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Rheumatoid Arthritis: Clinical Features, ACR/EULAR Criteria & Treatment Options
# **RHEUMATOID ARTHRITIS (RA)** **Clinical Features β’ ACR/EULAR 2010 Criteria β’ Diagnosis β’ Management (stepwise) β’ Drugs with MoA, dosing, AEs, contraindications, interactions, monitoring & counselling** --- # **1. Definition** Rheumatoid arthritis is a **chronic, systemic, autoimmune inflammatory polyarthritis** primarily affecting **synovial joints**, causing **persistent symmetric polyarthritis**, progressive joint destruction, disability, and extra-articular complications. It is mediated by **autoantibodies (RF, anti-CCP)** and **pro-inflammatory cytokines (TNF-Ξ±, IL-6, IL-1)**. --- # **2. Pathophysiology (Short but Complete)** * Genetic: **HLA-DRB1 shared epitope** strongly associated * Autoantibodies: **RF (IgM anti-Fc)** and **anti-CCP** (highly specific) * Inflammatory cascade β **synovial hyperplasia (pannus formation)** β cartilage erosion β bone destruction * Cytokines: **TNF-Ξ±, IL-6, IL-1**, JAK-STAT pathway activation * Extra-articular: vasculitis, nodules, ILD, anemia of chronic disease, scleritis * Accelerated **atherosclerosis** β β CV mortality --- # **3. Clinical Features** ## **A. Articular** * **Symmetric small joint polyarthritis** (MCP, PIP, wrists; usually spares DIP) * **Morning stiffness > 1 hour** * Joint tenderness, boggy swelling * **Warm joints but not red** * **Deformities** (late): * Ulnar deviation * Swan-neck deformity * BoutonniΓ¨re deformity * Z-thumb deformity * Reduced grip strength * In advanced disease: rheumatoid nodules, tendon rupture (e.g., **extensor tendon**) ## **B. Extra-articular** * **Rheumatoid nodules** * **Felty syndrome**: RA + neutropenia + splenomegaly * Ocular: **scleritis, episcleritis, keratoconjunctivitis sicca** * Pulmonary: **ILD, pleural effusion (exudative, low glucose)** * Cardiac: **pericarditis, β CAD risk** * Hematology: anemia of chronic disease, thrombocytosis * Neurological: carpal tunnel syndrome, cervical spine (C1βC2) subluxation * Skin: vasculitic ulcers --- # **4. Investigations & Diagnosis** ### **A. Blood Tests** * **ESR/CRP** β * **RF** positive in ~70β80% * **Anti-CCP**: highly specific (~95%), predicts severe disease * **CBC**: anemia of chronic disease, thrombocytosis * **LFT/RFT** baseline before DMARD therapy ### **B. Imaging** * **X-ray early**: soft tissue swelling, peri-articular osteopenia * **X-ray late**: joint space narrowing, erosions * **Ultrasound / MRI**: detects early synovitis & erosions --- # **5. ACR/EULAR 2010 Classification Criteria for RA** A score **β₯ 6/10 = definite RA** ### **A. Joint involvement (0β5 points)** * 1 large joint β 0 * 2β10 large joints β 1 * 1β3 small joints β 2 * 4β10 small joints β 3 * > 10 joints (β₯1 small) β 5 ### **B. Serology (0β3 points)** * RF negative & anti-CCP negative β 0 * Low-positive RF or low-positive anti-CCP β 2 * High-positive RF or anti-CCP β 3 ### **C. Acute-phase reactants (0β1 point)** * Normal ESR/CRP β 0 * Abnormal ESR/CRP β 1 ### **D. Duration of symptoms (0β1 point)** * <6 weeks β 0 * β₯6 weeks β 1 --- # **6. Differential Diagnoses** * Osteoarthritis * Psoriatic arthritis * SLE arthritis * Reactive arthritis * Viral polyarthritis (parvovirus B19, chikungunya) * Gout/pseudogout * Polymyalgia rheumatica --- # **7. Management (Stepwise & Evidence-Based)** ## **A. General Principles** * **Early aggressive treatment** with DMARDs * Aim: **remission or low disease activity** * Regular **DAS28** monitoring * Combination DMARDs if inadequate response * Avoid long-term steroids --- # **8. Pharmacologic Treatment (Full drug-level details)** # **1) First-line: Conventional DMARDs** --- ## **A. Methotrexate (MTX) β cornerstone** **Indication:** First-line DMARD for all moderate-severe RA **Mechanism:** Inhibits dihydrofolate reductase β β purine synthesis; β adenosine (anti-inflammatory) **Dose:** * Start 7.5β15 mg once weekly β titrate to **25 mg weekly**; give **folic acid 1 mg/day** **PK:** Hepatic metabolism, renal excretion **Common AEs:** GI upset, stomatitis, hair loss **Serious AEs:** Hepatotoxicity, myelosuppression, pneumonitis **Contraindications:** Pregnancy, liver disease, alcohol use disorder, severe renal impairment **Interactions:** TMP-SMX β MTX toxicity; avoid NSAID excess **Monitoring:** CBC, LFT, RFT every 6β12 weeks **Counselling:** Once weekly dosing, avoid alcohol, report dyspnea --- ## **B. Leflunomide** **MoA:** Inhibits dihydroorotate dehydrogenase β β pyrimidine synthesis **Dose:** 10β20 mg daily **AEs:** Hepatotoxicity, diarrhea, alopecia, teratogenic **Contra:** Pregnancy; need cholestyramine washout **Monitoring:** CBC, LFT every 8 weeks --- ## **C. Sulfasalazine** **MoA:** Anti-inflammatory; modulates cytokines **Dose:** 500 mg/day β 2β3 g/day **AEs:** Rash, GI upset, reversible oligospermia **Contra:** Sulfa allergy **Monitoring:** CBC, LFT --- ## **D. Hydroxychloroquine** **MoA:** Inhibits antigen presentation & TLR pathways **Dose:** 200β400 mg/day **AEs:** Retinopathy (dose-dependent) **Monitoring:** Baseline eye exam + annual screening after 5 yrs **Use:** Mild RA or combination therapy --- # **2) Biologic DMARDs (if inadequate response to MTX)** --- ## **A. Anti-TNF Agents** * **Etanercept** * **Infliximab** * **Adalimumab** * **Golimumab** * **Certolizumab** **MoA:** TNF-Ξ± blockade **AEs:** TB reactivation, infections, demyelination, CHF worsening **Contra:** Active infection, demyelinating disease **Monitoring:** TB screening, CBC, LFT **Counselling:** Report fever; maintain vaccination --- ## **B. Anti-IL-6 (Tocilizumab, Sarilumab)** **MoA:** IL-6 receptor blockade **AEs:** β cholesterol, infections, GI perforation (esp. diverticulitis) --- ## **C. Anti-CD20 (Rituximab)** **MoA:** B-cell depletion **Use:** Refractory RA or when biologics contraindicated **AEs:** Infusion reactions, hepatitis B reactivation --- ## **D. CTLA-4 Fusion Protein (Abatacept)** **MoA:** Inhibits T-cell activation **AEs:** Infections, COPD exacerbation --- # **3) Targeted Synthetic DMARDs β JAK Inhibitors** * **Tofacitinib** * **Baricitinib** * **Upadacitinib** **MoA:** JAK-STAT inhibition β β cytokine signaling **AEs:** Herpes zoster, β LDL/HDL, thrombosis risk **Monitoring:** CBC, lipids, LFT **Counselling:** Vaccinate for zoster before therapy --- # **4) Glucocorticoids** * Used as **bridge therapy** until DMARDs act * Dose: **Prednisolone 5β10 mg/day short-term** * AEs: osteoporosis, weight gain, infection, HTN * Avoid chronic use * Provide **calcium + vitamin D** --- # **5) NSAIDs** * Symptomatic relief only * Do NOT prevent joint damage * Contra: renal disease, peptic ulcer, CVD --- # **9. Non-Pharmacologic Management** * Physiotherapy + joint-protection exercises * Smoking cessation (smoking worsens RA) * Weight optimisation * Vaccination: influenza, pneumococcal before biologics * Occupational therapy * Surgery: joint replacement in advanced destruction --- # **10. Follow-Up & Monitoring** * DAS28 scoring every 3 months * Monitor DMARD toxicity: CBC, LFT, RFT * Eye exams for hydroxychloroquine * TB screening annually for biologics --- # **11. Prognostic Factors** **Poor prognosis indicators:** * High RF/anti-CCP titers * Early erosions on X-ray * High disease activity (DAS28) * Extra-articular disease * Smoking * Early disability ---
What Causes High Blood Pressure? Common Reasons, Risk Factors & Hidden Causes Explained
High blood pressure (**hypertension**) develops when the force of blood pushing against artery walls stays too high over time. It usually results from a **combination of causes and risk factors**, not a single reason. --- ## πΉ Main Causes of High Blood Pressure ### 1οΈβ£ **Primary (Essential) Hypertension** β *Most common* * No single identifiable cause * Develops gradually over years * Strongly linked to lifestyle and genetics --- ### 2οΈβ£ **Secondary Hypertension** β *Due to an underlying condition* Caused by a specific medical problem and often appears suddenly. **Common causes include:** * **Kidney disease** (CKD, renal artery stenosis) * **Hormonal disorders** * Hyperaldosteronism * Cushing syndrome * Pheochromocytoma * Thyroid disorders * **Obstructive sleep apnea** * **Pregnancy-related hypertension** * **Certain medications** * NSAIDs * Oral contraceptives * Steroids * Decongestants --- ## πΉ Major Risk Factors ### 𧬠**Non-modifiable** * Family history (genetics) * Increasing age * Male sex (younger age), females (post-menopause) ### π§ **Modifiable (Lifestyle-related)** * High salt (sodium) intake * Obesity and overweight * Physical inactivity * Excess alcohol intake * Smoking * Chronic stress * Poor sleep --- ## πΉ How These Factors Raise Blood Pressure * **Narrowing of blood vessels** β increased resistance * **Increased blood volume** (salt & fluid retention) * **Overactive sympathetic nervous system** * **Hormonal imbalance** (RAAS activation) --- ## πΉ Key Takeaway > **High blood pressure is usually caused by long-term lifestyle factors combined with genetic susceptibility, but sometimes it is a warning sign of another disease.** --- If you want, I can also provide: * β **Causes by age group** * β **Flowchart of hypertension pathophysiology** * β **Difference between primary vs secondary hypertension** * β **When to suspect secondary hypertension** Just tell me π
Disorders of Parathyroid Gland Complete Clinical Guide for Medical Students
--- # **DISORDERS OF THE PARATHYROID GLAND** --- ## **1. Physiology of Parathyroid Hormone (PTH)** **Parathyroid glands (4)** β secrete **PTH** β maintain **serum calcium and phosphate balance** ### **Normal actions of PTH** | Target organ | Action | | ------------- | ----------------------------------------------- | | **Bone** | β Osteoclastic bone resorption β β CaΒ²βΊ release | | **Kidney** | β CaΒ²βΊ reabsorption, β phosphate reabsorption | | **Kidney** | β 1-Ξ± hydroxylase β β calcitriol | | **Intestine** | Indirectly β CaΒ²βΊ absorption via vitamin D | **Net effect:** **β Serum calcium, β serum phosphate** --- # **CLASSIFICATION** 1. **Hyperparathyroidism** * Primary * Secondary * Tertiary 2. **Hypoparathyroidism** 3. **Pseudohypoparathyroidism** 4. **Parathyroid crisis** --- # **PRIMARY HYPERPARATHYROIDISM (PHPT)** ## **Definition** Autonomous excessive PTH secretion β **hypercalcemia** ## **Causes** | Cause | % | | ----------------------- | ------ | | Parathyroid adenoma | 85% | | Parathyroid hyperplasia | 10β15% | | Parathyroid carcinoma | <1% | | MEN-1, MEN-2A | Rare | --- ## **Pathophysiology** Excess PTH β * β Bone resorption β osteoporosis * β Renal Ca reabsorption * β Vitamin D β β gut Ca absorption β **Hypercalcemia + hypophosphatemia** --- ## **Clinical Features** **βStones, Bones, Groans, Thrones, Psychiatric Overtonesβ** | System | Features | | ------ | ---------------------------------------------- | | Kidney | Nephrolithiasis, polyuria | | Bone | Bone pain, fractures, osteitis fibrosa cystica | | GIT | Constipation, pancreatitis, peptic ulcer | | CNS | Depression, confusion | | Heart | Short QT | --- ## **Investigations** | Test | Result | | -------------------- | ---------------- | | Serum Ca | β | | Serum phosphate | β | | PTH | β | | ALP | β | | 24-hr urine Ca | β | | DEXA | Osteoporosis | | Neck USG / Sestamibi | Localize adenoma | --- ## **Differential Diagnosis** | Condition | PTH | Ca | | ------------------------ | --- | -------- | | PHPT | β | β | | Malignancy hypercalcemia | β | β | | FHH | β | Normal/β | --- ## **Management** ### **A. Acute hypercalcemia** | Step | Treatment | | ---- | ----------------- | | 1 | IV normal saline | | 2 | Loop diuretic | | 3 | IV bisphosphonate | | 4 | Calcitonin | ### **B. Definitive** **Parathyroidectomy** **Indications** * Ca >1 mg/dL above normal * Kidney stones * Osteoporosis * Age <50 --- # **SECONDARY HYPERPARATHYROIDISM** ## **Definition** Compensatory β PTH due to **hypocalcemia** ## **Causes** * Chronic kidney disease (most common) * Vitamin D deficiency * Malabsorption --- ## **Biochemistry** | Parameter | Result | | --------- | ---------- | | Calcium | β | | Phosphate | β (in CKD) | | PTH | β | | Vitamin D | β | --- ## **Management** * Oral calcium * Vitamin D (calcitriol) * Phosphate binders * Dialysis if CKD --- # **TERTIARY HYPERPARATHYROIDISM** Long-standing secondary β autonomous glands | Ca | PTH | | -- | --- | | β | β | **Treatment:** Parathyroidectomy --- # **HYPOPARATHYROIDISM** ## **Definition** Deficient PTH β hypocalcemia ## **Causes** * Post-thyroid surgery (most common) * Autoimmune * DiGeorge syndrome * Hypomagnesemia --- ## **Pathophysiology** Low PTH β β calcium, β phosphate β neuromuscular excitability --- ## **Clinical Features** | Feature | Mechanism | | --------------- | ------------------------------ | | Tetany | Hypocalcemia | | Chvostek sign | Facial nerve hyperexcitability | | Trousseau sign | Carpopedal spasm | | Seizures | Low Ca | | QT prolongation | Hypocalcemia | --- ## **Investigations** | Test | Result | | --------- | -------- | | Ca | β | | Phosphate | β | | PTH | β | | Mg | May be β | --- ## **Management** ### **Acute** IV **calcium gluconate** ### **Chronic** * Oral calcium * Calcitriol --- # **CALCIUM GLUCONATE** | Parameter | Value | | ------------ | -------------------- | | Indication | Acute tetany | | Mechanism | Raises serum Ca | | Dose | 10 ml of 10% IV slow | | Side effects | Arrhythmia | | Monitoring | ECG | --- # **CALCITRIOL (Vitamin D)** | Feature | Detail | | ------------ | -------------------------- | | Action | β Intestinal Ca absorption | | Dose | 0.25β1 mcg/day | | Side effects | Hypercalcemia | | Monitoring | Serum Ca | --- # **PSEUDOHYPOPARATHYROIDISM** ## **Definition** Target organ resistance to PTH | Ca | PTH | Phosphate | | -- | --- | --------- | | β | β | β | ## **Clinical** * Short stature * Round face * Brachydactyly * Mental retardation **Treatment:** Calcium + Vitamin D --- # **PARATHYROID CRISIS** Severe hypercalcemia (>14 mg/dL) ### **Features** * Dehydration * Arrhythmia * Coma ### **Management** 1. IV saline 2. Loop diuretic 3. Calcitonin 4. Bisphosphonates 5. Dialysis if refractory --- # **EXAM PEARLS** | Scenario | Diagnosis | | --------------------------------- | --------------------------- | | High Ca + high PTH | Primary hyperparathyroidism | | Low Ca + high PTH | Secondary HPT | | Low Ca + low PTH | Hypoparathyroidism | | Low Ca + high PTH + short fingers | Pseudohypoparathyroidism | ---
Pancreatic Neuroendocrine Tumor Symptoms Diagnosis Treatment Prognosis
--- # **PANCREATIC NEUROENDOCRINE TUMOR (pNET)** --- ## **1. Definition** Pancreatic neuroendocrine tumors (pNETs) are **neoplasms arising from endocrine (islet) cells of the pancreas** that secrete peptide hormones or amines. They are biologically distinct from pancreatic adenocarcinoma and may be **functioning (hormone-secreting)** or **non-functioning**. --- ## **2. Pathophysiology** pNETs originate from **enterochromaffin cells** of pancreatic islets. They show: * **Neuroendocrine differentiation** * **Dense-core secretory granules** * **Expression of chromogranin A and synaptophysin** Tumor behavior depends on: * **Hormone secretion** * **Tumor size** * **Ki-67 index (mitotic rate)** * **Invasion and metastasis** Tumors may be: * **Well differentiated (NET G1βG3)** * **Poorly differentiated (Neuroendocrine carcinoma)** MEN1 mutation commonly involved β parathyroid, pituitary, pancreas tumors. --- ## **3. Classification** ### **A. By hormone secretion** | Type | Hormone | | --------------- | ------------ | | Insulinoma | Insulin | | Gastrinoma | Gastrin | | Glucagonoma | Glucagon | | VIPoma | VIP | | Somatostatinoma | Somatostatin | | Non-functioning | None | ### **B. By WHO grading** | Grade | Ki-67 | | ----- | ----- | | G1 | <3% | | G2 | 3β20% | | G3 | >20% | --- ## **4. Causes and Risk Factors** * MEN-1 syndrome * Von HippelβLindau * Neurofibromatosis-1 * Tuberous sclerosis * Smoking * Chronic pancreatitis --- ## **5. Clinical Features** ### **A. Insulinoma** * Hypoglycemia * Sweating * Palpitations * Confusion * Weight gain ### **B. Gastrinoma (Zollinger-Ellison)** * Severe recurrent peptic ulcers * Diarrhea * GERD ### **C. Glucagonoma** * Diabetes * Necrolytic migratory erythema * Weight loss * Anemia ### **D. VIPoma** * Profuse watery diarrhea * Hypokalemia * Achlorhydria ### **E. Somatostatinoma** * Diabetes * Gallstones * Steatorrhea ### **F. Non-functioning** * Abdominal pain * Weight loss * Jaundice * Abdominal mass * Metastasis symptoms --- ## **6. Investigations** ### **Blood Tests** | Test | Use | | ------------------ | --------------- | | Chromogranin-A | Tumor marker | | Insulin, C-peptide | Insulinoma | | Gastrin | Gastrinoma | | Glucagon | Glucagonoma | | VIP | VIPoma | | Somatostatin | Somatostatinoma | | Fasting glucose | Hypoglycemia | ### **Imaging** * Contrast CT * MRI pancreas * Endoscopic ultrasound (best for small tumors) * Ga-68 DOTATATE PET-CT (gold standard) * Octreoscan ### **Biopsy** * EUS-guided biopsy * Ki-67 index --- ## **7. Differential Diagnosis** * Pancreatic adenocarcinoma * Islet cell hyperplasia * Metastatic carcinoid * Chronic pancreatitis * Insulin autoimmune syndrome --- ## **8. Management** ### **A. Curative β Surgery** * Enucleation (small insulinomas) * Distal pancreatectomy * Whipple procedure * Liver metastasis resection ### **B. Medical Therapy** Used when metastatic, unresectable or hormone excess. --- ## **9. Drugs Used** ### **1. Octreotide** **Indication:** Hormone control and tumor stabilization **Mechanism:** Somatostatin analog β inhibits hormone secretion **Dose:** Adult: 100β500 mcg SC 2β3 times/day or 20β30 mg IM monthly Paediatric: 1β10 mcg/kg/day **Adverse effects:** Gallstones, diarrhea, hyperglycemia **Contraindication:** Severe gallbladder disease **Monitoring:** LFT, glucose **Counsel:** May cause GI upset --- ### **2. Lanreotide** Same as octreotide Dose: 120 mg SC every 4 weeks --- ### **3. Everolimus** **Indication:** Advanced pNET **Mechanism:** mTOR inhibitor **Dose:** 10 mg daily **Adverse:** Mouth ulcers, hyperglycemia, infections **Contra:** Active infection **Monitor:** CBC, glucose **Counsel:** Avoid live vaccines --- ### **4. Sunitinib** **Indication:** Metastatic pNET **Mechanism:** VEGF receptor inhibitor **Dose:** 37.5 mg daily **Adverse:** Hypertension, fatigue **Contra:** Cardiac failure **Monitor:** BP, ECG --- ### **5. Diazoxide (for insulinoma)** **Mechanism:** Inhibits insulin release **Dose:** 100β600 mg/day **Adverse:** Fluid retention, hyperglycemia **Monitor:** Glucose, edema --- ### **6. Streptozocin + 5-FU (Chemotherapy)** **Indication:** High-grade metastatic disease **Adverse:** Nephrotoxicity, nausea --- ## **10. Non-Pharmacologic** * Surgical resection * Radiofrequency ablation of liver mets * Peptide receptor radionuclide therapy (PRRT) * Dietary glucose support in insulinoma --- ## **11. Prognosis** * Localized pNET: 80β90% 5-year survival * Metastatic: 30β40% Better than pancreatic adenocarcinoma --- ## **12. Key Exam Points** * Insulinoma = most common pNET * Gastrinoma = most malignant * MEN1 = 3 Pβs: Parathyroid, Pituitary, Pancreas * Chromogranin A is universal tumor marker * Ga-68 DOTATATE PET = best imaging ---
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