KJN_Clinpharm-PrelimMiterm.pdf

KHRISHA C. EPISTOLA Respiratory infection – viral respiratory infection - nfluenza virus CLINICAL PHARMACY 2...

KHRISHA C. EPISTOLA Respiratory infection – viral respiratory infection - nfluenza virus CLINICAL PHARMACY 2 can exacerbate or worsen AR symptoms AR : sinisipon lang GERD RESPIRATORY DISEASES Irritant exposure – exposed in cleaning chemicals and fumes Allergic rhinitis 4. Genetic predisposition families have AR, you will be susceptible to allergic Hay fever (commonly known) rhinitis Inflammatory disorder of the nasal mucosa 5. Stress / emotional factors Inhaled substances that cause allergic rhinitis (allergens) may not cause allergic rhinitis “Rhino” nose not considered the main cause to AR because not exposed to allergen HOW DOES IT WORK? umiiyak ka – sinisipon animal dander (dumi ng hayop) 6. Hormonal Changes cause immune response during pregnancy or menstruation once exposed or sensitization to allergen 7. Food allergies 8. Age and developmental factors antigen presenting cells found in nasal mucosa, present n T-cells / TH2 cells (activate the release of cytokines early exposure – autacoids (IL4, IL3) infants body ay masasanay na may allergic rhinitis if cytokines are released it ill produce immunoglobulin E (specific to allergen) CLINICAL MANIFESTATION IGE will circulate in the blood streams and to the surface 1. Sneezing of mast cells and basophils, specifically found in nasal hahatching lang pag na-exposed mucosa repetitive dapat if may Allergic rhinitis mast cells and basophils 2. Rhinorrhea / runny nose will now release inflammatory mediators (causes excessive production of liquid nasal discharge inflammation) such as histamine and leukotrienes clear and watery na sipon once histamine and leukotrienes are released, cause 3. Nasal congestion vasodilation, increase vascular permeability causing swelling of nasal tissue inflammation increase mucus production Increased in blood flow kay inflamed barado na ilong dinadilate yung ugat para maincrease yung blood flow 4. Itchy nose it will lead to the symptoms of allergic rhinitis itching inside the nose Histamine – vasodilation (tutulo ung sipon) TH2- 5. Watery or itchy eyes cytokines – IGE – BASOPHILS / MAST CELLS – referred to as allergic conjunctivitis inflammatory mediators – inflammation – allergic rhinitis tear duct in a vessel (caused by pollen or allergens si allergic rhinitis lahat ng vessel ay nag-oopen if open ang tear duct may tears na lumalabas PATHOPHYSIOLOGY unconsciously because dilated Allergic rhinitis is an IgE-mediated inflammatory response 6. Sore throat triggered by allergens such as pollen, dust mites, animal -post nasal drip is common in Allergic rhinitis dander, or mold. -scratchy throat 7. Coughing Allergens bind to IgE on mast cells and basophils, leading 8. fatigue to the release of inflammatory mediators (e.g., histamine). chronic symptoms causes daytime sleepiness This causes nasal mucosal inflammation, resulting in hindi makatulog , tired body symptoms like sneezing, rhinorrhea, nasal obstruction, 9. Impaired sense of smell and itching. nasal congestion is the cause 10. Ear symptoms POTENTIATING FACTORS feeling mo barado yung ear 1. Environment Factor 11. facial pressure pollen levels (common sa tagsibol usually in mangoes) can cause headache pollen can cause inflammation in nasal mucosa 12. Exacerbation of Asthma Air Pollution if may asthma and exposed sa allergens it will lead to air pollutants allergic rhinitis and mawoworsen yung asthma Mold spores and dust mites allergen found 2. Lifestyle factors DIAGNOSTIC AND LABORATORY TEST Smoking – exposure to smoke can increase AR or can 1. skin prick test worsen its symptoms identify specific allergens triggered in the body Occupational exposure – if gardener, farmer, or -allergens pollen dust construction worker 2. Blood test 3. Medical factors -IGE blood test  -IGE an allergen Identify the allergen 3. CBC (Complete count blood) Eosinophils and basophils in the blood if elevated and WBC / RBC exposed to allergen 4. Nasal smear cytology Dobe to assess the presence of inflammatory mediators smear in nasal mucosa 5. Nasal endoscopy Papasok yung camera sa nasal mucosa/ nasal passage 6. Allergen challenge testing patient exposing to environment to identify the allergen in chronic allergic rhinitis THERAPEUTICS OUTCOME 1. Symptoms relief 2. Improve quality of life 3. prevention of complications 4. Functional improvement 5. Enhance sleep 6. Patient education and empowerment 7. prevention of allergic symptoms TREATMENT AND MANAGEMENT 1. Allergic Rhinitis Antihistamines - block the effect of histamine and relieve the symptoms Nasal corticosteroids to lower inflammation in the nasal passages Decongestant - alleviate nasal congestion MANAGEMENT 1. Allergen avoidants - minimise the exposure immunotherapy - allergy shot  Asthma 9. Hormonal changes Not curable, only treatable 10. Food allergies Treat the symptoms of asthma 11. Poor air quality in indoor environments Chronic inflammatory disorder CLINICAL MANIFESTATIONS Chronic means long term 1. Wheezing Disorder of the airways characterized by reversible airflow obstruction, bronchial hyperresponsiveness, and high pitch whistling sound heard during expiration or exhalation (“agberberber”) respiratory symptoms due to narrowing of airways PATHOPHYSIOLOGY 2. Coughing 1. Airway Inflammation persistent coughing or recurrent (tuloy-tuloy at hindi Chronic inflammation in the airways nawawalang ubo) Inflammation due to immune cells such as eosinophils 3. Shortness of breath (Dyspnea) and other mediators occur during physical activity Exposure to allergens causing airway inflammation stress or exercise Specific IgE antibody will be release and bind to mast 4. Chest tightness cells and basophils found in the airway passage that will 5. Increased in respiratory rate lead to inflammation rapid breathing Passageway of air, results to obstructed breathing body tries to compensate decreased outflow Histamine results to bronchoconstriction (constriction of 6. Fatigue bronchial vessels or passageway of air) mabilis na paghinga kaya napapagod The air will be blocked hence the patient will 7. Night-time symptoms 8. Peak Expiratory Flow (PEF) have shortness of breath 2. Bronchial Hyperresponsiveness (BHR) measures the maximum speed which air are inhaled Excessive response of bronchial obstruction due to non- ↓PEF, Exacerbate asthma symptoms specific environment such as cold environment, exercise, 9. Mucous production irritants, etc. Leading to phlegm or mucus production (Sticky kaya IgE cannot be activated hindi makalabas) Not allergen-specific triggers Nebulizer 3. Airway Remodelling LABORATORY AND DIAGNOSTIC TESTS Due to chronic exposure leading to inflammation 1. Spirometry Can cause subepithelial fibrosis Can cause smooth muscle hypertrophy test that assess lung function Change in blood vessel structures Measure the amount and speed of air that can be inhaled and exhaled POTENTIATING FACTORS patient breathes in and inhales it to spirometer and measures by FVC (Forced vital capacity) and FEV (forced 1. Allergens expiratory volume in 1 second) can exacerbate or alleviate asthma symptoms it includes dander, dust mites, and pollens ↓FVC/FEV, Indication of airway obstruction so patient may have asthma 2. Respiratory infections for example common colds and influenza PEF is reduced, it is severe because of obstructed airway 3. Irritant and environmental factors 2. Bronchoprovocation Test (BPV Test) 4. Exercise and physical activities can exacerbate asthma methacholine challenge or exercise challenge during or after exercise induce the bronchoconstriction to assess the hyperresponsiveness of bronchial vessels Excessive exercise 3. Fractional exhaled nitric oxide (FeNO) measurement For asthma management they must do regular exercise It indicates airway inflammation if the result is high only 5. Weather changes it help to assess the use eosinophilic inflammation in the airway Bronchial hyperresponsiveness 4. Allergy Testing 6. GERD It include skin prick testing and IgE blood test to identify can worsen asthma symptoms the specific allergen that triggers asthma 7. Medications 5. Chest X-Ray non-steroidal anti-inflammatory drugs, beta CT scan blockers, and antihypertensive agents can cause or trigger asthma symptoms recommended because sometimes asthma is not the cause, but the disease or the symptoms is due to other Dextromethorphan (MOA: Bronchoconstriction) bronco diseases Hypertensive medications ( vessels are constricted) 6. Arterial Blood Gas (ABG) Analysis Neozep® and Bioflu® (Constricts) measures the level of oxygen and carbon dioxide in the 8. Emotional factors blood stress can cause bronchial hyperresponsiveness if the oxygen is low the patient will have a hard time patients are required to undergo stress management breathing 7. CBC if the inflammatory mediators are elevated in the body that causes asthma THERAPEUTIC OUTCOMES (same as AR) 1. Improved lung function Stable PEF and FEV Prevention of progressive decline in lung function over time TREATMENT 1. Long Term control medications A. Inhaled corticosteroids Reduce inflammation in the nasal passages Fluticasone, budesonide, beclomethasone B. Long Acting Beta Agonists (LABA) Relax muscle around the airways make it easier to breath LABA + ICS — salbutamol and formoterol C. Leukotrienes Modifiers Blocks the action of certain chemicals such as inflammatory mediators that contributes to inflammation and bronchoconstriction montelukast 2. Short acting and control medications A. Short acting beta agonists (SABA) Quick relief from acute asthma symptoms by relaxing the muscles in the airways LABA: chromic SABA: acute 3. Combination Inhalers In a single inhalers (SABA + CABA) 4. Biologics - Parentals for severe asthma attacks that cannot be controlled by medications COPD (chronic obstructive pulmonary disease) 9. Malnutrition No cure, only treated Impact several health Diagnose pt with COPD dies with COPD 10. Physical Inactivity A progressive disease (may levels) Lack of exercise affecting respiratory function Irreversible respiratory condition Sedentary lifestyle Characterised by persistent airflow limitation CLINICAL MANIFESTATIONS PATHOPHYSIOLOGY 1. Chronic Cough Obstructive A persistent and chronic cough is a early symptom of 1. Chronic Bronchitis COPD Inflammation of bronchial vessels or tubes due to Long-term cough exposure to irritants such as smoke leads to long-term Produces sputum or mucus inflammation 2. Characterized by increased mucus production in the airways If it swells to level 1, it won’t return to its original state 3. Shortness of breath Cause excessive mucus production 4. Wheezing Asthma: increased mucus production 5. Chest tightness 6. Limited exercise tolerance Because there's a lot of phlegm,the patient will have 7. Frequent respiratory infection more difficulty breathing, so oxygen is given, unlike in asthma where only a nebulizer is used Such as bronchitis and pneumonia 2. Emphysema 8. Barrel Chest 9. Fatigue Destruction of alveoli in the lungs 10. Weight loss Changes in gas exchange, results to enlarged surface 11. Morning headaches Lose its elasticity – leads to elastic fibers in the lung tissue Caused by hypoxemia (low oxygen level) - lungs will not able to recoil 12. Cyanosis Limitation in the airflow Bluish color in lips, nails, due to low oxygen levels - narrowing the airways, cause obstruction of airflow, hypersecretion of mucous due to loss of LABORATORY AND DIAGNOSIS elasticity 1. Spirometry - Loss of elasticity (Hyperinflation of lungs) Measures FEV and FVC - Air Trapping within the lungs - The lungs will expand FVC/FEV results to obstructed airways - The lungs expanded (Barrel Chest Syndrome) 2. PIK - Emphysema due to inflammatory response due to 3. Post-bronchodilator testing 4. Chest X-ray release of proteases, due to cigarette smoke 5. ABG analysis Proteases - inflammatory mediator 6. CBC - breaks down connective tissue causes emphysema - COPD can cause PULMONARY HTN Used to check the levels of inflammatory mediators - as it narrows pulmonary blood vessels Inflammatory Mediators - It can’t just be CB, there should also be RBC Counts emphysema If RBC is high – chronic hypoxia in COPD RBC - carries the oxygen POTENTIATING FACTURE 7. Alpha-1 Antitrypsin Testing 1. Smoking Test alpha-1 deficiency which indicates patients having Passive or active smoking COPD Mostly males are COPD patient Recommended for patients with history of COPD Second hand smoker can have COPD or Manifest 8. Chest CT-Scan 2. Environmental / Occupational Exposure Visualize the lung structure and identify emphysematous 3. Air Pollution changes 4. Generic Factor 9. ECG (Electrocardiogram) Alpha-1 antitrypsin deficiency can predispose an Assess electrical activity of the heart if it has right sided individual to manifest COPD heart strain or pulmonary HTN Balances enzymes in the lungs 5. Respiratory Infection THERAPEUTIC OUTCOME Can contribute to progression of COPD 1. Improve lung function 6. Aging 2. Prevent disease progression Basically aging can cause changes in lung function Slow the progression of COPD mostly if the lifestyle is not healthy 3. Reduce exacerbation 7. Socio-Economic Factors 4. Reduce Hospitalization Individuals may exposed to environmental factors 5. Maintain optimal oxygenation 8. Comorbidities Oxygen tanks are used CVD 6. Smoking cessation Diabetes Improve quality of life to achieve optimum health of HTN patient 7. Enhance or Improve Quality of life TREATMENT 1. Antihistamines Cetirizine Loratadine Block the effects of histamine which are inflammation 2. Nasal Corticosteroids Reduce inflammation in the nasal passages 3. Decongestants Alleviate nasal congestion MANAGEMENT 1. Allergen avoidance Infinite exposure to allergens 2. Immunotherapy Allergy shots which are patients who have persistent symptoms TREATMENT 1. Bronchodilators Short-acting beta agonists Long-acting beta agonists 2. Inhaled Corticosteroids 3. Combination inhalers 4. Phosphodiesterase 4 inhibitor Ex. roflumilast Inhibit PDEA MANAGEMENT 1. Oxygen Therapy Supplemental oxygen for patients with low oxygen The alveoli is destroyed so the level of oxygen is low 2. Pulmonary rehabilitation Exercise training They try to restore the function of lungs 3. Vaccination Annual vaccination Flu and Pneumonia Vaccines 4. Lifestyle Modifications Avoid exposure to environmental factors 5. Nutritional support Maintain a healthy diet 6. Medication adjustment and monitoring 7. End-of-life Planning Discuss with the patient's family GASTOINTESTINAL DISEASE inflamed mucosal damage leads to imbalance fluids that leads to diarrhea Diarrhea 6. Neuro endocrine factors Diarrhoea, as a symptom, can be due to many causes “ enteric nervous system” and conditions. A definition of diarrhoea is the abnormal Disruption of enteric nervous system can cause changes passing of loose or liquid stools, with increased in GI motility ( increase motility in GIT, increase frequency and/or increased volume. Increased frequency absorption of fluid which can cause intolerance of fluid is defined as the presence of three or more abnormally and lead to diarrhea) loose or watery stools in the preceding 24 hours Similar to constipation, diarrhea is an abnormality in the FACTOR regular functioning of the intestines. Diarrhea symptoms 1. Infection include increased stool frequency or bulk. In cases of Bacteria acute diarrhoea, symptoms such as anorexia, nausea, Viral vomiting, abdominal pain, flatulence, or bloating may Parasitic in GI tract occur with loose or watery stools. → anything ingested in GI tract can cause infection 2. Diarrhea factor PATHOPHYSIOLOGY Consuming food high in fat, fibers can cause diarrhea 1. Increased fluid secretion caffeine/alcohol which can worsen diarrhea Increase fluid secretion in the small intestine due to 3. Medications toxins/irritants found in the GI tract that causes Medications with side effects like diarrhea (antibiotics) increased absorption of fluid from ingested foods. 2. Impaired absorption Medications with effects like pampatae (laxatives: bisacodyl), antacids containing magnesium, Decrease absorption of fluids and electrolytes in the chemotherapeutic drugs intestine due to damage intestinal lining 4. Underlying conditions Abnormal balance of fluid /electrolytes Inflammatory bowel disease Conditions: Irritable bowel syndrome - Celiac: A flare-up of celiac disease can cause Crohn's disease digestive symptoms, including diarrhea and bloating Lactose intolerance - Inflammatory Bowel disease: a term for two 5. Stress and anxiety conditions (Crohn's disease and ulcerative colitis) Physiological factor due to Nervous system (PNS & CNS that are characterised by chronic inflammation of effect) the gastrointestinal (GI) tract. Prolonged 6. Travel and changes in routine inflammation results in damage to the GI tract. “Traveller’s diarrhea” 3. Increased motility Dietary food ingested in other countries can cause Hormonal rhythmic contraction of the intestine renewing the bioflora (is a pathogen) which can cause Motility causes peristalsis diarrhea. It is safe to bring your own water at home Increase speed of motility (contraction) can cause before travelling 7. Allergies and intolerance diarrhea which can lead to watery stool Conditions: Lactose intolerance can cause diarrhea - Irritable bowel syndrome which can cause Food may cause diarrhea hypermotility and can lead to diarrhea 8. Intestinal disorders 4. Osmotic diarrhea Disorder in intestine (damage/disrupt of intestine which unabsorbed substances in intestine which prevents the can lead to diverticulitis, intestinal ischemia, radiation draws water in the intestine enteritis) Poorly absorbed carbohydrates prevents the reabsorption CLINICAL MANIFESTATION of water due to osmotic force attracts water in the gut instead of absorption it by small intestine causes watery 1. Increase frequency bowel movements stool Acute - < 4 days Conditions: Frequent - > 7 days but LT 8 days - Lactose intolerance is when your body can't break Chronic - > 8 days down or digest lactose. The lactose doesn't 2. Loose or watery stool absorbed in the small intestine and attracts water Consistency of stool / fluid along with peristalsis which causes - Normal: “buo” diarrhea - diarrhea : watery 5. Inflammation of mucosal damage 3. Abdominal cramps & pain Inflammatory process in GIT can damage mucosal lining Increase motility which can cause disrupt the normal secretory function 4. Urgency of the intestine Urgency of bowel movement Conditions & disease: 5. Bloating and gas - Crohn's diseases ( an inflammatory bowel disease Feel bloated means bloated with water that causes chronic inflammation of the GI tract, 6. Nausea & vomiting which extends from your stomach all the way down 7. Fever to your anus) / ulcerative colitis can cause One mechanism of body to fight infection 8. Dehydration (if diarrhea is chronic) Metronidazole, mebendazole - parasitic drugs Kids: pedialyte (oral rehydration) 3. Viral infections Adults: offer gatorade /pocari sweat Vaccines 9. Electrolyte imbalance Abnormalities (Decrease electrolyte can cause MANAGEMENT hyponatremia, hypokalemia which can cause metabolic 1. Treatment of underlying conditions acidosis) 2. Preventive measures - practise good hygiene 10. Weight loss 3. Monitoring & follow up conditions LABORATORY AND DIAGNOSTIC TEST THERAPEUTIC OUTCOMES 1. Stool analysis 1. Relief symptoms Evaluate to identify infectious agents, inflammatory Prevent lose watery stool markers, indication of abnormality in intestine and Abdominal cramps prevention parasites 2. Rehydration of fluid & electrolyte a. Microscopic examination - stool detection if there is a 3. Prevention of complications presence of parasites 4. Prevention of transmission b. Culture and sensitivity - culture is to identify parasite or 5. Long term management and prevention bacterial pathogen using sensitivity test 6. Improve quality of life c. Ova and parasite examination - To see the egg of a parasite 2. Stool for clostridium difficile Toxin antibiotic associated with patients with diarrhea 3. Blood test Detect abnormalities in blood which cause by infection increase infection mediators can cause inflammations Increase WBC can cause infections Increase basophils indicates inflammations 4. Serological test Enzyme-linked immunosorbent assays, indicates specific pathogens which can cause diarrhea Immunoassays are the most commonly used serological assays is Point-of-care tests (POC tests), both for antigens and antibodies. 5. Imaging studies CT scan: to detect less common causes of acute diarrhea such as inflammatory bowel disease (IBD), intestinal lymphoma, carcinoid syndrome, and other neuroendocrine tumors. 6. Endoscopic medications Visualise GIT to obtain biopsy for chronic disease 7. Breathe test (done by doctors) Bad breath indicate stomach problems (unless the patient doesn't brush/gargle 😜😜) Bacterial overgrowth in intestines Can be done to people with lactose intolerance causes bacterial overgrowth) TREATMENT AND MANAGEMENT 1. Rehydrate 2. Dietary modification BRAT diet: banana, rice, apple, toast (to harden the stool) 3. Avoiding irritants Spicy foods, caffeines, artificial sweeteners 4. Probiotics Has lactobacillus which helps restore the balance in gut MEDICATIONS 1. Antimotility agents Control movement and contraction of intestine e.g. loperamide: 2 capsules at once, 1 hr interval. max: 5 capsule a day 2. Antibiotics Infections causing diarrhea Constipation LABORATORY AND DIAGNOSTIC TEST Infrequent bowel movement 1. Blood Tests (CBC, Thyroid FT) Difficulty passing stool CBC - infection, inflammation, anemia Thyroid FT - underlying condition, constipated if PATHOPHYSIOLOGY hyperthyroidism 1. Reduce intestinal motility 2. Stool analysis Reduction to frequency in motility Infection in the body, presence of blood and abnormal Delayed passing stool in the colon/large intestine in the body A. Slow transit of constipation Ex. Stool Occult BT - Abnormalities in the colon Indicate GI bleeding B. Pelvic Dysfunction 3. Colonoscopy or flexible sigmoidoscopy - Pelvic floor dysfunction Insertion of camera in the rectum C. Neurological Disorders tumors , impactions, lesions Ex. Parkinson’s, multiple sclerosis Flexible Sigmoidoscopy 2. Inadequate Fluid and Fiber Intake - sigmoid colon and rectum - the motility is not good 4. Anorectal Manometry 3. Obstruction / Impaction Evaluate the sphincter muscle and anal muscle - the flow is not good or smooth 5. Colonic Transit Studies - Ex. tumor, impacted stool Tracking the markers 4. 4. Medications for medical conditions Transit the stool to the colon - Iron Supplement 6. Defecography - Side effect of certain medication Radiographic - Ex. Hypothyroidism, Diabetes, IBS of Hyper Evaluate rectum and pelvic floor during defecation 5. Hormonal Changes TREATMENT AND MANAGEMENT - Hyperthyroidism 1. Lifestyle Modification - Pregnant Dietary changes 6. Physiological Factor High fiber intake, food and vegetables, food that promote - ENS effects small intestine stool movement 2. Hydration POTENTIATING FACTORS Drink fluid/water soften the stool 1. Dietary Factors 3. Regular Exercise Inadequate fluid and fiber intake Walking 2. Sedentary Lifestyle 4. Establishing regular toilet habit No physical activity Slow bowel movement MEDICATIONS Modify intestinal motility Laxatives 3. Medications Relieve constipation Side effects (slows down the intestinal motility of A. Bulk-forming Laxative - forms the unabsorbed (Ex. intestine) Psyllium - Metamucil® ) 4. Psychological B. Osmotic Laxative - attracts water (Ex. Lactulose) 5. Age C. Stimulant Laxative - stimulates motility (Ex. Bisacodyl, Elderly or Adults - age related changes in motility Sennal) 6. Pregnancy D. Stool softener- softens poop 7. Ignoring the urge to defecate Prokinetic Agents Suppress the bowel movement / food / stool in - Same as stimulant laxative the intestine, causing constipation - The one that given to the patient is with chronic constipation CLINICAL MANIFESTATION MANAGEMENT 1. Infrequent bowel movement 1. Pelvic Floor Rehabilitation 2. Difficulty passing stool If the reason for constipation is dysfunction in pelvic 3. Straining during bowel movement floor 4. Abdominal discomfort or pain 2. Rectal Interventions 5. Rectal bleeding Direct 6. Abdominal bloating and gas accumulation Ex. Rectal suppositories or enema for faecal or stool 7. Rectal prolapse infection Rectum is slowly showing Ex. fleet enema - inserts fluid in the enema 8. Decrease appetite and nausea 3. Surgery 9. Fatigue and Malaise If the cause is structural abnormalities (Ex. colectomy) 10. Changes in stool consistency and appearance 4. Treatment of Underlying Conditions Diabetes, neurological condition, hyperthyroidism 5. Behavioral and Psychological Rehabilitation Therapy and counselling 6. Regular Monitoring THERAPEUTIC OUTCOMES 1. Relieve Symptoms Relief in infrequent bowel movement 2. Improve bowel function - twice a day 3. Prevention of complication Underlying condition 4. Improve quality of life GERD (Gastroesophageal reflux disease) a chronic condition in which the stomach contents move CLINICAL MANIFESTATIONS up into the esophagus. 1. Heartburn - burning sensation because of acid reflux May result in heartburn, chest pain, sore throat and radiates esophagus into the throat other symptoms 2. Dysphagia - difficulty in swallowing due to chronic mucosal injury PATHOPHYSIOLOGY 3. Regurgitation - involuntary passage of gastric content 1. Lower Esophageal Sphincter Dysfunction 4. Chest pain - due to acid reflux LES: prevents the backflow of stomach content to AKA: non-cardiac chest pain esophagus. 5. Chronic cough - often accompanied by mucus If dysfunction: The lower esophageal sphincter doesn't 6. Hoarseness/voice changes - due to impaired larynx close properly. As a result, stomach acid and contents 7. Asthma exacerbation flow backward into your esophagus. 8. Dental erosion - tooth enamel is disrupted Hiatal hernia - occurs when part of the stomach protrudes up into the chest through the sheet of muscle LABORATORY & DIAGNOSTIC TEST called the diaphragm. 1. Esophagogastroduodenoscopy - direct visualization of the Obesity - excess body weight may increase the intra- GIT/LES/esophagus using a camera abdominal pressure, decreasing the LES pressure and 2. Barium Swallow - radiographic involves ingesting a barium increasing esophageal acid exposure. agent to visualize and detect the structural abnormalities 3. Esophageal Manometry - evaluates the esophageal motility Pregnancy - pregnancy hormones cause the LES to relax, 4. Esophageal Biopsy allowing stomach acids to flow back up into your 5. Serum Markers - conditions associated with the increase of esophagus. gastrin levels leading to hypergastrinemia 2. Impaired Esophageal Clearance 6. Complete Blood Count (CBC) - signs of anemia leading to coordinated contraction of swallowed food into the chronic intestinal bleeding stomach. stomach esophageal peristalsis: increases the risk of TREATMENT AND MANAGEMENT mucosal injury. Prolong influx time disrupts the esophagus to the Management: stomach. 1. Lifestyle Modifications dysfunctional LES + impaired esophageal clearance = 2. Weight loss causes reflux 3. Esophageal Mucosal Injury Medication: Erosive esophagitis - inflammation, irritation, or swelling 1. Antacids - e.g. Kremil-S of the lining of the esophagus provides temporary relief by mild to neutralize gastric acid Chronic exposure to gastric acid causes irritation and taken after meal erosion. 2. H2 receptor Antagonist - e.g. Famotidine, Ranitidine, causes heartburn, chest pain, dysphagia Cimetidine 4. Delayed Gastric Emptying reduce gastric acid secretion AKA: gastroparesis prevents reflux slow or stop the movement of food from the stomach 3. Proton Pump Inhibitors (PPIs) - e.g. Omeprazole, Pantoprazole to small intestine most effective prolong the retention of gastric content in the stomach, causing the food to stay in the stomach for a longer Surgical Intervention: period of time 1. Fundoplication - the top part of your stomach — called the fundus — is folded and sewn around the lower POTENTIATING FACTORS esophageal sphincter 1. Hiatal hernia - inborn, during birth, since childhood, 2. Endoscopy Treatment - a healthcare provider places a congenital long, thin tube (endoscope) inside your body until it 2. Obesity - abdominal obesity reaches the organ or area they need to check. 3. Dietary factors 3. Esophageal pH Monitoring - A thin tube is passed High fat foods causes delay in gastric emptying time through your nose or mouth to your stomach. The tube Spicy/Acid food irritates the esophageal mucosa is then pulled back into your esophagus. A monitor 4. Smoking - weaken LES, impaired esophageal peristalsis attached to the tube measures the acid level (pH) in 5. Alcohol - exacerbate GERD your esophagus. Large amount of alcohol increases gastric acid secretion 4. Regular Monitoring & Follow-Up during bedtime 6. Medications THERAPEUTIC OUTCOMES Side effects: CCB relaxes smooth muscle such as LES 1. Relief of symptoms Nitrates: same as CCB and impairs esophageal motility 2. Healing of esophageal mucosa 7. Pregnancy 3. Prevent complication 8. Delayed gastric emptying 4. Reduce the risk of esophageal cancer 5. Improve quality of life 9. Stress/Anxiety - alteration in gastric secretion; requires stress management technique 10. Posture & Body position - lying down after eating Hepatitis 9. Poor nutrition - decrease immune system Is an inflammation of the liver that is caused by a variety 10. Genetic factors - variations with genes of infectious viruses. CLINICAL MANIFESTATIONS TYPES OF HEPATITIS 1. Prodromal Phase - nonspecific symptoms (e.g. fatigue, malaise, anorexia, nausea) Hepatitis A Virus 2. Abdominal discomfort - where the liver is located (upper right transmitted via fecal route quadrant of the body) transmitted through ingestion of contaminated food and 3. Jaundice - yellowish skin & eye, increase bilirubin water 4. Dark urine 5. Hepatomegaly - enlargement of liver the virus replicates into the liver then enters in the bloodstream 6. Abdominal pain 7. Fatigue targets infected hepatocytes or liver cells, causing 8. Pruritus inflammation 9. Flu-like symptoms does not establish chronic infection 10. Coagulopathy resolve without further medication Chronic Hepatitis (B & C) Hepatitis B Virus asymptomatic for years and decades transmitted through contact with infected body fluids like leads to different complications in liver blood, saliva, vaginal fluids and semen. It can also be abnormal enlargement of stomach (ascites) passed from a mother to her baby. LABORATORY & DIAGNOSTIC TEST it can also be transmitted via infected needles (e.g. 1. History & Physical Examination tattoo) 2. Blood Test targets hepatocytes, liver cells, and immune cells Liver Function Test Two types: measures liver enzymes and bilirubin Acute - HBV can be dormant within 6-8 months LAT & AST Chronic - leads to liver cirrhosis indicate damage in the liver if elevated (injury, dysfunction, etc.) Hepatitis C Virus spread through contact with infected blood (e.g. blood Viral Serological Test transfusions with unscreened blood products) identify antibodies found in the body targets whole immune system HAV - IgM (acute infection); IgG (past infection, past vaccination) causes persistent recurrence of infection HBV - HBsAg (acute chronic HB) liver cirrhosis, liver failure HCV - anti-HCV (HCV RNA testing for confirmation) Hepatitis D Virus HDV/HEV - IgG antibody detective virus 3. Imaging Studies - abdominal ultrasound (liver) 4. Liver Biopsy requires HBV to replicate only infect people who are also infected by the hepatitis TREATMENT AND MANAGEMENT B virus (HBV). HAV exacerbate liver injury or cirrhosis cause by HBV no specific antiviral therapy supportive treatment Hepatitis E Virus supplements transmitted via fecal oral route common in contaminated water rest & adequate hydration (water) HBV self-limiting can cause acute liver failure in pregnants Acute - no need for treatment and individuals with present liver diseases. monitoring of their function and test if there are POTENTIATING FACTORS improvements 1. Poor hygiene & sanitation (HAV, HEV) Chronic - needs treatment 2. Injection drug use - direct blood-blood contact (HBV, HCV) Antiviral medications (e.g. Tenofovir for HBV) 3. Unsafe sexual practices - especially with multiple partners regular monitoring of liver function 4. Occupational exposure - Doctors and other healthcare liver transplant if severe workers, laboratory personnel, etc. (HBV, HCV) HCV 5. Blood transfusion and organ transplant crucial if chronic 6. Mother-child transmission - during child birth Antiviral Therapy with Direct Acting Antiviral if the child is vaccinated, Hepatitis virus will be dormant HDV immediately limited treatment (e.g. Interferon alpha) 7. Immune suppression - those with HIV/AIDS if treating HBV, HDV may suppress Immunosuppressive therapy HEV 8. Alcohol consumption - can exacerbate HBV and HCV (liver self-limiting damage - chronic) supportive care (supplement, good lifestyle habit) liver fibrosis = cirrhosis adequate hydration  symptom management THERAPEUTIC OUTCOMES HAV develop life-long immunity to the virus self-limiting low rates of mortality HBV Acute - complete recovery Chronic - achieve suppression of viral complication reduce the risk of cirrhosis improve liver function lifelong treatment can’t detect in the blood HCV viral clearance and prevention of chronicity HDV treat HB to cancel HD HEV suppress the transmission to other individual ENDOCRINE SYSTEM Focused on the hormones in the body POTENTIATING FACTORS Chemical messenger in the body (hormones) 1. Autoimmune factors Signals the actions or reactions inside our body Such as diseases like Grave’s Disease Part of the endocrine system or hormones produced by 2. Iodine intake endocrine system Patient with hyperthyroidism must reduce iodine intake because it can elevate or trigger the release of thyroid Thyroid Hormones hormones Produced by our thyroid glands Because elevated T3 can 3. Family history 1. HYPERTHYROIDISM If a member has hyperthyroidism, it can be pass on to Excessive production of thyroid hormones by thyroid next generation glands 4. Gender These overproduction disrupts the normal balance, hence Women are commonly affected with hyperthyroidism there is an imbalance 5. Age Thyroid hormones is produced by hypothalamus pituitary individuals between 20 to 40 y/o thyroid axis, hypothalamus release trirotophrine releasing hormone (TRH) that stimulates the pituitary glands CLINICAL MANIFESTATIONS Pituitary glands release the thyroid stimulating hormone METABOLIC SYMPTOMS (TSH) Persons or individual experiencing hyperthyroidism TSH will act on the thyroid gland to produce T3 and T4, 1. Weight loss despite increase appetite then it will produce its biological effect 2. Heat intolerance 3. Increased sweating and basal metabolic rate Due to pathophysiological factors causing hyperthyroidism Mabilis maiinitan ang body CARDIOVASCULAR SYMPTOMS Hypothalamus à thyrotropin (TRH) Stimulateà pituitary 1. Palpitations gland releaseà thyroid stimulating hormone (TSH) 2. Tachycardia 3. Atrial fibrillation stimulateà T3(triiodothyronine) &T4(dominant) = produce biological effect. NEUROMUSCULAR SYMPTOMS Factors: graves disease (autoimmune thyroid disease) 1. Tremors mimics TSH and stimulate à thyroid gland to produce 2. Hyperactivity increase t4 & t3 = unregulated stimulation. 3. Muscle weakness PATHOPHYSIOLOGY GASTROINTESTINAL SYMPTOMS There is an overproduction because of specific diseases 1. Diarrhea or increased bowel movement 1. Graves disease Hence it will lead to weight loss Aka autoimmune thyroid disease There is a production of thyroid stimulating DERMATOLOGICAL SYMPTOMS immunoglobulin (TSI) 1. Warm moist skin Body produces TSI that mimics TSH which results to unregulated thyroid hormone synthesis and secretion OPHTHALMIC SYMPTOMS Thyroid glands is enlarged due to overstimulation of 1. Proptosis thyroid hormones Eye bulging (lumalaki yung mata, naka wide open yung Increased in thyroid hormones eyes) Decreased TSH, increased TSI that causes 2. Double vision hyperthyroidism 2. Toxic multinodular goiter DIAGNOSTIC AND LABORATORY TESTS Aka. Plummer's disease 1. Thyroid function test Multiple nodules in the thyroid glands produces Checks the TSH level autonomous (produces on its own) thyroid hormones Check TSH versus T3 and T4 without the command of pituitary glands Not balance in T3 and T4 levels because it is elevated Nodules operate independently in the thyroid gland in this test Thes autonomous nodules continuously produce thyroid 2. Thyroid autoantibody test hormones elevating T3 and T4 levels causing Test the TSI found in the body hyperthyroidism High TSI can lead to problem (Grave’s disease) 3. Toxic adenoma 3. Radioactive iodine uptake test There is benign tumor found in the thyroid glands that Helps differentiate causes of hyperthyroidism produces thyroid hormones Assess the presence of tumor These tumor disrupts the normal release of thyroid 4. Imaging studies hormone in thyroid glands Such as ultrasound Elevate the levels of thyroid hormones in the body Assess thyroid glands if may tumors or inflammation TREATMENT AND MANAGEMENT 1. Medications SECONDARY OR CENTRAL HYPOTHYROIDISM Methimazole and propylthiouracil (PTU) Involves the dysfunction in hypothalamic pituitary axis They inhibit thyroid hormone synthesis dysfunction 2. Radioactive iodine therapy Insufficient production of TRH, hence hindi ma-stimulate Destroys thyroid tissue to reduce hormone production ang pituitary glands However, it can often result to hypothyroidism due to Low level of thyroid hormone in the body excessive damage to thyroid glands because of excessive loss of thyroid hormones CLINICAL MANIFESTATIONS Thyroid hormone replacement must be done METABOLIC SYMPTOMS 3. Thyroidectomy Slowing down of metabolic effect in the body Removal of thyroid gland 1. Weight gain despite decrease appetite Can be partial or total surgery 2. Cold intolerance 3. Experience fatigue and lethargy Done to individuals that are not reactive to medications or treatment because they are resistant CARDIOVASCULAR SYMPTOMS RELIEF OF SYMPTOMS 1. Bradycardia 2. Hypotension Beta blockers is given for the relief of cardiovascular 3. Pericardial effusion symptoms NEUROMUSCULAR SYMPTOMS MANAGEMENT MONITORING AND REGULAR FOLLOW UP 1. Muscle weakness 1. Regular follow up of thyroid function test 2. Cramps 2. Long term monitoring for potential monitoring of 3. Delayed relaxation of deep tendon reflexes treatments GASTROINTESTINAL SYMPTOMS EXPECTED THERAPEUTIC OUTCOMES 1. Constipation 1. Symptoms 2. Normalize thyroid function Slow peristalsis 3. Prevention of complications (osteoporosis, hypothyroidism, atrial fibrillation) DERMATOLOGICAL SYMPTOMS 1. Dry coarse and brittle skin 4. Improve quality of life 2. Brittle nails 2. HYPOTHYROIDISM 3. Hair loss 4. Experience psychiatric symptoms Characterized by insufficient production of thyroid hormones Loss of concentration Slowing down of metabolic processes and various Depression systemic functions in the body Impaired memory Happens due to certain pathophysiological diseases DIAGNOSTIC AND LABORATORY TEST PATHOPHYSIOLOGY 1. Thyroid function test 1. Autoimmune thyroiditis Elevated TSH Aka. Hashimoto thyroiditis TREATMENT AND MANAGEMENT Attacks thyroid glands 1. Thyroid hormone replacement therapy Common cause of hypothyroidism worldwide Levothyroxine (a medication which is a synthetic form of Immune system mistakenly attacks the thyroid glands (it thyroid hormone) will lead to chronic inflammation and destruction of thyroid cells) MANAGEMENT Thyroid glands will not be able to release thyroid 1. Regular monitoring hormones (thyroid hormones decrease the pituitary gland Adjust the dosage of levothyroxine to be given to response) patients with low thyroid hormone level Elevated TSH levels in the blood, as compared to T3 and T4 EXPECTED THERAPEUTIC OUTCOME 2. Iodine deficiency 1. Symptom resolution Known to be the cause 2. Improve energy level Not sufficient intake of iodine 3. Weight management Can lead to decrease of production of thyroid hormones 4. Stabilize mood 3. Iatrogenic hypothyroidism 5. Normalize thyroid function Result from the surgical removal 6. Achieve normal state of thyroid with appropriate Caused by radioactive iodine therapy levothyroxine therapy 4. Congenital hypothyroidism 7. Prevent complication of hypothyroidism During birth (defect, enzyme deficiency) 8. Improve quality of life Occurs due to defect of thyroid glands and it is during infancy Baby should be screened for hypothyroidism 3. GROWTH HORMONE DEFICIENCY (GHD) 3. Imaging study (Brain imaging test) Impact growth and development in childrena dn adults Pituitary gland in the brain Released and secreted by the pituitary gland, which is Assess the brain such as MRI, evaluate the structure important for regularting metabolism and body hypothalamus and pituitary glands PATHOPHYSIOLOGY TREATMENT AND MANAGEMENT FOR CHILDREN: CONGENITAL GHD 1. GH Replacement therapy There is genetic mutation Administered parenterally Congenital or during birth Mimics the natural growth hormone secretion in the body 1. Genetic mutation Improvement in growth velocity achieving normal height potential 2. Pituitary dysgenesis FOR ADULT: Abnormal development of the pituitary gland leading to 1. GH Replacement Therapy insufficient production of growth hormone based on symptoms and GH level found in the body ACQUIRED GHD THERAPEUTIC OUTCOMES Malaki na nung nakuha Children - 1. Pituitary tumor/ Lesions Adult - improvement in body composition (decrease fat and Caused by surgery, trauma, radiation therapy, increase muscles) Pituitary glands is inside the brain Improve quality of life 2. Hypothalamic disorder Can impair GH secretion 4. REPRODUCTION Release GSRH stimulate the release of sex hormone If GSRH is not released, therefore GRH cannot be Female Reproduction released in pituitary glands Ovarian Function Hypothalamus triggers the various glands to release 1. Oogenesis (follicle) - where the egg or ova develop ovaria, 24 hrs where the egg stay and undergo in the specific hormones ovary POTENTIATING FACTORS Development of egg inside the body 1. Genetic factors Development and regulation 1. Follicle stimulating hormone - maturity in the ovary, to Family history develop the eggs produce in the ovary 2. (LH) - ovulation of eg release out of your ovary - 24 2. Medical history hrs ovulation only Previous brain surgery or head trauma Oogenesis developing - first the egg in the ovary will mature Radiation therapy to the head and neck can potentiate Ovarioan - menstrual cycle GHD 3. Follicular phase - dominating FSH Day 1 to Day D14 Infections can also trigger GHD because it can sometimes 4. Ovulation - lumabas ang egg 5 days window, 28 days affect the brain leading to brain damage cycle 3. Autoimmune disorders 2 weeks after follicle phase maximum of 5 days 5. Luteal Phase - formation of corpus luteum and produce CLINICAL MANIFESTATIONS progesterone which helps to maintain the endometrium (the lining FOR CHILDREN: of the uterus) to support a potential pregnancy - 5 days then 1. Stunted growth fertilize - ready the menstruation, Implantation For children Growing slower than normal growth rate compared to Uterus function normal person in your age Endometrial cycle - endometrium (the inner lining of the uterus) 2. Delayed puberty Proliferative phase - thickening of the endometrium - end 3. Chubbiness with short stature of menstruation to ovulation (day 5-14 of a 28 day Dwarfism GHD cycle) 4. Delayed tooth development Secretory - maturation did preparation of the developing embryo FOR ADULTS: Pregnancy start once the embryo meets the 1. Decreased muscle mass and increased in fat mass endometrium 2. Fatigue and reduced exercise tolerance FSH and LH - release by the pituitary gland by the 3. Impaired psychological stimulation of gonadotropin DIAGNOSTIC AND LABORATORY TEST MALE 1. Growth hormone stimulation test Testicular function Measure GH levels in response to stimulants such insulin 1. hypoglycemia or GHRH 2. Insulin light growth factor Stimulates the liver to produce IgF1 which can indicate GHD POTENTIATING FACTORS IVF and IVL (Intrauterine Valuable Liquor) 1. Age 4. Surgical interventions Declines with age due to sperm quality Varicoceles abnormalities 2. Health conditions 5. Successful contraception leading to childbirth can affect fertility resolution of infertility issues for example hormonal disorders and obesity the patient must diet 3. Lifestyle factors 5. Diabetes mellitus Smoking, excessive alcohol consumption, and stress disruption in glucose metabolism leading to increase in 4. Environmental factors glucose level in the body due to defects in insulin secretion CLINICAL MANIFESTATIONS FEMALE: Types: 1. Menstrual irregularities Type 1 Diabetes mellitus Oligomenorrhea (infrequent) or amenorrhea (absence) an autoimmune destruction of beta cells found in 2. Ovulatory disorder pancreas anovulation or irregular ovulation beta cells - creates insulin 3. Pelvic pain pancreas - synthesizes insulin Due to endometriosis and inflamed pelvic area immune cells mistakenly attacks beta cells 4. Infertility cause is due to genetic susceptibility and environmental Inability to conceive after trying for 1 year factors MALE: Type 2 Diabetes mellitus 1. Decrease libido known as insulin resistance — less responsive to insulin Reduced sexual desire leading to increase in glucose level 2. Abnormal semen analysis 1. Hyperinsulinemia - there is a higher amount of insulin in Color or texture of semen your blood than what's considered normal due to insulin 3. Infertility resistance. 2. Chronic hypoglycemia - β-cell dysfunction promotes DIAGNOSTIC AND LABORATORY TESTS/METHODS decreased insulin production leading to hyperglycemia FEMALE: then later Type 2 DM. 1. Ovulation tracker 3. Gestational DM - due to hormonal changes during ovulation tracker kits pregnancy 2. Hormonal assessment Diabetes baby - GDM mother while pregnant Evaluation of FSH (Follicle-Stimulating Hormone), LH (Luteinizing Hormone), and progesterone POTENTIATING FACTORS MALE: 1. Genetics 1. Sperm counting 2. Obesity - excess fat contribute to insulin resistance 2. Laboratory semen analysis 3. Physical Inactivity - cause insulin resistance Sperm motility and morphology 4. Dietary Factors - high intake of sugars and Evaluation of FSH (Follicle-Stimulating Hormone), LH carbohydrates increases glucose level (Luteinizing Hormone), and testosterone 5. Age - high risk if getting older MALE AND FEMALE: 6. Ethnicity 1. Imaging ultrasound CLINICAL MANIFESTATIONS 1. Polyuria TREATMENT AND MANAGEMENT 2. Polydipsia FEMALE: Increased thirst 1. Lifestyle modification due to dehydration stress reduction and smoking cessation 3. Polyphagia 2. Ovulation induction Increased hunger that will lead to hypotension Medications: Clomiphene Citrate (Stimulate ovary to 4. Weight Loss produce egg) diabetes mellitus type 1 3. Assistive refractory 5. Fatigue IVF (In Vitro Fertilization) 6. Blurred Vision intracytoplasmic sperm injection changes in eye fluids due to hyperglycemia 4. Surgical interventions enlargement of veins DIAGNOSTIC & LABORATORY TEST APAS (Antiphospholipid Antibody Syndrome) pregnancy 1. FBlood Glucose Monitoring MALE: Fasting blood sugar (FBS) 1. Lifestyle change Blood glucose measurement after fasting Obesity, smoking cessation, and reduce alcohol intake fasting is about 16 hours 2. Medications 2. Oral Glucose Tolerance Test (OGTT) balanced hormonal therapy This test is used for pregnant 3. Assistive refractory technique  it measures the glucose in the blood after consuming foods with glucose 3. Hemoglobin A1c (HbA1c) Average blood glucose level is tested for the past 2-3 months TREATMENT AND MANAGEMENT TYPE 1 DM 1. Insulin Therapy - replace deficient insulin Management: Regular Monitoring blood glucose Self-monitoring of glucose intake Lifestyle modifications TYPE 2 DM 1. Oral Medications Metformin Sulfonylureas improves insulin sensitivity and blood glucose production 2. Insulin Therapy - if oral medications is not effective Management: Lifestyle modifications GDM 1. Blood Glucose Monitoring - if not achieved through exercise, etc. — insulin therapy is recommended 2. After birth - postpartum monitoring might lead to Type 2 if there are no postpartum THERAPEUTIC OUTCOMES 1. Prevent complications / long term effects which affects eyes or cardiovascular system 2. Improve quality of life BONE AND JOINTS DISORDERS POTENTIATING FACTORS GOUT AND HYPERURICEMIA 1. Diet Closely related excessive consumption of food that contain purines such Characterized by elevated uric acid levels in the blood as seafood and liver Can lead to the formation of monosodium urate crystals 2. Obesity Foreign body of immune cells Adipose tissue produces substances that increases uric This crystals will be deposited in bones and ligament acid and reduces secretion spaces causing inflammation of the joints and tendons 3. Genetics Results to not flexible bones From family 4. Medications 1. URIC ACID METABOLISM Diuretics, aspirins, and some anti Uric acid 5. Medical conditions end product of urine formation in the body Chronic kidney disease (CKD) Found in organic compounds rich in purines (such as CLINICAL MANIFESTATIONS liver, seafoods) ACUTE GOUTY ARTHRITIS Purine to xanthine oxidase Xanthine oxidase Sudden onset of severe joint pain often in the big toe, ankle, knee, wrist or elbow an enzyme that will convert hypoxanthine to xanthine and then to uric acid and will be Appearance or presence of tophi (urate crystals deposits around the joints) excreted by the kidney CHRONIC GOUTY ARTHRITIS HOW IS IT REGULATED? Renal excretion Recurrent attacks Kidney filters unwanted minerals coming from the blood There is also joint deformities and chronic pain into the urine Kidney stones, urate crystals can cause stones in the kidney Uric acid is excreted to the kidneys and the remainder will be eliminated Gout flares (acute attacks of gout) Maintains the production and secretion of uric acid TREATMENT AND MANAGEMENT hence it is regulated and balanced ACUTE ATTACKS The patient is given an NSAIDs (Aspirin, Ibuprofen (Alaxan® , paracetamol, Flaxan (Naproxen®), Diclofenac) 1. Increase in uric acid intake Dietary intakes of purine and excessive production of The patient is given colchicine (an anti inflammatory uric acid medications specific for acute gout attack) 2. Decrease uric acid secretion SEVERE ATTACKS due to renal dysfunction or kidney damage Given corticosteroids (such as prednisone and methylprednisolone) Medications that affects exception of uric acid like diuretics LONG TERM MANAGEMENT OR CHRONIC ATTACKS Genetics Xanthine oxidase inhibitor (such as allopurinol, Certain medical condition such as metabolic syndrome februiostal), reduce uric acid production and hypertension Uricosuric agents (such as probenecid), increases uric acid excretion PATHOPHYSIOLOGY OF GOUT 1. Formation of crystals THERAPEUTIC OUTCOMES Monosodium urate crystals can precipitate out or deposit 1. Lifestyle modification in joints or tendons and surrounding tissues of the body Avoid high purine foods like beans Have an inflammatory response from the body because these urate crystals are considered as foreign body by Weight loss immune cells Reduce alcohol consumption 2. Resolve acute attacks Immune cells will combat crystals Cytokines Reduce the pain and inflammation cause by gout 3. Prevent recurrent attacks First immune cells that will combat that foreign body Maintain low level of uric acid in blood to prevent recurrent attacks Causes inflammation 4. Prevent joint damage Inflammatory mediator of the body 5. Improve quality of life of the patient Neutrophils More chronic than cytokines as it causes tissue damage Exacerbate the formation of inflammatory response of cytokines causing tissue damage Hence gouty arthritis starts caused by hyperuricemia  persistent joint pain that worsens with activity improves OSTEOARTHRITIS with rest Degenerative joint disease 2. Stiffness Degenerative (breakdown of joint cartilage) Cannot move 3. Swelling PATHOPHYSIOLOGY Mild to moderate joint swelling NORMAL CARTILAGE Inflamed synovial fluids Articular cartilage (connective tissue that covers joints 4. Decreased range of motion and connective tissue Difficulty in moving the joints properly Consists of chondrocytes 5. Joint deformities Embedded in a matrix filled with collagen fibers Joint enlargements and malformations (gives elasticity to bones) Hydrolysed collagen (gives whitening effect) DIAGNOSTIC AND LABORATORY TESTS Undergoes progressive degradation: 1. Clinical evaluation based on history symptoms and physical 1. Loss of proteoglycans examinations Proteoglycans and collagen works together in protecting 2. Imaging studies articular cartilage x-ray that can assess joint spacing and narrowing Collagen matrix that protects the articular cartilage will MRI or CT scan (cartilage and soft tissue damage) lose its ability to retain water and maintain the elasticity Joint fluid analysis 2. Collagen breakdown Collagen fibers will be degraded, particularly the type 2 TREATMENT AND MANAGEMENT collagen NON PHARMACOLOGICAL No structural integrity 1. Weight management 3. Fibrillation and erosion Lose weight Formation of erosion and cracks in cartilage surface as 2. Exercise a result of mechanical tear and wear Improve joint flexibility and strength 4. Bone Remodelling Physical therapy to improve joint function and reduce Degenerative changes the pain (knee caps and knee braces) Undergoes dynamic remodelling There will be formation of osteophytes PHARMACOLOGICAL Osteophytes will form new bones in response to 1. Analgesic inflammatory stress and cytokines Reduce inflammation 2. Topical medications There will also be subchondral sclerosis Bone cysts