Pathology Exam 1 PDF

Chapter 1: Etiology is the precise cause of the disease. - Pathogen- a disease causing microorganism - Multifactorial- more than one cause for disease - Idiopathic- no known cause - Nosocomial- disease results from exposure to infection in the...

Chapter 1: Etiology is the precise cause of the disease. - Pathogen- a disease causing microorganism - Multifactorial- more than one cause for disease - Idiopathic- no known cause - Nosocomial- disease results from exposure to infection in the healthcare environment - Iatrogenic- disease from medical treatment 1. Primary prevention: Prohibits the disease from happening or occuring. Ex. Wearing a helmet, flu shots, prophylaxis 2. Secondary prevention: early detection through screening and early treatment.footage Ex. doing self breast exams & testicular exams 3. Tertiary prevention: rehabilitation after diagnosis of a disease/injury. Preventing complications/progression of the condition. Ex. Physical therapy for stroke Chapter 2: Cell Function: 1. Transport- movement of molecules across membranes. 2. Ingestion - (intake) controlling what comes in (endocytosis) 3. Secretion - (removing) controls what leaves cells (exocytosis) 4. respiration - anaerobic and aerobic 5. communication - exchange of information 6. Reproduction - Mitosis, single cell divide into two identical daughter cells. Meiosis, germ cells (sperm + egg) form gametes with half chromosomes as parent cells. fifty Passive Transport (no energy required) : Osmosis, Diffusion Osmosis - Solvent (the water) moves from low to high solute concentration, through a semipermeable membrane. ageemaggarrager Diffusion - Solute (the salt) moves from high to low concentration. ing Facilitated transport - proteins aid substance movement across the membrane, no energy. (ex. glucose) Active transport - moves particles against concentration gradient, energy. (Na/K- ATPase pump) What are Feedback mechanisms? Regulates the gene activity and controls the cells from overproduction or underproduction. Proliferation- Increase # of cells (helps maintain population, tissue growth, tissue repair) Differentiation- Change in physical function & properties. Special functions (influenced by cell microenvironment / signals) Cellular adaptation and response to stress Atrophy - Shrunken cell, decrease in SIZE. (Ex. Menopause) - Decrease demand ; immoble - Decrease blood supply ; ischemia - Lack of hormones and nutrients Hypertrophy - enlarged, increase in SIZE, in response to stress. (Ex. Pregnancy) > increased sex hormones; hypertrophied reproductive cells for location. Hyperplasia - Increase in NUMBER of cells (Ex. Puberty) > increase number of cells on the uterus; high altitude > increase number of RBC. Metaplasia - Transform from one type to another caused by external stress. When stressor is removed it can return to normal Ex. bronchial tubes change from epithelial to squamous from smoking. Dysplasia - Transform to abnormal & mutated cell types. (change in cell shape, size, uniformity, arrangement, structure; CAUSED BY ABNORMAL MUTATION OF DIVIDING CELLS) (ex. Cancer cells) Cell Injury & Death Apoptosis - “cell suicide” programmed cell death. (damaged genetic mutation/materials, old age etc) Necrosis - Unplanned death, due to cell injury. (chemicals & pathogens, infections, physical injury, serum deficit) Chapter 3: Inflammation and tissue repair First Line of Defense- Physical & chemical barrier to protect pathogens from entry. (ex: skin, mucous membrane, tears, saliva) Second Line of Defense - Inflammatory Response. Vasodilation & increased capillary permeability causing redness and swelling. Phagocytes move in to engulf harmful substances. (nonspecific) Third Line of Defense - Immune response.Provides a specific and effective response to provide long term protection against disease. (if unsuccess will cause disease to spread)  Acute inflammation (heat, pin, redness, swelling, loss of function) 1. Vascular response - vessels dilate to increase blood flow, and lining becomes more permeable this allows WBC to phagocytize the harmful agents. Inflammatory Mediators: REGULATORS & first responders.They regulate vessel dilation, blood flow, and the start/end of vascular regulation. Mast cells: They are by the epithelium and have receptors that recognize pathogens so they can also be first responders. 2. Cellular response - alert products of healing to injured sites. Chemotaxis - transporting cells to the site of injury. Cellular Adherence - stick to the line of the epithelium. Cellular Migration - leaving blood vessels to migrate out to the blood vessel. 3. Prepair - remove the damaged tissues and prepare the site for healing. Manifestations: (referred to as Cardinal Signs) LOCAL: Erythema (redness), heat, swelling, pain, loss of function, lymphadenitis (enlarged and inflammation of lymph nodes for draining harmful substances) SYSTEMIC : Fever: helps kill some microorganism/Bacteria. Also increases blood flow. FATIGUE, loss Appetite LAB: High level CBC, Blood Test , CRP, ESR (erythrocyte sediment rate) Treatment : Reduce blood flow, swelling, pain, block mediators. RICE: rest, ice, compression, elevation. Treat underlie condition, diet, NSAIDS & Glucocorticoids. Healing and Tissue Repair Primary Intention - Wound is close together (papercut). The wound is connecting and healing simultaneously. Secondary Intention - Big opening; they must heal from the bottom up, more likely to lead to infections. Chapter 4 : Altered Immunity Immune function: Body Recognizes SPECIFIC foreign substances and neutralizes them to prevent damage in the body. Antigens: They SIGNALS the antibodies to recognize and approach the invader. Antibodies: Proteins that bind to the antigen, which will deactivate and stop the pathogens. Innate immunity: Non-specific, it will fight against any pathogen that comes in contact with. Adaptive Immunity: Acquired immunity; it takes time to develop and it only can attack certain pathogens. (specific & memory) Specificity: seek and destroy specific invaders. Memory: remembers more easily and attacks returning invaders. Bone Marrow : Produces lymphocytes, matures B lymphocytes Thymus: Differentiation & maturation of T lymphocytes Humid Cellular AHP antibody antigen or CD 8 CD 4 Humoral: Produces ANTIBODIES/immunoglobulin by B cells. These antibodies target and neutralize pathogens. Cell Mediated: Activates the T cells (cytotoxic). Secretes signal molecules that cause apoptosis. Active immunity: (forever protection) The body already has an immune response for it. 1. Body has already faced it and now has memory to fight it (natural) 2. Received a vaccine and now body has memory of it (artificial) vasthe weakversion ofVirus Passive immunity: (short term protection) transferred from a host to a recipient. 1. Transferred via mother to infant 2. Antibody injections (ex. Donated blood with antibody) Hypersensitivity - Inappropriate excessive immune response Autoimmunity - Inappropriate attack to “self”. Fail to distinguish self from nonself. Alloimmunity - reaction directed at tissue antigens from others of the same species (ex. Rejection after transplant or blood transfusion)  1. Graft Rejection - The recipient body attacks the donated tissue. 2. Graft Vs. Host Disease: The skin graft is rejecting the body, it attacks the recipient. Manipulating the immune response : Take medication, manage the autoimmune disease, take vaccines. in Iembrane againstToxin G Bacteria Virus 0 E allergies Chapter 5: infections Microbes - Living organisms; some cause harm & some dont. Bacteria, virus, fungi protozoa. Resident Flora don't cause harm and are actually helpful. Pathogen - DISEASE producing microbes. They need to bind to specific receptors of the host to cause harm. 1. direct destruction of the host cell by the pathogen 2. Interfere with host cell metabolic function 3. Expose the host cell to the toxic pathogen Types of pathogens Bacteria - Most can survive outside of the host cell. Anaerobic survives in deep tissues. Some can survive both. They have cell walls and human cells don't. So the best treatment is to inhibit their cell wall. Virus - Intracellular parasites. THEY NEED TO INVADE THE HOST CELL to replicate. Cervical metaplasia/dysplasia 1. Pathophysiology: Cervical metaplasia/dysplasia refers to abnormal changes in the cells of the cervix. Risk factors: Multiple sex partner, Smoking, HPV Virus, early onset of sex. If left untreated Dysplasia can turn into cancer. 2. Clinical Manifestations:  may not present with any symptoms initially and is often detected through routine cervical cancer screening, such as a Pap smear or HPV testing. In some cases, individuals may experience abnormal vaginal bleeding, especially after intercourse or between periods. pelvic pain, abnormal vaginal discharge, or bleeding after menopause. 3. Diagnosis: Diagnosis of cervical metaplasia/dysplasia involves cervical cancer screening methods, including Pap smear (Pap test) and HPV testing. During a Pap smear, a sample of cells is collected from the cervix and examined under a microscope for abnormal changes. HPV testing detects the presence of high-risk strains of HPV DNA in cervical cells, which is often performed in conjunction with Pap smear screening. If abnormalities are detected, further evaluation may include colposcopy, a procedure that allows visualization and biopsy of the cervix for more detailed assessment. 4. Treatment: Mild dysplasia may resolve spontaneously without intervention and may be monitored with regular follow-up Pap smears. Treatment modalities include loop electrosurgical excision procedure (LEEP), cryotherapy, laser therapy, or surgical excision (conization) of the abnormal tissue. surgery, radiation therapy, chemotherapy Rheumatoid arthritis 1. Pathophysiology: autoimmune response where the body's immune system mistakenly attacks its own tissues, particularly the synovium (lining of the joints). Inflammation in the synovium leads to synovitis, causing swelling, pain, and eventually damage to the cartilage and bone within the joint. Immune cells, particularly T-lymphocytes and macrophages, play a central role in the inflammatory cascade, releasing cytokines and other inflammatory mediators that perpetuate joint inflammation and destruction. Over time, chronic inflammation can lead to irreversible joint damage, deformities, and systemic complications affecting other organs such as the heart, lungs, and skin. 2. Clinical Manifestations: joint pain, swelling, stiffness, and decreased range of motion.HeatatJoint RA typically affects multiple joints symmetrically, commonly involving the small joints of the hands, wrists, and feet, although larger joints such as the knees and shoulders may also be affected. Morning stiffness lasting more than 30 minutes is a characteristic feature of RA. Systemic symptoms such as fatigue, low-grade fever, and weight loss may also occur, especially during periods of active disease flares. 3. Diagnosis: No definitive test; rheumatoid arthritis is based on a combination of clinical evaluation, laboratory tests, and imaging studies.  Laboratory tests may include rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies, which are commonly elevated in RA. Imaging studies such as X-rays, ultrasound, or magnetic resonance imaging (MRI) may reveal joint erosions, synovitis, and periarticular changes characteristic of RA. 4. Treatment: Treatment of rheumatoid arthritis aims to reduce inflammation, relieve symptoms, prevent joint damage, and improve overall function and quality of life. Nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroids Physical therapy, occupational therapy, and lifestyle modifications, including exercise and joint protection techniques, are essential components of RA management to maintain joint function and mobility. In severe cases of RA with significant joint damage and disability, surgical interventions such as joint replacement surgery (arthroplasty) may be considered to improve joint function and relieve pain. Gastritis 1. Pathophysiology: inflammation of the lining of the stomach Acute gastritis often results from irritants such as alcohol, nonsteroidal anti-inflammatory drugs (NSAIDs), or H Pylori Chronic gastritis may develop over time and is often associated with persistent infection by H. pylori, autoimmune diseases, or long-term use of NSAIDs. Disrupt the protective mucous layer of the stomach, allowing acid and digestive enzymes to injure the gastric mucosa, leading to symptoms such as pain, bleeding, and ulceration. 2. Clinical Manifestations: Common symptoms include abdominal pain or discomfort. nausea, vomiting, bloating, loss of appetite, and a feeling of fullness after eating small amounts. In severe cases or with complications such as gastric bleeding or ulceration, symptoms may include hematemesis (vomiting blood) or melena (black, tarry stools). 3. Diagnosis: Endoscopy with biopsy. Other diagnostic tests may include blood tests to assess for H. pylori infection (e.g., serology, urea breath test), stool tests for occult blood, and imaging studies such as upper gastrointestinal (GI) endoscopy or barium swallow. 4. Treatment: Treatment of gastritis aims to alleviate symptoms, promote healing of the gastric mucosa, and address underlying causes. For acute gastritis caused by irritants such as alcohol or NSAIDs, care such as antacids or proton pump inhibitors (PPIs) to reduce gastric acid secretion. Chronic gastritis associated with H. pylori infection may require eradication therapy with a combination of antibiotics (e.g., clarithromycin, amoxicillin) and acid-suppressing medications (e.g., PPIs, H2-receptor antagonists).  Lifestyle modifications such as avoiding irritants, following a healthy diet, and reducing stress may help prevent gastritis and promote gastric mucosal healing. Pancreatitis 1. Pathophysiology: Acute pancreatitis often results from gallstones or excessive alcohol consumption, leading to activation of pancreatic enzymes within the pancreas itself, causing autodigestion and tissue damage. Pancreatic enzymes (e.g., amylase, lipase) become activated prematurely, leading to inflammation, edema, necrosis, and, in severe cases, hemorrhage and pseudocyst formation. 2. Clinical Manifestations: abdominal pain, nausea, vomiting, and fever. upper abdomen and radiating to the back. bloating, indigestion, diarrhea, and unintentional weight loss. In severe cases, complications such as pancreatic necrosis, pseudocysts, or systemic inflammatory response syndrome (SIRS) may occur, leading to shock and multiorgan failure. 3. Diagnosis: Blood tests, including serum amylase and lipase levels Imaging studies such as abdominal ultrasound (CT) (MRI) may be used to visualize the pancreas and assess for signs of inflammation, necrosis, or complications. Endoscopic retrograde cholangiopancreatography (ERCP) may be performed to evaluate the pancreatic duct and biliary tree if gallstones are suspected as a cause. 4. Treatment: fasting, intravenous fluids, and pain control with analgesics. nasogastric suction, bowel rest, and nutritional support. lifestyle modifications (e.g., alcohol cessation, dietary changes), enzyme replacement therapy to aid digestion Hepatitis 0 0 viral infections, alcohol consumption, autoimmune diseases, and toxic exposures.  Viral hepatitis typically involves the invasion of liver cells by the respective viruses, leading to inflammation and injury. The immune response to viral infection contributes to liver damage Chronic hepatitis may develop if the immune response is unable to clear the virus, leading to persistent inflammation, fibrosis, and eventually cirrhosis or liver failure. 2. Clinical Manifestations: Common symptoms include fatigue, jaundice, dark urine, pale stools, abdominal pain, and loss of appetite. nausea, vomiting, fever, and weight loss. Acute hepatitis = flu-like symptoms, while chronic hepatitis may be asymptomatic or present with nonspecific symptoms until complications such as cirrhosis or liver failure develop. 3. Diagnosis: Blood tests are used to assess liver function (e.g., serum aminotransferases, bilirubin, albumin) and to detect specific markers of viral infection (e.g., hepatitis B surface antigen, hepatitis C antibodies). (CT), (MRI) may be performed to evaluate liver size, texture, and the presence of focal lesions or complications. 4. Treatment: - A & B can be prevented by vaccines. AVOID contact sports antiviral therapy, immunosuppressive agents, or lifestyle modifications. rest, adequate nutrition, hydration, and avoidance of hepatotoxic substances such as alcohol and certain medications. corticosteroids or immunosuppressants. liver transplantation may be necessary to prevent mortality. Tuberculosis 1. Pathophysiology: Mycobacterium tuberculosis primarily affects lungs but can also involve other organs. When M. tuberculosis enters the body through inhalation of infectious droplets, it is engulfed by alveolar macrophages in the lungs. The bacterium can evade destruction by macrophages and replicate within them, leading to the formation of granulomas, which are aggregates of immune cells and bacteria. Within granulomas, M. tuberculosis may exist in a dormant or latent state, allowing it to persist within the host for years without causing active disease. immunosuppression or systemic illness can lead to reactivation of latent TB, resulting in active tuberculosis disease 2. Clinical Manifestations: Latent TB infection is asymptomatic and is characterized by a PPD Active TB disease typically presents with symptoms such as cough, fever, night sweats, weight loss, fatigue, and hemoptysis (coughing up blood). Pulmonary TB is the most common form and may cause symptoms such as pleuritic chest pain, productive cough (often with purulent sputum), and breathlessness.  Extrapulmonary TB can affect other organs such as the lymph nodes, bones, joints, meninges, and genitourinary system, depending on the site of involvement. 3. Diagnosis: Microbiological confirmation of TB is achieved through sputum smear microscopy, culture, and molecular testing (IN THE MORNING FOR 3 CONSECUTIVE DAYS) Chest X-ray may reveal characteristic findings such as upper lobe infiltrates, cavitation, and lymphadenopathy in pulmonary TB. PPD SKIN TESTING Additional tests such as chest CT, bronchoscopy with bronchoalveolar lavage, or biopsy may be needed to evaluate for extrapulmonary TB or complications. 4. Treatment: Treatment of tuberculosis involves combination antimicrobial therapy with multiple drugs to prevent the development of drug resistance. Standard treatment regimens for drug-susceptible TB typically include a combination of isoniazid, rifampin, pyrazinamide, and ethambutol Directly observed therapy (DOT) is recommended to ensure adherence to treatment and minimize the risk of treatment failure and drug resistance. Bacillus Calmette Ghrelin (BCG) is a TB vaccine, will show false positives with PPD. Urinary tract infection 1. Pathophysiology: Escherichia coli (E. coli) aerobic & gram-negative urinary tract and multiply. Female more likely bc ureter is shorter & closer to the anus. Blockages: Kidney stones, enlarged prostate gland, use of catheters. 2. Clinical Manifestations: dysuria (painful urination), increased frequency and urgency of urination, suprapubic pain, hematuria (blood in the urine), and cloudy or foul-smelling urine (leukocytes). fever, chills, flank pain, nausea, vomiting, and systemic symptoms of infection. 3. Diagnosis: Urinalysis: of white blood cells (indicative of inflammation), bacteria, red blood cells, and other abnormalities. A urine culture is used to identify the specific bacteria causing the infection and determine their antibiotic susceptibility. (CT) (MRI) may be performed in cases of complicated or recurrent UTIs to evaluate for structural abnormalities or urinary tract obstructions. 4. Treatment: Diuretics to FLUSH out the bacteria. Commonly prescribed antibiotics against gram negative bacteria. Symptomatic relief measures such as pain management, hydration, and urinary analgesics (e.g., phenazopyridine) may be used to alleviate discomfort while undergoing antibiotic therapy. Meningitis 1. Pathophysiology:  Meningitis is an inflammation of the meninges, the protective membranes covering the brain and spinal cord. It is AIRBORNE, enters the respiratory tract and attracts epithelial cells. Then it would go into the bloodstream. In the CNS, the bacterias multiply in the meninges and CSF. This causes edema, blood, and exudate. This causes obstruction leading to no oxygen leading to septic shock. 2. Clinical Manifestations: Common symptoms include fever, headache, neck stiffness (nuchal rigidity), photophobia (sensitivity to light), and altered mental status. INCREASED INTRACRANIAL PRESSURE > less oxygen > less conscious neurological deficits, seizures, focal neurologic, Fever, leukocytosis, anorexia. 3. Diagnosis: Lumbar puncture (LP) is performed to obtain CSF for analysis CSF analysis typically reveals an elevated white blood cell count (pleocytosis), elevated protein levels, and decreased glucose levels in bacterial meningitis CT & MRI complications such as hydrocephalus, abscess formation, or cerebral edema. Kernig Sign - lift leg up & extend it, if it is painful. (+) Brudzinski Sign - Lift up the Neck a little bit, their legs will bend. 4. Treatment: Antimicrobial, corticosteroid, etc to reduce inflammation and mortality. Maintain adequate BP and vital signs. Supportive care measures include maintenance of cerebral perfusion, control of intracranial pressure, and management of complications such as seizures or shock. Close monitoring of clinical status, neurological examination MUST BE QUARANTINED/ISOLATED TO PREVENT THE SPREAD. H. influenzae is a vaccine to prevent or lessen the chance of getting it. HIV/AIDS (WHEN THE CD4 IS BELOW A CERTAIN NUMBER IT IS AIDS) 1. Pathophysiology: (HIV) is a retrovirus that primarily infects CD4+ T lymphocytes, macrophages, and dendritic cells, leading to progressive immune system dysfunction. HIV is transmitted through contact with infected bodily fluids, including blood, semen, HEY vaginal secretions, and breast milk. Upon entry into the body, HIV targets and binds to CD4 receptors on the surface of nters replicate immune cells, facilitating viral entry and replication. insideCD4 CD8 kills the CD4 bc it is infected apoptosis. Viral replication within CD4+ T cells leads to their depletion, causing a progressive decline in immune function (AIDS). it susceptible to opportunistic infections, malignancies, and other complications. D8 Kills 2. Clinical Manifestations: Early HIV infection may present with flu-like symptoms such as fever, fatigue, headache, Bified sore throat, swollen lymph nodes, and rash.  As the disease progresses, individuals may experience chronic symptoms such as weight loss, diarrhea, night sweats, recurrent infections, oral thrush, and fungal infections. Advanced HIV infection, characterized by low CD4+ T cell counts and/or the presence of AIDS-defining illnesses, may present with severe opportunistic infections (e.g., Pneumocystis pneumonia, cytomegalovirus retinitis, cryptococcal meningitis) and malignancies (e.g., Kaposi's sarcoma, non-Hodgkin lymphoma). 3. Diagnosis: Diagnosis of HIV infection is typically made through serological testing for HIV antibodies or antigens in blood or oral fluid samples. Monitoring of HIV disease progression involves measurement of CD4+ T cell counts and viral load, which provide information on immune status and viral replication levels. 4. Treatment: – THERE IS PREPALAXIS !!! Antiretroviral therapy (ART) combination therapy ART suppresses viral replication, preserves immune function, reduces the risk of opportunistic infections and complications, and improves overall survival. Anaphylaxis (IMMUNOGLOBULIN E) 1. Pathophysiology: Systemic allergic reaction that occurs rapidly after exposure to an allergen. It is an exaggerated immune response mediated by immunoglobulin E (IgE) antibodies. Allergen binds to IgE antibodies attached to mast cells and basophils, triggering the release of inflammatory mediators such as histamine, leukotrienes, and cytokines. Leads to vasodilation, increased vascular permeability, smooth muscle contraction, and recruitment of inflammatory cells, causing systemic manifestations of anaphylaxis. asodialation Activation of the complement system and coagulation cascade may also contribute to the pathophysiology of anaphylaxis, leading to further tissue damage and organ dysfunction. 2. Clinical Manifestations: overBP (depends on the amount of antigen specific Ig E antibodies) Common manifestations are hives, itching, flushing, and angioedema (swelling of the face, lips, tongue, or throat). Respiratory symptoms may include wheezing, shortness of breath, chest tightness Cardiovascular manifestations can range from mild symptoms such as palpitations and Taihylardia tachycardia to severe hypotension, shock, and cardiac arrest. Neurological symptoms such as dizziness, confusion, or loss of consciousness 3. Diagnosis: Diagnosis of anaphylaxis is primarily based on clinical presentation and a detailed patient history of exposure to an allergen. Laboratory tests such as serum tryptase levels may be helpful in confirming the diagnosis and assessing the severity of anaphylaxis. Allergy testing, including skin prick tests or serum-specific IgE assays, may be performed to identify the causative allergen and guide allergen avoidance strategies. 4. Treatment: epinephrine (adrenaline) as the first-line therapy  airway management, supplemental oxygen, intravenous fluids, and positioning the patient in a supine position with legs elevated to improve venous return. Antihistamines (e.g., diphenhydramine) and corticosteroids (e.g., methylprednisolone) In cases of severe anaphylaxis with refractory hypotension or shock, vasopressors such as dopamine or norepinephrine may be required to maintain adequate perfusion pressure. Vasopressor increases BP Lupus 1. Pathophysiology: Systemic lupus erythematosus (SLE), is a chronic autoimmune disease characterized by dysregulation of the immune system>inflammation and tissue damage in multiple organs and tissues. The exact cause of lupus is not fully understood, but it is believed to involve a combination of genetic predisposition, environmental triggers, and dysregulated immune responses. In lupus, the immune system produces antibodies that target self-antigens, such as nuclear antigens (e.g., DNA, RNA, histones), resulting in the formation of immune complexes. These immune complexes deposit in various tissues and organs, including the skin, joints, kidneys, heart, lungs, and central nervous system, triggering inflammation and tissue damage. Dysfunctional clearance of apoptotic cells and defective immune regulation contribute to the perpetuation of inflammation and the development of clinical manifestations in lupus. 2. Clinical Manifestations:. Fatigue, fever, joint pain and swelling (arthritis), skin rashes (Butterfly rash), photosensitivity, and oral or nasal ulcers. Lupus can also affect various internal organs, leading to complications such as nephritis (lupus nephritis), cardiovascular disease, pleuritis or pericarditis, hematologic abnormalities (e.g., anemia, leukopenia, thrombocytopenia), and neuropsychiatric manifestations (e.g., cognitive dysfunction, seizures). proteinuria Disease flares and remissions are characteristic of lupus 3. Diagnosis: Diagnosis of lupus is based on a combination of clinical criteria, laboratory tests, and assessment of organ involvement. malar rash, discoid rash, oral ulcers, arthritis, photosensitivity, hematologic disorders, renal involvement, immunologic abnormalities (e.g., presence of autoantibodies), and neurologic manifestations. Laboratory tests commonly used in the diagnosis and monitoring of lupus include antinuclear antibodies (ANA), anti-double-stranded DNA (anti-dsDNA) antibodies, anti-Smith (anti-Sm) antibodies, complement levels (C3, C4), and erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) to assess inflammation. 4. Treatment: Treatment of lupus aims to control disease activity, minimize symptoms, prevent organ damage, and improve quality of life.  Medications commonly used in the treatment of lupus include nonsteroidal anti-inflammatory drugs (NSAIDs), antimalarial agents (e.g., hydroxychloroquine), corticosteroids (e.g., prednisone), immunosuppressive agents (e.g., methotrexate, mycophenolate, azathioprine), and biologic therapies (e.g., rituximab). Lifestyle modifications such as sun protection, regular exercise, smoking cessation, and stress management may also be recommended to help manage symptoms and improve overall well-being. Close monitoring of disease activity, organ function, and medication side effects is essential for optimizing treatment outcomes and preventing disease complications. Influenza 1. Pathophysiology: IT IS A VIRUS, attached to the host on the epithelial cells of the airway. Influenza viruses primarily target respiratory epithelial cells in the upper and lower respiratory tract. Upon infection, the virus enters the host cell, replicates, and spreads to neighboring cells, leading to epithelial cell damage and inflammation. The host immune response is triggered, leading to the release of pro-inflammatory cytokines, recruitment of immune cells, and activation of the adaptive immune system. The resulting inflammation and immune response contribute to the characteristic symptoms of influenza, including fever, malaise, cough, sore throat, headache, myalgia, and nasal congestion. 2. Clinical Manifestations: Abrupt onset of symptoms, often characterized by high fever, chills, and generalized malaise. Respiratory symptoms such as cough, sore throat, nasal congestion, and rhinorrhea (runny nose) are common. Systemic symptoms may include headache, myalgia (muscle aches), arthralgia (joint pain), fatigue, and weakness. Gastrointestinal symptoms such as nausea 3. Diagnosis: Diagnosis of influenza is primarily based on clinical presentation during periods of increased influenza activity (e.g., flu season) and epidemiologic factors. Rapid influenza diagnostic tests (RIDTs) are commonly used for point-of-care testing in clinical settings. These tests detect viral antigens from respiratory specimens (e.g., nasal swabs) and provide results within minutes. 4. Treatment: Antiviral medications are available for the treatment of influenza and may be prescribed to reduce the severity and duration of symptoms, especially if initiated early in the course of illness. Anti Supportive care measures, including rest, hydration, and symptomatic relief (e.gAntipyretics for fever, analgesics for pain), are essential for managing influenza symptoms and promoting recovery. BET ANNUAL VACCINATION  Ch 10: Altered Neural Function Parts of the neuron, function of the neuron recieve tᵈ sendsignalaway Cell Body: Main part with the nucleus. Dendrites: Receive signals. Axon: Sends signals away. Axon Terminal: Releases signals to other cells Receive Information: Dendrites receive signals. Integrate Information: Cell body decides what to do with signals. Transmit Information: Axon sends signals. Communicate with Other Cells: Axon terminal releases signals to other cells. Main job of supporting neuroglial cells (e.g., neuroglia, Schwann cells) It provides support and nutrients, maintains homeostasis, and forms the myelin that covers the neurons of the brain. Basics of neurotransmission Action potential - electrical signal that travels along the axon through the membrane to communicate with other neurons. Depolarization - More influx of positive charge (Na+) Repolarization - Outflow of potassium ions out of the cell, returning to normal state. Communication between cells(information from neuron flow between synapse) Electrical synapses - They are connected by GAP JUNCTIONS and they communicate in between. (MULTI–directional) Chemical synapses - Communications are carried out by NEUROTRANSMITTERS. (UNI- directional) Neural injury – how can neurons suffer injury? When neurons are damaged, they can not regenerate or be replaced, this means they summer with permanent damage. It can be damaged by… Chromatolysis: The swelling of a neuron because of injury Atrophy: Decrease in the size of the cell (neuron) Neuronophagia: Phagocytosis and inflammatory responses caused by a dead neuron damaging neighboring cells Intraneuronal inclusions: Distinctive structures formed in the nucleus or cytoplasm Protective structures: blood-brain barrier: Protects the brain by reducing/selecting the permeability of substances to get into the brain. It consists of tight junctions that line the epithelial cells that line the capillaries of the brain. cerebrospinal fluid: Clear substance that surrounds the brain & spinal cord. It provides protection, reduces pressure on the brain structure, removes harmful substances, and transports hormones to remote areas of the brian. What are types of trauma or injury to CNS? Traumatic CNS injury- Direct trauma to the brain or to the spine. ISCHEMIA CNS injury - lack of perfusion to the brain bc of thrombus or atherosclerosis Excitation Injury - may result from things like stroke/epilepsy causing imbalance in excitatory and inhibitory neurotransmitters. Prolonged exposure to GLUTAMATE. What happens when intracranial pressure increases? It will compress blood flow to the brain. It also presses the brain lower triggering the vomiting zone that's why they may feel nausea or vomit. What is decerebrate and decorticate posturing? Why do they happen? core Decorticate A = Decorticate B= Decerebrate This happens because of damage or disruption to certain areas of the brain. Triggering these involuntary movements. Decerebrate Basics of peripheral nervous system (PNS) organization Somatic nervous system - Voluntary muscle movement and processes sensory information Autonomic nervous system: They are involuntary and their purpose is to maintain homeostasis. Sympathetic - increase HR, pupils dilate, redirects blood flow from digestion sites to muscles. Parasympathetic - Promotes digestion, decreases HR, pupils constrict stc. Reflexes- what do they represent and why do we test them? Reflexes are rapid involuntary movements in response to sensory stimuli that help protect the body. They are able to test the central nervous system. outsideBrain Spine How do PNS (peripheral nervous system) neurons sustain injury? 1. Physical Injury: Like getting hit hard, cut, or squeezed too much. 2. Compression: When nerves get squished for too long, like in carpal tunnel syndrome when the wrist puts pressure on a nerve. 3. Stretching Too Far: Sometimes nerves can get pulled too much, like in accidents or sports injuries, which can damage them. 4. Chemicals: Exposure to harmful substances like certain drugs or toxins can hurt nerves. 5. Inflammation and Immune Reactions: Conditions where the body's immune system mistakenly attacks the nerves can cause damage.  attacking toproblems Multiple sclerosis (MS) autoimmune leading neuro 1. Pathophysiology: ownmyelin slow MS is an autoimmune disorder characterized by inflammation, demyelination, and neurodegeneration within the central nervous system (CNS), particularly the brain and spinal cord. In MS, the immune system mistakenly attacks the myelin sheath, the protective covering of nerve fibers, leading to demyelination. Demyelination disrupts nerve conduction, slows down or blocks nerve signals, and causes a variety of neurological symptoms. 2. Clinical Manifestations: Fatigue, weakness, numbness or tingling, visual disturbances (such as optic neuritis, nystygmus), balance and coordination problems, muscle stiffness or spasms, bladder and bowel dysfunction, cognitive impairment, and mood disturbances. MS can manifest as relapsing-remitting episodes of neurological symptoms followed by periods of partial or complete recovery, or as a progressive accumulation of disability without distinct relapses and remissions (progressive forms of MS). 3. Diagnosis: Criteria for diagnosing MS include evidence of dissemination of lesions in space (lesions located in different areas of the CNS) and time (new lesions or clinical relapses occurring at different time points). Diagnostic tests commonly used in the evaluation of MS include magnetic resonance imaging (MRI) of the brain and spinal cord, cerebrospinal fluid (CSF) analysis for IgG, and evoked potential tests (to evaluate nerve conduction). 4. Treatment: The goals of treatment for MS are to reduce the frequency and severity of relapses, slow disease progression, manage symptoms, and improve quality of life. NO CURE ONLY DRUGS THAT HELP TH SYMPTOMS Symptomatic treatments may be prescribed to manage specific symptoms such as fatigue, spasticity, pain, bladder dysfunction, and cognitive impairment. Rehabilitation strategies, including physical therapy, occupational therapy, speech therapy, and cognitive rehabilitation, play a crucial role in maximizing functional abilities and independence in individuals with MS. Parkinson disease 1. Pathophysiology: Neurodegenerative disorder characterized by the loss of dopamine-producing neurons in the BASAL GANGLIA, a region of the brain involved in movement control. The exact cause of Parkinson's disease is not fully understood, but it is believed to involve a combination of genetic predisposition, environmental factors, and aging-related changes. The loss of dopamine-producing neurons leads to imbalanced neurotransmission within the basal ganglia, a group of brain structures involved in motor control. Reduced dopamine levels result in impaired regulation of movement, leading to the characteristic motor symptoms of Parkinson's disease, such as bradykinesia (slowness of movement), rigidity (muscle stiffness), resting tremor, and postural instability. 2. Clinical Manifestations: Parkinson's disease is characterized by both motor and non-motor symptoms that can vary in severity and progression.  Motor symptoms include bradykinesia (slowness of movement), rigidity (muscle stiffness), resting tremor (typically seen in the hands), and postural instability (difficulty maintaining balance and coordination). Non-motor symptoms may include cognitive impairment, mood disturbances (such as depression or anxiety), sleep disturbances, autonomic dysfunction (such as constipation or orthostatic hypotension), and sensory symptoms (such as loss of sense of smell). Parkinson's disease is often described as a "movement disorder," but the non-motor symptoms can have a significant impact on quality of life and overall functioning. 3. Diagnosis: Diagnosis of Parkinson's disease is primarily based on clinical evaluation and assessment of characteristic motor symptoms. There are no specific diagnostic tests for Parkinson's disease, but neuroimaging studies such as MRI or DaTscan (a type of nuclear medicine imaging) may be used to support the diagnosis and rule out other conditions that mimic Parkinsonism. The diagnosis of Parkinson's disease is often made by a neurologist or movement disorder specialist based on the presence of specific motor symptoms, their progression over time, and the exclusion of other possible causes. 4. Treatment: Treatment of Parkinson's disease aims to alleviate symptoms, improve quality of life, and slow disease progression. Medications used in the management of Parkinson's disease include levodopa (a precursor of dopamine), dopamine agonists, MAO-B inhibitors, COMT inhibitors, and anticholinergic agents. Deep brain stimulation (DBS) surgery may be considered for individuals with advanced Parkinson's disease who experience motor fluctuations or medication-resistant symptoms. Physical therapy, occupational therapy, and speech therapy can help improve mobility, functional abilities, and communication skills in individuals with Parkinson's disease. STILL NO CUREEE  Ch 13: Altered Hormonal and Metabolic Regulation What do hormones do? How do they know what to do? Travel through bloodstream and bind to receptors on cells or organs for specific effects monetary to maintain homeostasis Know the hormones that we talked about in class, like ADH, ACTH, epinephrine & norepinephrine, glucocorticoids, insulin, thyroid hormones 1. ADH (Antidiuretic Hormone): Produced by the hypothalamus and released by the posterior pituitary gland. Regulates water balance by promoting water reabsorption in the kidneys, reducing urine volume, and increasing blood volume and blood pressure. 2. ACTH (Adrenocorticotropic Hormone): CRH Produced by the anterior pituitary gland. Stimulates the adrenal glands to release glucocorticoid hormones, primarily cortisol, in response to stress or low blood glucose levels. ACH 3. Epinephrine and Norepinephrine: Produced by the adrenal medulla (inner portion of the adrenal glands) and also by nerve endings. Known as "fight or flight" hormones, they are released in response to stress and prepare the body for immediate action by increasing heart rate, blood pressure, and energy availability. 4. Glucocorticoids (e.g., Cortisol): Produced by the adrenal cortex (outer portion of the adrenal glands). Regulate metabolism, immune function, and stress response. They increase blood glucose levels, suppress inflammation, and modulate the body's response to stress. 5. Insulin: Produced by the beta cells of the pancreas. Regulates blood glucose levels by promoting glucose uptake into cells, where it is used for energy production or stored as glycogen. Insulin also inhibits gluconeogenesis (production of glucose from non-carbohydrate sources) in the liver. 6. Thyroid Hormones (T3 and T4): Produced by the thyroid gland. Regulate metabolism, growth, and development by influencing cellular energy production and protein synthesis. Thyroid hormones increase basal metabolic rate, heat production, and oxygen consumption in cells. Hypothalm pituitary Hypothalamus-pituitary axis : controls the synthesis and secretion of many hormones. The hypothalamus produces and releases releasing hormone & inhibiting hormones (somatostatin & dopamine) When the pituitary senses the release of hormones from the hypothalamus, it releases stimulating hormones that target the specific organ to do things. Negative Feedback: When it is too hot, it shuts down to become cooler. (bring it back to homeostasis) Positive feedback: Increases the production of hormones until the business is done. Receptors and cell-cell communication Direct Communication: Some cells are in direct physical contact with each other, allowing molecules to move directly from one cell to another through specialized structures like gap junctions or plasmodesmata. Paracrine Signaling: In this type of signaling, cells release signaling molecules (paracrine factors) into the extracellular fluid, where they diffuse locally to nearby cells and influence their behavior. Endocrine Signaling: Endocrine signaling involves the release of hormones into the bloodstream by endocrine glands. These hormones travel through the bloodstream to target cells in distant parts of the body, where they bind to receptors and initiate cellular responses. Autocrine Signaling: In autocrine signaling, cells release signaling molecules that bind to receptors on their own surface, affecting their own behavior or that of nearby cells of the same type. Synaptic Signaling: Synaptic signaling occurs in the nervous system, where neurotransmitters are released from the synaptic terminals of neurons. These neurotransmitters diffuse across the synaptic cleft and bind to receptors on the membrane of the target cell (usually another neuron, muscle cell, or gland cell) to transmit a signal. Neurologic and hormonal responses to stress Neurological - Increases brain activity in response to stress. And it activates the Autonomic nervous system in response to stress. So increase BP, blood flow to heart and brain, pupil dilate, etc. Hormonal - Stress triggers the release of CRH from the hypothalamus> stimulates the release of ACTH> adrenal gland secrete cortisol. (cortisol increases metabolism, regulates blood glucose for energy, acts as a potent anti-inflammatory) Catecholamines (dopamine, epinephrine, norepinephrine) which increase alertness, BP, HR, etc. General adaptation syndrome 1. Alarm Stage: When you encounter a stressor, your body goes into high alert. Your brain signals your adrenal glands to release hormones like adrenaline and cortisol, which prepare your body to deal with the stress. This stage is like sounding the alarm in response to a threat. 2. Resistance Stage: If the stress continues over time, your body tries to adapt to it. Your hormone levels may remain high as your body works to cope with the ongoing stress. You might feel like you're managing okay, but your body is still under strain. 3. Exhaustion Stage: If the stress persists for too long, your body's resources become depleted. Your hormone levels may drop, and you may start to feel exhausted and overwhelmed. This stage can lead to physical and mental health problems if the stress isn't relieved. Alterations in hormonal function- Damaged endocrine organ, excessive hormone production, impaired receptor binding, damaged feedback mechanisms. How is damage sustained? And how would you expect systems to be altered after damage?  BPby syndrome of inappropriate antidiuretic hormone secretion (SIADH) Vasopressor Water 1. Pathophysiology: Retaining SIADH is a disorder characterized by the excessive release of antidiuretic hormone (ADH) from the pituitary gland or non-pituitary sources, leading to water retention and dilutional hyponatremia (low sodium levels in the blood). (increase permeability in nephron) ADH causes the kidneys to retain water, resulting in increased water reabsorption and decreased urine output. Too mush 2. Clinical Manifestations: HYPOTONIC HYPONATREMIA, decreased and concentrated urine output (high levels of wanna sodium & urea in urine) Symptoms may include nausea, vomiting, headache, lethargy, confusion, muscle weakness, loodDiluted seizures, and in severe cases, coma , gait. Physical examination findings may include signs of volume overload such as edema, ascites, or so Hypo Nat jugular venous distension. stuff Concentrated 3. Diagnosis: - Hypotonicity (plasma osmolality less than 280 mOsm/kg) - Hyponatremia (serum sodium less than 135 mEq/L) - Decreased urine output - Highly concentrated urine with high sodium content - No renal , adrenal, thyroid abnormalities 4. Treatment: Treatment of SIADH aims to correct hyponatremia, restore fluid balance, and address the underlying cause. Management strategies may include fluid restriction to limit water intake, administration of 0 hypertonic/isotonic saline solution to raise serum sodium levels, and pharmacological interventions such as vasopressin receptor antagonists (e.g., conivaptan, tolvaptan) to block the effects of ADH.  In cases where SIADH is caused by an underlying condition such as a tumor or malignancy, treatment may involve addressing the primary pathology through surgery, radiation therapy, or chemotherapy. Diabetes Nothingtodo w diabetes insipidus (DI) 1. Pathophysiology: Diabetes insipidus (DI) is a disorder characterized by insufficient production or action of antidiuretic hormone (ADH), also known as vasopressin, resulting in excessive urination and thirst. amount DI can be classified into central DI (CDI), caused by a deficiency of ADH secretion from the hypothalamus or posterior pituitary gland, and nephrogenic DI (NDI), caused by kidney resistance large Urine to the effects of ADH. diluted of In CDI, the lack of ADH leads to the inability of the kidneys to reabsorb water properly, resulting in the excretion of large volumes of dilute urine. In NDI, although ADH is produced and released normally, the kidneys fail to respond to its effects, leading to the excretion of large volumes of dilute urine despite elevated levels of ADH. 2. Clinical Manifestations: The hallmark symptom of DI is polyuria, characterized by the production of large volumes of urine (exceeding 3 liters per day in adults). Hyponatremia Polyuria can lead to polydipsia body attempts to compensate for fluid loss. df.ee nocturia (frequent urination at night), dehydration, hypernatremia (high blood sodium levels), and ratB watfgood in symptoms of electrolyte imbalance such as weakness, fatigue, and confusion. 3. Diagnosis: Diagnosis of DI involves clinical evaluation, laboratory tests, and specialized diagnostic studies. Laboratory tests may include measurement of serum and urine osmolality, serum sodium levels, and urine specific gravity. A water deprivation test may be performed to assess the kidney's response to dehydration and ADH levels. Additional tests such as magnetic resonance imaging (MRI) of the brain or genetic testing may be indicated to determine the underlying cause of DI, particularly in cases of suspected central DI. 4. Treatment: Treatment of DI aims to replace or augment ADH levels and manage symptoms to prevent dehydration and electrolyte imbalances. Central DI is typically treated with synthetic ADH analogs such as desmopressin (DDAVP) administered orally, intranasally, or intravenously to replace deficient ADH levels. Nephrogenic DI may require a combination of dietary modifications (such as low-sodium diet), thiazide diuretics (which enhance water reabsorption in the kidneys), and supportive measures to manage symptoms and prevent dehydration. Hyperthyroid (graves disease) 1. Pathophysiology: Hyperthyroidism is a condition characterized by excessive production and secretion of thyroid hormones (triiodothyronine - T3 and thyroxine - T4) by the thyroid gland. autoimmune disorder in which autoantibodies IgG stimulate the thyroid gland to produce more hormones. Other causes include toxic multinodular goiter, toxic adenoma (a single overactive nodule), and thyroiditis (inflammation of the thyroid gland).  Excess thyroid hormone leads to a hypermetabolic state, affecting multiple organ systems and increasing the body's overall metabolic rate. 2. Clinical Manifestations: Common symptoms include weight loss despite increased appetite, heat intolerance, sweating, palpitations, tremors, anxiety, irritability, insomnia, fatigue, muscle weakness, and frequent bowel movements. Physical examination findings may include an enlarged thyroid gland (goiter), fine tremor of the hands, warm and moist skin, hair thinning or loss, and signs of thyroid eye disease (e.g., proptosis, eyelid retraction, or diplopia). 3. Diagnosis: Laboratory levels (T3, T4) and thyroid-stimulating hormone (TSH) levels. In hyperthyroidism, T3 and T4 levels are elevated, while TSH levels are low or undetectable. Additional tests such as thyroid ultrasound, radioactive iodine uptake (RAIU) scan, or thyroid scintigraphy may be performed to evaluate thyroid gland structure and function and to differentiate between different causes of hyperthyroidism. 4. Treatment: Options may include antithyroid medications (such as methimazole or propylthiouracil) to inhibit thyroid hormone synthesis, radioactive iodine therapy to destroy overactive thyroid tissue, or thyroidectomy (surgical removal of part or all of the thyroid gland). Beta-blockers may be used to manage symptoms such as palpitations, tremors, and anxiety. Management of Graves' disease may also involve immunosuppressive therapy or thyroid eye disease management for individuals with ocular manifestations Hypothyroid 1. Pathophysiology: Hypothyroidism is a condition characterized by insufficient production and secretion of thyroid hormones ( T3 & T4) by the thyroid gland. Hashimoto's thyroiditis, an autoimmune disorder in which the immune system attacks and damages the thyroid gland, leading to decreased hormone production. Other causes include thyroidectomy (surgical removal of the thyroid gland), radioactive iodine therapy, iodine deficiency, medications (such as lithium or amiodarone), or pituitary dysfunction affecting thyroid-stimulating hormone (TSH) secretion. Insufficient thyroid hormone levels lead to a hypometabolic state, affecting various organ systems and slowing down the body's overall metabolic rate. 2. Clinical Manifestations: Common symptoms include fatigue, weight gain, cold intolerance, constipation, dry skin, hair loss, brittle nails, hoarseness, muscle weakness, joint pain, menstrual irregularities, and depression. bradycardia, delayed relaxation phase of deep tendon reflexes, cool and dry skin, facial puffiness, and a firm or  enlarged thyroid gland (it enlarges and tries to increase function). MYXEDEMA - protein and carbs accumulate in the extracellular matrix drawing water into tissues, skin turns coursed, hard, and non pitting. 3. Diagnosis: Laboratory tests typically include measurement of serum thyroid hormone levels (T3, T4) and thyroid-stimulating hormone (TSH) levels.T3 and T4 levels are low, while TSH levels are elevated as the body attempts to stimulate thyroid hormone production. Additional tests such as thyroid ultrasound or thyroid antibody testing may be performed to evaluate thyroid gland structure and to confirm autoimmune thyroid disease. 4. Treatment: Treatment of hypothyroidism aims to restore thyroid hormone levels to normal and alleviate symptoms. The mainstay of treatment is thyroid hormone replacement therapy with synthetic thyroid hormone medications, such as levothyroxine (T4) , lifelong. Regular monitoring of thyroid function tests is essential to adjust medication dosage as needed and to ensure optimal thyroid hormone levels. Cushing syndrome 1. Cushing syndrome results from prolonged exposure to high levels of cortisol, a hormone produced by the adrenal glands. There are several causes, including: Adrenal gland overproduction: The most common cause is excessive cortisol production by the adrenal glands, often due to tumors such as adrenal adenomas or carcinomas. Pituitary adenoma: pituitary adenoma (Cushing disease) that stimulates the adrenal glands to produce excessive cortisol. Ectopic ACTH production: In rare cases, tumors outside the pituitary gland (ectopic tumors) can produce adrenocorticotropic hormone (ACTH), which stimulates the adrenal glands to produce cortisol excessively. 2. Clinical Manifestations: Weight gain: Particularly in the trunk, face ("moon face"), and between the shoulders (buffalo hump). Muscle weakness: Especially in the proximal muscles of the arms and legs. Skin changes: Thin, fragile skin prone to bruising, stretch marks (striae), and acne. Hyperglycemia: Increased blood glucose levels due to cortisol's effects on glucose metabolism. Hypertension Osteoporosis: Weakening of the bones, increasing the risk of fractures. Menstrual irregularities: In females, menstrual cycles may become irregular or stop altogether. 3. Diagnosis: Laboratory tests: Measurement of cortisol levels in urine, blood, or saliva, typically done over a 24-hour period to assess cortisol production. Dexamethasone suppression test: In this test, the patient takes a synthetic glucocorticoid (dexamethasone) to suppress cortisol production. Failure to suppress cortisol secretion suggests Cushing syndrome. Imaging studies: MRI or CT scans may be used to visualize abnormalities in the pituitary gland or adrenal glands. 4. Treatment: Surgical removal: If the cause is an adrenal tumor or pituitary adenoma, surgical removal may be necessary.  Medication: In cases where surgery is not possible or effective, medications such as ketoconazole, metyrapone, or mifepristone may be used to block cortisol production or its effects. Radiation therapy: This may be an option for pituitary tumors that cannot be surgically removed. Lifestyle modifications: Managing weight, controlling blood glucose levels, and reducing stress can help manage symptoms. Addison disease Pathophysiology: AUTOIMMUNE The ACTH can be elevated as a compensatory mechanism when there is low cortisol & aldosterone. 1. Addison's disease, also known as primary adrenal insufficiency, is characterized by the inadequate production of cortisol and aldosterone due to damage to the adrenal glands. Without sufficient cortisol, the body's ability to respond to stress, regulate metabolism, and maintain blood pressure is impaired. Additionally, the lack of aldosterone leads to electrolyte imbalances, particularly low sodium (hyponatremia) and high potassium (hyperkalemia). 2. Clinical Manifestations: Fatigue and weakness: Due to decreased cortisol levels, individuals may experience chronic fatigue and muscle weakness. Weight loss and decreased appetite: Loss of appetite and unintentional weight loss are common symptoms. Hyperpigmentation: In some cases of autoimmune adrenalitis, increased production of adrenocorticotropic hormone (ACTH) can lead to hyperpigmentation of the skin, particularly in sun-exposed areas, gums, and scars. Hypotension: Low blood pressure, especially upon standing (orthostatic hypotension), can occur due to insufficient aldosterone production. Salt craving: Due to low sodium levels (hyponatremia) resulting from aldosterone deficiency, individuals may crave salty foods. Nausea, vomiting, and abdominal pain: These symptoms may occur due to electrolyte imbalances and gastrointestinal disturbances. Hypoglycemia: Decreased cortisol levels can lead to low blood sugar levels. Dizziness or fainting: Resulting from orthostatic hypotension. 3. Diagnosis: Blood tests: Measurement of cortisol and aldosterone levels in the blood. Low levels of cortisol and aldosterone support the diagnosis of Addison's disease. ACTH stimulation test: This test measures the adrenal gland's ability to respond to ACTH stimulation. In Addison's disease, the adrenal glands typically do not produce an adequate cortisol response. Electrolyte tests: Monitoring sodium, potassium, and other electrolyte levels can help detect imbalances associated with adrenal insufficiency. Imaging: CT scans of the abdomen may be performed to assess the size and condition of the adrenal glands. 4. Treatment: Hormone replacement therapy: Lifetime replacement of cortisol and aldosterone is necessary to manage Addison's disease. This typically involves daily oral corticosteroid medications, such as hydrocortisone or prednisone, to replace cortisol, and mineralocorticoid medications, such as fludrocortisone, to replace aldosterone. Stress management: During periods of illness, injury, or surgery, individuals with Addison's disease may require additional doses of corticosteroids to help the body cope with stress. Dietary sodium supplementation: Some individuals may need to increase their sodium intake to help manage low blood pressure and sodium levels. Regular medical monitoring: Close monitoring of symptoms, blood pressure, electrolyte levels, and hormone replacement dosages is essential to ensure optimal management of Addison's disease. sina.ii.ie ii foe momentted