What is Medicine – Acute Coronary Syndromes NSTE -ACS ( Unstable Angina and NSTEMI)
ACUTE CORONARY SYNDROMES: NSTE-ACS (UNSTABLE ANGINA AND NSTEMI) ESSENTIAL DESCRIPTION Acute coronary syndromes without ST-segment elevation (NSTE-ACS) include unstable angina (UA) and non-ST-segment elevation myocardial infarction (NSTEMI). ● NSTEMI is defined by the rise and fall of cardiac biomarkers (preferably troponin I or T) with at least one value above the 99th percentile upper reference limit and accompanied by one of the following: symptoms of ischemia, new ST-segment/T-wave changes (such as ST depression or T-wave inversions), development of pathologic Q waves on 12-lead ECG, or noninvasive imaging with evidence of myocardium at risk for ischemia or a new regional wall motion abnormality. The presence of clinical signs of cardiac ischemia (new-onset angina, alteration in the pattern of angina, development of angina while resting, or alteration in the typical anginal equivalent) without signs of myocardial necrosis as shown by normal cardiac biomarkers of injury (troponin) defines UA. There could be ECG alterations such ST segment depression or T wave inversions. EPIDEMIOLOGY New and recurrent MI are estimated to occur 605,000 and 200,000 times per year, respectively. The average age at the onset of MI in the United States is 65.6 years for men and 72.0 years for women (1). Prevalence According to estimates, 16.5 million Americans under the age of 20 have CAD. Mortality: With an overall age-adjusted mortality rate of 98.8/100,000, CAD is the top cause of adult mortality in the United States. Men have a greater death rate. NSTE-ACS is primarily caused by a sharp drop in myocardial blood flow caused by acute plaque rupture or plaque erosion, which results in a partially occluding thrombus. Other mechanisms include (i) dynamic obstruction brought on by a severe spasm of an epicardial coronary artery (prinzmetal angina or coronary vasospasm caused by tobacco use, hyperventilation, magnesium deficiency, cocaine, or methamphetamine use In general, genetic CAD is a complicated, polygenic condition. Age is the biggest risk factor, followed by male sex, prior MI, hypertension (HTN), cigarette use, diabetes mellitus (DM), dyslipidemia, and a family history of premature CAD (defined as age of onset prior to 55 years for men and 65 years for women). Sedentary behaviour, being overweight or obese (metabolic syndrome), inflammation (psoriasis, rheumatoid arthritis), psychosocial variables (anxiety/depression), chronic kidney disease (CKD), obstructive sleep apnea, and environmental contaminants are some of the new or increasing risk factors. GENERAL PREVENTION Quitting smoking, eating a diet low in saturated fat, keeping a normal body mass index, and engaging in regular exercise while managing risk factors: glycemic control for diabetics, blood pressure (BP) control for those with HTN, risk-based statins, and aspirin for those with CAD are all recommended. CONDITIONS OFTEN Associated with Chronic kidney disease and vascular disease DISEASE HISTORY A 10-minute-long tightness or heaviness in the chest that can happen with or without effort. Typically retrosternal in origin, pain or discomfort may radiate to the neck, jaw, interscapular region, upper extremities, or epigastrium. Common adjectives for pain include pressure, tightness, weight, squeezing, or fullness. Palpitations, dyspnea, nausea, diaphoresis, lightheadedness, syncope, or dysphoria are possible accompanying symptoms. Patients, particularly the elderly, diabetics, and women, may present without chest discomfort and with "anginal equivalents" of dyspnea, diaphoresis, and excessive exhaustion. Cocaine or amphetamine usage as CAD risk factors MEDICAL ANALYSIS Note any abnormal vital signs, including tachycardia, bradycardia, HTN, hypotension, tachypnea, fever, and poor dental hygiene. Dysrhythmia, jugular venous distention (JVD), new murmur, rub, or gallop, reduced peripheral pulses, carotid bruits are among cardiovascular symptoms. Tachypnea, difficulty breathing, crackles are respiratory symptoms. Musculoskeletal: It is doubtful that a sharp pain that is reproduced with movement or palpation is cardiac. Skin: xanthomas and xanthelasmas (signs of dyslipidemia), pallor, diaphoresis, and cold skin Cardiac differential diagnoses include: mitral valve disease, aortic dissection, myocarditis, pericarditis, pericardial effusion/cardiac tamponade, heart failure with preserved and reduced ejection fraction, hypertensive emergency Psychiatric: panic attacks, anxiety; musculoskeletal: costochondritis; rib fracture; gastroenterology: gastroesophageal reflux disease; esophageal spasm; esophagitis; esophageal rupture or perforation; hiatal hernia; penetrating or perforating peptic ulcer; biliary or pancreatic pain; pulmonary: pulmonary embolism; pneumot DETECTION & INTERPRETATION OF DIAGNOSIS Initial examinations (lab, imaging) When applicable to both NSTEMI and UA, a 12-lead ECG should be obtained within 10 minutes after presentation. A transmural STEMI of the posterior wall may be indicated by new ST-segment depressions of less than 0.5 mm in two or more adjacent leads and/or T-wave inversions of less than 1 mm in two or more adjacent leads with a significant R wave or R/S ratio of greater than 1. Perform an ECG using the posterior leads (V7-V9). – Perform serial ECGs at intervals of 15 to 30 minutes if the initial ECG is nondiagnostic but symptoms continue and there is a suspicion of ACS. A full blood count and serum biomarkers (which are invariably negative in UA) - The rise in troponin levels occurs 3 to 6 hours after the onset of ischemia symptoms, but it can be postponed for up to 8 to 12 hours (troponin T is not specific in patients with renal failure). - Ultra-high sensitive troponins are more sensitive than conventional assays, but additional validation is necessary. - It has been demonstrated that in post-PCI MI, CK-MB has more specificity than troponins. In 3 to 10 days, the troponin elevation will go away, and in 3 to 4 days, the CK-MB level will return to normal. Repeat biomarkers 8–12 hours after the start of symptoms. A chest x-ray and computed tomography with contrast to rule out any other causes, if necessary. It is advised to undergo transthoracic echocardiography. Tests in the Future & Special Considerations A lipid profile taken while fasting, ideally within 24 hours. TSH, HgbA1c, and activated partial thromboplastin time (aPTT) Urine drug testing in a subset of patients Other/Diagnostic Procedures Consider noninvasive cardiac testing with a standard exercise treadmill test, exercise stress echocardiography, or myocardial perfusion imaging with single-photon emission computed tomography for low- to intermediate-risk patients with improved symptoms and nondiagnostic ECGs with negative biomarkers. In addition, coronary computed tomography angiography can be done on the same demographic of people who are at low to moderate risk. Treatment and general precautions Risk stratify (using the TIMI or GRACE score) to decide whether to use an early invasive approach (coronary angiography within 24 hours of admission) or ischemia-guided therapy; urgent invasive management is needed for very high-risk patients, such as those with hemodynamic instability or cardiogenic shock, persistent chest pain that is resistant to medical treatment, life-threatening arrhythmias or cardiac arrest, mechanical complications, acute heart failure, and recurrent dynamic ST-T wave changes Bed or chair rest with continuous ECG monitoring, keep O2 saturation over 90%, and strictly manage blood pressure. Stop using NSAIDs if at all possible. Promote quitting smoking. Correct K+ and Mg++ electrolyte imbalances. First Line: MEDICATION All patients with NSTE-ACS should receive dual antiplatelet treatment, according to the recommendation. Aspirin, nonenteric coated, first dose of 162–325 mg chewed or crushed for all patients; maintenance dose of 75–100 mg/day forever; reduces mortality and morbidity P2Y12 inhibitors: Ticagrelor, 180 mg PO as a loading dose, followed by 90 mg PO twice daily; avoid in patients with 2nd and 3rd degree heart block; should be given at the time of diagnosis unless invasive approach is planned in a patient with very high bleeding risk. can in some patients lead to dyspnea. Patients with severe liver impairment should not take this medication. A reversal agent can be PB2452, a monoclonal antibody fragment that binds ticagrelor, OR - Prasugrel 60 mg PO, followed by 10 mg PO daily. Indicated in patients under 75 years of age or those with a history of CVA or TIA OR - Clopidogrel, loading dose 300 to 600 mg PO, followed by 75 mg PO daily. Frequently reserved for post-PCI patients treated with coronary stents. In patients with thrombocytopenia and CKD, use with caution. roughly 15% of the general populace are clopidogrel "nonresponders." P2Y12 assay can be used to test for resistance, although routine screening is not currently advised (1). – P2Y12 inhibitors should be given as a loading and maintenance dose to those who cannot take aspirin. - GP IIb/IIIa inhibitors: After PCI, add eptifibatide or tirofiban in some high-risk patients (persistent chest discomfort, significant thrombus burden). If oxygen saturations are below 90% or in patients who are showing signs of heart failure, more oxygen may be administered. Sublingual nitroglycerin 0.4 mg every 5 minutes for a total of 3 doses, and then determine whether IV nitroglycerin is necessary. Avoid if you have hypotension or have taken phosphodiesterase inhibitors. Right ventricular infarction may lessen the hypotension brought on by nitroglycerin. Patients with persistent ischemic chest discomfort should receive morphine sulphate 1 to 5 mg IV, followed by increments of 2 to 8 mg repeated every 5 to 30 minutes. In patients without evidence of heart failure, cardiogenic shock, or other contraindications to -blockade (second or third degree heart block without a pacemaker, active asthma), oral -blocker medication should be started within 24 hours. Metoprolol tartrate 25 to 50 mg every 6 to 12 hours is the recommended dosage. Patients with severe ischemia may want to explore IV treatment. Metoprolol succinate, carvedilol, and bisoprolol are suggested -blockers in individuals with concurrent ACS, stabilised heart failure, and diminished systolic function (LVEF 40%). Lipid-lowering therapy: Regardless of the patient's baseline LDL level, begin or continue high-intensity statin medication with atorvastatin 80 mg daily or rosuvastatin 20 to 40 mg daily (preferred due to nonlipid benefit on vascular function). In statin-intolerant patients or as an adjunctive therapy, ezetimibe, omega-3 fatty acids, PCSK9 inhibitors (evolocumab, alirocumab), and/or fibrates may be investigated. All ACS patients should take an ACE inhibitor (ACEi), especially if they also have diabetes, LV dysfunction, or heart failure. Patients with NSTEMI who are on a therapeutic dose of ACEi/ARB and -blocker and have LVEF 40%, DM, or heart failure are advised to take an aldosterone antagonist (spironolactone or eplerenone) if they do not have substantial renal impairment or hyperkalemia. Start anticoagulant therapy with fondaparinux, enoxaparin, unfractionated heparin (UFH), or bivalirudin. Lower bleeding risk has been linked to bivalirudin. Next Line Verapamil or diltiazem, a non-dihydropyridine calcium channel blocker (CCB), to lower myocardial oxygen demand when beta-blockers are contraindicated and the left ventricular ejection fraction is normal. Use oral long-acting CCB only following complete use of -blockers and nitrates. When treating individuals with epicardial or microvascular coronary artery spasm, long-acting CCBs are advised. Avoid around those who have heart blocks. Long-term nitrate therapy for recurrent angina; sublingual nitroglycerin as needed for angina Ranolazine, 500 to 1,000 mg twice daily, is recommended for the treatment of persistent angina that is unresponsive to other drugs. Patients who have cocaine/methamphetamine intoxication should take benzodiazepines. Patients who use cocaine or methamphetamine should avoid -blockers. QUESTIONS FOR REFERENCE Consultation with a cardiologist is advised for NSTE-ACS. A cardiologist will need to closely monitor patients. Prior to hospital release, referral to an exercise-based cardiac rehabilitation programme is linked to lower morbidity and death. It should be thought about referring someone to a dietician. SURGICAL AND OTHER PROCEDURE Coronary reperfusion techniques include CABG surgery and PCI with stenting. Patients with refractory shock should get mechanical circulatory support. CONSIDERATIONS FOR ADMISSION, THE INPATIENT, AND NURSING Admit patients who have NSTE-ACS suspicions. Special populations are taken into account - Elderly population (75 years) - Early invasive management benefits the elderly - Older population Pharmacotherapy needs to be tailored based on a patient's weight, pre-existing conditions, and comorbidities. - Pregnancy: Preeclampsia/eclampsia, gestational diabetes, and advanced maternal age are specific risk factors for ACS during pregnancy. In evaluating pregnant women with ACS, spontaneous coronary artery dissection and thromboembolism should be taken into account. Statins, ACEi, and ARBs should not be used. CONTINUING CARE AFTERCARE RECOMMENDATIONS Within 72 hours of being discharged, patients with low-risk suspected ACS who have normal serial ECGs and cardiac troponins may undergo a treadmill ECG, stress myocardial perfusion imaging, or stress echocardiography. 2 to 6 weeks of follow-up (low risk) and 14 days (high risk) are recommended. Patients who have an LVEF below 40% are more likely to experience ventricular arrhythmias. One to three months after discharge, perform a second LVEF test to assess function and decide if an ICD should be implanted. DIET The link between diet and coronary artery disease (CAD) is complicated; patients should follow a fiber-rich, sodium- and trans-fat-free diet. Patient education on nutrition, exercise, quitting smoking, and changing one's lifestyle. After an outpatient reevaluation, it is safe for asymptomatic patients to resume exercise and sexual activity. Encourage vaccination against influenza and pneumococci. Patients with UA/NSTEMI had lower in-hospital mortality than STEMI patients, but their long-term prognosis is the same or worse. COMPLICATIONS Depression (increases mortality risk), acute thromboembolic stroke, pericarditis/Dressler syndrome, dysrhythmia, cardiogenic shock, and heart failure
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What is Medicine – Acne Vulgaris
Pilosebaceous unit dysfunction and chronic inflammatory dermatosis in acne vulgaris is characterised by open/closed comedones, papules, pustules, and nodules. Aspects of Geriatrics Favre-Racouchot syndrome: sun-induced comedones on the face or head pregnant women's issues Acne may flare up or go away; typically gets better in the first trimester; may get worse in the third; can be treated with topical benzoyl peroxide, azelaic acid, erythromycin, or clindamycin; orally with erythromycin, azithromycin, or cephalexin; avoid topical tretinoin and adapalene as they may cause retinoid embryopathy; class C; contraindicated with t Child Safety Considerations Neonatal acne (neonatal cephalic pustulosis) affects newborns up to 8 weeks old; lesions are confined to the face and are typically self-limited. Infantile acne: lesions on the face, neck, back, and chest; topical/systemic prescription; infant to one year Early to middle childhood acne (rare; 1 to 7 years old); take hyperandrogenism into account. Preadolescent acne affects 7 to 12 year olds; it is prevalent, affecting 47% of kids, and is typically caused by comedonal lesions. Tetracyclines shouldn't be used in children under 8; instead, employ therapy more suited to adolescents. EPIDEMIOLOGY Male > Female (teen), Female > Male (adult) Predominant age: early to late puberty, may remain in 20- 40% of affected persons beyond 4th decade Prevalence 80–95% of teenagers are affected, 8% of adults are 25–34 years old, 3% are 35–44 years old, and 37% of African Americans and 24% of Caucasians are affected. PATHOPHYSIOLOGY AND AETIOLOGY Androgens (testosterone and dehydroepiandrosterone sulphate [DHEA-S]) increase keratinocyte proliferation, sebum production, and qualitative alterations in sebum in follicles. Keratin plug blocks follicle growth, resulting in sebum buildup and follicular distention. An anaerobe called Cutibacterium acnes phylotype Ia colonises and multiplies within a biofilm in the blocked follicle. C. acnes encourages proinflammatory mediators, which inflames the dermis and hair follicles. Genetics 50% of cases include family ties Increased endogenous androgenic impact, oily cosmetics, cocoa butter, polyvinyl chloride, chlorinated hydrocarbons, cutting oil, and polyvinyl chloride are risk factors. Cell phones, hands against the skin, pandemic masks ("maskne"—a subset of acne mechanica), occluding skin surface (e.g., sports equipment such as helmets and shoulder pads), androgenic steroids (e.g., steroid abuse, some birth control pills), lithium, and phenytoin; and endocrine disorders such as PCOS, Cushing syndrome, congenital adrenal hyperplasia, androgen-secreting tumours Stress Diets high in dairy products (skim milk), high glycemic loads, and whey protein supplements may aggravate acne. With smoking, severe acne could get worse. DURATIONAL PREVENTION avoiding risk elements COMMONLY ASSOCIATED CONDITIONS Pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA), as well as seborrhea, acne, hirsutism, and alopecia (SAHA), include acne conglobata, hidradenitis suppurativa, pomade acne, and SAPHO syndrome (synovitis, acne, pustulosis, hyperostosis, and o Patients with dark skin had 50% keloidal scarring and 50% hyperpigmented acne macules. DIAGNOSIS HISTORY Obtain information on the duration, relationship to menstruation, medications, cleaning agents, stress, smoking, exposures, food, and family history. PHYSICAL EXAM: Nodules or papules, pustules, cysts, closed comedones (whiteheads), open comedones (blackheads), Scars include sinus tracts, ice pick, rolling, boxcar, hypertrophic, depressed, and atrophic macules. Although guidelines don't specify a particular global grading system, consistent grading is helpful. The American Academy of Dermatology's 1990 grading scale - Mild: a few pustules/papules but no nodules - Moderate: a few nodules and a few papules/pustules - Serious: many papules, pustules, and nodules incredibly severe acne: acne conglobata, acne fulminans, and acne inversa The most frequently affected body parts are the face, chest, back, and upper arms (where sebaceous glands are most concentrated). Adult females have face lesions that are similar to those in teenagers and do not just occur in the mandibular and perioral regions. DIFFERENTIAL DIAGNOSIS Folliculitis: gram-negative and gram-positive, perioral dermatitis, pseudofolliculitis barbae, drug eruption, keratosis pilaris, sarcoidosis, seborrheic dermatitis, lupus erythematosus, and acne (rosacea, cosmetica, steroid-induced). DETECTION & INTERPRETATION OF DIAGNOSIS Initial examinations (lab, imaging) Only recommended if there are further indicators of androgen overproduction; in that case, test for free and total testosterone, DHEA-S, and take into account LH and FSH (PCOS). TREATMENT Mild inflammatory acne (grade 2): benzoyl peroxide +/- topical retinoid or benzoyl peroxide +/- topical antibiotic +/- topical retinoid. Comedonal (grade 1): keratinolytic agent Moderate inflammatory acne (grade 3): Upgrade the grade 2 treatment to include a time-limited systemic antibiotic. The first-line treatment for more severe cases of the condition is topical retinoid combined with a topical antibacterial agent, such as Severe inflammatory acne (grade 4): as in grade 3 or isotretinoin. For mild to moderate, topical retinoid plus antibiotic (topical or oral) is preferable to either one alone. The first-line treatment for maintenance therapy is topical retinoids. Don't use prolonged antibiotics for maintenance. Steer clear of using oral or topical antibiotics alone. Use with topical retinoids or BP. Recommended automobile class - Creams, lotions, or ointments for dry or sensitive skin - Gel, solution, wash for oily skin and humid conditions - Areas that bear hair: foam, hydrogel, or lotion Use topical medications to treat the entire affected area, not just any apparent lesions. Use gentle soap everyday to manage oiliness; stay away from abrasives. To reduce MEDICATION ALERT, stay away from drying chemicals and use gentle cleansers and noncomedogenic moisturisers. The majority of topical prescription drugs carry high prices. Keratinolytic drugs (-hydroxy acids, salicylic acid, topical retinoids, azelaic acid) (Side effects include dryness, erythema, and scaling; start with lower strength or alternate day prescription; increase as tolerated.) Tretinoin comes in a variety of strengths and formulations (Retin-A, Retin-A Micro, Avita, and Atralin): To lessen irritation, wash the skin and let it air dry for 30 minutes before applying. At bedtime, use a pea-sized amount. - The BP-stable Retin-A Micro, Atralin, and Avita are less irritating. Apply every other day for the first 2 to 4 weeks to relieve the first flare-up of lesions; avoid using on pregnant or nursing women. - Prices vary depending on formulation; generic tubes cost $50 to $150 each. Adapalene (Differin): 0.1%, topically applied HS - May be used with benzoyl peroxide (Epiduo) 0.1 or 0.3%/2.5%—very effective for skin of colour - Effective; less irritant than tretinoin or tazarotene - Available over-the-counter (OTC); significantly less expensive ($10–$15) than other prescription retinoids Apply tazarotene (Tazorac) before going to bed. Most irritating and ineffective; teratogenic, $400 per tube 20% topical BID azelaic acid (Azelex, Finevin) Reduces postinflammatory hyperpigmentation in people with dark skin due to keratinolytic, antimicrobial, and anti-inflammatory compounds. - Erythema, dryness, scaling, and hypopigmentation are side effects. - Safe during pregnancy-risk Category B - Effective in treating post-adolescent acne - 20% Rx >$400 per tube; OTC 10% and 15% versions cost $10 to $40 each tube. Salicylic acid (2%), while less irritating and less efficacious than tretinoin. -Hydroxy acids: over-the-counter Topical benzoyl peroxide has no resistance in C. acnes; 2.5% formulations are just as efficient as stronger ones, and gel penetrates the follicles more thoroughly. – Apply benzoyl peroxide in the morning and tretinoin at night when using with tretinoin. - Negative effects irritation that varies with dosage; garments that may fade; and photosensitivity Different types of topical antibiotics from benzoyl peroxide Due to antibiotic resistance, avoid using as a monotherapy (2)[A]. - Once daily use of metronidazole gel or cream, erythromycin 2%, and clindamycin 1%. - Benzamycin (benzoyl peroxide-erythromycin), which works best when combined with azelaic acid. - Clindamycin with benzoyl peroxide (BenzaClin, DUAC, Clindoxyl) - Benzoyl peroxide-salicylic acid (Cleanse & Treat, Inova): comparable to benzoyl peroxide in terms of efficacy–clindamycin - Sodium sulfacetamide (Sulfacet-R, Novacet, Klaron) is effective for treating rosacea or acne with seborrheic dermatitis. - Dapsone (Aczone) 5% gel: effective for treating adult females with inflammatory acne; when combined with BP, it may induce yellow or orange skin pigmentation; also highly expensive ($350 per bottle). Oral antibiotics: Use for the shortest time possible, often 6 to 12 weeks of therapy, with a maximum of 6 months if necessary (2); use when acne is more severe, involves the trunk, is resistant to topical medications, or is more likely to leave scars. Do not use as a monotherapy. - Tetracycline: 500 to 1,000 mg/day divided BID; initially high dose, taper in 6 months; less effective than doxycycline or minocycline (2); use while fasting or without dairy; photosensitivity and esophagitis are side effects. - Minocycline: adverse effects include photosensitivity, urticaria, gray-blue skin, vertigo, autoimmune hepatitis, and lupus; prolonged release preparation is better tolerated. - Sarecycline (Seysara): 60 to 150 mg (1.5 mg/kg) taken once daily, narrow spectrum, $1,000/month - Doxycycline: 20 to 200 mg/day, divided daily—BID; photosensitivity - Erythromycin's effectiveness is diminishing due to C. acnes resistance; 500 to 1,000 mg/day, divided BID-QID. Trimethoprim-sulfamethoxazole: QD or BID (Bactrim DS, Septra DS) - Azithromycin (Zithromax): 500 mg three times per week for the first month, then 250 mg every other day for the next two months. Oral retinoids - Isotretinoin: 0.5 to 1.0 mg/kg/day divided BID to maximum 2 mg/kg/day divided BID for very severe disease; usually given for 12 to 20 weeks; maximum cumulative dose = 120 to 150 mg/kg; 20% of patients relapse and require retreatment (1), 0.25 to 0.40 mg/kg/day in moderately severe acne Night blindness, erythema multiforme, Stevens-Johnson syndrome, pancreatitis, excessive skin dryness, hypertriglyceridemia, hepatitis, blood dyscrasias, hyperostosis, premature epiphyseal closure, night blindness, psychosis, and teratogenic consequences are only a few of the side effects. Avoid taking vitamin A or tetracyclines while taking isotretinoin. At baseline and once a month, check for pregnancy, psychiatric/mood changes, CBC, lipids, glucose, and LFTs. The iPLEDGE programme (www.ipledgeprogram.com) requires that both the patient and the physician sign up, and two types of reliable contraception are needed. FDA-approved oral contraceptives (listed in order of potential effectiveness) for women exclusively[B] Drospirenone/ethinyl estradiol (Yaz) or drospirenone/ethinyl estradiol/levomefolate (Beyaz) are superior than norethindrone acetate/ethinyl estradiol (Estrostep) and norgestimate/ethinyl estradiol (Ortho Tri-Cyclen). The majority of combination contraceptives work well and can last for three to six months. Spironolactone (Aldactone); 25 to 200 mg/day; antiandrogen; lowers production of sebum; not FDA-approved for acne Rx ISSUES FOR REFERRAL Acne scar management ADDITIONAL THERAPIES Topical hydroquinone (1.5-10%), topically applied azelaic acid (20%), topical retinoids, low-dose corticosteroids, topical dapsone 5% gel (Aczone): anti-inflammatory; usage in patients over 12 years old, sunscreen The best evidence is for photodynamic therapy using 5-aminolevulinic acid. Other light-based treatments include pulse dye, infrared laser, and ultraviolet A/ultraviolet B (UVA/UVB), blue or blue/red light. SURGICAL AND OTHER PROCEDURE Comedo extraction is performed after the epithelial layer covering a closed comedone is cut. Large cystic lesions are then injected with 0.05 to 0.30 mL triamcinolone (Kenalog 2 to 5 mg/mL) using a 30-gauge needle to slightly enlarge the cyst. Retinoids, steroid injections, cryosurgery, electrodesiccation, micro-/dermabrasion, chemical peels, laser resurfacing, pulsed dye laser, microneedling, fillers, punch elevation are all methods for treating acne scars. ALTERNATIVE & COMPLEMENTARY MEDICINE Tea tree oil, seaweed extract, Kampo formulations, Ayurvedic formulations, rose extract, basil extract, epigallocatechin gallate, barberry extract, gluconolactone solution, and green tea extract may all be helpful, according to the evidence (2). Limited data for dermocosmetics' acne treatment SUCCESSIVE RECOMMENDATIONS Utilise oral antibiotics for no more than three months; take off topical antibiotics as lesions heal. DIET Skim milk and foods with a high glycemic index may make acne worse. EDUCATION OF PATIENTS In the first two weeks of treatment, lesions may get worse; after at least four weeks of treatment, lesions usually get better. PROGNOSIS gradual progress over time (often 8 to 12 weeks after starting therapy) Acne conglobata, a severe form of confluent inflammatory acne with systemic signs, is a complication. psychological suffering, such as anxiety, sadness, and suicide thoughts, together with facial scarsScars, keloids, and post-inflammatory hyperpigmentation are more prevalent in those with darker skin. What is Medicine – Acne Rosacea ACNE ROSACEA Rosacea is a chronic condition that causes recurrent bouts of facial flushing, erythema (caused by dilated small blood vessels in the face), papules, pustules, and telangiectasia (caused by increased reactivity of capillaries) in a symmetric, central facial distribution. There are four subtypes: - Phymatous rosacea - Erythematotelangiectatic rosacea (ETR) - Papulopustular rosacea (PPR) - Ocular rosacea Skin/exocrine system(s) impacted; rosacea as synonym Aspects of Geriatrics Chronic inflammatory dermatosis with middle-aged onset: Aging-related effects may worsen the side effects of oral isotretinoin therapy (at this time, data are limited due to the dearth of clinical research in senior patients over 65 years old). EPIDEMIOLOGY Prevalence Females are more likely than men to develop the condition in people between the ages of 30 and 50. However, males are more likely to advance to subsequent stages. Fitzpatrick skin types I and II are more prevalent. No known cause. Possible aetiologies and pathophysiologies include the following: - Disturbance of the thyroid and sex hormones - Excessive consumption of alcohol, coffee, tea, and spicy foods (unproven) - Suspected Demodex follicular parasite - Exposure to heat and cold - Emotional stress - GI tract dysfunction (potential link to Helicobacter pylori) Genetics Commonly affects people of Northern European and Celtic ancestry Linked to three human leukocyte antigen (HLA) alleles: (MHC class II) HLA-DRB1, HLA-DQB1, and HLA-DQA1 RISK ELEMENTS Consumption of spicy foods and hot beverages Environmental elements: heat, cold, wind, and sunlight GENERAL PREVENTION No known preventive measures COMMONLY ASSOCIATED CONDITIONS include seborrheic dermatitis of the scalp and eyelids, keratitis with photophobia and lacrimation, and uveitis. DISEASE HISTORY Are typically episodically flushed with an increase in skin temperature in reaction to heat stimuli in the mouth (hot liquids), spicy foods, alcohol, and sun exposure. The main presenting symptoms of rosacea are excessive facial warmth and redness. Although acne may have developed years before the start of rosacea, this is not always the case. In most cases, itching is nonexistent. MEDICAL ANALYSIS Four subtypes of rosacea exist: - Episodic erythema and "flushing and blushing" are symptoms of the rosacea diathesis. ETR is an acronym for persistent erythema with telangiectases. - PPR: papules, pustules, telangiectases, persistent erythema - Phymatous: long-lasting deep erythema, dense telangiectases, papules, pustules, and nodules; in rare cases, long-lasting "solid" edoema of the centre area of the face. It is speculative to assume that one subtype will progress to another. Erythema on the face, especially on the cheekbones, chin, and nose. Sometimes the entire face could be affected. Pustules and telangiectasia may be present, and inflammatory papules are predominant. In contrast to acne vulgaris, comedones are not present. Women typically have lesions on their chins and cheeks, whereas men typically have them on their noses. 50% of patients have ocular signs, which include mild dryness and irritation with blepharitis, conjunctival injection, burning, stinging, and tears, as well as inflammation, swelling, and redness of the eyelids. Differential diagnoses include granulomas of the skin, drug eruptions (iodides and bromides), carcinoid syndrome, acne vulgaris, seborrheic dermatitis, steroid-induced rosacea, systemic lupus erythematosus, and lupus pernio (sarcoidosis). DETECTION & INTERPRETATION OF DIAGNOSIS Physical exam results are used to make the diagnosis. ● In order to better focus treatment options that are intended to address the primary clinical presentation, a categorization modification has recently been proposed based on the phenotype that reflects the clinical presentation (1). Interpretation of Tests Histology of the affected skin may show: Papules, pustules, and cysts produced by inflammation around hypertrophied sebaceous glands; Absence of comedones and clogged ducts; Vascular dilatation and dermal lymphocytic infiltrate; Granulomatous inflammation. GENERAL TREATMENT MEASURES Adequate sun protection and skin care are crucial elements of management plan (1)[B]. Local skin irritants should be avoided; moderate, nondrying soap is advised. Steer clear of triggers Reassurance that rosacea has absolutely nothing to do with bad hygiene; treatment of any psychological stress that may be present. Topical steroids shouldn't be applied since they might make rosacea worse. Avoid using cosmetics with oil bases; other products are acceptable and may help women cope with discomfort. Support for physical fitness; electrodesiccation or chemical sclerosis of permanently dilated blood arteries; potential future laser therapy. First Line: MEDICATION Patients with moderate to severe rosacea responded considerably better to topical metronidazole preparations given once (1% formulation) or twice (0.75% formulations) daily for 7 to 12 weeks compared to placebo. Compared to metronidazole, a rosacea treatment system (cleanser, metronidazole 0.75% gel, moisturising complexion corrector, and sunscreen SPF 30) may be more effective and tolerable. Finacea, which contains azelaic acid, is particularly successful as an initial treatment; azelaic acid topical alone is excellent as a maintenance treatment. Topical ivermectin 1% cream has recently been found to treat PPR more effectively than metronidazole. Topical brimonidine tartrate 0.5% gel works well to lessen the erythema brought on by ETR. Oxymetazoline 1% cream, a potent 1A-adrenergic receptor agonist, was recently approved for the treatment of persistent erythema associated with rosacea in adults. Doxycycline 40 mg dose is at least as effective as 100 mg dose and costs much more, but it also carries a lower risk of side effects. Tetracyclines may cause photosensitivity; wearing sunscreen is advised. ● Important potential interactions - Tetracyclines: Steer clear of taking them at the same time as iron, dairy products, or antacids. - Broad-spectrum antibiotics: may lessen the efficacy of oral contraceptives; nevertheless, rifampin is the only antibiotic where this finding has been verified; think about incorporating barrier technique. Next Line Topical clindamycin (lotion preferable) - Can be used in conjunction with benzoyl peroxide; commercial topical combinations are available. Topical erythromycin, topical timolol maleate 0.5%, and topical clindamycin. The potential usage of pimecrolimus and tacrolimus, two calcineurin inhibitors. Inflammatory rosacea can be effectively treated with 1% pimecrolimus. Permethrin 5% cream, which has equal effectiveness to metronidazole for severe cases and isotretinoin oral solution at 0.3 mg/kg for at least three months. Pediatric Considerations Tetracyclines: not to be used in children under the age of 8 pregnant women's issues Tetracyclines should not be used during pregnancy. Isotretinoin is teratogenic and should not be used by women of reproductive age who are not taking effective contraception. It is also necessary to register with the iPLEDGE programme. ADVANCED THERAPIES For ocular rosacea, cyclosporine 0.05% ophthalmic emulsion might be superior to artificial tears. SURGICAL AND OTHER PROCEDURE Progression of rhinophyma or telangiectasias may be treated with laser therapy. Telangiectases and erythema can be effectively treated with pulsed dye laser (585 or 595 nm). Rhinophyma can be treated with a CO2 fractional ablative laser. CONTINUING CARE /AFTER CARE /RECOMMENDATIONS Outpatient therapy patient observation According to the prescribing guidelines and the iPLEDGE program's advice, patients using isotretinoin occasionally and as needed should have close follow-up and laboratory assessments. Consider having patients with eye complaints evaluated by an ophthalmologist. Avoid drinking alcohol and any form of hot beverage. PROGNOSIS: Slowly progressing; occasionally subsides on its own COMPLICATIONS Rhinophyma (dilated follicles and enlarged bulbous skin on nose), particularly in men, is a problem. Conjunctivitis, blepharitis, keratitis, and a decline in vision PRINCIPLES OF ACETAMINOPHEN POISONING
A condition marked by liver necrosis after consuming excessive amounts of paracetamol. Acetaminophen toxicity clinical manifestations are divided into four stages based on the time since consumption. The majority of paracetamol poisoning results from a single, big dose, although it can also happen from smaller doses in people who routinely abuse alcohol, have chronic malnutrition, or take drugs that affect hepatic metabolism. The hepatic system is predominantly affected by toxicity, which is likely to occur with doses greater than 12 g in adults and more than 250 mg/kg in children. Rarely, cardiotoxicity and nephrotoxicity may occur, but there is little conclusive proof that these organ systems have been specifically damaged. A similar term is "paracetamol poisoning." EPIDEMIOLOGY Intentional ingestion accounted for 67% of hospitalisations for paracetamol toxicity from 1998 to 2011; accidental ingestion accounted for 16% of cases, and unspecified causes accounted for 17% (1). 83% of hospitalisations for paracetamol toxicity from 1998 to 2011 were for adults, and 69% of those patients were female (95% CI: 68–69%) (1). ● About 49% of unintended acetaminophen-related poison control calls between 2008 and 2012 involved children under the age of five (1). Incidence Prior to 2009, hospitalisation rates for paracetamol use gradually rose. In 2011, there were 108.6 discharges for every 100,000 people, down from 119.8 for every 100,000 in 2009 (1). Prevalence Data from the American Association of Poison Control show that there were on average 111,632 acetaminophen-related occurrences each year nationwide from 2008 to 2012 (1). According to estimates, 10% of these incidents had liver damage, and 1% had fatal outcomes (1). PATHOPHYSIOLOGY AND AETIOLOGY Pharmacokinetics Acetaminophen is completely absorbed from the duodenum during oral therapeutic ingestion and reaches peak serum concentrations of 10 to 20 g/mL within as little as 2 hours. Toxic ingestions may cause this peak to be delayed. Acetaminophen therapeutic adult doses range from 325 to 1,000 mg every four to six hours, with a daily maximum of 4 g. Therapeutic paediatric doses are 10 to 15 mg/kg every four to six hours, with a maximum of five doses per day or 75 g/kg per day. The elimination half-life of paracetamol is 2 to 4 hours, while extended-release formulations have the potential to postpone this time. PathophysiologyAcetaminophen poisoning and the ensuing hepatic damage are brought on by the consumption of supratherapeutic quantities of acetaminophen or subtherapeutic doses in people with impaired liver function. 96% of acetaminophen consumed is metabolised by the liver, and just 2-4% is eliminated in urine unaltered. N-acetyl-p-benzoquinone imine (NAPQI), a hazardous metabolite, accounts for 5- 10% of the breakdown of therapeutic dosages and 90-95% of the breakdown of benign metabolites. NAPQI quickly combines with glutathione stored in the liver to generate a harmless metabolite that is eliminated in the urine. Consuming excessive amounts of acetaminophen damages hepatocellular tissue by overloading the glucuronidation and sulfation pathways, diminishing glutathione reserves. RISK FACTORS include concurrent toxicity with other substances that affect hepatic metabolism, mental illness or a history of suicide attempts, excessive alcohol consumption on a regular basis, chronic malnutrition, and potential risks from prior weight loss surgery. DURATIONAL PREVENTION Poison Control can be reached at (800) 222-1222 for advice and consultations. FDA labelling recommendations are available at: http://www.fda.gov/ Drugs/ GuidanceCompliance RegulatoryInformation/ Guidances/ default.htm. Aspects of Geriatrics Due to impaired hepatic metabolism and concomitant administration of other hepatotoxic drugs, there is an increased risk of liver injury in frail, elderly individuals. people with liver illness, alcohol consumption disorders, and/or elderly people should not take more than 3,000 mg of paracetamol each day. Child Safety Considerations Young children may experience less severe liver damage from hazardous paracetamol doses, maybe because they have larger glutathione reserves. pregnant women's issues Acetaminophen intoxication increases the risk of spontaneous abortion in pregnant women, especially when the overdose occurs at a young gestational age. Delaying acetylcysteine (NAC) medication increases the risk of abortion and potential foetal mortality. Because IV NAC has a higher bioavailability during pregnancy, it is often favoured. DIAGNOSIS Poisoning signs and symptoms appear within the first 24 hours of significant ingestions. In those who have a history of long-term consumption of doses close to supratherapeutic doses, symptoms may appear gradually. There are four stages in which symptoms can present themselves (3). Stage 1: the first 24 hours following consumption Patient may have no symptoms for the first eight hours after ingesting. Nausea, emesis, anorexia, and diaphoresis are possible symptoms. – At this point, laboratory findings are typically uninteresting. Stage 2—days two to three after intake Right upper quadrant pain and hepatomegaly may become obvious. - Usually less nausea, vomiting, diaphoresis, and malaise than in stage 1. – Usually, elevated aminotransferases are detected. Stage 3—days three to four after intake - Recurrence of Stage I symptoms such nausea, vomiting, and malaise. – Jaundice, disorientation, sleepiness, and coma are possible symptoms of severe poisonings. - Significant increases in liver enzymes that normally peak at this time; extended PT/INR; and frequently low paracetamol levels – In this stage, multiorgan failure and death are most frequent. Stage 4: days 5+ following ingestion - A potential stage of recovery in patients whose stage 3 symptoms are subsiding - Recovery may take a while, but it usually goes smoothly and without any aftereffects. Laboratory anomalies usually go away. - Fulminant hepatic failure is extremely rare in children under the age of six and occurs in about 1% of adults. HISTORY What was ingested (extended release, hydrocodone-acetaminophen, coingestants, etc.), how much was ingested, and when was ingested should be the main topics of inquiry. Was the ingesting deliberate or unintentional? Additionally, inquire about any past or present hepatitis, alcohol addiction, and surgery. MEDICAL ANALYSIS The results of a physical test may probably change depending on the level of toxicity. A thorough physical examination is generally necessary, along with a vitals assessment. Examine the person's general appearance for indicators of dehydration, such as diaphoresis, pallor, weariness, and somnolence. Look out for hepatomegaly and RUQ discomfort, which are symptoms of hepatotoxicity. DISTINCTIVE DIAGNOSIS Amanita phalloides, products containing yellow phosphorus or carbon tetrachloride, as well as other ingested toxins that cause severe acute hepatic injury, should all be taken into account. You should also take into account the presence of coingestants, especially alcohol, opiates, and aspirin. DETECTION & INTERPRETATION OF DIAGNOSIS Initial examinations (lab, imaging) All patients should have their plasma paracetamol levels measured 4 hours after administration (the peak time). If an extended-release version was consumed, draw additional levels at 6 and 8 hours. The frequency of physical examinations, vital signs checks, and any additional tests that might be necessary can be guided by Poison Control (3). – Obtain two serum paracetamol values, 4 to 6 hours apart, if a sustained-release product has been consumed. If either level exceeds the potential toxicity line, treat. – Treat patients with persistent toxicity or those who show up 24 hours after intake based on the clinical effects, LFTs, and acetaminophen level. Alanine transaminase (ALT), aspartate transaminase (AST), prothrombin time (PT)/international normalised ratio (INR), bilirubin, and lactate dehydrogenase (LDH) are among the liver function tests that can be performed. Along with LFT alterations, PT/INR increases with severe poisonings. – - Improvement in ALT with therapy is an optimistic clinical indicator. AST, ALT, and bilirubin levels rise with hazardous ingestions and peak in stage 3. Additional lab tests include those for serum alcohol, electrolytes, glucose, BUN, creatinine, urinalysis, and urine drug screening (UDS). - Based on the clinical history, screen for coingestants with the aforementioned labs and take additional drugs or substances into consideration. – Get a urine or serum pregnancy test in females because it may affect treatment. - Take an arterial blood gas (ABG) into consideration: Anion-gap metabolic acidosis caused by a buildup of 5-oxoproline may occasionally be observed. Imaging: No particular imaging is necessary. Tests in the Future & Special Considerations Liver tests should return to normal during the healing process, and full liver function restoration without long-term consequences is anticipated. Other/Diagnostic Procedures When acute hepatitis or renal injury are evident, advanced imaging of the liver and/or kidney with ultrasound or CT can be thought about to rule out alternative explanations. If aberrant results are discovered without imaging, they could be nonspecific. TREATMENT Request advice right away from a nearby Poison Control Centre. Dial (800) 222-1222 to reach someone in the US. NAC is a safe prodrug that gives cysteine as a substrate for the detoxification of acetaminophen metabolites and replenishes glutathione reserves in the liver. Taking NAC may lower mortality from 5% to 0.7%. According to the Rumack-Matthew nomogram (3): – A plot used to assess whether paracetamol levels during acute hazardous ingestions are high enough to call for treatment with NAC. – The nomogram is not meant for long-term use or for products with sustained release. – When paracetamol plasma levels are at the "treatment line" or above on the Rumack-Matthew nomogram and tested 4 hours after intake, provide NAC. – At 4, 8, and 12 hours after intake, the treatment line acetaminophen plasma levels on the nomogram correspond to >150 g/mL (993 mol/L), >75 g/mL (497 mol/L), and >37 g/mL (244 mol/L), respectively. Whenever possible, start NAC (Mucomyst) within 8 hours of ingestion. Single-dose activated charcoal (1 g/kg PO) may also be useful if administered within 1 to 4 hours of ingestion. Never wait to take oral NAC after taking activated carbon. The routine use of ipecac and gastric lavage at home or in healthcare settings is no longer advised. First Line: MEDICATION Start NAC empirically within 8 hours, even if you're awaiting lab results. It might still work 36 hours after consumption. NAC may be administered IV or PO, depending on the circumstance and what is available. Compared to PO NAC, IV NAC has been demonstrated to shorten hospital stays. – To lessen the negative effects of NAC treatment, a 2-bag regimen should be employed to provide a total of 300 mg/kg IV NAC (Acetadote, Cetylev) over a 20-hour period. Start by administering 200 mg/kg IV over four hours, then 100 mg/kg IV over sixteen hours (5). – Use an oral loading dosage of 140 mg/kg, followed by 17 doses of 70 mg/kg every four hours (72-hour schedule). NAC safety measures: - Due to its sulphur content, PO NAC frequently causes substantial nausea and vomiting and is poorly tolerated; try using a nasogastric tube. - Anaphylactoid reactions to IV NAC (Acetadote) are possible (3-6%) and can include rash, bronchospasm, pruritus, angioedema, tachycardia, or hypotension (atopic dermatitis and asthmatics are more likely to experience these reactions). Reactions frequently happen after the loading dose. Slow or briefly stop the infusion to avoid this; you can also treat it with antihistamines at the same time. - Metoclopramide, 1 to 2 mg/kg IV, or ondansetron, 0.15 mg/kg IV, can be used to relieve nausea. - The percentage of NAC failures varies from 3% to 7% (4). Within 1 to 4 hours of intake (particularly in situations of coingestants), administer a single dosage of activated charcoal. Don't delay administering NAC because you're using activated charcoal. Next Line Hemodialysis may increase survival in cases of severe ingestions (levels >1,000 mg/L, severe acidosis, coma/hypotension), severe renal failure, or both. QUESTIONS FOR REFERENCE Child abuse reporting if negligence resulted in an overdose; Behavioural health assessment for purposeful ingestions; CONSIDERATIONS FOR ADMISSION, THE INPATIENT, AND NURSING For hazardous ingestions accompanied by vital instability and/or test abnormalities, hospitalisation should be considered. When medically stable, take into account admission to a mental health facility for purposeful ingestions. IV fluids are typically offered to help patients stay hydrated. CONTINUING CARE AFTERCARE RECOMMENDATIONS In a hospital that has been granted accreditation, evaluate each patient. • Assess patients for emergency liver transplantation (ELT) in a transplant facility who have signs of organ failure, elevated LFTs, or coagulopathy. For nontoxic accidental ingestions, outpatient care is sufficient; limit activity if liver damage is severe. No particular diet is required, unless you have serious liver disease. EDUCATION OF PATIENTS Encourage patients to stay away from acetaminophen (Tylenol, among other brands) and other acetaminophen-containing products, especially if they are using combination products that contain acetaminophen. Inform parents and carers about proper OTC dosage and drug storage during well-child checkups. Give carers, family members, and roommates of possibly suicidal patients proactive advice. Patients should be informed about long-term paracetamol therapy. PROGNOSIS In stage 4 of toxicity, complete recovery is both achievable and more likely with early therapy (3). In 10% of adult patients with significant liver problems, necrosis, hepatic encephalopathy, or transplantation are required (1). Children under the age of six rarely get hepatic failure. COMPLICATIONS After an acute poisoning, recovery is complete, and complications are uncommon. CERVICAL DYSPLASIA AND ABNORMAL PAP
ESSENTIAL DESCRIPTION Precancerous epithelial alterations in the transformation zone of the uterine cervix are known as cervical dysplasia, also known as cervical intraepithelial neoplasia (CIN), and they are virtually always linked to human papillomavirus (HPV) infections. The term "CIN" refers to a variety of histologic diagnosis. - CIN I: moderate dysplasia; low-grade lesion; the lowest third of the squamous epithelium only exhibits cellular abnormalities. - CIN II: moderate dysplasia; high-grade lesion; the lower 2/3 of the squamous epithelium alone exhibits cellular abnormalities. - CIN III, or carcinoma in situ, is a high-grade disease characterised by severe dysplasia and cellular alterations that affect the entire thickness of the squamous epithelium. Affected systems: reproductive Child Safety Considerations Only 0.1 percent of cervical cancers develop before the age of 20. When compared to starting screening at age 21, screening anyone with a cervix younger than 21 years old (regardless of sexual history or debut) had no effect on cervical cancer incidence or mortality. Aspects of Geriatrics Anyone with a cervix who is older than 65, has had an adequate amount of screening in the past, and has no history of CIN II+ in the previous 20 years should not be checked for cervical cancer. Three consecutive negative cytology-only results, two consecutive negative HPV testing results, negative cytology "cotesting" with negative HPV results within 10 years before the termination of screening (with the most recent test within the last 5 years), are all considered adequate prior screening. Even if this pushes screening past the age of 65, routine screening should continue for at least 25 years at 3-year intervals with HPV testing or cotesting after spontaneous regression or proper care of a high-grade precancerous lesion. pregnant women's issues Squamous intraepithelial lesions can advance during pregnancy, however they frequently recover after delivery. Colposcopy is only performed on high-risk patients to rule out the existence of invasive cancer. Pregnancy is not a time for CIN therapy unless cancer has been detected or is suspected. EPIDEMIOLOGY The fourth most prevalent form of cancer among women overall is cervical cancer. Cervical cancer is now the 20th leading cause of cancer-related death in the US as of 2021. Between the ages of 25 and 29, CIN III incidence increases, while invasive disease incidence peaks 15 years later. Ages 35 to 44 are the most typical ranges for cervical cancer occurrence. More than 15% of instances of cervical cancer in people over 65 (who did not receive routine screening) occur in this age group. Incidence It was predicted that 14,480 new instances of cervical cancer will be identified in 2021, and 4,290 women would pass away from the condition. Because of the widespread use of cervical cancer screening tests, the incidence of cervical cancer has fallen by more than 50% in the United States during the past 40 years. Prevalence High-grade dysplasia prevalence has considerably decreased in HPV-immunized individuals, according to numerous research conducted in populations across the globe. PATHOPHYSIOLOGY AND AETIOLOGY Most sexually active men and women will contract at least one kind of HPV at some point in their lives since HPV is so widespread. High-risk HPV types: Cervical cancer is frequently caused by the oncogenic virus types 16, 18, 31, 33, 35, 45, 52, and 58. About 70% of all cervical malignancies are linked to HPV 16 and 18. The majority of HPV infections are transitory and go undetected in 1 to 2 years. Women are at a higher than average risk of acquiring precancerous lesions because of persistent illnesses. Women over 30 are less likely to successfully treat a new HPV infection than younger women. Low-risk individuals: Genital warts can be brought on by the commonly seen low-risk HPV virus strains 6, 11, 42, 43, and 44. Low-grade squamous intraepithelial lesions (LSIL) and CIN I can be caused by HPV 6 and 11, which account for 90% of benign anogenital warts. HIV infection and other immunosuppressive diseases are risk factors. Diethylstilbestrol exposure during pregnancy; smoking; having several partners; and some link with low socioeconomic position, high parity, oral contraceptive use, and inadequate nutrition. DURATIONAL PREVENTION Immunisation has not yet been proven to reduce cervical cancer, but it does reduce high-risk HPV infections and CIN II/III cervical pathology for at least 5 to 7 years. Within a few years, it's conceivable that invasive cancer prevention will be proven. Girls, boys, and anybody with a cervix should ideally start receiving HPV vaccinations before having their first sexual encounter. According to the Advisory Committee on Immunisation Practises (ACIP), adolescents between the ages of 11 and 12 should receive the HPV vaccine, however children as young as 9 can begin receiving it. Gardasil 9: In October 2018, the FDA approved it for use in both genders and in both sexes between the ages of 9 and 26 and via shared clinical decision between the ages of 27 and 45. It is 88% effective in preventing dysplasia caused by HPV types 16 and 18, which account for 75% of cases of cervical cancer, as well as types 6 and 11 (anogenital warts), and it offers protection against five additional HPV types, which are responsible for 25% of CIN II Vaccine schedule: If the first dose was administered before the age of 15, only 2 doses, spaced 6 to 12 months apart, are needed to finish the series. If vaccination started on or after the age of 15, receive three doses at 0, 2, and 6 months. 3 doses are required in immune-compromising disorders. Use of condoms is a safe sex practise. Advise people to stop smoking. With or without co-testing for HPV, the primary screening test for cervical cellular abnormalities has been the Pap smear. For women between the ages of 30 and 65, the U.S. Preventive Services Task Force advises either primary HPV testing with an authorised assay rather than cotesting at 3-year intervals. Depending on the availability of assays, clinicians will decide which screening and testing technique is the most practical. – Recommendations for screening by age and source (see algorithm "Pap, Normal and Abnormal in Nonpregnant Women Ages 25 Years and Older" and separate algorithm "Pap, Normal and Abnormal in Women Ages 21-24 Years"). - Don't screen if you're under 21. – The guideline for screening frequency varies by age and screen. 21 to 29 years: Cytology screening every three years. For patients under the age of 25, screening should be done every three years with cytology or every five years with primary HPV testing using an assay method that has been specifically authorised for primary HPV testing. Every five years, conduct a primary HPV test or cotest on those aged 30 to 65 (1)[C]. If cotesting or HPV-only testing are not available, cytology every three years is likewise acceptable. Do not examine anyone over 65 who have had sufficient prior screening and are not at high risk. Patients who have undergone hysterectomy procedures that included cervix removal and who have no prior history of CIN II+ should not be screened Patients with a history of CIN II+ or who are receiving therapy should maintain screening for at least 25 years after receiving a CIN II+ diagnosis Patients who are HIV-positive: Those who have had three consecutive normal annual Pap tests should be screened every three years, and those under the age of 30 should have cotesting every three years. DIAGNOSIS HISTORY typically asymptomatic until an aggressive illness develops MEDICAL ANALYSIS External HPV lesions are occasionally seen during a pelvic exam. Check for bleeding or not, exophytic or ulcerative cervical lesions. DISTINCTIVE DIAGNOSIS Cervicitis, whether acute or chronic; cervical glandular hyperplasia; and uterine cancer DETECTION & INTERPRETATION OF DIAGNOSIS According to the most recent data, there are no clinically significant differences between liquid-based cytology and traditional cytology when it comes to identifying cervical cancer precursors. A cervical sample from a traditional Pap smear is plated with fixative onto a microscope slide. A thin-layer preparation and collection method is called ThinPrep. Use a cytobrush and an extended tip spatula to ensure that a sufficient sample of the ecto- and endocervix is obtained. ● When HPV and cytology tests are combined (cotesting), the sensitivity and specificity for dysplasia are close to 100% and 92.5%, respectively. Compared to cytology alone, cotesting allows for an earlier identification of CIN III+ and cancer. For those with cervix ages 25 years, it is preferred to test for high-risk HPV using an assay specially approved for primary screening without cytology, particularly for underscreened or unscreened groups. When HPV or cotesting is not practical, the 2019 ASCCP recommendations state that cytology screening alone is likewise appropriate. Components of the cytology report include the specimen's type (a traditional Pap smear or a liquid-based sample), suitability (the presence of endocervical cells), and classification (the absence of intraepithelial lesions, malignancies, or abnormalities of the epithelial cells, such as squamous/glandular lesions) System of Bethesda 2014 (cytologic grading) Atypical squamous cells (ASC) are epithelial cell abnormalities in squamous cells, which cannot rule out high-grade squamous intraepithelial lesions (HSIL) in ASCH. Moderate/severe dysplasia, CIN I, mild dysplasia, and HPV Atypical glandular cells (AGCs), which are not further characterised, favour neoplasia in cases of CIS, CIN II, and CIN III. Adenocarcinoma in situ (AIS), other diagnostic techniques for adenocarcinoma Clinical intervention for cases younger than 25 years relies on the immediate risk of CIN III+ (1)[C]. For women aged 21 to 24, different algorithms from the 2012 ASCCP guidelines are offered below. ASC-US: (25 years of age or older) Tests for HPV are Option 1 (recommended). If HPV positive, take clinical intervention based on the risk for CIN III+ right away (1),(4)[C]. Repeat cotesting at 3 years if HPV testing is negative (4)[C]. Repeating the cytology at a year is Option 2 and is acceptable (4)[C]. If the imminent risk of CIN III+ is known and the repeat cytology ASC is larger, perform a colposcopy or take other therapeutic steps. If a second cytology test comes out negative, move on to routine screening. LSIL (25 years of age): colposcopy is necessary for ASC-H (25 years of age). - Repeat cotesting at one year (recommended) for LSIL with negative HPV test results. If the second cotest is negative, the third cotest should be performed. If the cotest is positive, either get a colposcopy or do it again in a year. - LSIL with a negative HPV test or a positive HPV test: Colposcopy is recommended. - Colposcopy is preferred for LSIL in pregnancy, but postpartum colposcopy is acceptable - Colposcopy is likely for HSIL/CIN II or III+/AGCs/atypical endometrial cells (21 years), but clinical action ultimately depends on immediate CIN III+ risk - Clinical action is only taken for age 25 years/special populations/rarely screened/status posttreatment/history of CIN II, CIN III, AIS, or invasive cancer ASCCP's smart phone app for treatment incorporates 2019 guidelines: Pap smear and postcolposcopic diagnoses and therapies are guided by algorithms in the evidence-based management phone application, which is accessible online at https:// www.asccp.org/ mobile-app and https:// www.asccp.org/ management-guidelines. UNSPECIFED MEASURES Office evaluation and observation, smoking reduction, safe sex practises, and immunisation promotion are all encouraged. MEDICATION Treat the organism or condition indicated on the results of an infected or reactive Pap smear. Treatment options for condyloma acuminatum: See "Condylomata Acuminata" chapter. SURGICAL AND OTHER PROCEDURE For non-pregnant patients with an immediate CIN III+ risk of >60%, expedited treatment that omits colposcopy biopsy is advised. However, shared decision-making is crucial for patients with an immediate CIN III+ risk between 25% and 60% as well (1). For CIN I, observation is preferred over treatment (1). For some patients, colposcopy can be postponed, and repeat HPV testing or cotesting in a year is advised if the chance of developing CIN III+ right away is minimal (4%). For histologic HSIL (CIN II or CIN III), ablative treatment is favoured to excisional treatment. Excision is advised for AIS. CONTINUING CARE AFTERCARE RECOMMENDATIONS Women should resume screening with HPV testing or cotesting after treatment (excision or ablation) for HSIL, CIN II or III, or AIS and initial posttreatment management every three years for at least 25 years (1). PATIENT EDUCATION HPV vaccination, smoking cessation, protected sexual activity, and routine Pap smear screening in accordance with recommendations PROGNOSIS The rate of remission in CIN is high and the rate of progression to invasive cervical cancer is slow: Lesions in CIN II and III may regress by up to 43% and 32%, respectively. Over a 30-year period, CIN III has a 30% chance of developing invasive cancer, but only around 1% if it is treated. CIN III starts to intrude: Early-stage lesions are treatable with excellent outcomes and few recurrences. The survival percentage for cervical cancer patients after five years is 66.3%. For patients with a diagnosis of localised illness, the 5-year relative survival rate is 91.9%. COMPLICATIONS Cervical stenosis, cervical incompetence (which can result in preterm labour), and scarring that affects cervical dilatation in labour can all be brought on by aggressive cervical surgery. Abnormal Uterine Bleeding
Abnormal uterine bleeding (AUB), often known as heavy, protracted, or recurrent menstrual-like bleeding, is a kind of abnormal uterine bleeding. Can be acute or chronic (lasting more than six months) Instead of dysfunctional uterine bleeding (DUB), the International Federation of Gynaecology and Obstetrics (FIGO) now refers to AUB. EPIDEMIOLOGY Women who are adolescent or perimenopausal are more frequently afflicted. Incidence In any given year, 5% of women in reproductive age will visit a doctor for AUB. Prevalence AUB affects 3–30% of reproductive-age women. PATHOPHYSIOLOGY AND AETIOLOGY 90% of AUB is caused by anovulatory cycles, which are typically brought on by an underdeveloped hypothalamic-pituitary-ovarian (HPO) axis in adolescents. The acronym PALM-COEIN was created to remember AUB in women of reproductive age. PALM stands for Polyp, Adenomyosis, Leiomyoma, and Malignancy and/or Hyperplasia (structural causes) COEIN (nonstructural causes): Coagulopathy, Iatrogenic, Endometrial, Ovulatory problems, and Coagulopathy is currently unclassified. 20% of people who experience severe menstrual bleeding also suffer from a bleeding condition. The two most typical: Blood clotting issues and thrombocytopenia - Conditions that affect ovulation PCOS, eating problems, prolactinoma, hypothyroidism, hyperparathyroidism, and thyroid disorders - Drugs (iatrogenic factors) Blood thinners, steroids, oestrogen receptor antagonists like tamoxifen, hormonal contraceptives like copper IUDs, first-generation antipsychotic drugs, postmenopausal hormone replacement therapy, and antiemetics like metoclopramide and domperidone Ectopic pregnancy, threatened or unfinished abortions, hydatidiform moles, upper genital tract infections, advanced or fulminant liver disease, chronic renal disease, nutritional deficiencies, inflammatory bowel disease, excessive weight gain, and increased exercise are some additional causes of AUB not listed in PALM-COEIN. Genetics-Unknown but may include hereditary hemostasis diseases Age, usually >40 years old; obesity; PCOS; diabetes mellitus; nulliparity; early menarche or late menopause (>55 years of age); chronic anovulation or infertility; history of breast cancer or endometrial hyperplasia; use of tamoxifen; family history of gynecologic, breast, or colon cancer; thyroid disease are all risk factors for endometrial cancer. DURATIONAL PREVENTION There is no specific prevention for AUB COMMONLY ASSOCIATED CONDITIONS. Endometrial polyps, adenomyosis, leiomyoma, endometrial cancer, coagulopathy, PCOS, thyroid issues, malnutrition (eating disorders), hyperprolactinemia, ovarian follicle decline (perimenopause), pregnancy, and endometriosis are some of the conditions that can affect the uterus. DISEASE HISTORY Menstrual history, including the start, severity (measured by pad/tampon use, the presence and size of clots), and timing of bleeding (unpredictable or episodic) for the previous six months; also determine menopausal status. Association with additional factors, such as coitus, contraception, and weight gain or loss Review of systems (excluding symptoms of pregnancy, bleeding disorders, stress, exercise, recent weight change, vision changes, headaches, galactorrhea) Gynecologic history: gravidity and parity, STI history, prior Pap smear findings ALERT Any bleeding that occurs more than a year following the previous menstrual period is referred to as postmenopausal bleeding; malignancy must always be ruled out. MEDICAL ANALYSIS Body mass index, pallor, vital signs, faults in the visual field (pituitary lesion), vaginal discharge, hirsutism or acne, goitre, galactorrhea, purpura, and ecchymosis are all things to look out for. Pelvic exam: Tanner stage, foreign bodies, irregularities in the uterus, ruling out rectal or urinary tract bleeding, Pap test, and tests for STIs (1)[C] Child Safety Considerations Children who are premenarchal and have vaginal bleeding should be examined for foreign objects, symptoms of physical or sexual abuse, potential infections, and early signs of puberty. Initial Tests (lab, imaging) Diagnostic Tests & Interpretation For acute heavy/hemorrhagic bleeding, a type and cross should be acquired in all patients. A partial thromboplastin time (PTT), prothrombin time (PT), activated partial thromboplastin time (aPTT), and fibrinogen level should be obtained if a disorder of hemostasis is suspected; if abnormal, von Willebrand factor, ristocetin cofactor assay, and factor VIII should also be obtained. - STI testing, KOH preparation, follicle-stimulating hormone (FSH), prolactin level, and vaginitis panel – 17- Testosterone and/or dehydroepiandrosterone sulphate (DHEA-S) if PCOS is suspected. - Hydroxyprogesterone if congenital adrenal hyperplasia is detected. TVUS in postmenopausal AUB: Postmenopausal endometrial thickness (ET) 4 mm does not necessitate endometrial sample unless bleeding is continual or recurrent, but ET >4 mm should warrant further investigation. - Negative predictive value (NPV) for excluding endometrial cancer at 99.6% for ET 5 mm (2) - Postmenopausal women who discover an endometrial measurement of >4 mm incidentally should not be evaluated; nonetheless, a risk factor assessment based on each person is appropriate. In premenopausal women with AUB, TVUS, sonohysterography, and hysteroscopy may all be equally successful at spotting intrauterine disease. Tests in the Future & Special Considerations Prior to performing an endometrial biopsy (EMB), it is advisable to begin medical treatment in females under the age of 35 if there is a low risk of uterine anatomic/histologic abnormalities or adenomyosis. Other/Diagnostic Procedures If you are older than 21 years, get a Pap test to check for cervical cancer (1).[C] EMB - Women over 45 with AUB to rule out cancer or premalignancy - Postmenopausal women with ET 4 mm - Women between the ages of 18 and 45 with AUB, a history of unopposed oestrogen, and unsuccessful medical management - Women of any age without risk factors if imaging results show abnormalities (1) - If known, perform on or after day 18 of the cycle; secretory endometrium verifies ovulation. Hysteroscopy with targeted biopsy is recommended in cases of suspected intrauterine lesions and negative EMB; the NPV for endometrial cancer in these cases is 99.5%. Interpretation of Tests A Pap smear may show cervicitis-related inflammation or cancer. Anovulation is typically indicated by proliferative or dyssynchronous endometrium in EMBs, but endometrial cancer or simple or complicated hyperplasia can also be present. NSAIDs (naproxen sodium 500 mg BID, mefenamic acid 500 mg TID, and ibuprofen 600 to 1,200 mg/day) Decreases amount of blood loss and pain compared to placebo "Surgical" techniques (including LNG-IUD) are typically preferable to medical approaches for long-term control First Line: MEDICATION Acute, urgent, nonovulatory bleeding: Conjugated equine oestrogen (Premarin) 25 mg IV every four hours (maximum six doses) stops bleeding in 72% of people in eight hours; 2.5 mg Premarin given orally every six hours should cease bleeding in 12 to 24 hours.[A]. TXA 1.3 g PO or 10 mg/kg IV (maximum dose of 600 mg) If there is no improvement after two to four Premarin doses, or sooner if bleeding is more than one pad per hour, do an intrauterine tamponade by filling a 26F foley bulb with 30 mL saline (1). Then switch to an oral contraceptive pill (OCP) or progestin for cycle regulation. Acute, nonemergent, nonovulatory bleeding is stopped in 88% of women by monophasic combination OCPs with 35 g of oestrogen TID for 7 days. Non-acute, nonovulatory bleeding can be stopped in 76% of women in 3 days with medroxyprogesterone acetate 20 mg PO TID for 7 days (3)[A]. Levonorgestrel IUD (Mirena) is the most efficient type of progesterone delivery, reducing blood loss by 71% to 95%, and is not less successful than surgical treatment. Medroxyprogesterone acetate (Provera), 10 mg/day for 5–10 days per month, is a progestin. Progesterone is taken daily for 21 days per cycle, which greatly reduces blood loss. - OCPs: 20 to 35 g of daily oestrogen plus progesterone (pay special attention to anovulatory females under the age of 18 who are not yet engaged in sexual activity). - TXA 1.0-1.5 g PO 3 times per day; refrain from administering to patients with hypercoagulable conditions. If there are any contraindications to using oestrogen, including those for smoking in women over 35 (relative contraindication), a history of DVT, migraines with aura, or suspicion of endometrial hyperplasia or cancer. Precautions: If medical treatment proves unsuccessful, additional investigation and surgical intervention should be considered. – When using high dose oestrogen therapy, take DVT prevention into consideration. Next Line Gonadotropin-releasing hormone (GnRH) agonists include Elagolix 300 mg BID and Leuprolide (various dosages and durations of action). Danazol (200 to 400 mg/day for a maximum of 9 months), while more effective than NSAIDs, was constrained by androgenic side effects and cost; it has since been replaced by GnRH agonists. Add-back therapy (1 mg estradiol/0.5 mg norethindrone acetate once a day) is now FDA-approved for heavy menstrual bleeding caused by uterine fibroids in premenopausal women. Clomifene (Clomid) or metformin, either alone or in combination, for PCOS patients who want to ovulate and become pregnant QUESTIONS FOR REFERENCE Consult a paediatric gynaecologist or endocrinologist if a child's vaginal bleeding does not have an obvious reason. Additional treatments include antiemetics when using high doses of oestrogen or progesterone, iron supplementation if anaemia (usually iron deficiency) is found, and ulipristal acetate 5 mg or 10 mg (selective progesterone receptor modulator), which has been found to be effective but is currently being suspended while being assessed for a potential severe liver injury. SURGICAL AND OTHER PROCEDURE Endometrial ablation, which is less expensive than hysterectomy and is associated with high patient satisfaction; this is a permanent procedure and should be avoided in patients who desire continued fertility. Hysterectomy in cases of endometrial cancer, if medical therapy fails, or if other uterine pathology is found. If bleeding is unresponsive to medicine or fibroids have been diagnosed, uterine artery embolisation CONSIDERATIONS FOR ADMISSION, THE INPATIENT, AND NURSING Significant bleeding that results in acute anaemia and hemodynamic instability; restore volume with crystalloid and blood as needed in cases of acute bleeding. To estimate and keep track of the quantity of bleeding, pad counts and clot sizes can be helpful. Hemodynamic stability and management of vaginal bleeding are the conditions for discharge. CONTINUING CARE AFTERCARE RECOMMENDATIONS Once the patient is stable following acute care, a follow-up evaluation in 4 to 6 months is advised for additional assessment. patient observation Menstrual diaries should be kept by women on OCPs or oestrogen to track bleeding patterns and how they relate to treatment. No limitations on diet, albeit a 5% weight loss can trigger ovulation in women with PCOS-related anovulation. The majority of anovulatory cycles can be treated with medicinal therapy and do not need surgical intervention, however the prognosis varies with the pathophysiologic process. COMPLICATIONS Anaemia due to a lack of iron and mood disorders What is Medicine – Stable Angina
Stable Angina is a narrowing of the coronary arteries. The narrowing of the coronary arteries may lead to the reduction of blood flow to the heart muscle / myocardium. In times of high demand, such as physical exertion, there is insufficiency blood supply to meet the demand. Angina may be presented with chest pain with or without radiation to arms or jaw. Stable angina is different from unstable angina as stable angina’s symptoms are relieved by rest or the intake of glyceryl trinitrate while unstable angina / acute coronary syndrome may present on randomly whilst at rest. Physical examination is needed for patient with stable angina to look for any signs of abnormalities in heart sound, or signs of heart failure. ECG, full blood count for anemia, urea and electrolytes ( prior to starting an ACE inhibitor) and liver function test ( prior to starting statins), lipid profile, thyroid function test( hypo or hyperthyroid) or HbA1C and fasting glucose ( diabetes) are needed for patient with stable angina. The investigation needed for stable angina include CT coronary angiography which is considered as a gold standard of diagnostic investigation. CT coronary angiography includes the injection of contrast and taking CT images timed with the heart beat to give detailed view of the coronary arteries. Any narrowing of the coronary arteries will be highlighted. The management of stable angina include referral to cardiology, advise the patient about the diagnosis, management and when to call for ambulance, medical treatment and procedural as well as surgical intervention. The medical treatment for stable angina include immediate symptomatic relief, long term symptomatic relief and secondary prevention of cardiovascular disease. Immediate symptomatic relief will focus on GTN spray which causes vasodilation and help to relieve the symptoms. Long term symptomatic relief include beta blocker or / and calcium channel blocker. Long acting nitrates such as isosorbide mononitrate, ivabradine, nicorandil and ranolazine are considered. The secondary prevention includes, aspirin, atorvastatin and ACE inhibitor. Surgical / procedural intervention may include percutaneous coronary intervention with coronary angioplasty. This involves dilating the blood vessel with a balloon and or inserting a stent. This intervention is considered in patient who based on CT coronary angiography reveals a proximal or extensive disease. The procedure involves the catheter being put into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under the guidance of the x ray and injecting contrast so that any stenosis of the coronary arteries can be highlighted on the image of the x ray. Later balloon dilation is considered and followed by stent insertion. Coronary Artery Bypass Graft surgery is considered in severe cases of stenosis (recovery is slower and complication rate is higher than percutaneous coronary intervention The chest along the sternum is opened, a graft vein from the patient’s leg such as the great saphenous vein is taken and sewed it on the affected part of the coronary artery to bypass the stenosis. What is Medicine –Achilles Tendinitis
Achilles Tendinitis is a common overuse injury. Achilles tendinitis occurs among competitive athletes such as distance runners or in recreational activities.6% of the runners may develop Achilles tendinitis. Active middle aged individuals are at high risk of developing Achilles tendinitis. Any changes in the training regimen such as sudden increase in training regimen ( mileage) change in terrain or shoewear may lead to the condition. Running hills, rough terrain or uneven surface may also lead to Achilles Tendinitis. Improper shoe wear and adverse weather conditions such as snow, cold or ice may also contribute to this condition. Cavus foot, hyperpronation and leg- length discrepancy which are biochemical abnormalities of the lower extremity from lumbar spine to foot are also causes of Achilles Tendinitis. It can be avoided by avoiding any excessive running uphill or overly rapid increase in running mileage. In general Achilles tendon consists of 95% type 1 collagen with wavy configuration at rest. The tendon is surrounded throughout its length by a thin gliding paratenon which functions as an elastic sleeve, permitting the free movement of the tendon. The blood supplies of the Achilles tendon include intrinsic vascular system at the osteotendinous and musculotendinous junctions and the extrinsic vascular system via paratenon.2-6 cm proximal to the tendon insertion is a zone of hypovascularity. Achilles tendinitis is a spectrum of disorders and it involves Achilles tendon, paratenon and retrocalcaneal bursa. Achilles Tendinitis may include, Achilles tendinitis, paratenonitis, retrocalcaneal bursitis and tendonitis. Paratenonitis is an inflammation of the paratenon. Achilles tendinitis is an acute inflammation of the tendon with paratenon inflammation. Tendinosis is an intrasubstance degeneration of the tendon and retocalcaneal bursitis is an inflammation of the retrocalcaneal bursa sparing tendon. Achilles tendinitis ranges from painful inflammation of the Achilles tendon and its sheath to chronic degenerative tendinosis and tearing. The risks of developing Achilles Tendinitis include connective tissue disorders, hemodialysis or peritoneal dialysis, microvascular disorders such as diabetes, rheumatoid arthritis, lupus and large posterosuperior calcaneal tuberosity. Achilles Tendinitis is associated with Achilles Tendinitis rupture. The signs and symptoms of Achilles Tendinitis include, a gradual increase in painful swelling and warmth at any point along the tendon substance from the musculotendinous junction to the bony insertion. The pain is usually 3-5 cm proximal to the insertion onto the calcaneus. Pain is relieved by rest. The complications of Achilles Tendinitis may include degeneration of the tendon and eventual rupture with loss of function. This may lead high rate of surgical failure. The differential diagnosis of Achilles Tendinitis may include, inflammatory arthritis, partial or complete Achilles tendon rupture,posterior tibialis tendinitis or rupture, peroneal tendinitis or rupture, retrocalcaneal bursitis and precalcaneal bursitis. The physical examination of the patient may include the tenderness on dorsiflexion of the ankle. The tendon sheath may be swollen and crepitant with ankle motion in severe cases. Nodular swelling may be detected. Retrocalcaneal bursitis may present with swelling, warmth or bogginess immediately anterior to the tendon insertion. It is also important to identify any ankle, leg and foot deformities such as leg –length discrepancies, equinus deformity and scoliosis. Other tests need to be considered are Thompson test to rule out the rupture of the tendon and single limb heel rise test. The investigations that is needed include blood test for any sign of inflammatory arthritis. The imaging techniques include standing foot radiographs and MRI as well as ultrasound. The standing foot radiographs may include AP , lateral and oblique views. It is important to assess the Haglund prominence and identify any intratendinous calcification to show chronic tendinosis or insertional spurring of the calcaneus. MRI of the Achilles tendon may reveal homogenous low signal on all sequences, the normal thickness is less than 8 mm,crescentic shape, flat or concave anterior margin and ovoid shape at its insertion onto the calcaneus. MRI of chronic Achilles Tendinopathy may reveal thickness more than 8 mm, enlarged tendon, heterogeneous increased signal intensity within tendon on T1 weighted views and loss of normal concave margin anteriorly. MRI of acute paratenonitis reveals loss of sharp interface between tendon and pre –Achilles fat. There will be low signal intensity within the tendon itself. On T2 weighted views, high signal intensity around the tendon and pre – Achilles fat. MRI of Achilles rupture reveals the rupture at 3-5 mm above calcaneal insertion. In case of complete rupture MRI shows a loss of continuity with gap formation while partial rupture may reveal focal areas of high signal intensity on T2 weighted sequence images within the tendon substance with preservation of continuity of the tendon. Ultrasound may reveal the fluid around the tendon, tendon tear, tendon abnormalities and peritendinous adhesions. The treatment of Achilles Tendinitis in early acute phase may include NSAIDS, heel lift, ice, rest, footwear modification and orthotic correction of the foot and leg abnormality. It is important to modify the activities and perform Achilles stretching. Symptoms and inflammation may be relieved with retrocalcaneal bursa injection. A trial of cast or boot immobilization is considered if patient remains unresponsive to any treatment. Corticosteroid injection should be avoided as it may cause tendon sheath rupture. Ultrasound therapy, phonophoresis, iontophoresis and short term heel wedge are considered as physical therapy. In term of medication NSAIDS and analgesic are considered to treat Achilles Tendinitis. If any non operative treatment has failed after 3 -6 months trying., consider removal or release of the paratenon through a straight medial incision in case of paratenonitis. In Achilles Tendinosis, it requires intratendinous debridement, retocalcaneal bursectomy and Haglund exostectomy. It may also require augmentation or local tendon transfer such as plantaris or flexor hallucis longus . The prognosis of Achilles Tendinitis is good but with prolonged recovery. What is Medicine – Accessory Navicular
This is an anatomical condition due to the present of an accessory ossicle located at the medial edge of the navicular. It is also known as Os tibiale, os tibiale externum, prehallux and naviculare secundum. Accessory ossicle derives from the unfused ossification centers. Patients remain asymptomatic and the finding is incidental on radiograph. The incidence of accessory navicular is 4-21% with 90% of the cases are bilateral. Less than 1% of patients are symptomatic. It is commonly seen over the medial pole of the navicular bone in adolescent patient. It is the common accessory ossicles in the foot. Accessory navicular is common in adolescent patients or young adults with arch pain or flat foot deformity . It appears more frequent in females compared to males. May also appears in older adults as incidental finding or appears symptomatic together with degenerative changes in the synchondrosis, posterior tibialis tendinosis and bursitis. It can only be symptomatic due to overuse or any forms of trauma in children and adult which is known as ‘accessory navicular syndrome’. Accessory navicular is associated with flatfoot deformity and secondary Achilles tendon contracture. There are three major types of accessory navicular adjacent to the posteromedial navicular tuberosity. There are type I, II and III. Type I (30%) also known as ‘os tibiale externum’ is presented as small, 2-3 mm sesamoid bone in the posterior tibial tendon. There is no cartilaginous connection to the navicular tuberosity . Type II of Accessory Navicular can be divided into type IIa and type IIb.It is divided based on the location. It is most commonly symptomatic. There will be a larger ossicle than type I. the cause is due to the secondary ossification center of the navicular bone. There is a heart shaped or triangular ossicle which forms a synchondrosis with the navicular. Type III may present with enlarged navicular tuberosity. Type III of Accessory Navicular is considered as a fused variant of a type II with a pointed shape. Accessory navicular is a variant of normal anatomy. The symptom appears due to the impingement of the bony prominence against the shoe wear. The patient may present with diffuse medial and plantar arch pain. Accessory navicular cause problem by destabilizing the insertion and diminishing the pull of the posterior tibial tendon. Lateral pain may occur secondary to impingement of the calcaneus against the fibula mostly in patient with associated severe flatfoot deformity. Any traumatic event may lead to the injury to the fibrocartilaginous synchondrosis which attaches the ossicle to the main navicular. The signs and symptoms of accessory navicular are pain which is localized to the medial aspect of the navicular. The pain may begin after wearing ill-fitting shoes, with weight bearing activities or athletics or after trauma to the foot. The pain or weakness when the patient attempts to run, rise on toes or jump. The pain and tenderness along the medial aspect of the foot in the region of accessory navicular. In young athletes, symptomatic accessory tarsal navicular may develop. Swelling and redness may present on the bony prominence. The pain is often relieved by rest. On physical examination, tenderness is localized to the medial pole of the navicular. This tenderness might be exacerbated by abducting and adducting the foot. It is important to assess the insole of the shoe. As it may exacerbate the symptoms. Identify any contracture of the Achilles tendon and assess the motion of the ankle and subtalar joint. The strength of the posterior tibialis tendon, is assessed by manual resistance testing against plantarflexion-inversion or by determining ability to perform multiple single limb heel rises. Differential diagnosis of accessory navicular include posterior tibial tendinitis, acute avulsion fracture of the tuberosity of the navicular, stress fracture of navicular, Pathologically, there is osteoblastic or osteoclastic activity in the tissue between the main body of the navicular and the ossicle. In type II accessory navicular there is proliferation of cartilage and vascular mesenchymal tissue. The important imaging technique include the X-Ray and MRI. X-Ray include standing AP, external oblique and lateral radiographs of the foot. The image produced by X Ray in Type II accessory ossicle, include smooth borders and triangular or heart shaped. The base is 1-2mm from the medial and posterior aspect of the navicular bone. The accessory ossicle is best visualized on the internal oblique view. It may resemblance the characteristic of acute fracture. The differences between acute fracture and accessory navicular is the present of smooth margins with well-formed cortex in accessory navicular. MRI has the higher sensitivity and specificity. MRI may show an alteration in signal intensity and bone marrow edema which are the signs suggesting In type II accessory navicular, the MRI shows soft tissue edema consistent with a synchondrosis sprain or tear. MRI may show posterior tibialis tendon degeneration. The complications of accessory navicular are continued deformity, incomplete pain relief and weaknesses. General treatment may include prescription of anti -inflammatory medication, patient need to rest and avoid any aggravating activities such as athletics. Use of a softer and wider shoe. A medial arch support may be useful in flatfoot cases. However, the patient may not tolerate due to the direct pressure on the ossicle. For persistent symptoms consider below the knee walking case or removable fracture boot for 3-6 weeks. Physical therapy, cryotherapy or strengthening exercises may be considered. Surgical excision may be considered if pain is progressive or does not remit with non operative treatment. Excision of accessory navicular and naviculoplasty is considered. Naviculoplasty is a partial resection of medial edge of navicular bone. The contemporary surgical treatment may include the excision of the ossicle and reattachment of the posterior tibial tendon insertion to the navicular with suture anchors or sutures passed through drill holes. In the kidner procedure, the accessory navicular is excised and the posterior tibial tendon is re routed into a more plantar position. Concomitant osteotomy of the calcaneus or medial column of the foot is considered in severe flatfoot deformity with lateral impingement symptoms. Hoping to improve the alignment and decrease mechanical stress of the posterior tibial tendon insertion. Percutaneous drilling of the synchondrosis of accessory navicular for bone union is acceptable in adolescent athletes with immature basal phalanx of the great toe. What is Medicine – What is Anterior Uveitis ?
Uvea includes the choroid, ciliary body and iris. Choroid is the layer between the sclera and retina all the way around the eye An inflammation of the anterior part of the uvea is known as anterior uveitis. Anterior uveitis is also known as iritis. The anterior chambers being infiltrated with lymphocytes, neutrophils and macrophages. This happens due to infection, malignancy, autoimmune and ischemia. Patients may present with floaters in their vision due to the present of the inflammatory cells. There are two forms of anterior uveitis such as acute anterior uveitis and chronic anterior uveitis. Acute anterior uveitis is associated with HLA B27 linked conditions such as ankylosing spondylitis, reactive arthritis and inflammatory bowel disease. Chronic anterior uveitis is more granular in nature due to it has more macrophages. Chronic anterior uveitis is associated with herpes virus, tuberculosis, syphilis and sarcoidosis. However it is less severe with longer duration of symptoms which lasted more than 3 months. The common symptoms and signs of anterior uveitis include painful dull aching red eye, reduction in visual acuity, ciliary flush ( a red ring spreading from the cornea outwards), floaters and flashes, miosis / constricted pupils due to contraction of sphincter muscle, lacrimation / excessive tear production, pain on movement, photophobia due to spasm of ciliary muscle and abnormally shaped pupil due to posterior synechiae / adhesions pulling the iris into abnormal shapes All the symptoms and signs are usually unilateral in nature and happen spontaneously In terms of management patients are referred to ophthalmologist. The treatments include, oral, topical or intravenous steroids and cycloplegic mydriatic medications (paralyzing ciliary muscle and dilating the pupils) such as atropine eye drops or cyclopentalone. Cyclopentolate and atropine are anti muscarinic agents which block the action of the ciliary body and the iris sphincter muscles. As a result dilate the pupil and stopping the action of the ciliary body to avoid any pain due to ciliary spasm. The other treatments include DMARDS and TNF inhibitors which are immunosuppressant, cryotherapy, laser therapy or surgery such as vitrectomy. |
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