localized or widespread, and it can affect different parts of the body.
5. Severe sepsis: Severe sepsis is a more severe form of sepsis that is characterized by severe organ dysfunction and a higher risk of death. Patients with severe sepsis may require intensive care unit (ICU) admission and mechanical ventilation.
6. Septic shock: Septic shock is a life-threatening condition that occurs when there is severe circulatory dysfunction due to sepsis. It is characterized by hypotension, vasopressor use, and organ failure.
Early recognition and treatment of sepsis are critical to preventing serious complications and improving outcomes. The Sepsis-3 definition is widely used in clinical practice to diagnose sepsis and severe sepsis.
These animal models allow researchers to study the underlying causes of arthritis, test new treatments and therapies, and evaluate their effectiveness in a controlled environment before moving to human clinical trials. Experimental arthritis models are used to investigate various aspects of the disease, including its pathophysiology, immunogenicity, and potential therapeutic targets.
Some common experimental arthritis models include:
1. Collagen-induced arthritis (CIA): This model is induced in mice by immunizing them with type II collagen, which leads to an autoimmune response and inflammation in the joints.
2. Rheumatoid arthritis (RA) models: These models are developed by transferring cells from RA patients into immunodeficient mice, which then develop arthritis-like symptoms.
3. Osteoarthritis (OA) models: These models are induced in animals by subjecting them to joint injury or overuse, which leads to degenerative changes in the joints and bone.
4. Psoriatic arthritis (PsA) models: These models are developed by inducing psoriasis in mice, which then develop arthritis-like symptoms.
Experimental arthritis models have contributed significantly to our understanding of the disease and have helped to identify potential therapeutic targets for the treatment of arthritis. However, it is important to note that these models are not perfect representations of human arthritis and should be used as tools to complement, rather than replace, human clinical trials.
Endotoxemia can occur in individuals who have a severe bacterial infection, such as pneumonia or meningitis, or those who have a prosthetic device or other foreign body that becomes infected with gram-negative bacteria. Treatment of endotoxemia typically involves antibiotics and supportive care to manage symptoms and prevent further complications. In severe cases, medications such as corticosteroids and vasopressors may be used to help reduce inflammation and improve blood flow.
Endotoxemia is a serious medical condition that requires prompt diagnosis and treatment to prevent complications and improve outcomes for patients.
The symptoms of myocarditis can vary depending on the severity of the inflammation and the location of the affected areas of the heart muscle. Common symptoms include chest pain, shortness of breath, fatigue, and swelling in the legs and feet.
Myocarditis can be difficult to diagnose, as its symptoms are similar to those of other conditions such as coronary artery disease or heart failure. Diagnosis is typically made through a combination of physical examination, medical history, and results of diagnostic tests such as electrocardiogram (ECG), echocardiogram, and blood tests.
Treatment of myocarditis depends on the underlying cause and severity of the condition. Mild cases may require only rest and over-the-counter pain medication, while more severe cases may require hospitalization and intravenous medications to manage inflammation and cardiac function. In some cases, surgery may be necessary to repair or replace damaged heart tissue.
Prevention of myocarditis is important, as it can lead to serious complications such as heart failure and arrhythmias if left untreated. Prevention strategies include avoiding exposure to viruses and other infections, managing underlying medical conditions such as diabetes and high blood pressure, and getting regular check-ups with a healthcare provider to monitor cardiac function.
In summary, myocarditis is an inflammatory condition that affects the heart muscle, causing symptoms such as chest pain, shortness of breath, and fatigue. Diagnosis can be challenging, but treatment options range from rest and medication to hospitalization and surgery. Prevention is key to avoiding serious complications and maintaining good cardiac health.
There are several types of radiation injuries, including:
1. Acute radiation syndrome (ARS): This occurs when a person is exposed to a high dose of ionizing radiation over a short period of time. Symptoms can include nausea, vomiting, diarrhea, fatigue, and damage to the bone marrow, lungs, and gastrointestinal system.
2. Chronic radiation syndrome: This occurs when a person is exposed to low levels of ionizing radiation over a longer period of time. Symptoms can include fatigue, skin changes, and an increased risk of cancer.
3. Radiation burns: These are similar to thermal burns, but are caused by the heat generated by ionizing radiation. They can cause skin damage, blistering, and scarring.
4. Ocular radiation injury: This occurs when the eyes are exposed to high levels of ionizing radiation, leading to damage to the retina and other parts of the eye.
5. Radiation-induced cancer: Exposure to high levels of ionizing radiation can increase the risk of developing cancer, particularly leukemia and other types of cancer that affect the bone marrow.
Radiation injuries are diagnosed based on a combination of physical examination, medical imaging (such as X-rays or CT scans), and laboratory tests. Treatment depends on the type and severity of the injury, but may include supportive care, medication, and radiation therapy to prevent further damage.
Preventing radiation injuries is important, especially in situations where exposure to ionizing radiation is unavoidable, such as in medical imaging or nuclear accidents. This can be achieved through the use of protective shielding, personal protective equipment, and strict safety protocols.
There are five types of PsA:
1. Asymptomatic psoriatic arthritis - This type of psoriatic arthritis does not cause any symptoms and is typically diagnosed during routine blood tests or imaging studies.
2. Symptomatic psoriatic arthritis - This type of psoriatic arthritis causes painful joints, stiffness, and swelling in the hands and feet.
3. Distal interphalangeal predominant psoriatic arthritis - This type of psoriatic arthritis affects the joints at the tips of the fingers and toes.
4. Polyarticular psoriatic arthritis - This type of psoriatic arthritis causes inflammation in multiple joints throughout the body, including the hands, feet, knees, elbows, and spine.
5. Sulfur-shoulder psoriatic arthritis - This type of psoriatic arthritis primarily affects the shoulders and upper back.
Symptoms of PsA may include:
1. Joint pain and stiffness
2. Swollen and warm joints
3. Redness and warmth in the affected area
4. Fatigue
5. Low-grade fever
6. Loss of range of motion
7. Skin rashes or lesions
PsA is diagnosed based on a combination of physical examination, medical history, and laboratory tests such as blood tests to check for inflammatory markers (e.g., ESR and CRP) and X-rays or imaging studies to assess joint damage. There is no cure for PsA, but various treatments can help manage symptoms, slow the progression of the disease, and improve quality of life. These may include medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs) or biologic agents that target specific proteins involved in inflammation. In severe cases, surgery may be necessary to repair damaged joints or correct deformities.
It's important for people with PsA to work closely with their healthcare provider to develop a personalized treatment plan that addresses their individual needs and monitors their disease activity over time. With appropriate treatment and self-care, many people with PsA are able to manage their symptoms, maintain joint function, and lead active and fulfilling lives.
In conclusion, psoriatic arthritis (PsA) is a chronic inflammatory disease that affects both the skin and joints, causing pain, stiffness, and swelling in various parts of the body. Early diagnosis and appropriate treatment can help manage symptoms, slow the progression of the disease, and improve quality of life.
Example sentences:
1. The outbreak of birnaviridae infections in the local wildlife population has been linked to the consumption of contaminated water sources.
2. The researchers are studying the effects of birnaviridae infections on the reproduction rates of infected birds.
3. The veterinarian suspects that the sudden death of several zoo animals may be due to birnaviridae infections.
The definition of AKI has evolved over time, and it is now defined as a syndrome characterized by an abrupt or rapid decrease in kidney function, with or without oliguria (decreased urine production), and with evidence of tubular injury. The RIFLE (Risk, Injury, Failure, Loss, and End-stage kidney disease) criteria are commonly used to diagnose and stage AKI based on serum creatinine levels, urine output, and other markers of kidney damage.
There are three stages of AKI, with stage 1 representing mild injury and stage 3 representing severe and potentially life-threatening injury. Treatment of AKI typically involves addressing the underlying cause, correcting fluid and electrolyte imbalances, and providing supportive care to maintain blood pressure and oxygenation. In some cases, dialysis may be necessary to remove waste products from the blood.
Early detection and treatment of AKI are crucial to prevent long-term damage to the kidneys and improve outcomes for patients.
Symptoms of MHN may include jaundice (yellowing of the skin and eyes), loss of appetite, nausea, vomiting, abdominal pain, fatigue, and confusion. The condition can progress rapidly, leading to multi-organ failure and death if left untreated.
Treatment options for MHN depend on the underlying cause, but may include supportive care such as fluid replacement, antibiotics, and medication to manage symptoms. In severe cases, a liver transplant may be necessary. The prognosis for MHN is generally poor, with high mortality rates reported in some studies.
Prevention measures for MHN include avoiding alcohol, maintaining a healthy diet, and getting vaccinated against hepatitis A and B viruses. Early detection and management of underlying conditions such as viral hepatitis can also help prevent the development of MHN.
Osteoarthritis (OA) is a degenerative condition that occurs when the cartilage that cushions the joints breaks down over time, causing the bones to rub together. It is the most common form of arthritis and typically affects older adults.
Rheumatoid arthritis (RA) is an autoimmune condition that occurs when the body's immune system attacks the lining of the joints, leading to inflammation and pain. It can affect anyone, regardless of age, and is typically seen in women.
Other types of arthritis include psoriatic arthritis, gouty arthritis, and lupus-related arthritis. Treatment for arthritis depends on the type and severity of the condition, but can include medications such as pain relievers, anti-inflammatory drugs, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy and lifestyle changes, such as exercise and weight loss, can also be helpful. In severe cases, surgery may be necessary to repair or replace damaged joints.
Arthritis is a leading cause of disability worldwide, affecting over 50 million adults in the United States alone. It can have a significant impact on a person's quality of life, making everyday activities such as walking, dressing, and grooming difficult and painful. Early diagnosis and treatment are important to help manage symptoms and slow the progression of the disease.
Spondylitis, ankylosing can affect any part of the spine, but it most commonly affects the lower back (lumbar spine) and the neck (cervical spine). The condition can also affect other joints, such as the hips, shoulders, and feet.
The exact cause of spondylitis, ankylosing is not known, but it is believed to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks healthy tissue in the joints. Genetics may also play a role in the development of the condition.
Symptoms of spondylitis, ankylosing can include:
* Back pain and stiffness
* Pain and swelling in the joints
* Limited mobility and flexibility
* Redness and warmth in the affected area
* Fatigue
If you suspect that you or someone you know may have spondylitis, ankylosing, it is important to seek medical attention for proper diagnosis and treatment. A healthcare professional can perform a physical examination and order imaging tests, such as X-rays or MRIs, to confirm the diagnosis and rule out other conditions.
Treatment for spondylitis, ankylosing typically involves a combination of medications and physical therapy. Medications may include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs). Physical therapy can help improve mobility and flexibility, as well as strengthen the muscles supporting the affected joints.
In severe cases of spondylitis, ankylosing, surgery may be necessary to repair or replace damaged joints. In some cases, the condition may progress to the point where the joints become fused and immobile, a condition known as ankylosis.
While there is no cure for spondylitis, ankylosing, early diagnosis and appropriate treatment can help manage symptoms and slow the progression of the disease. With proper care and support, individuals with spondylitis, ankylosing can lead active and fulfilling lives.
Brain neoplasms can arise from various types of cells in the brain, including glial cells (such as astrocytes and oligodendrocytes), neurons, and vascular tissues. The symptoms of brain neoplasms vary depending on their size, location, and type, but may include headaches, seizures, weakness or numbness in the limbs, and changes in personality or cognitive function.
There are several different types of brain neoplasms, including:
1. Meningiomas: These are benign tumors that arise from the meninges, the thin layers of tissue that cover the brain and spinal cord.
2. Gliomas: These are malignant tumors that arise from glial cells in the brain. The most common type of glioma is a glioblastoma, which is aggressive and hard to treat.
3. Pineal parenchymal tumors: These are rare tumors that arise in the pineal gland, a small endocrine gland in the brain.
4. Craniopharyngiomas: These are benign tumors that arise from the epithelial cells of the pituitary gland and the hypothalamus.
5. Medulloblastomas: These are malignant tumors that arise in the cerebellum, specifically in the medulla oblongata. They are most common in children.
6. Acoustic neurinomas: These are benign tumors that arise on the nerve that connects the inner ear to the brain.
7. Oligodendrogliomas: These are malignant tumors that arise from oligodendrocytes, the cells that produce the fatty substance called myelin that insulates nerve fibers.
8. Lymphomas: These are cancers of the immune system that can arise in the brain and spinal cord. The most common type of lymphoma in the CNS is primary central nervous system (CNS) lymphoma, which is usually a type of B-cell non-Hodgkin lymphoma.
9. Metastatic tumors: These are tumors that have spread to the brain from another part of the body. The most common types of metastatic tumors in the CNS are breast cancer, lung cancer, and melanoma.
These are just a few examples of the many types of brain and spinal cord tumors that can occur. Each type of tumor has its own unique characteristics, such as its location, size, growth rate, and biological behavior. These factors can help doctors determine the best course of treatment for each patient.
The exact cause of cachexia is not fully understood, but it is thought to be related to a combination of factors such as inflammation, hormonal imbalances, and changes in metabolism. Treatment for cachexia often focuses on addressing the underlying cause of the wasting, such as managing cancer or HIV/AIDS, as well as providing nutritional support and addressing any related complications.
In the medical field, cachexia is a serious condition that requires careful management to improve quality of life and outcomes for patients. It is important for healthcare providers to be aware of the signs and symptoms of cachexia and to provide appropriate treatment and support to affected individuals.
Liver neoplasms, also known as liver tumors or hepatic tumors, are abnormal growths of tissue in the liver. These growths can be benign (non-cancerous) or malignant (cancerous). Malignant liver tumors can be primary, meaning they originate in the liver, or metastatic, meaning they spread to the liver from another part of the body.
There are several types of liver neoplasms, including:
1. Hepatocellular carcinoma (HCC): This is the most common type of primary liver cancer and arises from the main cells of the liver (hepatocytes). HCC is often associated with cirrhosis and can be caused by viral hepatitis or alcohol abuse.
2. Cholangiocarcinoma: This type of cancer arises from the cells lining the bile ducts within the liver (cholangiocytes). Cholangiocarcinoma is rare and often diagnosed at an advanced stage.
3. Hemangiosarcoma: This is a rare type of cancer that originates in the blood vessels of the liver. It is most commonly seen in dogs but can also occur in humans.
4. Fibromas: These are benign tumors that arise from the connective tissue of the liver (fibrocytes). Fibromas are usually small and do not spread to other parts of the body.
5. Adenomas: These are benign tumors that arise from the glandular cells of the liver (hepatocytes). Adenomas are usually small and do not spread to other parts of the body.
The symptoms of liver neoplasms vary depending on their size, location, and whether they are benign or malignant. Common symptoms include abdominal pain, fatigue, weight loss, and jaundice (yellowing of the skin and eyes). Diagnosis is typically made through a combination of imaging tests such as CT scans, MRI scans, and ultrasound, and a biopsy to confirm the presence of cancer cells.
Treatment options for liver neoplasms depend on the type, size, location, and stage of the tumor, as well as the patient's overall health. Surgery may be an option for some patients with small, localized tumors, while others may require chemotherapy or radiation therapy to shrink the tumor before surgery can be performed. In some cases, liver transplantation may be necessary.
Prognosis for liver neoplasms varies depending on the type and stage of the cancer. In general, early detection and treatment improve the prognosis, while advanced-stage disease is associated with a poorer prognosis.
In animals, hepatitis can be caused by a variety of agents, including:
1. Viral hepatitis: Caused by viruses such as feline infectious peritonitis (FIP) in cats and canine infectious hepatitis (CIH) in dogs.
2. Bacterial hepatitis: Caused by bacteria such as Leptospira spp., which can be transmitted through contact with contaminated water or soil.
3. Parasitic hepatitis: Caused by parasites such as liver flukes (Fasciola spp.) and tapeworms (Taenia spp.).
4. Toxic hepatitis: Caused by exposure to certain drugs, chemicals, or environmental toxins.
5. Genetic hepatitis: Caused by inherited genetic disorders such as hemophilia in dogs and cats.
The clinical signs of animal hepatitis can vary depending on the cause and severity of the disease, but may include lethargy, loss of appetite, vomiting, diarrhea, abdominal pain, and jaundice (yellowing of the skin and eyes). Diagnosis is based on a combination of physical examination, laboratory tests (such as blood tests and liver biopsy), and imaging studies.
Treatment of animal hepatitis depends on the underlying cause and may include supportive care, antibiotics, anti-inflammatory medications, and in some cases, surgery or liver transplantation. In severe cases, animal hepatitis can be fatal if left untreated, so early diagnosis and aggressive treatment are essential for a successful outcome.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
There are several types of disease susceptibility, including:
1. Genetic predisposition: This refers to the inherent tendency of an individual to develop a particular disease due to their genetic makeup. For example, some families may have a higher risk of developing certain diseases such as cancer or heart disease due to inherited genetic mutations.
2. Environmental susceptibility: This refers to the increased risk of developing a disease due to exposure to environmental factors such as pollutants, toxins, or infectious agents. For example, someone who lives in an area with high levels of air pollution may be more susceptible to developing respiratory problems.
3. Lifestyle susceptibility: This refers to the increased risk of developing a disease due to unhealthy lifestyle choices such as smoking, lack of exercise, or poor diet. For example, someone who smokes and is overweight may be more susceptible to developing heart disease or lung cancer.
4. Immune system susceptibility: This refers to the increased risk of developing a disease due to an impaired immune system. For example, people with autoimmune disorders such as HIV/AIDS or rheumatoid arthritis may be more susceptible to opportunistic infections.
Understanding disease susceptibility can help healthcare providers identify individuals who are at risk of developing certain diseases and provide preventive measures or early intervention to reduce the risk of disease progression. Additionally, genetic testing can help identify individuals with a high risk of developing certain diseases, allowing for earlier diagnosis and treatment.
In summary, disease susceptibility refers to the predisposition of an individual to develop a particular disease or condition due to various factors such as genetics, environment, lifestyle choices, and immune system function. Understanding disease susceptibility can help healthcare providers identify individuals at risk and provide appropriate preventive measures or early intervention to reduce the risk of disease progression.
There are several types of vasculitis, each with its own set of symptoms and characteristics. Some common forms of vasculitis include:
1. Giant cell arteritis: This is the most common form of vasculitis, and it affects the large arteries in the head, neck, and arms. Symptoms include fever, fatigue, muscle aches, and loss of appetite.
2. Takayasu arteritis: This type of vasculitis affects the aorta and its major branches, leading to inflammation in the blood vessels that supply the heart, brain, and other vital organs. Symptoms include fever, fatigue, chest pain, and shortness of breath.
3. Polymyalgia rheumatica: This is an inflammatory condition that affects the muscles and joints, as well as the blood vessels. It often occurs in people over the age of 50 and is frequently associated with giant cell arteritis. Symptoms include pain and stiffness in the shoulders, hips, and other joints, as well as fatigue and fever.
4. Kawasaki disease: This is a rare condition that affects children under the age of 5, causing inflammation in the blood vessels that supply the heart and other organs. Symptoms include high fever, rash, swollen lymph nodes, and irritability.
The exact cause of vasculitis is not fully understood, but it is thought to be an autoimmune disorder, meaning that the body's immune system mistakenly attacks its own blood vessels. Genetic factors may also play a role in some cases.
Diagnosis of vasculitis typically involves a combination of physical examination, medical history, and diagnostic tests such as blood tests, imaging studies (e.g., MRI or CT scans), and biopsies. Treatment options vary depending on the specific type of vasculitis and its severity, but may include medications to reduce inflammation and suppress the immune system, as well as lifestyle modifications such as exercise and stress management techniques. In severe cases, surgery or organ transplantation may be necessary.
In addition to these specific types of vasculitis, there are other conditions that can cause similar symptoms and may be included in the differential diagnosis, such as:
1. Rheumatoid arthritis (RA): This is a chronic autoimmune disorder that affects the joints and can cause inflammation in blood vessels.
2. Systemic lupus erythematosus (SLE): This is another autoimmune disorder that can affect multiple systems, including the skin, joints, and blood vessels.
3. Polyarteritis nodosa: This is a condition that causes inflammation of the blood vessels, often in association with hepatitis B or C infection.
4. Takayasu arteritis: This is a rare condition that affects the aorta and its branches, causing inflammation and narrowing of the blood vessels.
5. Giant cell arteritis: This is a condition that causes inflammation of the large and medium-sized blood vessels, often in association with polymyalgia rheumatica (PMR).
6. Kawasaki disease: This is a rare condition that affects children, causing inflammation of the blood vessels and potential heart complications.
7. Henoch-Schönlein purpura: This is a rare condition that causes inflammation of the blood vessels in the skin, joints, and gastrointestinal tract.
8. IgG4-related disease: This is a condition that can affect various organs, including the pancreas, bile ducts, and blood vessels, causing inflammation and potentially leading to fibrosis or tumor formation.
It is important to note that these conditions may have similar symptoms and signs as vasculitis, but they are distinct entities with different causes and treatment approaches. A thorough diagnostic evaluation, including laboratory tests and imaging studies, is essential to determine the specific diagnosis and develop an appropriate treatment plan.
Psoriasis can affect any part of the body, including the scalp, elbows, knees, and lower back. The symptoms of psoriasis can vary in severity, and the condition can have a significant impact on quality of life. In addition to physical discomfort, psoriasis can also cause emotional distress and stigma.
There is no cure for psoriasis, but there are several treatment options available, including topical creams and ointments, light therapy, and systemic medications such as biologic drugs. With proper treatment, many people with psoriasis are able to manage their symptoms and improve their quality of life.
Psoriasis is relatively common, affecting approximately 2-3% of the global population, with a higher prevalence in Caucasians than in other races. It can occur at any age, but typically starts in the late teenage years or early adulthood. Psoriasis is often associated with other health conditions, such as diabetes, heart disease, and depression.
Overall, psoriasis is a complex and multifactorial condition that requires a comprehensive approach to management, including both physical and emotional support. With appropriate treatment and self-care, people with psoriasis can lead full and active lives.
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the World Health Organization (WHO). In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
In this article, we will explore the definition and impact of chronic diseases, as well as strategies for managing and living with them. We will also discuss the importance of early detection and prevention, as well as the role of healthcare providers in addressing the needs of individuals with chronic diseases.
What is a Chronic Disease?
A chronic disease is a condition that lasts for an extended period of time, often affecting daily life and activities. Unlike acute diseases, which have a specific beginning and end, chronic diseases are long-term and persistent. Examples of chronic diseases include:
1. Diabetes
2. Heart disease
3. Arthritis
4. Asthma
5. Cancer
6. Chronic obstructive pulmonary disease (COPD)
7. Chronic kidney disease (CKD)
8. Hypertension
9. Osteoporosis
10. Stroke
Impact of Chronic Diseases
The burden of chronic diseases is significant, with over 70% of deaths worldwide attributed to them, according to the WHO. In addition to the physical and emotional toll they take on individuals and their families, chronic diseases also pose a significant economic burden, accounting for a large proportion of healthcare expenditure.
Chronic diseases can also have a significant impact on an individual's quality of life, limiting their ability to participate in activities they enjoy and affecting their relationships with family and friends. Moreover, the financial burden of chronic diseases can lead to poverty and reduce economic productivity, thus having a broader societal impact.
Addressing Chronic Diseases
Given the significant burden of chronic diseases, it is essential that we address them effectively. This requires a multi-faceted approach that includes:
1. Lifestyle modifications: Encouraging healthy behaviors such as regular physical activity, a balanced diet, and smoking cessation can help prevent and manage chronic diseases.
2. Early detection and diagnosis: Identifying risk factors and detecting diseases early can help prevent or delay their progression.
3. Medication management: Effective medication management is crucial for controlling symptoms and slowing disease progression.
4. Multi-disciplinary care: Collaboration between healthcare providers, patients, and families is essential for managing chronic diseases.
5. Health promotion and disease prevention: Educating individuals about the risks of chronic diseases and promoting healthy behaviors can help prevent their onset.
6. Addressing social determinants of health: Social determinants such as poverty, education, and employment can have a significant impact on health outcomes. Addressing these factors is essential for reducing health disparities and improving overall health.
7. Investing in healthcare infrastructure: Investing in healthcare infrastructure, technology, and research is necessary to improve disease detection, diagnosis, and treatment.
8. Encouraging policy change: Policy changes can help create supportive environments for healthy behaviors and reduce the burden of chronic diseases.
9. Increasing public awareness: Raising public awareness about the risks and consequences of chronic diseases can help individuals make informed decisions about their health.
10. Providing support for caregivers: Chronic diseases can have a significant impact on family members and caregivers, so providing them with support is essential for improving overall health outcomes.
Conclusion
Chronic diseases are a major public health burden that affect millions of people worldwide. Addressing these diseases requires a multi-faceted approach that includes lifestyle changes, addressing social determinants of health, investing in healthcare infrastructure, encouraging policy change, increasing public awareness, and providing support for caregivers. By taking a comprehensive approach to chronic disease prevention and management, we can improve the health and well-being of individuals and communities worldwide.
Crohn disease can occur in any part of the GI tract, from the mouth to the anus, but it most commonly affects the ileum (the last portion of the small intestine) and the colon. The inflammation caused by Crohn disease can lead to the formation of scar tissue, which can cause narrowing or blockages in the intestines. This can lead to complications such as bowel obstruction or abscesses.
The exact cause of Crohn disease is not known, but it is believed to be an autoimmune disorder, meaning that the immune system mistakenly attacks healthy tissue in the GI tract. Genetic factors and environmental triggers such as smoking and diet also play a role in the development of the disease.
There is no cure for Crohn disease, but various treatments can help manage symptoms and prevent complications. These may include medications such as anti-inflammatory drugs, immunosuppressants, and biologics, as well as lifestyle changes such as dietary modifications and stress management techniques. In severe cases, surgery may be necessary to remove damaged portions of the GI tract.
Crohn disease can have a significant impact on quality of life, and it is important for individuals with the condition to work closely with their healthcare provider to manage their symptoms and prevent complications. With proper treatment and self-care, many people with Crohn disease are able to lead active and fulfilling lives.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
The exact mechanism of the Shwartzman Phenomenon is not fully understood, but it is thought that the cancer cells that have spread to other parts of the body may be less susceptible to treatment because they are more aggressive and faster-growing than the original tumor. Additionally, these cells may have developed resistance mechanisms that make them less sensitive to chemotherapy and radiation.
The Shwartzman Phenomenon can make it more difficult to treat certain types of cancer, such as breast cancer, lung cancer, and melanoma. It is particularly common in cases where the cancer has spread to the liver or lymph nodes.
To overcome the Shwartzman Phenomenon, doctors may use higher doses of chemotherapy and radiation, or they may use different combinations of treatments. In some cases, surgery may be necessary to remove tumors that have spread to other parts of the body.
Overall, the Shwartzman Phenomenon is an important consideration for doctors treating cancer patients, as it can affect the success of treatment and the patient's prognosis.
Types of experimental neoplasms include:
* Xenografts: tumors that are transplanted into animals from another species, often humans.
* Transgenic tumors: tumors that are created by introducing cancer-causing genes into an animal's genome.
* Chemically-induced tumors: tumors that are caused by exposure to certain chemicals or drugs.
The use of experimental neoplasms in research has led to significant advances in our understanding of cancer biology and the development of new treatments for the disease. However, the use of animals in cancer research is a controversial topic and alternatives to animal models are being developed and implemented.
Gastric dilatation can occur for various reasons, including:
1. Eating too quickly or consuming large amounts of food in a short period of time.
2. Swallowing air, which can happen when eating or drinking too quickly or sucking on hard candies.
3. Eating certain types of foods that are difficult to digest, such as beans or cabbage.
4. Medical conditions such as irritable bowel syndrome (IBS), gastroparesis, or hiatal hernia.
5. Inflammation or infection of the stomach lining, such as gastritis.
Symptoms of gastric dilatation may include:
* Bloating and discomfort in the abdomen
* Pain or cramping in the abdomen
* Feeling nauseous or vomiting
* Gas and belching
* Diarrhea or constipation
Treatment for gastric dilatation usually involves making lifestyle changes, such as eating smaller, more frequent meals, avoiding foods that trigger symptoms, and reducing stress. In some cases, medications may be prescribed to help manage symptoms. If the condition is caused by an underlying medical condition, treating the underlying condition can help resolve the gastric dilatation.
In severe cases of gastric dilatation, surgical intervention may be necessary. This may involve laparoscopic or open surgery to repair any anatomical abnormalities or to remove any blockages in the digestive tract.
It's important to note that gastric dilatation can lead to more serious complications, such as gastric rupture or perforation, which can be life-threatening. If you experience severe abdominal pain, fever, or vomiting blood, seek medical attention immediately.
Preventing gastric dilatation involves maintaining a healthy diet and lifestyle, managing stress, and avoiding trigger foods. It's also important to drink plenty of water and exercise regularly to promote digestive health. If you experience any symptoms of gastric dilatation, it's important to seek medical attention promptly to prevent complications.
The term "acute-phase" describes the rapid onset and short duration of this reaction, which typically lasts for hours to days before resolving as the body's inflammatory response subsides. APR is characterized by a series of molecular events that result in altered expression of genes involved in inflammation, immune response, and tissue repair.
Some key components of an acute-phase reaction include:
1. Cytokine production: Cytokines are signaling molecules released by immune cells, such as white blood cells, that coordinate the immune response. During an APR, cytokine levels increase, triggering a cascade of downstream effects.
2. Leukocyte trafficking: White blood cells migrate towards sites of inflammation or infection, where they phagocytose (engulf and digest) pathogens and cellular debris. This process helps to limit the spread of infection and initiate tissue repair.
3. Coagulation cascade: The APR triggers a complex series of events involving blood coagulation factors, leading to the formation of blood clots and preventing excessive bleeding.
4. Anti-inflammatory response: As the APR progresses, anti-inflammatory cytokines, such as interleukin-10 (IL-10), are produced to dampen the inflammatory response and promote tissue repair.
5. Cellular proliferation: To replace damaged cells and tissues, the APR stimulates cellular proliferation and tissue regeneration.
6. Nutrient mobilization: The APR enhances nutrient uptake and utilization by immune cells, allowing them to mount an effective response to the stress.
7. Hormonal changes: The APR is accompanied by changes in hormone levels, such as the increase in corticotropin-releasing factor (CRF) and cortisol, which help to mobilize energy resources and regulate metabolism.
8. Immune tolerance: The APR helps to establish immune tolerance, preventing excessive or inappropriate immune responses that can lead to autoimmune diseases or allergies.
9. Tissue remodeling: The APR stimulates the remodeling of damaged tissues, allowing for the restoration of normal tissue function.
10. Memory formation: The APR sets the stage for the formation of immunological memory, which enables the immune system to mount a more effective response to future infections or stressors.
The most common type of colitis is ulcerative colitis, which affects the rectum and lower part of the colon. The symptoms of ulcerative colitis can include:
* Diarrhea (which may be bloody)
* Abdominal pain and cramping
* Rectal bleeding
* Weight loss
* Fever
* Loss of appetite
* Nausea and vomiting
Microscopic colitis is another type of colitis that is characterized by inflammation in the colon, but without visible ulcers or bleeding. The symptoms of microscopic colitis are similar to those of ulcerative colitis, but may be less severe.
Other types of colitis include:
* Infantile colitis: This is a rare condition that affects babies and young children, and is characterized by diarrhea, fever, and vomiting.
* Isomorphic colitis: This is a rare condition that affects the colon and rectum, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Radiation colitis: This is a condition that occurs after radiation therapy to the pelvic area, and is characterized by inflammation and symptoms similar to ulcerative colitis.
* Ischemic colitis: This is a condition where there is a reduction in blood flow to the colon, which can lead to inflammation and symptoms such as abdominal pain and diarrhea.
The diagnosis of colitis typically involves a combination of physical examination, medical history, and diagnostic tests such as:
* Colonoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the colon and rectum.
* Endoscopy: This is a test that uses a flexible tube with a camera on the end to visualize the inside of the esophagus, stomach, and duodenum.
* Stool tests: These are tests that analyze stool samples for signs of inflammation or infection.
* Blood tests: These are tests that analyze blood samples for signs of inflammation or infection.
* Biopsy: This is a test that involves taking a small sample of tissue from the colon and examining it under a microscope for signs of inflammation or infection.
Treatment for colitis depends on the underlying cause, but may include medications such as:
* Aminosalicylates: These are medications that help to reduce inflammation in the colon and relieve symptoms such as diarrhea and abdominal pain. Examples include sulfasalazine (Azulfidine) and mesalamine (Asacol).
* Corticosteroids: These are medications that help to reduce inflammation in the body. They may be used short-term to control acute flares of colitis, or long-term to maintain remission. Examples include prednisone and hydrocortisone.
* Immunomodulators: These are medications that help to suppress the immune system and reduce inflammation. Examples include azathioprine (Imuran) and mercaptopurine (Purinethol).
* Biologics: These are medications that target specific proteins involved in the inflammatory response. Examples include infliximab (Remicade) and adalimumab (Humira).
In addition to medication, lifestyle changes such as dietary modifications and stress management techniques may also be helpful in managing colitis symptoms. Surgery may be necessary in some cases where the colitis is severe or persistent, and involves removing damaged portions of the colon and rectum.
It's important to note that colitis can increase the risk of developing colon cancer, so regular screening for colon cancer is recommended for people with chronic colitis. Additionally, people with colitis may be more susceptible to other health problems such as osteoporosis, osteopenia, and liver disease, so it's important to work closely with a healthcare provider to monitor for these conditions and take steps to prevent them.
Example sentence: The patient had a hemorrhage after the car accident and needed immediate medical attention.
There are several types of gliomas, including:
1. Astrocytoma: This is the most common type of glioma, accounting for about 50% of all cases. It arises from the star-shaped cells called astrocytes that provide support and nutrients to the brain's nerve cells.
2. Oligodendroglioma: This type of glioma originates from the oligodendrocytes, which are responsible for producing the fatty substance called myelin that insulates the nerve fibers.
3. Glioblastoma (GBM): This is the most aggressive and malignant type of glioma, accounting for about 70% of all cases. It is fast-growing and often spreads to other parts of the brain.
4. Brain stem glioma: This type of glioma arises in the brain stem, which is responsible for controlling many of the body's vital functions such as breathing, heart rate, and blood pressure.
The symptoms of glioma depend on the location and size of the tumor. Common symptoms include headaches, seizures, weakness or numbness in the arms or legs, and changes in personality, memory, or speech.
Gliomas are diagnosed through a combination of imaging tests such as CT or MRI scans, and tissue biopsy to confirm the presence of cancer cells. Treatment options for glioma depend on the type and location of the tumor, as well as the patient's overall health. Surgery is often the first line of treatment to remove as much of the tumor as possible, followed by radiation therapy and/or chemotherapy to kill any remaining cancer cells.
The prognosis for glioma patients varies depending on the type and location of the tumor, as well as the patient's overall health. In general, the prognosis is better for patients with slow-growing, low-grade tumors, while those with fast-growing, high-grade tumors have a poorer prognosis. Overall, the 5-year survival rate for glioma patients is around 30-40%.
Example sentence: The patient was diagnosed with experimental sarcoma and underwent a novel chemotherapy regimen that included a targeted therapy drug.
Fibrosis can occur in response to a variety of stimuli, including inflammation, infection, injury, or chronic stress. It is a natural healing process that helps to restore tissue function and structure after damage or trauma. However, excessive fibrosis can lead to the loss of tissue function and organ dysfunction.
There are many different types of fibrosis, including:
* Cardiac fibrosis: the accumulation of scar tissue in the heart muscle or walls, leading to decreased heart function and potentially life-threatening complications.
* Pulmonary fibrosis: the accumulation of scar tissue in the lungs, leading to decreased lung function and difficulty breathing.
* Hepatic fibrosis: the accumulation of scar tissue in the liver, leading to decreased liver function and potentially life-threatening complications.
* Neurofibromatosis: a genetic disorder characterized by the growth of benign tumors (neurofibromas) made up of fibrous connective tissue.
* Desmoid tumors: rare, slow-growing tumors that are made up of fibrous connective tissue and can occur in various parts of the body.
Fibrosis can be diagnosed through a variety of methods, including:
* Biopsy: the removal of a small sample of tissue for examination under a microscope.
* Imaging tests: such as X-rays, CT scans, or MRI scans to visualize the accumulation of scar tissue.
* Blood tests: to assess liver function or detect specific proteins or enzymes that are elevated in response to fibrosis.
There is currently no cure for fibrosis, but various treatments can help manage the symptoms and slow the progression of the condition. These may include:
* Medications: such as corticosteroids, immunosuppressants, or chemotherapy to reduce inflammation and slow down the growth of scar tissue.
* Lifestyle modifications: such as quitting smoking, exercising regularly, and maintaining a healthy diet to improve overall health and reduce the progression of fibrosis.
* Surgery: in some cases, surgical removal of the affected tissue or organ may be necessary.
It is important to note that fibrosis can progress over time, leading to further scarring and potentially life-threatening complications. Regular monitoring and follow-up with a healthcare professional are crucial to managing the condition and detecting any changes or progression early on.
Neoplasm refers to an abnormal growth of cells that can be benign (non-cancerous) or malignant (cancerous). Neoplasms can occur in any part of the body and can affect various organs and tissues. The term "neoplasm" is often used interchangeably with "tumor," but while all tumors are neoplasms, not all neoplasms are tumors.
Types of Neoplasms
There are many different types of neoplasms, including:
1. Carcinomas: These are malignant tumors that arise in the epithelial cells lining organs and glands. Examples include breast cancer, lung cancer, and colon cancer.
2. Sarcomas: These are malignant tumors that arise in connective tissue, such as bone, cartilage, and fat. Examples include osteosarcoma (bone cancer) and soft tissue sarcoma.
3. Lymphomas: These are cancers of the immune system, specifically affecting the lymph nodes and other lymphoid tissues. Examples include Hodgkin lymphoma and non-Hodgkin lymphoma.
4. Leukemias: These are cancers of the blood and bone marrow that affect the white blood cells. Examples include acute myeloid leukemia (AML) and chronic lymphocytic leukemia (CLL).
5. Melanomas: These are malignant tumors that arise in the pigment-producing cells called melanocytes. Examples include skin melanoma and eye melanoma.
Causes and Risk Factors of Neoplasms
The exact causes of neoplasms are not fully understood, but there are several known risk factors that can increase the likelihood of developing a neoplasm. These include:
1. Genetic predisposition: Some people may be born with genetic mutations that increase their risk of developing certain types of neoplasms.
2. Environmental factors: Exposure to certain environmental toxins, such as radiation and certain chemicals, can increase the risk of developing a neoplasm.
3. Infection: Some neoplasms are caused by viruses or bacteria. For example, human papillomavirus (HPV) is a common cause of cervical cancer.
4. Lifestyle factors: Factors such as smoking, excessive alcohol consumption, and a poor diet can increase the risk of developing certain types of neoplasms.
5. Family history: A person's risk of developing a neoplasm may be higher if they have a family history of the condition.
Signs and Symptoms of Neoplasms
The signs and symptoms of neoplasms can vary depending on the type of cancer and where it is located in the body. Some common signs and symptoms include:
1. Unusual lumps or swelling
2. Pain
3. Fatigue
4. Weight loss
5. Change in bowel or bladder habits
6. Unexplained bleeding
7. Coughing up blood
8. Hoarseness or a persistent cough
9. Changes in appetite or digestion
10. Skin changes, such as a new mole or a change in the size or color of an existing mole.
Diagnosis and Treatment of Neoplasms
The diagnosis of a neoplasm usually involves a combination of physical examination, imaging tests (such as X-rays, CT scans, or MRI scans), and biopsy. A biopsy involves removing a small sample of tissue from the suspected tumor and examining it under a microscope for cancer cells.
The treatment of neoplasms depends on the type, size, location, and stage of the cancer, as well as the patient's overall health. Some common treatments include:
1. Surgery: Removing the tumor and surrounding tissue can be an effective way to treat many types of cancer.
2. Chemotherapy: Using drugs to kill cancer cells can be effective for some types of cancer, especially if the cancer has spread to other parts of the body.
3. Radiation therapy: Using high-energy radiation to kill cancer cells can be effective for some types of cancer, especially if the cancer is located in a specific area of the body.
4. Immunotherapy: Boosting the body's immune system to fight cancer can be an effective treatment for some types of cancer.
5. Targeted therapy: Using drugs or other substances to target specific molecules on cancer cells can be an effective treatment for some types of cancer.
Prevention of Neoplasms
While it is not always possible to prevent neoplasms, there are several steps that can reduce the risk of developing cancer. These include:
1. Avoiding exposure to known carcinogens (such as tobacco smoke and radiation)
2. Maintaining a healthy diet and lifestyle
3. Getting regular exercise
4. Not smoking or using tobacco products
5. Limiting alcohol consumption
6. Getting vaccinated against certain viruses that are associated with cancer (such as human papillomavirus, or HPV)
7. Participating in screening programs for early detection of cancer (such as mammograms for breast cancer and colonoscopies for colon cancer)
8. Avoiding excessive exposure to sunlight and using protective measures such as sunscreen and hats to prevent skin cancer.
It's important to note that not all cancers can be prevented, and some may be caused by factors that are not yet understood or cannot be controlled. However, by taking these steps, individuals can reduce their risk of developing cancer and improve their overall health and well-being.
The main symptoms of FMF include:
1. Recurrent fever, usually during childhood and adolescence, which can range from 38°C to 40°C (100°F to 104°F).
2. Serositis, which can involve the heart (endocarditis), lungs (pleuritis), and/or peritoneum (peritonitis).
3. Painful joints, particularly in the hands, knees, and ankles.
4. Abdominal pain, diarrhea, and vomiting.
5. Rash, which may be present during fever episodes.
6. Enlarged spleen and liver.
7. Elevated levels of inflammatory markers in the blood, such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP).
8. Skin rashes or lesions, which may be present during fever episodes.
9. Kidney problems, such as kidney stones or chronic kidney disease.
10. Eye problems, such as uveitis or retinal vasculitis.
There is no cure for FMF, but the symptoms can be managed with medications and other therapies. Treatment typically involves colchicine, a drug that reduces inflammation and prevents flares. Other medications, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids, may also be used to manage symptoms. In some cases, surgery may be necessary to remove the affected organ or to repair damaged tissue.
It is important for individuals with FMF to work closely with their healthcare provider to develop a treatment plan that is tailored to their specific needs and symptoms. With proper management, many people with FMF are able to lead active and fulfilling lives. However, it is important to note that FMF can be a chronic condition, and ongoing management is typically necessary to control symptoms and prevent complications.
Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.
There are several different types of pathologic neovascularization, including:
* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.
The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.
In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.
Necrosis
Heparin necrosis
Piecemeal necrosis
Necrosis (album)
Centrilobular necrosis
Fibrinoid necrosis
Acral necrosis
Liquefactive necrosis
Coagulative necrosis
Necrosis (film)
Avascular necrosis
Pulp necrosis
Warfarin necrosis
Caseous necrosis
Necrosis (disambiguation)
Fat necrosis
Acute tubular necrosis
Ulcerative dermal necrosis
Temporal lobe necrosis
Acute esophageal necrosis
Cortical pseudolaminar necrosis
Intrauterine epidermal necrosis
Infectious pancreatic necrosis
Tumor necrosis factor
Acute retinal necrosis
Beet vascular necrosis
Renal papillary necrosis
Contraction band necrosis
Subcutaneous fat necrosis
Cocoa necrosis virus
Coagulative necrosis - Wikipedia
Renal Cortical Necrosis: Background, Etiology, Epidemiology
Necrosis: MedlinePlus Medical Encyclopedia
Pulp Necrosis: Symptoms, Tests, Causes, Risks, and Treatments
Tuberculosis Associated with Blocking Agents Against Tumor
Necrosis Factor-Alpha --- California, 2002--2003
Subcutaneous Fat Necrosis of the Newborn: Background, Pathophysiology, Etiology
Amiodarone induced skin necrosis | Heart
Prognostic markers in acute pancreatitis: can pancreatic necrosis be predicted?
Browsing by Subject "Necrosis"
Bone Necrosis
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Nontuberculous Mycobacterium Infection and Tumor Necrosis Factor-α Antagonists - Volume 15, Number 10-October 2009 - Emerging...
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Tumor Necrosis Factor Receptor Superfamily, Member 11A - CAGS
Mucosal tumour necrosis factor alpha and interleukin-6 in patients with Helicobacter pylori associated gastritis. | Gut
RePub, Erasmus University Repository:
Tumor Necrosis Factor-Alpha Inhibitor Etanercept Does Not Alter Methotrexate-Induced...
Inhibition of Soluble Tumor Necrosis Factor Prevents Chemically Induced Carcinogenesis in Mice | Cancer Immunology Research |...
bone necrosis - General Practice notebook
A Truncated Singleton NLR Causes Hybrid Necrosis in Arabidopsis thaliana
Necrosis avascular
AVASCULAR NECROSIS | Buyxraysonline
Necrosis aseptica de la cabeza femoral<...
Journal: Vaccine / Subject: Infectious spleen and kidney necrosis virus and Seriola dumerili / Subject term: Seriola dumerili -...
Periapical repercussion of pulpal necrosis
Avascular necrosis - Knowledge @ AMBOSS
Interactions between rheumatoid arthritis antibodies are associated with the response to anti-tumor necrosis factor therapy |...
Avasular Necrosis
Avascular necrosis4
- Avascular necrosis is a condition in which bone tissue becomes ischemic and begins to suffer pathologic decomposition , leading to joint dysfunction. (amboss.com)
- Avascular necrosis ( AVN ) affects all age groups and is caused by direct trauma, medications, cellular insult, or mechanical compression, often in the context of predisposing conditions. (amboss.com)
- Glucocorticoid use and chronic heavy drinking are the most common causes of nontraumatic avascular necrosis . (amboss.com)
- Avascular necrosis is defined as the localized death of cells in the bone due to lack of blood supply to it. (drnaveenreddyortho.com)
Tumor necro2
Pulp necrosis11
- Pulp necrosis refers to a condition where the pulp inside your teeth die. (healthline.com)
- Once pulp necrosis develops, you can't feel cold at all. (healthline.com)
- Before testing for pulp necrosis, your dentist will first perform an examination of your teeth, gums, and other surrounding tissues. (healthline.com)
- Dental X-rays are also helpful in narrowing down areas of decay or abscess that may be harboring pulp necrosis. (healthline.com)
- Pulp necrosis usually starts off with tooth decay. (healthline.com)
- Another cause of pulp necrosis is chronic pulpitis. (healthline.com)
- Treatment options for pulp necrosis may vary based on the stage and severity of the condition. (healthline.com)
- This is a method of treatment used in pulp necrosis from irreversible pulpitis. (healthline.com)
- Depending on the severity of pulp necrosis, your dentist may remove the entire tooth. (healthline.com)
- Pulp necrosis occurs when the pulp's vital functions are interrupted, starting a degenerative process. (bvsalud.org)
- These periapical lesions related to pulp necrosis result from the same etiologic factors, but they present particular clinical and radiographical features and diverse symptoms that are important to differentiate the diagnosis that will determine the treatment. (bvsalud.org)
Pancreatic necrosis11
- Prognostic markers in acute pancreatitis: can pancreatic necrosis be predicted? (nih.gov)
- The value of six prognostic markers was assessed prospectively in 198 attacks of acute pancreatitis with specific attention to their ability to predict pancreatic necrosis. (nih.gov)
- None of the measured parameters were helpful in distinguishing patients who subsequently developed pancreatic necrosis from patients who had other severe outcomes. (nih.gov)
- These methods are unlikely to distinguish pancreatic necrosis from other severe outcomes, but they may supplement clinical judgment in selecting a high risk group of patients for contrast enhanced computed tomography. (nih.gov)
- Endotherapy for pancreatic necrosis: An update. (bvsalud.org)
- Approximately 20% of patients with acute pancreatitis develop pancreatic necrosis . (bvsalud.org)
- Pancreatic necrosis is associated with high mortality and morbidity . (bvsalud.org)
- In the last few decades, there has been a significant revolution in the treatment of infected pancreatic necrosis . (bvsalud.org)
- Endoscopic intervention for pancreatic necrosis is being increasingly performed with good success and a lower complication rate. (bvsalud.org)
- However, techniques of endotherapy are still not uniform and vary as per local expertise, and there are still many unresolved questions with regard to the interventions in patients with pancreatic necrosis . (bvsalud.org)
- The objective of this paper is to critically review the literature and update the concepts of endoscopic interventional therapy of pancreatic necrosis . (bvsalud.org)
Ischemic3
- Renal cortical necrosis is a rare cause of acute renal failure secondary to ischemic necrosis of the renal cortex. (medscape.com)
- Many cases of subcutaneous fat necrosis of the newborn have been reported in newborns who sustained perinatal hypoxic-ischemic injury and were treated by hypothermia to prevent encephalopathy and serious brain injury. (medscape.com)
- It is also called osteonecrosis or ischemic bone necrosis and most commonly occurs in the hip. (drnaveenreddyortho.com)
Occurs3
- Coagulative necrosis occurs in most bodily organs, excluding the brain. (wikipedia.org)
- Subcutaneous fat necrosis of the newborn (SFNN) occurs in the first several weeks of life. (medscape.com)
- Focal neuronal degeneration with necrosis occurs, leading to the development of glial nodules. (medscape.com)
Tumour3
- Mucosal tumour necrosis factor alpha and interleukin-6 in patients with Helicobacter pylori associated gastritis. (bmj.com)
- The production of tumour necrosis factor alpha (TNF alpha) and interleukin-6 by human antral mucosa during short term culture in vitro has been measured by enzyme linked immunosorbent assay. (bmj.com)
- Details for: Tumour necrosis factor and related cytotoxins. (who.int)
Bone1
- The bone tissue ischemia and necrosis characteristic of AVN most commonly affect the epiphysis of long bones . (amboss.com)
Ischemia2
- Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction . (wikipedia.org)
- It is important to note that while ischemia in most tissues of the body will cause coagulative necrosis, in the central nervous system ischemia causes liquefactive necrosis , as there is very little structural framework in neural tissue. (wikipedia.org)
Subcutaneous8
- Subcutaneous fat necrosis of the newborn (SFNN) is an uncommon disorder characterized by firm, mobile, erythematous nodules and plaques over the trunk, arms, buttocks, thighs, and cheeks of full-term newborns. (medscape.com)
- Subcutaneous fat necrosis of the newborn usually runs a self-limited course, but it may be complicated by hypercalcemia and other metabolic abnormalities. (medscape.com)
- The exact pathogenesis of subcutaneous fat necrosis of the newborn (SFNN) is not known. (medscape.com)
- when the PGE1 was discontinued, the subcutaneous fat necrosis of the newborn resolved. (medscape.com)
- The cause of subcutaneous fat necrosis of the newborn (SFNN) is not known. (medscape.com)
- IMSEAR at SEARO: Hypercalcemia and metastatic calcification in a neonate with subcutaneous fat necrosis. (who.int)
- Nair Sajitha, Nair Sathyajith G, Borade Ashwin, Ramakrishnan K. Hypercalcemia and metastatic calcification in a neonate with subcutaneous fat necrosis. (who.int)
- We report a 30-day-old baby with subcutaneous fat necrosis and symptomatic hypercalcemia, who developed metastatic calcification in the subcutaneous tissue, kidneys, pericardium and brain. (who.int)
Characteristic1
- Protein denaturation results in exposure of hydrophobic regions normally sequestered within the three-dimensional center of the molecules and may explain why necrotic cells display an increased capacity to bind the hydrophobic Eosin pigment) [4] Also, it is characteristic of coagulative necrosis to not have a zone in between necrotic cells and viable cells. (wikipedia.org)
Complications1
- Acute renal failure is typical in patients with renal cortical necrosis, with associated complications (eg, hyperkalemia, fluid overload). (medscape.com)
Pathology1
- Histopathology of a pheochromocytoma with coagulative necrosis, displayed at gross pathology (upper left) and light microscopy at low (upper right), medium (lower left) and high magnification (lower right). (wikipedia.org)
Commonly1
- Coagulative necrosis is most commonly caused by conditions that do not involve severe trauma , toxins or an acute or chronic immune response . (wikipedia.org)
Femoral1
- Díaz-Bertrana, C & Tordesilla, C 2007, ' Necrosis aseptica de la cabeza femoral ', Revista del Grupo de especialistas veterinarios en ortopedia , vol. 11, pp. (uab.cat)
Occur3
- Like most types of necrosis , if enough viable cells are present around the affected area, regeneration will usually occur. (wikipedia.org)
- Renal cortical necrosis is usually extensive, although focal and localized forms occur. (medscape.com)
- Most of the symptoms that indicate issues with your tooth and inner pulp occur before necrosis. (healthline.com)
Onset1
- This is because once the onset of necrosis happens, the nerves may stop sending signals that alert you to any pain or discomfort, because the pulp has died. (healthline.com)
Treatment2
- [3] Both of these treatments use coagulative necrosis in treatment of cancer. (wikipedia.org)
- We report pulmonary M . haemophilum infection in a woman who had been immunosuppressed by tumor necrosis factor-α antagonist (TNF-αA) (adalimumab) treatment for rheumatoid arthritis. (cdc.gov)
Tissue4
- In coagulative necrosis, the architectures of dead tissue are preserved for at least a couple of days. (wikipedia.org)
- The macroscopic appearance of an area of coagulative necrosis is a pale segment of tissue contrasting against surrounding well vascularized tissue and is dry on cut surface. (wikipedia.org)
- To achieve coagulative necrosis in tumor tissue, it only takes around 20 minutes of application with the RF probe. (wikipedia.org)
- Necrosis is the death of body tissue. (medlineplus.gov)
Treatments1
- Coagulative necrosis can be induced for treatments of cancers. (wikipedia.org)
Patients3
- Studies have shown that patients with HUS with thrombotic microangiopathy (TMA) involving arteries have a higher likelihood of progressing into acute cortical necrosis compared with patients with predominant glomerular TMA. (medscape.com)
- Blocking of the Tumor Necrosis Factor (TNF) activity is a successful therapeutic approach for 50-60% of rheumatoid arthritis (RA) patients. (biomedcentral.com)
- Cette étude a permis de déterminer la fréquence et l'étiologie de l'insuffisance rénale aiguë chez des patients hospitalisés en Arabie saoudite sur une période de 2 ans. (who.int)
Clinical1
- The objective of this study was to expose and discuss, through a review, the etiological factors and histological, clinical and radiographical features of the periapical illnesses resulting from necrosis. (bvsalud.org)
Examination1
- Renal cortical necrosis was detected by postmortem examination in 5% of infants aged 3 months or younger at death. (medscape.com)
Results2
- If this vasospasm is brief and vascular flow is reestablished, acute tubular necrosis results. (medscape.com)
- It is postulated that cold or stress-induced injury to immature fat cells results in the development of solidification and necrosis. (medscape.com)
Central1
- Tumor necrosis factor (TNF) is a proinflammatory cytokine that is central to the inflammatory process of RA. (biomedcentral.com)